NP4 Theory Final Exam

Internal disaster vs External disaster; Mass Casualty vs Multi-casualty Disaster

-Internal disaster: event inside a HC facility or campus that could endanger the safety of pts or staff; creates need for evacuation or relocation. Often requires extra personnel & activation of emergency prep & response plan (AKA emergency management plan). --Ex. fire, explosion, loss of critical utilities (electricity, water, computers, communication capabilities), & violence (active-shooter). --Each facility develops policies & procedures for preventing events through facility & security management plans. --Most important outcome for any internal disaster is to maintain pt, staff, & visitor safety. -External disaster: event outside the HC facility or campus, somewhere in community, requires activation of emergency management plan. --Staff # & resources may not be adequate for incoming ED pts. --Ex. natural= hurricane, earthquake, or tornado; technologic= terrorism w/ explosives or malfunction of nuclear reactor w/ radiation exposure. Also COVID-19 pandemic; mass shootings; Hurricane Harvey. -Internal & external disasters result in many casualties, + death. Multi-casualty & mass casualty (disaster) are not the same; difference based on scope & scale of incident, # of victims or casualties & severity of effects. -Both types require specific response plans to activate resources. Multi-casualty can be tx at hospital w/ local resources; a mass casualty event overwhelms local capabilities & may require collab. multiple agencies & facilities to handle crisis.

MAP Formula; Rule of 9's; Parkland Formula

-MAP= (2xDBP + SBP)/3; Factors that influence MAP include: Total blood vL (viscosity); CO (HR × SV); Size & integrity of vascular bed, esp. capillaries. --Gas exchange & perfusion depend on how much O2 from arterial blood perfuses the tissue; Perfusion is r/t MAP. -Rule of nines: quickest method for calculating the size of burn injury in adults w/ normal wt-ht proportion; body divided into areas as multiples of 9%. Useful at site of injury; more accurate evaluations using other methods made in burn unit. -Extent of Burn Injury: severity of a burn is ID by how much of BSA is involved. -Head & Neck A+P= 4.5+4.5 (9%); Chest, ABD, Back A+P= 18+18 (36%); Arms A+P= 4.5+4.5 (9% x 2= 18%); Legs A+P= 9+9 (18% x 2= 36%). Genitals= 1%. -Parkland Formula for fluid replacement: 4 ml/kg/% TBSA burned= Total fluid requirement for lst 24 hours. --1/2 Total in 1st 8 hours; 1/2 of total over the next 16 hours. --NOTE: calculate from the time of injury - not the time you are starting resuscitation. -Ex. 70KG man with 50% TBSA Burn; 4 ml X 70 X 50% = 14,000 ml --1/2 total 1st 8 hours = 7000 ml --1/4 total 2nd 8 hours = 3500 ml --1/4 total 3rd 8 hours - 3500 ml --MONITOR URINE OUTPUT -Fluid Therapy: Severity of Burn is a factor; 15-20% TBSA require fluids. Crystalloids (.9% NS, Lactated Ringers, D5W); Colloids (albumin, dextran, FFP).

Mission statement; Statement of competitive challenges & strategy

-Mission statement: development is the 1st step in strategic management for an org; focuses on definition of what the org. does & aspires to do. For some orgs. its further divided into a vision= tells where the org. wants to be in future. Many also create a values statement= behaviors of importance in the org. -Statement of competitive challenges & strategy: part of strategic planning process, it is vital for org. to be aware of competitive environment; accomplished through strategic analysis [environmental scan]= conducting a review of orgs. environment (political, social, economic, & technical). -Planners carefully consider driving forces in environment; increasing competition, changing demographics, etc; also look at strengths, weaknesses, opportunities, & threats regarding the org= SWOT. -Other info collected for strategic planning process comes from past performance & info collected from all stakeholders; ex. satisfaction surveys (HCAPS; pt, employees, physicians, community), focus groups w/ members of community to ID issues, & other means of listening to desires of local community. -Org. then ID strategic challenges & strategic opportunities. --Most orgs. use 6 pillars: people, service, quality, community, finance, & growth, but w/ teaching role, a 7th pillar added reflecting that activity. Pillars used to align strategic objectives, strategic initiatives, & performance measures & targets for system & in business units from top to individual employee. --Competitive strategy is orgs. plan for achieving goals; states what services will be provided to whom. Decided on as a direct result of info from strategic analysis & environmental scan. --Org. evaluates its mission, vision, & goals in light of environmental scan info, ID strengths & challenges, & demand for service. Make plan which includes strategic goals that need to be achieved. --Based on competitive strategy, the org. makes a plan that allows it to take advantage of ID strengths & needs of stakeholders. Product of process is conclusions about what the org. must do as a result of major issues & opportunities facing it; include overall accomplishments (or strategic goals) the org. should achieve.

Team nursing & Modular Nursing

-Team nursing: group of staff led by a RN to provide care; team= HC workers w/ diversity of skills, education, licensure, & ability who work collaboratively to provide care to group of pts. RN is team leader; supervises & evaluates team; leader can provide care to pt w/ complex needs, but usually does not provide hands-on care. Strong communication skills essential; model supports group work & productivity. -Care delivered by group of staff, all report back to leader; leader has decision-making responsibility for care delivered to pt group. -Advantages: Facilitation & overseeing of novice RNs. Smaller group of pts allows for higher quality care vs functional nursing. Team leader has knowledge of pt needs & can provide coordination of care. Fixed teams relate to higher quality care. -Disadvantages: Increased time needed to communicate w/in team. Expensive bc increased #staff needed. Increased time required to supervise, coordinate, & delegate. Can lead to omissions in care. Most educated staff relegated to supervisor, not direct care. --Modular Nursing: variation of team nursing; based on physical layout of unit. Some units designed to house a # of smaller pt pods, so structurally divided into smaller pt care areas or substations. RNs stationed near pts. Essential components: module= group of staff & group of pts; Pts grouped by spatial or floor plan clustering; RN/pt assignment standardized by cluster. --Advantages: physical layout of assignment & ease of working in environment. --Disadvantages: need for consistent #'s staff in physical environment.

Total pt care; Functional nursing

-Total pt care: oldest care method; AKA case method (not CM). Primary care delivery model until 1930s; resurgence in 1990s. 1 RN accountable for complete care of group of pts; described as type of primary nursing, but accountability for coordination of care does not extend beyond the assigned shift. Seen in private duty nursing & some ICUs; model used by Florence Nightingale. -Advantages: Quality; all care by RN. Continuity for a given shift. High pt satisfaction. Decreases communication time required between staff. Reduces need for supervision. Allows 1 person to perform >1 task. -Disadvantages: May not be cost effective bc # RNs needed. Some RNs dislike bc some care done safely & effectively by others w/ less skill. -Functional nursing: work allocated per specific tasks & technical skills; popular from late 1800s→ end of WWII. "Charge RN" ID tasks/work to be completed during shift. Tasks/work then divided & assigned; ex. med RN, dressing RN, etc. Oriented to accomplishment of tasks; efficient in staff shortages, & pt care units revert to it during staff shortage, ex. snow emergencies- #staff limited. Some institutions w/ lg. variation in staff classification (RN, LPN, RN aides, & techs) to deliver care may also use. -Everyone accountable for portion of care; challenge is all aspects of pt care need to be communicated to next shift, & charge RN must ensure all pertinent info known by staff & it's communicated to next shift. Can lead to fragmented pt knowledge & lack of holistic care. -Advantages: lg. # tasks completed in a shift. Ability to mix staff classifications. Efficient financially. Staff trained to master 1 task. -Disadvantages: Charge RN may be only 1 w/ total view of pt. Decreased pt satisfaction. Decreased RN satisfaction. Fragmented communication. Unit coordination is responsibility of charge RN. Fragmented accountability.

3 Phases of Burn care

3 Phases of Burn care: emergent (resuscitation), acute (healing), & rehab (restorative). -Emergent (resuscitation) phase: begins at injury onset & continues for 24-48hrs; injury is evaluated & priorities of care ID based on extent & severity. --Priorities: (1) securing airway, (2) supporting circulation & perfusion, (3) maintaining body temp., (4) keeping comfortable w/ analgesics, & (5) providing emotional support. -Acute (healing) phase: begins 36-48hrs after injury, when fluid shift resolves, & lasts until wound closure complete. RN coordinates IP care→ continued assessment & maintenance of the CV & resp. systems, & nutrition status, wound care to preserve tissue integrity, pain control, & psychosocial txs. -Rehabilitative (restorative) phase: rehab efforts started at admit, but technical rehab phase begins w/ wound closure & ends when at highest level of functioning. Emphasis on psychosocial adjustment, prevention of scars & contractures, & resumption of pre-burn activity, + resuming work, family, & social roles. Phase may take yrs→ lifetime, depending on degree & impact of burn(s). OT/PT, focus on walking, moving, & ADLs. -Superficial 1st or 2nd-degree burns are cared for various locations depending on severity. Localized burns may be tx as outpatient like urgent care or ED.

Perfusion Concept Exemplar; Acute Coronary Syndrome (UA)

ACS: unstable angina or acute MI. Believed that atherosclerotic plaque in coronary artery ruptures→ plt aggregation (clumping), thrombus (clot), & vasoconstriction. Amount of plaque disruption→ degree of coronary artery obstruction & specific dz process. Artery reaches 50% occlusion→ BF impaired→ myocardial ischemia when myocardial demand is increased. -Unstable angina (UA): CP or discomfort; at rest or exertion & causes severe activity limits. Increase in # attacks & pressure intensity, indicates UA. Pressure may last >15min or be poorly relieved by rest or NTG. Can include new-onset angina, vasospastic angina, & pre-infarction angina. --UA may present w/ ST changes on 12-lead ECG but do not have changes in troponins bc it's ISCHEMIA not infarction. --Ischemia present but not severe enough to cause detectable myocardial damage or cell death. As assays for troponins become more sensitive, Dx of UA is decreasing. --S/S: ST changes on 12-lead ECG, w/o changes in troponin or CK levels. S/S have changed from stable angina (resolve at rest or w/ NTG) to occurring at rest, stress, or activity & do not always respond to rest & NTG. USA is a medical emergency. --New-onset angina: 1st angina s/s, usually after exertion or increased demands on heart. --Vasospastic angina: AKA variant or Prinzmetal angina; CP or discomfort from coronary artery spasm, usually after rest. --Pre-infarction angina: is CP in days or wks before MI.

ALI Leading to ARDS; Preventing ARDS

ALI Leading to ARDS; Preventing ARDS: -ALI→ ARDS has many causes; sepsis is the most common. Some causes result in direct injury to lung tissue; others do not directly involve the lungs. --Direct lung injury; ex. gastric acid aspiration, pneumonia, near-drowning, or inhaling toxic fumes. Surfactant production is impaired & remaining surfactant is diluted; leads to atelectasis, decreased lung compliance, & shunting (movement of blood in the lungs w/o gas exchange & oxygenation). --Indirect injury; ex. sepsis, pancreatitis, trauma, & other conditions, result in inflammatory mediators→ lungs→ damage ("cytokine storm"). -All causes result in systemic inflammatory response that produce a cytokine storm that maintain inflammation: Thick, swollen tissue + Lung fluid increases= Reduces gas exchange & oxygenation. -Health Promotion & Maintenance: ID those at high risk; Monitor pts on tube feedings to prevent aspiration & pts w/ impaired swallowing & gag reflex; Infection control guidelines (ex. handwashing, invasive catheter & wound care, & Contact Precautions, teach UAPs). Monitor pts tx for health problems associated w/ ARDS. Swallowing problems or a poor gag reflex→ use a suction toothbrush for oral care.

American Nurses Association Code of Ethics

ANA Code of Ethics: ANA Code of Ethics for RNs does not distinguish cause from effect. -RN suspects a practitioner may be impaired→ duty is to take action designed to protect pts & to ensure impaired individual receives assistance in regaining optimal function. -Advocacy role does not stop once impairment is ID. RNs in all roles should advocate for colleagues, whose job performance may be impaired, to ensure they receive assistance, tx, & access to fair org. & legal processes; includes supporting the return to practice if sought assistance & is ready to resume duties. -Many boards of nursing have set up advocacy programs for impaired RNs to provide w/ assistance to overcome addiction. Info about programs is on state board websites. -What do you do immediately when you suspect co-worker is working impaired? Call your immediate supervisor, follow policy. -Hospitals have differing procedures on handling situations, & it is important to follow procedure. What you do not do is nothing. -If complaint is found valid, the state board will have the RN surrender license to practice. RN is then referred to assistance & is monitored by state board. -Reinstatement of license can occur depending on rules & regulations of state board. RNs can also voluntarily surrender license if they think they need assistance. -In late 1970s, the ANA began efforts to secure assistance for chemically and mentally impaired RNs. Assistance is in form of diversion programs, intervention, or peer assistance programs. It is a voluntary, confidential program for RNs whose practice may be impaired bc of chemical dependency or mental illness.

ARDS pathophysiology

ARDS is ARF w/ these features: Hypoxemia that persists even when 100% O2 is given (refractory hypoxemia= cardinal feature; how to differentiate PE vs ARDS); Decreased pulmonary compliance; Dyspnea; Non-cardiac associated bilateral pulmonary edema; Dense pulmonary infiltrates on x-ray (ground-glass appearance). --AKA: adult respiratory distress syndrome, "stiff lungs," shock lung, & acute respiratory dysfunction syndrome. --ARDS often occurs after acute lung injury (ALI) in people w/ no pulmonary disease as a result of other conditions; ex. sepsis, burns, pancreatitis, trauma, & transfusion. -Causes of ALI in ARDS; trigger is a systemic inflammatory response→ activates pro-inflammatory cytokines→ maintain continuing inflammation in the alveoli & pulmonary vasculature; response= "cytokine storm". If prolonged→ thick, swollen tissues→ hinder gas exchange & promote scar tissue; why ARDS s/s similar regardless of cause. --Alveolar-capillary membrane= main site of lung injury; normally is permeable only to small molecules; injured during sepsis, PE, shock, aspiration, severe COVID inflammation, or INH injury. Injury to AC membrane→ more permeable to large molecules→ allows debris, proteins, & fluid into the alveoli. --Lung tissue normally remains relatively dry; ARDS= lung fluid increases & contains more proteins. ARDS + COVID-19= results in thick exudate→ inhibits gas exchange. -Other changes in alveoli & bronchioles. Type II pneumocytes produce surfactant; increases lung compliance (elasticity & recoil of lung tissue) & prevents alveolar collapse. --Surfactant activity is reduced in ARDS; type II pneumocytes are damaged & surfactant is diluted by excess lung fluids→ unstable alveoli that tend to collapse→ collapsed or fluid-filled alveoli cannot exchange gases. --Edema then forms around terminal airways→ compressed, closed, & can be destroyed→ lung vL & compliance are further reduced. --Fluid continues leaking in more lung areas→ fluid, protein, & BCs collect in the alveoli & spaces between→ lymph channels are compressed, & more fluid collects. --Poorly inflated alveoli receive blood but cannot oxygenate it, increasing the shunt→ hypoxemia & V/Q mismatch. -Transfusion-related acute lung injury (TRALI): sudden onset (w/in 6hrs of transfusion) of extreme hypoxemic lung disease w/ infiltrates on x-ray w/o cardiac problems. Activation of inflammatory response; cause= recent plasma transfusion-containing blood products; ex. PRBCs, platelets, & FFP.

Activities That May Not Be Delegated

Activities That May Not Be Delegated: RN activities that may not be delegated include: • Performing initial pt assessment & subsequent assessments or RN interventions that require specialized RN knowledge, judgment, &/or skill. • Formulating RN Dx. • ID RN care goals & developing RN plan of care w/ pt &/or family. • Updating pts plan of care. • Providing pt education to pt &/or family. • Evaluating pt progress, or lack thereof, toward achieving desired goals & outcomes. • Discussing pt issues w/ physician. • Communicating w/ physicians or implementing orders from physician. • Documenting pts assessment or response to txs in pts plan of care. • Admin meds. • Providing direct RN care.

Management of Burns

Acute Phase of Burn Injury tx: Begins about 36-48hrs after injury & lasts until wound closure completed. Care directed toward continued assessment & maintenance of all systems & healing processes. -Wound Care Management: --Debridement: wound care RNs provide this to get dead tissue out. Ex. wet to dry dressing (sterile H2O, NS). --Mechanical debridement 2x/day by hydrotherapy through tub or shower water treatment; encourages tissue sloughing. --Enzymatic debridement by autolysis or the application of enzyme agents, such as collagenase. -Surgical tx: Surgical excision is done w/in 5 days after injury to excise very thin layers of necrotic burn surface; bed of healthy dermis or SQ fat is then reached. For permanent wound covering by autograft (pts own skin, if available; prevents rejection). -Risk for Infection tx for Burns: -Autocontamination of burn wound from client's own normal flora. -Cross-contamination of burn wound from the external environment; why units & tx are sterile. --Burn wounds promote growth of Clostridium tetani. -Drugs for prevention: Tetanus toxoid, Ig Topical ABs (Silvadene, flamazine, Sulfamylon- assess allergy to sulpha drugs); Systemic ABs. -Topical AB tx: Silver Sulfadizine (Silvadene) for Gram +/- Bacteria; Painless; no dressing needed. Not as effective on eschar bc it's dead. Watch for allergy & depression of WBCs. Not effective against a Pseudomonas. -Collagenase Polysporin powder Topical enzymatic debriding agent; Used on deep partial-thickness wound with eschar. Digests collagen in necrotic tissue; Painless; Daily dressing changes. Side effects - rare. Easy to apply BUT Expensive! -Impaired Physical Mobility: -Positioning: Maintain in neutral body position with minimal flexion (flexion is most comfortable for patients but this is one reason contractures occur). -Diet tx: Need high kcals. Frequent high calorie, high protein meals. For regeneration & repair. Enteral tube feedings if cannot swallow. Parenteral nutrition IV; TPN 20% dextrose; PPN is 10%. Anything >10% end up w/ phlebitis bc glucose is caustic. Accu-check Q6h; DM on TPN may have insulin given w/ it. RN checks label on bag vs order. Dedicated lines; cant use them for anything else bc contamination & risk for infection; high glucose can feed bacteria. -Rehabilitative Phase of Burn: begins w/ wound closure & ends when pt returns to highest level of functioning. Emphasis on psychosocial adjustment, prevention of scars & contractures, & resumption of preburn activity. May last yrs or lifetime if pt needs to adjust to permanent limits.

Adaptive Responses & Events During Hypovolemic Shock

Adaptive Responses & Events During Hypovolemic Shock: -Initial Stage: Decreased MAP of 5-10 from baseline value; Increased SNS stimulation; Mild vasoconstriction; Increased HR. --Ask about fluid I&Os during previous 24hrs; UO is esp. important bc reduced during 1st stg. of shock, even if intake is normal.(<30 mL/hr or 0.5 mL/kg/hr) --Increased HR is often 1st s/s shock; SV decreased→ peripheral pulses difficult to palpate & easily blocked. Shock progresses→ peripheral pulses may not be palpable; Doppler may be needed. -Compensatory Stage: Decreased MAP of 10-15 from baseline value; Continued SNS stimulation; Moderate vasoconstriction; Increased HR; Decreased pulse pressure; Chemical compensation; Renin, aldosterone, & ADH secretion; Increased vasoconstriction; Decreased UO; Stimulation of thirst reflex; Some anaerobic metabolism in non-vital organs; Mild acidosis; Mild hyperkalemia. SpO2 90-95%. -Progressive Stage: Decreased MAP of >20 from baseline value; Anoxia of non-vital organs; Hypoxia of vital organs; Overall metabolism is anaerobic; Moderate acidosis; Moderate hyperkalemia; Tissue ischemia. SpO2 75-80%. -Refractory Stage: Severe tissue hypoxia w/ ischemia & necrosis; Release of myocardial depressant factor from pancreas; Buildup of toxic metabolites; Multiple organ dysfunction syndrome (MODS); Death. --Any value <70% is a life-threatening emergency & may signal refractory stage.

Amputations

Amputations: elective or traumatic. Most elective & r/t complications of PVD resulting in decreased perfusion (ischemia) to distal areas of LE. DM often underlying cause. Trauma to limb is 2nd leading cause of amputation. Amputation considered only after other txs have not restored circulation to LE, AKA limb salvage procedures (percutaneous transluminal angioplasty; PTA). -Traumatic amputations often from accidents or war & are primary cause of UE amputation. Ex. power equipment injuries; MVA or industrial machine accident. -Common complications of amputations: Hemorrhage leading to HvLS; Infection; Phantom limb pain; Neuroma; Flexion contractures. --Flexion contractures of hip or knee most frequent in amputations of LE; must be avoided so can ambulate w/ prosthetic. Proper positioning & active ROM exercises in early post-op help prevent this. -Critical Rescue: If decreased tissue perfusion, notify surgeon or RRT immediately to communicate findings! If BP drops & pulse increases, suspect covert bleeding. To check for overt bleeding, lift residual limb & feel under pressure dressing for dampness or drainage. If bleeding occurs, apply direct pressure & notify RRT or PHCP immediately. Continue to monitor until help arrives.

Anti-venoms for Pit viper & Coral Snakes

Anti-venoms for Pit viper (rattlesnakes, cottonmouths, copperheads): -Oldest is Antivenin Crotalidae Polyvalent Convention therapy and still plays a role on a more limited basis today. Best if admin w/in 4hrs of envenomation but may be helpful in coagulopathy up to 24hrs. --Check for allergies to papaya, pineapples, sheep, horses, dust mites, or latex. It is made from blood or plasma of healthy horses or sheep. -Crotalids - tx w/ CroFab antivenom (2001) txs bites of all NA & SA crotalids. --Anaphylaxis w/ CroFab is rare but can occur. Most effective if given w/in 4-6hrs, & less effective after 12hrs. --When pt comes in, Poison control is called & directions are followed. Dosage is according to envenomation. --BEFORE CROFAB INFUSION STARTS: Assess if patient is allergic to ovine (sheep) products or papain or papaya (use in manufacturing process of the drug)- if so CroFab is --Can give cautiously to: pts w/ Hx allergic rx to conventional antivenom, allergy to bromelain (pineapple enzyme), renal or hepatic problems, pregnancy, sensitivity to mercury products. -Antivenom for Coral Snakes: -Antivenin Micrurus fulvius (made from horse serum); good for all coral snakes, except Sonoran coral snake found in Arizona (supportive care recommended for the Sonoran coral). -Critical Rescue: most significant risk to snakebite victim is airway compromise & respiratory failure. Respond by ensuring IV lines are patent & resuscitation equipment is immediately available. Contact Poison Control in collab. w/ HCP to receive guidance for possible antivenin (AKA antivenom) admin & pt management.

Aortic Regurgitation (Insufficiency)

Aortic Regurgitation (Insufficiency): aortic valve leaflets do not close properly during diastole; annulus (valve ring that attaches to leaflets) is dilated, loose, or deformed→ allows BF from aorta back into LV during diastole. LV, in compensation, dilates to accommodate greater BvL & eventually hypertrophies. -Usually results from nonrheumatic conditions like infective endocarditis, congenital anatomic aortic valvular abnormalities, HTN, & Marfan synd. (rare, generalized, systemic connective tissue dz). -S/S: asymptomatic for many yrs bc compensation of LV. As dz progresses & LV failure occurs→ major s/s are DOE, orthopnea, & paroxysmal nocturnal dyspnea. Palpitations w/ severe dz, esp. when lie on Lt. Nocturnal angina w/ diaphoresis often occurs. "Bounding" arterial pulse; pulse pressure usually widened, w/ elevated SBP & diminished DBP. Classic auscultatory s/s is high-pitched, blowing, decrescendo diastolic murmur.

Aortic stenosis

Aortic stenosis: most common valve dysfunction in US; often considered dz of "wear & tear"; aortic valve orifice narrows & obstructs LV outflow during systole. Increased resistance to ejection or afterload→ V hypertrophy. As stenosis worsens, CO is fixed & cannot increase to meet demands during exertion→ development of s/s. -Eventually LV fails, blood backs up in LA, & pulmonary system is congested. Rt-HF can occur in late dz. When SA of valve is 1cm or less, surgery is indicated on urgent basis! -Congenital bicuspid or unicuspid aortic valves are primary causes for aortic stenosis in many. Rheumatic aortic stenosis occurs w/ rheumatic dz of MV & develops in young & middle-age adults. Atherosclerosis & degenerative calcification of aortic valve are major causative factors in elderly. Aortic stenosis is most common valvular ds in all countries w/ aging pts. -Classic s/s: result from fixed CO= dyspnea, angina, & syncope on exertion. When CO falls in late stg.→ marked fatigue, debilitation, & peripheral cyanosis. Narrow pulse pressure when BP measured. Diamond-shaped, systolic crescendo-decrescendo murmur usually noted.

Assessing AF

Assessing AF: -Hx: assess Hx of AF or other dysrhythmias. AF recurrence common; assess previous conduction issues→ helpful in developing care plan. Assess Hx CVD; AF risk is much higher w/ hx HTN, HF, obesity, or ACS. Assess hx PE, VTE. -Physical; S/S: apical pulse may be irregular. S/S depend on ventricular rate. Uncontrolled AF→ loss of atrial kick→ greater risk inadequate CO. S/S poor perfusion may be seen; assess for fatigue, weakness, SOB, dizziness, anxiety, syncope, palpitations, chest discomfort or pain, hypotension. Some pt asymptomatic. -Psychosocial: AF pts, esp. w/ high ventricular rate→ very anxious; increased HR, CO decreases→ dyspnea, contributing to anxiety. Assess pts w/ chronic AF for coping methods w/ a LT conduction issue. Chronic AF may have anxiety r/t anticoagulation meds & potential for emboli. -Other Dx: Definitive Dx w/ 12-lead ECG. AF classified into 5 categories based on length of time in the rhythm: --Paroxysmal: has an episode w/in 7 days that converts back to sinus rhythm. Episode lengths vary but do not continue beyond a wk. --Persistent: experienced as episodes that occur for >7 days. --Long-standing persistent: sustained for >12mo. --Permanent: remain in AF, & decision made not to restore or maintain sinus rhythm by medical or surgical tx. --Nonvalvular: occurs in absence of mitral valve dz or repair. -Analysis: priority collaborative problems for most w/ AF are: 1.) Potential for embolus formation due to irregular cardiac rhythm. 2.) Potential for HF due to altered conduction pattern.

Assessing Strokes

Assessing Strokes: -Health Promotion & Maintenance: most strokes are preventable. CDC & other CV organizations recommend to apply ABCS of heart health to prevent strokes: Aspirin use when appropriate; BP control; Cholesterol management; Smoking cessation. -1st assess: time of onset; what pt was doing; s/s progression; medical hx (head trauma, DM, HTN, CVD, anemia, obesity); meds, social hx, jobs, travel, habits; LOC, cognition, sensory & motor impairments. --LOC suddenly decreased or altered→ immediately ID if hypoglycemia or hypoxia present bc may mimic emergent neuro ds; easily tx & reversed, unlike brain injury from inadequate perfusion or trauma. --W/ SAH, esp. when hemorrhage from ruptured (leaking) aneurysm, often reports onset of sudden, severe headache "worst headache of my life." --S/S SAH or cerebral aneurysmal & AVM bleeding→ N/V, photophobia, CN deficits, stiff neck, & MS change; may be family Hx of aneurysms. -Critical Rescue: In ED, assess stroke w/in 10min of arrival; std. also applies to already hospitalized for other conditions. Priority is assessment of ABCs. Many hospitals have stroke teams & centers; experts in acute strokes. --RN also performs complete neuro assessment on ED arrival. National Institutes of Health Stroke Scale (NIHSS; 0-40, 40= most deficits) commonly used valid & reliable assess tool; RNs complete ASAP after ED arrival; IDs eligibility for IV fibrinolytics.

Atrial dysrhythmias: PAC

Atrial dysrhythmias: focus of impulse generation shifts away from SA node→ atrial tissues. Shift changes axis (direction) of atrial depolarization→ Abnormal P-wave. Most common are: PAC; SVT; AF. Atrial dysrhythmias: focus of impulse generation shifts away from SA node→ atrial tissues. Shift changes axis (direction) of atrial depolarization→ Abnormal P-wave. Most common are: PAC; SVT; AF. -Premature Atrial Complexes [contraction]: PAC; atrial tissue becomes irritable; ectopic focus fires impulse before next SA impulse is due. Premature P wave may not always be clearly visible bc hidden in preceding T wave. Examine T wave closely for shape change & compare w/ other T waves. PAC usually followed by pause. -Atrial irritability causes: Stress; Fatigue; Anxiety; Inflammation; Infection; Caffeine, nicotine, or alcohol; Drugs= epi, sympathomimetics, amphetamines, digoxin, or anesthetics. --PACs may also result from myocardial ischemia, hypermetabolic states, electrolyte imbalance, or atrial stretch. --Atrial stretch can result from CHF, valvular dz, & pulmonary HTN w/ cor pulmonale. -Assess: usually no s/s except for possible palpitations. -Tx: none needed, except to tx causes [ex. HF]. If PACs frequent→ may cause more serious atrial tachydysrhythmias→ may need tx. Admin antidysrhythmics may be necessary.

Automatic Advancement Levels I & II

Automatic Advancement Levels I & II: -Clinical Nurse I: Clinical ladder entry level for new grad bedside RN. After successful completion of dept. orientation, a RN will automatically advance to a Clinical Nurse I. --Description: new bedside RN developing nursing skills, expanding knowledge, & assuming job responsibilities. -Clinical Nurse II: After completion of a yr of employment, & receiving a satisfactory evaluation, a bedside RN will automatically advance to Clinical Nurse II level. Newly hired, experienced RN (w/ 1yr+ of recent RN experience) will be placed at Clinical Nurse II level. After successful completion of dept. orientation and 1st successful evaluation, may advance to higher ladder levels following all program requirements. All RNs will remain at Nurse II level if they do not choose to advance to higher levels. --Description: experienced bedside RN capable of independent pt care. Actively developing more advanced RN skills & knowledge via education & involvement in RN activities beyond basic job requirements & responsibilities.

Automatic Advancement Levels III, IV, & V

Automatic Advancement Levels III, IV, & V: -Clinical Nurse III: Requires annual portfolio submission & complying w/ all ladder program requirements. Advancement to level requires self-paced & self-motivated participation. --Description: a bedside RN highly skilled in pt care. Demonstrates leadership & mentorship abilities. Active involvement in continuing education & RN activities beyond basic job requirements & responsibilities. -Clinical Nurse IV: Requires annual portfolio submission & compliance w/ all ladder program requirements. Advancement to level requires highly self-paced & self-motivated participation. --Description: A bedside RN w/ broad base of advanced experience. Recognized for leadership & knowledge. Leadership extends to education & development of others. Involvement in multiple RN activities beyond basic job requirements & responsibilities. Acquiring research skills by participating in evaluation of clinical outcomes to improve nursing via EBP. -Clinical Nurse V: Requires annual portfolio submission & compliance w/ all ladder program requirements. Advancement to highest level on ladders requires extraordinary & exceptional self-paced & self-motivated participation. (Must be nationally certified in RN specialty.) --Description: A bedside RN w/ exceptional advanced experience. Recognized for expert leadership & knowledge. Leadership is recognized at role-model level. Involvement in multiple RN activities beyond basic job requirements & responsibilities. Active & ongoing involvement in improving nursing via EBP; research, writing published RN article, etc. All submitted EBP submissions & research materials must be presented in professional format w/ extensive info like charts, graphs, studies, stats, outcomes, etc. -As RNs move up ladder, the educational progression is more specific. Org-wide specific education goes beyond requirements of regulators to those that are specific to needs & current performance of org. Orgs. required to perform annual needs assessments to ID educational needs of staff; assessments need to go beyond what staff "wants" to learn, needs to move toward outcomes-based model, where "needs to know" education is planned.

BOX 9-3: Model for Managing Conflict

BOX 9-3; Model for Managing Conflict: -Determine the Basis of the Conflict: Intrapersonal. Interpersonal. Group. Intergroup. Organizational. -Analyze Sources of the Conflict: Cultural differences. Different facts. Separate pieces of info. Different perceptions of the event. Defining the problem differently. Divergent views of power & authority. Role conflicts. # of organizational levels. Degree of association. Parties dependent on others. Competition for scarce resources. Ambiguous jurisdictions. Need for consensus. Communication barriers. Separation in time & space. Accumulation of unresolved conflict. -Consider Alternative Approaches to Conflict Management: Avoiding. Accommodating. Compromising. Collaborating. Competing. -Choose the Most Appropriate Approach: Implement the Conflict Management Strategy. Evaluate Results.

Benner 5 Stages

Benner 5 Stages: RN moves through 5 stages of clinical competence: novice, advanced beginner, competent, proficient, and expert nurse. -Different levels reflect changes in 3 general aspects of skilled performance: 1.) One is a movement from reliance on abstract principles to the use of past concrete experience as paradigms. 2.) Second is a change in the learner's perception of demand situation; situation is seen less & less as a compilation of equally relevant bits, & more & more as a complete whole; only certain parts are relevant. 3.) Third is a passage from detached observation to involved performer; performer no longer stands outside the situation, but is now truly engaged in the situation. -BOX 10-1; 5 Stages of Transition from Novice to Competent Practitioner: -Stage I Novice: The nurse is overwhelmed by the number of potentially relevant details that pertain to a patient's care. -Stage II Advanced Beginner: The new nurse may suffer exhaustion while trying to manage their patients within the confines of the unit guidelines and protocols. -Stage III Competent: Successfully embracing policy and protocol enables feelings of confidence and serves as a critical marker of readiness. -Stage IV Proficient: A period of transition in the preceptee-preceptor relationship. The preceptor serves as a resource, frequently retreating from the forefront of patient care. -Stage V Expert: The "comfort zone" of a preceptor is withdrawn as orientation is successfully completed.

Budgeting Process

Budgeting Process: responsibility of RN manager; part of overall strategic planning process; Org. budget cascades down to individual depts. & units. Budgets developed annually for 12-mo period. Budget cycle based on orgs. definition of fiscal year (calendar= 1/1-12/31 or fiscal= 7/1-6/30). -Economic stability of org. depends on management of resources required to deliver care in cost-effective & safe manner. -Resources required to deliver pt care are costly & often managed at POS (unit). RNs need to understand how to manage cost of pt care r/t their clinical practice & workings of particular unit. Also, accrediting agencies require collab. input from staff in development of annual budgets. 2 major types of budgeting processes: -0-based budgeting: requires entire budget to be re-created annually starting from zero; allows for consideration of alternatives in service delivery. --Ex. How many FTEs, xerox machines leased (units charged for copies, maintenance fees, equipment is mostly leased). --All portions of 0-based budget need to be justified annually. --Demands proactive evaluation of need for services. -Incremental budgeting: more traditional; builds on previous yrs budget. Use it or lose it; more difficult to do in a for-profit. --If 10% increase in funds is available→ budget may be increased by 10%. --Easier process, but at times it allows budgets to become bloated w/ min. justification of service or at times it does not reflect actual changes anticipated for unit. -Budgeting process can be divided into phases: 1.) Info gathering & planning. 2.) Development of org. & unit budgets. 3.) Development of cash budgets, negotiation, & revision. 4.) Evaluation.

Burn Classification

Burn Classification: by depth of destruction; amount of tissue integrity loss is r/t agent causing the burn, temp. of heat source, & how long the skin is exposed to source. -2 primary systems of classification: (1) degree of burn (1st, 2nd, 3rd, & 4th degree), & (2) degree of thickness (superficial or deep, w/ thickness designations). Also classified as minor, moderate, or major, depending on injury depth, extent, & location. -Classification of Burn Depth: -Superficial 1st-degree burns: Damage is Above basal layer of epidermis; Appears Dry, Pink to red; No edema or blistering; have Pain; No eschar; Healing= Injured epidermis peels away & reveals new epidermis, takes 1wk. Ex. sunburn. -Superficial 2nd-degree burns (superficial partial-thickness): Damage= all epidermis & Into dermis; Appears Moist, Red, Blanching Blistering; Edema is Mild to moderate; have (much) pain; No eschar. Healing= Re-epithelialization from skin adnexa, takes 2wks; pigment changes but no scar. -Deep second-degree burns (deep partial-thickness): Damage= Deeper into dermis; Appears Less moist, Less blanching, Less painful; Moderate edema; Blistering is rare; some pain; Eschar= Yes, soft & dry. Healing= Scar deposition, contraction, limited re-epithelialization, may need grafting; BV constriction can lead to deeper injury bc hypoxia & ischemia; takes 2-6 wks. -[Deep] 3rd-degree burns (full-thickness): Damage= Entire thickness of skin [dermis & epi] destroyed, into fat; Appearance= Any color (black, red, yellow, brown, white), Dry; Severe edema; No blistering or pain; Eschar= Yes, hard & inelastic, must slough off for healing; Healing= Contraction & scar deposition, will not re-epithelialize many wont contract bc no BVs; requires grafting, takes wks to months. --Circumferential (around chest; circulation & breathing problems) may require escharotomy (incision into eschar, release tension) or fasciotomy (incision into eschar & fascia); almost like compartment syndrome, breathing issues. --Can appear waxy white, deep red, yellow, brown, or black, & thrombosed BV may be visible -[Deep] 4th-degree burns: Damage= Damage extends into muscle, tendon, bone; Appears Black; Severe edema; No blistering or pain; has eschar; Healing= Need specialized care, grafting does not work, takes wks to months, if at all. --Can occur w/ electrical, chemical, or flame injury.

Burns

Burns: Extent of injury r/t age, health, size & depth of burn, & area injured. Even after healing, may cause late complications→ contracture & scarring. -Care priorities: closure of burn wound & preventing infection. Lack or delay in wound healing is key factor for all systemic problems & major cause of disability & death. -Less complicated burns can be tx & released; severe burns may need comprehensive care for wks→ months to survive. -Epidermis does not have BVs; but can regrow after burn bc epidermal cells surrounding sweat & oil glands & hair follicles extend into dermal tissue. Skin regrows as long as parts of dermis present bc of BVs. -Sweat & oil glands in palm & sole extend deep into dermis; allows healing of deep burns in these areas. If entire dermal layer is burned, all cells and dermal appendages destroyed, & skin can no longer restore itself. -SQ tissue lies below dermis & is separated from dermis by basement membrane= thin, noncellular protein surface. Bone, tendon, & muscles maybe exposed if burns are deep. -Extent of Burn Injury: severity of a burn is ID by how much of BSA is involved. -Rule of 9's: quickest method for calculating the size of burn injury in adults w/ normal wt: ht proportion; body is divided into areas that are multiples of 9%. Useful at site of injury; more accurate evaluations using other methods are made in burn unit. -Temp: Skin can tolerate up to 140F for 5s; Brain cell death at >107.6 F→ seizures. Cell damage depends on temp & time exposed.

CAB; CPB; CABG Intra-op

CAB OP: general anesthesia for cardiopulmonary bypass (CPB) & off-pump surgery. Traditional→ begins w/ median sternotomy incision & visualization of heart & great vessels. Another team begins harvesting vein if used for graft (CABG); or synthetic grafts used. -Cardiopulmonary bypass (CPB): provides oxygenation, circulation, & hypothermia during induced cardiac arrest. Blood diverted from heart to bypass machine→ heparinized, oxygenated, & returned via cannula in ascending aortic arch or femoral artery. -During bypass, core temp. remains between 95°F (35°C; cold cardioplegia)→ normal temp (warm cardioplegia). Cooling decreases metabolism rate & O2 demand, but keeping heart warm decreases post-op complications; more common w/ cold cardioplegia. -Heart perfused w/ K+ solution→ decreases myocardial O2 consumption & causes heart to stop during diastole; ensures motionless OP field & prevents myocardial ischemia. -Heart arrested→ grafting begins. Surgeon uses internal mammary artery (IMA), saphenous vein, &/or radial artery to bypass blockages in CAs. Distal end of vessel graft is dissected & attached below clot in the CA. If surgeon uses venous graft or radial artery→ anastomosed (sutured) proximally to aorta & distally to CA just beyond occlusion→ improving myocardial perfusion. -After flow rates through grafts are measured→ heart is rewarmed slowly; cardioplegic solution flushed from heart. Heart regains rate & rhythm, or defibrillated to return normal rhythm. -OP completed→ may be rewarmed (if cold cardioplegia used) & weaned from bypass machine while grafts observed for patency & leakage. Surgeon may place A&V PM wires & mediastinal & pleural chest tubes. -Finally surgeon closes sternum w/ wire sutures.

CABG Pre-op

CABG Pre-op: planned elective or performed as emergency; traditional or MIS. Elective→ admit morning of OP. Pre-op prep & teaching completed during pre-hospitalization interviews. Teach drugs changed after OP. Ensure drugs admin before OP. -Complication is sternal wound infection. Decrease risk→ shower w/ 4% CHG; decreases # of skin microbes. Sites prep by clipping hair & applying CHG w/ isopropyl alcohol (0.5% or 2%). IV ABs admin 1hr before OP. -Familiarize pt & family w/ cardiac surgical-critical care unit (AKA open heart unit) & prep for post-op care. If elective→ demo & return demo's of how to splint chest incision, cough, DB, & perform arm & leg exercises. -Stress that: report any pain; Most of pain in harvested vessel site; use of endovascular vessel harvesting [EVH] & 1 or 2 sm incisions→ pain & edema less vs previous OPs. -Analgesics to decrease pain. Coughing & DB essential to prevent pulmonary complications. Early ambulation important to decrease risk for thrombus & embolism. -Traditional: explain will have sternal incision; possibly lg. leg incision; 1, 2, or 3 CTs; foley; PM wires; & invasive HDM. ETT w/ MV during OP. ETT removed once awake & stable. Tell pt & family that pt will not be able to talk w/ ETT. Describing post-op→ emphasize close monitoring & equipment are Std. tx. -Pre-op anxiety common & can negatively affect post-op outcomes. RN ID anxiety level & past coping methods; may be helpful to define fears. Fear sources→ unknown, bodily harm, & death. -Elective OP; benefit from detailed OP info, depending on preferences & culture; others feel overwhelmed by material. Some discuss feelings in detail or describe experiences of others w/ CABG. Assess anxiety level & help cope.

Capnometry & capnography; PETCO2

Capnometry & capnography: noninvasive methods that measure the amount of CO2 present in exhaled air, it's an indirect measurement of arterial CO2 levels. Measure the partial pressure of end-tidal CO2 levels (PETCO 2; ETCO 2) in intubated & spontaneously breathing patients. --Provide info about CO2 production, pulmonary perfusion, alveolar ventilation, respiratory patterns, ventilator effectiveness, & possible rebreathing of exhaled air. -Capnometry: exhaled air sample is tested w/ a sensor that changes the CO2 level into a color or # for analysis. -Capnography: CO2 level is graphed as a specific waveform along w/ a #. More sensitive indicator of gas exchange adequacy than pulseOx; useful in early detection of respiratory depression. -Normal PETCO2: 20-40 mm Hg; alterations reflect changes in breathing effectiveness & gas exchange. Changes occur before hypoxia, can be detected using pulseOx because CO2 moves out of the body more easily than O2 moves into it. PulseOx & PETCO2 for patients at risk for respiratory problems can provide info to direct early intervention. -Increased PeTCO2: conditions that reflect inadequate gas exchange or an increase in cellular metabolism; increase production of CO2. --Ex. Gas exchange- hypoventilation, partial airway obstruction, & rebreathing exhaled air. Metabolism- fever, acidosis, & heavy exercise. -Decreased PETCO2: conditions w/ poor pulmonary ventilation. --Ex. pulmonary embolism, apnea, total airway obstruction, & malposition of an ET tube. --Ex. hyperventilation not based on O2 need, CO2 is blown off faster than it is generated in the tissues. --Ex. CP arrest decreases PETCO2; PETCO 2 may be used to determine the effectiveness of CPR & whether there is a spontaneous return of circulation.

Cardiomyopathy

Cardiomyopathy: subacute or chronic dz of cardiac muscle; cause may be unknown. 4 categories; based on abnormalities in structure & function: -Dilated cardiomyopathy (DCM): most common structural abnormality. Extensive damage to myofibrils & interference w/ myocardial metabolism. Ventricular wall thickness is normal, but ventricles dilated (LV usually worse) & systolic function impaired. --Causes: alcohol abuse, chemo, infection, inflammation, poor nutrition. --Decreased CO r/t inadequate pumping→ DOE, decreased exercise capacity, fatigue, palpitations. -Hypertrophic cardiomyopathy (HCM): Cardinal features= asymmetric ventricular hypertrophy & disarray of myocardial fibers. LV hypertrophy→ stiff LV→ diastolic filling abnormalities. S/S result of hypertrophied septum→ diminished space→ reduces SV & CO. --Obstruction in LV outflow tract seen in most w/ HCM. Mitral valve structural abnormalities commonly associated w/ HCM & contribute to ventricular outflow obstruction. --1-gene autosomal-dominant trait occurring in 1: 500 pts. Some die w/o any s/s; others have DOE, syncope, dizziness, & palpitations. Many athletes who die suddenly probably had hypertrophic cardiomyopathy. -Restrictive cardiomyopathy: rarest cardiomyopathy; characterized by stiff ventricles→ restrict filling during diastole. S/S similar to Lt or Rt HF or both. Can be primary or caused by endocardial or myocardial dz [sarcoidosis or amyloidosis]. Px is poor. -Arrhythmogenic RV cardiomyopathy (dysplasia): from replacement of myocardial tissue w/ fibrous & fatty tissue. Name implies RV dz, but about 1/3 pts also have LV involvement. Has familial association & most often affects young adults. Some pts have s/s, & others do not.

Care of Neurogenic Shock & AD

Care of Neurogenic Shock & AD: -Critical Rescue: Monitor acute SCI at least Q1h for indications of neurogenic shock: PulseOx (SpO2) <95% or s/s of aspiration (stridor, garbled speech, or inability to clear airway); Symptomatic bradycardia, + reduced LOC & deceased UO; Hypotension w/ SBP <90 or MAP <65. Notify the RRT or PHCP immediately if these s/s occur bc this problem is an emergency! --Respiratory compromise from aspiration tx w/ intubation or bronchial endoscopy. Similar to txs for any shock type, neurogenic shock is tx symptomatically by providing fluids to circulating BvL, adding vasopressor IV tx, & providing supportive care to stabilize. -In addition to observing for shock or hypotension, monitor high-level SCI for additional risk of AD. AD is neuro emergency & must be promptly tx to prevent a HTN stroke! Reduce potential causes by preventing bladder & bowel distention, managing pain & rm temp, & monitoring for early VS changes. --Critical Rescue: If AD occurs→ raise HOB immediately to reduce BP as 1st action. Notify RRT or PHCP immediately for drug tx to quickly reduce BP as indicated. ID cause of AD & manage promptly. --Place in sitting position (1st priority!), or return to previous safe position. --Assess for & remove/manage the cause: urinary retention or catheter blockage; urinary cath for kinks or obstruction. If urinary cath not present, check for bladder distention & catheterize immediately if indicated; Consider using anesthetic ointment on cath tip before insertion to reduce urethral irritation. --ID if UTI or bladder calculi are contributing to GU irritation. Check for fecal impaction or other colorectal irritation, using anesthetic ointment at rectum. Disimpact if needed. Exam skin for new or worsening pressure injury s/s. --Monitor BP Q10-15min. Give nifedipine or nitrate as prescribed to lower BP PRN; w/ recurrent AD→ may receive clonidine or other centrally acting alpha-agonist agent prophylactically.

