Objective 10.txt

fluid in the lung, life-threatening, acute, flash pulmonary edema

crackles, dyspnea, distortion, tachycardia, hyper/hypo tension, reduced urinary output, cough with frothy pink sputum, PVSc, anxiety, restlessness, lethargy

start at bottom and work up

high fowlers unless hypotension then lay flat

2-5L is nasal cannula, 5-6 mask, 10-15 respirator with goal to get O2 above 90%

respiratory distress, anxiety, increased HR (weak), JVD, agitation and confusion due to not enough oxygen

cardiac; overload, respiratory status, left ventricular function

nitro (vasodilator), rapid acting diuretics, morphine 1-2 mg which reduces preload

left ventricle fails to eject sufficient blood and pressure causes fluid to leak across the pulmonary capillaries and into the lung airways and tissues

decrease volume overload, increase ventricular function, increase respiratory exchange

in Afib the loss of coordinated contractions can lead to stagnation of blood resulting in PE; clot would move from right atrium to right ventricle to lungs

chest pain, SOB, tachycardia, change in LOC, symptoms of DVT

assess, keep pt calm, anticoagulant therapy

c venous catheter, age, hx of clots

dyspnea, chest pain, restlessness, impending doom, cough, hemoptysis

tachypnea, crackles, pleural friction rub, tachycardia, S3 or S4, diaphoresis, fever, petechiae, decreased O2 sats

rt sided HR, respiratory failure, death

increases with inhalation and decreases with exhalation

shorten diastolic time, increased workload of heart, can lead to HF

reduced O2 demand, hypotension

early rhythm dinctions, decreased cardiac output

epi and atropine

hypoxia, MI, dig, BAB agents

meds, IV fluids, atropine may be drug of choice, DON’t stimulate vagal response

if they don’t convert, give adenosine to get into sinus rhythm and then cardiovert

cardiogenic shock, angina

rapid uncontrolled twitching of atria, AV node is bombarded, high chance of clots, usually use IV meds to convert to sinus

amiodarone, also Cardizem, dig and veraprimil, anticoagulants

block at AV node

low BP, SOB, treat like afib, sawtootk

lost protection of AV node

impulse starts in ventricle, not atria; acidosis; drug is amiodarone or lidocaine

3 or more PVCs in a row, cardiovert if necessary, lethal rhythm

Can turn into vfib

quivering of ventricles, no atrial, absent heartbeat and palpable pulses

immediate defib

200 joules

NO

first-all sinus impulses reach ventricles; second-some do; third none do

baseline of EKG is depressed

baseline of EKG is elevated

emergent situation, myocardial death

plaque at least 40% before it stops blood flow

might not have changes in troponin or CK levels

assess, compare to baseline, monitor EKG

ineffective cardiac tissue perfusion, risk for fluid imbalance, risk for ineffective peripheral tissue perfusion

acute pulmonary edema, HF, cardiogenic shock, cardiac arrest, pericardial effusion, cardiac tamponade, pleural effusion

relieve pain, prevent further damage, good respiratory, reduce anxiety, adhere to self care program, know early indicators

smoking, diet, cholesterol, physical activity, diabetes, BP, obesity

AFA and Hispanic women more than white women

elevated LDL and low HDL increase risk for MI

angina-less than 15 minutes, MI more than 30 minutes and relieved only by opiods

CK (CK-MB), troponin T and I, myoglobin

aspirin 325 mg, nitro, morphine, beta blockers, ACE inhibitors within 24 hours, evaluate thrombolytic therapy, give bed rest

cardiac tamponade

excess fluid within pericardial activity, restriction of heart function, pericardial effusion

chest pain, engorged neck veins, falling systolic BP, narrowing pulse pressure, muffled heart sounds, paradoxal pulse

pericardiocentesis to remove fluid and relieve the pressure on the heart

increases pressure within pericardial sac and compresses the heart; increases pressure in all chambers, decreases venous return due to atrial compression and ventricles cannot distend and fill adequately

MI, cardiac arrest, vfib, vetch, cardiac amyloidosis, cardiacmyopathies

H and RR increase or slight increase in diastolic BP may be only objective manifestation

rt or left fails to pump oxygenated blood into systemic circulation; necrosis of more than 40% of left ventricle

necrotic area impairs contractility and cardiac output; oxygenated blood not moved forward into systemic circulation

ejects too little blood into left ventricle, tissues decrease O2

decreased HR and RR, vasoconstriction, increase in pulse pressure, MAP and urinary output; tissue hypoxia in nonvital organs

rapid changes, BP decrease, weak pulse, MAP decrease and O2 stats, decreased ABGs, heart dysrhythmias, all organs begin to fail

increases as shock progresses

decreased tissue oxygenation (decreased PH, decreased PaO2, increased PaCO2)

arterial line insertion to monitor continuous BP, pulmonary artery cath

dobutamine-strengthens cardiac contraction and increases cardiac output

nipride, reduces afterload and preload, causes vasodilation, decreases cardiac output and afterload