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Transcript
Heart Failure heart failure is characterized by inadequate blood flow from the heart .As the heart is unable to provide adequate perfusion of peripheral organs to meet their metabolic requirements Factors contributing to CHF Ischemic Heart Disease Coronary AD: less blood flow to heart, increased damage. Myocardial Infarct: damaged tissue. Hypertension: “overworked” heart. Diabetes. Lung Diseases. Cardiomyopathies: heart muscle disease dilated - enlarged chambers (ventricle/atria) hypertrophic - thickened ventricle walls Abnormal heart valves: inefficient pumping ,causes are genetic, infection or disease. Congenital heart defects: present at birth Severe Anemia Hyperthyroidism Cardiac Arrhythmia. Examples of CHF factors Hypertrophic Cardiomyopathy Congenital Heart Defects Types of Heart Failure include left, right or both sides left ventricular heart failure most common systolic failure: unable to contract diastolic failure: unable to relax right ventricular heart failure usually occurs after left failure less pumping by right side venous pooling of blood in legs Right heart vs. Left heart failure Left Heart failure Pulmonary congestion Reduced forward cardiac output: Fatigue Renal insufficiency Cool extremities Decreased mentation Right Heart failure Neck vein distension Hepatic congestion Peripheral edema Also may result in reduced forward cardiac output, but with clear lung fields Systolic vs. Diastolic Dysfunction Systolic dysfunction Decreased stroke volume Decreased forward cardiac output Almost always associated with diastolic dysfunction as well Diastolic Dysfunction One third of patients with clinical heart failure have normal systolic function – i.e. “pure” diastolic dysfunction The common causes of left-sided failure -Ischemia (old or recent myocardial infarct, ischemic muscle disease) -Aortic stenosis -Mitral valve disease -Systemic hypertension (uncontrolled) Myocardial disease: MI, Myocarditis ....... Specefic clinical symptomes of left-sided failure -Dyspnea (from pulmonary edema and total-body hypoxia) -Cough -Fatigue -Tachycardia -Cold pale skin &may have cynotic extremities. -Hypoxic encephalopathy: diziness, blurred vision &syncope. -Sodium overload and systemic dependent edema (from hypoperfused kidneys: why do you think?) The common causes of right-sided failure: Cardiac causes Pulmonic valve stenosis RV infarction Parenchymal pulmonary causes COPD Cystic fibrosis Pulmonary vascular disease Pulmonary embolism Primary Pulmonary hypertension Specefic clinical symptomes of right-sided failure Edema in lower limb Dyspepsia & anorexia Splanchnic congestion (you'll feel big livers & spleens ) Jugular venous distention Total-body dependent edema (from increased venous hydrostatic pressure, etc.) Effusions (transudates, of course; notably pleural, notably more on the right side than on the left; why?) Impaire d Contrac tility 1. Myoc ardial Infarc tion 2. Trans ie nt myoc ardial is c he mia 3. Chronic Volume ove rload 4. Dilate d Cardiomyopathy Pre s s ure Ove rload 1. Aortic S te nos is 2. Unc ontrolle d hype rte ns ion L.V. Sys tolic dys func tion Left Heart Failure L.V. Diastolic dysfunction 1. Left ventricular hypertrophy 2. Hypertrophic cardiomyopathy 3. Restrictive cardiomyopathy 4. Transient myocardial ischemia Pre s s ure Ove rlo a d 1 . Ao rtic S te no s is 2 . Unc o ntro lle d hype rte ns io n Pathophysiology In HF, the heart dose not provide tissues with adequate blood for metabolic need, and cardiac-related elevation of pulmonary or systemic venous pressures may result in organ congestion In LV failuir: CO decreases and pulmonary venous pressure increases. As pulmonary capillary , pressure exceeds the oncotic pressure of plasma proteins , fluid extravasates from the capillaries into the interstitial space and alveoli, reducing pulmonary compliance and increasing the work of breathing. Lymphatic drainage increases but cannot compensate for the increase in pulmonary fluid. Marked fluid accumulation in alveoli (pulmonary edema) Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli and causing dyspnea decreases and blood pH increases (respiratory alkalosis). respiratory failure. .In RV Failuir: systemic venous pressure