Best Practice for Pt Safety & Quality Care: Care of Pt Receiving MV

Care of Pt Receiving MV: -Remember why they're using MV→ management also focuses on correcting causes of RF; require different tx to successfully wean. Use explanations, & acknowledge feelings to reduce anxiety; sensitive RN care promotes emotional wellness & synchrony w/ MV; reassure that ETT prevents speech only temporarily. --MV in ICUs often experience delirium, or "ICU psychosis"; need frequent, repeated explanations & reassurance. --Always assess pt 1st, MV 2nd. MV alarm sounds→ examine pt for breathing, color, & O2sat before assessing ventilator. -Critical Rescue: always assess MV pt for indications of respiratory distress & poor gas exchange. S/S respiratory distress develop during MV→ immediately remove MV & provide ventilation w/ BVM device; allows quick ID of problem w/ MV or pt. If no MV problem ID, reconnect pt & request RT assistance. -Assess respiratory status & gas exchange at least Q4h for the first 24hrs & then PRN: VS Q4h + O2sat & lung auscultation (assess Q1h or more often for ICU). Be alert for the possibility of unintended extubation or self-extubation. If the pt requires sedation or restraints, follow institution guidelines for pt safety. Assess color around the lips & nail beds, & observe for bilateral chest expansion. Assess placement of the ETT. Evaluate ABGs as available. -Maintain HOB >30 degrees when supine to decrease risk for aspiration & VAP. -Review ventilator settings at least Q8h, + alarm settings, w/ RT. -Review pt info on the ventilator display to confirm they are receiving the prescribed set tidal vL & that peak pressures are not elevated (→ obstruction or decreased lung compliance). -Empty ventilator tubings when moisture collects. -Ensure cuff is adequately inflated to ensure tidal vL. Concern for overinflation→ have RT check cuff pressure. -Assess need for suctioning Q2hrs & suction only PRN (must pre-oxygenate before suctioning). -Assess mouth around ETT for pressure injuries. -Perform mouth care at least Q12hrs using std. ventilator bundles. -Perform tracheostomy care at least Q8hrs, changing ETT holder or tape PRN, & moving the oral ETT to the opposite side of the mouth daily [prevent ulcers]. -Assess for GI distress (diarrhea, constipation, tarry stools). -Turn at least Q2hrs & get out of bed as prescribed to prevent immobility complications. -Monitor progress on current settings & promptly relay concerns to the respiratory HCP or RT. -Monitor for AEs of MV: infection, barotrauma, reduced CO. -Position to facilitate ventilation-perfusion (V/Q) matching ("good lung down"), as appropriate. -Monitor effects of ventilator changes on gas exchange, pts subjective responses, & readiness to wean. -Provide communication method. Request consultation w/ SLP for assistance, if necessary. -Admin muscle-paralyzing agents, sedatives, & narcotic analgesics, as prescribed, using lowest possible dose to achieve comfort w/o oversedation. -Include pt & family whenever possible (esp. suctioning & tracheostomy care).

Case management

Case management: mixes process + care delivery. In hospital nursing= focuses on achievement of pt outcomes w/in an effective & appropriate time frame. Focused on entire illness episode & can cross all units where pt receives care. Associated w/ use of care pathways, order sets, care maps, protocols, practice guidelines= written plans that ID critical & predictable events that must occur throughout & after hospitalization. CM works w/ assigned RN staff to coordinate pt progress through transition of care pathway. -CM Society of America defines CM as: "collab. process of assessment, planning, facilitation & advocacy for options & services to meet individual's health needs through communication & available resources to promote cost-effective outcomes". -CM model also extends beyond hospital setting, w/ CM working w/ pts & families in all transitions of care. Some orgs. use CMs w/ chronically ill at high risk for continued readmits. CMs work w/ pts to coordinate entire spectrum of care in all settings. Associated w/ decreased readmits for chronically ill. -CMs often population based, so 1 CM may work w/ all surgical pts in a hospital, but some orgs. do use unit-based CMs. CM assigned to pt on admit & follows for entire hospital stay & performs all post-hospital care coordination. Not all CMs are RNs. -Advantages: Provides professional practice model for RNs. Is cost effective. -Disadvantages: May lead to fragmented communication. Needs to be integrated into care delivery model. May lead to RNs caring for pts to become more skills focused if CM makes all decisions.

Causes & Types of Shock by Functional Impairment (tbl 34.1)

Causes & Types of Shock by Functional Impairment: -HvLS: Overall Cause is total body fluid decreased (in all fluid compartments). Specific Cause or Risk Factors; Hemorrhage, Trauma, GI ulcer, Surgery, Inadequate clotting, Hemophilia, Liver disease, Cancer tx, Anticoagulation tx, Dehydration, Vomiting, Diarrhea, Heavy diaphoresis, Diuretic tx, NG suction, DI. -Cardiogenic Shock: Overall Cause is Direct pump failure (fluid vL not affected). Specific Cause or Risk Factors; MI, Cardiac arrest, Ventricular dysrhythmias, Cardiomyopathies, Myocardial degeneration, Cardiac tamponade. -Distributive Shock: Overall Cause is Fluid shifted from central vascular space (total body fluid vL normal or increased). Specific Cause or Risk Factors; Neural induced, Pain, Anesthesia, Stress, Spinal cord injury, Head trauma, Chemical induced, Anaphylaxis, Sepsis, Capillary leak, Burns, Extensive trauma, Liver impairment, Hypoproteinemia. -Obstructive Shock: Overall Cause is Cardiac function decreased by noncardiac factor (indirect pump failure); total body fluid not affected, but central vL is decreased. Specific Cause or Risk Factors; Cardiac tamponade, Arterial stenosis, PE, Pulmonary HTN, Constrictive pericarditis, Thoracic tumors, Tension pneumothorax.

Changes Resulting from Burn Injury; Assessing Burn pts Skin, CO poisoning, Renal

Changes Resulting from Burn Injury: -Cardiac (s/s similar to HvLS); r/t electrical burn. -Pulmonary problems caused by superheated air, steam, toxic fumes, or smoke (black under nose). -GI (Curling's ulcer): r/t physical stress of body from trying to regenerate; pours acid out→ ulcer. -Increase kCal needs: Increase metabolism; give body more kCal to repair itself. --Burns increase metabolism by secreting catecholamines, cortisol, & ADH. Catecholamines break down proteins & increase kcal needs. Core body temp increases due to hypermetabolism. -Immunologic (infection): always a main concern w/ burns. Assessing the Burn; Skin: Assess skin to ID extent & depth of burn injury; injury size first est. in comparison w/ TBSA; ex. burn involves 40% of TBSA= 40% burn. Injury size important for Dx & Px & for calculating drug doses, fluid replacement vLs, & kcal needs. --Inspect skin integrity to ID injured areas & changes in color & appearance. Except w/ electrical burns, initial size assessment usually made accurately w/ specific tools & charts. --Specific txs are r/t depth of burn, initial assessment of skin includes est. of burn depth. Criteria for injury depth based on appearance and characteristics. -CO Poisoning: a leading COD from fire; colorless, odorless, tasteless gas released in during combustion. INH injury is risk for CO poisoning. --CO rapidly transported across lung membrane & binds tightly to Hgb in place of O2 to form carboxyhemoglobin (COHb)→ impairs O2 unloading at tissue level; O2-Hgb disocociation curve shifts to the Lt. --O2-carrying capacity of Hgb is reduced, but ABGs of PaO2 is normal. Vasodilating action of CO causes "cherry red" color in pts. S/S vary w/ concentration of COHb. Admin high-flow O2 for at least 6hrs to suspected or confirmed CO poisoning. -CO 1%-10% (normal): Increased threshold to visual stimuli; Increased BF to vital organs. -CO 11%-20% (mild poisoning): Headache; Decreased cerebral function; Decreased visual acuity; Slight breathlessness. -CO 21%-40% (moderate poisoning): Headache; Tinnitus; Nausea; Drowsiness; Vertigo; Altered MS; Confusion; Stupor; Irritability; Decreased BP, increased & irregular HR; Depressed ST segment on ECG & dysrhythmias; Pale to reddish-purple skin. -CO 41%-60% (severe poisoning): Coma; Convulsions; CP instability. -CO 61%-80% (fatal poisoning): Death. -Renal/Urinary Assessment: Release of Myoglobin; Assess renal function; Assess urine. Cellular debris & decreased renal BF; tissue breaks down→ kidneys filter debris→ possible AKI bc of prolonged conditions or excessive vL of debris. Assess UO Q1H.

Classification of post-MI HF

Classification of post-MI HF: Several systems used to categorize HF after MI. Classic Killip system ID 4 classes based on px; system complements ACC/AHA HF classification of function assessment. -Killip Classification of Heart Failure: I.) Absent crackles & S3. Class I respond well to reduction in preload w/ IV nitrates & diuretics. Monitor UO hourly, check VS hourly, continue to assess for s/s HF, & review serum K+. II.) Crackles in lower half of lung fields & possible S3. Class II & III may require diuresis & more aggressive tx; ex. afterload reduction &/or enhancement of contractility. IV nitroprusside or NTG to decrease preload & afterload; given as continuous infusions in specialized units w/ HDM. Intra-arterial BP monitoring preferred for nitroprusside. III.) Crackles > 1/2 way up lung fields & frequent pulmonary edema. Classes II & III usually on 1x/day BB. Dosing titrated, depending on goal achievement & drug tolerance. Other drugs; ACEIs & ARBs, common to inhibit ventricular remodeling. IV.) Cardiogenic shock. Class IV cardiogenic shock= necrosis of >40% of LV. Most w/ stuttering pattern of CP→ extension of ACS.

Clinical Ladders

Clinical Ladders: are programs that reward RNs for advancement in nursing; permits horizontal advancement, allowing excellent clinicians to remain in role at bedside. -RNs advance through determined # of levels w/in position category based on predetermined criteria. -When level is reached→ additional advantages for the RN. When highest level for position reached→ advancement requires additional education in nursing. -Clinical ladders developed in orgs. in rx to Benner's concept of From Novice to Expert (1984); means to promote individual's growth as professional RN on path to expert status. -Using org. estab. criteria + an interview, HC orgs. decide on merits of individual clinical advancement. Process for Professional Clinical Career Ladder progression is usually clinically & academically based. --Encourages RN to continue specialization, education, broadening horizon; given more $ to encourage you to do it; sometimes it's a certification. Block of things you must achieve to move up; you have to keep updating this every yr, quarter, etc.

Common Dysrhythmias & their broad categories; Premature Complexes

Common Dysrhythmias & their broad categories: Many dysrhythmias have no s/s, others have serious consequences if not tx. -Premature Complexes: early rhythm complexes; cardiac cell or cell group, other than SA node, becomes irritable & fires an impulse before the next sinus impulse is produced. -Abnormal focus= ectopic focus; may be generated by atrial, junctional, or ventricular tissue. -After the premature complex→ pause before next normal complex→ irregularity in rhythm. -May be unaware or feel palpitations or skipping of heartbeat. -If premature complexes, esp. ventricular, become more frequent→ possible s/s of decreased CO. -May occur repetitively in a rhythmic fashion: --Bigeminy: normal complexes & premature complexes occur alternately in repetitive 2-beat pattern, w/ pause occurring after each premature complex→ complexes occur in pairs. --Trigeminy: repeated 3-beat pattern, usually as 2 sequential normal complexes followed by premature complex & pause, w/ same pattern repeating in triplets. --Quadrigeminy: repeated 4-beat pattern, usually as 3 sequential normal complexes followed by premature complex & pause, w/ same pattern repeating in a 4-beat pattern.

Common Ex. of Anti-dysrhythmic Meds: Sodium Channel Blockers & Beta Blockers

Common Ex. of Anti-dysrhythmic Meds: -Class I, Sodium Channel Blockers: 3 subgroups of class I; Membrane stabilizing agents. -Type IA= Disopyramide phosphate. Type IB= Lidocaine (suppresses automaticity); Mexiletine hydrochloride. Type IC= Flecainide acetate; Propafenone hydrochloride. -Monitor BP & HR; hypotension & bradycardia can occur. -Monitor for arrhythmias; agents affect conduction patterns, may increase the frequency or severity of dysrhythmias. -Monitor for CNS SEs—dizziness, anxiety, ataxia, insomnia, confusion, seizures, GI distress; may require dose reduction or D/C. -Monitor for s/s HF; many class I 's can also cause HF. -Class II, Beta Blockers: Only 4 BBs approved for tx dysrhythmias. Propranolol; Acebutolol; Esmolol; Metoprolol; Sotalol. For control of dysrhythmias associated w/ excessive B-adrenergic stimulation. Slow HR, delay repolarization. -Monitor HR & BP; bradycardia & decreased BP are expected effects. -Assess for wheezing or SOB; effects on lungs can cause bronchospasm. -Assess for insomnia, fatigue, & dizziness; SEs may require a decrease in dosage or D/C. -Sotalol is a class II dysrhythmic & class III drug bc effect on QT interval & delay of repolarization. Assess ventricular arrhythmias bc can have pro-arrhythmic effects.

Common Ex. of Antidysrhythmic Meds: K+ Channel Blockers

Common Ex. of Anti-dysrhythmic Meds: -Class III, K+ Channel Blockers: 5 class III's. Each works to delay repolarization & prolongs QT interval. Effects similar, but SEs & mechanism of action vary greatly. Lengthens absolute refractory & prolongs repolarization. -For all class III K+ channel blockers: Monitor BP & HR; hypotension & bradycardia can occur. Monitor for arrhythmias; bc they affect conduction patterns, may increase the frequency or severity of dysrhythmias. -Sotalol: for A&V dysrhythmias. -Amiodarone: for A&V dysrhythmias. Continually monitor ECG rhythm during infusion; bradycardia & AV block can occur. Can cause serious toxicities (lung damage, visual impairment); as result, approval limited to life-threatening dysrhythmias. But bc of efficacy, use is very common. Corneal pigmentation occurs in most, but generally does not interfere w/ vision. -Dronedarone: for AF & a-flutter. Teach take w/ meals & avoid grapefruit juice; better absorbed w/ food, & grapefruit alters effect. Teach notify HCP w/ s/s HF; contraindicated for pts w/ HF. -Ibutilide: for AF & a-flutter. Stop infusion as soon as dysrhythmia terminated or w/ VT; may cause potentially fatal dysrhythmias. Assess K+ & Mg+ levels before infusion bc elec. balance must be corrected prior to & during use. -Dofetilide: for AF & a-flutter. Teach change positions slowly; orthostatic hypotension is common SE.

Common Ex. of Antidysrhythmic Meds: Ca+ Channel Blockers & Other drugs

Common Ex. of Antidysrhythmic Meds: -Class IV: Ca+ Channel Blockers: Only 2 CCBs approved for tx of dysrhythmias. Slow flow of Ca+ into cell during depolarization. -Verapamil; Diltiazem (Cardizem): Monitor HR & BP; bradycardia & hypotension common SEs. Teach change position slowly when receiving PO tx; orthostatic hypotension can occur until tolerance develops. For AF & a-flutter. -Teach report dyspnea, orthopnea, distended neck veins, or swelling of extremities; HF can occur, requires decrease in dosage or D/C. -Class Other: tx of dysrhythmias; fall outside of previous categories. Unclassified drugs for dysrhythmia tx. -Digoxin: for AF & a-flutter; cardiac glycoside, + inotrope; Increases contractility, reduces HR (increases filling time), slows conduction through AV node (prolonged PR), inhibits SNS & enhances PSNS. Assess apical HR before admin; decreased HR is an expected response. Early s/s toxicity= bradycardia, heart block, & loss of P wave. -Atropine sulfate: for bradycardia. Teach report N/V, diarrhea, paresthesias, confusion, or visual disturbance; can indicate digoxin toxicity. Monitor HR & rhythm after admin; increased HR is expected. -Adenosine: for paroxysmal SVT (intermittent; sudden onset r/t PC; stops suddenly). Push fast; have emergency equipment available bc short period of asystole is common after admin; bradycardia & hypotension may occur. Facial flushing, SOB, & CP common SEs. --Teach stress MGT measures & substances to avoid; ex. caffeine & alcohol, known to increase atrial irritability. (above vent. but causes VT; very rapid)

Common Ex. of Drugs for Hypovolemic Shock

Common Ex. of Drugs for Hypovolemic Shock: -Vasoconstrictors: Improve MAP by increasing peripheral resistance, increasing venous return, & increasing myocardial contractility. Ex. NE & Phenylephrine HCl. --Assess for chest pain bc drugs increase myocardial consumption & can cause angina or ischemia. --Monitor UO hourly bc higher doses decrease kidney perfusion & UO. --Assess BP Q15min bc HTN is a s/s of OD. --Assess for headache bc it is an early s/s of drug excess. --Assess Q30min for extravasation; check extremities for color & perfusion bc if drug gets into tissues, can cause severe vasoconstriction, tissue ischemia & necrosis. --Assess chest pain bc drug can cause rapid onset vasoconstriction in the myocardium & impair cardiac oxygenation. -Inotropic Agents: Directly stimulate beta-adrenergic receptors on heart muscle, improving contractility. Ex. Dobutamine & Milrinone. --Assess chest pain bc drugs increase myocardial O2 consumption & can cause angina or MI. Monitor for transient hypotension as both drugs may cause vascular dilation. --Assess BP Q15min bc HTN is s/s of OD. -Agents That Enhance Myocardial Perfusion: Improve myocardial perfusion by dilating coronary arteries rapidly for short time. Ex. Sodium nitroprusside & Nitroglycerin. --Protect drug container from light bc it degrades drug quickly. --Assess BP at least Q15min bc drug can cause systemic vasodilation & hypotension, esp. in elderly.

Commonly Used IV Vasodilators & Inotropes:

Commonly Used IV Vasodilators & Inotropes: Nitrates: -Nitroprusside sodium: potent, rapidly reversible vasodilator; acts on peripheral venous & arterial musculature. Monitor BP Q2-5min when initiating tx. Monitor PAOP, SVR, BP, HR, UO frequently. Titrate to obtain desired effect. Protect from light bc it's light sensitive. Admin in mcg/kg/min. Higher doses are associated w/ thiocyanate or cyanide toxicity. Monitor for metabolic acidosis, confusion, & hyperreflexia= s/s of toxicity. -Nitroglycerin: systemic vasodilation & dilates coronary arteries rapidly. Monitor BP Q1-3min when initiating bc BP may drop in 1min. Monitor RAP, PAOP, SVR, BP, HR, & UO frequently. Assess for headache bc frequent SE of initial tx. Tolerance to can develop w/ continued admin. -Milrinone; Fenoldopam: Assess BP & HR Q5min bc hypotension is a common AE. If SBP drops 30→ stop infusion & call HCP. Monitor I&O & wt bc it causes diuresis. Sympathomimetics: -Dopamine: dose-dependent activator of alpha, beta, & dopaminergic receptors. Assess reason for use & expected result. Observe HR, BP, PAOP, SVR, CO, & UO Q5min-1hr. Titrate to maintain dose range & obtain desired effect. Infuse through central line bc extravasation→ tissue necrosis & sloughing. Monitor for ectopy & angina. -Dobutamine: Observe continuously during admin bc it's a very strong beta 1 -receptor activator & a moderately strong beta 2 -receptor activator. Titrate on basis of adequate tissue perfusion: mentation, skin temp, peripheral pulses, PAOP, CO, SVR, & UO. Monitor for A&V ectopy bc dysrhythmias are an AE.

Communication after Stroke

Communication after Stroke: Language or speech problems usually result of stroke involving dominant hemisphere. Lt cerebral hemisphere is speech center in most. Speech & language problems may be result of aphasia or dysarthria. Aphasia caused by cerebral hemisphere damage; dysarthria is result of loss of motor function in tongue or speech muscles→ facial weakness & slurred speech. -Types of Aphasia: -Expressive: Referred to as Broca, or motor, aphasia; Difficulty speaking; Difficulty writing. -Receptive: Referred to as Wernicke, or sensory, aphasia; Difficulty understanding spoken words; Difficulty understanding written words; Speech often meaningless; Made-up words. -Mixed: Combo of difficulty understanding words & speech; Difficulty w/ reading and writing. -Global: Profound speech & language problems; Often no speech; or sounds that cannot be understood. -Aphasia classified many ways; most commonly, classified as expressive, receptive, or mixed. Few w/ only expressive or receptive aphasia; but usually 1 type is dominant. -Expressive (Broca or motor) aphasia: result of damage in Broca area of frontal lobe. Motor speech problem; understands spoken word but cannot speak; also has difficulty writing but may be able to read. Rote speech & automatic speech like responses to greeting often intact. Pt aware of deficit & may get frustrated & angry. -Receptive (Wernicke or sensory) aphasia: caused by injury involving Wernicke area in temporoparietal area; cannot understand spoken or written word. May be able to talk, but language often meaningless. -Mixed or Global aphasia: pt usually has some degree of this; dysfunction in areas of expression & reception. Reading & writing ability are equally affected. -Help communicate w/ aphasia pt, using these principles: Present 1 idea or thought in a sentence (I am going to help you get into the chair). Use simple 1-step commands rather than asking to do multiple tasks. Speak slowly but not loudly; use cues or gestures PRN. Avoid yes/no questions w/ expressive aphasia. Use alternative forms of communication if needed; ex. computer, mobile device, communication board, or flash cards (often w/ pics). Do not rush pt when speaking. -Care w/ Aphasia: w/ moderate-to-severe aphasia or dysarthria, consult w/ SLP who can complement your care w/ specialized knowledge of speech & language problems. SLP may ID problems that could trigger need for other team members to achieve positive outcomes for stroke pts. According to IP Education Collab. (IPEC), using unique & complementary abilities of HC members optimizes health & care.

Comparison of Triage Under Usual vs Mass Casualty Conditions:

Comparison of Triage Under Usual vs Mass Casualty Conditions: -Triage Under Usual Conditions: -Emergent: immediate threat to life. -Urgent: major injuries that require immediate tx. -Nonurgent: minor injuries that do not require immediate tx. Does not apply -Triage Under Mass Casualty Conditions: -Emergent or class I: red tag; immediate threat to life. -Urgent or class II: yellow tag; major injuries that require tx. -Nonurgent or class III: green tag; minor injuries that do not require immediate tx. -Expectant or class IV: black tag; expected & allowed to die.

Complications of Tracheostomy

Complications of Tracheostomy: -Tracheomalacia: Constant pressure exerted by the cuff causes tracheal dilation and erosion of cartilage, leading to loss of tissue integrity. --Indications: increased amount of air is required in the cuff to maintain the seal. A larger tracheostomy tube is required to prevent an air leak at the stoma. Food particles are seen in tracheal secretions. The patient does not receive the set tidal vL on the ventilator. --Tx: no special management is needed unless bleeding occurs. --Prevent: use an uncuffed tube as soon as possible. Monitor cuff pressure & air vLs closely & detect changes. -Tracheal stenosis: narrowed tracheal lumen is caused by scar formation from irritation of tracheal mucosa & impaired tissue integrity by the cuff. --Indications: stenosis is usually seen after the cuff is deflated or the tracheostomy tube is removed. The patient has increased coughing, inability to expectorate secretions, or difficulty breathing or talking. --Tx: Tracheal dilation or surgical intervention is used. --Prevent: prevent pulling of and traction on the tracheostomy tube. Properly secure the tube in the midline position. Maintain proper cuff pressure. Minimize oronasal intubation time. -Tracheoesophageal fistula (TEF): excessive cuff pressure causes erosion of the posterior wall of the trachea & loss of tissue integrity; hole is created between the trachea & the anterior esophagus. Highest risk also has a NGT present. --Indications: similar to tracheomalacia; Food particles are seen in tracheal secretions. Increased air in cuff is needed to achieve a seal. The patient has increased coughing & choking while eating. The patient does not receive the set tidal vL on the ventilator. --Tx: manually administer O2 by mask to prevent hypoxemia. Use a small, soft feeding tube instead of a NGT for tube feedings; a gastrostomy or jejunostomy may be performed by a physician. Monitor the patient with a nasogastric tube closely; assess for TEF and aspiration. --Prevent: maintain cuff pressure. Monitor the amount of air needed for inflation & detect changes. Progress to a deflated cuff or cuffless tube as soon as possible. -Trachea—innominate artery fistula: a poorly positioned tube causes its distal tip to push against the lateral wall of the tracheostomy. Continued pressure causes necrosis & erosion of the innominate artery. This is a medical emergency! --Indications: tracheostomy tube pulsates in synchrony with the heartbeat. There is heavy bleeding from the stoma. This is a life-threatening complication. --Tx: remove the tracheostomy tube immediately. Apply direct pressure to the innominate artery at the stoma site. Prepare the patient for immediate surgical repair. --Prevent: correct the tube size, length, & midline position. Prevent pulling or tugging on the tracheostomy tube. Immediately notify the surgeon of the pulsating tube.

Conflict resolution techniques

Conflict resolution techniques: -Avoiding: If you avoid problem, you can trick yourself into believing there is no problem. -Withholding or withdrawing: parties remove themselves from participation in solution; this does not resolve a conflict. -Reassuring: Parties do not withdraw, but try to make everyone feel good; used to diffuse strong conflicts; may be a way of hindering open communication. -Accommodating: often used in vertical conflict when there is a power differential; may also be used when 1 individual has vested interest in a solution that may be relatively unimportant to the other individual. -Competing: assertive strategy; 1 individual's needs are satisfied at another's expense. -Compromising: used when both individuals play a part in decision; basis of conflict management. -Confronting: Individuals will speak for themselves in a way that the other individual hears the concern. -Collaborating: Parties work together to find a mutually beneficial solution. -Bargaining & negotiating: involves both parties in a back-and-forth discussion to reach a level of agreement. -Problem solving: goal is to find a workable solution for all parties.

Contraindications to Thrombolytic Therapy

Contraindications to Thrombolytic Therapy: -Absolute: Any prior IC hemorrhage; Known structural cerebral vascular lesion (ex. AV malformations); Known malignant IC neoplasm (primary or metastatic); Ischemic stroke w/in 3mo EXCEPT acute ischemic stroke w/in 3hrs; Suspected aortic dissection; Active bleeding or bleeding diathesis (excluding menses); Significant closed-head or facial trauma w/in 3mo. -Relative: Hx chronic, severe, poorly controlled HTN; Severe uncontrolled HTN on presentation (SBP >180); Hx prior ischemic stroke w/in 3mo, dementia, or known IC patho not covered in contraindications; Traumatic or prolonged (≥10min) CPR or major OP (w/in 3wks); Recent (w/in 2-4wks) internal bleeding; Non-compressible vascular puncture; For streptokinase→ prior exposure (>5 days ago) or prior allergic rx to these agents; Pregnancy; Active peptic ulcer; Current anticoag. use→ higher INR= higher risk for bleeding.

Coral snakes

Coral snakes: Bands of black, red, & yellow that encircle snake's body; Small maxillary fangs. -Venom contains nerve & muscle toxins; Blocks neurotransmission; Toxic effects may be delayed up to 10-12hrs & then produce rapid clinical deterioration. -"red on yellow, kill a fellow"; (Some King Snakes can look like Coral Snake but are not dangerous). -1st Aid; Pre-hospital care: Move to safety, away from snake. Call for immediate emergency assistance. Encourage rest to decrease venom circulation. Remove jewelry & constrictive clothing. Take photos of snake from safe distance to aid in ID. ID snake as coral snake, if possible. Encircle affected extremity w/ elastic bandage or roller gauze (do not wrap so tightly that arterial flow is impeded; compression dressing bc tissue is not destroyed by venom); then splint. Leave on until tx at acute care facility. -Assess for: 1st s/s n/v & sweating; Neurotoxic s/s show 12-14hrs after bite; Weakness, CN deficits (ptosis, diplopia, swallowing difficulty), altered LOC, & respiratory paralysis. Pain at site, may be mild & transient. Fang marks that are difficult to locate bc small. -Tx: ID as coral snake if possible. If un-ID, tx as if venom were injected. Monitor for toxic effects, may be delayed. Monitor for CK level elevation from muscle breakdown & myoglobinuria. Monitor cardiac function, BP, & pulseOx. Anticipate admit to a critical care unit. Be prepared to provide aggressive airway management if respiratory insufficiency or severe neuro impairment occurs. Initiate txs to decrease risk for aspiration. Coral snake antivenin is not currently made in US (some existing stock may remain). Supportive care is recommended. Teach that effects of severe bite can persist for many days. Contact regional poison control for specific advice on tx.

Coronary Artery Bypass Graft Surgery

Coronary Artery Bypass Graft Surgery: Occluded CAs bypassed w/ pts own venous or arterial BVs or synthetic grafts. Internal thoracic artery (AKA internal mammary artery; IMA) often graft of choice bc excellent patency rate many yrs after OP. Arterial grafts more durable vs venous grafts. -If not responding to tx of CAD or dz progression evident. Drug-eluting stents (DESs)→ pts previously had no option but CABG, now vessels revascularized w/o OP. Decision for OP based on s/s & results of cardiac cath. -Candidates for OP: Angina w/ >50% occlusion of Lt main CA, cannot stent; UA w/ severe 2-vessel dz, moderate 3-vessel dz, or sm-vessel dz where stents cannot be introduced; Ischemia w/ HF; Acute MI w/ cardiogenic shock; S/S ischemia or impending MI after angiography or PCI; Valvular dz; Coronary vessels unsuitable for PCI. -CABG most effective if adequate V function remains & EF close to or >50%. Lower EF pts subject to more complications. For most, risk is low & benefits of bypass clear. OP tx of CAD does not affect life span. LV function is most important LT indicator of survival. CABG improves quality of life for most. Most are pain free 1yr post-op & remain so 5yrs post-op; % of pts w/ some pain increases sharply after 5yrs.

Coronary artery disease (CAD)

Coronary artery disease (CAD): broad term; includes chronic stable angina & acute coronary syndrome (ACS). Affects arteries that provide blood, O2, & nutrients to myocardium. -BF through coronary arteries is partially or completely blocked→ ischemia & infarction of myocardium. -Ischemia: insufficient O2 supplied for myocardium requirements. -Infarction: necrosis, or cell death; occurs when severe ischemia is prolonged & decreased perfusion→ irreversible tissue damage. -CAD, AKA coronary heart disease (CHD) or heart disease; largest killer of U.S. men & women in all ethnic groups. Arteries that supply myocardium are diseased→ heart cannot pump effectively to perfuse vital organs & peripheral tissues; which need O2 in arterial blood for survival. Perfusion impaired→ life-threatening s/s & possibly death. -CAD death rate declined over past decade; due to many factors, like increasingly effective tx & increased awareness & emphasis on reducing major CV risk factors; ex. HTN, smoking, high cholesterol. Some coronary events occur w/o common risk factors.

Costs other than personnel in Operating Budget (Capital expenditure budget & Revenue Budget)

Costs other than personnel in Operating Budget: RN manager has to calculate supply & expense costs; ex. supplies, education, travel to conferences, telephone, electricity, & minor equipment. -Some orgs. also require support services (indirect costs) to be included in budget; ex. info technology services by in-house dept. to a unit. --RN manager is dealing w/ only minor equipment purchases in this budget. --Major items there is capital expenditure budget; must have life span of at least 1yr, & usually a dollar limit for ID if equipment request is capital or minor. --Capital expenditure usually >$500 or $1000 (depending on org.) & includes equipment & renovation expenses needed to meet LT goals. --Orgs. often perform LT planning w/ capital expenditures→ org. ID priorities for such expenditures. -Revenue Budget: Each RN unit usually called cost center= organizational unit where costs can be ID & managed; in most large HC orgs. the revenue budget is prepared by CFO, but the RN manager must be aware of revenue anticipated by unit; RN in sm Out-pt center may create revenue budget. --Calculation requires knowledge of anticipated reimbursement for pt care & time of expected reimbursement. --Most HC orgs. orient the RN manager to financial aspects of position; also includes orientation to budget process of org. & role of RN manager in this process. --Some HC agencies have changed the org. structure of unit management to include clinical RN manager & business manager. Business manager may not be RN, but work w/ unit director to maintain $ efficiency in operations.

Cranial Nerves; how to test CNs

Cranial Nerves; how to test CNs: -I: Olfactory; Sensory= Smell. Have pt close eyes & ID scents. -II: Optic; Sensory= Central & peripheral vision. Snellen chart or peripheral vision. -III: Oculomotor; Motor to eye muscles= Eye movement via medial & lateral rectus & inferior oblique & superior rectus muscles; lid elevation via levator muscle. PSNS-motor= Pupil constriction; ciliary muscles. PERRLA. -IV: Trochlear; Motor= Eye movement via superior oblique muscles. Look down & in. -V: Trigeminal; Sensory= Sensory perception from skin of face & scalp & mucous membranes of mouth & nose. Motor= Muscles of mastication. Pt opens mouth, while you try to close it; or cotton on face. -VI: Abducens; Motor= Eye movement via lateral rectus muscles. Move eyes side to side. -VII: Facial; Sensory= Pain & temp from ear area; deep sensations from face; taste from anterior 2/3 of tongue. Motor= Muscles of the face & scalp. PSNS-motor= Lacrimal, submandibular, & sublingual salivary glands. Symmetry of facial expressions; ID salt or sugar taste. -VIII: Vestibulocochlear; Sensory= Hearing, Equilibrium. Tuning fork or whisper test; equilibrium= weber & rinne. -IX: Glossopharyngeal; Sensory= Pain & temp from ear; taste & sensations from posterior 1/3 of tongue & pharynx. Motor= Skeletal muscles of the throat. PSNS-motor= Parotid glands. Touch back of throat; pt swallows. -X: Vagus; Sensory= Pain & temp from ear; sensations from pharynx, larynx, thoracic & ABD viscera. Motor= Muscles of the soft palate, larynx, & pharynx (swallowing). PSNS-motor= Thoracic & ABD viscera; cells of secretory glands; cardiac & smooth muscle innervation to the level of the splenic flexure. Assess gag, swallow, & voice quality; "ah" uvula rises midline. -XI: Accessory; Motor= Skeletal muscles of pharynx & larynx & sternocleidomastoid & trapezius muscles (swallowing). Shrug shoulders; turn head side to side. -XII: Hypoglossal; Motor= Skeletal muscles of the tongue (swallowing). Stick out tongue & move side to side; assess articulation.

Dementia & Alzheimer's disease

Dementia: AKA chronic confusional state or syndrome; general term for progressive loss of brain function & impaired cognition; many types of dementia. -Alzheimer's disease (AD): most common type of dementia; typically affects >65yr olds. -Vascular dementia: 2nd most common type; ex. multi-infarct dementia; results from strokes or vascular ds→ decrease BF to brain. -Any type of dementia affects ability to learn new info & eventually impairs language, judgment, & behavior. Dz progresses→ functional ability declines & death occurs bc of complications of decreased mobility. -Dementia is not a normal physiologic change of aging. Elderly brain usually weighs less & occupies less space in cranium. Other brain changes w/ aging= widening cerebral sulci, narrowing gyri, & enlarged ventricles. W/ AD & dementia, these normal changes are greatly accelerated; brain wt reduced further; marked atrophy of cerebral cortex & loss of cortical neurons. -Microscopic changes of AD brain= neurofibrillary tangles, amyloid-rich senile or neuritic plaques, & vascular degeneration. --Neurofibrillary tangles are fibrous tissue that impairs ability of impulses transmitted from neuron→ neuron. --Neuritic plaques are degenerating nerve terminals; found in hippocampus; important part of limbic system. Deposited w/in plaques are increased amounts of abnormal protein= beta amyloid; tendency to accumulate & form neurotoxic plaques in brain→ impair neuronal transmission. --Vascular degeneration: occurs in normally aging brain; but presence significantly increased in dementia; accounts for at least partial loss of nerve cells ability to properly function. Pathologic change contributes to cognitive decline & mortality of AD. --Abnormalities in NTs: in addition to structural changes in brain associated w/ AD, abnormalities in NTs (ACh, NE, dop, & 5-HT) may occur. High levels of beta amyloid can reduce amount of acetyltransferase in hippocampus; decreased Ach interferes w/ cholinergic innervation to cerebral cortex→ impaired cognition, recent memory, & ability to acquire new memories.

Development of Cash Budgets, Negotiation, & Revision

Development of Cash Budgets, Negotiation, & Revision: Operating & capital budgets developed; then the cash budget. -Capital= excess items; defined by org. in $'s spent; 1-time expenditure= high cost items. Usually non-recurring (so not leased items). -Operating= cost of running business on day-to-day basis; ex. supplies, salaries, equipment, supplies, utilities, contracts for equipment, housekeeping contract, plumbing, etc. -Cash budget= developed after operating & capital budgets of unit or dept. developed; unit manager's negotiating & revising skills used. --Cash budget usually prepared by CFO; plan for actual anticipated cash receipts & disbursements of the org= the cash flow. --Org. must have sufficient cash to meet monthly obligations= the cash on hand. --Ideally, the RN manager must be able to predict when budgeted items needed. Unexpected expenditures occur & may put strain on a cash-poor system.

Disaster Prep & Evacuation

Disaster Prep & Evacuation: -Maintain disaster prep→ hospital staff participate in ER training & drills regularly. TJC mandates hospitals have ER prep plan that is tested w/ drills or participation in real event 2x/yr+. 1 of drills or events must involve community resources & influx of actual or SIM pts to assess ability of collab. efforts & command structures. --Accredited HC orgs. required to take "all-hazards approach" to disaster planning= prep activities must address all credible threats to safety of community that could result in disaster. -RN homes & LTC also mandated annual drills to prep for mass casualty events; agencies, HHC, & group homes, part of response plan must include method for evacuation from facility in timely & safe manner in disaster. --Evacuation plan: part of fire prevention & prep plans for HC facilities. Life Safety Code provides guidelines for bldg construction, design, maintenance, & evacuation. Medicare & Medicaid requires all HC facilities to practice 1 fire drill or actual response 1x/yr+. Pt evacuation not required if it's a drill. All staff mandated to have training in fire prevention & responsiveness each yr.

Drugs for VF

Drugs for VF: -Class I antidysrhythmics: are membrane-stabilizing agents used to decrease automaticity; 3 subclassifications: --Type IA drugs: moderately slow conduction & prolong repolarization, prolonging the QT interval. Tx or prevent supraventricular & ventricular premature beats & tachydysrhythmias, but not as commonly used as other drugs. Ex. procainamide hydrochloride. --Type IB drugs: shorten repolarization; Tx or prevent ventricular premature beats, VT, & VF. Ex. lidocaine & mexiletine hydrochloride. --Type IC drugs: markedly slow conduction & widen the QRS complex; used primarily to tx or prevent recurrent, life-threatening ventricular premature beats, VT, & VF. Ex. flecainide acetate & propafenone hydrochloride. -Class II antidysrhythmics: control dysrhythmias associated w/ excessive beta-adrenergic stimulation by competing for receptor sites→ decreasing HR & conduction velocity. --Beta-adrenergic blocking agents; ex. propranolol & esmolol hydrochloride. Tx or prevent supraventricular & ventricular premature beats & tachydysrhythmias. --Sotalol hydrochloride is an antidysrhythmic agent w/ both noncardioselective beta-adrenergic blocking effects (class II) & action potential duration prolongation properties (class III). An oral agent that may be used for tx of documented ventricular dysrhythmias [ex. VT], that are life threatening. -Class III antidysrhythmics: lengthen the absolute refractory period & prolong repolarization & action potential duration of ischemic cells. Ex. amiodarone & ibutilide; tx or prevent ventricular premature beats, VT, & VF. -Class IV antidysrhythmics: slow the flow of Ca+→ cell during depolarization→ depressing the automaticity of SA & AV nodes, decreasing HR, & prolonging AV nodal refractory period & conduction. --Ca channel blockers; ex. verapamil hydrochloride & diltiazem hydrochloride; tx SVT & AF to slow the ventricular response. -Mg sulfate is admin to tx refractory VT or VF bc they may be hypomagnesemic, w/ increased ventricular irritability. Also used for a life-threatening VT called torsades de pointes; can result from certain antidysrhythmics like amiodarone.

ECG & Lead Systems

ECG & Lead Systems: § Lead systems= + & - pole. Lead axis= imaginary line joining 2 poles. Cardiac axis= the direction of electrical current flow in the heart. § Relationship of cardiac axis & lead axis is responsible for deflections seen on ECG pattern: o Baseline= isoelectric line; occurs when there is no current flow in the heart after complete depolarization & also after complete repolarization. + deflections occur above this line, & - deflections occur below it. Deflections= depolarization & repolarization of cells. o Direction of electrical current flow in heart (cardiac axis) is toward the + pole→ see a + deflection (above baseline). o Direction of electrical current flow in the heart (cardiac axis) is moving away from the + pole toward the - pole→ see a - deflection (below baseline). o Cardiac axis is moving neither toward or away from the + pole→ see a biphasic complex (both above & below baseline). -ECG strip: each small block= 1mm Ht&W; recorders & monitors are std. at 25 mm/s. ---Time measured on horizontally; each sm block= 0.04s; 5 sm blocks= 1 lg block→ darker bold lines= 0.20s; 5 lg blocks= 1s; 30 lg blocks= 6s. Vertical lines on top margin of graph→ usually 15 lg blocks apart= 3s segments. --Waveforms measured in amplitude (voltage) & duration (time). Each segment between dark lines (above the strip) represents 3s when monitor set at speed of 25 mm/sec. To est. ventricular rate, count QRS complexes in a 6s strip x 10 to est. rate/1min.

ECG Rhythm Analysis (8 Steps)

ECG Rhythm Analysis: 1.) Determine HR. 2.) Determine heart rhythm. Assess for atrial &/or ventricular regularity. Rhythms can be regular or irregular. Irregular rhythms= regularly irregular, occasionally irregular, or irregularly irregular. Slight irregularity in the PP intervals, varying no more than 3 small blocks= essentially regular if P waves are all same shape. Alteration is caused by changes in intrathoracic pressure during the respiratory cycle. -QRS of different shapes (ectopic QRS complexes) [if present], create an irregularity & do not walk out w/ the other QRS complexes. Slight irregularity of no > 3 small blocks between intervals= essentially regular if the QRS complexes are all same shape. 3.) Analyze P waves. Check P-wave shape; is it consistent throughout strip= atrial depolarization occurring from impulses originating in 1 focus; normally SA node. ID if 1 P wave before each QRS complex; estab. relationship exists between P wave & QRS→ indicates impulse from 1 focus responsible for A&V depolarization. 4.) Measure PR interval. Place 1 caliper point at the beginning of the P wave & other point at the end of PR segment. PR interval normally measures 0.12-0.20s; measurement should be constant throughout strip. PR interval cannot be ID if there are no P waves or if P waves occur after QRS complex. 5.) Measure QRS duration. Place 1 caliper point at beginning of QRS complex & other at J point, where the QRS complex ends & ST segment begins. QRS duration normally measures 0.06-0.10s; measurement should be constant throughout the entire strip. -QRS narrow (0.10s or less)= impulse was not formed in the ventricles→ supraventricular or above the ventricles. -QRS wide (>0.10s)= impulse is of ventricular or SV origin w/ aberrant conduction [deviating from normal course or pattern]. 6.) Examine ST segment. Normal ST segment begins at the isoelectric line. ST elevation or depression is significant if displacement is >1 mm (1 small box) above or below the line & is seen in >2 leads. --ST elevation→ problems such as MI, pericarditis, & hyperkalemia. ST depression→ hypokalemia, MI, or ventricular hypertrophy. 7.) Assess T wave. Note shape & height of T wave for peaking or inversion. Abnormal T waves= problems such as MI & ventricular hypertrophy. 8.) Measure QT interval. Normal QT interval should be equal to or less than 1/2 the distance of the RR interval.

ED RN Roles & Responsibilities

ED RN Roles & Responsibilities: ED RN one of large IP team that provides care in ED; team approach to ED care using teamwork & collaboration is std. of practice. RN coordinates care w/ all HC team, from pre-hospital EMS to physicians & other providers, techs, & support staff. -ED RN interacts w/ staff, HCP specialists, & community HCPs involved in pt care, but in closest collab. w/ emergency medicine physicians→ directs overall care in ED. EDs also employ NPs & PAs to for roles in assessment & tx. Teaching hospitals have resident physicians who train in ED; in collab. or under supervision of emergency medicine physician to assist w/ care. --ED RN is accountable for communication w/ support staff of pertinent staff considerations, pt needs, & restrictions (physical limits, safety concerns, Transmission Precautions) to ensure that ongoing safety issues are addressed. -Providing concise but comprehensive report of pts ED experience is essential for hand-off communication process & pt safety. -Info includes the pts: Situation (reason for being in ED) & admit Dx; Pertinent medical Hx, + implantable devices & organ transplant Hx; Assessment & Dx findings, esp. critical results; Transmission Precautions & safety concerns (fall risk, allergies) as indicated; Txs provided in ED & response to txs. -Many use SBAR method (situation, background, assessment, response) or variation to ensure complete & clearly understood communication. -NPSG: TJC advocates hospitals & HC agencies use a std. approach to hand-offs to prevent errors caused by poor or inadequate communication.

ET Intubation

ET Intubation: Know how to contact intubation personnel in an emergency; explain procedure to the pt clearly. --Ensure each intubation attempt lasts no >30s [preferably <15s]; after 30s, provide O2 via mask & manual resuscitation bag to prevent hypoxia & cardiac arrest; suction PRN. --BLS measures, like obtaining patent airway & delivering 100% O2 by a manual resuscitation bag w/ a facemask, are crucial to survival until help arrives. --Critical Rescue: monitor pts at risk for airway obstruction & impaired ventilation. ID need for emergency intubation & ventilation→ bring code ("crash") cart, airway equipment box, & suction equipment (often on cart) to bedside. Maintain patent airway w/ positioning (head-tilt, chin-lift) & insertion of an OPA or NPA until intubated. Delivering manual breaths w/ a BVM may be required. --During intubation, RN coordinates the rescue response & continuously monitors for VS changes, s/s hypoxia or hypoxemia, dysrhythmias, & aspiration. --HCP tube placement, verification &, tube stabilization; RN, RT, or anesthesia provider stabilizes ETT at the mouth or nose; tube is marked where it touches the incisor tooth or naris. --After completion, verify & document the presence of bilateral & equal breath sounds & tube level. --Cuff at distal end is inflated after placement, creates a seal between trachea & tube; ensures delivery of set tidal vL for MV. Inflated w/minimal-leak technique; when inflated to an adequate sealing vL, a minimal amount of air can pass around it to the vocal cords, nose, or mouth; they cannot talk when cuff is inflated. --Pilot balloon w/ 1-way valve permits air insertion into cuff & prevents air from escaping. Balloon is a guide for ID if air is in cuff; it does not show how much or how little is present; it does not indicate how much pressure is exerted on trachea from cuff balloon.

