nurs 285 exam 4
Acute Decompensated Heart Failure
"Cold and Wet" Myocardial ischemia/infarction Inflammatory Heart Disease Valvular heart disease Severe systemic HTN Cardiac dysrhythmias Acute decompensation of chronic HF: most common cause is exacerbation of HF: prevent with fluids, meds, diet, wt monitoring, smoking cessation Ex: Pulmonary Edema, Cardiogenic Shock
CK or CPK to CPK-MB
(0% of CPK is normal) cardiac specific short interval back to normal in 3 days Isoenzymes: MB (heart), MM (skeletal muscles), BB (brain) CK-MB - very sensitive to myocardial injury
What is the MAP if... Your patient's blood pressure is 120/80? Your patient's blood pressure is 100/65?
(2 X 80) +120 / 3 = 93 (2 X 65) +100 / 3 = 76 big drop > 5-10mm = stimulate compensatory mechanisms
Troponin
(<0.03ng/ml) EBP focus on b/c most reliable stay elevated much longer = we can see for some time more speciic to heart muscle damage Rises quickly +stays elevated longer Very sensitive to myocardial injury (unstable angina, MI, blunt trauma, acute allograft rejection) Now considered the "gold standard"
Myoglobin
(<90 mcg/L) any muscle damage not specific to cardiac muscles
diastolic heart failure
(filling problem) -- the inability of the left ventricle to relax normally, resulting in fluid backing up into the lungs
systolic heart failure
(pumping problem) -- the inability of the heart to contract enough to provide blood flow forward
Maximizing Oxygen Delivery with drugs that Improve Cardiac Output
*all drugs increase world + 02 demand = creat problem while fixing problem use lowest dose that is effective *do not se unless pt has been adequate fluid resuscitated, don't want to vasoconstriction an empty vascular system Vasopressors/Inotropes -Dopamine -Norepinephrine (Levophed) -Phenylephrine (Neosynephrine) -Vasopressin -Dobutamine -Epinephrine Vasodilating meds -Nitroglycerine, Nitroprusside
Management of DKA/HHS
1. restore fluid volume, 2. potassium address, 3. Insulin
MI
12 lead - ST elevation or non ST elevation - positive troponin/ckmb
diagnostic tests
12 lead ekg chest x ray echocardiogram cardiac cauterization PA catheter
Prevention of Infection
1st defense skin is destroyed pt quickly becomes colonized by bacteria esp. bacteria that normally live on skin Minimal use of systemic antibiotics Use of topical antimicrobials Refer to posted guide of commonly used topical agents Early debridement w/ dead tissue Early excision and grafting w/ dead tissue
Anaphylactic Shock Pathophysiology
1st exposure: IgE antibodies markers are made on Mast cells i.e. Basophils Subsequent exposure leads to a release of immunological mediators specifically Histamine. also: leukotrienes, and prostaglandins Can take minutes to hours first airway problem then perfusion problem levy capillaries = lose volume form vascular space/3rd spacing = swell in interstitial space histamine is a vasodilation = hypotension +tachycardia
Central Venous Pressure Waveform
3-8 normal
rule of nines
A system that assigns percentages to sections of the body, allowing calculation of the amount of skin surface involved in the burn area.
A client is in the emergency department after being rescued from a house fire. After the initial assessment, the client develops a loud, brassy cough. What intervention by the nurse takes priority? A. Apply oxygen and continuous pulse oximetry. B. Allow the client to suck on small quantities of ice chips. C. Request an antitussive medication from the physician. D. Have the respiratory therapist provide humidified room air.
A. brassy cough in a burn pt is indicative of inhalation injury
The nurse assesses a client in the burn unit after the client was repositioned by the nursing assistant. The nurse intervenes after finding the client repositioned in what manner? A. Supine with one pillow behind the head B. Semi-Fowler's position with arms elevated C. Wrists extended to 30 degrees in a splint D. A towel roll placed under the neck or shoulder
A. no pillow positing prevents neck flexion
Anti-arrythmic therapy for ACS/AMI
ACLS Guidelines Defibrillation/Cardioversion Meds CPR Patients suffering AMI are at risk for ALL types of dysrhythmias. Approximately 50% of all people having an MI have a fatal Dysrhythmia within the first hour. Many more experience less serious dysrhythmias. Continuous ECG monitoring is essential
A young man comes into the foyer of the hospital and says that he has a container of anthrax, which he opens and pours on the floor. Which is the priority action for the nurse who first comes upon the scene? A. Dons a protective gown, mask, and goggles B. Escorts the young man to the decontamination room C. Begins evacuating the immediate area D. Notifies the local health department of a biohazard situation
ANS: C The highest priority is to evacuate the immediate area and prevent injury to those near the spill.
A client who recently lost his home in a fire becomes angry and screams at the nurse when his dinner tray is late. What is the nurse's best response? A. "Settle down, the dinner is still hot." B. "I will not be caring for you again." C. "I suggest that you get control of yourself." D. "Let's talk about this."
ANS: D Clients should be allowed to ventilate their feelings of anger and despair after a catastrophic event.
There has been an industrial explosion near the hospital and many victims are brought to the emergency room (ER) for treatment of their injuries. Which victim will be triaged with a red tag as emergent? A. An older adult with a dislocated right hip and an open fracture of the right lower leg B. A man with a large contusion on his forehead and a bloody nose C. A woman with a closed fracture of the right clavicle and numbness in her right arm D. A woman with multiple fractured ribs and shortness of breath
ANS: D Clients who have an immediate threat to life are given the highest priority, and placed in the emergent or class I category. The client with multiple rib fractures and shortness of breath most likely has developed a pneumothorax, which may be fatal if not treated immediately.
Which is the priority action for the nursing supervisor in the event of a mass casualty situation? A. Directing medical-surgical and case management nurses to assist emergency room staff with critically injured victims B. Calling additional medical-surgical and critical care nursing staff to come to the hospital to assist when the victims are brought in C. Informing the incident commander at the mass casualty scene about how many victims may be handled by the ER D. Directing medical-surgical and critical care nurses to assist with clients who are already in the ER while the ER staff prepares to receive the mass casualty victims
ANS: D The nursing supervisor should direct additional nursing staff to help care for the current ER clients while the ER staff prepares to receive the mass casualty victims.
Hypovolemic Shock/FVD
Actual fluid volume deficit Hemorrhagic, severe dehydration Typical hemodynamic parameters?- refer to stages of hypovolemic shock Interventions based on type of shock.