increases, causing fluid extravasation and consequent , edema, primarily in dependent tissues (feet and ankles) and abdominal viscera. fluid accumulation in the peritoneal cavity (ascites) can occur. RV failure commonly causes moderate hepatic dysfunction, The impaired liver breaks down less aldosterone, further contributing to fluid accumulation. COMPANSATORY MECHANISM IN HF As the heart fails, the low cardiac output and inadequately filled arteries activate the neurohormonal system leading to: 1- increased sympathetic activity and circulating catecholamines that increase heart rate, and causes vasoconstriction. In addition to increase in endothelin release, (neurohormone secreted primarily by endothelial cells), may exert direct toxic effects on the heart and result in myocardial cell proliferation. N.B. :The effects of baroreceptors in the aortic arch and carotid sinus that normally inhibit undue sympathetic stimulation are blunted in clients with HF, and the effects of the high levels of circulating catecholamines are intensified). 2-activation of the renin–angiotensin aldosterone system which cause: i-Arterial vasoconstriction impairs cardiac function by increase in the resistance (afterload), this increases stretch and stress on the myocardial wall, and predisposes to subendocardial ischemia. N.B.: Patients with severe HF have constricted arterioles in cerebral, myocardial, renal, hepatic, and mesenteric vascular beds. This results in increase organ hypoperfusion and dysfunction. ii-Venous vasoconstriction and increased diastolic ventricular filling pressures (preload) iii-Angiotensin II also promotes sodium and water retention by stimulating aldosterone and the release of vasopressin (antidiuretic hormone) .These increase blood volume and pressure in the heart chambers, stretch muscle fibers, and produce dilation, hypertrophy, and changes in the shape of the heart (cardiac remodeling) that make it contract less efficiently. Overall, the compensatory mechanisms increase preload, workload of the heart, afterload. General Symptoms of CHF shortness of breath blood pooling in pulmonary veins fluid in lungs occurs during activity, rest, or sleeping persistent coughing/wheezing produces white/bloody mucus edema (or excess fluid buildup in body tissues) venous pooling swelling in extremities necrosis Con. : Symptoms of CHF tiredness/fatigue decreased O2 supply diversion of blood supply from limbs lack of appetite/nausea decreased blood supply to digestive tract confusion/impaired thinking increased heart rate baroreceptor reflex SNS output Heart Failure Diagnosis medical history Any symptoms you may have Also,to confirm a heart failure diagnosis: Laboratory blood tests. Chest X-Rays Electrocardiogram (ECG) Treatment Pharmacological Chronic heart failure ACE inhibitors Beta-blockers ATII antagonists aldosterone antagonists digoxin diuretics Acute heart failure diuretics PDE inhibitors vasodilators Non-pharmacological Reduce cardiac work Rest Weight loss low Na+ diet Prototype drugs to know for treatment of heart failure Inotropes: Digoxin, inamrinone, dobutamine, dopamine Diuretics: Hydrochlorothiazide, furosemide, amiloride, spironolactone ACE inhibitors: Captopril, enalapril, lisinopril AGII receptor blockers: Valsartan, losartan Sympatholytics: Carvedilol , Bisoprolol Vasodilators: Glyceryl trinitrate, hydralazine, sodium nitroprusside Cardiac Glycosides derived from plants Strophanus – Ouabain Digitalis lanata - Digoxin, Digitoxin Direct effects -Inhibitor of Na+/K+ ATPase pump -Increased [Na+]I -Increased Ca2+ influx through -Na+/Ca2+ exchangernew -Ca2+ steady-state: increased Ca2+ release during cardiac action potential. Indirect effects -Increased parasympathetic tone -Decreased SA/AV node automaticity -Decreased AV node conduction velocity and increased refractory period Side Effects extremely low therapeutic index . most effects caused by inhibition of Na+/K+ ATPase in extracardiac tissues: CNS: malaise, confusion, depression, vertigo, vision GI: anorexia, nausea, intestinal cramping, diarrhea yellow-tinted vision or yellow corona-like spots Cardiac: bradycardia, arrhythmias anti-digoxin antibody in toxic emergencies Serum Electrolytes affect Toxicity Ca2+ hypercalcemia: increases toxicity K+ digitalis