Cardiac heart failure

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Cardiac heart failure

  1. 1. CARDIAC HEART FAILURE By M.MAHITHA
  2. 2. DEFINITION Heart failure is a clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body. Heart failure can result from any disorder that reduces ventricular filling (diastolic dysfunction) and/or myocardial contractility (systolic dysfunction).
  3. 3. Epidemiology  The incidence: 1 in 1000 population per year; increasing by about 10% every year. In >85y incidence is 10 cases per 1000.  The prevalence ranges from 3-20 cases per 1000 population, increasing to at least 80 cases per 1000 in people aged 75 years and over.  The male to female ratio is about 2:1.  The median age of presentation is 76 years.
  4. 4. Etiology INTRINSIC PUMP FAILURE :The important cause of heart failure is the weakening of ventricular muscle due to disease so that the heart fails to act as an efficient pump  Ischaemic heart disease (35-40%)  Cardiomyopathy (dilated) (30-34%)  Myocarditis  Metabolic disorders like beri beri INCREASED WORKLOAD ON THE HEART : It is due to either increased pressure load or volume load  Increased pressure load  Hypertension  Valvular disease:stenosis  Chronic lung disease  Increased volume load  Severe anaemia  Hypoxia due to lung disease IMPAIRED FILLING OF CARDIAC CHAMBERS:Cardiac failure may also result from defects in filling of heart
  5. 5. PATHOPHISIOLOGY  Heart failure is associated with complex neurohormonal changes including activation of the renin angiotensin aldosterone system and the sympathetic nervous system
  6. 6. Right sided heart failure  Right ventricle fails as effective pump  Right ventricle cannot eject blood returning through vena cavae  Blood backs up into systemic circulation The main causes are: 1. As a consequence of left ventricular failure 2. Pulmonary or tricuspid valvular disease 3. Congenital heart disease 4. Myocardial heart disease effecting right heart
  7. 7. Left sided heart failure It is initiated by the stress to the left heart.  Left ventricle fails as effective pump  Left ventricle cannot eject blood delivered from right heart through pulmonary circulation  Blood backs up into pulmonary circulation The major causes are : 1. Systemic hypertension 2. Mitral or aortic valve disease 3. Ischemic heart disease 4. Cardiac myopathies 5. Myocarditis
  8. 8.  To understand the pathophysiologic processes in heart failure, a basic understanding of normal cardiac function is necessary. Cardiac output (CO) is defined as the volume of blood ejected per unit time (L/min) and is the product of heart rate (HR) and stroke volume (SV): CO = HR × SV. Stroke volume, or the volume of blood ejected during systole, depends on preload, afterload, and contractility.
  9. 9. TYPES OF HEART FAILURE Heart failure may be classified into:  Acute heart failure  Chronic heart failure
  10. 10. Acute heart failure Sudden and radip development of heart failure occurs in following conditions: 1. Larger myocardial infarction 2. Valve rupture 3. Massive pulmonary embolism 4. Acute viral myocarditis In this type there is sudden reduction in cardiac output resulting in systemic hypotension but edema does not take place
  11. 11. Chronic heart failure It develops slowly as observed in following cases 1. Myocardial ischaemia 2. Multi valvular disease 3. Sytemic hypertension 4. Chronic disease 5. Progression of acute into chronic failure In this type of failure there is a well maintained arterial pressure and there is accumulation of edema
  12. 12. SIGNS ■ Pulmonary edema ■ Cool extremities ■ Tachycardia ■ Narrow pulse pressure ■ Cardiomegaly ■ Peripheral edema ■ Hepatomegaly
  13. 13. Symptoms ■ Hemoptysis ■ Abdominal pain ■ Anorexia ■ Nausea ■ Bloating ■ Poor appetite, early satiety ■ Ascites ■ Mental status changes ■ Nocturia ■ Dyspnea, particularly on exertion ■ Orthopnea ■ Paroxysmal nocturnal dyspnea ■ Exercise intolerance ■ Tachypnea ■ Cough ■ Fatigue
  14. 14. Laboratory Tests ■ BNP (brain natriuretic peptide) >100 pg/mL ■ Electrocardiogram may be normal or it could show numerous abnormalities including acute ST-T–wave changes from myocardial ischemia, atrial fibrillation , bradycardia , left ventricular hypertrophy. ■ Serum creatinine may be increased because of hypoperfusion . ■ Complete blood count useful to determine if heart failure is a result of reduced oxygen-carrying capacity ■ Chest radiography is useful for detection of cardiac enlargement , pulmonary edema, and pleural effusions ■ Echocardiogram assesses left ventricle size, valve function, pericardial effusion, and ejection fraction ■ Hyponatremia, serum sodium <130 mEq/L, is associated with reduced survival and may indicate worsening volume overload and/or disease progression
  15. 15. Goals of Management  Improve oxygenation, ventilation  Decrease venous return to heart  Decrease cardiac work, O2 demand  Improve cardiac output by  Reducing afterload  Increasing myocardial contractility
  16. 16. TREATMENT OF HEART FAILURE  General measures: Rest, salt restriction, stop smoking  Removal of the cause: This deserves top priority in all cases and includes surgical measures correcting valvular lesions or congenital malformations and medical measures for treating hypertension or infective endocarditis when Present  Removal of precipitating causes of heart failure
  17. 17. General lifestyle advice  Education:Effective counselling of patients and family emphasizing weight monitoring and dose adjustment of diuretics may prevent hospitalization.  Obesity control:Maintain desired weight and body mass index.  Smoking: Smoking should be stopped, with help from anti-smoking clinics if necessary.  Physical activity, exercise training and rehabilitation  Dietary modification: Large meals should be avoided and if necessary weight reduction instituted. Salt restriction is necessary and foods rich in salt or added salt in cooking and at the table should be avoided. A low- sodium diet is unpalatable and of questionable value. In severe heart failure fluid restriction is necessary. Alcohol has a negative inotropic effect and heart failure patients should moderate consumption.
