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<3failure/valve dise
NP4 Test 2
| Question | Answer |
|---|---|
| Preload is determined by | amount of venous return and ejection fraction (blood volume) |
| Some medications to decrease preload include | *Nitrates: cause venous pooling *Diuretics: down body fluid = down volume *Positive Inotropic Agents (digoxin): helps contractility of myocardial fibers *Beta Adrenergic Agonists (Dobutamine, Dopamine):up contractility, IV meds, dont down o2 consumptio |
| Afterload is the amount of | tension the ventricle must develop during contraction in order to eject blood from LV |
| Afterload is determined by | size of ventricles, ventricle wall tension, atrial pressure (PVR) |
| Afterload is increased in heart failure d/t | large ventricles, increased tension, incrased arterial pressure |
| An increase in afterload causes | hypertrophy and dilation of ventricles, muscle gets thicker and body is unable to supply enough oxygen so contractility decreases |
| Medications to decrease afterload includes | Phoshphodiesterase inhibitors (inocor, primacor): basodialate, improve myocardial contractility Vasodialators (nitrates, nitroprusside (icu med): dialate pulmonary vessels causing decrease wall tension Ace inhibitors: vasodialation, help renin-angiotens |
| Stroke Volume (SV)= | amount of blood ejected from one ventricle with one heartbeat |
| Avg. Stroke Volume = | 70 mL/beat |
| Cardiac Output (CO)= | amount of blood pumped by each ventricle in one minute |
| diastole= | relaxation |
| systole= | contraction |
| End diastolic volume (EDV)= | volume of blood in ventricle after relaxation and just before contraction |
| End systole volume (ESV)= | volume of blood in ventricle after ventricle contraction and before atrial contraction |
| Ejection fraction (EF)= | amount of blood ejected during systole compared to the amount of bloodin heart at end of diastole |
| Normal ejection fraction (EF)= | 50ml; 2/3 of EDV is ejected normally |
| Normal end diastolic volume (EDV)= | 120 ml |
| Normal ejection fraction (EF)= | 0.58 |
| Patho of right heart failure | increased workload placed on RV as it pumps blood against resistance in patients congested lungs or when there is pulmonary hypertension; backs up into rt. atrium and veins |
| Population at risk for right heart failure includes | dx. that increases pulmonary artery pressure & produces pulmonary htn. LV failure, COPD, tricuspid/pulmonic valve problelms |
| Rule of thumb for Right heart failure cause and effect is | |
| Patho of left heart failure | decreased capacity of LV to pump adequate volume of blood out of heart, causing backup into LA and pulmonary system |
| Population at risk for left heart failure (most common form of heart failure) includes | *Any weakness in LV- MI, anneurysm, aortic/mitral valve prob *Dysrhythmias *HTN *Cardiomyopathy *Anemia *Stress *Hyperthyroidism *Obesity *Pregnancy *Alcoholism |
| S/S of right heart failure include | dependent, pitting edema; JVD; weight gain; hepatomegaly (can cause cardiac serosis adn liver failure); ascites/fatigue (d/t increased amt. of waste products); weakness; anorexia, N/V |
| S/S of right heart failure are caused from | back-up of blood from RA into venous system, causing venous congestion |
| S/S of left heart failure include | Dyspnea; orthopnea; PND; moist rales; dry, hacking cough; S3/S4; fatigue; weakness; mental status changes (d/t lack of oxygen); nocturia; angina (d/t enlarged myocardium) |
| S/S of left heart failure are caused from | back-up of blood from LA into lungs, causing lung congestionm and decreased oxygenated blood from heart |
| Classifications of heart failure (4) include what limitations? | Class 1: No limitation of physical activity Class 2: Slight limitation; no symptoms at rest Class 3: Slight limitation; no symptoms at rest Class 3: Marked limitation Class 4: Inability to carry on any physical activity without discomfort |
| Avg. CO for a heart failure patient is | 3L |
| Avg. CO for a healthy person is | 5L |
| How would a persons body compensate for heart failure | increased HR, which causes increased CO; LV dialated, which causes hypertrophy |
| How does heart failure effect cardiac reserve? | decreases |
| When heart failure is decompensated what happens? | something i.e cold, flu puts more demand on heart which causes decreased CO which in turn causes renal problems |
| The first compensatory mechanisms for heart failure include | Tachycardia, Dilation, Hypertrophy |
| S/S of pulmonary edema include | sevrere dyspnea,tachycardia, frothy blood-tinged sputum, anxiety, restlessness, S3 |
| Normal Range for pulmonary artery wedge pressure (PAWP) is | 6-12 |
| Where does central venous pressure (CVP) reflect pressure of | right atria |
| For what cases is a pulmonary artery (PA) catheter better for | LV failure; more sensitive so it registers more info |
| How does Dopamine (Intropin) help with heart failure | increased cardiac contractility but doesn't increase oxygen demand *dose related increase's CO by positive intropic effect- selectively dilates renal & mesemteric vessels to increase profusion (1-3 mcg/kg/min) low does = renal and artery vasodialation |
| What are the stages of Cardiogenic shock? | Compensatory stage: reversible, compensatory mechanisms are effective Prgressive stage: compensatory mechanisms becoming ineffective, fail to maintain vitals organs |
| Manifestations of cardiogenic shock compensatory stage includes | NEURO: oriented, restless, agitated, change in LOC CARDIO: extensive vasoconstriction, increased HR RESP: hyperventalation blows off CO2 RENAL: decreased bld. flow causes: increased renin, increased aldosterone, fluid vol. excess, decreased urinary output |
