Скачать презентацию Heart Failure J B Handler M D Physician Скачать презентацию Heart Failure J B Handler M D Physician

e384ad46a1bc6ffcca1964e16698d7c5.ppt

  • Количество слайдов: 52

Heart Failure J. B. Handler, M. D. Physician Assistant Program University of New England Heart Failure J. B. Handler, M. D. Physician Assistant Program University of New England 1

Abbreviations n n n CO- cardiac output PCW- pulmonary capillary wedge SVR- systemic vascular Abbreviations n n n CO- cardiac output PCW- pulmonary capillary wedge SVR- systemic vascular resistance SVR PVR (peripheral vascular resistance) HR- heart rate JVD- jugular venous distension A+V- arterial and venous C- cardiac EF- ejection fraction ED- emergency department LHF- left heart failure BVF- biventricular failure n n n n n P- Pulmonary ACEI- angiotensin converting enzyme inhibitor ARB- angiotensin receptor blocker NYHA- New York Heart Association criterion BNP- beta natiuretic peptide MVO 2 - myocardial oxygen consumption ICD- implantable cardioverter defibrillator RHF- right heart failure CRT- cardiac resynchronization therapy 2

Heart Failure: Definition n A pathophysiologic state in which an abnormality of cardiac function Heart Failure: Definition n A pathophysiologic state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues and/or can do so only from an abnormally elevated diastolic volume/pressure. 3

Heart Failure Basics Over 5 million patients in U. S. with HF n 550, Heart Failure Basics Over 5 million patients in U. S. with HF n 550, 000 patients newly diagnosed each year n > 1 million hospitalizations/yr- HF as 1 st Dx; >2. 5 hospitalizations- HF among Dx. n number of HF deaths in spite of advances in Rx: n – Increased salvage of patients with acute MI – Numbers are rising as “baby boomers” age n Management must be individualized 4

Etiologies of Heart Failure (HF) Coronary Heart Disease: MI(s) or ischemia superimposed on prior Etiologies of Heart Failure (HF) Coronary Heart Disease: MI(s) or ischemia superimposed on prior infarction(s) 75% of all cases. n Primary pump failure - Cardiomyopathy, viral myocarditis n Valvular heart disease n Congenital heart disease n Long standing, uncontrolled hypertension n 5

Precipating Causes n n n n Progressive weakening of the myocardium and consequences heart Precipating Causes n n n n Progressive weakening of the myocardium and consequences heart failure Infection Anemia Thyrotoxicosis Arrhythmias Aggravation of hypertension Myocardial ischemia or infarction Physical, dietary (Na/fluid) or emotional excesses 6

HF: Systolic or Diastolic? n n n Systolic Failure (or dysfunction): Primary contraction abnormality; HF: Systolic or Diastolic? n n n Systolic Failure (or dysfunction): Primary contraction abnormality; inadequate delivery of O 2 to tissues and associated symptoms; e. g: large or multiple MI(s), dilated cardiomyopathy, chronic AR, MR. Diastolic Failure (or dysfunction) - Impaired ventricular relaxation- elevation of ventricular filling pressures and associated symptoms; e. g: long standing hypertension (with LVH), hypertrophic cardiomyopathy, acute ischemia, prior infarcts, restrictive cardiomyopathy. Systolic and diastolic failure often occur together. 7

HF: Acute or Chronic? n n n Acute - Large MI sudden onset of HF: Acute or Chronic? n n n Acute - Large MI sudden onset of symptoms, systolic failure, hypotension, pulmonary edema. Chronic - pathophysiology and symptoms develop slowly, BP usually maintained until late in course; peripheral edema common; e. g: dilated cardiomyopathy, chronic valvular insufficiency, large or multiple infarcts. Acute episodes may be superimposed on chronic HF development of pulmonary edema in patient with previously compensated (treated) HF. 8

HF: Rt Sided or Lt Sided? Lt sided failure e. g: post MI, aortic/mitral HF: Rt Sided or Lt Sided? Lt sided failure e. g: post MI, aortic/mitral valve disease. Inadequate CO with pulmonary congestion and related symptoms. n Rt. sided failure e. g: COPD/pulmonary hypertension, pulmonic stenosis; associated with peripheral edema, hepatic congestion, etc. n Most common cause of right sided failure is left sided failure/dysfunction! n 9