Anaphylactic Shock Always Epinephrine
Adrenergic Agonist: Alpha receptor stimulation -arterial vasoconstriction Beta2 receptor stimulation -bronchodliations Beta1 receptor stimulation -heart tachycardia, done want AE but need other parts of it
Injuries to the Respiratory System
Airway edema Pulmonary capillary leak Chest burns Carbon Monoxide Poisoning therein injury from that and inhalation of toxin from fire/smoke - can affect airway potency + oxygenation monitor with pt how has face burns, black teeth/mouth/nose, singed hair, voice change = inhalation injury most likely will need to be intubated b/c inflammation = severe swelling of airways watch for stridor and wheezing
Anaphylactic Shock interventions
Airway/Breathing -Bronchodilator—albuterol -Antihistamine—diphenhydramine/benadryl (not orla) -Corticosteroids - IV w/ prednisone oral taper over 10 days after -O2 by NRB -Intubation or emergency -tracheotomy Circulation Isotonic IV fluids Other vasopressors (dopamine, norepinephrine
Resuscitative Phase Fluid Resuscitation
American Burn Association accepted formula is the Baxter/Parkland formula First 24 hours Calculate fluid volume replacement wt in kg x tbsp burned x 4ml Administer Lactated Ringer's Replace ½ of calculated volume in first 8 hours Replace remaining half of calculated volume within next 16 hours fluid resuscitation done after assessing airway and breathing pt also lose a lot of albumin monitor: output, cvp, map, person
Abdominal Aortic Aneurysms
An AAA is an abnormal dilation in a weakened portion of the arterial wall occurs when thre is a weakening in abdominal aorta that creates an anergyms - can cause many porlbmes; tear or rupture = massive internal bleed develop slowly over eyars risk factors similar to other hear problem CVA, CAD, MI, *uncontrolled htn*
True or False: A physician must fulfill the role of triage officer during a mass-casualty event. True False
Answer: B (False) Rationale: This individual is generally a physician in a large hospital who is assisted by triage nurses. However, when physician resources are limited, an experienced nurse may assume this role.
During a large-scale multi-casualty situation, which patients usually make up the greatest number of patients? A. Red-tagged B. Yellow-tagged C. Green-tagged D. Black-tagged
Answer: C Green-tagged patients usually make up the greatest number in most large-scale multi-casualty situations.
During a multi- or mass-casualty event, triage is performed with which outcome in mind? A. Treat those with massive injuries first. B. Treat each injured person to save the most lives possible. C. Limited resources must be dedicated to saving the most lives. D. Save one life at the possible expense of many others.
Answer: C Rationale: In mass casualty or disaster situations, a military form of triage is implemented with the overall goal of doing the greatest good for the greatest number of people (Reisner, 2006). This means that patients who are critically ill or injured and might otherwise receive attempted resuscitation during usual operations could be triaged into an "expectant" or "black-tagged" category and allowed to die or not treated until others received care. Typical examples of black-tagged patients are those with massive head trauma, extensive full-thickness body burns, and high cervical spinal cord injury requiring mechanical ventilation. The rationale for this seemingly heartless decision is that the limited resources must be dedicated to saving the most lives rather than expending valuable resources to save one life at the possible expense of many others.
Burn patient 2: Estimate the % burn
Anterior and posterior trunk = 36% Anterior right arm = 4.5% Posterior Left arm = 4.5% Left palm = 1%
Anti-platelet Drugs for ACS/AMI
Aspirin COX1 in the platelet is involved in the formation of chemicals that increase a platelet's ability to cause platelet aggregation. ASA inhibits this enzyme and platelet aggregation is disrupted. clopidogrel (Plavix), ticlopidine (Ticlid) Platelets require a molecule called ADP to bind to the platelet in order to facilitate aggregation. Ticlid and Plavix inhibit the ability of ADP to bind to platelets. As a result, platelet aggregation is inhibited. eptifibitide (Integrilin) GPIIb/IIIa inhibitor Reversible when infusion stopped Abciximicab (Reopro) *if go to cath lab will be on 1 of these at least
Nursing Care for Patients Receiving Fibrinolytic Therapy
Assess for contraindications need good Secure vascular access, bliggauage needle for if we need to give blood Monitor EKG watch for resolution of ST elevation watch for re-perfusion arrythmias Monitor for complications bleeding, hemmorhagic stroke, anaphylaxis, re-occlusion -monitor for stroke like symptoms b/c risk for lbeeding -increase risk spontaneous hemp in brain
Pericarditis
Assessment -comp of acute mi, open heart surrey, cancer etc -Chest pain, pericardial friction rub (rub like sound walking crunch snow), fever (inflammatory response symptoms), ST segment elevation like with MI Treatment NSAIDS Pericardiocentesis Pericardial window Complications Pericardial effusion Cardiac tamponade inflammation of the sac surrounding the heart
Endocarditis
At risk: IV drug abusers, pts with valve replacements, systemic infections, and cardiac defects. Assessment Heart murmur, chills/fever, petechiae, CO Prevention Abiox prophylaxis in high risk patients Treatment Antibiotics, valve-replacement surgery
A client has a large burned area on the right arm. The burned area appears pink, has blisters, and is very painful. How does the nurse categorize this injury? A. Full thickness B. Partial thickness superficial C. Partial thickness deep D. Superficial
B. Partial thickness superficial
When providing care for a client with an acute burn injury, which nursing intervention is most important to prevent infection by autocontamination? A. Avoid sharing equipment such as blood pressure cuffs between clients. B. Change gloves between wound care on different parts of the client's body. C. Use the closed method of burn wound management for all wound care. D. Use proper and consistent handwashing by all members of the staff.
B. do you know about auto contamination?
Rehabilitative Phase
Begins with wound closure On going skin needs Activity needs Self-concept and depression Noncompliance with care Psycholocia support prospect with amputaiton
Other Medications Used for ACS/AMI
Beta Blockers! Anti-coagulants: heparin affect clotting factors (2nd defense) AE: bleeding Antiplatelet meds: Plavix, epitifamibide (Integrilin), Asprin affects platelets (1st defense) AE: bleeding ACE Inhibitors Anti-dysrhythmics Thrombolytics
Adverse effects of PTCA/Stent
Bleeding - over + hidden signs of fleeting; hematoma, retroperitoneal bleeding, pokes big hoel in femoral artery = high risk of bleeding esp b/c pt usually on anti platlet+coag Femoral Artery Occlusion - not enough blood to leg from occlusion Dysrhythmia - reperfusion dysrthmias LOC/Respiratory Depression - sedated for procedure, resp depression/LOC Re-occlusion - stand might loss + attract clotting and close up
The vascular capillary response to burn injury (early phase).
