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%