Cardiac Pressures 4 -12 8 -15 4 -12 Images. google. com Cardiac Pressures 4 -12 8 -15 4 -12 Images. google. com

HF: Backward or Forward? Backward failure: Inadequate ventricular emptying; pressures in the atrium and HF: Backward or Forward? Backward failure: Inadequate ventricular emptying; pressures in the atrium and venous system behind the failing ventricle rise resulting in transudation of fluid into interstitial spaces. n Forward failure: Inadequate forward CO; Na and water retention result from diminished renal perfusion and activation of renin-angiotensinaldosterone system. n 11

Compensatory Mechanisms n n Redistribution of CO: Blood flow redistributed to vital organs- brain Compensatory Mechanisms n n Redistribution of CO: Blood flow redistributed to vital organs- brain and myocardium with reduced blood flow to skin and muscle mediated via activation of the adrenergic nervous system and vasoconstriction to less vital tissues. Na and water retention: Complex sequence of adjustments occurs resulting in accumulation of fluid and increasing SVR: – Helps maintain CO via Starling mechanism – Cost is volume overload and afterload. 12

Adrenergic Nervous System n n n Activated in CHF-beneficial and harmful. Increase levels of Adrenergic Nervous System n n n Activated in CHF-beneficial and harmful. Increase levels of norepinephrine result in increase HR, contractility and SVR- helps maintain arterial perfusion pressure (BP) in presence of decreased CO. Elevation of SVR results in increased hemodynamic burden (afterload) and O 2 requirement of the failing ventricle. Long term elevation of catecholamines lead to progressive myocardial damage and fibrosis. BP = CO x SVR CO = BP/SVR 13

Renin-Angiotensin System n n Renin: enzyme released by kidneys if perfusion or BP. Angiotensinogen Renin-Angiotensin System n n Renin: enzyme released by kidneys if perfusion or BP. Angiotensinogen (renin substrate) converted to Angiotensin I by renin. Angiotensin I converted to Angiotensin II in lungs by angiotensin converting enzyme. Angiotensin II – extremely potent vasoconstrictor- leads to arteriolar constriction and increase in SVR, raising BP. 14

Renin-Angiotensin System n n Angiotensin II stimulates adrenal gland to secrete Aldosterone a mineralocorticoid Renin-Angiotensin System n n Angiotensin II stimulates adrenal gland to secrete Aldosterone a mineralocorticoid hormone increases renal Na and H 2 O reabsorption. Renin-angiotensin-aldosterone activation (by decreased cardiac output) in heart failure is a major factor in edema formation and increased SVR. Long term activation of angiotensin II and aldosterone lead to myocardial thinning and fibrosis (remodeling). 15

Functional Classification of Heart Disease: NYHA Criterion n n I: No limitation of physical Functional Classification of Heart Disease: NYHA Criterion n n I: No limitation of physical activity. No symptoms of SOB, CP dizzyness, etc. II: Slight limitation of physical activity. Some (ordinary) activities (exercise, exertion, etc) cause symptoms. III: Marked limitation of physical activity. Less than ordinary activities (walking, dressing, etc. ) cause symptoms. IV: Symptomatic at rest or minimal activity; unable to engage in any physical activity. 16

Clinical Manifestation of HF n n Dyspnea: Initially with activity, then at rest; due Clinical Manifestation of HF n n Dyspnea: Initially with activity, then at rest; due to elevation of pulmonary venous pressure. Orthopnea: Dyspnea in recumbent position; redistribution of fluid from abdomen and lower extremities into chest. Paroxysmal Nocturnal Dyspnea: Attacks of severe SOB, coughing and wheezing awakening patient from sleep. Unexplained weight gain: Sodium and water retention. Patients may note swelling of the legs. – Nocturia commonly occurs 17

n n n Fatigue, weakness, abdominal symptoms, decreased exercise capacity; reflects CO to muscles, n n n Fatigue, weakness, abdominal symptoms, decreased exercise capacity; reflects CO to muscles, GI tract and other organs. Cerebral symptoms (esp. in patients with coexisting cerebrovascular disease): Decreased perfusion to brain. Acute Pulmonary Edema : Severe dyspnea at rest as pulmonary congestion progresses; accompanied by marked elevation of pulmonary capillary pressure leading to alveolar edema; *PCW >20 interstitial edema; PCW > 25 alveolar edema. A medical emergency usually addressed in ED. *PCW: Pulmonary Capillary Wedge pressure 18