Emergency Care of the Patient With an Extremity Fracture

Emergency Care Extremity Fracture: -Assess ABCs; estab. any ABC affected by injury. -Perform quick H-to-T assessment. -Remove pts clothing (cut if necessary) to inspect affected area while supporting area above & below injury. Do not remove shoes bc can cause increased trauma unless foot or ankle is injured. -Apply direct pressure on area if bleeding & pressure over proximal artery nearest to fracture. -Remove jewelry on affected extremity in case of swelling. -Keep warm & in supine position. -Check NV status of area distal to fracture, + temp., color, sensation, movement, & cap-refill. Compare affected & unaffected limbs. Immobilize extremity by splinting; + joints above & below fracture site. Recheck circulation after splinting. -Cover any open areas w/ dressing (preferably sterile).

Emergency Care of Chest Discomfort:

Emergency Care of Chest Discomfort: Emergency Care of Chest Discomfort: -Assess ABCs. Defibrillate as needed. Provide continuous ECG monitoring. Obtain pts description of pain or discomfort. Obtain VS (BP, HR, RR). -Assess/provide vascular access. Consult chest pain protocol or notify HCP or RRT for specific tx. Obtain 12-lead ECG w/in 10min of report of chest pain. -Provide pain meds & aspirin (non-enteric coated) as prescribed. Admin O2-tx to maintain SpO2 >90%. Remain calm. Stay w/ pt if possible. -Assess VS & pain intensity 5min after med admin. Remedicate w/ prescribed drugs (if VS remain stable) & check pt Q5min. Notify HCP if VS deteriorate.

Emergency Care of Heat Stroke

Emergency Care of Heat Stroke: Restoring Thermoregulation -At the Scene: Ensure patent airway. Remove from hot environment (into air-conditioning or shade). Contact EMS to transport to ED. --Remove clothing. Pour or spray cold water on body & scalp. Fan pt (all surrounding people should fan pt w/ newspapers or whatever is available). --If available, place ice in cloth or bags & position packs on scalp, groin area, behind neck, & in armpits. --If immediate immersion in cold water is possible, support pt in water for rapid cooling & protect airway= best method to tx heat stroke. -At the Hospital: Give O2 by mask or NC; be prepared for ET intubation. Start 1+ IVs w/ large-bore needle or cannula. Admin fluids as prescribed, using cooled solutions if available (0.9% NS). Use cooling blanket or cool water; prevent shivering by avoiding ice water. --Obtain baseline labs as quickly as possible: urinalysis, serum electrolytes, cardiac enzymes, liver enzymes, & CBC. --Do not admin aspirin or antipyretics. Insert rectal probe to measure core temp. continuously or use rectal thermometer & assess temp. Q15min. --Insert an indwelling urinary cath. Monitor VS frequently as indicated. Assess ABGs. --Admin muscle relaxants or benzos (Diazepam) as prescribed if begin shivering. Measure & monitor UO & SG to ID fluid needs. Stop cooling txs when core temp. reduced to 102°F (39°C).

Emergency Preparedness & Response

Emergency Preparedness & Response: -ER management: actions or steps to decrease potential loss during disaster, & involves mitigation, prep, response, & recovery. --Mitigation: preplanning for disaster, analyzing potential risk & loss, & putting processes in place to minimize impact. --Preparedness: active steps to prep to handle emergency. --Response: actions to rescue and care for pts affected by disaster. --Recovery: steps taken to return to normal after event. -Protocols for Disasters: Before going to incident in field, all of IP team must have adequate training to prep to ID risks in an unstable environment. Risks= structural collapse, secondary target of terrorist attack, interpersonal violence in unsecured locales, & contagious dz & natural hazards (snake bites, mosquito illnesses). Disaster workers must take measures like obtaining prophylactic meds & vax, personal evacuation plan, & ensuring access to supplies & protective equipment so they do not become victims. -In triage area of hospital→ receive special bracelet w/ disaster #. Preprinted labels w/ # can be applied to chart forms & personal belongings. Digital pics used as part of ID process in some systems. Std. hospital registration & ID band applied after ID confirmed.

Emergency care of PE Hypoxemia

Emergency care of PE Hypoxemia: -Managing hypoxemia: sudden onset of dyspnea & chest pain, or other s/s of respiratory impairment, immediately initiate the RRT. Apply O2, reassure pt, & elevate HOB. Prep for ABG analysis while continuing to monitor & assess for other changes. -Management of PE: --Apply O2 by NC or mask. Reassure pt that correct measures being taken. Place in high-Fowlers. --Apply telemetry equipment. Obtain venous access. Assess oxygenation continuously w/ pulseOx. --Assess respiratory status at least Q30min by: Listening to lung sounds; Measuring RR, rhythm, & ease of respirations; Checking skin color & cap-refill; Checking position of trachea. --Assess cardiac status by: Comparing BP in right and left arms; Checking pulse quality; Checking cardiac monitor for dysrhythmias; Checking for distention of neck veins. --Ensure prescribed chest imaging & lab tests obtained immediately (may include CBC w/ differential, platelet count, PT, PTT, D-dimer level, ABGs). --Examine chest for presence of petechiae. Give prescribed anticoagulants. Assess for bleeding. Handle pt gently. Institute Bleeding Precautions.

Emergent care priorities of Burns

Emergent care priorities of Burns: -Still ABCs: Airway, then Circulation & Perfusion -Maintain body temp bc lost function of skin. -Comfort: pain big issue, unless it's a 4th degree where nerve endings burned. -Provide emotional support. -Pre-burn (dry= baseline) wt used to calculate fluid rates & drug admin -BSA (ht & wt): ID extent of burn via Rule of 9's. -Health Hx: MOI; smoke INH. Ask what pt was doing when burn occurred, time & place where it happened, & source & cause of injury; how burn occurred & events from time of injury until help arrived. Obtain age, wt, & ht, & full health Hx (+ pre-existing medical hx, alcohol or drug use, & Hx of other injuries). --Obtain list of allergies, current meds, & vax. Ask if other events occured at time of burn [fall], could indicate other injuries present. Remember rate of complications from burns is increased in elderly bc of age-related physiologic changes. -Fluid Therapy; Severity of Burn is a factor: 15-20% TBSA require fluids. Crystalloids (0.9% NS, Lactated Ringers, D5W). Colloids (albumin, dextran, FFP, hespan). --Parkland Formula for fluid replacement: 4mL/kg/% TBSA burned= Total fluid requirement for 1st 24hrs. 1/2 of Total in 1st 8 hrs from the TIME of INJURY, not from time of resucitation. 1/2 of total over the next 16hrs. Monitor UO!

Employee Assistance Programs

Employee Assistance Programs: All issues dealt w/ in this ch. may be supported by use of employee assistance programs (EAPs). Majority of HC employers in US have created EAPs. -EAP is confidential, ST counseling service for employees w/ personal problems that affect work performance. EAPs grew out of industrial alcoholism programs of 1940s. -EAPs should be part of larger company plan to promote wellness that involves written policies, supervisor & employee training, & an approved drug testing program. -Programs allow employees to confidentially deal w/ concerns that may be causing problems in personal or professional life. -As RN manager you may refer staff to this program; ex. of employee issue is continual patterns of lateness &/or attendance; More serious issues may be for drug or alcohol abuse. -Referral can also be a self-referral. EAPs always protect the employee's privacy, & assist in getting help they need w/o fear of break of confidentiality. Family may also use EAP in some orgs. Exact steps for referral process should be in hospital's policy & procedure manual. -EAP services provide counseling to employees & families in attempt to help employee & their family return to a functional unit; may provide assistance in dealing w/ these issues: Personal issues; Job stress; Relationship issues; Eldercare, childcare, parenting issues; Harassment. Substance abuse; Separation & loss; Balancing work and family; Financial or legal; Family violence. -Some EAP providers also able to offer other services, + retirement or layoff assistance & wellness/health promotion & fitness (wt control, nutrition, exercise, or smoking). -Others may offer advice on LT illnesses, disability issues, counseling for crisis situations (death at work), or advice for managers/supervisors in dealing w/ difficult situations.

Etiology & Genetic Risk for ACS

Etiology & Genetic Risk for ACS: -Atherosclerosis= primary factor in development of CAD. Numerous risk factors, nonmodifiable & modifiable, contribute to atherosclerosis & subsequently to CAD. -Nonmodifiable (uncontrollable) risks: age, gender, ethnicity, family hx CVD; chronic dz or illness. African-American & Hispanic women increased risk CAD; American Indians & Alaska natives have 46.7% more CAD risk factors. --Men= higher CAD risk than women of all ages; CAD risk factors similar for both, but women have several gender-specific risks, (ex. disorders of pregnancy & menopause). -Modifiable (controllable) risks: lifestyle habits; ex. cigarettes, physical inactivity, obesity, & psyc variables; cholesterol, HTN, DM, excessive alcohol, stress.CVD= leading cause of DM-related death; DM Adults have CVD death rates 2-4x higher. Stroke risk 2-4x higher w/ DM. -Metabolic syndrome: AKA insulin resistance synd. or synd. X; risk factor for CVD. Pts w/ 3 of factors→ Dx w/ metabolic synd.; increases risk for DM & CAD. --Central obesity, high BP, & hyperglycemia when Dx w/ metabolic syndrome→ highest risk for CVD. Females have higher prevalence of metabolic syndrome, & prevalence increases w/ age. --Incidence of metabolic synd. continues to increase. Management aimed at reducing risks, managing HTN, & preventing complications. -Indicators of Risk Factors for Metabolic Synd.: --HTN: Either BP 130/85+ or taking anti-HTN drug(s). --Decreased HDL-C (usually w/ high LDL-C): Either HDL-C <40 mg/dL for men or <50 mg/dL for women; or taking anti-cholesterol drug. --Increased triglycerides: Either 150 mg/dL+ or taking anti-cholesterol drug. --Increased FBS (caused by DM, glucose intolerance, or insulin resistance): Either 100 mg/dL+ or taking anti-DM drug(s). --Lg. waist size (excessive ABD fat→ central obesity): 40in+ (102cm) for men or 35in+ (88cm) for women.

Etiology of Dysrhythmias

Etiology of Dysrhythmias: occur for many reasons; ex. MI, electrolyte imbalances (esp. K & Mg), hypoxia, drug toxicity, & hypovolemia. --Pt use cocaine & illicit INH→ particularly at risk for potentially fatal dysrhythmias. --Stress, fear, anxiety, & caffeine→ increased HR (tachycardia or PVC). --Nicotine & alcohol excess→ abnormal HR or rhythm (A-Fib). Best Practice for Pt Safety & Quality Care: Care of the Pt w/ Dysrhythmias -Assess VS at least Q4h & PRN. Monitor for cardiac dysrhythmias. Evaluate & document response to dysrhythmias. -Encourage to notify RN when chest pain occurs. Assess chest pain→ location, intensity, duration, radiation, precipitating & alleviating factors. -Assess peripheral circulation→ palpate for presence of peripheral pulses, edema, cap-refill, color, temp. of extremity). -Provide antidysrhythmic tx according to unit policy, as appropriate; antidysrhythmic meds, cardioversion, defibrillation. -Monitor & document response to antidysrhythmic meds or tx. Monitor appropriate labs; cardiac enzymes, electrolyte levels. Monitor activity tolerance & schedule exercise/rest periods to avoid fatigue. Observe for respiratory difficulty→ SOB, rapid breathing, labored respirations. -Promote stress reduction. Offer spiritual support to pt &/or family, as appropriate; contact clergy.

Evaluation of Budget; variance analysis

Evaluation of Budget: occurs at org. & unit levels. Many orgs. have created dashboards that allow for monitoring of progress in meeting dept. goals= provide quick visual display of unit's performance. -Evaluation of budget performance obtained via variance analysis= difference between planned & actual costs. --Positive variance (favorable): budgeted amount was greater than actually spent. --Negative variance: budgeted amount was less than actual spending. -Variance analysis: complex process, unit environment is fully investigated; characterized in 4 ways. --vL variance: in hospital may occur in response to fluctuating in-pt days. --Efficiency variance: changes from anticipated hrs per pt day (HPPD). --Rate variances: difference between budgeted hourly rate of pay & actual rate paid. --Non-salary expenditure variance: caused by changes in pt mix, supply quantities & costs, & price paid. Negative variance may be seen in # of staff required during 2-wk period; but on further investigation, it may be ID that pt acuity was higher than anticipated, & expenses increased in response to increased acuity. -Ex. of variable costs in unit budgets: -Increased OT r/t greater-than-anticipated use of sick time. Increased use of part-timers r/t unanticipated increase in pt acuity. Increased expense for minor equipment bc of electrical malfunction that destroyed equipment. Increased expenses caused by staff resignation & orientation of replacement staff. -RN manager role: be aware of variances r/t unit & reasons for alt. in expected performance; & use data in prep of next yrs budget. -Many HC orgs. have flexible budgets that automatically adjust to environmental changes. -Goal is to proactively anticipate challenges via collection of info in environmental assessment. Ex. proactive budgeting is budgeting of increased staff during flu season. -Most orgs. provide RN manager w/ fiscal reports on routine basis (weekly, monthly, or quarterly per org); allows each cost center manager to carefully monitor $ activity of unit. -Budget process continually evolving work, requiring evaluation & continual improvement.

Event Resolution & Debriefing

Event Resolution & Debriefing: Last major casualties have been tx & no more expected to in #s that could overwhelm HC system, the incident commander considers "standing down" or deactivating ER response plan. Casualties may have left the ED, other areas in hospital may still be under stress & need resources of ER plan activation. Before terminating response, must ensure needs of hospital depts. met & all in agreement to resume normal ops. -Vital in event resolution to ID if staff & supply can meet ongoing needs. If RN staff & other personnel were called in from home during off hrs or if worked well beyond scheduled shifts, provision for rest periods should be made. Exhaustion poses risk to pt safety & to RNs when driving home. Sleeping quarters at hospital might be necessary, esp. if disaster contributed to treacherous travel conditions. -Severe shortages of supplies pose threat to ops. Taking inventory & restocking ED are high-priorities after disaster or mass casualties. Teamwork & collaboration between ED & central supply dept. are essential to resolving stock problems. Instrument trays must be washed, packaged, & re-sterilized. Contracts w/ key vendors outlining ER resupply expectations & arrangements are part of hospital's ER prep plan so service can be quick after event.

Extubation of an ETT

Extubation: removal of the ETT; removed when intubation need has resolved. -Before removal, explain the procedure. Set up prescribed O2 delivery system at bedside & bring in the equipment for emergency reintubation. Hyperoxygenate & thoroughly suction ETT & oral cavity. -Removal: Instruct pt to inhale deeply, then rapidly deflate the ETT cuff & remove tube during exhalation. Instruct pt to immediately cough; normal for large amounts of oral secretions to collect. -Afterwards: Continue O2 by FM or NC; FiO2 usually 10% higher than level used while ETT was in place. -Monitor VS after extubation Q5min at first & assess ventilatory pattern for s/s of respiratory distress. --Common to be hoarse & have sore throat for a few days after extubation. --Teach to sit in semi-Fowlers, take DBs Q30min, use IS Q2hrs, & limit speaking; measures help improve gas exchange, decrease laryngeal edema, & reduce vocal cord irritation. --Observe closely for respiratory fatigue & airway obstruction. -Early s/s of obstruction= mild dyspnea, coughing, & inability to expectorate secretions. Stridor= high-pitched, crowing during inspiration r/t laryngospasm or edema around glottis; late s/s of narrowed airway & requires prompt attention. Racemic epinephrine [topical aerosol vasoconstrictor] is given, & reintubation may be needed. --Critical Rescue: monitor frequently to ID s/s obstruction. When stridor or other s/s of obstruction occur after extubation, respond by immediately initiating RRT before airway is completely obstructed.

Fat Embolism Versus Blood Clot (Pulmonary) Embolism

Fat Embolism Versus Blood Clot (Pulmonary) Embolism: serious fracture complication; fat globules released from yellow BM into bloodstream w/in 12-48hrs after injury. Globules clog sm BVs supplying vital organs, [common= lungs], & impair organ perfusion. Usually results from fractures or fracture repair; less often, in pancreatitis, osteomyelitis, blunt trauma, or SCD. -Earliest s/s FES= low PaO2 (hypoxemia), dyspnea, & tachypnea. -Fat Embolism: Obstruction of pulmonary (or other organ) vascular bed by fat globules. --Origin: Most from fractures of long bones; occurs usually w/in 48hr of injury. --S/S: Altered MS (earliest sign); Increased RR, pulse, temp.; CP; Dyspnea; Crackles; Decreased SaO2; Petechiae (not in all pts); Mild thrombocytopenia. --Tx: Bedrest; Gentle handling; O2; Hydration (IV fluids); Possibly steroid tx; Fracture immobilization. -Blood Clot Embolism: Obstruction of PA by a blood clot[s]. --Origin: Most from DVT in legs or pelvis; can occur anytime. --S/S: Same as fat embolism, except no petechiae. --Tx: Preventive measures (leg exercises, antiembolism stockings, SCDs); Bedrest; O2; Possibly MV; Anticoags; Thrombolytics. Possible surgery: pulmonary embolectomy, vena cava umbrella.

Fracture

Fracture: break or disruption in bone continuity; often affects mobility & causes pain; can occur anywhere in body & at any age. All fractures have same basic patho mechanism & require similar pt-centered, IP collab. care, regardless of type or location. -Classification of Fractures: by extent -Complete fracture: across the entire width of bone in such a way that the bone is divided into two distinct sections. If bone alignment is altered or disrupted, the fracture is also referred to as a displaced fracture. The ends of bone sections of a displaced fracture are more likely to damage surrounding nerves, blood vessels, and other soft tissues. --Displaced fracture: bone alignment is altered or disrupted; ends of bone sections of a displaced fracture more likely to damage surrounding nerves, BVs, & soft tissues. -Incomplete fracture: does not divide bone into 2 portions bc break is through only part of bone; not typically displaced. -By extent of soft-tissue damage: -Compound fracture: skin surface over broken bone is disrupted; causes an external wound. Often graded to ID extent of tissue damage. -Simple fracture: does not extend through skin; no visible wound. -By their cause: -Fragility fracture (AKA pathologic or spontaneous fracture) occurs after minimal trauma to bone bc weakened by dz; ex. bone cancer or osteoporosis. -Fatigue (stress) fracture: from excessive strain & stress on bone; common in athletes. -Compression fractures: loading force applied to long axis of cancellous bone; common in vertebrae of elderly w/ osteoporosis; extremely painful.

GCS Scoring

GCS Scoring: range 3-15; 3= comatose; 15= normal/AO x 3; 8 or lower= prep for ET intubation & MV. -Eye response (E): 1. No eye opening. 2. Eye opening in response to pain (a peripheral pain stimulus, ex. squeezing lunula area of fingernail is more effective vs central stimulus, ex. trapezius squeeze, due to grimacing effect). 3. Eye opening to speech (not to be confused w/ awakening of sleeping person; such pts get score of 4, not 3). 4. Eyes opening spontaneously. -Verbal response (V): 1. No verbal response. 2. Incomprehensible sounds (moaning but no words). 3. Inappropriate words (random or exclamatory articulated speech, but no conversational exchange). 4. Confused (pt responds to questions coherently but w/ some disorientation & confusion). 5. Oriented (pt responds coherently & appropriately to questions like pts name & age, where they are & why, the yr, mo). -Motor response (M): 1. No motor response. 2. Extension to pain (extensor posturing: abduction of arm, external rotation of shoulder, supination of forearm, extension of wrist, decerebrate response). 3. Abnormal flexion to pain (flexor posturing: adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist, decorticate response). 4. Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied; pulls part of body away when nailbed pinched). 5. Localizes to pain (Purposeful movements towards painful stimuli; ex. hand crosses mid-line & gets above clavicle when supra-orbital pressure applied). 6. Obeys commands (pt does simple things as asked, ex. stick out tongue or move toes).

GCS

GCS: ex. of std. rapid neuro assessment tool. Used in acute care settings to estab. baseline data in each area: eye opening, motor response, verbal response; assigned a # score for each. The lower the score, the lower the neurologic function. If intubated & cannot talk, record score w/ "t" after the # for verbal response. -May respond to painful stimuli in several ways. Initial response to pain may be abnormal flexion or extension, continued application of pain for no >20-30s may show pt can localize or withdraw. If pt does not respond after 20-30s, stop applying painful stimulus. --Critical Rescue: decrease of 2+ in GCS total is significant & should be reported to PHCP immediately. Other findings requiring urgent communication w/ PHCP= new finding of abnormal flexion or extension, esp. of UE (decerebrate or decorticate); pinpoint or dilated nonreactive pupils; & sudden or subtle changes in MS. Change in LOC= earliest s/s of neuro deterioration! Communicate early ID of neuro changes to RRT or PHCP for best opportunity to prevent complications & preserve CNS function. -Decortication= abnormal motor movement seen in w/ lesions that interrupt corticospinal pathways; arms, wrists, & fingers flexed w/ internal rotation & plantar flexion of legs. -Decerebration= abnormal movement w/ rigidity; extension of arms & legs, pronation of arms, plantar flexion, & opisthotonos (spasm; body is bowed forward). Usually associated w/ dysfunction in brainstem area.

Gender Considerations for women w/ MI's

Gender Considerations for women w/ MI's: Many women w/ symptomatic ischemic heart dz or abnormal stress test do not have abnormal coronary angiography. -Studies implicate microvascular dz &/or endothelial dysfunction as causes for CAD risk in women. -Endothelial dysfunction is inability of arteries & arterioles to dilate due to lack of nitric oxide production by endothelium. -Nitric oxide is relaxant of vascular smooth muscle. -Women typically have smaller coronary arteries & frequently have plaque that breaks off & travels into small BVs to form embolus. -Positive remodeling, or outward remodeling (lesions protrude outward), may occur; outpouching may be missed on coronary angiography. -S/S: women frequently present w/ CAD differently vs men. Assess for nonspecific CV s/s; fatigue, malaise, anxiety, & SOB. CVD remains leading COD in women in US. -Risk Factors: most important risk for CAD in women is age. Older age→ more likely to have dz. Compared w/ men, women usually 10yrs older when have CAD. Only 56% women aware heart dz is leading COD in women, & fewer can ID s/s heart attack. Women w/ MIs have greater risk for dying. More women die w/in 1yr after MI. Female Survivors→ more develop complications [HF or stroke]; less likely to do cardiac rehabs. --Premenopausal have lower incidence of MI vs men; postmenopausal in 70s+, 2-3x increase in CAD; incidence= men. Family hx also risk factor; if parents had CAD→ more susceptible. Women w/ ABD obesity (androidal shape) & metabolic synd. also increased risk for CAD. Studies limited, but indicates LGBT adults have increased risk of CVD r/t increased incidence of modifiable risks; ex. smoking, alcohol, & drugs. --Many women of any age experience atypical angina; indigestion, pain between shoulders, aching jaw, or choking occurs w/ exertion. Other s/s→ unusual fatigue, SOB, dizziness, palpitations, generalized anxiety or weakness & flulike s/s. S/S typically w/ stressful circumstances or ADLs; may curtail activity bc angina, & HCP need to ask about changes in routine. S/S in women typically include chest discomfort, unusual fatigue, & dyspnea.

Guillain-Barré syndrome (GBS)

Guillain-Barré syndrome (GBS): Common Cause of Ventilatory Failure; rare acute inflammatory ds that affects axons &/or myelin of PNS resulting in ascending muscle weakness or paralysis. Priority= respiratory support; ex. ET & MV 10-14 days, if longer TT. LT Goal= prevent muscle atrophy. -Acute, rapidly progressing, & potentially fatal form of polyneuritis; affects PNS & results in loss of myelin & edema & inflammation of affected nerves, causing loss of neurotransmission to periphery. Believed to be cell-mediated immune rx directed at peripheral nerves; preceded by immune stimulation from viral infection, trauma, OP, viral vax, HIV, or lymphoproliferative neoplasms. -Usually preceded by respiratory or GI infection 1-4wks prior to onset of neuro deficits. -Pts w/ acute SCI or ascending GBS assessed Q1h until stable & then Q4h. As condition improves, neuro assessment may be needed only 1x/shift. Findings documented per agency protocol. -If GBS does not improve, respiratory failure may result in death. -Assess: DTR's; Hyporeflexia of LEs is classic s/s, paralysis ascends up LEs. Dx based on Hx & s/s; test CSF via LP= CSF normal or low protein initially, after 7-10 days elevated to 700 mg/dl (normal= 15-45) w/ normal cell count. --RN must monitor ascending paralysis; respiratory function; ABGs; gag, corneal, & swallowing reflexes during routine assessment. Reflexes usually decreased or absent. -Communication: system is estab. using available abilities; peak of severe episode= may be incapable of comunicating. RN explains all tcs before doing; reasure pt muscle function will return. -If ventilator malfunctions→ Acute Resp. Distress (SOB); RN must 1st ventilate w/ manual resuscitation bag until problem resolved. Next, notify other depts. (RT), then request labs (ABGs). Afterwards, lungs may assessed (sounds). -Improving: paralysis stops & descends; wean from MV bc resp. muscles not paralyzed. --Full recovery usually occurs w/in several mo to 1yr after s/s onset. --RN provides support & encouragement to family & pt. Residual problems & relapses uncommon except in chronic form of GBS, so complete recovery is anticipated; but slow process, takes months or yrs if axonal degeneration occurs. --Can breathe w/o MV & keeps improving→ rehab unit; refer to PT ASAP for gait training, muscle building, & transfer techs→ promote early D/C & reduce risk of injury.

Hazards & Complications of O2 Tx: O2 Toxicity

Hazards & Complications of O2 Tx: O2 Toxicity: rt the concentration delivered, tx duration, & degree of lung disease. Continuous O2 tx >50% for >24-48hrs, can injure lung & reduce tissue integrity. -Excessive tissue O2 levels increase the concentration of reactive O2 species (ROS: O2 free radical; damaging substances) which can combine w/ cellular elements & induce oxidative stress, causing cell damage & cell death. -Lung injury from O2 toxicity: causes & indications same as ARDS. --S/S start w/ dyspnea, nonproductive cough, chest pain beneath the sternum, GI upset, & crackles on auscultation. --As exposure to high levels of O2 continues, problems become more severe, w/ decreased vital capacity, decreased compliance, & hypoxemia. --Continued prolonged exposure leads to atelectasis, pulmonary edema [hemoptysis], hemorrhage, & hyaline membrane formation. --Surviving O2 toxicity depends on correcting the underlying disease process & decreasing the O2 amount delivered. -RN: toxic effects difficult to manage; prevention is key. Lowest level of O2 needed to maintain gas exchange & prevent toxicity is ordered. Monitor ABGs & notify the HCP when PaO2 is >90mmHg. Monitor the ordered O2 level & length of tx to ID patients at risk. --Use of noninvasive positive airway pressure techniques w/ O2 or use of MV may reduce the amount of O2 needed. --As soon as their condition allows, the ordered O2 amount is decreased.

Heart Blocks

Heart Blocks: o First-degree: prolonged pr >0.20 sec. If the R is far from the P, then it must be First Degree. o 2nd-degree Mobitz I (aka Wencheback); gradual prolongated PR until you drop a QRS & it startsall over again. If PR gets longer (longer, longer) then a QRS drop, then it must be a Type I Wenckebach. o 2nd degree Mobitz II; consistent PR, then a drop. If some of the P's don't get through, then you have Mobitz II. o 3rd degree (aka Complete HB) P's & Q's don't agree; A's & V's all doing their own thing. Ventricles run at a different rate (20-40) when not getting atrial impulse, it can only do its own inherent rate. If the P's & Q's don't agree, then you have a 3rd degree. --Remember: 3rd degree's need pacemaker= external PM, then internal when can get them into cath lab (no drugs will fix it).

Heart Failure & BNP

Heart Failure: AKA pump failure; general term for inability of heart to work effectively as pump. Results from acute & chronic CV problems. -Common chronic health problem, w/ acute episodes often causing hospitalization. Acute coronary dz & other structural or functional problems of heart can lead to acute HF. Acute & chronic HF can be life threatening if not tx adequately or if not responding to tx. -Major types: Lt-sided, Rt-sided, & High-output failure. Most HF begins w/ LV failure & progresses to failure of both V's. -Lt-HF (ventricular) causes: HTN, CAD, & valvular dz. Decreased tissue perfusion from poor CO & pulmonary congestion from increased pressure in pulmonary BVs= left ventricular failure (LVF). Formerly called CHF; but not all cases of LVF involve fluid accumulation. -Rt-HF (ventricular) causes: LV failure, RV MI, or pulmonary HTN. RV cannot empty completely. Increased vL & pressure in venous system, & peripheral edema results. -High-output HF Causes: increased metabolic needs or hyperkinetic conditions, like septicemia, high fever, anemia, & hyperthyroidism. CO remains normal or above normal; unlike Lt & Rt HF, which are typically low-output. . This HF type is not as common as other types. -Natriuretic peptides: neurohormones that promote vasodilation and diuresis via Na loss in renal tubules. --B-type natriuretic peptide (BNP; brain natriuretic peptide): produced & released by V's as they stretch in response to fluid overload from HF. NP binds to receptors in nephrons→ effects are opposite of aldosterone. Kidney reabsorption of Na inhibited at same time that UO is increased; outcome is decreased circulating BvL & decreased blood Osm. --BNP levels increase w/ age; generally higher in healthy women vs healthy men. --BNP used for Dx HF (esp. diastolic HF) in pts w/ acute dyspnea; part of body's response to decreased CO from LV or RV dysfunction. Absence of elevated BNP + H&P→ r/o HF as cause of acute dyspnea & points to primary lung dysfunction. In ambulatory care, BNP trends used over time to guide ambulatory care tx. -BNP: Normal <100 pg/mL. Dx tool; it's proportional→ shows HF is worsening or improving. --Acute HF BNP: 50yrs+= 450 pg/mL+; 50-75yrs= 900 pg/mL+; 75yrs+= 1,800 pg/mL+.

Heat exhaustion

Heat exhaustion: synd. resulting primarily from dehydration; caused by heavy perspiration & inadequate F&E intake during heat exposure over hrs→ days. Profuse diaphoresis can lead to profound, even fatal, dehydration & hyponatremia from excessive Na lost in perspiration. If un-tx, heat exhaustion can lead to heat stroke= true medical emergency w/ very high mortality rate. -S/S: Usually flulike w/ headache, weakness, N&/orV. Body temp. may not be significantly elevated; may continue to perspire despite dehydration. -Action Alert: should assess for orthostatic hypotension & tachycardia, esp. elderly bc can dehydrate quickly. Elderly w/ dehydration often have acute confusion & at risk for falls. -Tx: Instruct to immediately stop physical activity & move to cool place. Use cooling measures like cold packs on neck, chest, ABD, & groin. Soak in cool water or fan while spraying water on skin. Remove constrictive clothing. Sports drinks or ORT solution can be provided. Mistakenly drinking plain water can worsen Na deficit. Do not give salt tablets, bc can cause stomach irritation & N/V. If s/s persist, call ambulance to transport to hospital. -In clinical setting, monitor VS. Rehydrate w/ IV solution as prescribed if n/v persists. Draw blood for serum electrolyte analysis. Hospital admit indicated only for pts w/ other health problems worsened by heat-illness or for severe dehydration & s/s physiologic compromise.

Heat stroke

Heat stroke: medical emergency; body temp. may >104°F (40°C); high mortality rate if not tx in timely manner. Thermoregulation mechanisms fail & cannot adjust for critical elevation in temp. If condition not tx or not responding to tx, organ dysfunction & death can result. -Exertional heat stroke: sudden onset & often result of strenuous physical activity (esp. w/ heavy clothing) in hot, humid conditions. -Classic heat stroke: AKA nonexertional heat stroke; occurs over period of time bc of chronic exposure to hot, humid environment like home w/o air conditioning in high heat of summer. -S/S: profoundly elevated temp. (>104°F; 40°C); skin is hot & dry, but presence of sweating does not r/o heat stroke—may continue to perspire. MS changes occur bc of thermal injury to brain & are hallmark s/s in heat stroke. Cardiac troponin I (cTnI) frequently elevated in nonexertional heat-related illnesses; research indicates test can be used to cost effectively predict severity & organ damage at beginning of heat stroke, even in remote setting. -Key Features of Heat Stroke: Body temp. >104°F (40°C). Hot & dry skin; may [not] perspire. MS changes= Acute confusion; Bizarre behavior; Anxiety; Loss of coordination; Hallucinations; Agitation; Seizures; Coma. VS changes= Hypotension; Tachycardia; Tachypnea; Electrolyte imbalances, esp. Na & K; Decreased renal function (oliguria); Coagulopathy (abnormal clotting); Pulmonary edema (crackles).

Hemorrhage in TBI

Hemorrhage in TBI: causes brain hematoma or clot, may occur as part of primary injury & begin at moment of impact; may also arise later from vessel damage. Classically, bleeding caused by vascular damage from shearing force of trauma or direct physical damage from skull fractures or penetrating injury. All hematomas are potentially life threatening bc act as space-occupying lesions & are surrounded by edema. 3 major types of hemorrhage after TBI= epidural, subdural, intracerebral hemorrhage. Subarachnoid hemorrhage may also occur. -Epidural hematoma: results from arterial bleeding into space between dura & inner skull. Often caused by fracture of temporal bone= houses middle meningeal artery. Pts have "lucid intervals" that last for mins= awake & talking; follows momentary unconsciousness that can occur w/in mins of injury. --Critical Rescue: After initial interval, s/s of neuro impairment from hemorrhage can progress very quickly, w/ potentially life-threatening ICP elevation & irreversible structural damage to brain. Monitor pt suspected of epidural bleeding frequently (Q5-10min) for changes in neuro status. Can become quickly & increasingly symptomatic. Loss of consciousness from epidural hematoma is neurosurgical emergency! Notify PHCP or RRT immediately if these changes occur. Carefully document assessments & ID trends. -Subdural hematoma (SDH): results from venous bleeding into space beneath dura & above arachnoid; often from tearing of bridging veins w/in cerebral hemispheres, from laceration of brain. Bleeding occurs more slowly vs epidural hematoma. SDHs subdivided into acute, subacute, & chronic. Acute SDH presents w/in 48hrs after impact; subacute SDH between 48hrs-2wks, & chronic SDH from 2wks-several mo after injury. Have highest mortality rate bc often unrecognized until pt has severe neuro compromise. --Incidence of chronic SDHs (written as cSDH) nearly doubles w/ 65-75yrs old & increases w/ >80yrs old. Common causes of chronic SDHs in elderly= head trauma resulting from fall & anticoags or antiplt. Typical s/s= worsening headaches, paresis, acute confusion, & seizures. Some pts have decreased LOC, + coma. -Traumatic intracerebral hemorrhage (ICH): accumulation of blood w/in brain caused by tearing of small arteries & veins in subcortical white matter. Often acts as space-occupying lesion (tumor); potentially devastating, depending on location. ICH may also produce significant brain edema & ICP elevations. Traumatic brainstem hemorrhage occurs from blow to back of head, fractures, or torsion injuries to brainstem (VS center). Brainstem injuries have a very poor Px.

Horizontal Violence in the Workplace; Vertical Conflict

Horizontal Violence in the Workplace: Many issues that interfere w/ workplace safety arise from interactions routinely occurring w/ staff; during stress, often miscommunication among colleagues. Most of these conflicts can be resolved w/ open communication. -Horizontal violence: act of aggression toward another colleague; may range from verbal or emotional abuse, or extend to physical abuse. Subtle acts of horizontal abuse may include belittling, withholding info, or freezing out of group activities. --Horizontal conflict based on differences between colleagues. -Vertical conflict r/t differences between managers & staff; often r/t inadequate communication, opposing interests, & lack of shared attitudes.

Hospital Emergency Preparedness; Roles & Responsibilities

Hospital Emergency Preparedness; Roles & Responsibilities: RNs have major role in ER prep or ER management plan; multiple health system resources necessary to manage the disaster, so Hospital Incident Command System typically estab. for organization & structure. -Hospital incident commander: a primary role estab. at incident onset; assumes overall leadership for implementing institutions plan. Physician or admin who assumes overall leadership for implementing ER plan. Authority to activate resources; can be a RN supervisor as on-site hospital admin after usual business hrs until leadership arrives. HIC assists in organization of hospital services to rapidly expand capacity, recruit paid or volunteer staff, & ensure availability of supplies. Role is to take global view of entire situation & facilitate pt movement through system, while bringing in staff & resources to meet needs. -Medical command physician: typical role defined in hospital or HC ER prep plan; focuses on ID #, acuity, & resource needs of pts arriving from incident to hospital & organizing ER HC team response to injured or ill. Physician who decides #, acuity, & resource needs of pts. Responsibilities include ID need for & calling in specialty-trained providers. In smaller hospitals w/ limited specialty resources, MCP might help ID which pts should be transported to higher level of care or to specialty hospital (burn center). -Triage officer: Physician or RN who rapidly evaluate pts to ID priorities for tx. Closely affiliated w/ MCP; generally physician in large hospital who is assisted by triage RNs. If physicians limited, an experienced RN may assume role. Rapidly evaluates each pt coming in hospital, even if have triage tags in place. Pt acuity is re-evaluated for disposition to area w/in ED or hospital best suited to meet needs. -Community relations or public info officer: serves as liaison between the HC facility & media; esp. important role to delineate in advance. Mass casualties attract large amount of media attention; officer can draw media away from clinical areas so essential hospital ops not hindered. Also serve as liaison between hospital admin & media to release only appropriate & accurate info.

Preparing for Self-Management: How to Prevent or Decrease Dysrhythmias

How to Prevent or Decrease Dysrhythmias: -At Risk for Vasovagal Attacks Causing Bradydysrhythmias. Avoid doing things that stimulate vagus nerve; ex. raising arms above head, applying pressure over carotid artery, applying pressure on eyes, bearing down or straining during BM, & stimulating gag reflex when brushing teeth or putting objects in mouth. -W/ Premature Beats & Ectopic Rhythms. Take prescribed meds & report any AEs→ HCP. Stop smoking, avoid caffeinated beverages & energy drinks as much as possible, & drink alcohol only in moderation. Learn ways to manage stress & avoid getting too tired. -W/ Ischemic Heart Disease. Have an angina attack→ tx promptly w/ rest & nitroglycerin as prescribed by HCP→ decreases chances of a dysrhythmia. If chest pain is not relieved after taking prescribed amount of nitroglycerin→ seek medical attention promptly. Also seek prompt medical attention if pain becomes more severe; or other s/s of sweating, nausea, weakness, & palpitations. -At Risk for K+ Imbalance. Know s/s of decreased K+ levels; ex. muscle weakness & cardiac irregularity. Eat foods high in K+; ex. tomatoes, beans, prunes, avocados, bananas, strawberries, lettuce. Take K+ supplements that have been prescribed.

Imaging for ACS

Imaging for ACS: -CXR: not Dx for angina or MI, unless associated cardiac dysfunction (valve dz) or HF present. CXR performed to help rule out aortic dissection, bc may mimic MI. If CXR shows widened mediastinum→ further testing for aortic dissection w/ transesophageal echography (TEE) or CT scan is needed. -TEE: ????????? -Thallium scans: use radioisotope imaging to assess for ischemia or necrotic muscle tissue r/t angina or MI. Areas of decreased or absent perfusion→ cold spots, ID ischemia or MI. Thallium may be used w/ exercise tolerance test. Dipyridamole thallium scanning (DTS) may also be used. -Contrast-enhanced CV magnetic resonance (CMR): imaging tech. done as a noninvasive approach to detect CAD. -Echocardiography: used to visualize heart structures & anatomy; mainly structure of chamber & valves [if closing] & BF [ID regurgitation]; colors show BF direction & approx. CO; done at bedside. -CT coronary angiography (CTCA): use of 64-slice CTCA found helpful in Dx CAD. High-speed CT scanner is a highly reliable, noninvasive way to evaluate calcified plaque; plaque is quantified into calcium score. Calcium score (AKA Agatston score) >400→ higher risk of MI & death w/in next 2-5yrs. -Myocardial nuclear perfusion imaging (MNPI): use of radionuclide techniques in CV assessment; CV abnormalities can be viewed, recorded, & evaluated w/ radioactive tracers. Useful for ID MI & decreased myocardial BF & evaluating LV ejection. Conducting MNPI w/ exercise or admin vasodilators→ clearer ID of how heart responds to stress. -Electrophysiologic study (EPS): invasive tx; programmed electrical stimulation of heart to cause & evaluate lethal dysrhythmias & conduction abnormalities. Indicated if survived cardiac arrest, recurrent tachydysrhythmias, or unexplained syncopal episodes. Dysrhythmia induction helps find accurate Dx & aids effective tx. Risks similar to cardiac cath; performed in special cath lab, where conditions are strictly controlled & immediate tx is available for AEs. -Angiography of arterial vessels [arteriography]: invasive Dx tx w/ fluoroscopy & contrast media; performed when arterial obstruction, narrowing, or aneurysm is suspected. Interventional radiologist performs selective arteriography to evaluate specific areas of arterial system. Ex. coronary arteriography, performed during Lt- cardiac cath, assesses arterial circulation w/in heart. Can also be performed on arteries in extremities, mesentery, & cerebrum.

Impaired Practice

Impaired Practice: Sometimes issues of staff conflict are symptomatic of other personal issues that may be impairing staff member; may be stress at home, $ difficulties, or actual impairment r/t drugs &/or alcohol. -Staff will have personal issues that affect workplace at various times, but important to know when these personal issues interfere w/ workplace &/or pt safety. -Impaired practice r/t substance abuse AND mental health disorders or issues. -BOX 9-8 Signs of Nursing Drug Diversion: Arriving early, staying late, and coming to work on scheduled days off. Excessive wasting of drugs. Regularly signing out large quantities of controlled drugs. Volunteering often to give medication to other nurses' patients. Taking frequent bathroom breaks. Patients reporting unrelieved pain despite adequate prescription of pain medication. Discrepancies in the documentation of controlled substance administration. Medications being signed out for patients who have been discharged or transferred, or who are off the unit for procedures or tests. -BOX 9-9 Physical Symptoms of Alcohol or Drug Dependency: Shakiness, tremors of hands, jitteriness. Slurred speech. Watery eyes, dilated or constricted pupils. Diaphoresis. Unsteady gait. Runny nose. N/V, diarrhea. Wt loss or gain. Blackouts (memory losses while conscious). Wears long-sleeves continuously.

Implantable Cardioverter/Defibrillator (ICD); Automated wearable cardioverter/defibrillator (WCD)

Implantable Cardioverter/Defibrillator (ICD): indicated for 1+ episodes of spontaneous sustained VT or VF not caused by MI. Collab. w/ HCP & electrophysiology RN to prep pt. -Psychological profile ID if able to cope w/ discomfort & fear of internal defibrillation. Many report anxiety, depression, & decreased quality of life; improves for majority after 12mo. -2 types of lead systems: TV & SQ. -Traditional transvenous system→ leads introduced via subclavian vein & generator implanted in Lt pectoral area, similar to permanent PM. -SQ ICD→ leads tunneled underneath skin & placed Lt of sternum to form Rt angle just below xiphoid, where they attach to generator; generator implanted in Lt midaxillary chest wall. Recommended for younger pts (<40yrs), pts w/o venous access, & pts who do not require concomitant pacemaker tx. -Performed in EP lab. Experiences VT or VF after ICD placed & ICD tx not successful→ qualified RN or HCP promptly externally defibrillates & initiates CPR. Automated wearable cardioverter/defibrillator (WCD): lightweight, external vest worn 24hrs/day except w/ showering or bathing. Popular brand is Zoll Lifecore LifeVest; monitors for VT & VF. -Family must be present to call 911 & initiate CPR if pulseless VT or VF while showering. -If conscious w/ VT→ pt can press button to prevent shock; precaution is advantage over implantable devices bc ICDs always shock in VT or VF. -Generator is activated or deactivated by HCP placing magnet over site for few moments. Pt requires close monitoring post-op for dysrhythmias & complications; bleeding & cardiac tamponade. -RN must know if ICD is activated or deactivated. Care similar to after implantation of permanent PM. If implanted following sudden cardiac arrest→ driving usually restricted 6mo.

Increased ICP in TBI

Increased ICP in TBI: cranial contents= brain tissue, blood, & CSF; encased in rigid skull→ little room for any of them to expand or increase in vL. Normal ICP is 10-15. Periodic increases in pressure occur w/ straining on BM, coughing, or sneezing but do not harm the uninjured brain. Sustained ICP of >20 is detrimental to brain bc neurons begin to die. -Brain injury→ increase in vL of 1 component must be compensated for by decrease in vL of another. 1st response to increased vL→ CSF shunted or displaced from cranium to spinal subarachnoid, or rate of CSF absorption is increased. Additional response, if needed, is decrease in cerebral BvL by movement of cerebral venous blood into sinuses or jugular veins. If brain can compensate for increased vL & remain compliant, increases in ICP are minimal. -Increased ICP is leading COD from head trauma in pts who reach hospital alive. Occurs when compliance no longer takes place & brain cannot accommodate further vL changes. ICP increases→ cerebral perfusion decreases→ brain ischemia & edema. If edema remains un-tx→ brainstem may herniate downward through foramen of Monro or laterally from unilateral lesion w/in 1 hemisphere, causing irreversible brain damage & possibly death.

Increasing Myocardial Tissue Perfusion in ACS: Reperfusion tx

Increasing Myocardial Tissue Perfusion in ACS: Reperfusion tx; As time passes, myocardial tissue becomes more ischemic & necrotic; tx based on location & skill set w/in facility, 1 of 2 reperfusion txs used to open a blocked artery in acute MI: thrombolytic tx or percutaneous coronary intervention (PCI). PCI is tx of choice for most w/ STEMI. -Fibrinolytic tx: AKA thrombolytic tx; dissolves thrombi in CAs & restores myocardial BF. Agents target fibrin in coronary thrombosis; ex. Tissue plasminogen activator (tPA, alteplase); Reteplase; Tenecteplase. (activase, cathflo activase, streptokinase) --It converts plasminogen to plasmin= major enzyme of clot breakdown. --If can't receive timely PCI w/ s/s STEMI→ consider fibrinolytic tx. Benefit of fibrinolytics declines as time between onset to tx increases. Goal is to admin fibrinolytics w/in 30min of arrival. Not for NSTEMI pts. Absolute contraindications→ previous IC hemorrhage, active bleeding, & significant trauma w/in 3mo. --Drug Alert: During & after thrombolytic admin, immediately report any s/s bleeding to HCP or RRT. Observe for bleeding s/s by: Documenting neuro-status (IC bleeding); Observing IV sites for bleeding & patency; Monitoring clotting labs; Observing for s/s internal bleeding (monitor Hgb, Hct, BP); Testing stool, urine, & emesis for occult blood. --Pts receiving fibrinolytics require PCI for more definitive tx [ex. stents]. If criteria for PCI met→ go directly to cath lab where definitive tx, not just clot resolution performed. --Monitor for indications that clot is lysed (dissolved) & artery reperfused; ex: Abrupt cessation of pain or discomfort; Sudden onset of V dysrhythmias; Resolution of ST depression/elevation or T-wave inversion; A peak at 12hrs of markers of myocardial damage. --After clot lysis w/ fibrinolytics, lg. amounts thrombin released→ increasing risk for reocclusion. Maintain patency of CA after thrombolytics→ usually aspirin & IV heparin. Maintain heparin IV via pump to maintain aPTT 50-70s (= 1½-2x control). Heparin drip continued for min. 48hrs or until revascularization. LMWH (enoxaparin) may be substituted for IV heparin. Therapeutic dosing of LMWH based on wt.