  18. 18. NON-PHARMACOLOGICAL TREATMENT:  Revascularization  Biventricular pacemaker  Cardiac transplantation  Nutritional therapy  Diet/weight reduction recommendations-individualized and culturally sensitive  Dietary Approaches to Stop Hypertension (DASH) diet recommended  Sodium- usually restricted to 2.5 g per day  Potassium encouraged unless on K sparing diuretics (Aldactone)
  19. 19. PHARMACOLOGICAL TREATMENT  Drugs used in CCF:  Cardiotonic drugs: Cardiac glycosides (digitalis, digoxin,digitoxin.  Vasodilators: ACE-I, ARBs, Na- nitroprusside, nitroglycerine, prazosine.  Diuretics: Thiazides, loop diuretics, K+ sparing diuretics.  Miscellaneous:  Sympathomimetics: Dobutamine, dopamine.  Ionodilators: Amrinone, xanthines.  Aldosterone antagonist; spiranolactone.  Β blockers: Carvedilol, metoprolol.
  20. 20. Diuretics Loop diuretics,thiazide diuretics and potassium sparing diuretics These act by promoting the renal excretion of salt and water by blocking tubular reabsorption of sodium and chloride. The resulting loss of fluid reduces ventricular filling pressures (preload), produces consistent haemodynamic and symptomatic benefits and rapidly improves dyspnoea and peripheral oedema.
  21. 21. Diuretics Cortex Medulla Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle K-sparing Inhibit reabsorption of Na in the distal convoluted and collecting tubule Loop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle
  22. 22. Loop diuretics Drugs such as furosemide and bumetanide :  Have a rapid onset of action (i.v. - 5 min; oral - 1-2 h) and generally short-lived (4-6 h) diuresis as the concentrating power of the kidney is reduced.  These agents also produce potassium loss and promote hyperuricaemia, and renal function should be monitored.  Dose of
  23. 23. Loop diuretics
  24. 24. Thiazide diuretics:  Thiazides are less effective in patients with reduced glomerular filtration rates.  Thiazide diuretics in combination with loop diuretics have a synergistic action and greater diuretic effect. Associated metabolic abnormalities are more likely and close supervision is needed. Ex:Hydrochlorthiazide C.I:hepatic failure,renal impairment,electrolyte imbalance Dose:25-75mg daily in divided doses
  25. 25. Potassium-sparing diuretics:  Spironolactone is a specific competitive antagonist to aldosterone, producing a weak diuresis but with a potassium-sparing action.  Risk factors for developing hyperkalaemia include spironolactone dose > 50 mg/day, high-dose angiotensin-converting enzyme inhibitor (ACEI) and renal impairment.
  26. 26. Vasodilator therapy Actions of vasodilators in CCF:  Decrease in preload: preload is the amount of blood returning to the heart which the heart has to pump. Two types of drugs reduce pre-load.  Venodilators: Nitrates, Na nitroprusside, ACE- I, ARBs, prazosin.  Diuretics: Which reduce circulating volume.  Preload reduces the size of the ventricles, decreases ventricular EDV/P, increases ejection fraction and efficiency of the heart.  Decrease in after load: After load is the resistance against which the heart has to pump. Arterial dilators reduce the after load. Nifedipine, minoxidil,hydralazine.  Balanced (mixed) vasodilators: ACE-I, ARBs, Na- nitroprusside, prazosin
  27. 27. Vasodilator therapy ACE-I: are mixed vasodilators, they dilate both arteries, and veins. Arteriolar dilatation: This reduces after load. When load is decreased, efficiency of the heart to pump the blood improves- there is improvement in the ejection fraction. This is how, reduction in after load helps a patient of CCF. Venodilatation: This reduces preload. Preload means increased capacity of the veins to hold blood: venous return decreases. In CCF the ventricles are over stretched beyond the physiological limits. Over stretched muscles do not produce sufficient power. Due to reduction in venous return, ventricles size decreases and the length return to with in physiological limits. This increases the force generated by the ventricles. Thus reduction in preload is helpful in patients with CCF. .