Physical Exam (L+R sided HF) n n Symptoms vary depending on severity. Patient may Physical Exam (L+R sided HF) n n Symptoms vary depending on severity. Patient may be uncomfortable lying flat; BP normal or low; tachycardia common. Cyanosis of lips & nailbeds reflects hypoxemia. Crackles (Rales- older term)- moist inspiratory crackles; wheezes. Begin at bases and progress upwards through the lungs. S 3 gallop- low pitched sound in early diastole. 19

Physical Exam (L+R sided HF) Increased systemic venous pressure; JVD reflects JVP. n + Physical Exam (L+R sided HF) Increased systemic venous pressure; JVD reflects JVP. n + Hepato-Jugular Reflux. n Congestive hepatomegaly- enlarged, tender, pulsatile liver. n 20

Physical Exam Peripheral edema develops with progressive HF. n Hydrothorax and ascites- pleural effusions. Physical Exam Peripheral edema develops with progressive HF. n Hydrothorax and ascites- pleural effusions. n Cardiac cachexia- “Wasted appearance” occurs with severe chronic heart failure weight loss, anorexia, nausea; correlates with increased levels of cytokines like circulating tumor necrosis factor. n 21

Additional Findings Cx. R: Cardiomegaly; distension of pulmonary veins; venous redistribution to apices; interstitial Additional Findings Cx. R: Cardiomegaly; distension of pulmonary veins; venous redistribution to apices; interstitial alveolar edema; pleural effusions. n Echo-Doppler- findings unique to pathology responsible for HF; best non-invasive tool. Identifies ventricular dysfunction and EF. n ECG- may reflect underlying pathology i. e. infarct, LVH, arrhythmia, etc. n 22

n Cx. R: CHF n Cx. R: CHF

 -type Natriuretic Peptide n n n NP- hormone produced by heart (ventricle) in -type Natriuretic Peptide n n n NP- hormone produced by heart (ventricle) in response to wall stress- marker of decompensated heart failure in blood. Blood test for acute ventricular dysfunction symptomatic heart failure Useful in diagnosis of HF in patients presenting with SOB of uncertain (C vs P) etiology and confirming HF when suspected clinically. Has vasodilator (a&v) and diuretic properties- new Rx for treating refractory heart failure (below). Normal is < 100 pg/ml 24

Pathophysiologic Basis of Therapy Taylor treatment to the manifestations of heart failure in each Pathophysiologic Basis of Therapy Taylor treatment to the manifestations of heart failure in each individual patient. n Excessive increase in preload: diuretics, venodilators (nitrates). n Excess Na retention with edema: diuretics. n Increased afterload: Vasodilator therapy n – ACE inhibitors, Angiotensin Receptor blockers and others. 25

Pathophysiologic Basis of Therapy n n Myocardial systolic failure -Rx. to improve contractility- Digoxin; Pathophysiologic Basis of Therapy n n Myocardial systolic failure -Rx. to improve contractility- Digoxin; sympathomimetics. Slow progression of cardiac deterioration. ACE inhibitors Beta blockers Prevent Remodeling Spironolactone Improve diastolic dysfunction if possible: regression of LVH with treatment of co-existing HTN Treat arrhythmias as needed 26

Mortality in Heart Failure Overall poor prognosis once symptomatic n Severe failure (class IV)- Mortality in Heart Failure Overall poor prognosis once symptomatic n Severe failure (class IV)- 40 -50% mortality in 12 months n Moderate failure (class III)- 40 -50% mortality in 3 -4 yrs n Ejection Fraction (EF) is predictive n 30 -40% die suddenly- arrhythmia. n 27