Burn victims lose a LOT of intravascular volume. The higher the percentage of body surface area, the worse the fluid shift leaking of water + protein out of the blood vessel as they become more permeable ALSO profound vasodilation from systemic inflammation
Characteristics of an AMI
Chest pain (feels like a crushing pressure) lasting longer than 30 minutes -Unrelieved by rest or NTG -80% of people Many associated signs and symptoms: -N/V, weakness, dizziness, palpitations, dyspnea and sense of impending doom, "heartburn"
Cardiogenic Shock
Clinical Manifestations: -All the signs/symptoms of SEVERE acute heart failure -All the signs/symptoms of hypoperfusion -Decreased MAP "cold and wet and hypotensive"
Hospital Incident Command System
Common organizational model for disaster management Roles formally structured under the hospital or long-term care facility incident commander with clear lines of authority and accountability for specific resources Emergency Operations Center or Command Center Hospital incident commander Medical command physician Triage officer
JCAHO Requirements for Hospitals Regarding Disaster Preparedness
Communications - both internal and external to community care partners, state/federal agencies Supplies - Adequate levels and appropriateness to hazard vulnerabilities Security - Enabling normal hospital operations and protection of staff and property Staff - Roles and Responsibilities within a standard Hospital Incident Command Structure Utilities - Enabling self-sufficiency for as long as possible with a goal of 96 hours Clinical Activity - Maintaining care, supporting vulnerable populations, alternate standards of care
Hypo-perfusion
Complex syndrome of decreased blood flow to body tissues resulting in cellular dysfunction and eventual organ failure" also know as shock, shock is a hypo perfusion problem
Resuscitation Phase of Burn Injury
Continues for about 24 to 48 hours Goals of management: -Secure airway - patent airway, oxygenation well supplemental O2, mech ventilation if needed -Support circulation/perfusion (fluid replacement) - large 3rd spacing edema, secondary to systemic inflammation -Provide analgesia -Prevent infection - strict asps with bun pt, infection ot seen in first 24048 hrs b/c 1st defense is down -Maintain body temperature - b/c skin maintains temp watch for hypotermia -Provide emotional support
PTCA/Stent
Coronary artery stents are commonly used during PTCA Provide structural support to the coronaries Create a larger luminal diameter Drug-eluting stents can prevent platelets from adhering
Calculating % of Burn Injury
Count only the parts burned: example ½ total (A & P) arm = 4.5% Rapid estimate of scattered burns: the size of patient's palm = 1% This method does not apply to children
IV fluids
Crystalloids * LR—Isotonic-good volume expander * NS 0.9%--fluid replacement used to increase plasma volume when there has been no loss of RBC's. - monitor I+O, kidney function, electrolytes Colloids -stop 3rd spacing + hold volume in vascular space, prevent capillary leaking -Increase the colloidal osmotic pressure within the vascular space Ex: Albumin, hetastarch, dextran
example: Code Triage, Stage II
Current staffing levels are insufficient to manage the disaster. Department Managers and Directors are notified and activate emergency Associate call-in procedures, consistent with their department policy. Associates may not leave the facility until an "All Clear" is broadcast.
A client is receiving fluid resuscitation after a burn. Which finding indicates that fluid resuscitation is adequate for this client? A. Hematocrit = 60% B. Heart rate = 130 beats/min C. Increased peripheral edema D. Urine output = 50 mL/hr
D. hematocrit indicates FVD. tachycardia is abnormal and may be indicative of FVD or infection. increase edema would be an A.E. of fluid resuscitation
It has been 12 hours since a patient has been admitted for burns to his face and neck and for inhalation injuries. He had been wheezing audibly, but at this time the nurse notes that his wheezing has stopped. What should the nurse do? A. Document this improvement in the patient's condition. B. Re-assess his breathing in an hour. C. Check the patient's Spo2 level. D. Notify the physician immediately.
D. the sudden absence of wheezing indiacates that the pt is about to lose his/her airway. The pt will need to intubation asap
Prototypes for Hypovolemic Shock
DKA/HHNK Abdominal Aortic Aneurism
Event Resolution
Debriefing: Critical incident stress debriefing Administrative review Psychosocial response of survivors to mass casualty events PSTD Assessment Intervention
Intravenous Nitroglycerin for PT in acute coronary syndrome
Decreases afterload and preload Vasoactive med- Dilates the coronary arteries = heart works less harder non-PVC bottle, continuous monitoring titrate to effect on BP and chest pain - to lowest possible does at is effective stop tittering when something happens good or bad: stops chest pain, hypotension < 50 mcgs/min = pure venous titrate 5-10 mcgs/min q 5-10 mins Max dose 200mcgs/min -AE: low bp -will become dizzy, light hearted so sit down
Myocardial Infarction (MI)
Definition: Irreversible necrosis or death of myocardial tissue due to inadequate blood supply. Area(s) of infarction become nonfunctional and scar tissue forms. Irreversible death of tissue = will not come back STEMI or NSTEMI - if ST develop they are quick = we can intervene faster
Full Thickness
Destruction of entire epidermis and dermis Skin does NOT regrow can be all different colors black not uncommon possible pain if nerve ends not destroyed - no pain if destroyed healing = weeks to months graft required long rehabilitation
12/15 lead EKG
Diagnostic Tests for ACS Gold standard - st segment and t wave changes can tell us a lot Used to identify dysrhythmias and myocardial ischemia, injury or infarct. Not everyone has EKG changes initially! can have MI w/o EKG change, would then need lab values then to determine Does not reflect the severity of an MI Location of infarcted tissue - based on where lead is
Pharmacology Acute Decompensated Heart Failure
Diuretics Decrease preload monitor fluid/electrolytes closely Morphine (Pulmonary Edema) Decrease preload Decrease anxiety dial pulmonary vessels Oxygen Increase oxygen content and delivery to cells sometimes pt needs to be on ventilator or intubated Beta blockers Decrease renin release Decreases SNS effects vasodilation ACE Inhibitors and Angiotensin receptor blockers Block RAAS system Reduces re-modeling vasodilation Digoxin
Pain Management
Drug therapy -Opioid analgesics -Non-opioid analgesics CAM therapies - relaxation, music therapy Environmental changes
Surgical Management of Burns
Escharotomy - if scar non stretchable/dead tissue can create pressure if a lot, done to relieve scar make incision into and take away pressure Fasciotomy - if scar extends deep into muscle/ fascia, done to prevent compartment syndrome/ increase pressure cutting off blood supply to underneath increase risk of infection and complication of mobility
Impact of Recent Disasters
Events of September 11, 2001 HAZMAT training Emergency preparedness
An Acute MI
Evolution of an AMI Occlusion over 5-10 minutes damage Necrosis in 4-6 hours Healing begins in 24 hours; new collateral circulation develops Site of healing soft after 5-10 days soft spot may rupture Scar tissue replaces the necrotic area "Ventricular re-modeling" scar tissue mechanically and electrically dead small MI: 2 weeks; lrg MI: 5-8 weeks
Acute MI Therapies = "MONA"
First 10 minutes not done in this order 3. Morphine 2. Oxygen - if sat below 90, too much O2 = vasoconstriction this is bad; only if needed 3. Nitroglycerin 1. Aspirin - 160-325mg, 1-2tab chewed - powerful affect on platelets
Nonsurgical Management: Acute Phase
Focus on wound care, keep clean of exudate + necrotic tissue so can regranulate Mechanical débridement Hydrotherapy- can be done several x a day, painful medicate prior, use aseptic technique Enzymatic débridement Autolysis Collagenase
Discharge must haves for HF
Follow-up appointments Documented EF** Medication Information Activity S/Sx to report Daily weights (3lbs/2days...CALL) Smoking Cessation Alcohol consumption
Decrease Oxygen Consumption in Shock
Goal is to decrease oxygen demands of all tissues Intubation and mechanical ventilation - lower WOB by doing breathing for them -sedate and pain control don't have to worry about resp depress and pain = decrease O2 demand Neuromuscular blockade - paralysis to decrease O2 demand Analgesia and sedation Control hyperthermia - fever increases O2 demand Proper nutritional support - ideal
Classification of Shock
Hypovolemic (tank is low) Cardiogenic (pump problem) Distributive (vasodilation; relative hypovolemia) Obstructive (blood can't get out) ex: cardiac tamponade, tension pneumo
Maximizing Oxygen Delivery
Improve arterial oxygenation: -supplemental oxygen -manual ventilation -mechanical ventilation -high FIO2 initially in early shock to decrease aerobic metabolic + lattice acid; nonrebreathers Improve Cardiac Output: -Volume replacement, maximize preload with fluids +blood -Crystalloids, Colloids, Blood Products -**Cardiogenic shock requires less volume = don't treat with this
Emergency Preparedness and Response
In mass casualty or disaster situations, a military form of triage is implemented with the overall goal of doing the greatest good for the greatest number of people. Safety concerns for providers in the field
example: Code Triage, Standby
Indicates a disaster involving mass casualties could very likely happen, but is not confirmed. Associates must return to assigned departments, review department-specific policies and look to department management for information and instructions. Do NOT call Security or Switchboard for information during any Code Triage.