competes for K+ binding site on Na+/K+ ATPase contraindicated with K+ depleting diuretics or patients with hypo/hyperkalemia hypokalemia: increased toxicity hyperkalemia: decrease toxicity Phosphodiesterase Inhibitors primarily used for management of acute heart failure Amrinone (Inocor) and Milrinone (Primacor) -They are inhibitors of phosphodiesterase Increased [cAMP] Increased PKA phosphorylation of Ca2+ channels in cardiac muscle increased cardiac contraction (positive inotropic effects) & relaxes vascular smooth muscle (decrease total peripheral resistance and afterload) Side Effects: sudden death secondary to ventricular arrhythmia, hypotension and thrombocytopenia now only prescribed for acute cardiac decompensation in patients nonresponsive to diuretics or digoxin Direct acting sympathomimetics Dopamine: activates prejunctional D2 dopamine receptors, inhibit NE release of sympathetic nerves, vasodilation activates cardiac β1-adrenergic receptors, increase cardiac output used with furosemide in diuretic resistant patients (volume overload) Dobutamine: racemic mixture, stimulates β1-adrenergic receptors peripheral vasodilation used in patients with low cardiac output and increased left ventricular enddiastolic pressure Side Effects: restlessness tremor headache cerebral hemorrhage cardiac arrhythmias used with caution in patients taking β-blockers β-adrenergic receptor antagonists -Antagonizes β-adrenergic receptors on cardiac myocytes -Counterbalances increased SNS activity in CHF -Prevents development of arrhythmias -Reduces cardiac remodeling -Prevents renin release -Usually given in conjunction with other therapy (ACE inhibitors & Digoxin) -Effective in patients with chronic systolic heart failure in -Prevents remodeling and cardiac damage ACE inhibitors/AT1 receptor antagonists ACE inhibitors -Inhibits angiotensin converting enzyme (ACE) -Prevents conversion of ATI to ATII -Slows progression of left ventricular dysfunction in CHF AT1 receptor antagonists -Selectively inhibits ATI receptor activation. -More effective then ACE inhibitors -AT2 receptors still active: vasodilation, antiproliferative effects -Used in conjunction with ACE inhibitors for increased effectiveness Both classes are drugs of choice in heart failure •decreased preload •decreased afterload •decreased cardiac remodeling •decreased SNS effects •Side Effects: Cough , angioneurotic edema (with ACEI), hypotension & hyperkalemia ACE inhibitors and ATI receptor antagonists are both teratogenic Vasodilators Reduce TPR without ,reduce preload & reduce afterload Nitroglycerin acute ischemia or acute heart failure orally active also administered I.V. for peripheral vasodilation quick onset for acute relief Isosorbide dinitrate/hydralazine chronic administration for long-term symptom relief administered I.V. Nesiritide recombinant brain-natriuretic peptide (BNP) BNP is secreted from ventricular myocytes in response to stretch vasodilator: increases cGMP in SMCs decrease afterload/preload inhibits cardiac remodelling suppresses aldosterone secretion administered IV for acute decompensated CHF adverse effects: hypotension, renal failure. Diuretics used in CHF to reduce extracellular fluid volume primarily used in patients with acute CHF with volume overload IV infusion causes immediate and predictable diuresis for immediate relief Goal: reduce preload/afterload overdosing can result in excessive reduction in preload, overreduction in stroke volume thiazide and loop diuretics (i.e. Furosemide) commonly used as adjunct therapies in CHF Aldosterone Antagonists elevated AngII levels increase production of aldosterone in the adrenal cortex (~20X increase) aldosterone activates mineralocorticoid receptors in renal epithelial cells in kidney aldosterone promotes Na+ retention, Mg2+ and K+ loss increased SNS activity decreased PSNS activity , myocardial/vascular fibrosis. aldosterone receptor antagonists: Spironolactone & eplerenone both antagonists reduce mortality in patients with moderate to severe CHF only use in patients with normal renal function and K+ levels use with K+ sparing diuretic. Hyperkalemia , Agranulocytosis, Hepatoxicity , Renal failure Spironolactone: gynecomastia, sexual dysfunction Eplerenone: arrhythmia, myocardial infarct/ischemia