Interventions for AF; Preventing HF w/ Cardioversion

Interventions for AF: -Preventing HF: by restoration of normal conduction w/ controlled ventricular rate. Txs to prevent HF & improve CO begins w/ drugs; may require other nonsurgical or surgical tx if med not successful. -Nonsurgical: -Electrical cardioversion: synchronized countershock; restores normal conduction in new-onset AF; or scheduled electively for stable AF, resistant to tx. -AF onset >48hrs→ must take anticoags for >3wks (or until INR 2-3) before procedure; prevent clots moving from heart→ brain or lungs. -AF onset uncertain→ transesophageal echocardiogram (TEE) used to assess clot formation in LA. -Shock depolarizes lg. amount of myocardium during depolarization; intended to stop re-entry circuit & allow SA node to regain control. -Emergency equipment must be available during CV; HCP, APRN, or qualified RN→ explains tx. Help pt sign consent unless emergency tx for life-threatening dysrhythmia. Pt usually conscious, short-acting anesthetic admin for sedation. -Defibrillator set synchronized mode; dot or line over each QRS complex, confirms synchronized mode; avoids shock during T wave→ increase ventricular irritability→ VF. Charge defibrillator to level requested; usually starting at low rate of 120-200 joules for biphasic. -Critical Rescue: safety before cardioversion→ turn O2 off & remove it; fire could result. Shout "CLEAR" before shock for electrical safety! -After cardioversion→ assess response & rhythm. Repeated, PRN, until desired result obtained or alternative tx considered. If pt deteriorates into VF after→ check synchronizer is turned off so immediate defibrillation can be admin. -RN care after cardioversion: Maintaining patent airway; Admin O2; Assess VS & LOC; Admin antidysrhythmics; Monitor for dysrhythmias; Assess for chest burns from electrodes; Provide emotional support; Document results.

Interventions for AF

Interventions for AF: depend on severity & pts response. Individualize care; Drug tx often effective. -Preventing Embolus Formation: by restoring regular conduction. Correcting rhythm & controlling rate→ restore BF→ helps prevent embolus formation & increases CO. Drug tx often effective. -Action Alert: loss of coordinated atrial contractions in AF can lead to pooling of blood→ clotting. High risk for PE! Thrombi may form w/in RA→ RV→ lungs. If PE suspected→ remain w/ pt & monitor for SOB, chest pain, &/or hypotension→ Initiate RRT & notify HCP. --Risk for systemic emboli, esp. embolic stroke→ severe neuro impairment or death. Monitor carefully for s/s stroke. Initiate RRT if stroke suspected to facilitate timely Dx. --AF w/ valvular dz esp. at risk VTE→ may report LE pain & swelling. Anticipate US of vasculature & initiation of systemic anticoagulation. -Traditional AF tx: antidysrhythmic drugs to slow ventricular conduction or convert AF→ NSR.

Interventions for AF; Preventing Emboli w/ Drugs

Interventions for AF; Preventing Emboli w/ Drugs: -Slow conduction: CCBs [diltiazem]; for difficult-to-control AF, use amiodarone. Dronedarone similar to amiodarone, but better tolerated for maintenance of sinus rhythm after cardioversion; not used w/ HF→ exacerbation of cardiac s/s, or w/ permanent AF→ increases risk of stroke, MI, or CV death. --BBs [metoprolol & esmolol] slow ventricular response. Digoxin for HF + AF; useful controlling rate of ventricular response; does not convert AF→sinus rhythm. Carefully monitor PR. Interventions for AF; Preventing Embolis Formation with Drugs -Drugs to slow conduction: CCBs [diltiazem]; for more difficult-to-control AF, use amiodarone. Dronedarone is similar to amiodarone, but better tolerated for maintenance of sinus rhythm after cardioversion; not used if HF present→ can cause exacerbation of cardiac s/s, or w/ permanent AF→ increases risk of stroke, MI, or CV death. --BBs [metoprolol & esmolol] used to slow ventricular response. Digoxin used for HF + AF; useful in controlling rate of ventricular response; does not convert AF→sinus rhythm. Carefully monitor PR w/ these. -Rhythm control: flecainide, dofetilide, propafenone, ibutilide; usually started w/in acute care bc risk of prolonged QT intervals & bradycardia. Continuous cardiac monitoring & frequent 12-lead ECGs needed. --Amiodarone used but does not require acute care stay. Permanent AF present→ rhythm control antiarrhythmics should not be used. -Goal: convert AF→ SR; may not be possible for elderly→ require LT anticoags. to prevent stroke & thrombus. -Unpredictable drug response & many food-drug interx→ labs (ex. INR) required w/ warfarin. Teach importance of avoiding foods high in Vit-K & avoid herbs like ginger, ginseng, goldenseal, Ginkgo biloba, & St. John's wort→ could interfere w/ drug's action. -Problems w/ warfarin→ direct oral anticoags. (DOACs) like dabigatran, rivaroxaban, apixaban, or edoxaban may be given LT to prevent strokes from nonvalvular AF. Drugs achieve steady state→ no labs needed. PT & INR not accurate predictors of bleeding time w/ DOACs. -Bleeding risk lower w/ DOACs; important to be aware of reversal agents. Idarucizumab [IV monoclonal antibody]→ binds to dabigatran→ preventing it from inhibiting thrombin. SEs of idarucizumab= hypokalemia, confusion, constipation, fever, pneumonia. FDA approved andexanet alfa as reversal for rivaroxaban & apixaban; reversal agents significantly increase risk of clotting & stroke→ only used for life-threatening bleeding. -Drug Alert: Teach if on any type of anticoagulant to report bruising, bleeding nose or gums, & s/s bleeding→ PHCP immediately.

Interventions for AF; Preventing HF w/ LAA, Biventricular Pacing, & RCA

Interventions for AF; Preventing HF: Nonsurgical -Left atrial appendage closure: pt is high risk for stroke & not candidates for LT anticoags→ LAA occlusion device may be an option; small sac in LA wall. Complications similar to cardiac ablation. --Nonvalvular AF→ LAA most common site of clot development→ risk of stroke. --Inserted percutaneously via femoral vein; device to occlude LAA delivered via transseptal puncture. --Watchman (nitinol frame w/ fenestrated fabric) only device approved for AF. --After insertion, anticoag w/ aspirin & warfarin required. Repeat TEE (transesophageal echocardiogram) approx. 45 days after insertion→ assess for leaks around device. If no leak detected→ warfarin stopped & anti-plt tx continued. -Biventricular pacing: type of pacing; alt. for HF & conduction ds. Biatrial pacing, antitachycardia pacing, & implantable atrial defibrillators are other methods used to suppress or resolve AF. -Radiofrequency catheter ablation (RCA): invasive; destroys irritable focus in A or V conduction. --Must 1st do EPS & mapping to locate focus. Then radiofrequency waves delivered→ abolish irritable focus. --Ablation in AV nodal or His bundle area→ damage may occur to normal conduction system→ heart blocks & requiring implantation of permanent PM. --In AF, pulmonary vein isolation & ablation create scar tissue→ blocks impulses & disconnects pathway of abnormal rhythm. AF pts w/ rapid V rate not responsive to drugs→ AV nodal ablation, totally disconnects the conduction from A→ V; requires implantation of permanent PM. Ablation not performed if LT anticoag is contraindicated.

Interventions for ARDS

Interventions for ARDS: Often needs intubation & MV w/ PEEP or CPAP; best practice involves "open lung" & lung protective ventilation strategies. --Low tidal vLs (6 mL/kg) are shown to prevent lung injury. PEEP is started at 5cm H2O & increased to keep O2sat adequate; PEEP levels may need to be high. --Pressure-controlled is preferred over vL-controlled ventilation; promotes nonfunctional alveoli to participate in gas exchange. --SE of PEEP is tension pneumothorax; assess lung sounds Q1hr & suction PRN to maintain a patent airway. -Airway pressure release ventilation (APRV) & high-frequency oscillatory ventilation (HFOV) are alt. modes of MV; improve gas exchange w/ oxygenation & ventilation in moderate-to-severe ARDS. Airway pressure w/ APRV & HFOV is significantly higher than conventional MV. Sedation & paralysis may be needed for adequate ventilation & to reduce tissue O2 needs [esp. HFOV]; sedation & paralysis are not required w/ APRV but may be needed to prevent patient disruption of MV; method can allow for spontaneous breathing between mandatory breaths. -Positioning may be important in promoting gas exchange; exact position is controversial. Some do better in the prone position, esp. if it is started early in the disease course. Manually turning Q2hrs has shown to improve perfusion; often is not performed as frequently as needed. --Early progressive mobility also shown benefit in reducing ventilator needs, days on ventilator, & mortality. -Severe ARDS; extracorporeal membrane oxygenation (ECMO) w/ heart-lung bypass equipment has been a successful life-support technique, when traditional tx have failed. -ABs tx infections when organisms are ID; other drugs manage any underlying cause. No tx reverse the pathologic lung changes. -Conservative fluid tx: infusing smaller amounts of IV fluid & using diuretics to maintain fluid balance; liberal fluid tx often results in an increasingly positive fluid balance & more edema. Critically ill & at ARDS risk as a result of trauma, fluid management that involves slight hypotension is thought to help prevent ARDS. -Malnutrition risk; further reduces respiratory muscle function & immune response; must include RDN. EN or PN is started ASAP.

Interventions for Heat Stroke

Interventions for Heat Stroke: Coordinate w/ IP HC team to ID & tx immediately & aggressively to achieve optimal outcomes. -Critical Rescue: After ensuring patent airway, effective breathing, & adequate circulation, recognize that you must use rapid cooling as 1st priority of care. Respond by implementing methods for rapid cooling= removing clothing; placing ice packs on neck, axillae, chest, groin; immersing pt or wetting body w/ cold water; & fanning rapidly to aid in evaporative cooling. -First Aid/Prehospital Care: Do not give food or liquid by mouth bc vomiting & aspiration are risks if pt has neuro impairment. Immediate medical care using adv. life support is essential. -Hospital Care: 1st priority for IP collab. care is to monitor & support ABC status. --If shivering occurs during cooling process, midazolam or propofol may be prescribed. Midazolam has high risk for delirium, & propofol carries a risk of hypotension. --Seizure activity can further elevate temp. & is also tx w/ IV benzo. --Once stabilized, admit to critical care unit may be warranted to monitor for complications→ MODS & severe electrolyte imbalance→ both increase mortality risk.

Interventions for Strokes: Endovascular txs

Interventions for Strokes: -Endovascular txs: to improve perfusion; intra-arterial thrombolysis w/ drugs, mechanical embolectomy (OP blood clot/ thrombosis removal), & carotid stents. --Intra-arterial thrombolysis: advantage of admin fibrinolytics directly into thrombus w/in 6hrs of stroke onset. Esp. beneficial for occlusion of middle cerebral artery or if arrive in ED after window for IV alteplase. Pts having fibrinolytics or endovascular tx are admitted to critical care setting for intensive monitoring. --Carotid artery angioplasty + stenting: common to prevent or help manage an acute ischemic stroke. This IR tx usually w/ moderate sedation; performed by CV surgeon or IR. Technique using distal/embolic protection device has made this very safe. Device placed beyond stenosis through cath inserted into femoral artery (groin); device catches any clot debris that breaks off during procedure. Placement of carotid stent used to open blockage in carotid artery typically at division of common carotid artery into internal & external carotid arteries. Carefully assess neuro & CV status throughout the tx. -Action Alert: Before D/C after carotid stent placement, teach pt & family to report these s/s to PHCP immediately: Severe headache; Change in LOC or cognition (drowsiness, new-onset confusion); Muscle weakness or motor dysfunction; Severe neck pain; Swelling at neck incisional site; Hoarseness or dysphagia (r/t nerve damage). --When stroke is hemorrhagic & cause is r/t AVM or cerebral aneurysm, pt evaluated for optimal tx to stop bleeding. Some txs can be used to prevent bleeding in AVM or aneurysm that is discovered before s/s onset or SAH. Occur in IR suite or OR.

Interventions for Strokes: Fibrinolytic tx

Interventions for Strokes: -2 major tx modalities for acute ischemic stroke= IV fibrinolytic tx & endovascular txs. Regardless of immediate txs used, once stable, provide ongoing supportive care. Provide txs to prevent &/or monitor for early s/s complications; & prevent falls. -Fibrinolytic tx: For selected pts w/ acute ischemic strokes, early tx w/ IV fibrinolytics ("clot-busters") is care std. to improve BF to viable tissue around infarction or through brain. Success depends on interval between onset time & when tx available. IV (systemic) fibrinolytics (AKA thrombolytic tx) for acute ischemic stroke dissolves cranial artery occlusion to re-estab. BF & prevent cerebral infarction. --IV alteplase is only drug approved for tx of acute ischemic stroke. Most important factor in ID if you can give alteplase is time between s/s onset & time seen in stroke center. --FDA approves alteplase admin w/in 3hrs of stroke onset; American Stroke Association endorses 4.5hrs to admin this fibrinolytic unless they fall into 1+ of these categories: Age >80yrs; Anticoagulation regardless of INR; Imaging evidence of ischemic injury w/ >1/3 of brain tissue supplied by middle cerebral artery; Baseline NIHSS score >25; Hx of both stroke & DM; Evidence of active bleeding. --Clinical Guidelines for management of acute ischemic stroke recommend IV alteplase 90mg over 60min, w/ initial 10% of dose given as bolus over 1st min. Newest recommendation for door-to-needle time (ED→ fibrinolytic start) is 45min. The BP may be too high to admin, so given a rapid-acting anti-HTN drug until BP <185/110; BP must be maintained during fibrinolytic tx; give anti-HTN drugs [labetalol] as prescribed (IV recommended for faster response). -Drug Alert: In addition to frequent monitoring of VS, carefully observe for s/s intracerebral hemorrhage & other s/s of bleeding during fibrinolytic admin. --Prevent bleeding→ do not place invasive tubes [NGT or foley] until stable (usually for 24hrs). Discontinue infusion if reports severe headache or has severe HTN, bleeding, N/V; notify PHCP immediately. Obtain follow-up CTA or CTP scan after fibrinolytics & before starting anti-plt or anti-coags.

Interventions for Strokes: Increased ICP

Interventions for Strokes: -Monitoring for increased ICP: most at risk for increased ICP from edema during first 72hrs after stroke onset. Some may have worsening of neuro status starting w/in 24-48hrs after endovascular txs from increased ICP. --Reassess pts w/ acute stroke & after endovascular txs of stroke s/s Q1-4hrs, depending on severity of condition. Use approved assessment strategy & documentation tools. -Key Features of Increased ICP: -Decreased LOC (earliest s/s); Behavior changes: restlessness, irritability, & confusion; Headache; N/V (may be projectile); Aphasia; Change in speech pattern/dysarthria. -Change in sensorimotor status: Pupillary changes= dilated & nonreactive ("blown pupils") or constricted & nonreactive (very late s/s); CN dysfunction; Ataxia. -Seizures (usually w/in 24hrs after stroke). -Cushing triad (very late s/s): Severe HTN; Widened pulse pressure; Bradycardia. -Abnormal posturing (very late s/s): Decerebrate; Decorticate. -Critical Rescue: For ischemic strokes, if SBP >185, notify RRT or PHCP immediately & anticipate order of IV anti-HTN med. Monitor BP & MAP (normal MAP 70-100; at least 60 to perfuse major organs) Q5min until SBP adequate to maintain brain perfusion. Avoid sudden SBP drop to <120 w/ med admin, may cause brain ischemia.

Key Features of Angina & MI

Key Features of Angina & MI: -Angina: Substernal chest discomfort: Radiating to Lt arm; Precipitated by exertion or stress (or rest in vasospastic angina); Relieved by NTG or rest; Lasting <15min; Few, if any, associated s/s. -MI: Pain or discomfort: Substernal chest pain/pressure radiating to Lt arm; Pain or discomfort in jaw, back, shoulder, or ABD; Occurring w/o cause, usually in morning; Relieved only by opioids or tx; Lasting 30min+. --Frequent associated s/s of MI: N/V; Diaphoresis; Dyspnea; Fear & anxiety; Dysrhythmias; Fatigue; Palpitations; Epigastric distress; Anxiety; Dizziness; Disorientation/acute confusion; Feeling "SOB". --Common Terms Pts Use To Describe Angina: "Heaviness"; "Pressing"; "Suffocating"; "Squeezing"; "Strangling"; "Constricting"; "Bursting"; "Burning"; "Grip like"; "A band across my chest"; "A weight in the center of my chest"; "A vise tightening around my chest". -Older Adults: presence of associated s/s w/o chest discomfort is significant; more likely to have atypical s/s. Often w/ associated s/s instead of typical chest pain or pressure. Some may think it's indigestion & not ID having MI. Others report SOB as the only s/s. Ambiguity of s/s→ more likely to wait before seeking tx. Major manifestation of MI in pts >80yrs may be disorientation or acute confusion bc of poor CO & inadequate coronary perfusion. --Some older adults w/ MI, absence of chest pain may be caused by cognitive impairment or inability to verbalize pain; most cases it is probably result of increased collateral circulation. Silent myocardial ischemia increases incidence of new coronary events & should be tx aggressively.

Key Features of Shock

Key Features of Shock: -CV S/S: Decreased CO; Increased PR; Thready pulse; Decreased BP; Narrowed pulse pressure; Postural hypotension; Low central venous pressure; Flat neck & hand veins in dependent positions; Slow cap-refill in nail beds; Diminished peripheral pulses. -Respiratory S/S: Increased RR; Shallow depth of respirations; Decreased PaCO2 initially then progressing to increased PaCO2; Decreased PaO2; Cyanosis, esp. around lips & nail beds. -GI S/S: Decreased motility; Diminished or absent bowel sounds; N/V; Constipation. -Neuromuscular S/S: Early→Anxiety, Restlessness, Increased thirst. Late→ Decreased CNS activity (lethargy→ coma); Generalized muscle weakness; Diminished or absent DTRs; Sluggish pupillary response to light. -Kidney S/S: Decreased UO; Increased SG; Sugar & acetone present in urine. -Integumentary S/S: Cool→ cold; Pale→ mottled→ cyanotic; Moist, clammy; Mouth dry w/ pastelike coating present; Decreased cap-refill.

Laboratory Profile: Respiratory Assessment; ABGs

Laboratory Profile: Respiratory Assessment -ABGs: assesses gas exchange & perfusion as oxygenation (partial pressure of arterial O2; PaO2), alveolar ventilation (partial pressure of arterial CO2; PaCO2), & acid-base balance. Blood gas studies provide info for monitoring tx results, adjusting O2 tx, & evaluating the patient's responses. --PaO2: 80-100 mm Hg; Older adults: values may be lower ---Elevations indicate possible excessive O2 administration. ---Decreased indicate possible COPD, asthma, chronic bronchitis, cancer of the bronchi & lungs, cystic fibrosis, respiratory distress syndrome, anemias, atelectasis, or any other cause of hypoxia. --PaCO2: 35-45 mm Hg ---Elevations indicate possible COPD, asthma, pneumonia, anesthesia effects, or use of opioids (respiratory acidosis). ---Decreased indicate hyperventilation/respiratory alkalosis. --pH: Up to 60 yr: 7.35-7.45; 60-90 yr: 7.31-7.42; >90 yr: 7.26-7.43 ---Elevations indicate metabolic or respiratory alkalosis. ---Decreased indicate metabolic or respiratory acidosis. --HCO3: 21-28 mEq/L ---Elevations indicate possible respiratory acidosis as compensation for a primary metabolic alkalosis. ---Decreased indicate possible respiratory alkalosis as compensation for a primary metabolic acidosis. --SpO2: 95%-100%; Older adults: values may be slightly lower ---Decreased levels indicate possible impaired ability of Hgb to release O2 to tissues.

Laboratory Profile: Respiratory Assessment; CBCs

Laboratory Profile: Respiratory Assessment -Complete Blood Count: RBC count provides data about O2 transport. Hgb [w/in RBCs], transports O2 to the tissues. A deficiency of Hgb could cause hypoxemia. --RBCs: Females 4.2-5.4 × 106/mcL; Males 4.7-6.1 × 106/mcL --Hgb, total: Females 12-16 g/dL; Males 14-18 g/dL --Hct: Females 37%-47%; Males 42%-52% --Elevated levels (polycythemia) are often related to the excessive production of erythropoietin in response to a chronic hypoxic state (ex. COPD) & from living at a high altitude. --Decreased levels indicate possible anemia, hemorrhage, or hemolysis. -WBC count (leukocyte count): Total 5,000-10,000/mm3 --Elevations indicate possible acute infections or inflammations. --Decreased may indicate an overwhelming infection, autoimmune disorder, or immunosuppressant Tx.

Laboratory Profile: Respiratory Assessment; Differential WBC

Laboratory Profile: Respiratory Assessment -Differential WBC (Leukocyte) Count: --Neutrophils: 2500-8000/mm3, or 55%-70% of total, or 5-6.2 × 109/L ---Elevations indicate possible acute bacterial infection (pneumonia), COPD, or inflammatory conditions (smoking). ---Decreased indicate possible viral disease (influenza). --Eosinophils: 50-500/mm3, or 1%-4% of total, or 0.0-0.3 × 109/L ---Elevations indicate possible COPD, asthma, or allergies. ---Decreased indicate pyogenic infections. --Basophils: 15-50/mm3, or 0.5%-1% of total, or 0.02-0.05 × 109/L ---Elevations indicate possible inflammation; ex. chronic sinusitis, hypersensitivity rx. ---Decreased may be seen in an acute infection. --Lymphocytes: 1000-4000/mm3, or 20%-40% of total, or 1.0-4.0 × 109/L ---Elevations indicate possible viral infection, pertussis, & infectious mononucleosis. ---Decreased may be seen during corticosteroid tx. --Monocytes: 100-700/mm3, or 2%-8% of total, or 0.1-0.7 × 109/L ---Elevations: see Lymphocytes; also may indicate active TB. ---Decreased: see Lymphocytes.

Labs for ACS

Labs for ACS: no 1 test to Dx MI; most common lab→ troponins T&I; Troponin is specific for MI & cardiac necrosis, T&I rise quickly. If serial troponins negative→ nuclear medicine test. -Laboratory Profile; CV Assessment (Lipids & Markers): -Cholesterol <200 mg/dL; Elevation= increased CAD risk. -Triglycerides: Females 35-135 mg/dL; Males 40-160 mg/dL. Elevation= increased CAD risk. -Plasma HDLs: Females >55 mg/dL; Males >45 mg/dL; Older adults range increases w/ age. Elevations= protect against CAD. -Plasma LDLs: <130 mg/dL; Elevation= increased CAD risk. -HDL/LDL ratio 3:1; Elevated ratios= may protect against CAD. -VLDL: 7-32 mg/dL; Elevation= increased CAD risk. -CRP <1.0 mg/dL; Elevation= may indicate tissue infarction or damage. -Serum Markers; Cardiac troponin T <0.1 ng/mL; Cardiac troponin I <0.03 ng/mL. Elevations= indicate myocardial injury or infarction. --Troponin T & I. Troponin I more specific for cardiac dz. Troponin T more strongly associated w/ non-CVD; per NIH, preferred cardiac enzyme when evaluating for suspected MI. Troponin released into blood when heart muscle damaged; greater damage= higher troponin. -Highly sensitive C-reactive protein (hsCRP): most studied marker of inflammation. Any inflammatory process→ CRP in blood. Inflammation→ common & critical component to atherothrombosis. Elevations also seen w/ HTN, infection, smoking. --Level <1 mg/L= low risk; level >3 mg/L= high risk for heart dz. CRP is very helpful in ID tx outcomes in pts at CAD risk & w/ managing statin tx after acute MI. Most useful time to measure CRP for risk assessment in middle-age+. -PT & INR used when initiating & maintaining PO anticoagulant tx [warfarin]; measure activity of prothrombin, fibrinogen, & factors V, VII, & X. INR→ most reliable way to monitor anticoagulant status w/ warfarin. Therapeutic ranges vary significantly based on reason for use & pt history; normal INR is 0.8-1.1. -PTT is assessed if receiving heparin; measures deficiencies in all coagulation factors except VII & XIII.

Labs for Sepsis & Septic Shock; Planning

Labs for Sepsis & Septic Shock: No 1 test confirms sepsis & septic shock; hallmarks of sepsis= rising serum procalcitonin, increasing serum lactate, normal or low total WBCs, & decreasing segmented neutrophils w/ rising band neutrophils (Lt shift). Presence of bacteria in blood supports Dx of sepsis; may not be present. -Obtain specimens of urine, blood, sputum, & any drainage for culture to ID causative organisms. Blood cultures→ taken before ABs started, if it does not delay ABs by >45min. -Other abnormal labs w/ septic shock= WBC changes; differential leukocyte count may show Lt shift. Hct & Hgb usually do not change until late septic shock; when Hct & Hgb, fibrinogen, & plts are low from DIC. Serum lactate is above normal, & serum HCO3 lower than normal. -Blood culture results may not be available until progression to sepsis or septic shock→ other biomarkers are needed to help ID condition when management & cure is possible. 1 marker is serum lactate→ assess pts not yet hypotensive but at risk for septic shock. Lactate levels of 4 mmol/L+ (normal= 3-7mg/dL) associated w/ 30% mortality rate. --Actual Dx of sepsis is difficult; best outcome depends on early Dx & appropriate aggressive tx. -Planning: w/ appropriate tx, sepsis or septic shock pt is expected to have normal aerobic cellular metabolism. Indicators include: ABG (pH, PaO2, PaCO2) w/in normal range. Maintenance of UO >20 mL/hr. Maintenance of MAP w/in 10mmHg of baseline. Absence of MODS.

Levels & Functions of Trauma Centers

Levels & Functions of Trauma Centers: Not all EDs w/ 24/7 ER services are trauma centers. American College of Surgeons Committee on Trauma (2020) set forth national stds. for trauma center accreditation & categorizes resource requirements for highest-capability trauma center (Level I) to lowest (Level IV). -Level I: Usually in large teaching hospitals in densely populated areas. Provides full continuum of trauma services for adult &/or peds. Conducting research is requirement for trauma center verification. -Level II & Level III: Typically in community hospitals. --Level II: Provides care to most injured pts. Transfers if needs exceed resource capabilities. --Level III: Stabilizes pts w/ major injuries. Transfers if needs exceed resource capabilities. -Level IV: Usually in rural & remote areas. Provides basic trauma pt stabilization & adv. life support w/in resource capabilities. Arranges transfer to higher levels as necessary.

MV Indications, Goal, Ventilator Types, Modes of Ventilation

MV: support & maintain gas exchange. RN, pivotal role in care coordination & problem prevention. --Goal: improve gas exchange & decrease work for effective breathing; support until lung function is adequate or until acute episode passed. Does not cure lungs→ it supports until they can breath independently. Normal gas exchange w/ oxygenation, ventilation, & respiratory muscle strength is achieved→ can discontinue MV. -Positive Pressure: most common; usually ETT or tracheostomy is needed; can be pressure cycled, vL cycled, time cycled. During inspiration→ pressure generated→ drives gas flow to push air→ lungs & expand chest. NIPPV= use mask or nasal prongs to deliver gas flow. -Negative Pressure: air pressure is lower in 1 place in comparison to another; ex. iron lung→ create subatmospheric pressure [P<room air] around the chest→ lowers pleural & alveolar pressure→ facilitates air flow into lungs. -Assist-control (AC) ventilation: full support mode; ventilator takes over the work of breathing. Tidal vL & ventilatory rate are preset; called mandatory breaths. If pt does not trigger spontaneous breaths→ AC establishes a ventilatory pattern. --Disadvantage: continues to deliver preset tidal vL even when spontaneous breathing rate increases→ hyperventilation & respiratory alkalosis. Investigate & correct causes of hyperventilation, ex. pain, anxiety, or acid-base imbalances. -Synchronized intermittent mandatory ventilation (SIMV): similar to AC→ tidal vL & ventilatory rate are preset; used in pressure- or vL-regulated mode. If they do not breathe→ ventilatory pattern is established by SIMV. Unlike AC, it allows spontaneous breathing at their own rate & tidal vL between ventilator breaths. Used as main ventilatory mode or weaning mode. -Pressure support ventilation: for spontaneously breathing pts; no tidal vL set. Delivers the pts own breath w/ assistance from a set airway pressure & PEEP; used as a step in weaning process. -CPAP & BiPAP: noninvasive pressure support modes of ventilation (NIPPV); for spontaneously breathing pts; require a nasal mask or facemask. Both used for OSA, but BiPAP also for COPD, HF, respiratory muscle fatigue, or impending RF to avoid more invasive ventilation methods. --Normal CPAP levels= 5-15cm H2O. --Normal BiPAP levels= IPAP 10-20cm H2O; EPAP 4-8cm H2O.

Management of 3 phases of ARDS

Management of ARDS: general management focuses on the 3 phases of ARDS; phase timing varies by patient. -Exudative phase: includes early changes of dyspnea & tachypnea; results from the alveoli becoming fluid filled, pulmonary shunting, & atelectasis. --Early txs focus on support & providing O2 (via mask or NC). -Fibrosing alveolitis phase: increased lung injury leads to pulmonary HTN & fibrosis; body attempts to repair damage, & increasing lung involvement reduces gas exchange & oxygenation; multiple organ dysfunction syndrome (MODS) can occur. --Tx focus on delivering adequate O2, preventing complications, & lung support. -Resolution phase: usually occurs after 14 days, injury resolution is possible; if not, they die or have chronic disease; fibrosis is possible. Survivors often have neuropsychologic deficits.

Best Practice for Patient Safety & Quality Care: Management of Chest Tube Drainage System

Management of CT Drainage System: -Pt: • Ensure dressing on chest around tube is tight & intact. Per policy & surgeon, reinforce or change loose dressings. • Assess for difficulty breathing. • Assess breathing effectiveness by pulseOx. • Listen to breath sounds for each lung. • Check alignment of trachea. • Check tube insertion site for condition of skin. Palpate area for puffiness or crackling; may indicate SQ emphysema. • Observe site for s/s infection (redness, purulent drainage) or excessive bleeding. • Check if tube "eyelets" are visible (they should not be visible). • Assess for pain & its location & intensity & admin drugs for pain as prescribed. • Assist to DB, cough, perform maximal sustained INH, & use IS. • Reposition if reports "burning" pain in chest. -Drainage System: • Do not "strip" the CT; use hand-over-hand "milking" motion. • Keep system lower than level of pt chest. • Keep CT as straight as possible from bed→ suction unit, avoiding kinks & dependent loops. Extra tubing is loosely coiled on bed. • Ensure CT is securely taped to connector & connector is taped to tubing going into collection chamber. • Assess bubbling in water-seal chamber; should be gentle bubbling on exhalation, forceful cough, position changes. • Assess for "tidaling" (rise & fall of water in chamber 2 w/ breathing). • Check water level in water-seal chamber & keep at level recommended by manufacturer. • Check water level in the suction control chamber & keep at level prescribed by surgeon (unless dry suction system is used). • Clamp CT only for brief periods to change drainage system or if checking for air leaks. • Check & document amount, color, & characteristics of fluid in collection chamber as often PRN per pt condition & policy. • Empty collection chamber or change system before drainage contacts bottom of tube. • When sample of drainage needed for culture or labs, obtain it from CT; after cleaning CT, use 20g (or smaller) needle & draw up specimen into syringe. -Immediately Notify Surgeon or RRT for: • Tracheal deviation from midline. • Sudden onset or increased intensity of dyspnea. • SpO2 <90%. • Drainage >70 mL/hr. • Visible eyelets on CT. • CT falls out of chest (1st, cover area w/ dry, sterile gauze). • CT disconnects from drainage system (1st, put end of tube in container of sterile water & keep below level of chest). • Drainage in tube stops (in first 24hrs).

Managing LV Failure w/ drugs

Managing LV Failure w/ drugs: txs to relieve pain & decrease myocardial O2 requirements through preload & afterload reduction. -IV morphine→ decrease pulmonary congestion & relieve pain. O2 admin. Intubation & MV may be necessary. --Use info from HDM to titrate drugs. Preload reduction may be attempted cautiously w/ diuretics or NTG; Killip class III HF. Monitor SBP bc vasodilation→ further BP decline. Vasopressors & + inotropes to maintain organ perfusion, but increase myocardial O2 consumption & can worsen ischemia. Use extreme caution w/ drug tx. -Drug Alert: caution w/ + inotropes bc risk for increasing myocardial O2 consumption & further decreasing CO. Monitor frequently, w/ attention to development of CP. -Managing RV Failure: conditions other than LV failure may result in decreased CO after ACS. About 1/3 inferior MI pts→ RV infarction & failure; RV fails independently of LV. Decreased CO w/ paradoxical pulse, clear lungs, & JVD occurs in semi-Fowler position. --Desired outcome→ improve RV SV by increasing RV fiber stretch or preload. To enhance RV preload→ give sufficient fluids to increase RA pressure to 20. --Critical care unit, monitor PAOP, & auscultate lungs to assess for Lt-HF. If s/s of this complication occur→ notify HCP immediately. --If medical tx not sufficient to support RV & reverse shock state→ Rt percutaneous V assist device may be needed; temporary tx to support failing heart while tx cardiogenic shock w/ medical tx. --Normal RA pressure 0-8 mmHg. Increased RA pressures w/ RV failure; low RA pressures usually hypovolemia. --Normal PAP 15-30 systolic; 3-12 diastolic. --Normal PAOP 5-12. Elevated PAOP indicates LV failure, hypervolemia, mitral regurgitation, or intracardiac shunting; decreased PAOP w/ hypovolemia or afterload reduction.

Mandatory Reporting

Mandatory Reporting: Responsibility as RN & RN manager to report any issues of co-worker behaviors; be alert to any s/s of a co-worker under influence & be aware of methods of reporting. -Report the HC worker to immediate supervisor; supervisor's responsibility to take further action. -In keeping w/ orgs. policies & procedures, the HR dept. should be alerted to assist supervisor or RN manager w/ confronting employee. -Reporting laws & consequences vary per state. -Clear documentation about employee must be kept; include tardiness, absenteeism, pt or co-worker complaints, records of controlled substances on unit, & physical s/s, observed & reported. -HC workers who abuse drugs or alcohol place pt & staff at considerable risk; important to know responsibilities when dealing w/ impaired RN. -Safety of pt is paramount. Many state RN boards adopted mandatory reporting of suspected impairment. Look to rules & regulations in state to ID responsibility.

Mediastinal CTs

Mediastinal CTs: placed after heart surgery to prevent cardiac tamponade. -To access IMA→ pleural space entered & requires pleural CT w/ mediastinal CTs→ pulmonary assessment crucial. -Action Alert: Bleeding after CABG occurs to limited extent in all pts. Measure mediastinal & pleural CT drainage at least Q1h. Report if >150 mL/hr to surgeon. Internal mammary artery (IMA) grafts may have more chest drainage vs saphenous vein grafts (from leg). -Maintain patency of CTs; to promote CT drainage by preventing dependent loops in tubing. If bleeding & mediastinal CTs not kept patent, fluid (blood) may accumulate around heart. Myocardium compressed→ cardiac tamponade. Fluid compresses A&Vs, preventing adequate filling→ reducing CO. -Critical Rescue: Assess for, document, & report s/s cardiac tamponade immediately: • Sudden cessation of previously heavy mediastinal drainage. Distant, muffled heart sounds. Hypotension. Equalizing of PAOP & RA pressure. CV collapse. Beck triad= Jugular venous distention but clear lung sounds. Pulsus paradoxus (BP >10 higher on E vs I). -May have LOC changes; permanent or transient. Transient r/t anesthesia, CPB, air emboli, or hypothermia occur in many. Assess for neuro deficits; slowness to arouse, memory loss, new-onset confusion. -Prep for echocardiogram or CXR to confirm Dx. Pericardiocentesis (withdrawal fluid from pericardium via large needle) may not be appropriate for tamponade after CABG bc blood in pericardium may have clotted. vL expansion & emergency sternotomy w/ drainage are txs of choice.

Meningitis

Meningitis: infection of meninges of brain & spinal cord, specifically pia mater & arachnoid. Bacteria & viruses most often responsible; fungal & protozoal meningitis can occur. Cancer & drugs, notably NSAIDs, ABs, & IVIG, can cause sterile meningitis. Regardless of cause, s/s are similar. -Organisms enter CNS via bloodstream or are directly introduced into CNS. Direct routes of entry occur bc of penetrating trauma, surgery on brain or spine, or ruptured brain abscess. -Basilar skull fracture may lead to meningitis bc of direct communication of CSF w/ ear or nasal passages→ otorrhea (ear discharge) or rhinorrhea (nasal discharge, or runny nose) that is actually CSF. Organisms follow tract created by skull damage to enter CNS & circulate in CSF. -Pt w/ infection in head (eye, ear, nose, mouth) or neck/throat→ increased risk for meningitis bc of proximity of structures. -Organism may spread to CNs & SNs, causing irreversible neuro damage. Increased ICP may occur bc of blockage of flow of CSF, change in cerebral BF, or thrombus. -Bacterial Meningitis: most frequent organisms causing bacterial meningococcal meningitis= Streptococcus pneumoniae (pneumococcal dz) & Neisseria meningitidis. -N. meningitidis meningitis: AKA meningococcal meningitis; medical emergency w/ fairly high mortality rate, often w/in 24hrs. Unlike other types, it is highly contagious. Outbreaks most likely w/ high population density→ college dormitories, military barracks, & crowded living areas. -Action Alert: 16-21yrs old have highest rates of infection from life-threatening N. meningitidis meningococcal infection. CDC recommends initial meningococcal vax between 11-12yrs w/ booster at 16yrs. Adults advised to get initial or booster vax if living in shared residence (residence hall, military barracks, group home) or traveling or residing in countries where the dz common or if immunocompromised bc of damaged or removed spleen or serum complement deficiency. If baseline vax status is unclear & immediate risk for exposure to N. meningitidis infection is high, CDC recommends vax. Safe to receive booster as early as 8wks after initial vax. -Action Alert: bacterial meningitis is transmitted by droplets→ place pt on Droplet Precautions & Std. Precautions. If possible, place in private rm. Stay at least 3ft from pt unless wearing mask. Pts transported outside of rm should wear mask. Teach visitors about need for these precautions & how follow them. -Std. Precautions appropriate for all w/ meningitis unless have bacterial type transmitted by droplets [N. meningitides & H. influenzae].

Mild, Moderate, & Major Burn Injuries & Burn Center Referral Criteria

Mild, Moderate, & Major Burn Injuries & Burn Center Referral Criteria: Referral Criteria: for going to specialized burn center. Need opening & insurance to cover/approve it. -Minor Burns: Partial-thickness burns <10% TBSA; Full-thickness burns <2% TBSA. -No burns of eyes, ears, face, hands, feet, or perineum; No electrical burns; No INH injury; No complicated additional injury. -Pt is <60yrs & has no chronic cardiac, pulmonary, or endocrine ds. -Pts should receive emergency care at scene & be taken to clinic or ED for evaluation; tx w/ outpatient management. -Moderate Burns: Partial-thickness burns <10% TBSA; Full-thickness burns 2-10% TBSA. No burns of eyes, ears, face, hands, feet, or perineum. No electrical burns. No INH injury. -No complicated additional injury. -Pt <60yrs & has no chronic cardiac, pulmonary, or endocrine ds. -Pts should receive emergency care at scene & be transferred to hospital or burn center. -Major Burns: Partial-thickness burns >10% TBSA; Burns involve face, hands, feet, genitalia, perineum, or major joints. -3rd-degree burns in any age-group. Electrical burns, including lightning injury; Chemical burns; INH injury. Burn injury w/ Hx medical ds that could complicate tx, prolong recovery, or affect mortality. -Any pt w/ burns & concomitant trauma (fractures) where burn injury is greatest risk of morbidity or mortality; but if trauma is greater immediate risk, may be initially stabilized in trauma center before transfer to burn unit; HCP judgment will be necessary & in concert w/ regional medical control plan & triage protocols. -Burned kids in hospitals w/o qualified staff or equipment for care of peds. -Burn injury & requires special social, emotional, or rehab tx. -Pts meet any 1 of criteria above should receive emergency care at nearest ED & then transferred to burn center once stable.

Mitral Stenosis

Mitral Stenosis: usually results from rheumatic carditis, can cause valve thickening by fibrosis & calcification. Rheumatic fever most common cause. -Valve leaflets fuse & stiffen & chordae tendineae contract & shorten; valve opening narrows, preventing normal BF from LA→ LV. Result= LA pressure rises, LA dilates, PAP increase, & RV hypertrophies. Pulmonary congestion & Rt-HF occur 1st. Later, when LV receives insufficient BvL, preload is decreased & CO falls. -S/S: Mild mitral stenosis usually asymptomatic. As valvular orifice narrows & pressure in lungs increases→ DOE, orthopnea, paroxysmal nocturnal dyspnea (sudden; at night), palpitations, & dry cough. Hemoptysis & pulmonary edema occur as pulmonary HTN & congestion progress. Rt-HF can cause hepatomegaly, neck vein distention, and pitting dependent edema late in ds. -Pulse may be normal, rapid, or irregular (in AF). AF indicates pt may decompensate, so HCP notified immediately of rhythm changes Rumbling, apical diastolic murmur noted.

Mitral valve prolapse (MVP)

Mitral valve prolapse (MVP): valvular leaflets enlarge & prolapse into LA during systole; abnormality usually benign but may progress to pronounced mitral regurgitation in some. -Etiology of MVP is variable; associated w/ conditions like Marfan synd. & congenital cardiac defects; also has familial tendency. But usually no other cardiac abnormality found. -Most MVP are asymptomatic; but some may report CP, palpitations, or exercise intolerance. CP usually atypical; pts describe sharp pain localized to Lt chest. Dizziness, syncope, & palpitations may be associated w/ A or V dysrhythmias. -Normal HR & BP usually found; midsystolic click & late systolic murmur may be at apex. Intensity of murmur is not r/t severity of prolapse.

Mobile or portable CT drainage systems; CT Removal

Mobile or portable CT drainage systems: lightweight, "dry" systems w/o water seal to prevent air re-entering lung via CT. Instead use dynamic control "flutter" valve to prevents air back-flow. --When pt exhales, air forced from chest cavity into CT under pressure, the soft flutter valve opens, & air moves into harder surrounding tube shell, where it's vented. --Portable units allow ambulation & can go home w/ CT in place. -CT Removal: performed when drainage minimal & lung expansion stable. Usually surgeon removes CT at bedside; causes short period of procedural pain. --After removal, site dressed & sealed w/ occlusive dressing & observed for drainage. --Assess Q1h for respiratory distress for 1st few hrs after CT removal. Respiratory distress may signal lung collapse & need for CT reinsertion.

Monitoring for & Managing HF in ACS

Monitoring for & Managing HF in ACS: pt will be free of HF; if HF occurs, HF will be ID & tx early to prevent complications. Heart loses ability to contract adequately, it begins to fail. -Decreased CO r/t HF is common complication after MI result of LV dysfunction, rupture of intra-V septum, papillary muscle rupture w/ valvular dysfunction, or RV infarction. Most severe form of acute HF, cardiogenic shock, causes most hospital deaths after ACS. Tx type used to increase CO depends on location of ACS & type of HF that resulted from infarction. -Always assess for s/s of HF in a pt s/p MI. -Managing LV Failure: ACS pt w/ damage to LV, intraventricular septum rupture, or papillary muscle tear→ amount of blood that heart can eject reduced. When vL & pressure are markedly increased in pulmonary BVs→ pulmonary complications develop. Fluid backed up in pulmonary system. --Assess for s/s of LV failure & pulmonary edema by listening for crackles & ID location in lungs. Wheezing, tachypnea, & frothy sputum may also occur w/ pulmonary edema. Auscultate heart, assess for S3 sound. --Critical Rescue: Monitor, report, & document s/s inadequate organ perfusion that may result from decreased CO: change in orientation or MS; UO <0.5 to 1 mL/kg/hr; Cool, clammy extremities w/ decreased or absent pulses; Unusual fatigue; Recurrent CP. -Monitor for cardiogenic shock: most severe form of HF. S/S Cold, clammy skin, poor peripheral pulses, agitation, pulmonary congestion, tachypnea, hypotension, tachycardia, decreased UO. --Critical Rescue: Monitor, report, & document s/s cardiogenic shock immediately. Early ID essential bc un-Dx cardiogenic shock has high mortality! Tachycardia; Hypotension; SBP <90 or 30 less than baseline; UO <0.5-1 mL/kg/hr; Cold, clammy skin w/ poor peripheral pulses; Agitation, restlessness, or confusion; Pulmonary congestion; Tachypnea; Continuing chest discomfort.

Multiple Sclerosis

Multiple Sclerosis: chronic dz caused by immune, genetic, &/or infectious factors that affects myelin & nerve fibers of brain & SC. A leading cause of neuro disability in young & middle-aged. -Cause: complex & involves multiple immune, genetic, &/or infectious factors; changes in immunity [autoimmune] likely etiology. Environment may contribute to development; ex. MS more often in colder climates of NE, Great Lakes, & Pacific NW states & Canada. MS common in areas of N. European ancestry. -MS characterized by periods of remission & exacerbation (flare); pts progress at different rates & over different lengths of time. -Severity & duration of dz progress→ periods of exacerbation more frequent. -Normal life expectancy as long as effects of dz managed effectively. -Characterized by demyelination (loss of myelin sheaths). Diffuse random or patchy areas of plaque in white matter of CNS are the definitive finding. Initially, remyelination takes place to some degree, & s/s decrease; over time→ new lesions develop & neuronal injury & muscle atrophy occur. -Myelin= responsible for electrochemical transmission of impulses between brain & SC & body; demyelination→ slowed or stopped transmission. White fiber tracts= connect neurons in brain & spinal cord also usually involved in MS. -Areas affected: optic nerves, spinal pyramidal tracts, spinal posterior columns, brainstem nuclei, & ventricular region of brain. -4 major types: Relapsing-remitting; Primary progressive; Secondary progressive; Progressive-relapsing.

NPSGs & Sentinel Events

NPSGs: 1. Improve Accuracy of Pt ID: use 2+ identifiers to ID correct pt & procedure; name, ID #, telephone #, or person-specific ID. 2. Improve Effectiveness of Communication Among CGs: Report critical results of tests & Dx procedures on timely basis. 3. Improve Safety of Using Meds: Label all meds, med containers, & solutions on/off the sterile field in peri-op & procedural settings; ex. containers= syringes, med cups, basins. 4. Reduce Risk of HAIs: Comply w/ current CDC hand hygiene guidelines, or current WHO hand hygiene guidelines. 5. ID pts at risk for suicide: Hospital ID's Safety Risks Inherent in its pt pop; pt suicide in a staffed, ATC care setting is a frequently reported type of sentinel event. 6. Intro to Universal Protocol for Preventing Wrong Site, Wrong Procedure, & Wrong Pt Surgery: applies to all surgical & nonsurgical invasive procedures; highest risk= general anesthesia or deep sedation. 1.) Conduct pre-procedure verification process. 2.) Mark procedure site. 3.) Time-out performed before the OP. -Sentinel Event: Unexpected occurrence involving death or serious physical or psychological injury, or the risk thereof. Called "sentinel" bc signal need for immediate investigation & response. Serious injury specifically includes loss of limb or function. --Sentinel event ID→ root-cause analysis performed by team that includes those directly involved in the process; retrospective review of event, to evaluate potential causes of problem or sources of variation in the process. Team looks at every process along the way that lead up to the event. What factors & processes were in place that allowed this error to occur; where the processes okay & RN just didn't perform 2 ID's; is it a process error or an individuals error? -Terms "sentinel event" & "medical error" are not synonymous; not all sentinel events occur bc of an error, & not all errors result in sentinel events.

