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312 Chapter 35
Exam 2
| Question | Answer |
|---|---|
| Heart failure is characterized by... | Ventricular dysfunction reduced exercise tolerance diminished quality of life Shortened life expectancy |
| Primary Acute causes of HF | acute MI; dysrythmias, pulmonary emboli, thyrotoxicosis, hypertensive crisis, rupture of papillary muscle, ventricular septal defect, myocarditis |
| Primary Chronic causes of HF | CAD, HTN, Cor pulmonale, Anemia, Bacterial endocarditis, valvular disorders, congenital heart disease, rheumatic heart disease |
| Primary risk factors for HF | CAD and advancing age |
| Contributory risk factors for HF | HTN, obesiay, diabetes, smoking, high cholesterol, african american descent |
| The major contributing factor of HF | HTN |
| Largest predisposing factor for HF | diabetes |
| HF caused by interference of... | normal mechanisms regulating cardiac output (CO) |
| CO depends on...(5 things) | preload afterload myocardial contractility heart rate (HR) metabolic state of individual |
| Precipitating causes of HF increase... | workload of the ventricals |
| HF classified as.. | systolic failure/dysfunction diastolic failure/dysfunction |
| Features of systolic failure | Most common cause of HF LV loses ability to generate enough pressure to eject blood forward |
| Hallmark of systolic failure | ↓ in LV ejection fraction |
| Features of Diastolic failure | Impaired ability of the ventricles to fill during diastole Usually the result of LV hypertrophy Decreased filling -->decreased stroke volume and CO |
| Diagnosis of diastolic failure based on... | Pulmonary congestion Pulmonary HTN Normal ejection fraction |
| Features of Mixed systolic and diastolic failure | Seen in dilated cardiomyopathy Biventricular failure Patient has extremely poor ejection fractions |
| Compensatory mechanisms of HF | Ventricular dilation Ventricular hypertrophy Increased SNS stimulation Neurohormonal responses |
| One-sided failure eventually leads to... | biventricular failure |
| Most common for of HF | Left-sided failure |
| Features of L-sided HF | Blood backs up through the left atrium into the pulmonary veins-->Pulmonary congestion and edema |
| Most common cause of L-sided HF | HTN |
| What is ejection fraction? | The percentage of total ventricular filling volume that is ejected during each ventricular contraction |
| Diastolic failure primarily seen in... | older adults, primarily women |
| The patient with ventricular failure of any type has... | low systemic arterial BP, low CO, and poor renal perfusion |
| SNS compensatory for low CO | release of epi & noripi-->increased HR and contractility; ok for short term but Over time actually worsens ventricualar performance |
| Neurohormonal response compensatory for low CO (RAAS) | CO falls-->less blood flow to kidneys; sensed by kidney as decreased volume-->release of renin-->angiotensin 1-->angiotensin 2-->adrenal cortex releases aldosterone-->Na & H20 retention-->increased BP |
| Neurohormonal response compensatory for low CO (decreased cerebral profussion) | posterior pitutary secretes ADH-->increased H20 reabsorption in renal tubules-->increased blood volume |
| Endothelin | results in further vasoconstriction-->increase in cardiac contractility and hypertrophy |
| Compensatory dilation | enlargement of heart chambers (LV) elevates-->stretch occurs. effective at first until muscle fibers become overstretched |
| Hypertrophy as compensatory | increases CO but lessens contractility |
| Manifestations of acute decompensated HF | Pulmonary edema |
| Most common cause of pulmonary edema | Acute left ventricular failure secondary to CAD; lungs are engorged and become less compliant-->resistance in airways |
| Clinical manifestations of pulmonary edema | anxious, pale, cyanotic, cold clammy skin, severe dyspnea, use of accessory muscles, RR>30, orthopena, wheezing, coughing, crackles, wheezes, elevated BP |
| Clinical manifestations of HF (both R&L) | fatigue, anxiety, depression, elevated HR (tach) heaves, edema, nocturia, skin changes, |
| Clinical manifestations for R-sided HF | murmers, JVD, edema, weight gain, ascites, anasarca, hepatomegaly, dependent bilateral edema, RUQ pain, anorexia and GI bloating, Nausea |
| Clinical manifestations for L-sided HF | alternating pulses (strong/weak), PMI displaced, low PaO2, low PaCO2, Crackles (pulmonary edema), S3/S4 sounds, pleural effusion, restlessness, confussion, changes in mental status, dypsnea shallow/fast resp, orthopnea, frothy pink speutum, nocturia |
| Complications of HF | pleural effusion, dysrythmias, L ventricualar thrombus, hepatmegaly, renal failure |
| Pleural effusion | pressure from pleural capillaries into pleural space |
