1 / 33

Heart Failure Chapter 19

Heart Failure Chapter 19. Hear Failure. Complex clinical syndrome ventricles don’t work properly not enough blood pumped to support body’s needs manifestations dyspnea (breathlessness) fatigue fluid retention -> pulmonary congestion/peripheral edema. Hear Failure continued.

eshana
Download Presentation

Heart Failure Chapter 19

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Heart Failure Chapter 19

  2. Hear Failure • Complex clinical syndrome • ventricles don’t work properly • not enough blood pumped to support body’s needs • manifestations • dyspnea (breathlessness) • fatigue • fluid retention -> pulmonary congestion/peripheral edema

  3. Hear Failure continued • ~ 5 million have HF • #1 discharge diagnosis in medicare population • high mortality - 30% to 50% dead within one year, 80% with in 5 years • mortality rates improved with ACEI and B-blockers

  4. Low vs. High Output failure • Table 19-1 • in both types, heart cannot provide adequate tissue perfussion • low is much more common (> 90%) • Low means the heart is weakened • High out put means healthy heart but because of high metabolic demand (eg.hyperthyroidism, anemia) heart cannot keep up

  5. Left vs. Right Ventricular dysfunction • Left more common than right • may have both sided HF • Pulmonary arterial hypertension (PAH) right sided failure • increased pulmonary pressures increases right ventricle workload • can be drug induced -heroin, IV ritalin, redux • Cor pulmonale -COPD causing PAH and right sided HF

  6. Systolic vs. Diastolic dysfunction(both components of LVD) • Systolic -LVEF -<40% (NL 60-70%) • Diastolic - LVEF > 40% to 45% • volume is reduced but high fraction is ejected • Digoxin can worsen HF • B-blockers help

  7. Cardiac Workload (PRELOAD) • Refers to venous side of circulation • if elevated can aggravate HF • eg. Sodium load can increase preload • aortic stenosis can cause regurgitation of blood back to ventricle -> increase volume of blood

  8. Cardiac Workload (Afterload) • Tension in ventricular wall as systole (contraction) occurs • affected by intraventricular pressure, ventricular diameter and wall thickness • SVR (systemic vascular resistance) pressure against which the ventricle must pump (chiefly determined by arterial blood pressure) • hypertension, atherosclerosis increase afterload • 75% of HF pts have history of hypertension

  9. Cardiac contractility, AKA inotropic state • describe cardiac muscle ability to develop force and/or shorten its fibers • contractility decreases when myocardial fibers are diminished or poorly functioning (eg post MI, CAD)

  10. Pathogenesis of HF • Figure 19-1 • “remodeling” = cardiac hypertrophy • body’s response to decreased cardiac output is to release sympathetic catecholamines such as norepinephrine (NE) • NE increases contractility (intropy) and increases heart rate (chronotropy) • This increases CO, however, eventually increases workload and heart can’t keep up

  11. Pathogenesis continued • NE also cause vasoconstriction and decreased perfusion to skin, GI tract, and renal circulation, this cause increases SVR • NE also decreases sodium excretion by kidneys, restricted ability of coronary arteries to supply blood to ventricular wall, increase automaticity of cardiac tissue(increase arrhythmia), hypokalemia

  12. Renal Function • When CO decreases and vasoconstriction occurs, renal blood flow decreases -> then Na + water retention -> increase blood volume • As GFR decreases more Na reabsorbed • ADH (antidiuretic hormone) also released from pituitary • Renin is released, see fig. 19-1, angiotensin II causes coronary remodeling, aldosterone causes fibrosis in atria and ventricles (fig. 19-2)

  13. Natriuretic Peptides (cardiac Neurohormones) • A-type - secreted by atrial myocardium • B-type - produced by ventricles when increased pressure and volume • antagonize renin-angiotensin, inhibits sympathetic outflow, vasodilation, decreased preload, decreased afterload, diuretic properties • plasma levels of BNP - biologic marker for presence and severity of HF, when > 200 helps to differentiate from chronic bronchitis, pneumonia etc.

  14. Classifying HF • Table 19-3 • Important to monitor pt, some drugs are added when function decreases, certain drugs contraindicated by class (EG glitazones not for use in NYHA class III and IV) • studies may exclude class I and II or class III and IV and this gives idea bout pt types.