National Council of State Boards of Nursing; Nursing Licensure Compact

National Council of State Boards of Nursing (NCSBN): 2 licensure exams= National Council Licensure Exam for RNs or PNs; used by state & territorial boards of nursing to assist in making licensure decisions. -New RN needs to decide where to be licensed. Most take the exam in intended state of work. 1st contact state board of nursing in state intend to work. -Many states require RNs to take exam in that state or to apply via state board for reciprocity, the Nurse Licensure Compact of NCSBN moving toward mutual recognition of licensure by the states; 24 states, legislation pending in 4 others. Not all state boards have enacted. -If you move to another state & 1 of states has compact agreement: -Non-compact to compact: apply for licensure by endorsement in new residency state. You license from non-compact state not effected, remains active if maintained, & if so provided by the non-party state laws. -Compact to non-compact: apply for licensure by endorsement in new residency state. Compact license changed to 1-state license, valid only in that state. Must notify board you have moved out of state. -Compact to compact: can practice in former state for max 30 days. Required to: apply for licensure by endorsement (best if 1-2mo before move); pay any fees; declaration of primary state of residency in new state. Issued a new multi-state license & former is inactive. Notify board in former state that you have moved. May require proof of residency.

Natural Pacemakers; heart physiology

Natural Pacemakers; heart physiology: specialized myocardial cells; regulate HR & rhythm. -SA node: usual PM; 60-100 BPM. -Other potential PMs (if SA node fails): atrial PMs w/ inherent rates of 60-80 BPM, AV node (40-60 BPM), or ventricular pacer (20-40 BPM). -Certain conditions w/ ectopic (out of place) PMs can go much faster at 150-250 cycles/min. o Automaticity (pacing function)= ability of cardiac cells to generate electrical impulse spontaneously & repetitively. Normally only SA node can generate an electrical impulse. § Under certain conditions, ex. myocardial ischemia (decreased BF), electrolyte imbalance, hypoxia, drug toxicity, & infarction (cell death)—any cardiac cell may produce electrical impulses independently & create dysrhythmias. § Automaticity disturbances may involve an increase or decrease in pacing function. o Excitability= ability of non-PM heart cells to respond to an electrical impulse that begins in PM cells. o Depolarization= when normally - charged cells w/in heart muscle develop a + charge. o Conductivity= ability to send an electrical stimulus from cell membrane→ cell membrane. Result→ excitable cells depolarize in rapid succession from cell to cell until all cells have depolarized. § Depolarization wave→ deflections in ECG waveforms= P wave & QRS complex. § Disturbances in conduction result when conduction is too rapid or too slow, pathway is totally blocked, or when electrical impulse travels an abnormal pathway. o Contractility= ability of atrial & ventricular muscle cells to shorten fiber length in response to electrical stimulation→ sufficient pressure to push blood forward through heart. Contractility is the mechanical activity of the heart.

Noninvasive Positive-Pressure Ventilation (NPPV)

Noninvasive Positive-Pressure Ventilation (NPPV): type of noninvasive ventilation (NIV); uses positive pressure to keep alveoli open & improve gas exchange w/o the dangers of intubation. Can deliver O2 or RA; nasal mask, nasal pillows, or full-face mask system allows mechanical delivery. -3 common modes: 1.) CPAP; delivers a set PAP throughout each cycle of inhalation & exhalation. Opens collapsed alveoli; benefits patient's w/ post-op atelectasis, cardiac-induced pulmonary edema, & COPD. Not helpful for respiratory failure following extubation. 2.) vL-limited or flow-limited; delivers a set tidal vL w/ the inspiratory effort & won't give anything more than that; in-between the effect of CPAP & BiPAP. 3.) Pressure-limited; includes pressure support, pressure control, & bi-level PAP (BiPAP), which cycles different pressures at inspiration & expiration. BiPAP: cycling machine delivers a set inspiratory PAP each time the patient begins to inspire; when they begin to exhale, the machine delivers a lower set end-expiratory pressure; 2 pressures improve tidal vL, reduce RR, & relieve dyspnea. -CPAP & BiPAP are both commonly used after extubation to prevent respiratory failure & need for reintubation. -Used to manage dyspnea, hypercarbia, & acute exacerbations of COPD, cardiogenic pulmonary edema, & acute asthma attacks. -NPPV prevents the complications associated w/ intubation (ex. VAP: ventilator-associated pneumonia; VAEs: ventilator-associated events); still has risks & complications. -Masks must fit tightly to form a proper seal; can lead to loss of tissue integrity w/ skin breakdown over the nose or face. Full face masks cause fewer skin problems than nasal-oral masks. -Leaks can cause uncomfortable pressure around the eyes, & gastric insufflation can lead to vomiting & aspiration. -NPPV is recommended only for use in alert patients who have the ability to protect their airway, although a NGT may still be required for safety. -NPPV is used commonly for sleep apnea; holds open the upper airways. Those using CPAP or BiPAP at home often bring their home equipment to the hospital; feel more comfortable using their own equipment. -RN: patients using NPPV tx is increasing in every setting; RN must be knowledgeable about the equipment, technique, & potential complications. RT support can help safely manage a patient receiving NPPV.

NSR, Sinus bradycardia, Sinus tachycardia, Sinus Arrhythmia

Normal Sinus Rhythm: -Rate: Atrial & ventricular rates of 60-100 BPM -Rhythm: Atrial & ventricular rhythms regular -P waves: Present, consistent configuration, 1 P wave before each QRS complex -PR interval: 0.12-0.20s & constant -QRS duration: 0.06-0.10s & constant -Sinus Bradycardia: HR <60; Regular; PR 0.12-0.20; QRS 0.08-0.12. -Sinus Tachycardia: HR >100; Regular; PR 0.12-0.20; QRS 0.08-0.12. -Sinus Arrhythmia: Variant of NSR; results from changes in intrathoracic pressure during breathing. In this context→ arrhythmia does not mean absence of rhythm; instead, HR increases slightly during inspiration & decreases slightly during exhalation. This irregular rhythm is frequently observed in healthy adults. --Has all NSR characteristics except for irregularity. PP & RR intervals vary, w/ the difference between the shortest & longest intervals being >0.12s (3 small blocks): -Rate: Atrial & ventricular rates 60-100BPM -Rhythm: Atrial & ventricular rhythms irregular, w/ shortest PP or RR interval varying >0.12s from longest PP or RR interval -P waves: 1 P wave before each QRS complex; consistent configuration -PR interval: Normal, constant -QRS duration: Normal, constant --Sinus arrhythmias are occasionally due to nonrespiratory causes; ex. digoxin or morphine; drugs enhance vagal tone & cause decreased HR & irregularity unrelated to respiratory cycle.

OSA: Patho, S/S, RN Assessment

OSA: type of breathing pattern disruption during sleep; lasts >10sec & occurs min. of 5x/hr; usually occurs w/ sleep time hypopnea= lower-than-normal RR & depth insufficient for effective gas exchange. -Reduced Gas Exchange [O2sat <80%]→ Increases CO2→ Decreases pH→ stimulates neural centers to breathe & pt awakens after 10+sec of apnea→ corrects obstruction & respiration resumes→ falls asleep & cycle resumes (often as Q5min)→ daytime sleepiness→ LT reduction in deep sleep→ reduced body restoration→ fatigue, irritability, depression. -S/S: chronic excessive daytime sleepiness, inability to concentrate, morning headache, & irritability. LT chronic→ increased risk HTN, stroke, cognitive deficits, wt gain, DM, pulmonary & CVD, metabolic issues. -Most common cause is UAO by the soft palate or tongue. Contributing factors; obesity, large uvula, short neck, smoking, enlarged tonsils or adenoids, & oropharyngeal edema. -Assess: Hx- Persistent daytime sleepiness, snoring, GERD; nightmares; awakened by snoring (ask family); use of sleep aids; evening alcohol consumption; awakened by heartburn (GERD s/s). Physical- appearance, ht/wt; retracted lower jaw, smaller chin, & shorter neck; tonsils, adenoids, pillars, soft palate are swollen or enlarged; HTN (BP x2 if un-Dx). Psyc- irritability & personality changes (ask family); depression, social disinterest, memory loss, can't concentrate.

Other Dx tests for ACS

Other Dx tests for ACS: 12-lead ECGs allow HCP to examine heart from varying perspectives; by ID lead(s) ECG changes occurring in→ ID occurrence & location of ischemia (angina) or necrosis (MI). In addition to 12-lead ECG, HCP may request "Rt-sided" or 18-lead ECG to ID if ischemia or infarction occurred in RV. ECG should be obtained w/in 10min presentation w/ chest discomfort! -Ischemic myocardium does not repolarize normally; 12-leads obtained during angina episode→ ST depression, T-wave inversion, or both. Vasospastic angina, caused by coronary vasospasm (vessel spasm)→ [usually] elevation of ST segment during angina attacks. ST & T-wave changes usually subside when ischemia resolved & pain relieved. But T wave may remain flat or inverted for a period. If not experiencing angina at moment of test→ usually ECG normal unless evidence of old MI. -Infarction occurs→ 1 of 2 ECG changes usually observed: ST-elevation MI (STEMI), or non-ST-elevation MI (NSTEMI). Abnormal Q wave, wider than 0.04s or >1/3 the height of QRS complex, may develop, depending on amount of myocardium necrosed. Women having MI often present w/ NSTEMI. -Q wave may develop bc necrotic cells do not conduct electrical stimuli. Hrs-days after MI→ ST-segment & T-wave changes return to normal; when Q wave exists→ may be permanent. Q waves may disappear after #yrs, but absence does not mean pt has not had MI. -After acute stages of unstable angina episode, HCP often requests an exercise tolerance test (stress test) on treadmill to assess for ECG changes consistent w/ ischemia, evaluate medical tx, & ID pts who benefit from invasive tx. Pharm stress-testing agents [dobutamine] may be used instead of treadmill. Treadmill testing is only moderately accurate for women. Results are not as reliable in tall, obese men vs. short, thinner men. Women w/ suspected CAD→ perform stress echocardiography or single-photon emission CT (SPECT). -Cardiac Cath: imaging w/ fluoroscopy (dye), how CAs are filling; to ID extent & exact location of coronary artery obstructions; allows cardiologist & cardiac surgeon to ID pts who benefit from percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). Take pics; Dx; do balloon angio, stent, etc.

Other Management Considerations for ACS

Other Management Considerations for ACS: -Increasing functional ability: Cardiac rehab; 3 phases (1= hospital; 2= d/c to convalescing at home; 3= LT). Sex after MI is frequent concern. Refer to HCP/cardiologist for individualized tx. Assessing for problems post-D/C; Activity intolerance if 20+ in SBP, changes of 20BPM, dyspnea or CP. -Increasing ability to cope: Assess anxiety level, coping abilities & support systems. -ID & Managing Dysrhythmias: pt will be free of dysrhythmias. If dysrhythmias occur, ID & tx early to prevent complications or death. ID dysrhythmia→ assess HDS, CP or discomfort. --Dysrhythmias= leading cause of prehospital death in most w/ ACS. Even in early period of hospitalization, most w/ ACS experience some abnormal rhythm. --Dysrhythmias tx-ed if causing HD compromise, increase myocardial O2 requirements, or predispose to lethal V dysrhythmias. --Typical dysrhythmias w/ inferior ACS are bradycardias & 2nd degree AV blocks result of ischemia in AV node; rhythms usually intermittent. Monitor rhythm & HR & HDS. If HD unstable→ temporary PM may be necessary. --Anterior ACS: likely PVCs caused by V irritability. 3rd degree or bundle branch block is serious complication bc indicates lg. portion of LV involved. HCP may insert PM. Observe closely to ID HF.

Other Multitiered Models for Triage

Other Multitiered Models for Triage: further sort conditions w/in acuity classification or triage priority system, 4 & 5-tier triage models exist; based on comprehensive lists of conditions that indicate triage priority assignment or on nature of resources they will use in ED. A pt situation may generate various triage classifications in different hospitals, depending on triage priority system used. Some schemes may take into account pre-existing conditions like Hx of anticoagulants, DM, CVD, & organ transplant. -No universally triage system in US & no standardization of triage data to compare pt acuity among hospitals. HCPs, health insurance, & pts often disagree on definition of emergent vs nonurgent ED visit, making it essential to use practical triage system to maintain dept. efficiency & allocation of resources. -Emergency Nurses Association in collab. w/ American College of Emergency Physicians studied research on acuity scales & concluded that 2 std. 5-level systems were most reliable: Emergency Severity Index (ESI) & Canadian Triage Acuity Scale (CTAS). -ESI model uses algorithm that fosters rapid, reliable, and clinically pertinent categorization into 5 groups, from Level 1 (emergent)→ Level 5 (non-urgent). -CTAS model differs from ESI bc lists of descriptors used to estab. triage level. -Whatever triage model used, triage RNs must use systematic approach, apply decision-making skills, & maintain caring ethic. -Compassion fatigue: AKA burnout; can hinder objectivity in ED pt care; bias threatens the ED RNs ability to triage accurately→ Mis-triage is pt safety risk; can be "root cause" of delayed or inadequate tx, w/ potentially deadly consequences.

PE Severity & Management Options (tbl 29.1)

PE Severity & Management Options (tbl 29.1): -RN management of PE; rapid categorization of PE severity & prompt management are required. PE Severity & Management Options (tbl 29.1): -Massive PE; Mortality as high as 65%: --S/S: severe hypotension (SB <90 for >15min); cardiac arrest, cardiopulmonary collapse; severe bradycardia; shock; severe dyspnea, respiratory distress. --Tx: CPR; Inotropic and/or vasopressor support, fluids; Fibrinolytic tx; Tissue plasminogen activator (tPA); Alteplase; Unfractionated heparin initial tx. -Submassive PE: --S/S: normotension; RV dysfunction on echocardiography; RV dilation on echocardiography or CT; Rt bundle branch block; ST elevation or depression; T-wave inversion; Elevated BNP or troponin. --Tx: is controversial; some agents not approved for this group; must weigh benefits of thrombolytic tx against risk for bleeding; fibrinolytics may be preferred if patient appears to be decompensating or if there is RV dysfunction (hypokinesis) or elevation in BNP or troponin; LMWH (preferred agent); Fondaparinux; Unfractionated heparin. -Low-risk PE; Mortality ranges from 1-8%: --S/S: normotension; no RV dysfunction; no elevation in BNP or troponin. --Tx: fibrinolytics not warranted because of risk for bleeding; LMWH; Direct thrombin inhibitor; Inpatient hospitalization not usually required. --Heparin antidote= protamine sulfate; Warfarin antidote= vitamin K1, available as an injectable drug, phytonadione. Fibrinolytic tx antidotes= clotting factors, FFP, & aminocaproic acid. (Alteplase= Aminocaproic acid).

Parkinson disease (PD)

Parkinson disease (PD): AKA Parkinson's disease & paralysis agitans; progressive neurodegenerative dz & 1 of most common neuro-ds of elderly. -Parkinson's: dopamine & Ach; dopamine is inhibitory, so w/o it tremors. -Debilitating dz affecting mobility; characterized by 4 cardinal s/s: tremor, muscle rigidity, bradykinesia or akinesia (slow or no movement), & postural instability. Changes in cognition, like dementia & psychoses, can occur in some w/ late-stg PD. -Young & middle-age adults w/ s/s may be mis-Dx w/ Huntington dz= rare hereditary ds; is characterized by progressive dementia & choreiform movements (uncontrollable rapid, jerky movements) in limbs, trunk, & facial muscles. -Most pts have primary [idiopathic] dz; a few have secondary parkinsonian s/s from conditions [brain tumors] & antipsychotic drugs. -Normally→ motor activity occurs by integrating actions of cerebral cortex, basal ganglia, & cerebellum. Basal ganglia= group of neurons, deep w/in cerebrum at base of brain near lateral ventricles. When basal ganglia stimulated→ muscle tone is inhibited & voluntary movements refined; occurs by dopamine & ACh secretion. -Dopamine produced in substantia nigra & adrenal glands; transmitted to basal ganglia along neural pathway for secretion when needed. ACh produced & secreted by basal ganglia & nerve endings in periphery of body. ACh-producing neurons transmit excitatory messages throughout basal ganglia. Dopamine inhibits these neurons, allowing control over voluntary movement. System of checks & balances usually allows refined, coordinated movement, like picking up pencil & writing. -Widespread degeneration of substantia nigra leads to decrease in amount of dopamine in brain. When dopamine levels decreased to 70-80% of usual levels→ symptomatic & loses ability to refine voluntary movement. Large #s excitatory ACh-secreting neurons remain active, creating imbalance between excitatory & inhibitory neuronal activity. Resulting excessive excitation prevents controlling or initiating voluntary movement. -Interferes w/ movement bc of dopamine loss in brain; also reduces SNS influence on heart, BVs, & other areas. Loss→ orthostatic hypotension, drooling, nocturia, & other autonomic s/s frequently seen. -Staged by s/s & disability degree. Stage 1= mild dz w/ unilateral limb involvement; stage 5= completely dependent in all ADLs. Other classifications refer to mild, moderate, severe.

Patho, S/S, & Tx of Common Cardiomyopathies

Patho, S/S, & Tx of Common Cardiomyopathies: -Dilated Cardiomyopathy: Fibrosis of myocardium & endocardium; Dilated chambers; Mural wall thrombi prevalent. --S/S: Fatigue & weakness; HF (Lt side); Dysrhythmias or heart block; Systemic or pulmonary emboli; S3 & S4 gallops; Moderate→ severe cardiomegaly. --Tx: S/S tx of HF; Vasodilators; Control of dysrhythmias. Surgery= heart transplant. -Hypertrophic Cardiomyopathy: --Nonobstructed: Hypertrophy of all walls; Hypertrophied septum; Relatively sm chamber size. --S/S: Dyspnea; Angina; Fatigue, syncope, palpitations; Mild cardiomegaly; S4 gallop; Ventricular dysrhythmias; Sudden death common; HF. --Obstructed: Same as nonobstructed except for obstruction of LV outflow tract associated w/ hypertrophied septum & mitral valve incompetence. --S/S: Same as for nonobstructed except w/ mitral regurgitation murmur; AF. -Tx for both: S/S tx; BBs; Conversion of AF. Surgery= ventriculomyotomy or muscle resection w/ mitral valve replacement. Nitrates & other vasodilators contraindicated w/ obstructed form.

Pathophysiology & evolution of a MI

Pathophysiology & evolution of MI: Irreversible cardiac damage begins after 20min of O2 deprived state.Infarction= dynamic process that does not occur instantly; it evolves over period of several hrs. -Hypoxemia from ischemia→ local BV vasodilation & acidosis. K, Ca, & Mg imbalances, & acidosis at cellular level→ changes in normal conduction & contractile functions. -Catecholamines (epi & NE) released in response to hypoxia & pain→ increase HR, contractility, & afterload→ increase O2 requirements in tissue that is already O2 deprived; may lead to life-threatening ventricular dysrhythmias. -Area of infarction may extend into zones of injury & ischemia. Actual extent of zone of infarction depends on 3 factors: collateral circulation, anaerobic metabolism, & workload demands on myocardium. -Obvious physical changes do not occur in heart until 6hrs after infarction; infarcted region appears blue & swollen. Changes explain need for tx w/in 4-6hrs of s/s onset! -After 48hrs→ infarcted area turns gray w/ yellow streaks as neutrophils invade tissue & begin removing necrotic cells. -By 8-10 days after infarction→ granulation tissue forms at edges of necrotic tissue. -Over 2-3mo period→ necrotic area eventually is shrunken, thin, firm scar. Scar tissue permanently changes size & shape of entire LV [ventricular remodeling]. Remodeling may decrease LV function→ HF, & increase morbidity & mortality. Scarred tissue does not contract or conduct electrically. Area is often cause of chronic ventricular dysrhythmias surrounding the infarcted zone. -Pt response to MI also depends on which coronary artery[s] were obstructed & which part of ventricle wall was damaged: anterior, septal, lateral, inferior, or posterior. -Lt anterior descending (LAD) artery obstruction→ anterior or septal MIs bc it perfuses the anterior wall & most of septum of LV. Anterior wall MIs (AWMIs)→ highest mortality rate bc most likely to have LV failure & dysrhythmias from LV damage. -Circumflex artery supplies the lateral wall of LV & possibly portions of posterior wall or SA & AV nodes. Circumflex artery obstruction→ posterior wall MI (PWMI) or lateral wall MI (LWMI) & sinus dysrhythmias. -In most pts→ Rt coronary artery (RCA) supplies [most of] the SA & AV nodes,+ RV & inferior or diaphragmatic portion of LV. RCA obstruction→ often have inferior wall MIs (IWMIs). About 1/2 of all IWMIs are associated w/ RCA occlusion→ significant RV damage; important to obtain a "Rt-sided" ECG to assess for RV involvement.

Perfusion Exemplar; Atrial Fibrillation

Perfusion Exemplar; Atrial Fibrillation: most common dysrhythmia. Can impair quality of life & cause morbidity & mortality, r/t clotting concerns [embolic stroke, DVT, or PE]. -Multiple rapid impulses from many atrial foci→ depolarize atria in disorganized manner 350-600x/min; ventricular response usually 120-200BPM. -Result in chaotic rhythm w/ no clear P waves, no atrial contractions, loss of atrial kick, & irregular ventricular response. Atria quiver in fibrillation (A fib). -Often ventricles beat w/ rapid & irregular rate in response to numerous atrial impulses→ decreases ventricular filling & reduces CO. Cardiac function alteration allows blood to pool→ risk for clotting (DVT, PE). AF frequently associated w/ underlying CVD. -Etiology & Genetic Risk: associated w/ atrial fibrosis & loss of muscle mass; changes are common in heart dz [HTN, HF, CAD]. For pt w/o underlying ds→ AF, 30 genetic mutations potential cause. As AF progresses→ CO decreases by 20-30%. -Incidence & Prevalence: most common dysrhythmia in developed world; 2.7-6.1mil in US. Incidence increases w/ age→ predicted # will double in next 25yrs. AF→ serious problems in older pts→ stroke &/or HF. --Risk factors: HTN, previous ischemic stroke, TIA or other TE event, CAD, DM, HF, obesity, hyperthyroidism, CKD, excessive alcohol, & mitral valve disease.

Assessing the Burn Patient: Respiratory

Physical; S/S w/ Burns: findings in resuscitation phase differ greatly from later in course of injury. -Respiratory: Assessment of resp. system is most critical to prevent life-threatening complications w/ INH injuries. Even if you think a burn is minor, inspect mouth, nose, & pharynx. Continuous airway assessment is RN priority. Degree of INH damage depends on fire source, temp, environment, & types of toxic gases generated. Facial burns & singed hair, eyebrows, & /or eyelashes= strong indicators of INH injury. Black carbon particles in nose, mouth, & sputum & edema of the nasal septum= smoke INH; also "smoky" smell to pts breath. -Change in resp. pattern, drooling, or difficulty swallowing may indicate pulmonary injury & impairment of gas exchange. Listen for hoarseness, cough, wheezes, & stridor. Place upright, apply O2, & report any of these s/s immediately to HCP. -Critical Rescue: Monitor resp. efforts closely to ID airway involvement, even if you think burn injury is minor. Burn pt in resuscitation phase who is hoarse, has brassy cough, drools, difficulty swallowing, or audible breath sound on exhalation, respond by immediately placing upright, applying O2, & notifying RRT. -Upper airway edema & INH injury most common in trachea & mainstem bronchi, even if appears like a minor skin burn injury. Auscultation of these areas may reveal wheezes= partial obstruction impairing gas exchange. --Severe INH injuries may have rapid obstruction & in short time they cannot force air through narrowed airways→ wheezing disappears= airway obstruction & demands immediate intubation. --Many intubated when INH injury is first suspected. Waiting for s/s hypoxia may make intubation difficult or impossible. --Action Alert: Heat damage of pharynx often severe enough to produce edema & upper airway obstruction, esp. epiglottitis, impairing gas exchange; can occur at any time in resuscitation phase. If airway exposed to heat, early intubation may be performed before obstruction occurs. If intubation not performed in pt w/ upper airways mildly exposed to heat or toxic gases, continually assess upper airway for edema & obstruction. --Critical Rescue: Monitor resp. efforts closely to ID pulmonary edema. When s/s pulmonary edema present, respond by elevating HOB to at least 45 degrees, applying O2, & notifying burn team or RRT.

Pneumothorax; hemothorax (simple/massive); open/closed; tension pneumothorax

Pneumothorax: air in pleural space causing loss of negative pressure in chest cavity, rise in chest pressure, & reduction in vital capacity; can lead to lung collapse. -Often caused by blunt chest trauma & may occur w/ degree of hemothorax (bleeding into chest cavity); can be a complication of medical procedures. -Simple hemothorax is a blood loss of <1000 mL into the chest cavity. -Massive hemothorax is a blood loss of >1000 mL. -Open Pneumothorax: pleural cavity exposed to outside air, like an open wound in the chest wall. -Closed Pneumothorax: pt w/ COPD has a spontaneous pneumothorax. -Tension Pneumothorax: life-threatening complication of pneumothorax; air continues to enter pleural space during inspiration & does not exit during expiration. --Result= air collects under pressure, completely collapsing the lung & compressing BVs; limits blood return→ decreased filling of the heart & reduced CO. --If not promptly ID & tx, tension pneumothorax is quickly fatal.

Politics & Policy

Politics & Policy: ways RNs can influence quality, safety, & accessibility of HC. Magnet requires that RNs are involved in decision-making groups throughout org., & in community. -Arenas of political action in nursing: Workplace; Professional orgs.; Government. --RN Practice & Stds. Committee: focuses on definition of stds., policies, & procedures for practice, & care delivery across institution. Most policies deal w/ pt care, but others develop policy on issues of workplace safety, professional development of RNs, & staffing. RNs review policies by looking at current practice & comparing it to current best evidence from literature review. Policy evaluation usually occurs on 3yr cycles w/in orgs. New policies brought forward by anyone in org. --Professional Orgs: Membership important for continued development. Magnet orgs. expected to document their RNs belong to professional orgs., & improve RN practice bc of participation. Est. a low % of practicing RNs belong to professional orgs. Orgs. play role in continued upgrading of nursing & HC. ANA represents RNs interests & follows HC bills across all states. Issues: Rights of RNs handling drugs; Workplace violence; Process for optimal RN staffing in acute care. --Government: enormous role in nursing & HC. RN practice acts determined via state legislation. Reimbursements for HC determined at federal level. RNs increasingly entering government at local, state, & federal levels. -What Can a Nurse Do to Influence Policy: Keep abreast of issues in community & country. Write & publish articles. Join professional orgs. that match interests & share positions. Know who key players are in local, regional, & national govt. Know key RN positions & networks in your org. where you can influence policy. RNs often asked to serve on local boards of health, & boards of education. IOM report challenges RNs & society to ensure RNs represented in leadership positions in HC, + governing boards. Know what is happening in community & country generally. ID RNs in influential positions outside nursing (ex. dept. of health). Keep up-to-date w/ public issues by attending public meetings & reading newspapers & journals. RNs in influential positions outside of nursing can be useful resources to help you achieve your health policy goals. -Communicate your position through: Ongoing representation on policy-making; Committees or boards; Lobbying; Making submissions; Meeting w/ people in positions of influence.

Post-op CAB

Post-op CAB: After traditional→ transported to post-open heart OP unit; requires highly skilled care from qualified RNs. Use sterile technique w/ changing sternal or donor-site dressings. - Infections: tx underlying infections prior to OP. Pt shower or bathe w/ soap or antiseptic agent the night before OP. CHG for skin prep. Clip hair PRN immediately prior to OP. Pre-op ABs or antimicrobials used prior to incision. Use alcohol antiseptics to prep skin before incision. Antimicrobials should not be applied to incisions. Maintain peri-op BG <200 mg/dL even in pts w/o DM. Maintain normothermia. -Connect mediastinal tubes to water-seal drainage systems & ground epicardial pacing wires by connecting to PM generator. Cardiac RN monitors PAP & arterial pressures, & HR & rhythm; displayed on HDM. -Closely assess for dysrhythmias; ex. bradydysrhythmias, AF, or heart block. Manage symptomatic dysrhythmias per protocol or order. Hypoxemia & hypokalemia frequent causes of V dysrhythmias. Symptomatic bradydysrhythmias or heart block→ turn on PM & adjust PM settings as prescribed. -Monitor, report, & document other complications of CABG: F&E imbalance; Hypotension; Hypothermia; HTN; Bleeding; Cardiac tamponade; Decreased LOC; Anginal pain. -Managing F&E imbalance. Assessing F&E balance is high priority in early post-op. Edema common; but decisions w/ fluid admin based on BP, PAOP, RA pressure, CO, cardiac index, systemic vascular resistance, blood loss, & UO. Experienced specialized RN interprets findings & adjusts fluid admin on basis of unit policies or HCP prescription. --Serum elecs. (esp. Ca, Mg, K) may be decreased after OP & are monitored carefully. Serum K can fluctuate dramatically, so elecs. checked frequently, since imbalances→ dysrhythmias. K & Mg depletions common & may result from hemodilution or diuretic tx.

Preparing for Licensure Exam & Professional Growth

Preparing for Licensure Exam: -National Council of State Boards of Nursing (NCSBN) develops 2 licensure exams: the National Council Licensure Examination (NCLEX) for RNs & PNs; used by state & territorial boards of nursing to assist in making licensure decisions. --Nurse Licensure Compact of NCSBN is moving toward mutual recognition of licensure by states; 24 such states, w/ legislation pending in 4 others. Not all state boards have enacted such legislation. --Licensure should be in state of employment; ex. you live in Florida but work in Alabama. -Professional Growth: Professional orgs. are a good way to maintain currency in the profession. Many RN orgs. offer members an official journal that may contain peer-reviewed clinical articles & research relevant to the specialty. --Reasons to join: Education; Annual conventions; Networking; Certification; Targeted products & resources; Career assistance; Access to Internet sites. --RN decided on specialty→ highly recommended once eligible, to sit for cert exam in your specialty. Specialties have differing requirements for eligibility for exam. Adv. level exams for NPs & RN specialists. Also specialty exams for specific practice areas; ex. ANCC certs. --Many states require contact hrs of continuing education to maintain licensure. --Many orgs. reimburse tuition if return to school. When hired→ important to ask about policy on funding for continuing education, w/in facility & out of facility. Ask if they pay travel allowance for RN to go to out-of-state conference. Contact hrs listed in RN magazines & online-classes. RN must be aware of state's licensure requirements for renewal.

Preventing Contractures w/ amputations & promoting mobility

Preventing Contractures w/ amputations & promoting mobility: -AKAs or BKAs: teach ROM exercises for prevention of flexion contractures, esp. of hip & knee. A trapeze & overhead frame aid in strengthening arms & allow independent movement in bed. Teach how to do ROM exercises. Turn Q2h or teach to turn independently. Move pt slowly to prevent muscle spasms. -Firm mattress essential for preventing contractures w/ leg amputation. Assist into prone position Q3-4h for 20-30min if tolerated & not contraindicated; uncomfortable initially but helps prevent hip flexion contractures. Instruct to pull residual limb close to other leg & contract the gluteal muscles of buttocks for muscle strengthening. After staples removed, PT may begin resistive exercises, also done at home. -For AKA & BKA, teach how to push residual limb down toward bed while supporting it on soft pillow at first. Then instruct to continue activity using firmer pillow & then progress to harder surface. Helps prepare residual limb for prosthesis & reduces incidence of phantom limb pain & sensation. -Elevation of lower-leg residual limb on pillow while in supine is controversial. Some advocate avoiding at all times bc promotes hip or knee flexion contracture. Others allow elevation for first 24-48hrs to reduce swelling & pain. Inspect residual limb daily to ensure lies completely flat on bed. -For wrapping to be effective, reapply bandages Q4-6h or more often if loose. Figure-eight wrapping prevents restriction of BF. Decrease tightness of bandages while wrapping in distal-to-proximal direction. After wrapping, anchor bandages to highest joint, ex. above the knee for BKAs.

Preventing and Monitoring for Neurovascular Compromise:

Preventing and Monitoring for Neurovascular Compromise: -Perform NV assessments (AKA "circ checks" or CMS assessments) frequently before & after fracture tx. --Pts w/ extremity casts, splints w/ elastic bandage wraps, & open ORIF or external fixation, esp. at risk for NV compromise. --If perfusion to distal extremity impaired, pt reports increased pain, impaired mobility, & decreased sensory perception. If s/s allowed to progress, risk for ACS. -In some, compartment pressure may be monitored on 1x basis w/ handheld device w/ digital display, or pressure monitored continuously. Monitoring recommended for comatose or unresponsive high-risk w/ multiple trauma & fractures. -Critical Rescue: Monitor for & document early s/s ACS. Assess "six Ps" (i.e., pain, pressure, paralysis, paresthesia, pallor, and pulselessness) (rare or late stage). Pain increased even w/ passive motion & may seem out of proportion to degree of injury. Analgesics that had controlled pain become less effective or noneffective. Numbness & tingling (paresthesia) often 1 of 1st s/s of problem. Affected extremity then becomes pale & cool bc of decreased arterial perfusion to affected area. --If ACS suspected, notify PHCP immediately, if possible, implement txs to relieve pressure. Ex. tight, bulky dressings→ loosen bandage or tape. If pt has cast→ follow protocol about who can cut cast. Do not elevate or ice the extremity bc could compromise BF.

Best practices for preventing or managing increasing ICP for stroke include:

Preventing or managing increasing ICP for stroke: -Elevate HOB per agency or PHCP protocol to improve perfusion pressure. -Provide O2-tx to prevent hypoxia for SpO2 <95% or per protocol or prescription. -Maintain head in midline, neutral position to promote venous drainage from brain. -Avoid sudden & acute hip or neck flexion during positioning. Extreme hip flexion may increase intrathoracic pressure→ decreased cerebral venous outflow & elevated ICP. Extreme neck flexion also interferes w/ venous drainage from brain & IC dynamics. -Avoid clustering of care; multiple activities clustered in narrow time period→ ICP can dramatically elevate. -Hyperoxygenate before/after suctioning to avoid transient hypoxemia & resultant ICP elevation from dilation of cerebral arteries. -Provide airway management to prevent unnecessary suctioning & coughing bc can increase ICP. -Maintain quiet environment for pt w/ headache; common w/ cerebral hemorrhage or increased ICP. -Keep lights low to accommodate any photophobia. -Closely monitor BP, heart rhythm, SpO2, BG, & pt temp. to prevent secondary brain injury & promote positive outcomes after stroke.

Professional Organizations

Professional Organizations: Another arena for political action is via professional org; very important to continue RN professional development & to belong to a professional org→ major role in continual shaping of RN practice across the world & in continued upgrading of RN & HC. Magnet orgs. expected to document that their RNs in professional orgs., & improve RN practice bc of participation. -RNs are one of largest workforces in US at 3.1mil, but est. that only 5% in ANA. Many in specialty RN org., but est. is only 30% of total RNs. -Orgs. play a role in the continued upgrading of nursing and health care; along w/ state boards, effect outcome of RN practice. -ANA represents interests of RNs w/ many issues; Each yr track >1000 RN & HC-related bills in all states, exam priority issues, & trends. Also release position statements on issues of importance to RNs & HC. --In 2012, these issues brought forward to ANA House of Delegates for policy development: Rights of RNs handling drugs. Workplace violence. A process for optimal RN staffing in acute care settings. --ANA also supports worthy candidates for federal office who show belief in legislative & regulatory agenda of ANA via Political Action Committee (ANA-PAC).

Professional practice model

Professional practice model: driving force of RN care; schematic description of a theory, phenomenon, or system; how RNs practice, collaborate, communicate, & develop to provide highest quality care for those served by org. -Professional practice model of an org. illustrates alignment & integration of RN practice w/ mission, vision, & values of org. & RN dept; overarching conceptual framework for RNs, RN care, & IP pt care. -How RNs deliver care that meets 3 aims of effectiveness, efficiency, & pt experience; w/ pt & family at center/forefront of the model. -Models= team nursing, functional nursing, & primary nursing; describe how actual delivery of care is organized & environment where the RN practices. -Care delivery system: integrated into professional practice model; continually improved to adjust to NPSGs, value-based outcomes, regulatory requirements, & current best evidence. Manner in which care is delivered, context of care, & expected outcomes of care. RNs create care delivery systems that describe RNs accountability & shared authority for EBP, decision making & outcomes, PI initiatives, & staffing & scheduling processes.

Psychosocial Management of Mass Casualty Survivors

Psychosocial Management of Mass Casualty Survivors: RNs caring for survivors w/ s/s of ASD or PTSD perform further assessment w/ tool like Impact of Event Scale—Revised (IES-R); IES-R is 22-item self-admin questionnaire w/ several subscales like avoidance. -Before using tool, ID reading level bc it's 10th-grade reading level; should not be used w/ ST memory loss→ why many elderly not adequately assessed for post-disaster PTSD. Depending on s/s & results of assessment, remember BH evaluation & referral to counseling may be appropriate. -Action Alert: total score of 33+ (out of 88) on IES-R= probable PTSD; refer to psychiatrist, PMHNP, or qualified MH counselor. High score on any IES-R subscale= need for further evaluation & counseling; make appropriate referral to MH specialist to evaluate current or past trauma, like abuse or neglect.

Pt Care Team Members & Their Roles

Pt Care Team Members & Their Roles: -RN: ID scope of RN practice (ADPIE); responsible & accountable for provision of RN services. Supervise & ID appropriate use of any UAP in pt care. Define & supervise education, training, & use of any UAP. -LVN/LPN: 1yr to 18mo program; basic care, includes, but not limited to= VS, changing dressings, phlebotomy, & assisting w/ ADLs, under supervision of RN. --Can't perform ADPIE; can teach general handwashing; can care for stable pts, routine tx & dressings, admin prescribed therapies. -UAP: under direct supervision of RN to implement delegated aspects of RN care. Assist RN in providing care. Enable RN to provide RN care for pt. -5 Rights of Delegation: 1.) Right task. 2.) Right circumstance. 3.) Right person. 4.) Right direction/communication. 5.) Right supervision. -Direct Pt Care Activities: VS; daily wt; Apply leads & connect to cardiac monitor; I&O; Collect specimens; ADLs; bed bath; perineal care; Shave; Wash hair; mouth care; Change linen & assist w/ making occupied bed; Nutrition; Feeding; kcal count; Skin care; back care; Prep skin for procedure; skin prep for OP; Activity & mobility; Assist in ambulating; passive & active ROM; Position; Turn & reposition; Assist w/ transfer; Respiratory support; Set up O2; Assist w/ IS; Assist w/ C&DB exercises. Procedures; Set up rm (suction canisters, cables for continuous cardiac monitoring, tubing for CTs); Orient to rm; Obtain supplies for sterile tx; postmortem care. -Indirect Pt Care Activities: Cleaning; Clean equipment in use & stored equipment; Clean environment; Clean & defrost food refrigerators; Clean pt care area after transfer or D/C; Clean pt care area after txs completed; Empty waste baskets in rm & unit; Empty hampers; Remove meal trays; Clean supply carts; Clean & restock tx rm; Make unoccupied beds. Errands; Deliver meal trays.; Obtain & deliver supplies. Obtain & deliver equipment; Obtain & deliver blood products; Check lab specimens for labeling; Deliver specimens to lab. Clerical tasks; Place pages; Place & answer phone calls; Assemble, disassemble, & maintain pt charts; Transcribe HCP & RN pt care orders; Schedule Dx tests & txs; Order office supplies & forms; Sort & deliver mail; Keep unit log books up to date w/ admissions, transfers, & D/C; Maintain awareness of RN bed assignments. Stocking & maintenance; Stock bedside supplies, unit supplies, utility rooms, tx, exam, & procedure rms, nourishments & kitchen supplies. Check electrical equipment for inspections due dates; Stock linen cart.

Pulmonary Embolism Assessment:

Pulmonary Embolism Assessment: -Physical; S/S: range from vague, nonspecific discomforts to hemodynamic collapse & death; important to remember that many w/ PE do not have "classic" s/s, often leads to it being overlooked. --W/ possible PE; assess for sudden SOB, dry or productive cough w/ hemoptysis, syncope, hypotension, & fainting; sharp, pleuritic inspiratory chest pain. -Classic S/S: Sudden onset of dyspnea; Sharp, stabbing chest pain (on inspiration); Apprehension, restlessness; Feeling of impending doom; Cough; Hemoptysis [if infarction present]; Diaphoresis; Increased RR; Crackles; Pleural friction rub; Tachycardia; S3 or S4; Fever, low grade; Petechiae over chest & axillae (usually only w/ fat embolism syndrome [FES]); Decreased SaO2. -Respiratory: mostly r/t decreased gas exchange; Dyspnea, tachypnea, tachycardia, pleuritic chest pain (stabbing on inspiration), dry cough [or productive], hemoptysis. Crackles, wheezes, or pleural friction rub; or normal. -Cardiac: r/t decreased tissue perfusion; Tachycardia, Distended neck veins, syncope, cyanosis, systemic hypotension [ bc pulmonary HTN & reduced forward BF], abnormal heart sounds [S3/S4], abnormal ECG [nonspecific & transient; T-wave & ST-segment changes may occur, as Lt or Rt axis deviations]. RV dysfunction & failure are extreme complications; may have cardiac arrest or frank shock. -Critical Rescue: monitor pts at risk to ID s/s of PE (ex. SOB, chest pain, &/or hypotension w/o an obvious cause). If s/s present, respond by initiating the RRT. If PE is strongly suspected, prompt categorization & management strategies are started before Dx studies have been completed. -Psychosocial: s/s of PE are abrupt→ Anxiety; Hypoxemia can trigger anxiety & sense of impending doom. Life threat + ICU admit→ anxiety & fear.

Pulmonary Embolism

Pulmonary Embolism: Collection of particulate matter→ enters venous circulation→ lodges in pulmonary vessels. -Any substance can cause embolism; blood clot is most common. Ex. Blood, fat, oil, air, tumor cells, cholesterol, amniotic fluid & fetal debris, foreign objects (ex. broken IV catheters), injected particles, & infected clots can enter a vein & cause PE. -Embolism: blood clot [thrombus] or other object that is carried in the bloodstream & lodges in another area. Lg. emboli in lung vessels→ obstruct pulmonary BF→ reduces gas exchange & O2→ pulmonary tissue hypoxia, decreased perfusion, & potential death. -Thrombus: inappropriate blood clotting→ VTE (DVT) formed in leg or pelvis vein→ breaks off→ travels to rt-heart→ lodges in PA (or its branch)→ obstructing alveolar perfusion & outflow→ increased alveolar dead space & V/Q mismatch. Plts collect on embolus→ triggers release of substances→ BV constriction. Widespread pulmonary vessel constriction & pulmonary HTN impair gas exchange & tissue perfusion. Deoxygenated blood→ arterial circulation→ hypoxemia; but some w/ PE do not have hypoxemia. --Some have ongoing issues or residual problems after acute problems have resolved; continue to impair gas exchange & perfusion. --Common cause of preventable death bc s/s may be vague, & it may be mis-Dx→ high risk pts may not receive appropriate initial care.

RN Interventions for Various Causes of Ventilator Alarms: Major alarms indicate high pressure or low exhaled vL.

RN Interventions for Various Causes of Ventilator Alarms: Major alarms indicate high pressure or low exhaled vL. -High-Pressure Alarm (PIP reaches set alarm limit; usually 10-20 mmHg above baseline PIP) --Increased secretions or mucus plug in airways. S/S= Secretions; Increased peak airway (inspiratory) pressure (PIP); Rhonchi; Decreased breath sounds. Suction PRN. --Pt coughs, gags, or bites on oral ETT. Insert oral airway to prevent biting on ETT; provide pain management & sedation as prescribed. --Pt anxious or fights ventilator. Provide emotional support to decrease anxiety; increase flow rate; explain all procedures to pt; provide sedation or paralyzing agent as prescribed. --Airway size decreases r/t wheezing or bronchospasm. Auscultate breath sounds; collab. w/ RT dept. to provide bronchodilators. --Pneumothorax. Alert pulmonary HCP or RRT about new onset of decreased breath sounds or unequal chest excursion, may be caused by pneumothorax; auscultate breath sounds. --Artificial airway displaced; ETT may have slipped into Rt mainstem bronchus. Assess chest for unequal breath sounds & chest excursion; obtain CXR as ordered to ID position of ETT; after proper position verified, secure tube. --Obstruction in tubing bc pt lying on tubing or there is water or kink in tubing. Assess system, beginning w/ artificial airway & moving toward ventilator. --Increased PIP associated w/ a sigh. Empty water from tubing & remove kinks; coordinate w/ RT or pulmonary HCP to adjust pressure alarm. --Decreased compliance of lungs noted; trend of gradually increasing PIP noted over several hrs or a day. Evaluate reasons for decreased lung compliance; increased PIP in ARDS, pneumonia, or worsening of pulmonary dz. -Low-Exhaled vL (or Low-Pressure) Alarm (disconnection or leak in MV circuit or leak in artificial airway cuff) --Leak in MV circuit prevents breath delivery. Assess all connections & all ventilator tubing for disconnection. --Pt stops spontaneous breathing in SIMV or CPAP mode or on pressure support. Evaluate tolerance of mode; evaluate for overmedication w/ sedation or analgesics. --Cuff leak in ET or TT. Evaluate pt for cuff leak= suspected if can talk (air escapes from mouth) or if pilot balloon on artificial airway is flat.

RN Role in Responding to Health Care Facility Fires

RN Role in Responding to HC Facility Fires: -Remove any pt or staff from immediate danger of fire or smoke. -D/C O2 for all who can breathe w/o it. -On life support→ maintain respiratory status manually until removed from fire area. -Direct ambulatory pts to walk to safe location. -If possible, ask ambulatory pts to help push wheelchair pts out of danger. -Move bedridden from fire area in bed, stretcher, or wheelchair; if needed, have 1-2 staff move pts on blankets or carry them. -After everyone is out of danger, seek to contain fire by closing doors & windows & using ABC extinguisher (puts out any type of fire) if possible. -Do not risk injury to yourself or staff while moving pts or attempting to extinguish fire.