| Diagnostics for HF | cardia enzymes, BNP, serum chemistries, liver function studies, ECG, hemodynamics, stress tests, cardiac cath. |
| Ejection Fraction as diagnostic | to differentiate btwn diastolic or systolic HF. measured by ECG or nuclear studies |
| Four core measures for HF | written discharge instructions, LV function assessed, prescription for ace inhibitors as applicable, smoking cessation counciling |
| Nursing/collaborative management | decrease intravascular volume, decrease venous return, decrease afterload, improve gas exchange, improve cardiac function |
| Decrease intravascular volume: meds (management) | loop diruetics (lasix), bumex; acts within kidney and decreases venous rtn to LV-->reduce preload-->overfilled LV-->increased CO: improves gas exchange. Assess for renal function and hemodynamics |
| Decrease intravascular volume: Ultrafiltration (management) | via hemodialysis or central venous access |
| Decrease venous return: manual (management) | venous return (preload) reduces volume returned to LV during diastole: high fowler's and feet horizontal or dangling |
| Decrease venous return: meds (management) | IV nitroglycerin decreased preload and increase coronary artery circulation: reduces preload and afterload and increases O2 to myocardium. Monitor BP every 10-15 minutes |
| Decreaseing afterload: meds (management) | IV sodium nitroprusside (Nipride): potent vasodilator, rapid onset. Alert: rapid rate of IV can reduce BP to quickly, thiocyante toxicity; assess BP prior and during |
| Afterload (def) | the resistance against which the LV must pump; the amount of work the LV has to produce to eject blood into the systemic circulation. |
| Decreasing afterload: more meds (managment) | morphine sulfate: dilates pulmonary and systemic blood vessels-->decreases pulmonary pressure. reduces anxiety and dypsnea |
| Decreasing afterload: more meds | Nesiritide (Natrecor)IV; recombinate form of BNP arterial and venous dilation. increase CO, decrease PAWP, enhance renal profusion. Adverse effect: hypotension: monitor BP |
| Improving gas exchange and oxygenation (managment) | IV morphine, O2, bipap, intubaton, mechanical ventilation |
| improving cardiac function (management) | digitalis inotropic therapy, dopamine, dobutamine(tissue sloughing), epi, norepi, hemodynamic monitoring, PAWP of 14-18 mm Hg, |
| reduce anxiety | benzos, morphine (ease breathing), O2, rest, |
| Other colaborative measures | oxygen therapy, rest, bi ventricular pacing: increase exercise capacity, transplantation, intraaortic ballon pump, VAD's (destination therapy, a bridge to transplantation)up to 2 yrs |
| Diuretics | mobilize fluid, excrete Na and H20, thiazide are 1st choice, loops: lasix, bumex, demadex, spironolactone (aldactyone): potassium sparing (use with caution in hyperkalemia and digoxin, avoid foods high in potassium)combined with ace inhibitors. |
| Vasodilators | Increase venous capacity, decrease heart size, improve ventricular contraction: ACE inhibitors, Nesirtide, Beta blockers |
| Positive inotropes: increase force of contraction & decrease conduction speed | digitalis glycocides for a-flutter and a-fib (digoxin), B-andronergic agonists, calcium sesitizers |
| Signs of digoxin toxicity | visual disturbances, yellow vision, dysrhythmias, premature ventricular beats, atrial fib, 1st degree heart block |
| Angiotensin 2 receptor blockers | Cozaar, diovan prevent vasoconstriction and aldosterone secretion. |
| BilDil | used in African Americans already being treated with standard therapy. antihypertensive agent, relaxes arteries. Side effects: headache and dizziness |
| Nutritional therapy | Na restriction, DASH diet, 2.5g Na diet, refrain from milk, cheese, bread, cereals,canned soup, daily weights, |
| Nursing implementation | Health promotion, acute intervention, ambulatory and home care, |
| Cardiac transplantation | for refractory and end-stage HF, cardiomyopathy and inoperable CAD, understanding of lifestyle changes, based on heart size and ABO type, avoidance of CMV pos/neg crossing, immuniosupressive therapy: prograf, steroids, cyclosporine. biopisies from RV |
| Heartsbreath test | for transplant recipients: measures methalated alkanes; breath into plastic mouthpiece, used in first year following transplantation. |
| Bridge devices for transplant | AB5000, BVS 5000, VAD system |
| Artificial Heart | For short-term survival: CardioWest Total Artificial Heart (no immunosupressive drugs needed), AmioCor implantable replacement heart |
| Ongoing research | stem cells to regenerate heart muscle focusing on cardiomyocytes (contractile cells) and vascular endothelial cells. |
Created by:
daledee
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