  28. 28. Arteriolar vasodilators:  Drugs such as α-adrenergic blockers (e.g. prazosin) and direct smooth-muscle relaxants (e.g. hydralazine) are potent arteriolar vasodilators but are not very effective in heart failure.  Calcium-channel blockers also reduce afterload, but first-generation calcium antagonists (diltiazem, nifedipine) may have a detrimental effect on left ventricular function in patients with heart failure.
  29. 29. Venodilators:  Short- and long-acting nitrates act by reducing preload and lowering venous pressure, with resulting reduction in pulmonary and dependent oedema but tolerance occurs.  Only combination therapy of nitrate with hydralazine has been shown to improve mortality and exercise performance, and may be useful when ACEI are contraindicated.  Nitroglycerin 10 mcg/min increased by 5-10 mcg/min q 5 min
  30. 30. β-Adrenoceptor blocking agents  There is considerable evidence to support the use of beta-blockers in patients with chronic stable heart failure.  Initial doses should be low, e.g. carvedilol 3.125 mg twice daily.  Nebivolol is used in the treatment of stable mild–moderate heart failure in patients over 70 years old Beta blockers should not be used in the following conditions  Patients not receiving diuretics.  If iv ionotropic is required.  heart block.
  31. 31. Ionodilators  Amrinone- Ionodilator is an agent with both positive inotropic and vasodilator effects. They inhibit phoshodiesteraeIII enzyme. This increases the concentration of cAMP, -> more Ca++ influx.  This is responsible for for +ve ionotropic action. Vasodilator effect of amrinone is the result of direct relaxant effect on vascular smooth muscle. The drug reduces both the after load and preload.  ADRS:Thrombocytopenia ,adominal pain,nausea,liver damage  Dose:0.75mg/kg/i.v  C.I:hypersensitivity
  32. 32. Sympathomimetics:  Dobutamine, dopamine. Dobutamine is a selective β1 agonist. These drugs have positiv inotropic and vasodilator properties through activation of adenylyl cyclase  Due to development of tolerance these drugs have a limited role Dobutamine:2-8ug/kg/min  C.I:acute myocardial infarction  ADRS:incresase in HR Dopamine:3-10ug/kg/min  C.I:pheochromocytoma
  33. 33. ALDOSTERONE ANTAGONIST  SPIRANOLACTONE:It antagonises the effects of aldosterone like:  Expansion of e.c.f  Fibrotic change in myocardium  Hypokalemia and hypomagnesemia Contraindications :in renal insufficiency Adr :gynaecomastia,headache,ataxia Dose:25-200mg daily for adults
  34. 34. Cardiac glycosides  Digitalis glycosides have been used for many years in patients with heart failure and atrial fibrillation.  Digoxin acts as a positive inotrope by competitive inhibition of Na+/K+- ATPase, producing high levels of intracellular sodium. This is then exchanged for extracellular calcium. High levels of intracellular calcium result in enhanced actin- myosin interaction and increased contractility. Digoxin also improves baroreceptor responsiveness, and reduces sympathetic activity and circulating renin.
  35. 35. Digitalis They have narrow safety margin Anorexia, nausea, vomiting abdominal discomfort or pain and diarrhea. Headache, malaise, fatigue, drowsiness, confusion, delirium, hallucination or rarely convulsions. Blurred vision, mostly for yellow and green vision, diplopia.
  36. 36. Any type of arrhythmia may be produced including:  Bradycardia,  Heart block,  Ventricular extrasystole  Ventricular fibrillation. May be due to steroidal structure.
  37. 37. Treatment Of Digitalis Toxicitiy:  1) Stop the responsible drug.  2) KCl syrup or slow release or I.V. with ECG monitoring if plasma potassium is low or normal.  3) If due to calcium injection give disodium edetate I.V. which is chelating agent for calcium.  4) Cholestyramine binds to digitalis in gut, thus inhibit absorption and decreases the toxicity especially of digitoxin.  5) In acute toxicity give specific digitalis antibodies (Fab fragment).  6) Treatment of associated arrhythmia: Partial heart block is treated by atropine.  Ventricular arrhythmia without A-V block is treated by lidocaine I.V. or beta blockers.  Ventricular arrhythmia with A-V block & atrial arrhythmia is treated by Diphenylhydantoin (phenytoin)
  38. 38. THANK YOU

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