RN Care for the ETT: Priority, Complications, Positioning

RN care for ETT: Assess placement, cuff leak, breath sounds, indications of adequate gas exchange & oxygenation, & chest wall movement regularly. Maintain patient airway= PRIORITY action! --Critical Rescue: assess intubated to ID indications of decreased gas exchange (cyanosis, decreased O2sat, increased ETCO2, anxiety); indications present→ check DOPE: displaced tube, obstructed tube (often w/ secretions), pneumothorax, & equipment problems. ETT generally displaced into the Rt mainstem bronchus→ absent breath sounds on Lt. -Monitor for complications: [ETT or NTT] during placement, while in place, during extubation, or after extubation (either early or late); common complications are tube obstruction, tube dislodgment, pneumothorax, tracheal tears, bleeding, & infection. --Trauma & other problems: face, eye, nasal & paranasal areas; oral, pharyngeal, bronchial, tracheal, & pulmonary areas; esophageal & gastric areas; CV, musculoskeletal, & neurologic systems. -Assess ET tube position: prevent pulling or tugging on tube to avoid tube dislodgment, & check pilot balloon for cuff inflation; common cause of unplanned extubation in adults is confusion & agitation. --Monitor cuff pressure; ensure it's 20-30cm H2O to stabilize w/o causing tracheal injury; suctioning, coughing, & speaking→ dislodgment; neck flexion, neck extension, & head rotation→ tube movement. --Pt position changes→ affect cuff pressures; may require more frequent monitoring. Tongue movement→ change tube's position. Other measures fail→ need order for soft wrist restraints & apply if pulling on tube. Restraints→ last resort to prevent accidental extubation. --NPSG: compliance w/ TJC-NPSGs→ reassess restraint need daily. Need continues→ get new prescription daily. Adequate sedation (chemical restraint) may be needed to decrease agitation or prevent extubation. Obtain permission for restraints from pt or family.

Regulatory Agencies;

Regulatory Agencies: Multiple regulatory & advisory agencies w/ impact on stds. of HC. -Such agencies regulate the manner in which a hospital implements workplace standards. -Occupational Safety & Health Administration (OSHA): regulate manner a hospital implements workplace safety stds; stds. then become part of accreditor's management of environment of care std. -Centers for Disease Control & Prevention (CDC): agency w/in USDHHS; charged w/ promotion of health & quality of life via prevention & control of dz, injury, & disability; created multiple infection control stds. part of std. accreditation & practice stds. of most hospitals. -Food & Drug Administration (FDA): federal agency that regulates drugs, medical devices, & radiation-emitting products; regulations form basis of med management std. of accreditors. -Licensing Bodies: HC orgs. licensed to perform services by state dept. of health. Most state depts. of health undertake: -Regulate wide range of HC settings for quality of care, like hospitals, RN homes, assisted living, ambulatory care, HHC, medical day care, etc. -Investigate complaints from pts, consumers, & state & federal agencies. -Provide consumer info in form of report cards & other performance info. -RNs often called to assist hospital admin regarding complaints lodged w/ state dept. of health.

Regulatory Agencies & Accreditation Agencies

Regulatory Agencies: charged by federal and state govts. to: -Set stds. for operation of HC orgs. -Ensure compliance w/ federal & state regulations of govt. admin agencies. -Investigate & make judgments regarding complaints of consumers & the public. -HC orgs. work w/ myriad accrediting & regulatory agencies so optimum stds. of care & delivery can be met -Licensing of HC agencies to maintain practice occurs via state depts. of health; usually oversee outcomes of care in HC facilities, investigate consumer complaints, & deal w/ issues of importance to public health. -Agencies monitor basic compliance w/ specific HC regulations of state. Compliance w/ regulatory stds. on national & state levels is mandatory, & fines can be leveled against orgs. for noncompliance, or org. can be shut down. -Accreditation agencies evaluate HC orgs. against a set of stds. validated against best practice. Accreditation is voluntary, but mandatory for continued CMS reimbursement; can't shut down org., but can deny accreditation. . --Medicare conditions of participation require hospitals be accredited by org. w/ "deeming authority"= authority granted by CMS to accrediting orgs. to ID, on CMS's behalf, if org. is in compliance w/ Medicare regulations. --"Deeming authority" is granted by CMS to accrediting orgs. to ID, on CMS's behalf, whether an org. evaluated by accreditor is in compliance w/ corresponding Medicare regulations. ---3 major HC accrediting agencies: TJC, Det Norske Veritas, & American Osteopathic Association Healthcare Facilities Accreditation Program.

Role of RN in Community Emergency Prep & Response

Role of RN in Community Emergency Prep & Response: During disaster, RNs & other ER staff may be needed for triage, 1st aid or ER care, & shelter assistance. -Initial action of 1st responders in disaster is to remove pts from danger, both injured & uninjured. Firefighters & other disaster-ER personnel typically manage this; unless have specific prehospital search-&-rescue training, RNs not usually part of process. In all cases, developing & maintaining situational awareness are critical for priority setting & safety in rapidly changing environment. -After removal from danger, pts triaged by HC staff; after triage, RNs provide on-site first aid & ER care; may be involved in teaching & supervising volunteers. -American Red Cross sets up shelters for pts who lost homes or evacuated from homes. RNs may need to teach pts living in shelters about procedures needed for safety when return home. --Ex. Clean drinking water may not be available for several days+, so residents may need to boil water before drinking. If electricity & gas not available, an outdoor grill or camp stove can be used. Alternative procedures; water purification filters, sterilizing UV pens, or 10-20 drops of chlorine bleach added to gal water will make it safe to drink. -Human waste management is challenge if toilets do not flush. If not managed safely, enteric pathogens spread dz. --Toilet bowl or bucket lined w/ plastic bag can be used for human waste. To sanitize & control odor→ add chlorine bleach & tie/seal bag. Portable toilet chemicals or chlorinated lime used as alternative. --To prevent toxic gas rx, remind not to mix any chemicals. Treated human waste bags can be buried in ground. In austere environment, dig pit in ground as improvised toilet. --In all cases, emphasize importance of handwashing w/ soap+water or using hand sanitizer to prevent dz transmission.

SCI Fixed Skeletal Traction

SCI Fixed skeletal traction: used to realign vertebrae, facilitate bone healing, & prevent further injury, often after OP stabilization. Most common device for immobilization of cervical spine= halo fixator device; AKA halo crown; worn for 6-12wks; static device affixed by 4 pins (screws) into outer aspect of skull & is connected to vest or jacket. Pts not having OP→ addition of traction helps to reduce fracture. -Action Alert: Never move or turn pt by holding or pulling on halo device. Do not adjust screws holding it in place. Check skin frequently to ensure jacket is not causing pressure. Pressure is avoided if 1 finger can be inserted easily between jacket & pts skin. Monitor neuro status for changes in movement or decreased strength. Special wrench needed to loosen vest in emergencies [CP arrest]. Tape wrench to vest for easy & consistent accessibility. Do not use sharp objects (coat hangers, knitting needles) to relieve itching under vest; skin damage & infection slows recovery. -Common complications of halo device: pin loosening, local infection, & scarring. More serious but less common complications: osteomyelitis (cranial bone infection), subdural abscess, & instability. Hospital policy followed for pin-site care; may specify use of solutions [saline]; vaseline dressings may be used. Monitor VS for indications of infection (fever, purulent drainage from pin sites) & report any changes to PHCP immediately.

SOFA & qSOFA

SOFA & qSOFA: -Sepsis-3 task force recommends Sequential Organ Failure Assessment (SOFA) score in critical care & quick SOFA (qSOFA) in non-intensive care. The qSOFA score is not a defining tool for sepsis, it's a predictor of mortality; + score requires further assessment for organ failure. -Calculate SOFA score, the following labs are needed: bilirubin, Cr, coagulation studies, & ABGs. Labs + clinical assessment data are then scored from 0 (normal function) to 4 (organ failure). Higher score→ greater risk. Score 2+ in any system= increased risk for organ failure, poor outcome, or death. -The following parameters are abnormal, & each would receive score of 2+: -Respiratory: PaO2/FiO2 <300 mmHg -Coagulation: Plt <100 × 10^3/mm^3 -Liver: Bilirubin ≥2 mg/dL -CV: Hypotension requiring vasopressor support -CNS: Glasgow Coma Scale score ≤12 -Renal: Creatinine ≥2 mg/dL, or UO <500 mL/day -Quick Sequential Organ Failure Assessment: qSOFA can quickly alert clinicians to need for further assessment for organ dysfunction. 3 parameters, & get 1 point for each abnormal parameter. Abnormal parameters include: SBP ≤100 mm Hg; RR ≥22 breaths/min; Any change in MS. --Non-ICU pts w/ score of 2 or 3 require additional assessment using SOFA & are at risk for extended ICU stay or death.

Secondary Survey & Resuscitation Txs

Secondary Survey & Resuscitation Txs: After ED resuscitation team has addressed immediate life threats, other activities the RN can anticipate are insertion of gastric tube for decompression of GI tract to prevent vomiting & aspiration, insertion of urinary cath to allow careful measure of UO, & prep for Dx studies. -Resuscitation team performs a more comprehensive H→T= secondary survey, to ID other injuries or medical issues that need to be managed or might affect tx course. -Splints applied to fractured extremities, & temporary dressings placed over wounds while in Dx testing or prep for definitive tx.

Prep for Self-Management: Use of Halo Fixator w/ Vest

Self-Management: Use of Halo Fixator w/ Vest -Wt of halo device alters balance; careful when leaning forward or backward. Wear loose clothing, preferably w/ hook & loop (Velcro) fasteners or large openings for head & arms. Bathe in bathtub or take sponge bath; some PHCPs allow showers. -Wash under liner of vest to prevent rashes or sores; use powders or lotions sparingly under vest. Have someone change liner if it's odorous. Support head w/ small pillow when sleeping to prevent pressure & discomfort. -Try to resume usual activities to extent possible; keep active as possible; wt of device may cause fatigue or weakness; avoid contact sports & swimming. -Do not drive bc vision impaired w/ device. Keep straws for drinking fluids. Cut meats & food into small pieces to facilitate chewing & swallowing. Before going outside in cold temp, wrap pins w/ cloth to prevent metal getting cold. -Have someone clean pin sites as recommended by PHCP or hospital. Observe pin sites daily for redness, drainage, or loosening; report changes to PHCP. Increase fluids & fiber in diet to prevent constipation. Use position of comfort during sexual activity.

Sepsis S/S

Sepsis S/S: often has mild hypotension, low UO, & increased RR→ hypodynamic state w/ decreased CO. Body temp. varies w/ sepsis duration & WBC function; some have low-grade fever, others have high fever; may have below-normal temp. Compensate w/ reduced UO & increased RR bc of impaired gas exchange & perfusion. Often has elevated WBCs→ expected w/ systemic infection. -Inappropriate clotting w/ microthrombi forming in some organ capillaries→ hypoxia & reduces organ function; hard to ID, but if sepsis is stopped at this point→ organ damage is reversible. Microthrombi increase hypoxic conditions→ more toxic metabolites, can amplify inflammation & create vicious repeating cycle of poor gas exchange & perfusion. S/S subtle, & indicate sepsis; will progress unless tx begins immediately. -Early hypodynamic state has a relatively short duration; indicators are subtle→ condition is often missed or mis-Dx. Early sepsis is ID & tx aggressively→ cycle of progression can be stopped, & outcome is good. Sepsis is not ID & tx at this stage→ much harder to control. -RNs & all HC workers have a responsibility to ID cues that indicate sepsis before it progresses to organ failure. --Critical Rescue: Monitor pts at risk for sepsis to ID s/s indicating sepsis & septic shock. If any s/s present→ notify HCP or RRT. -Sepsis amplified→ all tissues involved & hypoxic to some degree; some organs have cell death & dysfunction at this time. Microthrombi formation is widespread, w/ clots forming where not needed→ uses up (consumes) available plt & clotting factors= disseminated intravascular coagulation (DIC). Anaerobic metabolism continues, & cell uptake of O2 is poor. Continued stress response→ continued glucose release from liver→ hyperglycemia; More severe response= higher blood glucose. -Despite patho severity, some s/s may be missed; bc cardiac function is hyperdynamic in this phase. Pooling of blood & widespread capillary leak stimulate heart→ CO is increased w/ more rapid HR & elevated SBP; also the extremities may feel warm, w/ little or no cyanosis. May "look" better, but changes at tissue level are serious & have caused significant damage. WBCs may no longer be elevated bc prolonged sepsis exceeded BMs ability to produce & release new mature neutrophils & other WBCs. WBCs may be extremely low, esp. segmented neutrophils (segs). -S/S: lower SpO2, rapid RR, decreased-to-absent UO, & change in cognition & affect. -Appropriate & aggressive tx at this stage can still prevent septic shock; mortality after reaching this stage is much higher vs. sepsis. At this point→ downhill course to septic shock is extremely rapid.

Sepsis & Septic Shock

Sepsis: extreme response to infection; can cause tissue damage, organ failure, & death if not tx promptly & appropriately. -Septic shock: distributive sock; subset of sepsis; higher risk of death vs. sepsis alone. Associated w/ systemic inflammatory response synd. (SIRS) & sepsis w/ MODS. -Infection: confined to local area, should not lead to sepsis & shock. Adult w/ effective immunity & inflammatory responses→ organism invasion 1st starts helpful, local inflammation response→ confines & eliminates organism & prevents infection becoming worse or widespread. -WBCs in invasion area secrete cytokines→ trigger local inflammation & bring more WBCs to kill pathogens. Response constricts small veins & dilates arterioles in the area→ increases perfusion to locally infected tissues. -Capillary leak occurs→ allowing plasma to leak into tissues→ swelling (edema). Duration of inflammation depends on infection size & severity; but usually subsides w/in few days, when infection managed by responses. Inflammation benefit= limited only to infection area & stops as soon as no longer needed. Pt does not have fever, tachycardia, decreased SpO2, or reduced UO. -Sepsis-3: std. defines sepsis as life-threatening organ dysfunction brought on by dysregulated infection response; septic shock= subset of sepsis→ circulatory, cellular, & metabolic abnormalities substantially increase risk of death vs. sepsis alone. -Etiology: syndrome of sepsis & septic shock is a complex systemic response that begins when infectious organism enters the bloodstream & causes an infection. If infection escapes local control→ sepsis develops. Bacteria increases→ triggers widespread inflammation (SIRS= systemic inflammatory response syndrome). --SIRS criteria are not used to Dx sepsis anymore, bc SIRS can present w/ infectious & noninfectious pathologies.

Shared Governance

Shared Governance: everyone in facility (RNs) participate in policy making, procedures, managing, etc. -Governance: power, control, authority, & influence; answers question of "Who rules?". -RN shared governance extends that rule to nurses; RN shared governance models have always focused on RNs controlling their practice (autonomy). Theme that flows consistently via shared governance research & literature. -Structure is of vital importance to success of shared governance. ANCC (2013) states that shared leadership/participative decision making is model where RNs are formally organized to make decisions about practice stds., QI, staff & professional development, & research. -RN autonomy implies that every RN is trained to be "in charge" of their unit or area, and shares that role with other professional team members. -Accountability is core of shared governance & RN empowerment. As RN grows, advancement through decision-making structure is expected. -Shared governance activities: participatory scheduling, joint staffing decisions, &/or shared unit responsibilities (every RN is trained to be "in charge" of their unit or area, & shares that role w/ other members, perhaps on a rotating schedule) to achieve best outcomes. -Same control over practice, at unit level, requires transition from historically hierarchical design of HC decision making to more decentralized decision-making process; to happen employee partnership, equity, accountability, & ownership must occur at POS (pt care units). -1st step in participation in shared governance is membership in unit-based council; allows new RN to become aware of major operational & practice issues in unit. Also allow opportunity to contribute to decisions impacting the unit. Membership usually all members of RN staff of a unit. -Shared governance is much more than set of committees; #, titles, & arrangements of committees not as important as people who make up membership. --Success in terms of shared governance & pt care is the control of practice leading to better pt outcomes.

Types of Shock

Shock types vary bc it's a problem caused by a pathologic condition [not a dz state]; >1 shock type can be present at same time. Ex. trauma from MVA may trigger hemorrhage (→ hypovolemic shock) & a MI (→ cardiogenic shock). -HvLS: too little circulating blood vL decreases MAP→ inadequate total body perfusion & gas exchange. Common problems→ hypovolemic shock= dehydration & poor clotting w/ hemorrhage. -Cardiogenic shock: the heart muscle is unhealthy & pumping is impaired. Most often associated w/ acute MI. Any type of pump failure decreases CO & MAP. -Distributive shock: when blood vL is not lost, but is distributed to interstitial tissues where it cannot perfuse organs. Caused by→ BV dilation, blood pooling in venous & capillary beds, & increased capillary leak; factors decrease MAP & may be started by nerve changes (neural induced) or presence of chemicals (chemical induced). Septic shock= most common cause of distributive. -Anaphylaxis: extreme type of allergic rx; begins w/in sec-mins after exposure to specific allergen in a susceptible adult→ widespread loss of BV tone, w/ decreased BP & CO. -Sepsis: life-threatening organ dysfunction from dysregulated response to infection. Septic Shock is a subset of sepsis in which circulatory, cellular, & metabolic abnormalities substantially increase risk of death vs. sepsis alone. -Obstructive shock: problems impair ability of normal heart to pump effectively. Heart remains normal, but conditions outside the heart prevent adequate filling or contraction of healthy heart muscle. Most common cause is cardiac tamponade. -Causes & initial s/s associated w/ different types vary; eventually effects of hypotension & anaerobic cellular metabolism (w/o O2)→ common key features of shock.

Shock; patho, classification, s/s

Shock= widespread abnormal cell metabolism; when gas exchange w/ oxygenation & tissue perfusion needs are not met to maintain cell function. It is a condition [not a dz]; "whole-body" response when too little O2 is delivered to tissues. -All organs are affected; work harder to adapt & compensate for reduced gas exchange, or perfusion, or fail to function bc of hypoxia. It's a "syndrome" bc resulting problems occur in a predictable sequence. -Any problem that impairs perfusion & gas exchange to tissues & organs can start the shock syndrome & lead to a life-threatening emergency. -Often a result of CV problems. Pts in acute care settings are at higher risk; can occur in any setting. Ex. older pts in LT care→ risk for sepsis & septic shock r/t UTIs & pneumonia. -Body's adaptive adjustments (compensation) or HC tx are not effective or exhausted & shock progresses→ cell loss, MODS, & death. -Classified by impairment type causing it; hypovolemic shock, cardiogenic shock, distributive shock (includes septic shock, neurogenic shock, anaphylactic shock), obstructive shock. -S/S: similar regardless of what starts process or which tissues affected 1st; s/s result from physiologic adjustments (compensatory mechanisms) that body makes to ensure continued perfusion of vital organs. Compensation triggered by SNS stress response activating endocrine & CVS. S/S unique to any 1 type result from specific tissue dysfunction.

Sinus Bradycardia

Sinus Bradycardia: excessive vagal (PSNS) stimulation to heart→ decreased SA node rate. May result from carotid sinus massage, vomiting, suctioning, Valsalva (w/ BM or gagging), ocular pressure, or pain. -Stimuli→ slow HR & decrease conduction speed through heart. SA node rate <60BPM. -Assess: may be asymptomatic except decreased PR; cause usually unknown. Assess EHR to ID if receiving meds that slow conduction through SA or AV node. S/S: Syncope ("blackouts", fainting); Dizziness & weakness; Confusion; Hypotension; Diaphoresis; SOB; Chest pain. -Tx: pt stable→ ID & tx underlying cause. Pt has any s/s & cause cannot be ID→ admin IV atropine, increase IV fluid vL, & apply O2 if SpO2 <94% or if short of air. --Discontinue drugs suspected of causing bradycardia. BB OD suspected→ admin glucagon; helps by increasing HR & BP. --HR does not increase sufficiently→ prep for transcutaneous or transvenous pacing to increase HR. --Tx of underlying cause does not restore NSR→ require permanent pacemaker implantation.

Sinus Tachycardia

Sinus Tachycardia: SNS stimulation or vagal (PSNS) inhibition→ increased SA node discharge rate→ increases HR. SA node rate is >100BPM. --Sinus tachycardia 1st increases CO & BP; continued increases in HR→ decrease coronary perfusion time, diastolic filling time, & coronary perfusion pressure while increasing myocardial O2 demand. --Increased SNS stimulation= normal response to physical activity; also caused by anxiety, pain, stress, fever, anemia, hypoxemia, & hyperthyroidism. --Drugs→ epi, atropine, caffeine, alcohol, nicotine, cocaine, aminophylline, & thyroid meds may also increase HR. --May be a compensatory response to decreased CO or BP; ex. dehydration, HvLS, MI, infection, & HF. -Assess for s/s of hypovolemia & dehydration [increased PR], decreased UO, decreased BP, & dry skin & mucosa; may be asymptomatic except increased PR. If rhythm not well tolerated→ may have s/s instability. -Desired outcome→ decrease HR to normal by tx underlying cause. Remind to remain on bedrest if tachycardia→ hypotension or weakness. Teach to avoid substances that increase HR [caffeine, alcohol, nicotine]. Help w/ stress-management or refer to MHP.

Staff Competency

Staff Competency: TJC states hospital must provide right # of competent staff to meet pt needs. Competent staff= qualified & able to perform work per professional stds. -Meet goal of providing adequate competent staff→ hospital must carry out these processes & activities: Providing competent staff via traditional employer-employee arrangements, or contractual arrangements w/ other entities or persons. Orienting, training, & educating staff. Providing ongoing in-service & other education & training to increase staff knowledge of specific work issues. Assessing, maintaining, & improving staff competence. Ongoing, periodic assessing of competence to evaluate staff members' continuing abilities to perform during association w/ org. Promoting self-development & learning. Staff encouraged to pursue ongoing professional development goals, & provide feedback about work environment. -High risk problem prone skills; ex. midline, access & de-access metaport. When you get hired, job must document that you can do these (key indicators the preceptor will sign you off on; ex. Transfusions). Litigation happens when not done correctly. -BOX 10-2 New Employee Orientation, Mandatory Content: Mission and governance. Service excellence requirements. Code of conduct. Fire safety. Safe environment. Culture of safety. Age-specific patient content. Infection control. Blood borne pathogens. Process improvement. Corporate compliance. Just workplace. Health Insurance Portability and Accountability Act (HIPAA). Benefits.

Stages of Parkinson Dz

Stages of Parkinson Dz: -Stage 1: Initial Stage; Unilateral limb involvement, Minimal weakness, Hand & arm trembling. -Stage 2: Mild Stage; Bilateral limb involvement, Mask-like face, Slow shuffling gait. -Stage 3: Moderate Dz; Postural instability, Increased gait disturbances. -Stage 4: Severe Disability; Akinesia, Rigidity. -Stage 5: Complete ADL Dependence.

ST & LT Goals; Action Planning

Statement of Short-Term & Long-Term Goals: competitive strategy is plan for achieving goals, & LT & ST goals may be used as method (or strategies) to achieve the overall strategic goals. -Goals should be designed & worded to be: Specific, Measurable, Acceptable to those working to achieve the goals, Realistic, Timely, Extending the capabilities of those working to achieve the goals, & Rewarding to them, as well. ("SMARTER.") -Action Planning: process where specific goals are matched w/ each strategic goal; overall strategic goals cascade down to all depts. & units &, possibly employees. Action planning requires specifying expected outcomes w/ each strategic goal; outcomes then form basis of performance scorecards used in most orgs. Anticipated outcomes usually based on competitive strategy & often benchmarked against "best in class performers" or to where the org. wants to be in performance. --Often, each objective is associated w/ tactic; 1 of methods needed to achieve objective. Implementing strategy involves implementing a set of tactics along the way; tactic is still a strategy, but on a smaller scale. --Action planning includes specifying responsibilities & timelines w/ each objective, or who needs to do what & by when; also include methods to monitor & evaluate the plan→ knowing how the org. will know who has done what & by when. --Common to develop an annual plan (AKA operational plan or management plan); includes the strategic goals, strategies, objectives, responsibilities, & timelines implemented in coming yr= ST goals of org. --Difference between ST & LT plans & objectives r/t time expected to accomplish them; times vary by institution, but ST plans usually extend up to 1yr. LT plans vary from 3-5yrs. --Budgets usually in strategic & annual plan, & w/ individual dept. & unit plans; specify funds needed for resources, necessary to implement annual plan; also show how the funds will be spent. --Performance indicators list measures that will be used to measure progress toward goal achievement. Benchmarks relate performance of competitors or "best in class," & targets are the ST & LT goals. --Org. plan cascades down to depts. & units→ becomes more specific w/ action plans & timelines for measures of achievement.

Stationary chest tube drainage systems

Stationary chest tube drainage systems: ex. Pleur-evac; use water-seal mechanism that acts as 1-way valve to prevent air or liquid back-flowing into chest cavity. -1st chamber of 3= drainage collection chamber; tube(s) from pt connected to it. Measure fluid Q1h during 1st 24hrs. --Drainage must never fill to where it contacts any tubes! If tubing from pt enters fluid, drainage stops & can lead to tension pneumothorax. -2nd chamber= water seal chamber to prevent air back-flowing into chest. Trapped air leaves pleural space, goes through chamber 1 (collection) then chamber 2 (water-seal; 1-way valve; bubbling). --Action Alert: for water seal system; always has 2cm H2O+ to prevent air returning to pt. Check water level 1x/shift & add sterile water to level marked on indicator (per manufacturer). --Bubbling in water seal: air drainage from pt; Bubbling seen when intrathoracic pressure > atmospheric pressure, ex. exhales, coughs, sneezes. Excessive bubbling may be air leak. Blocked or kinked CT can cause bubbling to stop. --If all air is evacuated from pleural space, bubbling of water seal stops. --Water in water-seal column normally rises 2-4in during I & falls during E= tidaling. No tidaling may be bc lung has fully re-expanded or bc CT obstruction. -3rd chamber= if suction applied, suction regulator or control system. Different types of suction; usually wet or dry. --Wet: fluid level in chamber 3 per surgeon. Chamber connected to wall suction; turned up until gentle bubbling in chamber; -20cm H2O (measured w/ pipet). --Dry: prescribed suction dialed in on device. When connected to wall suction, regulator set to amount per manufacturer; no water but dial turns to desired pressure (10, 20, 30, 40). --Check Q1h to ensure sterility & patency. Sterile gauze at bedside to cover & occlude the insertion site immediately if CT dislodged. Padded clamps at bedside; used if system interrupted. --Check water-seal chamber for unexpected bubbling from air leak in system. Bubbling normal during forceful expiration or coughing bc air in chest is expelled. Continuous bubbling= air leak; Notify surgeon if bubbling continuous in water-seal chamber.

Steps recommended to stop the cycle of Horizontal Violence

Steps recommended to stop the cycle of Horizontal Violence: As a new RN leader, it will be your responsibility to stop a pattern of horizontal violence. No federal std. that requires workplace violence protections, effective 1/09, TJC created new std. in "Leadership" ch. that addresses disruptive & inappropriate behaviors. --Some states sought legislative solutions, + mandatory estab. of a comprehensive prevention program for HC employers, in addition to increased penalties for those convicted of assaults of RN &/or HC staff. -Analyze culture of work unit: observe for verbal and NV cues in behavior of staff. -Name problem when you see it, & use term "horizontal violence." -Raise issue at staff meetings & educate staff about horizontal violence to help break silence. -Allow staff to tell stories if horizontal violence is part of culture of unit. -Ensure there is process for dealing w/ this issue if it occurs in your unit & be responsive when issues brought to your attention. -Engage in self-awareness activities & reflective practice to ensure that your leadership style does not support horizontal violence. -Provide your RN staff w/ training about conflict management skills, & empower them to defend themselves against bullying behavior.

Strategic planning

Strategic planning: process of an org./RN dept. or unit decides where it is going over next yr+ & how it is going to get there; usually organization-wide & the outcome of it cascades down to pt care dept. & units & employees. "Map" of where the organization, dept., or unit is going over the next yr+. --Strategic planning used to be done by financial managers; now by all org. stakeholders. RN managers have important role in strategic plan of org. & in implementation of action plans at unit level that assist org. in meeting goals. -Strategic management: process of setting goals & objectives for org./dept./unit; ID resources necessary to meet goals, creating action plan, & evaluating goal progress. Defining LT objectives of org. & setting priorities. Timeline is future-oriented & predicts org. activities over several yrs. --Org. Leaders need to focus on series of key questions when beginning strategic planning process: --Why does the org. exist? What is the org. currently? What would it like to be? How can we make the transformation to what we want to be? How will we know when the transformation is done? -Elements of a Strategic Plan: -Mission statement. -Statement of competitive challenges & strategy. -Statement of ST &LT goals. -Statement of org. policies. -Statement of needed resources. -Statement of key assumptions.

Best Practice For Patient Safety & Quality Care: Suctioning the Artificial Airway

Suctioning the Artificial Airway: -Assess the need for suctioning. -Wash hands. Don protective eyewear. Maintain Std. Precautions. -Explain to the patient that sensations such as SOB & coughing are to be expected but that any discomfort will be very brief. -Check the suction source. Occlude the suction source, & adjust the pressure dial to between 80-120mmHg to prevent hypoxemia & trauma to the mucosa. -Set up a sterile field. -Preoxygenate the patient with 100% oxygen for 30sec-3min (>3 hyperinflations) to prevent hypoxemia. Synchronize hyperinflations w/ inhalation. -Quickly insert the suction catheter until resistance is met. Do not apply suction during insertion. -Routine instillation of NS is not supported. Gas exchange is impaired due to hypoxia & there is an increased infection risk. -Withdraw the catheter 0.4-0.8in (1-2cm), & begin to apply suction. Apply continuous suction & use a twirling motion of the catheter during withdrawal to avoid impairing tissue integrity. Never suction >10-15sec. -Hyperoxygenate for 1-5min or until the patient's baseline HR & O2sat are w/in normal limits. -Repeat PRN for up to 3 total suction passes. -Document secretion characteristics & patient responses.

Atrial dysrhythmias: SVT

Supraventricular Tachycardia (SVT): rapid stimulation of atrial tissue at 100-280BPM. P waves may not be visible, esp. if 1:1 conduction w/ rapid rates, bc P waves embedded in preceding T wave. May occur in healthy young pt, esp. women. -Usually caused by re-entry mechanism= 1 impulse circulates repeatedly throughout atrial pathway→ re-stimulating atrial tissue at a rapid rate. -Paroxysmal SVT (PSVT): rhythm intermittent; initiated suddenly by a premature complex (PAC) & terminated suddenly w/ or w/o tx. --Adenosine: for PSVT. Have emergency equipment available bc short period of asystole common after admin; bradycardia & hypotension may occur. Facial flushing, SOB, & chest pain common SEs. -S/S depend on SVT duration & ventricular response rate. --Sustained rapid ventricular response→ assess for palpitations, chest pain, weakness, fatigue, SOB, nervousness, anxiety, hypotension, syncope. CV deterioration may occur if rate does not sustain adequate BP→ angina, HF, & cardiogenic shock. --Nonsustained or slower ventricular response→ may be asymptomatic except for occasional palpitations. --SVT in healthy person & stops on its own→ no tx may be needed other than eliminating causes. --SVT continues→ studied in electrophysiology study (EPS) lab. --Preferred tx for recurrent SVT→ radiofrequency catheter ablation (also an AF tx). --Sustained SVT w/ rapid ventricular response→ desired tx outcomes are to decrease ventricular response, convert dysrhythmia→ sinus rhythm, & tx cause. --If s/s of poor perfusion are severe & persistent→ may require synchronized cardioversion to immediately terminate SVT. [Also an AF tx] --For LT tx→ referred to electrophysiologist for radiofrequency catheter ablation. [Also an AF tx]

Surgical Management for CABG

Surgical Management for CABG: -MI direct CAB. may be indicated w/ lesion of Lt anterior descending (LAD) artery. In most common MIDCAB OP, a Lt thoracotomy incision made, & rib retraction required. Then Lt IMA dissected & attached to still-beating heart below level of lesion. CPB is not required. --After OP, assess for CP & ECG changes (Q waves & ST-segment & T-wave changes in leads V2 to V6) bc occlusion of IMA graft occurs acutely in only a small % of pts. If there is any question of acute graft closure, immediately notify HCP. --Tend to have more incisional pain after MIDCAB vs traditional CABG, bc of thoracotomy incision & required rib retraction. Pts have thoracotomy incision & CT or smaller-lumen vacuum chest device; encouraged to cough, DB, & use IS for 1wk post-op. Most spend <6hrs in critical care unit & are D/C in 2 or 3 days. -Endovascular (endoscopic) vessel harvesting. Regardless of whether traditional CABG or MIDCAB performed, the donor vessel may be obtained w/ endoscope rather than large incision; radial artery or vein in leg may be taken w/ this method. Instead of lg, painful incision, pt has 1 or 2 very sm incisions in leg or arm. Decreased hospital stay length, post-op complications, & pain. -Transmyocardial laser revascularization: Laser created narrow channels through ventricular muscle to facilitate BF to tissue. -Off-pump coronary artery bypass: OPCAB procedure in which open-heart OP is performed w/o heart-lung bypass machine. -Advantages= shorter hospital stays & decreased mortality, infection risk, & cost. -Disadvantage= requires surgeons to have increased skill to master technique. -Robotic-assisted heart OP: less invasive open-heart OP; endoscopically via very sm incisions in chest wall. Use of robotics provides surgeons w/ capabilities that simplify the process, eliminate tremors of hands, increase ability to reach inaccessible sites, & improve depth perception & visual acuity. --Other advantages= shorter hospital stays (average stay 2-3 days), less pain bc smaller incisions, no need for heart-lung bypass machine, less pt anxiety, & greater pt acceptance. Allows surgeons to perform telesurgery; heart OP over long distances. --Disadvantages= computer failure, limited #s of surgeons skilled in these techniques, & length of OP time (about 50min longer vs conventional OP).

Surgical Management for Fractures

Surgical Management for Fractures: some types of fractures, closed reduction not sufficient. Surgical tx needed to realign bone to enhance healing process. -Pre-op: orthopedic OP similar to OP w/ general or epidural anesthesia; may also receive regional nerve blockade, to promote comfort immediately after OP→ little or no pain immediately after OP for about 18-24hrs. -OP: ORIF common method of reducing & immobilizing fracture; preferred bc of early mobility; open= direct view of site; Internal fixation= metal pins, screws, rods, plates, or prostheses inside body to immobilize fracture during healing. External fixation w/ closed reduction used w/ soft-tissue injury (open fracture); External fixation= pins or wires inserted through skin & affected bone & then connected to rigid external frame outside body to stabilize fracture during healing. --External fixation advantages: min. blood loss vs internal fixation. Device allows early ambulation & exercise of affected part while relieving pain. Maintains alignment in closed fractures that will not maintain position in cast & stabilizes comminuted fractures that require bone grafting. --External fixation disadvantages: increased risk for pin-site infection; can lead to osteomyelitis, serious & difficult to tx. -Post-op External Fixation: assess pin sites every 8-12hrs for drainage, color, odor, & severe redness= inflammation & possible infection. In first 48-72hrs, clear fluid drainage or weeping is expected, creates crusting around pins. No std. method or EBP protocol for pin-site care estab., current evidence= pin site crusts not removed bc protect from infection. Disturbed body image; Teach about alt. to clothing.

Temporary Pacing

Temporary Pacing: nonsurgical tx; provides timed electrical stimulus→ heart, when impulse initiation or conduction system is defective. Stimulus spreads throughout heart to depolarize cells→ contraction & CO should follow. Stimuli delivered to RA or RV (single-chamber PM) or both (dual-chamber PM). -Txs symptomatic bradydysrhythmias not responding to atropine; or asystole. -Transcutaneous pacing: 2 large external electrodes, attached to external pulse generator. Generator emits electrical pulses→ through electrodes→ transcutaneously→ ventricular depolarization; when HR slower than PM set rate. --Emergency tx to provide demand ventricular pacing in profoundly bradycardic or asystolic until invasive pacing can be used or HR returns to normal. --Painful & may require pain & sedative meds for toleration. --Used only as temporary tx to maintain HR & perfusion until a more permanent pacing method used. -Temporary transvenous system: inserted in emergency as bridge until permanent PM can be inserted. External battery-op pulse generator & pacing electrodes, or lead wire. Wire attaches to generator; other wire end threaded to RV via subclavian or femoral vein.

The Interview Process

The Interview Process: Best way of determining the "fit" of the individual for the job and for your unit and organization. Before the interview process, a professional résumé is shared with individuals in the recruitment process. -Credentials reviewed before or during the interview: Copy of résumé; Copy of license or notice of passing board scores; 2 copies of all references & previous managers; Permission for a criminal background check; Permission for a drug and alcohol screen; For new RNs, copy of cumulative GPA. --1 copy of references is for HR dept, & 1 is for hiring manager. --New RNs should take a copy of a grade report to demonstrate that they are candidates for graduation & not at risk for failing board certification. -Initial interview may be w/ RN recruiter; Prep for interview: Self-assessment of abilities, strong points, & challenges (not "weaknesses"). Review of org.; one competitive technique is to have a question for them at the end of the interview. --Interview goal is to ID capabilities of individual, & to ID if they would be an asset to the unit. --Behavior-based interviews allow the manager to evaluate capabilities by asking interviewee to give ex. & describe previous experiences. -Unlawful inquiries by interviewer: Promises that can't be kept; Anything that law prohibits for job consideration; Respect applicant's privacy. Interviewee may bring up delicate topic, but interviewer may not. Not allowed to ask about race or religion. -Recruitment Strategies: Final stg. of interview process relies on recruitment activities of the org; important role in job satisfaction. Ex. Flexible hrs; Bonus or relocation $; Scholarships for continued education; Career opportunities. --Many strategies reflect compensation, benefits, or work alternatives that are important to RNs whom the org. is trying to recruit. A new RN should ID qualities of work environment that are important before the interview. Although $ is an important issue, it is generally not an acceptable 1st or early question to ask an interviewer. --New RN should ID qualities of a work environment that are important before the interview. Pay is important, but not an acceptable 1st or early question to ask interviewer.

Tracheostomy effect on swallowing; how to prevent aspiration

Tracheostomy effect on swallowing: TT sometimes tethers the larynx in place, making it unable to move effectively; result is difficulty in swallowing. When the cuff is inflated, it can balloon backward & interfere w/ food passage in the esophagus because the wall between the trachea & esophagus is thin. Keep the HOB elevated >30min after eating. -If balloon is inflated, can interfere w/ food passage through the esophagus. Consider liquids & soft foods; provide nutrition w/ less difficulty & discomfort. -Preventing Aspiration While Swallowing: -Avoid serving meals when they're fatigued. -Provide smaller & more frequent meals. -Provide adequate time; do not "hurry" them. -Closely supervise the self-feeding patient. Keep suctioning equipment close at hand & turned on. -Avoid H2O & "thin" liquids, & straws. Thicken all liquids, including H20. Thin liquids may be permitted after a swallowing evaluation by a speech-language pathologist. -Avoid foods that generate thin liquids during the chewing process (ex. fruit). -Position them in the most upright position possible. -When possible, completely (or at least partially) deflate the tube cuff during meals. -Suction after cuff deflation to clear the airway & allow comfort during the meal. -Feed each bite or encourage to take each bite slowly. -Encourage the patient to "dry swallow" after each bite ("double swallowing") to clear residue from the throat. -Avoid consecutive swallows of liquids. Provide controlled small vLs of liquids w/ a spoon. -Tell them to "tuck" the chin down & move the forehead forward while swallowing. -Allow them to indicate when they're ready for the next bite. -If coughing occurs, stop the feeding until they indicate that the airway is clear. -Assess RR, ease of swallowing, pulseOx, & HR during feeding.

Tracheotomy Post-op care

Tracheotomy Post-op care: Immediate needs are airway maintenance & respiratory assessment; focus on ensuring a patent airway; then confirm the presence of bilateral breath sounds. Perform a respiratory assessment at least Q1hr; assess for complications. -Tube obstruction: result of secretions or by cuff displacement. -Indicators: difficulty breathing; noisy respirations; difficulty inserting a suction catheter; thick, dry secretions; and high peak pressures (if a mechanical ventilator is used). --Assess the patient at least Q1hr for tube patency. Prevent obstruction by helping the patient cough & DB, providing inner cannula care, humidifying O2, & suctioning. If tube obstruction results from cuff prolapse over the end of the tube, the respiratory HCP repositions or replaces the tube. -Tube dislodgment & accidental decannulation: can occur when the tube is not secure. Prevent by securing the tube in place to reduce movement & traction or accidental pulling. --Tube dislodgment in the first 72hrs post-op is an emergency because the tracheostomy tract has not matured & replacement is difficult; tube may end up in the SubQ tissue instead of in the trachea ("false passage"). The patient will not be able to be ventilated. --Obese or those w/ short, large necks may be particularly difficult to recannulate if the tube is dislodged. --Critical Rescue: For safety, ensure that a TT of the same type (including an obturator) & size (or 1 size smaller) is at the bedside at all times, along w/ a tracheostomy insertion tray. Monitor the patient for tube placement. When tube is dislodged on an immature tracheostomy, respond by ventilating the patient using a manual resuscitation bag & facemask while another RN calls the RRT, as well as the surgical service that placed the tracheostomy. If a stay suture technique was used during the tracheostomy procedure, gentle tension on the sutures can reopen the trachea. --If decannulation occurs after 72hrs, extend the patient's neck & open the tissues of the stoma w/ a curved Kelly clamp to secure the airway. W/ the obturator inserted into the tracheostomy tube, quickly & gently replace the tube & remove the obturator. Check for airflow through the tube & for bilateral breath sounds. --If you cannot secure the airway, notify a more experienced RN, RT, or respiratory HCP for assistance. Ventilate with a bag-valve-mask. If the patient is in distress, call the RRT for help. To reduce tube dislodgment problems, many institutions have a "difficult airway" cart for high-risk patients.

Traction

Traction: pulling force to part of body to provide bone reduction or a last resort to decrease muscle spasm (reducing pain); often hospitalized, but in some, home care possible even for skeletal traction. -2 major types of traction= skin & skeletal traction. -Skin traction: use of Velcro boot (Buck traction), belt, or halter; usually secured around affected leg. Purpose of skin traction is to decrease painful muscle spasms w/ hip & proximal femur fractures. Weight used as pulling force; limited to 5-10 lb (2.3-4.5kg) to prevent injury to skin. -Skeletal traction: screws surgically inserted directly into bone (femoral condyles for distal femur fractures); allow use of longer traction time & heavier weights, usually 15-30lb (6.8-13.6kg). Aids bone realignment but impairs mobility. Use pressure-reduction measures & monitor for impaired tissue integrity. Pin site care is important part of RN tx to prevent infection. Keep pin sites clean & document nature of any drainage. Follow agency or PHCPs protocol for pin care. -Action Alert: in traction, weights not removed w/o prescription; should not be lifted manually or allowed to rest on floor. Weights freely hanging at all times. Teach to UAPs, to other personnel like radiology dept., & visitors. Inspect skin at least Q8h for s/s irritation or inflammation. When possible, remove belt or boot used for skin traction Q8h to inspect under device. Assess NV status of affected part per agency or PHCP protocol to ID impaired perfusion & tissue integrity. Circulation usually monitored Q1h for first 24hrs after traction applied & Q4h thereafter.

Triage concepts in mass casualty

Triage concepts in mass casualty differ from "civilian triage"= practiced during usual ER operations. Disaster triage practices can vary widely based on local EMS protocols, some concepts fairly universal. -Action Alert: In mass casualty or large-scale disaster, implement military form of triage w/ desired outcome of doing greatest good for greatest # of pts. If resources severely limited, this means that critically ill or injured & might receive attempted resuscitation during usual operations may be triaged into "expectant" or "black-tagged" & allowed to die or not be tx until others receive care. -Most mass casualty teams in field (at disaster site) & in hospital use disaster triage tag system that categorizes triage priority by color & #: -Emergent (class I): red tag; immediate threat to life [airway obstruction, shock]; require immediate tx. -Urgent (class II): yellow tag; major injuries [open fractures w/ distal pulse, large wounds] need tx 30min-2hrs. -Nonurgent or "walking wounded" (class III): green tag; minor injuries can be tx after a delay, generally >2hrs; ex. closed fractures, sprains, strains, abrasions, contusions. Usually the greatest # in most large-scale multi-casualty situations; can overwhelm system. self-transport may unknowingly carry contaminants from [nuclear, biologic, chemical] incident into hospital, w/ potentially disastrous consequences. -Expectant (class IV): black tag; expected (& allowed) to die or are dead; massive head trauma, extensive full-thickness burns, & high cervical SCI necessitating MV. Rationale is difficult decision but limited resources must be dedicated to saving most lives vs using valuable resources to save 1 life at expense of many others.

Triage in ED

Triage in ED: an organized system for sorting or classifying pts into priority levels, depending on illness or injury severity; organization of ER care & ED is structured via triage principles. -Based on triage priority→ rushed into tx rm, directed to lower-acuity area in ED, or asked to sit in waiting rm. -Variations include: Triage RN-initiated protocols for labs or Dx studies may be performed before actual evaluation by ED provider; Initiation of care while on stretcher in hallway of crowded ED. -Emergent (life threatening): Chest pain w/ diaphoresis; Hemorrhage; Respiratory distress; Stroke; VS instability. -Urgent (needs quick treatment, but not immediately life threatening): ABD pain (severe); Fractures (displaced or multiple); Renal colic; Respiratory infection (esp. pneumonia in elderly); Soft-tissue injuries (complex or multiple). -Nonurgent (could wait several hours if needed without fear of deterioration): Fracture (simple); Rashes; Strains & sprains; UTI.

Tx of ACS

Tx of ACS: Average wait time before seeking tx >2hrs; lessens 4-6hr window for most advantageous tx w/ percutaneous tx. -Managing Acute Pain: priority; address the cause; decrease pain, decrease myocardial O2 demand, & increase perfusion (myocardial O2 supply). Evaluate reports of pain, obtain VS, ensure IV access, & notify HCP of pt condition. -NTG: relieve episodic anginal pain. --In 5min increments→ total of 3 dose admins in attempt to relieve angina pain. --After 5min→ recheck pain intensity & VS. If BP is <100 sys. or 25 lower than previous→ lower HOB & notify HCP. ---Angina usually responds to NTG; states pain is relieved or markedly diminished. If simple measures, like 3 SL NGT, in timed increments, 1 after other, do not relieve chest discomfort→ may be MI. ---Ischemia persists→ HCP may prescribe IV NTG for tx chest pain. Begin infusion slowly, checking BP & pain level Q3-5min. NTG dose increased until pain relieved, BP falls excessively, or max prescribed dose is reached. ---Pain or s/s subsided & pt stabilized→ HCP may change to PO or topical nitrate. During admin of LT PO & topical nitrates→ 8-12hr nitrate-free maintained to prevent tolerance. May initially report headache→ Give acetaminophen before nitrate to ease discomfort. --Drug Alert: Before admin NTG, ensure not taken phosphodiesterase inhibitors for ED [ex. sildenafil, tadalafil, avanafil, or vardenafil] w/in past 24-48hrs. NTG w/ these inhibitors→ profound hypotension. Remind not to take w/in 24-48hrs of eachother. Some phosphodiesterase inhibitors also used to tx pulmonary arterial HTN (PAH). PAH pts cannot stop taking phosphodiesterase inhibitor→ NTG is contraindicated. -Morphine sulfate (MS): relieve discomfort that's unresponsive to NTG; decreases pain, decreases myocardial O2 demand, relaxes smooth muscle, & reduces circulating catecholamines. Persistent cardiac pain→ admin MS in doses of 2-4mg, slow IV push Q5-15min. Monitor for AEs→ respiratory depression, hypotension, bradycardia, & severe vomiting. -O2-tx: Hypoxemia→ O2 at 2-4 L/min to maintain SpO2 of 90%+. Use of O2 in absence of hypoxemia, shown to increase coronary vascular resistance, decrease coronary BF, & increase mortality. -Comfort: Monitor VS & cardiac rhythm every few min. BP stable→ help assume any position of comfort. Semi-Fowlers often enhances comfort & tissue oxygenation. -Quiet, calm environment & txs explanations reduce anxiety & help relieve CP; if needed, remind to take several DBs to increase O2. --Experiencing MI→ pain relief strategies + txs to increase myocardial perfusion is essential.