  15. Classifying HF continued • Objective to go from higher to lower class • III to II • Keep someone at lower class from progressing • I to II

  16. Treatment Principles • ACC/AHA routinely use 1) diuretic 2) ACEI 3) B-blocker 4) +/- digoxin 5) aldosterone antagonist (advanced disease) • no treatment is curative (only transplant can cure) • need to address risk factors (hypertension, ischemic heart disease, lipid disorders, anemia, hyperthyroidism

  17. Treatment Principles continued • immunize with influenza and pneumococcol vaccine, discontinue drugs which may harm condition, encourage physical activity • Na restricted diet and diuretics for fluid retention • Amiodarone- treatment for ventricular tachycardia and atrial fibrillation

  18. Sodium • Human body requires <1 gram Na/day to function • U.S. diet ~ 10grams/day • No evidence that Na restriction in normotensive or asymptomatic patients will prevent HF • However, if have hypertension/edema then salt restriction is prudent • 1 teaspoon salt is about 2 grams sodium • salt restriction may help diuretics to work better • decreased blood volume & decrease Na to retain • Eliminate cooking salt decreases intake to about 2-4 grams /day

  19. Diuretics • Provide symptomatic relief more rapidly than other drugs • Indicated for pulmonary and peripheral edema - decrease vascular volume • will activate RAAs (renin-angiotensin-aldosterone system) • which will make HF worse so, need to add ACEI/B-blocker • Goal- decrease excess vascular volume while not overdiuresing (dehydration) and then maintain balance

  20. Diuretics continued • Overdiurese-intravascular volume depletion, hypotension, decrease CO (not enough fluid to push around) • weight loss > 1 kg /day to be avoided unless pulmonary edema • diuretic effect depends on Na delivered to kidney, so if renal blood flow compromised (kidneys not working well, kidney disease) diuretics can’t work

  21. Diuretics continued • Thiazides - stop working @ CRCL <50-30 ml/min • Loops - will work till Crcl < 5ml/min • also has vasodilating properties • IV loop - 10 minute onset, 30 minute peak, lasts ~ 2 hours • oral loop - 30 - 90 minutes onset, 1-2 hour peak, lasts ~ 6-8 hours • Dosing Table 19-4 • “Ceiling”dose - beyond a certain dose, at one time may not improve effect, may be better to use more frequent doses

  22. Diuretics continued • Aldosterone antagonists • mild diuretic, effectiveness in HF probably related to aldosterone inhibition

  23. ACEI/AFBs • Arterial dilators - • decrease afterload • Venous dilators • decrease preload • This concept similar to earlier modality: hydralazine (arterial dilator) and nitrate (venous dilator), (hydral-Nit)

  24. ACEI/ARBs continued • ACEI/ARB also decrease cardiac remodeling and are more tolerable and decrease mortality more than hydral-Nit combo.

  25. ACEI/ARBs continued • ARBs candesartan (atacand), eprosartan (tevetan), irbesartan (avapro), losartan (cozaar), olmesartan (benicar), telmisartan (micardis), valsartan (diovan) • Specific to angiotensin II blockade and decreased risk of cough • reserved for ACEI failures (cough, angioedema?) or during pregnancy

  26. B-Blcokers • Used to be contraindicated in HF • Now, should be used in all pts with mild to moderate symptoms unless contraindiction • come pts can have temporary worsening of symptoms when started. But when continued - increase QOL, decrease hospitalization, increase survival

  27. Digoxin • Binds and inhibits Na-K+ ATPase in cardiac cells, this decrease outward Na transport and increases intracellular calcium. Ca++ binds to sarcoplasmic reticulum and increases contractile state of heart • increases contraction ( + inotrope) • also decreases sympathetic tone and indirectly suppresses renin

  28. Digoxin continued • also, prolongs refractory period of AV node • slows ventricular response rate • At high level - digoxin increases automaticity and irritability and can have rhythm disturbance. • Monotherapy with digoxin - not recommended • Digoxin PK - table 19-5

  29. Other Agents • Hydralazine/Nitrate combo • secondary agents • CCB- decrease afterload but also are negative inotrope • only amlodipine and felodipine don’t make HF worse.

  30. Heart Failure • Complex clinical syndrome • ventricles don’t work properly • not enough blood pumped to support the body’s needs • Manifestations • dyspnea • fatigue • fluid retention -> pulmonary congestion/ peripheral edema

  31. Heart Failure • ~ 5million have heart failure • #1 discharge diagnosis in medicare population • high mortality -

More Related