HF: Goals of Therapy n n Removal of precipitating factors. Treatment of underlying cause HF: Goals of Therapy n n Removal of precipitating factors. Treatment of underlying cause active ischemia, valvular disease, cardiomyopathy, etc. Control of the HF state: Reduction of cardiac workload Control of excessive Na/water retention Enhancement of cardiac contractility Early initiation of ACEI therapy for most patients – Hydralazine and nitrates in black populations; added to ACEI if needed. 28

Treatment of HF Reduction of cardiac workload – decreased/limited activity; elastic stockings, anxiolytic therapy; Treatment of HF Reduction of cardiac workload – decreased/limited activity; elastic stockings, anxiolytic therapy; anticoagulation for prolonged bed rest. n Control excessive dietary sodium (4 gram Na diet or less). n – No added salt; no salt in preparation of foods; avoid foods with high sodium content. 29

Diuretics Early addition of diuretics beneficial in relieving symptoms (shortness of breath) and reducing Diuretics Early addition of diuretics beneficial in relieving symptoms (shortness of breath) and reducing preload- does not mortality. n Loop diuretics: Most potent diuretics and cornerstone of diuretic Rx in CHFFurosemide, Bumetanide, Torsemide n – Metolazone - similar to thiazide diuretics; added to and potentiate loop diuretics in severe, refractory heart failure; caution K 30

Diuretics n n Loop diuretics remain effective in renal failure. Must monitor renal function Diuretics n n Loop diuretics remain effective in renal failure. Must monitor renal function (BUN, Cr. ) serum electrolytes (esp. K), uric acid and glucose; loop diuretics can cause hypokalemia, and hyperuricemia as well as metabolic alkalosis. Over aggressive diuresis can lead to pre-renal azotemia impaired renal fx from hypovolemia and perfusion. Triamterene and Amiloride are weak diuretics that are K sparing - elevate K levels; may be used in combination with loop diuretics to offset K losses 31

Vasodilator Therapy in HF n n n LV afterload always elevated in HF due Vasodilator Therapy in HF n n n LV afterload always elevated in HF due to neural and humoral influences that act to constrict the peripheral vascular bed and elevate SVR; preload also increased from Na/H 20 retention. In presence of impaired cardiac function, increasing afterload will reduce cardiac output further and lead to elevation of pulmonary pressures and pulmonary congestion. In patients with acute and chronic HF, treatment with vasodilators results in: decreasing SVR, increasing CO, decreasing PCW, and relief of symptoms; also decreases mortality. 32

Angiotensin Converting Enzyme Inhibitors Activation of the Renin-Angiotensin-Aldosterone system in heart failure results in Angiotensin Converting Enzyme Inhibitors Activation of the Renin-Angiotensin-Aldosterone system in heart failure results in marked vasoconstriction via Angiotensin II and Na and H 2 O retention via Aldosterone. n ACE Inhibitors dramatically reduce afterload, and to a lesser degree, preload in patients with HF by ing the production of Angiotensin II and aldosterone. n CO= BP/SVR n 33

ACE Inhibitors Superior to all other treatment of HF in terms of long-term symptomatic ACE Inhibitors Superior to all other treatment of HF in terms of long-term symptomatic improvement and outcome - Reduce mortality by >25+%. n Long term ACEI has significant natriuretic effects resulting in improved diuresis. n Captopril, enalapril, lisinopril, ramipril, fosinopril, perindopril et al; all equally beneficial. n 34

ACE Inhibitors ACEI decrease remodeling of the LV post MI and in HF by ACE Inhibitors ACEI decrease remodeling of the LV post MI and in HF by reducing wall thinning, fibrosis and interfering with programmed cell death (apoptosis) result is mortality. n Elevation of kinins from ACE inhibition may also have beneficial effects on hemodynamics (vasodilation) and remodeling – increased levels of prostaglandins and nitric oxide – vasodilation. n 35