Tx of ACS; Increasing Myocardial Tissue Perfusion w/ Anti-platelet Tx

Tx of ACS; Increasing Myocardial Tissue Perfusion w/ Anti-platelet Tx: MI is dynamic process, so restoring perfusion to injured area (usually w/in 4-6hrs for NSTEMI; 60-90min for STEMI) often limits amount of extension & improves LV function. Complete, sustained reperfusion of CAs after ACS has decreased mortality rates. -Antiplatelets: (aspirin, Plavix, Brillinta, Effient). -Aspirin (ASA) tx: recommended by ACC & AHA; inhibits plt aggregation & vasoconstriction→ decreasing likelihood of thrombosis. If new-onset angina at home→ teach to chew aspirin 325mg (4 baby aspirins, 81mg each) immediately & call 911! Anti-plt effect of ASA begins w/in 1hr & continues for several days. In hospital→ aspirin on arrival to ED or if MI occurs in hospital. All w/ suspected CAD should receive low-dose, non-enteric-coated aspirin daily unless absolutely contraindicated. Instruct chew & swallow & continue taking as prescribed unless AEs occur. -P2Y12 plt inhibitors: PO agents; ex. clopidogrel or ticagrelor; given w/ initial loading dose followed by daily dose for up to 12mo after Dx. Prevent plts aggregating (clumping) together to form clots. If dual anti-plt tx used→ significant reduction in mortality. Take w/ food bc can cause diarrhea & GI upset. Do not confuse Plavix w/ Paxil. --Drug Alert: Dual anti-plt tx (DAPT) is suggested for all ACS; incorporating aspirin w/ P2Y12 receptor blocker [clopidogrel, ticagrelor]; Major SE for each is bleeding. Observe for bleeding; ex. nosebleeds or blood in stool. Meds need to be D/C if bleeding occurs. Teach s/s bleeding & when to contact HCP. Receiving DAPT→ pts w/ high risk for GI bleeding may be prescribed a PPI [omeprazole]. -Protease-activated receptor inhibitor (PAR-1): ex. vorapaxar; an antiplatelet, shown to decrease risk of recurrent MI when added to regimen of aspirin & clopidogrel. Main SE is bleeding; increased risk of IC hemorrhage.

Tx of ACS; Increasing Myocardial Tissue Perfusion w/ Nitrates, GP IIb/IIIa inhibitors, ACEIs, ARBs, Anticoagulants, & CCBs.

Tx of ACS; Increasing Myocardial Tissue Perfusion: -Nitrates: NTG, Isosorbide; relieve episodic anginal pain. Increases collateral BF, redistributes BF toward subendocardium, & dilates coronary arteries; it decreases myocardial O2 demand by peripheral vasodilation→ decreases preload & afterload. -Glycoprotein (GP) IIb/IIIa inhibitors: ex. abciximab, eptifibatide, tirofiban; Integrilin, aggrastat, Reopro; admin IV to prevent fibrinogen attaching to activated plts at site of thrombus; blocks plt aggregation. Used in unstable angina & NSTEMI; also before & during PCI to maintain patency of artery w/ lg. clot & admin w/ fibrinolytics after STEMI. --Drug Alert: giving GP IIb/IIIa inhibitors→ assess closely for bleeding or hypersensitivity rx. If either occurs→ notify HCP or RRT immediately. Monitor plts 4hrs after starting & daily thereafter. Notify cardiologist if pt develops significant decrease in plts per protocol. -Angiotensin-converting enzyme inhibitors (ACEIs; prils...lisinopril, enalapril, captopril) or angiotensin receptor blockers (ARBs; losartan, valsartan "tan"): frequently prescribed w/in 24hrs of ACS to prevent ventricular remodeling & HF. After STEMI, all pts w/o contraindications→ receive ACEI or ARB; increase survival after MI. Monitor for decreased UO, hypotension, & cough. Check for changes in serum K, Cr, & BUN. If ACEIs or ARBs initiated, should be continued on D/C indefinitely. -Anticoagulation tx: in addition to antiplatelet tx; used to prevent clot formation. Drug choice per HCP preference; U.S. guidelines do not recommend 1 agent over another. Anticoagulation is stopped before cardiac cath & usually not continued following coronary tx unless high risk for clot reformation following tx. -CCBs: pts w/ angina; prescribed to promote vasodilation & myocardial perfusion. Indicated for vasospastic angina or have HTN & angina despite BB tx (unstable angina). Not indicated after acute MI unless beta blockade is contraindicated. Monitor for hypotension & peripheral edema & review frequency of angina episodes. Also used for chronic stable angina (CSA). When not successful in managing CSA→ ranolazine may be added to drug regimen; has antiangina & anti-ischemic properties & often effective in relieving pain associated w/ CSA.

Tx of ACS; Increasing Myocardial Tissue Perfusion w/ BBs & Statins

Tx of ACS; Increasing Myocardial Tissue Perfusion: -1x/day BBs: ex. metoprolol XL, carvedilol CR; AKA beta blockers. Decrease size of infarct, occurrence of V dysrhythmias, & mortality in MI. Usually prescribes a cardioselective BB agent w/in 1-2hrs after MI if HD stable. Slow HR & decrease force of contraction→ prolong diastole & increase myocardial perfusion while reducing force of contraction. Beta blockade→ heart performs more work w/o ischemia. --During BB tx, monitor for: Bradycardia; Hypotension; Decreased LOC; Chest discomfort. --Assess lungs for crackles (→ HF) & wheezes (→ bronchospasm). Hypoglycemia, depression, nightmares, & forgetfulness are also problems w/ beta blockade, esp. elderly; many SEs decrease w/ time. --Unless contraindicated, all experiencing NSTEMI & STEMI→ D/C on BB tx. If hx or new onset HF→ ER metoprolol succinate, carvedilol, or bisoprolol used bc reduce mortality in HF. --Drug Alert: Do not give BBs if HR <50BPM or SBP <100 w/o 1st checking w/ HCP. BB may lead to persistent bradycardia or further reduction of SBP, leading to poor peripheral & coronary perfusion. -Statins: reduces risk of recurrent MI, mortality, & stroke. Before D/C, all pts Dx w/ ACS should be started on high-intensity statin tx despite results of lipid panels. High-intensity→atorvastatin & rosuvastatin.

Interventions for pneumothorax, tension pneumothorax, hemothorax

Tx of Pneumothorax: Stable w/ small pneumothorax, has mild s/s & no continuing air leak→ no tx may be needed. -Severe pneumothorax, tension pneumothorax, & hemothorax→ chest tube tx is essential. --Initial management of tension pneumothorax→ immediate needle thoracostomy, w/ a large-bore needle inserted by PHCP into the 2nd ICS in MCL of affected side; changes tension pneumothorax→ simple pneumothorax & is only a temporary measure. When you suspect a tension pneumothorax, call RRT immediately! --More definitive tx is mandatory, w/ chest tube placement into the 4th ICS, & the other end attached to a water seal drainage system until the lung reinflates. -Tx for hemothorax→ chest tube placement to remove blood in the pleural space→ normalize breathing & prevent infection; multiple CTs may be placed. --Closely monitor chest tube drainage. Serial CXR used to ID tx effectiveness. --Other care: pain control, pulmonary hygiene, & continued assessment for RF. --Open thoracotomy: needed for initial blood loss of 1000 mL from the chest or persistent bleeding at 150-200 mL/hr over 3-4hrs. Monitor VS, blood loss, I&O; assess response to chest tubes & infuse IV fluids & blood as prescribed. Blood lost through chest drainage can be infused back into pt after processing if needed.

Types of Budgets: Overall & Operating (personnel)

Types of Budgets: -Overall budget: # of smaller budgets; represent specific areas of concern in $ objective setting of org. -Operating (expense) budget: includes (1) personnel budget, (2) costs other than personnel, & (3) revenue budget. Not all units prep a revenue budget; may be done by finance dept. --Personnel budget requires RN manager forecast the anticipated workload for yr; based on info from environmental assessment, review of previous workload, & ID of services to be provided. -1st, the average daily census & occupancy rate calculated; then total required pt-care hrs calculated. -2nd, the # of FTEs required to provide care calculated per expected # of pt care hrs; FTE= 2080hrs of work/yr. -3rd, the # of full-time, part-time, & shifts calculated; adjustments made for benefits & nonproductive time (vacation, orientation, education, sick time, etc.) -4th, prep daily staffing plan; staff mix required to provide pt care (RN, LPN, unit clerks, care associates, etc); skill mix of staff & staffing requirements are regulated (RN:Pt ratio). --RN manager must be compliant w/ all regulatory boards in determining budget. --Once RN manager decides positions required for care, then other labor costs included in personnel budget; benefits, shift differential, OT, raises, premium pay, etc. Benefits close to additional 40-50% of individual's pay. --Staffing plan based on distributing the # FTEs needed in accordance w/ staffing requirements & regulations. -Workload Calculation: Total required pt care hrs. -Productive Hours Calculation: # of FTEs, PTEs, & shifts needs to be calculated so that the total FTEs needed are achieved. -Non-productive hrs: not making $ for hospital but getting paid; vacation, sick time, etc. -How many FTEs needed: required pt care hrs/ productive hrs per FTE. -Ex. Pt acuity= pt care hrs/day (HPPD); HPPD x pt days= workload (total #hrs care needed for pt acuity & #pt days). -Ex. 1 FTE= 2080hrs/yr; 26 nonproductive days x8hrs/day= 208hrs. 2080-208= 1872 productive hrs per FTE. --Required pt care hrs / productive hrs per FTE= total # FTEs needed. Ex. 82420 care hrs / 1872 productive hrs= 44 FTEs (for 8hr shift). -$ management of unit, & the entire institution, is responsibility of RN leaders & staff RNs. Careful balance of delivery of quality HC & $ stewardship is delicate balance that RN leaders juggle daily= goal of "Triple Aim"; a learning system that all RNs work w/ on daily basis.

Types of Burns

Types of Burns: -True electrical injury if electrical current enters body. Tissue injury occurs if electrical energy converts to heat energy as it travels through body; "iceberg effect" bc surface injuries may look small, but internal injuries can be significant. High voltage is >1000 volts; electric energy converts to heat energy. Entry wound is small; exit wound is large & charred. --Current penetrates skin→ entry wound→ flows through body & damages tissues until it leaves→ exit wound (larger). --Extent of injury depends on type of current, pathway of flow, local tissue resistance, & duration of contact. Longer the electricity in contact w/ body= greater the damage. Skin= most resistant; fat & bone= high resistance; BVs & nerves= least resistant. --Duration of contact is increased by tetanic contractions of strong flexor muscles in forearm→ can prevent releasing the electrical source. -Smoke-related burn injuries: on INH. Orofacial burns can cause edema→ impairs breathing. Even if you think it's only a minor burn, it is critical to assess the mouth, throat, & nose for soot. Listen for coughing, SOB, or hoarseness, may indicate smoke INH. -Thermal burns: caused by contact w/ flames (dry heat), hot liquids (moist heat; scald), or hot objects or substances (contact). Thermal burns to RT usually limited to upper airway above glottis (nasopharynx, oropharynx, larynx). -Contact burns: from hot metal, tar, or grease, often full-thickness injury. Hot metal injuries occur body contacts hot surface [space heater, iron]. Also in industrial settings from molten metals. Tar & asphalt temp. usually >400°F (204.4°C), & deep injuries occur w/in seconds. Hot grease injuries r/t cooking usually deep bc of high temp. -Chemical Burns: Acids & alkalines are most common chemicals that can inflict burns. --Acids: bathroom cleaners, rust removers, pool chemicals, & industrial drain cleaners. Damaged tissue integrity caused by coagulating cells & skin proteins, can limit depth of tissue damage. Injury r/t acid's concentration. --Alkalines: oven cleaners, fertilizers, drain cleaners, & heavy industrial cleaners; damage by causing skin & proteins to liquefy→ allows deeper injury below skin + tissue & muscle. --Some chemicals cause systemic effect, can damage internal organs. --Decontamination is focus for EMS. Contaminated clothing is removed & powdered chemicals are brushed off; then burn is cautiously irrigated w/ large amounts of water.

Types of MS; Key Features of MS

Types of MS: -Classic picture of relapsing-remitting multiple sclerosis (RRMS): occurs in most cases. Course may be mild or moderate, depending on degree of disability. S/S develop & resolve in few wks→ months, & pt returns to baseline. During relapsing phase, pt reports loss of function & continuing development of new s/s. -Primary progressive multiple sclerosis (PPMS): steady & gradual neuro deterioration w/o remission of s/s; progressive disability w/ no acute attacks. Pts tend to be 40-60yrs at onset. -Secondary progressive multiple sclerosis (SPMS): begins w/ relapsing-remitting course that later is steadily progressive. About 1/2 of RRMS develop SPMS w/in 10yrs. Current addition of dz-modifying drugs as part of management may decrease development of SPMS. -Progressive-relapsing multiple sclerosis (PRMS): frequent relapses w/ partial recovery but no return to baseline; seen only small % of pts. Progressive, cumulative s/s & deterioration occur over several yrs. -Key Features of Multiple Sclerosis: -Muscle weakness & spasticity; Fatigue w/ continuous sensitivity to temp; Intention tremors= tremor when performing activity; Flexor muscle spasms; Dysmetria= inability to direct or limit movement; Numbness or tingling; Hypoalgesia= decreased sensitivity to pain. -Ataxia= decreased motor coordination; Dysarthria= difficulty speaking due to slurred speech; Dysphagia= difficulty swallowing; Diplopia= double vision; Nystagmus= eyes make repetitive uncontrolled movements. -Scotomas= changes in peripheral vision; Decreased visual & hearing acuity; Tinnitus= ringing in ears), vertigo= dizziness; Bowel & bladder dysfunction= flaccid or spastic. -Alt. in sexual function [impotence]; Cognitive changes= [over time] memory loss, impaired judgment, & decreased ability to solve problems or perform calculations; Depression.

Types of debriefing

Types of debriefing: 2 types of debriefing, or formal systematic review & analysis, occur after mass casualties or disaster. 1.) bringing in crisis support teams to provide sessions for small groups of staff, to promote effective coping. 2.) admin review of staff & system performance during event to ID if opportunities for improvement in ER management plan exist. -Crisis Support: Crisis workers w/ special education & training in psychological first aid & BH address pre-crisis via post-crisis tx for small-to-large groups, + communities. After working through turmoil & emotional impact of incident & aftermath, the staff may find it difficult to "get back to normal." --W/o tx during & after ER→ risk for ASD or PTSD. ASD is similar PTSD, but has dissociative s/s like numbing, reduced awareness, depersonalization, derealization, or amnesia, w/in 1st mo after event. PTSD can lead to multiple psychological & physical effects, + flashbacks, avoidance, less interest in previously enjoyable events, detachment, rapid HR, & insomnia; great difficulty relating in usual way to family & friends. --Ultimately, professional "burnout" can stem from inability to cope w/ stress; resource is Int. Critical Incident Stress Foundation. --Research indicates education & training in disaster management before incident occurs is associated w/ improved confidence & better coping after incident. -Administrative Review: 2nd type of debriefing; admin evaluation, AKA "hot wash," directed at analyzing hospital or agency response to event while still in forefront of everyones minds. Goal is to ID what went right & what could be improved during activation & implementation of ER prep plan so needed changes can be made. --Typically, representatives from all groups involved come together soon after plan activation discontinued; given opportunity to hear & express +/- comments r/t experiences. --In days after plan activation, written critique forms also used to gain additional info after they've had time to consider impressions of response & impact it had on depts. or areas. --Drills are important, but implementing ER prep plan during actual mass casualty is most effective means of "reality testing" the plan's utility. Feedback from participants can be used to modify or revise the plan & create new processes in prep for future events.

VAP; Ventilator-associated pneumonia

VAP: Infection prevention through strict adherence to infection control, esp. handwashing during suctioning & care of the TT or ETT, is essential, as is meticulous oral care. -Prevent VAP, implement "ventilator bundle" order sets; typically include these actions: Keeping the HOB elevated >30 degrees. Performing oral care per policy; usually brushing teeth w/ a suction toothbrush > Q12hrs & antimicrobial rinse. Ulcer prophylaxis. Preventing aspiration. Pulmonary hygiene; ex. chest physiotherapy, postural drainage, & turning & positioning. -Using the ventilator bundle has greatly reduced overall VAP incidence. -Vigilant oral care w/ suction toothbrush is a key component of VAP prevention; actual practice varies regarding timing, products, & application methods. -Most requiring MV [except ARDS], are placed in a supine position w/ HOB elevated to >30 degrees; this backrest elevation does not appear to be associated w/ an increase in sacral skin breakdown when other skin protection practices are used.

Vagal maneuvers

Vagal maneuvers→ vagal stimulation of cardiac conduction system, specifically SA & AV nodes; not as common, may be attempted to tx SV tachydysrhythmias. Results often temporary & may cause "rebound" tachycardia or severe bradycardia. Further tx must be initiated. -Carotid sinus massage: HCP massages over 1 carotid artery for few sec, observing for cardiac rhythm change; causes vagal stimulation, slowing SA & AV nodal conduction. --Prep pt; Instruct to turn head slightly away from massaged side & observe monitor for rhythm change. ECG is recorded before, during, & after. After tx, assess VS & LOC. --Complications: bradydysrhythmias, asystole, VF, & cerebral damage→ risks are why, it's not commonly performed. Defibrillator & resuscitative equipment must be immediately available during procedure. -Stimulate vagal reflex: HCP instructs to bear down as if straining w/ BM. Assess HR, rhythm, & BP. Observe monitor & record ECG before, during, & after to ID effect of tx.

Vascular Changes Resulting from Burn Injuries

Vascular Changes Resulting from Burn Injuries: -Fluid shift: 3rd spacing or capillary leak synd., usually occurs in first 12hr & can continue 24→ 36hrs. Loss of plasma & plasma proteins decreases BvL & BP→ hypovolemia & shock state. -Fluid shift w/ excessive wt gain: in first 12hrs after burn can continue up to 24-36hrs. S/S Edema, even in sclera; give colloids to bring fluid back into BVs. -Hypovolemia; Metabolic acidosis; Hyperkalemia (direct cell injury); Hyponatremia. Aldosterone secretion increases But the Na passes to interstitial space & doesn't get to the vascular space. Hemoconcentration due to vascular dehydration. Look at all values; bc all values increase in dehydration. -Profound imbalance of F&E, & A/B: hyperkalemia & hyponatremia, & hemoconcentration bc of fluid shift & cell damage. Insult to the human body; why we assess/monitor constantly status, I&O, LOC, VS, etc. -Fluid Remobilization: after 24hrs. Diuretic stage begins 48-72hrs after injury. Capillary membrane integrity returning (trying to repair itself) & edema; fluid shifts from interstitial to vascular space. Normalize= VS, UO→ return to normal. --Hyponatremia bc increased renal Na excretion. Hypokalemia (K+ moves back into cell). Anemia result of hemodilution; Transfusions usually not needed.

Ventilator Controls & Settings: Tidal vL, Rate, FiO2, IPAP, PEEP, Flow Rate, & Other

Ventilator Controls & Settings: -Tidal vL (VT): vL of air received w/ each breath; measured on inspiration or expiration; average prescribed VT 6-8 mL/kg, based on IBW & accurate measure of Ht. -Rate (breaths/min): # ventilator breaths delivered per min; usually 10-14 breaths/min. Pt condition & ventilator mode can be factors if above or below this range. -Fio2: O2 level delivered to pt; FiO2 is based on ABGs & pt condition; 21-100% O2. -Peak airway (inspiratory) pressure: pressure used by the ventilator to deliver a set tidal vL at a given lung compliance; appears on the display. It's the highest pressure reached during inspiration. PIP trends reflect changes in lung resistance & ventilator resistance. --Increased PIP= increased airway resistance in pt or ventilator tubing (bronchospasm or pinched tubing, patient biting the ET tube), increased secretions, pulmonary edema, or decreased pulmonary compliance (lungs or chest wall is "stiffer" & harder to inflate). --Upper pressure limit is set to prevent barotrauma; limit is reached→ high-pressure alarm, & remaining vL is not given. -PEEP: + pressure exerted during expiration; improves oxygenation by enhancing gas exchange & preventing atelectasis. MV often have a set PEEP of 5-6 cm H2O to prevent alveolar collapse & improve arterial oxygenation; may be increased to 15 cm H2O+ when PaO2 remains low despite increasing FiO2. --Need for increased PEEP= severe gas exchange problem; important to lower FiO2 delivered whenever possible, prolonged use of high FiO2 can damage lungs from toxic effects of O2. Effect should be increase in PaO2 so FiO2 can be decreased. -Flow rate: how fast each breath is delivered; usually 40-60L/min. Agitated or restless, widely fluctuating inspiratory pressure reading, or other s/s air hunger→ flow may be too low. Increasing flow should be tried before using chemical restraints. -Other settings: used depending on ventilation mode & pt condition; ex. waveform, plateau, pressure-vL loop, trigger sensitivity, & alarm settings.

Ventilator Controls & Settings: 3 components; vL-cycled, pressure cycled, flow cycled.

Ventilator Controls & Settings: settings generally based on 3 components: 1.) Inspiratory trigger is the initiation of ventilator breath from pt effort; or as a set, timed breath from the ventilator. 2.) Gas delivery achieved by setting the tidal vL= specific target vL of gas; or setting a target pressure that delivers a variable vL of gas. 3.) Breath termination the transition between I&E; inspiratory breath is terminated by a set vL, pressure, time, or flow. -vL-cycled: pushes air into lungs until preset vL is delivered; constant tidal vL is delivered, regardless of pressure needed to deliver tidal vL; set pressure limit prevents excessive pressure from being exerted on lungs. Advantage of this mode, constant tidal vL is delivered regardless of changes in lung or chest wall compliance or airway resistance. -Pressure-cycled: pushes air into the lungs until a preset airway pressure is reached; tidal vLs & inspiratory time vary. -Time-cycled: push air into lungs until a preset time has elapsed; tidal vL & pressure vary. -Flow-cycled: used w/ pressure support ventilation; it will terminate the breath when it reaches a preset flow rate (% of pts max. inspiratory flow).

Ventricular Dysrhythmias: VF

Ventricular Fibrillation (VF): V fib; electrical chaos in ventricles; life threatening! Impulses from many irritable foci fire in totally disorganized manner→ ventricular contraction cannot occur. No ID ECG deflections present; ventricles quiver→ consuming tremendous amount of O2. -No CO or pulse→ no cerebral, myocardial, or systemic perfusion. Rapidly fatal if not successfully ended w/in 3-5min. -VF may be 1st manifestation of CAD. Pts w/ MI at great risk for VF; also occurs w/ hypokalemia, hypomagnesemia, hemorrhage, drugs, rapid SVT, or shock. OP or trauma may also cause VF. -S/S: VF begins→ become faint, immediately loses consciousness, & becomes pulseless & apneic (no breathing); no BP, & heart sounds absent. R&M acidosis develop; seizures may occur. W/in minutes→ pupils fixed & dilated, skin cold & mottled. Death w/o prompt tx. -Tx: Emergency care for VF is critical for survival. -Desired care outcomes are to resolve VF promptly & convert to organized rhythm→ priority is to defibrillate immediately according to ACLS protocol. -Defibrillator not readily available→ high-quality CPR must be initiated & continued until it arrives. -Automated external defibrillator (AED) frequently used bc simple for medical & lay personnel. Defibrillation + CPR. -Drug tx: dysrhythmias sustained &/or life threatening. Drugs from 1+ classes of antidysrhythmics often used. Vaughn-Williams classification commonly used to categorize drugs according to effects on action potential of cardiac cells (classes I-IV); other drugs also have antidysrhythmic effects but do not fit classification.

Ventricular Tachycardia (VT)

Ventricular Tachycardia (VT): V tach; repetitive firing of irritable ventricular ectopic focus, usually 140-180BPM+. May result from increased automaticity or a re-entry mechanism; intermittent (nonsustained VT) or sustained, lasting >15-30s. SA node may continue to discharge independently→ depolarizing the atria but not ventricles, but P waves seldom seen in sustained VT. -May occur in pts w/ ischemic heart dz, MI, cardiomyopathy, hypokalemia, hypomagnesemia, valvular heart dz, HF, drug toxicity (ex. steroids), or hypotension. Users of cocaine or illicit INH→ high risk for VT. -Pts who go into cardiac arrest, VT is commonly the initial rhythm before deterioration into VF as the terminal rhythm! -S/S of sustained VT partially depend on ventricular rate. Slower rates→ better tolerated. -Critical Rescue: some pts, VT causes cardiac arrest. Assess circulation & airway, breathing, LOC, & oxygenation level. Stable pt w/ sustained VT→ admin O2 & confirm rhythm via 12-lead ECG. Amiodarone or lidocaine may be prescribed. -Current ACLS guidelines: elective cardioversion is highly recommended for stable VT. PHCP may prescribe PO antidysrhythmic agent to prevent further occurrences. --Pt on digoxin→ drug withheld up to 48hrs before elective cardioversion. Digoxin→ increases ventricular irritability→ risk for VF after countershock. --Persist w/ stable VT episodes→ may require radiofrequency catheter ablation. --Unstable VT w/o a pulse→ tx same way as VF.

Best Practice for Patient Safety & Quality Care: Pt in Hypovolemic Shock

Best Practice for Pt Safety & Quality Care in HvLS: -Ensure patent airway. Insert IV catheter or maintain established catheter; large-bore catheter is suggested. -IV therapy: fluid resuscitation; primary HvLS tx. Type & amount are debated; type generally situational. Crystalloids & colloids often used for vL replacement; crystalloids= nonprotein substances (minerals, salts, sugars; NS, LR) maintain F&E & plasma vL; colloids= lg. molecules of proteins or starches. --LR: balanced Na solution (Na, Cl, Ca, K, & lactate); isotonic→ expands vL, & lactate buffers acidosis. --NS: only solution for blood/product admin. --Protein colloid fluids: restore osmotic pressure & fvL. --Blood products: if shock cause is blood loss; often PRBCs & plasma. PRBCs increase Hct & Hgb w/ some fvL. -Admin O2 to maintain SpO2 at 92-96%; supplemental O2 is no longer recommended if SpO2 is normal. ---O2-tx used at any shock stg; via mask, hood, NC, ETT, or TT. Maintain SpO2 94-96%. O2-tx w/ normal SpO2 no longer recommended; may be associated w/ increased mortality risk. -Elevate feet, keeping head flat or elevated to no >30-degrees. Examine for overt bleeding. If overt bleeding present→ apply direct pressure to site. --Monitoring VS & LOC major RN action to ID condition & tx effectively. Monitor these responses: Pulse (rate, regularity, quality); BP; PP; Central venous pressure (CVP); RR; Skin & mucosal color; SpO2; Cognition; UO. --Assess parameters at least Q15min until shock is controlled & their condition improves. Hemodynamic monitoring in critical care includes intra-arterial monitoring, mixed venous O2sat (SvO2), & PA monitoring. -Admin drugs as prescribed. Increase rate of IV fluids. Do not leave pt. --Drug tx: in addition to fluid tx when vL loss is severe & not responding to fluids & blood products. Drugs increase venous return, improve cardiac contractility, or improve cardiac perfusion by dilating coronary BVs. --Drug Alert: Monitor closely bc drugs that dilate coronary BVs [ex. nitroprusside, NTG] can cause systemic vasodilation & increase shock if vL depleted. Drugs that increase heart muscle contraction increase heart O2 consumption & can cause angina or MI. -Surgical: in addition to nonsurgical tx; may be needed to correct shock cause; ex. vascular repair, surgical hemostasis of major wounds, closure of bleeding ulcers, & chemical scarring (chemosclerosis) of varicosities. -Teach pts & family the early shock indicators: increased thirst, decreased UO, light-headedness, apprehension; & seek immediate medical attention if these appear.

Complications of CABG

Complications of CABG: hypotension, hypothermia, hypertension, bleeding, cardiac tamponade, change in LOC. -Hypotension (SBP <90) major problem bc may result in collapse of coronary graft. Decreased preload can result from hypovolemia or vasodilation. If hypovolemic→ might need to increase fluid admin or admin blood. May manage w/ vL replacement followed by vasopressors to increase BP. If hypotension is result of LV failure→ IV inotropes. -Hypothermia common problem after OP. Warm cardioplegia usual tx, but body temp may drift downward after leaving OR. Monitor body temp & institute rewarming tx if it drops <96.8°F (36°C). Rewarming accomplished w/ warm blankets, lights, or thermal blankets. Danger of rewarming too quickly; begin shivering→ metabolic acidosis, increased myocardial O2 consumption, & hypoxia. Prevent shivering→ rewarming should proceed at rate no faster than 1.8°F/hr (1°C); D/C when body temp approaches 98.6°F (37°C) & extremities warm. --Hypothermia significant risk after CABG OP bc it promotes vasoconstriction & HTN. -HTN: SBP >140-150; many in post-op. May be from hypothermia, CPB, drugs, & increased SNS activity. Dangerous bc increased pressure promotes leakage from sutures & may cause bleeding. Drugs [nitroprusside or fenoldopam] to decrease afterload, ease workload of heart, & prevent HF. -Bleeding; Action Alert: Bleeding after CABG OP occurs to limited extent in pts. Measure mediastinal & pleural CT drainage at least Q1h. Report amounts >150 mL/hr to surgeon. IMA grafts may have more chest drainage vs saphenous vein grafts (leg). Maintain patency of mediastinal & pleural CTs; effective way of promoting CT drainage is to prevent dependent loops. --If pt bleeding & mediastinal tubes not kept patent→ fluid (blood) may accumulate around heart→ myocardium compressed→ cardiac tamponade. Fluid compresses A&Vs, preventing adequate filling→ reducing CO. --Critical Rescue: Assess, document, & report s/s cardiac tamponade immediately: Sudden cessation of previously heavy mediastinal drainage. Beck triad= JVD but clear lung sounds; Distant, muffled heart sounds; Hypotension. Pulsus paradoxus (BP >10 higher on E vs I); equalizing of PAOP & RA pressure; CV collapse. --Prep for echo or CXR to confirm Dx. Pericardiocentesis (remove pericardium fluid via lg. needle) may not be appropriate for tamponade after CABG bc blood in pericardium may have clotted. vL expansion & emergency sternotomy w/ drainage are best txs. -LOC: changes in LOC; permanent or transient. Transient changes r/t anesthesia, CPB, air emboli, or hypothermia in many pts. Assess for neuro deficits; ex. slowness to arouse, memory loss, & new-onset confusion. --Action Alert: After CABG, check neuro status Q30-60min until awakened from anesthesia. Then check Q2-4h or per policy. --Pts w/ transient neuro deficits usually return to baseline w/in 4-8hrs. --Permanent deficits associated w/ intraoperative stroke may manifest w/: Abnormal pupillary response; Failure to awaken from anesthesia; Seizures; Absence of sensory or motor function. -Managing pain. Differentiate between sternotomy pain [expected] & anginal pain [graft failure]. Typical sternotomy pain is localized, does not radiate, & worse w/ cough or DB. Describe pain as sharp, aching, or burning. Pain may stimulate SNS→ increases HR & vascular resistance while decreasing CO. --Admin analgesic in adequate doses to control pain. During MV weaning→ may need to use short-acting analgesics & limit pain meds bc respiratory depressant effects of analgesia. -Sternal wound infections develop 5 days→several wks post-op in small # pts & are responsible for increased costs & longer hospital stays. Be alert for mediastinitis by observing for: Fever beyond first 4 days after CABG; Instability (bogginess) of sternum; Redness, induration, swelling, or drainage from suture sites; Increased WBCs.

Complications of Fractures

Complications of Fractures: Regardless of type or location; several limb & life-threatening acute & chronic complications can result. S/S of beginning complications must be tx early to prevent serious consequences. In some, careful monitoring & assessment by RN can prevent complications from occurring or worsening. -Acute Complications of Fractures: common include VTE & bone or soft tissue infection. VTE= DVT & PE (major complication); most common complication of LE OP or trauma & most often fatal complication of MuSk OP. -ACS not limited to MuSk problems; also occurs in severe burns, extensive insect bites or snakebites, or massive infiltration of IV fluids; bc edema increases internal pressure in 1+ compartments. -ACS may need surgical tx= fasciotomy; surgeon cuts through fascia to relieve pressure & tension on vital BVs & nerves; wound remains open & requires care to begin healing from inside out. Usually closes wound w/ skin graft in several days. -LT problems from compartment syndrome: infection, persistent motor weakness in affected extremity, contracture, & myoglobinuric renal failure; extreme cases, amputation is necessary. -Trauma to tissues→ defense system disrupted. Wound infections= most common type of infection from orthopedic trauma; range from superficial skin infections to deep wound abscesses. Infection can be from implanted hardware used to repair fracture surgically [screws, pins, plates, rods]. Clostridia infections can result in gas gangrene or tetanus & can prevent bone from healing properly. --Osteomyelitis: Bone infection; most common w/ open fractures bc tissue integrity altered & after OP repair of fracture; w/ this type of trauma, risk for HC agency-acquired infections is increased. Infections are common, & many from multi-drug-resistant organisms (MRSA). Reducing MRSA infection is primary desired outcome for all HC agencies. -Several fracture complications are more rare but potentially life-threatening, like acute compartment syndrome and fat embolism syndrome. -Complex regional pain syndrome (CRPS): formerly reflex sympathetic dystrophy (RSD); dysfunction of CNS & PNS, causes severe, persistent pain & other s/s. Genetics possible role. Often bc fractures or traumatic MuSk injury; common in feet & hands. Specific nerve injuries present; others no injury ID. -Triad of s/s: Abnormalities of ANS (changes in color, temp., & sensitivity of skin over affected area, excessive sweating, edema); Motor s/s (paresis, muscle spasms, loss of function); Altered sensory perception s/s (intense burning pain, later intractable). -Tx: Facilitate soft tissue healing & prevent CRPS, PT has pt frequently apply various objects w/ various surface types directly to skin to desensitize it; rough, smooth, hard, soft, sharp (not enough to damage skin), or dull.

DMAT

DMAT: Disaster Medical Assistance Team; medical relief team of civilian medical, paraprofessional, & support staff, deployed to disaster area w/ enough medical equipment & supplies for 72hrs. --DMATs are part of National Disaster Medical System (NDMS) in US→ Provide relief services ranging from primary HC + triage to evacuation & staffing to assist HC facilities overwhelmed w/ casualties. Bc licensed HCPs [RNs] act as federal employees when deployed, their professional licenses are recognized & valid in all states.

Angina Pectoris: Chronic Stable angina

-Angina pectoris: CP caused by temporary imbalance in coronary arteries' ability to supply O2 & cardiac muscle's demand for O2. Ischemia (lack O2) occurring w/ angina is limited duration & does not cause permanent damage of myocardial tissue. -S/S: Chest discomfort associated w/ myocardial ischemia usually begins in central or Lt chest & then radiates to arm (esp. ulnar side of Lt arm), wrist, jaw, epigastrium, Lt shoulder, or between shoulder blades. Ischemic chest discomfort usually not sharp; not worsened by deep inspiration, not affected by moving muscles in area where discomfort localized, not positional in nature. --Angina has 2 main types: stable angina & unstable angina. -Chronic stable angina (CSA): Strangling of chest, chest discomfort; occurs w/ moderate-to-prolonged exertion in pattern familiar to pt. Frequency, duration, & intensity of s/s remain same over several mo. Only slight activity limits & usually associated w/ fixed atherosclerotic plaque; usually relieved by NTG or rest; often managed w/ drugs. Rarely requires aggressive tx. --Temporary imbalance between CA's ability to supply O2 & cardiac muscle's demand for O2. --Ischemia limited in duration & does not cause permanent damage to myocardial tissue.

Functional Nursing; Team Nursing; Primary Nursing; Total pt care

-Functional Nursing: task focused; Charge RNs make most decisions; work allocation= assigning tasks; time span= 1 shift. Communication= Hierarchical; charge RN gives & receives report. Tasks documented. Outcomes= Fragmented care. Quality= Omissions & errors can occur. -Team Nursing: group task focused; Team leader makes most decisions; work allocation= assigning tasks; time span= 1 shift. Communication= Hierarchical; charge RN to charge RN, or charge RN to team leaders, or team leaders to team members. Tasks & care plan documented. Outcomes= Fragmented care. Quality= Omissions & errors can occur. -Primary Nursing: Total pt care focus; Nurse at bedside makes decisions; work allocation= assigning pts; time span= 24hrs/7 days/wk. Communication= Lateral; CG to CG. Individualized plan documented. Outcomes= Continuity of care. Quality= Process oriented. -Total pt care: Total pt care focused. RN at bedside, charge RN makes some decisions; work allocation= assigning pts; time span= 1 shift. Communication= Hierarchical; charge RN gives & receives report. Unknown documentation. Outcomes= May lack continuity of care between CGs. Quality= High; all care delivered by RN.

Perfusion Concept Exemplar; ACS (MI)

ACS: MI most serious ACS; often called acute MI or AMI. Un-Dx or un-tx angina can cause MI. Occurs when myocardial tissue is abruptly & severely deprived of O2; BF quickly reduced by 80-90%→[3 stgs. of BF occlusion] ischemia→ injury→ necrosis of myocardial tissue if BF not restored. -Often MIs begin w/ infarction of subendocardial layer of cardiac muscle; has greatest O2 demand & poorest O2 supply. -Around initial area of infarction (zone of necrosis) in subendocardium are 2 other zones: (1) zone of injury= tissue injured but not necrotic; (2) zone of ischemia= tissue is O2 deprived. -2 types of MI: non-ST-segment elevation MI (NSTEMI) & ST-elevation MI (STEMI). -NSTEMI: typically ST segment & T-wave changes on 12-lead ECG; ST depression & T-wave inversion= myocardial ischemia. Initially troponin normal (-)→ elevates over 3-12hrs. ECG changes + cardiac troponin elevation= myocardial cell death or necrosis. --Causes: coronary vasospasm, spontaneous dissection, & sluggish BF bc narrowing coronary artery. Decreased BF, vessel tear. --ECG changes w/ troponin elevation should always be assessed w/ s/s & Hx. --Elevated troponin & ECG changes w/o typical s/s of ACS (chest discomfort, SOB, nausea)→ typically condition other than CAD (ex. sepsis), causing imbalance in myocardial O2 supply & demand. -STEMI: typically have ST elevation in 2 contiguous leads on 12-lead ECG= MI/necrosis. Attributable to rupture of fibrous atherosclerotic plaque→ plt aggregation & thrombus at site of rupture. --Thrombus causes abrupt 100% occlusion to coronary artery; medical emergency & requires immediate revascularization of blocked coronary artery. AHA door-to-balloon <90min. --Restoring BF can save heart muscle, if not necrotic. -Health Promotion & Maintenance: 90% of sudden cardiac arrest victims→ die before reaching hospital; many deaths attributed to v fib. Help combat problem→ AEDs in many public places.

Assessing TBI

Assessing TBI; Physical S/S: No 2 brain injuries are alike; TBI may have variety of s/s depending on severity of injury & resulting increase in ICP. -For any TBI, assess for s/s increased ICP, hypotension, hypoxemia, hypercarbia (PaCO2 >40-45) or hypocarbia (PaCO2 <40-45). -Hypercarbia can cause cerebral vasodilation & contribute to elevated ICP. Hypocarbia caused by hyperventilation & can lead to profound vasoconstriction w/ resulting ischemia. -CO2 levels in intubated pt can be ID w/ ETCO2 monitor [capnography]. Early ID of changes in neuro status enables HC team to prevent or tx life-threatening complications. -Subtle changes in BP, LOC, & pupillary rx to light can be very informative about neuro deterioration! -Mild TBI= possible LOC loss; Moderate= LOC loss 30min-6hrs, GCS 9-12; Severe= LOC loss >6hrs, GCS 3-8. -Airway & Breathing: 1st priority is ABC assessment! TBI occasionally associated w/ cervical SC injuries, so all head traumas are tx as if have cord injury until radiography proves otherwise. Elderly esp. prone to cervical injuries at 1st or 2nd vertebral level= life-threatening problem. Assess for indicators of SC injury, like loss of mobility & sensory perception, tenderness along spine, & abnormal head tilt. --Critical Rescue: upper cervical SNs innervate diaphragm to control breathing. Monitor all TBIs for resp. problems & diaphragmatic breathing, & diminished or absent reflexes in airway (cough, gag). Hypoxia & hypercapnia best ID via PaO2, SpO2, & ETCO2. Assess chest wall movement & breath sounds. Provide resp. support + O2-tx & bed positioning. Report any s/s resp. problems immediately to RRT or PHCP! Injuries to brainstem may cause major life-threatening change in breathing pattern→ Cheyne-Stokes &/or apnea. In unconscious→ artificial airway provides protection from aspiration & route for O2. MV often needed to bc of inadequate resp. effort. -Spine Precautions: w/ blunt trauma to head or neck, typically transported from injury scene to hospital w/ rigid cervical collar & long spine board. Expected outcome is prevent new & secondary spine injury. Spine precautions require placing supine & aligning spinal column in neutral position so there is no rotation, flexion, or extension. Long spine board removed ASAP on ED/ICU arrival; rigid cervical collar maintained until definitive Dx studies to r/o cervical spine injury completed. (1) bedrest; (2) no neck flexion w/ pillow or roll; (3) no thoracic or lumbar flexion; (4) manual control of cervical spine anytime rigid collar removed; (5) "log-roll" to reposition. -VS: autoregulation often impaired; more serious injury= more severe impact on autoregulation or ability of cerebral vasculature to modify systemic pressure such that BF to brain is sufficient. Monitor BP & HR frequently per protocol & status. May have hypotension or HTN. Cushing triad: classic but very late s/s of increased ICP; severe HTN, widened pulse pressure (increasing difference between SBP & DBP), & bradycardia; these CV changes usually indicates imminent death. -Neuro: Many hospitals use GCS to document neuro status; change of 2 points is important; notify PHCP if change is 2+ deterioration of GCS. Most important variable to assess w/ any brain injury is LOC! --Decrease or change in LOC typically 1st s/s of neuro status deterioration. Decrease in arousal, increased sleepiness, & increased restlessness or combativeness all s/s of declining neuro status. Early indicators of change in LOC= behavior changes (restlessness, irritability) & disorientation; often subtle. Report any of these s/s immediately to PHCP or RRT! --Critical Rescue: Check pupils of TBI for size & rx to light, esp. if unable to follow directions, to assess changes in LOC. Document any changes in pupil size, shape, & rx & notify RRT or PHCP immediately bc could indicate an increase in ICP! --Monitor for additional late s/s of increased ICP: severe headache, n/v (often projectile), & seizures. PHCP may evaluate for papilledema (via ophthalmoscope); edema & hyperemia (increased BF) of optic disc. It is always a s/s of increased ICP. --Headache & seizures are response to injury & may [not] be associated w/ increased ICP. Always note that brain injury at risk for potentially devastating ICP elevations during 1st hrs after event & up to 3-4 days after injury when cerebral edema can occur.

Assessment of ACS

Assessment of ACS: -Hx: If CAD s/s present at interview→ delay collecting data until txs are started to relieve s/s. If pt has pain→ ask how they've managed discomfort & other s/s & which drugs they may be taking. When pain free→ obtain info about family hx & modifiable risk factors—eating habits, lifestyle, & physical activity levels. Ask about smoking hx & how much alcohol consumed/day. Collaborate w/ RDN to assess current BMI & wt as needed. -Physical; S/S: Assess Pain; Rapid assessment of pt w/ chest pain or other presenting s/s is crucial. Important to differentiate among chest pain types & ID source. Question to ID pain characteristics; may deny pain & report feeling "pressure." Appropriate questions to ask about discomfort→ onset, location, radiation, intensity, duration, precipitating & relieving factors. --If Angina pain is ischemic pain→ usually improves when imbalance between O2 supply & demand resolved. Ex. rest reduces tissue demands, & NTG improves O2 supply. MI discomfort does not usually resolve w/ these measures. Ask about associated s/s—N/V, diaphoresis, dizziness, weakness, palpitations, & SOB. --Assess BP & HR. Interpret cardiac rhythm & dysrhythmias. Sinus tachycardia w/ PVCs frequently occurs in 1st few hrs after MI. --Next assess distal peripheral pulses & skin temp. Skin temp.; should be warm w/ all pulses palpable. In unstable angina or MI, poor CO→ cool, diaphoretic skin & diminished or absent pulses. Heart sounds; Auscultate for S3 gallop, often bc HF (fluid overload→ valves off-sync), serious & common MI complication; adults→ S3 heard w/ bell over apex. --Assess RR & breath sounds for s/s HF; increased RR common bc anxiety & pain; crackles or wheezes may indicate Lt-HF. Assess for JVD & peripheral edema. --MI→ may have temp. elevation for several days after MI; as high as 102°F (38.9°C) may occur in response to myocardial necrosis, indicating inflammatory response. -Psychosocial: Assess coping; common are denial, anger, depression. Denial→ common early rx to CP r/t angina or MI. On average, acute MI pt waits >2hrs before seeking tx; often rationalizes s/s caused by indigestion or overexertion; sometimes denial is normal part of adapting to stressful event. Denial that interferes w/ ID a s/s [CP] can be harmful. Explain importance of reporting any pain to HCP. Fear, anxiety, depression, & anger→ other common rx of pts & families. Assist in ID feelings. Encourage to explain understanding of event & clarify misconceptions.