| Manifestations of cardiogenic shock, compensatory stage includes | NEURO: decreased LOC, confusion, lethargy to coma CARDIO: decrease BP, dysrthymias, weak pules, decrease cap. refill, rapid thready HR, intersitital edema RESP: rapid shallow resp, pulmonary edema, acidosis, rales RENAL: oliguria, acidosis, up BUN & CR |
| Standard treatment goals for heart failure include | *eliminate or minimize underlying cause *reduce heart's workload by decreasing preload and afterload *increase cardiac contractility *optimize lifestyle *increase knowledge related to disease and treatment |
| Therapeutic serum digoxin level is | 0.5-2 gm/mL |
| Clinical manifestations of dig. toxicity include | anorexic, decreased HR, nausea |
| Demotropic | effect on conduction velocity of impulse through AV node and myocardium |
| Chronotropic | Effect on heart rate |
| Inoropic | Force on cardiac muscle contraction |
| Negative = Positive= | decrease increase |
| What is the action of ACE inhibitors? why are these useful for the CHF pt? | basodialation, block angiotension & aldosterone, better force of contraction |
| Why is Nesiritide (Natrecor) effective for the CHF pt? | synthetic BNP, peptide vasodialation used for heart failure causes diuresis |
| Other positive Intropc medications include Dobutamine and Milrinone (Primacor). What makes these so effective? | contractility, less oxygen consumption, vasodiatlation |
| AV valves anatomy consist of | annulus, leaflets, chordea tendineae, papillary muscles |
| Semilunar valves anatomy consist of | annulus, leaflets |
| The cardiac cycle consists of | Diastole- relaxation Systole- contraction S1- AV valves shut S2- Semilunar valves shut Murmurs |
| Acquired valvular heart disease patho includes | *ineffective endocardititis/Rheumatic heart disease *Staph/Strep/other organisms/AIDS/Meds *ischemia Large number of organisms enter the bloodstream and infect valves |
| S/S of valvular heart disease includes | *swelling and erosion of valve leaflets *fibrin, leukocytes, platelets, microbes adhere to the valve surface *fibrous thickening of leaflets then calcification |
| Functional alternations caused by valvular heart disease includes | -Stenosis: narrowing of orifice (constriction) impedes blood flow -Regurgitation: incomplete closure of valve causes backward flow of blood |
| Etiology of mitral valve stenosis | rheumatic heart disease, congenital mitral stenosis, rheumatoid arthritis |
| Pathophysiology of mitral valve stenosis | *scarring of valve leaflets & chordea tendoneae *contractions and adhesions develope between commisures (junctional areas) |
| Clinical manifestations of mitral valve stenoiss inlcudes | dyspnea, palpitations, fatigue, increased lt. atrial pressure, pulmonary HTN, RV failure, Lt. atrial hypertrophy, A.fib/A.flutter, Lt. ventricle decreased CO, SV, first heart sound is loud & low-pitched rumbling diastolic sound |
| Etiology of mitral valve regurgitation | MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic, papillary muscle dysfunction |
| Pathophysiology of mitral valve regrgitation | blood flows backward from left ventricle to left atrium d/t incomplete valve closure during systole; left atrium and left ventricle work harder |
| Clinical manifestations of mitral valvlve regurgitation | LV failure, dyspnea, fatigue, mitral regurgitation, weakness, palpations, increased lt. atrial pressure, acute pulmonary edema, papillary muscle rupture, lt. atrium & ventricle dilates & hypertrophies |
| Most common form of valve disease in the US is | mitral valve prolapse |
| Etiology of mitral valve prolapse | unknown |
| Patho of mitral valve prolapse | abnormality of mitral valve leaflets & papillary muscles or chordeae that allows leaflets to prolapse or buckle back into left atrium during systole; mumur from regurgitation that gets more intense through systole |
| Clinical manifestations of mitral valve prolapse include | asystomatic (most), one or more clicks usually heard in midsystole to late systole |
| Mitral valve prolapse causes a risk for | bacteral endocarditis so prophylactic antibiotic therapy is started |
| Etiology of aortic stenosis | rheumatic fever, senile fibrocalcific degeneration |
| Patho of aortic stenosis | fusion of the commisures (junctional areas) & secondary calcification cause the valve leaflets to stiffen and retract, causing stenosis which causes obstruction of flow from left ventricle to aorta during systole |
| Clinical manifestations of aortic stenosis | angina, syncope, exertional dyspnea, increase atrial pressure, pulmonary hypertension, RV failure, Left ventricular hypertophy, decreased CO, SV *can preciptate mycocardial ischemia |
| What medication is contraindicated in aortic stenosis | nitroglycerin bc it decreases preload which is necessary to help open stiffened aortic valvle |
| Etiology of acute aortic regurgitation includes | IE, trauma, aortic dissection, primary disease |
| Etiology of chronic aortic regurgitation includes | rheumatic heart disease, congenital bicuspid aortic valve, syphilis |
| Pathophysiology of aortic regurgitation | retrograde blood flow from ascending aorta into the left ventricle during diastole, resulitng in volume overload |
| Clinical manifestations of aortic regurgitation (general) | increased left atrial pressure, pulmonary HTN, orthopnea, increased RV pressure, RV failure, Lt ventricle hypertrophies, decreased CO, high SV |
| Clinical manifestations of acute aortic regurgitation | SV collapse, severe dyspnea, chest pain, hypotension *EMERGENCY |
| Clinical manifestations of chronic aortic regurtitation | water-hammer pulse, soft/absent S1, S3 or S4, a soft decreased high pitched diastolic murmur, asymptomatic |
| interventions for valvular heart disease includes | antidysrhytmics, anticoagulants, diuretics, digoxin, activity and lifestyle changes, valve repair (annuloplasty, valvuplasty, commisurotomy), valve replacement |
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