LV Remodeling NYer. RN LV Remodeling NYer. RN

Limitations of ACEI n n n Fall in systemic BP. ACEI usually well tolerated Limitations of ACEI n n n Fall in systemic BP. ACEI usually well tolerated if initiate with low dose and gradually increase. Cough- Drug related persistent cough resulting from elevated bradykinin levels; occurs in up to 15 -20% of patients, but only 5% need to DC the drug. Less effective in black populations. Hydralazine + long acting nitrates are added to ACEI prn. – Bi. Dil: Hydralazine + isosorbide dinitrate n Must monitor renal function; Cr and BUN often increase mildly (and expectedly) with ACEI. 37

Angiotensin II Receptor Blockers n n n Released and FDA approved for hypertension. Inhibit Angiotensin II Receptor Blockers n n n Released and FDA approved for hypertension. Inhibit angiotensin II receptor - reduce SVR, BP and afterload. Similar hemodynamic effects to ACEI. Do not increase bradykinen- no cough but less protection against remodeling. Useful as an alternative to ACEI (if pt intolerant); sometimes added to ACEI for severe HF. Comparison studies: ARB vs ACEI have demonstrated ACEI superiority in most large clinical trials. 38

Beta-Blocker Therapy Previously contraindicated in treating HF. n Now proven that -blockers are not Beta-Blocker Therapy Previously contraindicated in treating HF. n Now proven that -blockers are not only useful in treating HF, but reduce mortality as well as improve cardiac function and symptoms. n Multiple clinical trials using carvedilol, metoprolol and bisoprolol (MERIT et al). n Begin once patient stable and euvolemic; for chronic heart failure. n 39

Beta-Blocker Therapy n n Likely that chronic elevations of catecholamines and sympathetic nervous system Beta-Blocker Therapy n n Likely that chronic elevations of catecholamines and sympathetic nervous system activity cause progressive myocardial damage, fibrosis and dysfunction abnormal remodeling. Beneficial for all classes of heart failure with up to 30% decrease in mortality. Must begin with very low doses and gradually increase e. g carvedilol 3. 125 mgs b. i. d. Unclear if all -blockers are alike for HF. Carvedilol may be drug of choice because of its combined and blocking effects. 40

Aldosterone Antagonists Spironolactone: Competitive inhibitor of aldosterone; has mild diuretic properties and elevates K Aldosterone Antagonists Spironolactone: Competitive inhibitor of aldosterone; has mild diuretic properties and elevates K (often used in combination with loop diuretics which can cause hypokalemia). n In low dose (12. 5 -25 mgs/daily) spironolactone has been shown to decrease morbidity and mortality in patients with severe heart failure. n Has anti-androgenic properties. n Must monitor serum K to avoid hyperkalemia. n 41

Actions of Spironolactone n n Aldosterone mediates some of the deleterious effects of renin-angiotensin-aldosterone Actions of Spironolactone n n Aldosterone mediates some of the deleterious effects of renin-angiotensin-aldosterone system activation, such as myocardial remodeling and fibrosis. By blocking aldosterone, spironolactone should be considered as a neurohormonal antagonist rather than narrowly as a K sparing diuretic. Clinical trials (RALES et al) show 29% reduction in mortality in NYHA class III and IV patients. Eplerenone- released in 2003; aldosterone antagonist without anti-androgenic properties. 42

Aldosterone Blockade Post MI n Spironolactone and eplerenone post MI reduce morbidity and mortality Aldosterone Blockade Post MI n Spironolactone and eplerenone post MI reduce morbidity and mortality in patients with LV dysfunction/heart failure. – Mineralocorticoid blockade prevents remodeling, blocks collagen production, improves EF and decreases LV dilatation. n n Adjunct Rx to ACEI. Should be considered early in Rx of patients with large MI/LV dysfunction and heart failure. Must monitor K closely 43

Enhancement of Contractility Digitalis Glycosides - Digoxin most commonly used; only oral inotropic agent Enhancement of Contractility Digitalis Glycosides - Digoxin most commonly used; only oral inotropic agent available; improves cardiac contractility. n Increases automaticity of cardiac electrical tissue - can induce arrhythmias. n 44