Assessment of Sepsis & Septic Shock

Assessment of Sepsis & Septic Shock: -Hx: Age is important; sepsis develops more easily in older, debilitated. Ask about medical hx,& recent illness, trauma, invasive tx, or chronic conditions that may lead to sepsis. Check drugs taken this past wk; may directly cause changes→ shock. Drug regimen may indicate a disorder or problem that contributes to sepsis; ex. aspirin, corticosteroids, ABs, & cancer drugs. -Physical; S/S: sepsis & septic shock s/s occur over many hrs, & some change during progression. Some s/s are nonspecific & similar to conditions like pancreatitis or ARF. --CV: CO & BP low in early sepsis & very low in septic shock. Sepsis progresses→ CO, HR, & BP higher= worsening not improvement. --Progression→ DIC from excessive clotting, w/ 1,000s of small clots in tiny capillaries of liver, kidney, brain, spleen, & heart. Huge # of small clots uses clotting factors & fibrinogen faster than produced→ eventual poor clotting→ hemorrhage occurs in septic shock. Coupled w/ continued capillary leak, bleeding→ hypovolemia & dramatic decrease in CO, BP, & PP. Phase s/s are same as later stages of HvLS. --Respiratory: are 1st caused by compensation; trying to maintain oxygenation w/ increased rate. Lungs are susceptible to damage, & complication of ARDS may occur in septic shock. Septic Shock ARDS is caused by continued SIRS→ increasing O2 free radicals→ damage lung cells. ARDS in septic shock has a high mortality rate. --Skin: differ as sepsis progresses. Hyperdynamic stage→ warm skin & no cyanosis. Progression to septic shock & compromised circulation→ cool & clammy w/ pallor, mottling, or cyanosis. DIC→ petechiae & ecchymoses can occur anywhere; blood may ooze from gums, mucosa, & venipuncture sites & around IV catheters. --Renal: low UO vs. fluid intake= shock; no known kidney problems suddenly has low UO→ be suspicious of sepsis or septic shock. Reduced UO caused by low circulating vL & hormonal changes. Kidney function decreases, & serum Cr rises. --MODS: as sepsis & sepsis shock progress; progressive organ dysfunction in 2+ separate organ systems in acutely ill pt; homeostasis cannot be maintained w/o tx. MODS is severe end of illness spectrum of both infectious (sepsis, septic shock) & noninfectious (acute pancreatitis) conditions. -Psychosocial: indicator of sepsis progression often change in affect or behavior. Compare current behavior, verbal responses, & general affect w/ earlier in day or day before. May seem slightly different in rx to greetings, comments, or jokes; may be less patient or act restless or fidgety. May say, "Something is wrong, but I don't know what." Behavior changed from prior→ consider progressing sepsis & shock.

Pit viper (rattlesnakes, cottonmouths, copperheads)

Pit viper (rattlesnakes, cottonmouths, copperheads): Triangular head; 2 retractable curved fangs; Single row of ventral subcaudal scales; Rattlesnakes have vibrating horny rings in tails. --Venom immobilizes & aids in digestion of prey; may be lethal; local & systemic effects; Enzymes break down tissue proteins, alter tissue integrity; cell death. -1st Aid; Pre-hospital care: Move to safety, away from snake; Call for immediate emergency assistance; Encourage rest to decrease venom circulation; Remove jewelry & constrictive clothing; Take pics of snake from safe distance to aid in ID; Immobilize affected extremity in position of function—maintain at heart level (bellow the heart); Keep warm, provide calm environment; Do not incise or suck wound, apply ice, or use tourniquet. -Watch for anaphylaxis w/ bites (any kind) - s/s anxiety, chills, weakness, wheezing, stridor, vomiting, dyspnea, diaphoresis, throat constricting, sneezing or red streaking. Rx is Epi & Benadryl. -Assess for: Puncture wounds; Pain, swelling, redness, &/or bruising around bite(s); Vesicles or hemorrhagic bullae (may form later). Report of minty, rubbery, or metallic taste. Tingling or paresthesias on scalp, face, lips. Muscle twitching, weakness; N/V; Hypotension, seizures; Clotting abnormalities or DIC. -Tx: Obtain complete Hx of event (snake appearance, time of bite, prehospital txs, & past snakebites or antivenin tx); Give supplemental O2; Insert 2 large-bore IV lines; Infuse fluids (NS or LR) as prescribed; Continuous monitoring heart function & BP; Admin opioids to decrease pain; Obtain coag panel, CBC, CK, type & crossmatch, urinalysis; Obtain ECG; Mark, measure, & record circumference of bitten extremity Q15-30min; Contact regional poison control for specific advice on antivenin dosing & further management; Admin crotalidae polyvalent immune fab (if prescribed). --Tetanus; Broad spectrum ABs; Blood chems. Grades of Pit Viper Envenomation: -None: Fang marks, but no local or systemic rx. -Minimal: Fang marks, local swelling & pain, but no systemic rx. -Moderate: Fang marks & swelling progressing beyond bite site; systemic s/s such as N/V, paresthesias, or hypotension. -Severe: Fang marks & marked swelling of extremity; SQ ecchymosis; severe s/s + coagulopathy.

Info gathering & planning phase of Budgeting; then Development of Organizational & Unit Budgets

Info gathering & planning phase of Budgeting: RN manager provided w/ data necessary to budget development. -Environmental assessment is done→ provides org. & RN manager w/ info about changing needs of community, changing professional requirements, economic changes that will affect unit's function, community demographics, stakeholder needs & requirements, regulatory changes, & other items. --Provides context of needs that unit budgets for during next fiscal yr; provides materials for reassessment of orgs. mission, goals, & priorities. As org. priorities set, $ objectives are created, allocating resources to all units. Assessment provides context of needs that unit budgets for during next fiscal yr. -Development of Org. & Unit Budgets: Org. & unit budgets then created to match the $ objectives of org; important that both the $ & overall objectives of unit are in concert w/ org. objectives & goals. --Basic assumptions of org. need to be part of development of org. & unit objectives; assumptions may be negotiated union contract raise for all, cost of new EHR/EMAR, or similar items; important part of development of unit budget.

Mitral Regurgitation (Insufficiency)

Mitral Regurgitation (Insufficiency): fibrotic & calcific changes prevent MV closing completely during systole→ allows backflow into LA when LV contracts. During diastole, regurgitant output again flows from LA to LV along w/ normal BF. Increased vL must be ejected during next systole. To compensate for increased vL & pressure, the LA & LV dilate & hypertrophy. -Causes of primary mitral regurgitation= mitral valve prolapse, rheumatic heart dz, infective endocarditis, MI, connective tissue dzs [Marfan synd., & dilated cardiomyopathy]. -Secondary causes: ischemic & nonischemic heart dz that damage the valve. Rheumatic heart dz is #1 cause in developing nations. When results from rheumatic heart dz, usually coexists w/ degree of mitral stenosis. -Usually progresses slowly; may be s/s free for decades. S/S begin when LV fails from chronic BvL overload. -S/S: fatigue & chronic weakness from reduced CO. DOE & orthopnea develop later. Significant #pts report anxiety, atypical CP, & palpitations. May have normal BP, AF, or changes in respirations characteristic of LV failure. -Rt-HF develops→ neck veins distended, hepatomegaly, & pitting edema. High-pitched systolic murmur at apex, w/ radiation to Lt axilla. Severe regurgitation often has 3rd heart sound (S3).

Pacemaker systems; temporary

Pacemaker systems: electrical pulses [stimuli], emitted from - terminal of generator→ lead wire→ stimulate cardiac cells to depolarize. Current seeks ground by returning through other lead wire→ + generator terminal [completing a circuit]. Current intensity set by selecting output in milliamperes. -2 major modes: synchronous (demand) & asynchronous (fixed-rate). -Temporary pacing: usually synchronous (demand); PM sensitivity set to sense pts own beats. HR above set rate→ PM does not fire (inhibits itself). HR less than setting→ PM provides impulses (paces). --Pacing stimulus→ heart→ spike (or PM artifact) on monitor or ECG strip. Spike should be followed by evidence of depolarization (ex. P wave= atrial depolarization; or QRS complex= ventricular depolarization). Pattern referred to as capture= PM successfully depolarized [captured], the chamber.

Permanent Pacemaker & RN Care

Permanent Pacemaker: insertion txs conduction ds that are not temporary, ex. complete heart block. Usually have lithium battery; average life span 10yrs. Generator must be replaced at end of life span, w/ local anesthesia; some can be recharged externally. Combination PM/defibrillators are available. -Biventricular: coordinates contractions of RV & LV. Pacing in Rt-heart, & additional lead placed in LVs Lt-lateral wall through the coronary sinus. Allows synchronized depolarization of ventricles; used w/ moderate-to-severe HF to improve functional ability. -Electrophysiologist implants generator in surgical SQ pocket at shoulder in Rt or Lt subclavicular area; may create visible bulge. Leads introduced transvenously via cephalic or subclavian vein→ endocardium on Rt-heart. -RN Care: After tx, monitor ECG to check PM working correctly. Assess site for bleeding, swelling, redness, tenderness, infection. Dressing over site remains clean & dry. Pt is afebrile w/ stable VS. --HCP prescribes initial activity restrictions; then gradually increased. --Permanent PM complications: similar to temporary invasive pacing; pericardial effusion, pericardial tamponade, & diaphragmatic pacing. Diaphragmatic pacing→ pain diaphragm level; observe for muscle contractions over diaphragm that's synchronous w/ HR. --PM checks: ambulatory basis at regular intervals. Reprogramming may be needed w/ PM problems. Generator is interrogated w/ electronic device→ ID settings & battery life. Most manufacturers offer wireless home transmitters; Data sent via landline to database→ device clinic or PHCP. Stress need to keep follow-up appts. for detailed PM checks & reprogramming [PRN] & assessment. --Give written & verbal info about type & settings. Teach to report any HR lower than settings. Review care of insertion site & importance of reporting any fever or site redness, swelling, or drainage. If incision near shoulder→ advise to avoid lifting arm over head or lifting >10lb for 4wks→ dislodge wire. Encourage usual arm movement→ prevent shoulder stiffness. --Action Alert: Teach pts w/ permanent PM to: Avoid strong electromagnetic fields; ex. magnets & telecom transmitters→ interference & change settings→ malfunction. MRI usually contraindicated, depending on PM technology. Carry a PM ID card provided by manufacturer & wear medical alert bracelet at all times. --No special precautions for microwaves, communication devices, media players.

Primary nursing

Primary nursing: 1-to-1 approach to care. Each pt assigned a specific RN, who assumes 24hr responsibility for delivery, implementation, evaluation, & coordination of care. Primary RN works w/ RNs (associate RNs) on other shifts to coordinate all care for pt & family; primary RN responsible for development & evaluation of plan of care for pt. Decision making is decentralized & occurs bedside. It's a flexible model & can include variety of skill mixes. It does not mean only RNs care for pts. Primary RN plans, coordinates, & evaluates plan of care, but care can be delegated to appropriate staff depending on pt acuity. -Advantages: Improved care quality & continuity. Simplified communication. Increased RN satisfaction in RNs prepared for role. Pts perceive care to be more personalized. -Disadvantages: Increased #hrs of care/day requires a greater #RNs. Overall pt satisfaction results inconclusive. Can be difficult to implement if pt has multiple unit transfers.

Primary survey

Primary survey: Initial assessment of trauma pt; organized framework, rapidly ID & manages immediate threats to life. -Resuscitation efforts occur simultaneously w/ each primary element. May encounter multiple problems or injuries, but issues ID in primary are managed before providing txs of lower priority [splinting fractures, dressing wounds]. -1 exception to std. ABCDE trauma resuscitation approach; learned from military & research, if massive, uncontrolled external bleeding→ hemorrhage control txs are highest-priority. Priorities shifts to CAB (circulation, airway, breathing), & initial focus of resuscitation is to effectively stop the active bleeding. -A: Airway/cervical spine: Estab. patent airway by positioning, suctioning, & admin O2 PRN. Protect cervical spine by maintaining alignment; use jaw-thrust maneuver if risk for spinal injury. If GCS score is 8 or lower or at risk for airway compromise, prep for ET intubation & MV. --Critical Rescue: must clear airway of any secretions or debris w/ suction catheter or manually if necessary. Respond by protecting cervical spine by manually aligning neck in neutral, in-line position & using jaw-thrust maneuver when estab. airway. Provide supplemental O2 as ordered if require resuscitation. -B: Breathing: Assess breath sounds & respiratory effort. Observe for chest wall trauma or other physical abnormality. Prep for chest decompression if needed. Prep to assist ventilations if needed. --Assessment ID if ventilatory efforts are effective or not—not only if pt is breathing. -C: Circulation: Monitor VS, esp. BP & pulse. Maintain vascular access w/ large-bore cath. Use direct pressure for external bleeding; anticipate need for tourniquet for severe, uncontrollable extremity hemorrhage, wound packing, &/or hemostatic dressing. IO access excellent initial tx for critically ill if veins cannot be rapidly accessed by resuscitation team. --LR & 0.9%NS are crystalloids of choice for resuscitation; hypertonic saline may be prescribed, esp. w/ head trauma. Fluids & blood products should be warmed before admin, to prevent hypothermia. Anticipate need for rapid blood component admin in hemorrhagic shock using PRBCs, FFP, & plts to replace blood loss & prevent coagulopathy. But priority tx is always to stop bleeding. --In resuscitation pt→ SBP quickly & easily est. before manual BP obtained by palpating for presence or absence of peripheral & central pulses: Presence of radial pulse= BP at least 80 systolic. Presence of femoral pulse= BP at least 70 systolic. Presence of carotid pulse= BP at least 60 systolic. -D: Disability: Evaluate LOC using GCS. Re-evaluate LOC frequently. -E: Exposure: Remove all clothing for complete physical assessment. If evidence preservation needed, handle items per policy; ex. clothing, impaled objects, weapons, drugs, bullets. Prevent hypothermia (blankets, heating devices, warm solutions).

Pulse Oximetry

Pulse Oximetry: shows Hgb saturation w/ O2; normally Hgb is almost 100%sat w/ O2 in superficial tissues. Uses a wave of infrared light & a sensor placed on the finger, toe, nose, earlobe, or forehead. -Normal: 95% to 100%; little lower in older patients & in those with dark skin. Recorded as SpO2 (peripheral arterial O2sat) or SaO2. Can detect desaturation before s/s occur (ex. dusky skin, pale mucosa, pale or blue nail beds). -Causes for low readings: patient movement, hypothermia, decreased peripheral blood flow, ambient light (sunlight, infrared lamps), decreased Hgb, edema, & fingernail polish. --Impaired peripheral BF- test O2sat on the forehead. -Spo2 <91%: in an adult w/o a chronic respiratory problem (esp. <86%) are an emergency & require immediate assessment & tx. -Spo2 <85%: body tissues have a difficulty becoming oxygenated. -Spo2 <70%: is usually life threatening; some cases <80% may be life threatening. Pulse oximetry is less accurate at lower values.

S/S for any type of pneumothorax commonly include; Dx

S/S for any type of pneumothorax commonly include: Reduced (or absent) breath sounds of affected side; Hyperresonance on percussion; Prominence of involved side of the chest, moves poorly w/ respirations. -When severe, deviation of trachea away from midline & side of injury toward the unaffected side= pushing of tissues to the unaffected side [mediastinal shift] from increasing pressure w/in the injured side. -Tension pneumothorax, also may include: Extreme respiratory distress & cyanosis; Distended neck veins; Hemodynamic instability. W/ a hemothorax, percussion on involved side→ dull sound. -Dx: in addition to s/s; CXR, CT scans, or US may be used to Dx any type of pneumothorax or hemothorax. For a hemothorax; blood can be seen in the pleural space on a CXR, but definitive Dx comes from a thoracentesis.

S/S of Strokes & Dx

S/S of Strokes & Dx: -Stroke s/s can appear any time of AM/PM; 5 most common s/s: Sudden confusion or trouble speaking or understanding; Sudden numbness or weakness of face, arm, or leg; Sudden trouble seeing in 1 or both eyes; Sudden dizziness, trouble walking, or loss of balance or coordination; Sudden severe headache w/ no known cause. -Specific s/s depend on extent & location of ischemia & arteries involved. -Rt cerebral hemisphere is involved w/ visual & spatial awareness & proprioception (sense of body position); stroke w/ rt involvement→ unaware of any deficits, disoriented to time & place. Personality changes→ impulsivity & poor judgment. -Lt cerebral hemisphere, dominant hemisphere in all but 15-20% of pts; speech, language, math, & analytic thinking; problems in these expected w/ Lt stroke. -Embolic strokes: heart murmur, dysrhythmias (often AF), &/or HTN; not unusual for BP to be >180-200/110-120 at admit, esp. if have HTN bleeding. Higher BP of 150/100 needed to maintain cerebral perfusion after acute ischemic stroke, BP above this may lead to extension of stroke. -Imaging: Definitive evaluation of suspected stroke→ computed tomography perfusion (CTP) scan &/or computed tomography angiography (CTA) used to assess extent of ischemia of brain tissue. Cerebral aneurysms or AVM may be ID. --Magnetic resonance angiography (MRA) & multimodal techniques like perfusion-weighted imaging enhance sensitivity of MRI to ID early changes in brain, + confirming BF. --US (carotid duplex scanning) may be performed.

TBI Secondary Injury

Secondary Brain Injury: any processes that occur after initial injury & worsen or negatively influence outcomes; result from physiologic, vascular, & biochemical events that are an extension of primary injury. -Most common secondary injury from mild TBI [concussion] is postconcussion synd; reports headaches, impaired cognition, & dizziness continue for wks to months after initial brain injury. Other concussion pts may have only posttraumatic headaches or posttraumatic vertigo for wks to months after initial injury. -Some may not have been Dx w/ TBI bc not symptomatic; later may be Dx w/ chronic traumatic encephalopathy (CTE)= uncommon degenerative brain dz occurs mostly in veterans, athletes, & others w/ repetitive trauma to brain. CTE can lead to dementia, depression, suicidal thinking, & SUD. Usually Dx by Hx & s/s; can only be confirmed at autopsy when classic tau neurofibrillary tangles evident. -Moderate or severe TBI→ most common secondary injuries result from hypotension & hypoxia, IC HTN, & cerebral edema. Damage to brain tissue occurs primarily bc delivery of O2 & glucose to brain is interrupted from cerebral edema & increasing pressure.

Sepsis & Septic Shock Tx

Sepsis & Septic Shock Tx: focus on ID problem as ASAP, correcting cause, & preventing complications. Sepsis resuscitation bundle for tx of sepsis w/in 1hr is now Std. Bundle= 2+ specific tx shown to be effective when applied together or in sequence. -SSC care bundle guidelines developed to reduce sepsis deaths; previously incorporated into 3&6hr periods; tx sepsis as medical emergency w/ same degree of urgency as trauma & stroke, SSC combined 3&6hr bundles into 1hr bundle→ now the Std. -Hour-1 Bundle for Management of Sepsis: W/in 1hr.... -Measure lactate level. Remeasure if initial lactate elevated (>2mmol/L). -Obtain blood cultures before admin ABs. -Admin broad-spectrum ABs. -Begin rapid admin of 30 mL/kg crystalloid for hypotension or lactate ≥4 mmol/L. -Apply vasopressors if hypotensive during or after fluid resuscitation to maintain a MAP ≥65 mmHg. -O2-tx: useful when poor tissue perfusion & poor gas exchange are present. Pt w/ septic shock is more likely to be MV-ed. -Drugs: enhance CO & restore vascular vL is essentially the same as HvLS (see Drug tx: HvLS). Drug tx is needed to combat sepsis, adrenal insufficiency, hyperglycemia, & clotting problems. --Multiple ABs w/ broad-spectrum prescribed; based on infection site & most common geo. infections, until actual causative organism known. Goal, using Hour-1 Sepsis Bundle→ start ABs as prescribed w/in 1hr of ID sepsis. --Stress of sepsis can cause adrenal insufficiency. Adrenal support may involve providing low-dose corticosteroids during tx period; drugs used are IV hydrocortisone & PO fludrocortisone. --Sepsis or septic shock usually have elevated BG (>180 mg/dL); associated w/ poor outcome. Insulin tx maintains BG 140-180 mg/dL. Keeping BG <110 associated w/ increased mortality. --Severe sepsis→ microvascular abnormalities w/ many small clots. Heparin tx w/ fractionated heparin limits clotting & prevents excessive consumption of clotting factors. --Blood replacement: when poor clotting w/ hemorrhage occurs; clotting factors, plts, FFP, or PRBCs. Preferred tx→ plt transfusion recommended ahead of other blood products for septic shock to improve clotting.

Septic Shock

Septic Shock: a subset of sepsis; describes the circulatory, cellular, & metabolic abnormalities occurring that substantially increase risk of death vs. sepsis alone. -Septic shock ID in pts who: Require vasopressor tx to maintain MAP >65; or Have serum lactate level >2mmol/L (18 mg/dL), despite adequate fluid resuscitation. -Septic shock is the stage of sepsis when MODS w/ organ failure is evident & poor clotting w/ uncontrolled bleeding can occur. -Severe HvLS & hypodynamic cardiac function are present as result of inability of blood to clot bc plt & clotting factors were consumed earlier in sepsis response. -Vasodilation & capillary leak continue from vascular endothelial cell disruption, & cardiac contractility is poor from cellular ischemia. -S/S: resemble late stage of HvLS. --Sepsis can be complication of many conditions in acute care, so always consider its possibility. Early ID of sepsis before progression to septic shock is a major RN responsibility. ----RN most in contact w/ pt & can detect subtle changes in appearance & behavior that can indicate sepsis. Review qSOFA score; recommended in non-ICU settings to screen for progression of sepsis. Higher the score= greater the risk of morbidity & mortality. --MEWS developed to ID hospitalized pts at risk for clinical deterioration. All components of qSOFA are incorporated into MEWS, in addition to HR & temp. Scores of 5+→ higher risk of death & ICU admit. Scores can be calculated by RN, or many integrated into EHRs for prompt ID & tx of sepsis. Used appropriately→ MEWS can reduce # of codes by 50%. --Early detection can be by pts & family; esp. important for pts D/C home after invasive tx or OP. Teach s/s of local infection (local redness, pain, swelling, purulent drainage, loss of function) & early sepsis (fever, UO < intake, light-headedness). Teach how to use a thermometer & to take temp. 2x/day & when not feeling well. Urge pts w/ s/s of early sepsis to immediately contact HCP. Teach if ABs are prescribed, take as prescribed & complete entire course.

Stages of Shock

Stages of Shock; Syndrome of shock progresses in 4 stages when the causative conditions remain uncorrected & poor cellular oxygenation continues: -Initial Stage: the pts baseline MAP is decreased by <10. Compensatory mechanisms effective at returning SBP to normal; thus O2 perfusion→ vital organs maintained. Cellular changes→ increased anaerobic metabolism in some tissues w/ lactic acid production; overall metabolism is still aerobic. Compensation of vascular constriction & increased HR are effective; CO & MAP maintained w/in norm. Vital organ function is not disrupted→ shock indicators difficult to detect. --Action Alert: Be aware increased HR & RR or slight increased DBP may be only s/s of this stage. -Compensatory Stage: when MAP decreases by 10-15 from baseline. Kidney & hormonal compensation activated bc CV responses alone not enough to maintain MAP & supply O2→ vital organs. --Ongoing decrease in MAP → triggers release of renin, ADH, aldosterone, epi, & NE to start kidney compensation→ UO decreases, Na reabsorption increases, & widespread BV constriction occurs. ADH→ increases H2O reabsorption in kidneys, further reducing UO, & increases BV constriction in skin & less vital tissue. --Actions compensate for shock by maintaining FvL w/in central BVs. --Tissue hypoxia in nonvital organs (skin, GI tract) & in kidneys, not enough to cause permanent damage. Buildup of metabolites from anaerobic metabolism→ acidosis & increased K+ levels. --S/S: changes result of decreased tissue perfusion. Pt reports thirst & anxiety. Observe restlessness, tachycardia, increased RR, decreased UO, falling SBP, rising DBP, narrowing pulse pressure, cool extremities, & decreased SpO2. --Comparing these changes w/ values & earlier observations is critical to ID this stage. --Changes in MS & behavior occur early in shock. --If pt is stable & compensation is supported by tx→ can remain in this stage for hrs w/o permanent damage occuring. --Stopping conditions that started shock & providing supportive tx can prevent progression. --Effects of stage are reversible when RNs ID problem & coordinate HC team to start appropriate tx. -Progressive Stage: sustained decrease in MAP of >20 from baseline. Compensation functioning but can't deliver sufficient O2, even to vital organs. Vital organs→ hypoxia develops; less vital organs→ anoxic (no O2) & ischemic (cell dysfunction or death bc lack O2). Poor perfusion & buildup of metabolites→ some tissues die. --Indications: worsening changes resulting from decreased tissue perfusion. Pt may express impending doom; may be confused, thirst increases. Assess→ rapid, weak pulse; low BP; pallor→ cyanosis of oral mucosa & nail beds; cool & moist skin; anuria; 5-20% decrease in SpO2. Labs may show low pH, w/ rising lactic acid & K+. Lactic acid/ lactate (arterial) 3-7mg/dL; 0.3-0.8mmol/L; Increased: anaerobic metabolism w/ metabolite buildup. --Action Alert: progressive stg.→ life-threatening emergency. Vital organs tolerate situation only a short time before MODS w/ permanent damage. Immediate tx needed to reverse effects. Life usually can be saved if cause is corrected w/in <1hr of stage onset. Continuously monitor & compare w/ earlier findings to assess tx effectiveness & ID when tx changes are needed. -Refractory Stage & MODS: when too much cell death & tissue damage result from too little O2 reaching tissues. Vital organs have extensive damage & cannot respond effectively to tx, & shock continues. So much damage has occurred bc metabolites & enzymes→ damage to vital organs continues despite txs. --MODS: sequence of cell damage caused by massive release of toxic metabolites & enzymes. Once damage started→ vicious cycle as more dead cells open & release metabolites→ small clots (microthrombi) form→ block tissue perfusion & damage more cells, continuing devastating cycle. Liver, heart, brain, & kidney functions are lost 1st. Most profound change is damage to heart muscle. --S/S: rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow resp.; & unmeasurable SpO2. --Tx, [& fluid replacement], is not effective in saving life, even if cause is corrected & MAP temporarily returns to normal.

Stroke

Stroke: caused by interruption of perfusion to any part of brain→ infarction (cell death). National Stroke Association uses "brain attack" to convey urgency for acute stroke care similar to MI. Medical emergency & should be tx immediately to reduce or prevent permanent disability. -Brain cannot store O2 or glucose; must receive constant BF to provide these for normal function. BF is important for removal of metabolic waste (CO2, lactic acid). If perfusion to any part of brain interrupted for >few min→ infarction. -Brain metabolism & BF after stroke can be affected around infarction & in contralateral (opposite) hemisphere. Stroke effects on nonaffected side may be result of brain edema or global changes in brain perfusion. -Brain edema→ possible increased ICP & secondary brain damage. Secondary changes commonly occur from severe TBI.

Surgical tx for AF

Surgical tx for AF: in AF + HF→ may benefit from surgical maze; an open-chest technique often w/ coronary artery bypass grafting (CABG). Before OP, EP mapping studies done to confirm AF Dx. --Surgeon places maze of sutures in strategic places in A myocardium, PA, & possibly SVC to prevent electrical circuits from developing & continuing AF. --Sinus impulses can then depolarize atria before reaching AV node & preserve atrial kick. Post-op care similar to open-heart OP. --Surgical MAZE: being replaced by cath tx w/ MIS form. Catheter maze= insert cath through leg vein→ atria & dragging a heated ablating cath along the atria to create lines (scars) of conduction block. Pts w/ MIS form have fewer complications, less pain, & quicker recovery vs. open, surgical maze.

Types of TBIs; Primary Injuries

TBI: damage to brain from external mechanical force; not caused by neurodegenerative or congenital conditions. Can lead to temporary & permanent impairment in cognition, mobility, sensory perception, &/or psychosocial function. -Direct injury: force from a blow to head. Indirect injury: force applied to another body part w/ rebound effect to brain. Brain responds to forces by movement w/in rigid cranial vault; may also rebound or rotate on brainstem→ diffuse nerve axonal injury (shearing injuries). Brain may be contused (bruised) or lacerated (torn) as it moves over inner surfaces of cranium= irregularly shaped & sharp. -Movement or distortion w/in cranial cavity bc of multiple factors. 1st= how brain is supported by CSF w/in cranial cavity; External force applied to head→ brain injured by internal surfaces of skull. 2nd= consistency of brain tissue→ very fragile, gel-like, & prone to injury; Brain injury occurs from initial forces on cranium/brain & from secondary injury r/t mechanical pressure or cerebral edema. Type of force & MOI contribute to TBI. -Acceleration injury: caused by external force contacting head, suddenly head is in motion. -Deceleration injury: when moving head is suddenly stopped or hits stationary object -Forces can cause cerebrum to rotate about brainstem→ shearing, straining, & distortion of brain tissue, esp. axons in brainstem & cerebellum. Small areas of hemorrhage (contusion, IC hemorrhage) may develop around BVs that sustain force impact (stress), w/ destruction of adjacent brain tissue. Esp. affected are basal nuclei & hypothalamus; located deep in brain. -Primary Brain Injury: occurs at time of injury & results from physical stress (force) w/in tissue caused by blunt or penetrating force. Categorized as focal or diffuse. --Focal brain injury: confined to specific area of brain & causes localized damage; often can be ID w/ CT scan or MRI. --Diffuse injuries: damage in many areas of brain. Begin at microscopic level; not initially ID by CT scan. MRI has greater ability to ID microscopic damage, but areas may not be imaged until necrosis occurs. --Open TBI: skull is fractured or pierced by penetrating object; brain & dura integrity is violated, & exposed to contaminants. Damage may occur to underlying BVs, dural sinuses, brain, & CNs. --Closed TBI: skull integrity is intact, but damage to brain tissue still occurs bc of increased ICP. -TBI further defined as mild, moderate, or severe. Generally, ID of TBI severity result of GCS score immediately following resuscitation, presence (or absence) of brain damage imaged by CT or MRI following trauma, an est. of force of trauma, & s/s in pt. -Concussion: type of mild TBI; brain injury caused by blow to head; could result in period of unconsciousness. Military & sports pts esp. at risk for concussions. Some report no immediate s/s until later; typically impaired cognition (memory or thinking) & headache. -Veterans Health: in US increasing # of survivors of brain injury from blast injuries→ TBI major health problem among veterans & active duty. Chronic traumatic encephalopathy also more recognized as TBI from repetitive brain injuries among active duty & veterans.

TIA vs Stroke

TIA: Acute ischemic strokes often follow warning s/s like TIA= temporary neuro dysfunction resulting from brief interruption in cerebral BF. S/S of TIA easy to ignore or miss, esp. if s/s resolve at arrival to ED. Typically, s/s resolve w/in 30-60min; may last up to 24hrs. -Key Features of TIAs: -Visual: Blurred vision; Diplopia (double vision); Hemianopsia (vision in 1 or both eyes affected); Tunnel vision. -Mobility (Motor): Weakness (facial droop, arm or leg drift, hand grasp); Ataxia (lack muscle control & coordination; affects gait, balance, & ability to walk). -Sensory Perception: Numbness (face, hand, arm, or leg);Vertigo (spinning or dizziness). -Speech: Aphasia (problems w/ speech &/or language); Dysarthria (slurred speech bc of muscle weakness or paralysis). -On ED admit, have a complete neuro assessment. IP team admin NIHSS & agency assessment tools. Routine labs, + coags (PT, INR, aPTT) & lipids, ECG, & imaging. Initial scan typically head CT, then MRI brain scan w/o contrast. Depending on agency protocol & pts assessment, computed tomography angiography (CTA) or magnetic resonance angiography (MRA) of brain & neck also performed to ID patency of carotid arteries bc provide perfusion to brain, & arterial circulation w/in brain. -Common TIA or stroke causes: carotid stenosis= hardening & narrowing of artery→ decreases BF to the brain; often w/ atherosclerotic plaque buildup, & AF. Atherosclerotic plaque= fat & substances adhere to arterial wall & obstruct or restrict BF. -In addition to NIH score, often evaluated w/ ABCD assessment tool to ID risk of stroke in days-wks after TIA. Factors scored: Age >/= 60 (risk increases w/ age); BP >/= 140/90 (SBP or DBP or both); Clinical TIA features (unilateral weakness increases risk); Duration of s/s (longer TIA s/s last= greater risk). -Tx of TIA includes tx cause, if ID. Depending on pt, collab txs may include: --Traditional or MIS to remove atherosclerotic plaque buildup w/in CA & increase perfusion to brain. Carotid angioplasty w/ stenting to increase perfusion to brain. --Anti-plt drugs, typically aspirin or clopidogrel, to prevent thrombotic or embolic strokes (may be on both drugs). Reducing high BP (most common risk factor for stroke) by adding or adjusting drugs to lower BP. --Controlling DM & keeping glucose w/in target range, typically 100-180 mg/dL. Promoting lifestyle changes; smoking cessation, more heart-healthy foods, & increasing mobility & physical activity.

Tx of ACS: Increasing Myocardial Tissue Perfusion w/ Reperfusion tx via PCI

Tx of ACS: Increasing Myocardial Tissue Perfusion w/ Reperfusion tx via PCI: AKA PTCA; invasive but nonsurgical; tx of choice to reopen clotted CA & restore perfusion. -Goal: PCI w/in 90min of acute STEMI Dx. Associated w/ excellent return of BF through CA; if timely, decreases extent of myocardial damage. Can reduce frequency & severity of discomfort w/ angina & serve as bridge to CABG surgery. --Performed in cardiac cath lab; combines clot retrieval, coronary angioplasty, & stent placement. W/ fluoroscopic guidance, cardiologist performs initial coronary angiography, inserting arterial sheath & advancing catheter [retrograde] through aorta. --STEMI pt if clot seen→ clot retrieval device is inserted over guidewire, & clot removed. Once clot removed in STEMI pt or area of narrowing is ID in NSTEMI pt→ balloon-tipped catheter through guidewire to coronary artery occlusion. HCP activates compressor→ inflates balloon (angioplasty) to force plaque against BV wall→ dilating wall, & reduces or eliminates clot. --Balloon inflation repeated until angiography indicates decreased stenosis (narrowing) to <50% of BVs diameter. Balloon cath then withdrawn, & balloon cath w/ stent introduced. Once stent & balloon in position→ stent deployed by balloon inflation. --Balloon deflated & stent stays in place→ acts as scaffolding to hold Dz artery open. Stents= expandable metal mesh devices; maintain patent lumen created by angioplasty or atherectomy. Bare metal or drug-eluting stents (DESs) (drug coated) may be used. By providing scaffold, they prevent closure of BV from arterial dissection or vasospasm. --During PCI, may receive boluses of IV heparin or continuous infusion of bivalirudin (direct thrombin inhibitor). Heparin maintains elevated activated clotting time & prevent clotting on wires & caths during PCI. Heparin or anticoags usually stopped immediately after PCI, allowing access sheath removal once clotting time is normal. PCI initially reopens BV in most; but w/in 1st 24hrs, a sm % re-stenose. At 6mo, larger # have 1+ blockages. W/o stent placement→ artery often reoccludes bc normal elasticity & memory. --Pts most likely to benefit from PCI have 1 or 2-vessel dz w/ discrete, proximal, noncalcified lesions or clots. PCI often does not work for complex lesions. ID which lesions treatable→ cardiologist considers clot's complexity & location & amount of myocardium at risk. Tx-ing lesions in Lt main artery places lg. amount of myocardial tissue at risk if BV closes quickly; but these lesions now tx more w/ PCI; in past, CABG used for these pts. PCI used for evolving acute MI; alone or w/ thrombolytics or glycoprotein (GP) IIb/IIIa inhibitor, to reperfuse damaged myocardium. --PCI pts required to take dual antiplatelet therapy (DAPT)→ aspirin & plt inhibitor. HCP also prescribes LT nitrate & BB, & ACEI or ARB is added if pt had primary angioplasty after MI. Some have hypokalemia after PCI & require careful monitoring & K+ supplements. --RN care: for individual med SEs; & provide explanations of drug tx & lifestyle changes. --Critical Rescue: After PCI, monitor for potential problems→ acute closure of vessel (→ CP & ST elevation on 12-lead); bleeding from insertion (sheath) site; rx to contrast used in angiography. Also monitor for & document hypotension, hypokalemia, & dysrhythmias. Document & report any of these findings to HCP or RRT immediately!

Types of Strokes

Types of Strokes: generally classified as ischemic (occlusive) or hemorrhagic. Acute ischemic strokes= thrombotic or embolic in origin. Most strokes are ischemic. -Acute Ischemic Stroke (AIS): caused by occlusion of cerebral or carotid artery by thrombus or embolus. --Thrombotic stroke caused by thrombus (clot). Intermittent or stepwise improvement between episodes of worsening s/s. Completed stroke. Onset Gradual; mins→ hrs. LOC Preserved; pt is awake. Factors HTN; Atherosclerosis. Prodromal s/s TIA. Neuro May be deficits during 1st few wks; Slight headache; Speech deficits; Visual problems; Confusion. CSF Normal; possible presence of protein. Seizures no. Duration Improvements over wks→ months. Permanent deficits possible. --Embolic stroke caused by embolus (dislodged clot). Abrupt development of completed stroke. Steady progression. Onset sudden. LOC Preserved; pt is awake. Factors Cardiac dz. Prodromal s/s TIA. Neuro Max deficit at onset; Paralysis; Expressive aphasia. CSF Normal. Seizures no. Duration Usually rapid improvements. -Hemorrhagic Strokes: BV integrity interrupted, & bleeding occurs into brain tissue or into subarachnoid space. Usually abrupt onset; may be gradual if caused by HTN. LOC Deepening lethargy/stupor or coma. Factors HTN; BV ds; Genetic. Prodromal s/s Headache. Neuro Focal deficits; Severe, frequent. CSF Bloody. Seizures usually. DurationVariable; Permanent neuro deficits possible.

Ventricular Asystole [Cardiac Arrest]

Ventricular Asystole [Cardiac Arrest]: ventricular standstill; complete absence of any V rhythm. No impulses in V's→ no V depolarization, no QRS, no contraction, no CO, & no perfusion to body. -S/S: no pulse, respirations, or BP. In full cardiac arrest. In some, SA node may still fire & depolarize A, w/ only P waves on ECG; but SA impulses do not conduct to V's, & QRS's remain absent. In most, entire conduction system is electrically silent, w/ no P waves --Usually results from myocardial hypoxia; may be consequence of Adv. HF. May be caused by severe hyperkalemia & acidosis. If P waves seen→ asystole likely bc severe V conduction blocks. -Tx: cardiac arrest→ CO stops. Underlying rhythm usually VT, VF, or asystole. W/o CO→ pulseless & unconscious bc inadequate cerebral perfusion & gas exchange. Shortly after cardiac arrest→ respiratory arrest. CPR essential to prevent brain damage & death. -CPR & Defibrillation: CPR= BLS; must be initiated immediately in asystole. Unresponsive pt→ confirm unresponsiveness & call 911 (community or LTC) or emergency response team (hospital). --Gather AED or defibrillator before initiating CPR. Guidelines changed from ABC (airway-breathing-compressions) to initial priorities of CAB (compressions-airway-breathing). --Check for carotid pulse for 5-10s. Carotid pulse absent→ start compressions 100-120/min & 2-2.4in depth. Push hard & fast! Avoid leaning into chest after each compression to allow full recoil. --Maintain patent airway. Ventilate (breathing) w/ mouth-to-mask device→ rescue breaths 10-12/min. Adv. airway in place→ 1 breath given Q6-8s (8-10/min). V-to-C maintained at 30c: 2b if adv. airway not in place. Limit interruptions to compressions to <10s. When possible, compressors change Q2min to maintain effectiveness. --Use Std. Precautions w/ CPR. --Before defibrillation, loudly & clearly command to clear contact w/ pt & bed; check if its clear before shock. Deliver shock & immediately resume CPR for 5 cycles or 2min. --Reassess rhythm Q2min & if indicated. Charge defibrillator to deliver additional shock at same level previously used. --During 2min intervals while CPR delivered, ACLS team admins meds & txs to restore organized rhythm. -Complications of CPR: Rib fractures; Fractured sternum; Costochondral separation; Lacerations of liver & spleen; Pneumothorax; Hemothorax; Cardiac tamponade; Lung contusions; Fat emboli. --In VF or pulseless VT→ immediate priority is defibrillate! Defibrillation [asynchronous countershock], depolarizes critical mass of myocardium simultaneously to stop re-entry circuit→ SA node regains control. --After defibrillation, CPR resumed; must continue at all times except during defibrillation.

Ventricular Dysrhythmias: PVCs

Ventricular Dysrhythmias: potentially more life threatening vs. atrial dysrhythmias bc the LV pumps O2-blood throughout body→ perfuse vital organs & tissues. Most common or life-threatening ventricular dysrhythmias include: PVC; VT; FB; Ventricular asystole. -Premature Ventricular Complexes/Contractions (PVCs): result from increased irritability of ventricular cells, seen as early ventricular complexes followed by pause. --If multiple PVCs present→ QRS complexes may be unifocal [uniform; same shape]; or multifocal [multiform; different shapes]. --PVCs frequently occur in repetitive rhythms; bigeminy (2), trigeminy (3), & quadrigeminy (4). --2 sequential PVCs are a pair [couplet]. 3+ successive PVCs usually called nonsustained VT (NSVT). --PVCs common, & frequency increases w/ age. Insignificant or occur w/ problems like MI, chronic HF, COPD, & anemia. May be present in hypokalemia or hypomagnesemia. --Sympathomimetics, anesthesia drugs, stress, nicotine, caffeine, alcohol, fatigue, infection, or surgery can also cause PVCs, esp. in elderly. Postmenopausal often find caffeine causes palpitations & PVCs. -S/S: asymptomatic or have palpitations or chest discomfort caused by increased SV of normal beat after the pause. Peripheral pulses may be diminished or absent w/ the PVCs bc decreased SV of premature beats may decrease peripheral perfusion. -Action Alert: other dysrhythmias can cause widened QRS; assess if premature complexes perfuse to extremities. Palpate carotid, brachial, or femoral arteries while observing monitor for widened complexes or auscultating apical sounds. W/ acute MI, PVCs may be a warning, possibly triggering life-threatening VT or VF. -If no underlying heart dz present→ PVCs not usually tx, other than eliminating or managing contributing cause (caffeine, stress). K+ or Mg+ given for replacement tx if hypokalemia or hypomagnesemia is the cause. -If # PVCs/24hrs is excessive→ may be placed on BBs.

SCI Complications; Autonomic Dysreflexia

-Cervical SCI is at risk for breathing problems from interruption of spinal innervation to respiratory muscles. Collab w/ RT if available, perform complete respiratory assessment, + pulseOx for SpO2, Q8-12h; SpO2 92% or less & adventitious breath sounds may indicate complication→ atelectasis or pneumonia. --Cervical or high thoracic SCIs have upper motor neuron damage that spares lower spinal reflexes→ spastic bowel & bladder. -Lower thoracic & lumbosacral injuries usually have damage to lower spinal nerves→ flaccid bowel & bladder. -Autonomic dysreflexia (AD): AKA autonomic hyperreflexia; life-threatening condition; noxious visceral or cutaneous stimuli→ sudden, massive, uninhibited reflex sympathetic discharge in pts w/ high-level SCI. Severely elevated BP can cause hemorrhagic stroke. Key Features of AD: --Sudden, significant rise in SBP & DBP, w/ bradycardia. Profuse sweating above level of lesion—esp. in face, neck, shoulders; rarely below level of lesion bc of sympathetic cholinergic activity. --Goose bumps above or possibly below level of lesion. Flushing of skin above level of lesion—esp. in face, neck, shoulders. Blurred vision; Spots in visual field --Nasal congestion; Onset of severe, throbbing headache; Flushing about level of lesion w/ pale skin below level of lesion. Feeling of apprehension. -Causes of AD typically GI, GU, & vascular stimulation. Specific risk factors= bladder distention, UTI, epididymitis or scrotal compression, bowel distention or impaction [constipation], or irritation of hemorrhoids. Pain; circumferential constriction of thorax, ABD, or extremity (tight clothing); contact w/ hard or sharp objects; & temp. fluctuations can cause AD. Pts w/ altered sensory perception at great risk.

Initial & Priority Assessment of SCI; Spinal Shock; Level of Injury & Neuro Level

-Initial & Priority Assessment of SCI: focuses on ABCs. After airway estab., assess breathing pattern; cervical SCI at high risk for respiratory compromise bc cervical SNs (C3-5) innervate phrenic nerve controlling diaphragm. -Spinal shock: AKA spinal shock synd.; occurs immediately as SC response to injury. Complete but temporary loss of motor, sensory, reflex, & autonomic function; often lasts <48hrs, may continue for several wks. Spinal shock is not same as neurogenic shock. -Level of injury is lowest neuro segment w/ intact or normal motor & sensory function. -Tetraplegia (quadriplegia; paralysis) & quadriparesis (weakness) involve 4 extremities, seen w/ cervical cord & upper thoracic injury. -Paraplegia (paralysis) & paraparesis (weakness) involve only lower extremities, seen in lower thoracic & lumbosacral injuries or lesions. -Neuro level defined by ASIA refers to highest neuro level of normal function & is not same as anatomic level of injury. Neuro level is ID by evaluation of zones of sensory & motor function= dermatomes & myotomes. -May report complete sensory loss, hypoesthesia (decreased sensory perception), or hyperesthesia (increased sensory perception).

Partnership, Equity, Accountability, & Ownership

-Partnership: links HCPs & pts along all points in system; collab. relationship w/ all stakeholders & RNs required for empowerment. Partnership is essential to building relationships, involves all staff in decisions & processes, implies that each member has key role in fulfilling mission & purpose of org., & is critical to HC system's effectiveness. -Equity: best method for integrating staff roles & relationships into structures and processes to achieve + pt outcomes. Maintains focus on services, pts, & staff; foundation & measure of value; & says no 1 role is more important than another. Does not equal equality in terms of scope of practice, knowledge, authority, or responsibility, it does mean that each member is essential to providing safe & effective care. -Accountability: willingness to invest in decision-making & express ownership in decisions. Core of shared governance; often used interchangeably w/ responsibility, & allows for evaluation of role performance. Supports partnerships & is secured as staff produce + outcomes. -Ownership: recognition & acceptance of importance of everyone's work & that success is bound to how well individual staff perform their jobs. --Enable all members to participate, ownership designates where work is done, & by whom; requires staff to commit to contributing something, to own what they contribute, & to participate in devising purposes for work. --90%+ of decisions need to be made at POS; in matters of practice, quality, & competence, the locus of control in environment must shift to practitioners. --Only 10% of unit-level decisions should belong to management. Recent comparative analysis by who interviewed 279 RNs at 14 Magnet hospitals, found the highest staff RN ownership of issues & outcomes occurred where visible, viable, and recognized structures devoted to RN control over practice.

Assessment of ARDS

Assessment of ARDS: -Physical S/S: Assess the breathing of all those at increased ARDS risk; ID if increased work of breathing is present, as indicated by Hyperpnea, noisy respiration, cyanosis, pallor, retraction intercostally or substernally; VS. --Document sweating, respiratory effort, & any change in MS. --Abnormal lung sounds are not heard on auscultation because the edema occurs first in the interstitial spaces & not in the airways. Assess VS at least Q1hr for hypotension, tachycardia, & dysrhythmias. -Dx Assessment: -Lowered PaO2: ARDS Dx is established by a lowered PaO2 value (decreased gas exchange & oxygenation), done w/ ABGs. Bc a widening alveolar O2 gradient develops w/ increased shunting of blood, the pt has a progressive need for higher levels of O2. -Widening alveolar oxygen gradient= increased FiO2 does not lead to increased PaO2 levels. -P/F (<200 mmHg): another ARDS characteristic is a P/F ratio (PaO2/FiO2) of <200mmHg; develop refractory hypoxemia & often needs intubation & MV. -Sputum cultures: via bronchoscopy & transtracheal aspiration are used to ID if lung infection also is present. -CXR: may show diffuse haziness or a "whited-out" (ground-glass) appearance of the lung. -ECG: r/o cardiac problems & usually shows no specific changes.