heart Failure


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heart Failure

  1. 1. Cardiac failure By Dr. Osman Bukhari
  2. 2. <ul><li>Cardiac failure : - Occurs when the heart is unable to maintain sufficient cardiac output to meet the demands of the body. </li></ul><ul><li>- Incidence increases with age . </li></ul><ul><li>- Many pts. are admitted repeatedly . </li></ul><ul><li>- Despite improvement in management mortality is still high </li></ul><ul><li>Pathophysiology……. </li></ul>
  3. 3. <ul><li>Manifestations of cardiac failure : </li></ul><ul><li>1- Left cardiac failure : </li></ul><ul><li>- Symptoms include: fatigue, exertional dyspnoea, orthopnoea & paroxysmal nocturnal dyspnoea. </li></ul><ul><li>- Signs include: Cardiomegaly with displaced & often sustained apical impulse, triple & gallop rhythm, basal lung crackles, pulsus alternans, functional MR & pulmonary edema . </li></ul>
  4. 4. Cardiomegaly
  5. 5. LVF & pulmonary oedema
  6. 6. <ul><li>Causes :- </li></ul><ul><li>1- HT. </li></ul><ul><li>2- Ischemic heart disease. </li></ul><ul><li>3- Ao stenosis & regurgitation. </li></ul><ul><li>4- Mitral regurgitation. </li></ul><ul><li>5- Cardiomyopathy. </li></ul><ul><li>6- Myocarditis. 7- arrhythmias. </li></ul><ul><li>8- High output states (anemia , A-V fistula, thyrotoxicosis, PDA, pagets disease of bone, beri-beri & gram negative septicemia.) </li></ul>
  7. 7. <ul><li>2- Right cardiac failure : </li></ul><ul><li>- Symptoms include: - fatigue, anorexia and nausea related to distension and fluid accumulation in areas drained by systemic veins. </li></ul><ul><li>- Rt hypochondrial pain </li></ul><ul><li>- swelling of of the LLs </li></ul>
  8. 8. <ul><li>- Signs: include: - increased JVP - tender smooth hepatomegaly - dependent pitting edema - ascites & pleural transudates - tachycardia. - LPH, TR, Rt. S3 </li></ul>
  9. 9. Pitting oedema of the LL
  10. 10. <ul><li>Causes </li></ul><ul><li>1- Lt heart failure </li></ul><ul><li>2- Chronic lung disease (core pulmonale) </li></ul><ul><li>3- Pulm embolism </li></ul><ul><li>4- Pulm HT </li></ul><ul><li>5- Tricuspid valve dis. </li></ul><ul><li>6- Pulm valve dis </li></ul><ul><li>7- Lt to Rt shunts ( ASD , VSD) 8- isolated Rt. Vent. Cardiomyopathy </li></ul>
  11. 11. <ul><li>9- IHD. </li></ul><ul><li>10- Constrictive pericarditis & cardiac tamponade. </li></ul><ul><li>11- High output states . </li></ul><ul><li>3 - CCF: C ombines both Lt & Rt HF. </li></ul>
  12. 12. <ul><li>Acute heart failure </li></ul><ul><li>1- Extensive acute MI. </li></ul><ul><li>2- Rupture of IVS producing VSD. </li></ul><ul><li>3- Papillary or chordal rupture in endocarditis producing MR 4- Sudden Ao valve rupture in endocarditis 5- Acute pulmonary embolism & cardiac tamponade. </li></ul><ul><li>In all these conditions the heart size is relatively normal . </li></ul>
  13. 13. <ul><li>High output states are associated with tachycardia, gallop rhythm & patients are often warm with distended veins . </li></ul>
  14. 14. <ul><li>Factors precipitating HF in controlled patients. </li></ul><ul><li>1- Increased salt intake. </li></ul><ul><li>2- Uncontrolled HT. </li></ul><ul><li>3- Anaemia & pregnancy. </li></ul><ul><li>4- Fluid overload. </li></ul><ul><li>5- MI. </li></ul><ul><li>6- Arrhythmias specially AF. </li></ul><ul><li>7- Pulm. Embolism. </li></ul>
  15. 15. <ul><li>8- Infections sp. chest infections causing hyperdynamic circulation. 9-Thyrotoxicosis. </li></ul><ul><li>10- Drug non compliance . </li></ul><ul><li>11- Renal failure secondary to diuretic induced volium depletion or due to intrinsic renal disease. </li></ul>
  16. 16. <ul><li>Investigations in HF </li></ul><ul><li>This is to confirm HF & to establish the underlying cause. </li></ul><ul><li>1- CXR : Shows cardiac size & evidence of pulmonary congestion (upper lobe venous diversion; bat win appearance </li></ul><ul><li>in pulm oedema) </li></ul><ul><li>2- ECG : Shows arrhythmias, ischemia , chamber hypertrophy etc. </li></ul><ul><li>3- Echo : (2- dimentional & doppler echo) show valves, chambers size, ejection fraction, intracardiac thrombi. </li></ul>Establish evidence of systolic & diastolic impairment 0f z ventricles, etiology, intracardiac