example: Code Triage, Stage I
Indicates an unanticipated influx of victims, which may severely tax existing staffing levels, or an internal event that may jeopardize the safety of patients, visitors and/or Associates. Associates may not leave the facility until an "All Clear" is broadcast.
Lactate Levels
Indicator of cellular oxygen status Increased lactate levels = anaerobic metabolism! Normal levels are < 2 mmol/L ->4 = sigfnicant o2 delivery problem
Cardiac Biomarkers
Injury results in release of chemicals into plasma within 30-60 minutes that detect heart injury to myocardium The height and duration of the chemical changes correlates with the size of an MI (if uninterrupted by treatment) enzymes release in different phages to heart damage CPK-MB Myoglobin ***Troponin I EBP focus on b/c most reliable
Other meds: Acute Decompensated Heart Failure
Inodilator Milrinone (Primacor) monitor for arrythmias (QT intervals!) increase heart contractility + vasodialte monitor for hypotension may inhibit platelet aggregation, cause thrombocytopenia Nesiritide (Natrecor) Synthetic b. natriuretic peptide Results in: Vasodilation ( decreased afterload) Diuresis (decreased preload) Watch out! ProfoundHypotension Titrated only in ICUs
Non-Pharmacological Therapy
Intraaortic Balloon Pump Ventricular Assist Devices-LVAD Surgical Interventions--transplantation Hemodialysis - pt usually ends up in kidney failure/disease
Partial Thickness
Involves entire epidermis and dermis (varying depths) Categorized as: -Superficial partial-thickness - more of dermis involved -Deep partial-thickness injuries - patchy spot of dermis involvement
Progression of Shock: Refractory
Irreversible last stage high mortality rate Massive cellular death Response to interventions absent, catacomaines and fluids won't work MODS First kidneys, liver, heart, brain end of life prepartions/thinking about
Pericarditis lab and diagnostics
Labs CBC-Leukocytosis ESR elevated C-Reactive Protein elevated ECG-Gold Standard St elevation in ALL Leads - not just a few like with MI Chest X-Ray Pericardiocentesis or Biopsy
Superficial
Least damage; epidermis is only part of skin that is injured only top layer of food affected not usually blistering healing w/i few days Desquamation (peeling of dead skin) occurs 2 to 3 days after burn Think: Sunburn
"Cold and Wet"--Assessment Fluid Congestion (Wet)
Left Crackles Orthopnea/paroxysmal nocturnal dyspnea Signs/Symptoms of Hypoxemia Increased PA pressures Right JVD/NVD Peripheral edema Ascites Increased CVP
Other labs in Acute MI
Liver function Renal function Albumin ↓hgb/hct Thrombocytopenia (splenic congestion increase BUN/Creat with kidney damage elevated AST/ALT with liver
Progression of Hypovolemic Shock: Progressive
MAP decrease > 20mmHg life threatening, need quick response, can happen quickly Compensatory mechanisms begin to fail -Hypoxic vital organs -Anoxic non-vital organs - no O2 delivery; digestive tract -cellular death -lactic acid production -Worsening acidosis Multiple organ systems will begin to fail! Golden Hour! - 1 hr to save PT life at this stage
Progression of Hypovolemic Shock: Non-Progressive
MAP decrease by10-15 mmHg we can reverse - can prevent damage if we can identify + correct Neruo/Endocrine compensation begins- RAAS/ADH Anaerobic metabolism Non-vital organs Mild acidosis/hyperkalemia Assessment Findings -look for subtle change sin PT Compare to baseline! - compensation maintaining oxygenation @ minimum
Progression of Hypovolemic Shock:Initial/Early
MAP decrease less than 10mmHg Assessment Findings: 120/80- 108/84 Sinus tachycardia - increase HR Tachypnea - mild Vasoconstriction - most likely wound not see sign of except of PP narrow
EMERGENCY! Cardiac Tamponade
MEDICAL EMERGENCY pericardial sack fills with fluid so much ti compresses the heart and is unable to contract and relax b/c of the fluid Hallmark: Pulsus Paradoxus Pulses will be diminished or absent during inspiration Muffled heart tones, Tachycardia Distended neck veins ↓BP = C>o problem
Clinical Manifestations of AAA
Many are asymptomatic until they rupture ABD, flank, or back pain, may radiate to groin, buttocks, or legs - pain may indicate tear, pain can mimic chest pain Visible pulsation seen in the upper ABD Bruit can be heard over the mass - turbulent blood flow Possible diminished peripheral pulses if embolization occurs Avoid palpation, it can rupture
Role of Nursing in Hospital Incident Command System
Meet patient needs: Assess patients who can be discharged or moved to different level of care. This is to make sure that there is maximal room for incoming disaster victims. All patient care providers who are in the building, report immediately to their assigned floor and await further instructions. Med/Surg and Critical Care Nurses may be re-assigned to the ER during a disaster All nurses should be familiar with the hospital's disaster plan...many lives may depend on our ability to carry out the plan effectively Personal emergency preparedness plan Personal readiness supplies or "go bag"
Anaphylactic Shock Signs & Symptoms
Mucocutaneous Hives, angioedema (face, neck mouth swelling), pruritis, flushing Respiratory Cardiovascular GI
Significance of Abnormal Heart Sounds
Murmurs—interruption in bf to the valves, ischemia or infarct to muscles of valves may cause regurgitation S3, ventricular gallop (Ken(S1) Tuck(S2) y(s3) soft heart sounds heard after s2 -Heard best at apex and LSB -Decrease ventricular compliance + overstretching -Early sign of heart failure! S4, Atrial gallop -- before S1 Ten(S4) E(S1) See (S2) -Heard best at apex -Decrease ventricular compliance, increased afterload -not an early sign of HF Summation gallop -Combination of S3 and S4
Post-Operative Effects of Cardio-pulmonary Bypass
Myocardial depression = weak floppy heart Ventricular Arrythmias - vtach/vfib Decreased cerebral blood flow = risk of stroke Platelet dysfunction Acid-base disturbance post op care is intense 1st 24-48hrs
"Cold and Wet"--Assessment Poor Perfusion (Cold)
Narrow pulse pressure Proportional Pulse Pressure < 25% Decreased LOC Cool extremities, poor cap refill, pulses diminished Decreased BP with ACEI/ARBS Renal dysfunction Hyponatremia - RAAs = retains fluid Decreased MAP -Cardiogenic Shock
Those who do not tend to experience Chest Pain
Older adults Diabetics Women Psychiatric patients
Men and Acute MI: More "classical" impression
Pain radiating down left arm Crushing Chest Pain Diaphoretic Grey and Ashen (vasoconstriction-catecholamine release) Indigestion Sensation First thing in the morning (platelets get sticky want to tag together) Occur in severe stressful situations (even physically stressful situations)
Other Complications of AMI
Pericarditis- inflammation Endocarditis - inflammation Ruptured papillary muscle; cardiac rupture - infarcted area in the part of hear tis very weak; eventually will scar over to be stiff and strong Cardiogenic Shock aka extreme heart failure
Patient teaching/prevention endocarditis
Prophylactic antibiotics Teach patients how to admin ABX and the importance of completing the therapy as scheduled. Encourage proper hygiene, particularly oral hygiene. Teach patients how to monitor their temperature every day for up to 6 weeks and report fever, chills, fatigue, or malaise to their health care provider.