Digoxin n n Prolongs refractory period of AV node (vagal tone increased): slows rate Digoxin n n Prolongs refractory period of AV node (vagal tone increased): slows rate of Atrial fibrillation and flutter. Modest improvement in cardiac function in patients with LV dilatation and dysfunction. Falling out of favor for Rx of CHF; improves symptom but not mortality. Low Therapeutic/Toxic index- toxicity includes N, V, arrhythmias (PVC’s, atrial tachycardia) and 2 nd/3 rd degree A-V block. 45

Sympathomimmetic Amines n n n Indication: refractory HF. Must be given (short term) by Sympathomimmetic Amines n n n Indication: refractory HF. Must be given (short term) by continuous IV infusion in a hospitalized setting, preferably with invasive hemodynamic monitoring (rt. heart catheter). Dobutamine: Potent inotrope- stimulates Beta receptors, raises CO. Dopamine: Low dose-dilates renal and mesenteric blood vessels via Dopaminergic receptors Moderate dose- Stimulates B receptors High dose- Stimulates Alpha receptors. 46

Phosphodiesterase Inhibitors Indication: refractory HF. Improve cardiac contractility by inhibiting myocardial phosphodiesterase. n Potent Phosphodiesterase Inhibitors Indication: refractory HF. Improve cardiac contractility by inhibiting myocardial phosphodiesterase. n Potent inotropes administered IV for short term use. n Amrinone, Milrinone. n Trials using these and other newer inotropes orally for long term use have all demonstrated substantial increase in mortality. n 47

Nesiritide New- recombinant form of beta natriuretic peptide (BNP). Indication: refractory HF. n Potent Nesiritide New- recombinant form of beta natriuretic peptide (BNP). Indication: refractory HF. n Potent vasodilator (venous>arteriolar); decreases LV filling pressures (pre-load) and SVR (afterload); improves cardiac output. n Must monitor renal function- renal failure occurs. n Continuous IV infusion following a bolus. n May have diuretic effects in some individuals. n 48

Biventricular Pacing and ICD’s n n Abnormal IVCD results in dyssynchronous contraction. If QRS Biventricular Pacing and ICD’s n n Abnormal IVCD results in dyssynchronous contraction. If QRS > 120 ms and severe refractory CHF, synchronized biventricular pacing (CRT*) improves symptoms and quality of life; may decrease mortality. ICD decrease mortality in patients with LV dysfunction and symptoms of HF. Indications for ICD: – Secondary: Rescusitated cardiac arrest/Vfib or hemodynamically unstable Vtach – Primary: EF . 35 + mild to moderate HF symptoms n CRT-D’s address resynchronization pacing + ICD *CRT: cardiac resynchronization therapy 49

End-Stage Heart Failure n n n HF unresponsive to intensive medical Rx. LV assist End-Stage Heart Failure n n n HF unresponsive to intensive medical Rx. LV assist devices: Implantable assist device (pump) connected to external power supply. Decrease workload of native heart and buy time (“bridge”) to heart transplant. Allow mobility and discharge from hospital to await transplant. Heart may improve over time. Complications: Bleeding, infections, thromboembolism. Very expensive: $2 -300, 000 for up to 3 months. 50

Cardiac Transplantation n n Widely used. Problem: Not enough donor hearts. Living donor heart Cardiac Transplantation n n Widely used. Problem: Not enough donor hearts. Living donor heart replaces failing one. Improved immunosuppressive drugs yield 70% or greater 5 year survival with excellent quality of life. High cost- $200, 000 initially +$$$ Complications: – Rejection, infections, accelerated CHD in donor coronary arteries. – Immunospuppressive related cancers 51

Acute Pulmonary Edema n n Medical emergency Treatment modalities may include: – Morphine sulfate- Acute Pulmonary Edema n n Medical emergency Treatment modalities may include: – Morphine sulfate- reflex withdrawal of sympathetic tone; decreases anxiety – O 2 – IV loop diuretics - promote diuresis and have direct venodilator activity. – Afterload reduction: IV Nitroprusside – IV Inotropes -Dobutamine – Preload reduction- Nitrates – Invasive hemodynamic monitoring improves management. 52