Location of AMI
RCA perfuses AV +SA node + RV underneath LV LCA more branching + bifurcation, gives blood to more tissue/ left side of heart/LV = more prone to pump, hear, and C.O. problem MI problems based on location ex: RCA @90%, cath reports identify artery involved
review coronary artery anatomy
RCA: feeds R atrium + ventricle swings around to perfuse the inferior wall of the L ventricle + some of posterior wall ex: occlusion of RCA many areas could be damanged LCA: branches into the L anterior descending artery= L ventricular wall of ventricle + circumflex which swings onto posterior wall + lateral wall of L ventricle
Notification and Activation of Emergency Preparedness Plans
Radio or cellular communication between the ED and EMS providers at the scene Media broadcast message via radio, television, or electronic announcements DMAT team
Disaster Triage Tag System
Red Tag—emergent (class I) patients Yellow Tag—patients who can wait a short time for care (class II) Green Tag—nonurgent or "walking wounded" (class III) Black Tag—patients who are expected to die or are dead (class IV)
Valvular Heart Disease: Regurgitation
Regurgitation (a closing problem) - back up of blood Mitral regurgitation (insufficiency) Mitral valve prolapse Aortic regurgitation (insufficiency) Mitral and Aortic Regurgitation—Left Ventricular Failure = will need vegetation
Goals of MI Therapy in acute stage
Relieve pain Preservation of myocardium -Reperfusion of blocked artery -Reduction of cardiac workload O2 supply and demand! Control of lethal dysrhythmias - 50% in acute MI will die w/i 1st hour from v tach v fib systole Prevent or treat complications - major complication = acute heart failure-symptoms like pulmonary edema, decrease perfusion Return to functional life -Identify and manage risk factors *time is muscle - need to treat immediately
Surgical Management of Valvular Heart Disease
Reparative procedures Balloon valvuloplasty Direct or open commissurotomy Mitral valve annuloplasty Replacement
Nonsurgical Management of Valvular Heart Disease
Rest Drug therapy Diuretics Beta blockers Digoxin Oxygen Nitrates Vasodilators Anticoagulants
Routine Nursing Care—After Acute Episode is Over...
Rest vs. activity Daily wts/accurate I and O Fluid/Na restriction Pharmacological maintenance Patient and family teaching -Acute HF is # 1 cause of hospital adm. for ADHF -Outpatient/Homecare referrals essential!
General Treatment Goals for Acute Decompensated Heart Failure
Reverse ventricular re-modeling Decrease intravascular and extravascular volume Decrease vascular resistance (afterload!)
EBP: Proportional Pulse Pressure
SBP-DBP/SBP Desired: Greater than 25% poor CO/perfusion: <25% reliable indicator of decrease C.O. Ex: 105/80 105-80/105 = 24% = CO problem
Routes for Nitroglycerin: for PT in acute coronary syndrome
SL—very fast absorption, do not swallow, dissolve under tongue, expires, if doesn't work after 1st dose call 911, take every 3-5 min , for max of 3 dose Transdermal—no rubbing or massaging, no heat. Wear gloves. Dose may be removed at night and replaced in the morning. -AE: low bp -will become dizzy, light hearted so sit down
injury
ST segment elevation
Zone of Injury
ST segment elevation Seen first! some cardiac cells injured, not dead but in severe trouble ST seg elevation indicates the acuteness of situation - need to move fast or cells will die/infarrct *time is muscle - need to get repressed as quickly as possible
STEMI
ST-segment elevation myocardial infarction
Zone of Ischemia
ST-wave inversion and depression Occurs within hours and may persist for months blood/o2 supply to an area is interrupted BUT still some blood flow/o2 being delivered but not enough to meet demand but not to little to cause injury inflammation with ischemia as a result in interruption of bf = in trouble
Severity of Burn Injury
Severity determined -TBSA -Depth - different layers of skin, classify depth of burn according to the layers of skin that are affected Differences in skin thickness in various parts of the body also a factor
Dressing the Burn Wound
Standard wound dressings Biologic dressings: Homograft—human skin Heterograft—skin from other species Amniotic membrane Cultured skin Artificial skin Biosynthetic dressings Synthetic dressings
Diagnosis of Valvular Heart Disease
Sudden illness or slowly developing symptoms over many years Ask about rheumatic fever infective endocarditis possibility of IV drug abuse risk factors Chest x-ray, ECG, stress test, Echocardiography
Surgical Management
Surgical excision - usually done for deeper burns to get to a layer of vascularized tissue and gently scarp/take away layers not getting any blood flow healing won't occur + grafts won't take if there is no good vascularization of tissue Wound covering Skin graft - NEW GRAFT = dressing need to say on, bulky cause dressing, she is immobilized for some time for vascularization of graft and this can take a while
Assessment Findings of MI
Sympathetic nervous system effects -Respiratory rate, tachycardia, increased O2 demand + consumption Parasympathetic nervous system effects, sometimes seen if blockage to SA or AV node -Bradycardia, BP, AV blocks Signs/Sx of heart failure: dizzy, fatigue, inability to exercise, tachypnea, DOE, water retention, wt gain, swollen legs Heart Murmurs - indicate ischemia/Friction rub - indicate inflamed pericardia Dysrhythmias -90% of pt = common -50% of pt die w/i 1st hour from lethal dysrhtmias; v tach, v fib
Post-operative Care Priorities for AAA
Temp Urine output BP HR LOC Lung Sounds SaO2 CVP Cardiac rhythm Peripheral Vascular Status post op risk bleeding, thrombosis, emboss, AKI, impaired gas exchange, pain, bp variability
Management of Patients in Shock
Three main goals 1. Identify and treat the cause 2. Optimize oxygen delivery arterial oxygen content, cardiac output -CO -SaO2 -Hgb 3. Decrease oxygen consumption
Management of the Burn Patient
Three major phases of burn care: Resuscitative Phase Acute Phase Rehabilitative Phase
Female and Acute MI: More atypical symptoms (Framingham Heart Study)
Unexplained or unusual fatigue Sleep disturbances 43% in study said they did not experience chest pain 95% had new or different symptoms 1 month prior to heart attack that went away after the attack SOB 42% Indigestion 39% Anxiety 35% SCD (sudden cardiac death) 50% men, 63% women No previous warning symptoms at all Average time women delay seeking treatment 5.5 hours - (in 20-30 of occlusion necrosis starts)
Anaphylactic Shock Discharge teaching
Use of epi-pen -90 degree angle thru clothing -Hold for 10 seconds Call 911 b/c epic wears off Biphasic reaction - anaphalatic symptoms come back hrs/days later = need corticosteroids Medic-Alert Bracelet
Fibrinolytic Therapy for ACS/AMI
Used to dissolve clots/the lesions occluding the coronary artery very risky b/c risk of bleeding Often combined with antiplatelet therapy Contraindications:active bleeding, aortic dissection, recent trauma/surgery, acute hypertension -acute htn = risk for hemmorage = stroke very high
Cardiac catheterization
Used to evaluate the location of coronary artery lesions, to assess LV function, and to measure pressures within different heart chambers
Percutaneous transluminal coronary angioplasty (PTCA)
Used to increase the inner diameter of coronary arteries and to increase blood flow to the heart A balloon-catheter is advanced into the coronary artery and inflated to compress an area of plaque
Nitroglycerin - Acute Decompensated Heart Failure
Vasodilators Decrease afterload and preload titrate to effect on BP and chest pain < 50 mcgs/min = pure venous titrate 5-10 mcgs/min q 5-10 mins Max dose 200mcgs/min Adverse effects? if BB and ACE inhibitors and angiotensin receptor blockers don't work use nitro
Nitroprusside (nipride) - Acute Decompensated Heart Failure
Vasodilators For ICU PT potent arterial vasodilator 0.1-5 mcg/kg/min titrate q 5-15 minutes in increments of 0.5 to 1 mcg/kg/min MUST HAVE AN ARTERIAL LINE! b/c bp will drop quickly + drastically Watch for thiocynate toxicity - thiocynate is a metabolite of cyandie if used for 24-48hrs ill need velvets so see if any cyandie posioning last resort to decrease after load
DKA
Very high glucose and no insulin using fat for every acidosis = high K Polydipsia, polyuria,weakness, tachypnea (not kussmauls) and tachycardia. Dry mucous membranes, orthostatic hypotension, sunken eyes. Dehydration, hypovolemia and shock. + DYSRTHMIAS look at Serum osmolality, K+, Blood glucose, other electrolytes PH, abc, ketones
HHNK
Very high glucose just enough insulin to prevent ketones no acidosis Polydipsia, polyuria,weakness, tachypnea (not kussmauls) and tachycardia. Dry mucous membranes, orthostatic hypotension, sunken eyes. Dehydration, hypovolemia and shock. Serum osmolality, K+, Blood glucose, other electrolytes
Examples of Disaster
Violence Illness outbreaks Severe weather Earthquakes Avalanches Fire Multiple-vehicle accidents
Tissue Damage
Will not be complete at the time of injury - depth of injury can increase after admitted Tissue destruction can continue for 48 hours or more after the cause of the burn is removed due to -Release of local mediators -Immune inflammatory response -Coagulation system
Acute Phase of Burn Injury36-48 hrs—until wound closure
Wound care - clean, cleanse daily with routine care: clorahexadine, antimicrob agent, topical, silver- bread spectrum + pain relieve Nutritional support - internal, tube feeding Management of pain - opines, saids Prevention of contractures Psychosocial issues
atheroma
a deposit of plaque on or within the arterial wall
emergency operations center (EOC) or command center
a designated location in the hospital incident command system (HICS) with accessible communication technology, also called command center
emergency preparedness
a goal or plan to meet the extraordinary need for hospital beds, staff, drugs, pPE, supplies, and medial devices such as mechanical ventilaors
Valvular Heart Disease: Stenosis
a lot like heart failure with S+S Stenosis (an opening problem) - stiff valve has trouble opening, blood hard to get out -Mitral stenosis -Aortic stenosis Aortic Stenosis: SAD =Syncope, dyspnea, angina syncope - not enough blood to brain
mass casualty event
a situation affecting the public health that is defined based on the resource availability of a particular community or hospital facility. when the number of casualties exceeds the resource capabilities, a disaster is recognized to exists
disaster triage tag system
a system that categorizes triage priority by colored and numbered tags
Zone of Infarction
abnormal Q waves Present permanently on EKG after an MI dead/dead tissue - does not demoralize, electricity does not flow through it, does not contract large area = dysrthmias + pumping problems *time is muscle - St increase with injury may remain in infarct but abnormal Q is key healthy people do not have Q significant Q = 1 small box deep and wide Q wave remains for lifetime of pt does not ell you how recent infract is or was just that they had a q wave - will develop in hours
arteriosclerosis
abnormal hardening of the walls of an artery or arteries
infarct
abnormal/significant Q wave
Cardiogenic shock
acute decompensated heart failure, extreme failure of left ventricle decrease contractility - (pump problem) b/c extreme vasoconsiticon normal blood volume + decrease cap bed size
Debriefing
after a mass casuaty incident or disaster, the provision of sessions for small groups of staff in which teams are brought in to discuss effective coping strategies (critical incident stress debriefing), and the administrative review of staff and system performance during the vent to determine opportunities for improvement in the emergency management plan
Norepinephrine (Levophed)
alpha arterial vasoconstriction, not a much tacky or changes in C.O.
burns and its affect on body
alsmot every tissue + cell of body scan be affected when pt experiences significant burn b/c changes in metabolic rate + compensatory response in SNS, inflammation, fight or flight affects on the body in signficant
Special Considerations: Electrical Injury
always classified as a major burn
Disaster
an event in which illness or injuries exceed resource capabilities of a community or medical facility:
hospital incident command system (HICS)
an organisation model for disaster management in which roles are formally structured under the hostel or LTC facility incident command, with clear lines of authority and accountability for specific resources
Shock
any disease that impairs cellular oxygenation can lead to shock Whole body response due to poor cellular oxygenation Condition vs a disease state Any situation that impairs oxygen delivery to cells, tissues and organs can start a syndrome of shock and lead to a life threatening emergency
acute MI problems
at the beginning of occlusion of coronary artery @ tissue level heart cells already switching to anaerobic metabolism - not efficient way to produce energy = acidosis ventricle remodeling = increase risk for lethal dysrhtmias + pump prob dead tissue will turn into scar tissue = no electric/pumping flow will change shape of heart sooner we restore perfusion = the better
IABP
ballon pump caterer into aorta through femoral artery with bacon hooked up to machine that inflate and deflate with pt heart beat systole = deflate = collapse + pull blood out of ventricle into aorta to decrease hart work like a suction diastole =inflate = push blood back to coronary artery to increase perfusion
dopamine
beta affects heart and arterial system increase contractility + vasoconsticiton ae, tachcyardia + increased workload don't use unless we have to + if we already maximize pt volume status
Dobutamine
beta mainly for countability - good for cardiogenic shock
Epinephrine
beta + alpha 1st line anaphansis, can be IV causes vasocosnticiton and increases HR
beta vs alpha
beta improves contactility + hr alpha causes arterial vasoconstriction one drug is better than the other depending on hemodyanic problem: AL or contractility problem some drugs have more alpha or beta affects or are in between
Disseminated Intravascular Clotting
bleeding and thrombosis
Superficial Partial-Thickness Burn
blistering patchy dermis involvement
DKA + HHNK
both cause extreme dehydration, hypovolemia, shock, altered LOC + HTN both have osmotic diuresis - FVD losing urine/ diuresis = losing K+ Management = 1. restore fluid volume, 2. potassium address, 3. Insulin
Multi-Casualty Event
can be managed by a hospital using local resources.
Pericardiocentesis
catheter inserted in pericardial sack to remove fluid
left heart failure
causes: HTN, CAD, valve disease; mitral or aortic decrease tissue perfusion from poor C.O. + pulmonary congestion can be further divided into systolic or diastolic
right heart failure
causes: LV heart failure, RV MI, pulmonary htn RV cant empty completely increase volume + pressure in venous system = peripheral edema
Ventricular remodeling
changes in size, shape, structures, function of the heart from injury to heart thickening = less able to contract thinning = not strong unable to contract
Acute coronary syndrome
complication of a fracture characterized by increased pressure w/i one or more compartments and causing massive compromise of circulation to the area of the heart
Atherosclerosis
condition in which fatty deposits called plaque build up on the inner walls of the arteries
bundle branch block
conduction delay in one of the bundle branches that goes through the ventricle common consequence of acute MI sometimes are permanent after MI sometimes occur for other reasons wide QRS > 0.12 sec is a bundle branch block new BBB esp L side highly suggestive of acute MI want to monitor for
shock
defined as decrease in MAP + can be caused by many things
Organ perfusion : MAP
deiving force of blood flow that delivers o2 +nutients to organs and cells shock manifested by decrease in MAP -decrase of map 5-10mm will stimulate compensatory mechanism Mean Arterial Pressure Normal MAP = 70-110 MAP = (2x DBP) + SBP /3
stable angina
exertional angina relieved with rest or sublingual nitroglycerin
Facial Edema
get airway establish quickly b/c swelling = important
Facial Burn
high incidence for inhalation injury airway compromised face burns can require multiple reconstructive surgery + psychological support
Nitroglycerine and Nitroprusside
in cases of increase afterlaod/vasocnstricion is very high cardiogenic shock
Triage
in the ED, sorting or assigning pt into priority levels depending on illness o injury severity with the highest acute needs receiving the quickest evaluation and treatment
SNS stimulation
increased HR increased after load (resistance) increases contractility
RAAS
increases Afterload Na + fluid rendition systemic vasoconsitrcion
Hyponatremia and Acute MI
indicates severe activation of RAAS and BNP release can also be dilutional if patient is fluid overloaded poor prognostic indicator Other electrolyte imbalances are common
personal emergency preparedness plan
individual plan that outlines specific arrangements in the event of disaster; child care, pet care and older adult care
Endocarditis: Etiology
infection usually f hear valves or anywhere on endocardium - system b/c enters the blood stream Bacteria enter the bloodstream from the oral cavity, skin lesions, infections involving the GI/GU system, or invasive procedures and attach to susceptible areas in the heart, usually the valves. The valves of the heart are more likely affected due to the decreased blood supply and decreased immunity from WBCs. In patients with damaged valves, the body sends platelets, fibrin, and immune cells to try and heal the valves; This healing process traps microorganisms in the blood that causes clumps known as vegetations on the valves. affects valve function, vegetation beak of valves and sten out into system system - micro emboli now that cause problems
heart failure
is a complex clinical syndrome where the heart is unable to meet the metabolic demands of the body
post traumatic stress response
is a mental health condition that's triggered by a terrifying event — either experiencing it or witnessing it. Symptoms may include flashbacks, nightmares and severe anxiety, as well as uncontrollable thoughts about the event.
Heart Transplantation
last resort if heart not able to recover
Endovascular Repair for AAA
less risky than open heart surgery graft in placce/conduae for blood to flow through, makes pressure off aneurysm + prevents embolism from aneurysm if too much calfivaiton own tower similarly to cardiac cath procedure: same after care and monitoring done if not to big, assessable from femoral artery
petchaie in Endocarditis
little tiny clots that broke off and are now in capillary bed from vegetation from micro emboli can causes necrosis r/t vegetation ex: acute kidney injury - bun/creat increase b/c vegetation ex: abd pain distention - abdominal necrosis from vegetation
table of shock from beginning to end
local infection systemic infection (early sepsis) SIRS (systemic inflammatory response syndrome) organ failure (severe sepsis) multiple organ system failure (MODS) septic shock death
Mass Casualty Event
local medical capabilities are overwhelmed and may require the collaboration of multiple agencies and health care facilities to handle the crisis.
Prevent Contractures
maintaining motility is key can develop easily in areas of joints if thats where burns are ambulate asap: dr okay, decrease swelling, post grafting vasculariaiont, PT, position, ROM
Distributive Shock
massive vasodilation causes a relative hypovolemia - not enough volume to fill container after load problem to low = not enough pressure/ resistance neurogenic shock (not on this exam) anaphylactic shock septic shock
Distributive shock
massive vasodilation causing decrease volume b/c donation gets bigger with same amt of volume decrease in after load -(vasodilation; relative hypovolemia) normal blood volume and increase in cap bed size
ejection fraction
measures how well the heart contracts or pumps blood out with each beat recorded as a percentage. normal is equal to or more than 55% measured by nuclear stress tests, MUGA scan, *echocardiogram* or heart catheterization
Angina (stable and unstable)
mild to moderate substernal chest pain caused by ischemia or imbalance between oxygen supply vs demand to cardiac cell muscles
Deep Partial-Thickness Burn
more dermis invovled rare blistering edema may see scar formation healing time up to 6w grafting may be necessary
evidence for low perfusion
narrow pp cool extremities lethargic/obtunded hypotension decrease na level worsening renal function
shock causes shock
need to identify and intervene quickly shock becomes a vicious cycle poor perfusion causes other things to occur that weaken the perfusion state shock worsen shock
warm and dry
no congestion at rest no low perfusion at rest
cold and dry
no congestion at rest yes low perfusion at rest
Vasopressin
non adrenergic potent vasoconstrictor food for shock if not responding to meds abvoite it increase map
NSTEMI
non-ST elevation myocardial infarction
Inotropes - Acute Decompensated Heart Failure
not first choicest will use if previous meds are not working Dobutamine (Dobutrex) Beta adrenergic drug increase heart contraction to be stronger + faster sis simulates heart directly risky b/c weak floppy heart working harder can be harmful in long run Dose 2.5-20 mcg/kg/min titrate by 0.5-1 mcg/kg/min q 5-10 minutes Evaluate effectiveness with hemodynamic profile Dopamine—stimulates alpha, beta and dopaminergic receptors. Not usually used for heart failure stimulates more than heart ICU drug titratable meds: wtbased
eveidence fo confession
orhtopnea JVD edema ascites rales
stress test
performed to assess cardiovascular health and function during and after stress
hospital incident commander
person (emergency physician or administrator) who assumes overall leadership for implementing the institutional plan at the onset of the mass casualty incident. The hospital incident commander has a global view of the entire situation, facilities patient movements through the system and brings in resources to meet patient needs
medical command physician
person responsible for determining the number, acuity, and medical resource needs of victims arriving from the incident scene and for organizing the emergency health care team response to injured or ill patients
Triage officer
person who rapidly values each pt who arrives at the hospital, usually a physical with a triage nurse, but in situation when physician resources is limited can be nurse
BNP Assay and Acute MI
point of care test elevated in patients with LV dysfunction -released from ventricles in response to ventricular stretch and pressure overload now a gold standard for dx < 100--exclude heart failure 100-600--pulmonary vs. cardiac >600--heart failure!
Osmotic Diuresis
polyurina lose of a lot of volume = s+s fed
personal readiness supplies or go bag
preassembled sister supply kit for the home an for automobile that contains clothing and basic survival supplies also called go bag
aspirin
prevent platelets form aggregation increase oxygen to myocardium open up coronary arteries as much as possible
Open-Heart Surgery—Key Concepts
procedure has tremendous affect on the body post op stop heart from beating in procedure, need to be on bypass to artificially oxygenate heart and perfuse body: to pump blood out clean and oxygenate then bring back Hypothermia Extracorporeal circulation Hematological effects -reduces metabolic demands -can damage cells of body, blood wants to clot outside of body will be heperanized = increase risk of bleeding Cardioplegia- solution used to stop heart form beating
Phenylephrine (Neosynephrine)
pure alpha arterial constrictor, good for vasodilation w/o heart problem
brachytherapy
radiation therapy in which the source of radiation is implanted in the tissue to be treated
afterload
resistance left ventricle must overcome to circulate blood increase in: hypertension, vasoconstriction
Expected Outcome-PTCA/Stent
resolution of acute MI symtpms Chest pain should dissipate immediately St segment should come down to baseline Watch cardiac enzymes - will start to come down (Peak at time of intervention)
types of heart failure
right vs left heart failure acute vs chronic heat failure systolic vs diastolic
unstable angina
risk for MI or death, presents with low level activity or rest; exercise contraindicated very likely to have an MI in the next 12 months usually treated with aggressive repercussion strategies *12 lead no st elevation + troponin/ckmb negative*
regardless of shock symtpsm are the same
sever hypotension, cool clammy skin, edema, coma, oliguria, dyspnea, gi bleed, paralytic illeius *some exceptions
pulmonary artery cath
severe acute decompensation heart failure often require monitoring as well give more info for left side of the heart
Surgical Repair for AAA
sewing graft into aorta many potent complciaison open entire abdominal: stem to stern open aorta, graft put in, close up perfusion of legs decrease b/c clamps some pt at risk for AKI if clamped above kidney how long clamp time affects perfusion is important to know
Nursing and Medical Management of Acute Decompensated Heart Failure
shock caused by extreme heart failure all shock is a perfusion problem decrease af = extreme vasoconstriction causing low bp b/v blood can't get out of ventricles = treat with vasodilation even tho bp low to open up vessels
hypovolemic shock
shock resulting from blood or fluid loss decrease in preload - (tank is low) decerase in volume with normal cap bed size
ischemia
st depression + twave inversion can occur w/i hours and last for months depending on if we are able to resolve the ascetic process or not
Coronary Artery Bypass Graft
surgical intervetion for CAD/AMI open heart to create new pathway for blood Anastamosis of saphenous vein graft or internal mammary artery to create a conduit bypassing blockage within a coronary artery Selection criteria Angina unresponsive to medical therapy Left main disease/multiple lesions Failed PTCA/stent due to hemodynamic instability n/a for stent or area to narrow for stent
acute myocardial infarction
the condition in which a portion of the myocardium dies as a result of oxygen starvation; often called a heart attack by laypersons
narrow pulse pressure
the difference between S and D pressure as peripheral vasoconstrictor difference decreases narrow pp = earlier indicator of poor CO + poor perfusion than low BP ex: 120/80 to 120/85
Percutaneous transluminal coronary angioplasty
thread through the femoral artery, feeds through venous system and into coronary arteries balloon tipped cath will compress lesion against wall of artery, followed by stent, a mesh keeping plaque at wall so blood can pass through perferred perfusion thearephy over fibrolytics
Types of CAD or a facet of Coronary Artery Disease (CAD) that includes:
umbrella term used to describe various degrees of coronary artery occlusion: Unstable angina STEMI NSTEMI *underlying sense of urgency is the same = 1 term for all stages*
Meshed Autograft
used when not enough donor skin to cover all the burn areas can happen with large surface area burn meshing allows less skin to be used + stretched over a big area takes longer to heal
murmer
valves of heart also need blood + O2 delivery to work properly if bf to valves obstructed during an MI = murmer, this tells you heart valve being deprived of oxygen and is becoming dysfunctional symptoms of heart failure; syncope, etc
preload
volume of blood in ventricles at end of diastole (end diastolic pressure) increased in: hypervolemia, regurgitation of cardiac valves, heart failure
compensatory mechanism
when CO is insufficient to meet demands of bod, body will compensate initially will increase CO but will not in the long run -sympathetic nervous system (SNS) -renin angiotensin system (RAS) -ventricular remodeling (hypertrophy, cardiomyopathy) -other players (Bnp)
Deep Full-Thickness Burn
will not feel pain b/c nerve ending destroyed
Stents
wire mesh cylinder inserted into a clogged artery to hold it open
warm and wet
yes congestion at rest no low perfusion at rest
cold and wet
yes congestion at rest yes low perfusion at rest ex: acute decompensated heart failure
Burn patient 1: Estimate the % burn
½ posterior trunk = 9% all left arm = 9% all left leg = 18% right palm = 1%