  17. 17. CXR with right apical fibrosis
  18. 18. Electrocardiogram
  19. 19. Echocardiography
  20. 20. <ul><li>4- CBC, LFT & blood urea & electrolytes . </li></ul><ul><li>5- Cardiac enzymes in acute MI </li></ul><ul><li>6- Cardiac catherization . </li></ul><ul><li>7- Ambulatory ECG monitoring in suspected arrhythmias. </li></ul><ul><li>8- Stress ECG . </li></ul>
  21. 21. Coronary angiography
  22. 22. <ul><li>Treatment of HF </li></ul><ul><li>Preventive measures in HF include : - Cessation of smoking - Control of DM - Effective treatment of HT - TR of hypercholesterolemia - pharmacological TR following MI. </li></ul>
  23. 23. <ul><li>TR of chronic HF aims at : - Relieving symptoms, - Retarding disease progression, - Correction of the cause , -TR of aggravating factors, - Compliance with drug therapy. - Improving survival, </li></ul>
  24. 24. <ul><li>1- General TR : </li></ul><ul><li>- Physical activity : ranges from bed rest in severe HF to low level exercise in compensated HF . Avoid strenuous exercise. </li></ul><ul><li>- Dietary modifications : WT reduction, salt restriction, alcohol abstinence & fluid restriction in severe HF and dilutional hyponatraemia. </li></ul><ul><li>- Education . </li></ul>
  25. 25. <ul><li>2- Drug TR Of HF( Pharmacotherapy) </li></ul><ul><li>- Diuretics </li></ul><ul><li>- Vasodilators </li></ul><ul><li>- Digoxin </li></ul><ul><li>- Antiarrhythics </li></ul><ul><li>- Anticoagulants </li></ul><ul><li>- Inotropic drugs </li></ul><ul><li>- B B </li></ul><ul><li>- Statins </li></ul>
  26. 26. <ul><li>2- Drug TR Of HF( Pharmacotherapy) </li></ul><ul><li>1 - Diuretics : </li></ul><ul><li>Act by promoting renal excretion of salt and water reducing preload & rapidly improves dyspnoea & systemic congestion. They also cause arteriolar vasodilatation reducing after load. </li></ul><ul><li>- Loop diuretics : e.g. frusemide (lasix) have a rapid onset of action & short duration of action.They cause hypokalaemia ( add slow-K ) </li></ul>
  27. 27. <ul><li>b -Thiazide diuretics : e.g. hydrochlorothiazide and Chlorthalidone have mild diuretic effect, but act synergistically when combined with loop diuretics. Not effective in renal impairment. Metolazone is a powerful thiazide & is combined with loop diuretics in severe and resistant HF. </li></ul><ul><li>* Loop & thiazide diuretics have no proven survival benefit. They give symptomatic relieve </li></ul>
  28. 28. <ul><li>c - Potassium sparing diuretics : Care with ACE-I & avoided in renal impairment . Spironolactone reduces mortality in doses of up to 25 mg when added to conventional therapy in moderate to severe HF. Risk of hyperkalaemia is high with doses of > 50 mg.. </li></ul><ul><li>Ameloride & triamterene are weak but useful when combined with loop diuretics.. </li></ul>
  29. 29. <ul><li>2- Vasodilater therapy : </li></ul><ul><li>a- ACE-Is </li></ul><ul><li>- reduce after load & pre load - reduce circulating levels of catecholamines, - reduce BP - reduce cardiac dilatation & CCF after extensive MI - improve exercise tolerance & survival in pts. with severe HF. </li></ul>
  30. 30. <ul><li>- ACE-I should be carefully introduced in pts. on high doses diuretics & in the presence of hyponatraemia. - Care with K- sparing diuretics. </li></ul>
  31. 31. <ul><li>b- ARBs have similar effects to ACE-I but do not affect bradykinin metabolism. </li></ul><ul><li>c- Alpha blockers (prazocin) & direct smooth muscle relaxants (hydralazine) are not very effective in HF. CCBs reduce after load but have no prognostic benefit in HF. Diltiazem and verapamil are CI in HF. </li></ul><ul><li>d- Nitrates (glyceride trinitrates and isosorbide mononitrates) reduce preload and reduce pulm edema.Only </li></ul>
  32. 32. <ul><li>combination with hydralazine have proven prognostic value. </li></ul><ul><li>3- BB used in pts. with chronic stable HF (e.g. metoprolol, bisoprolol, atenolol and carvedilol), improve symptoms, exercise tolerance, LV function and mortality in pts. with HF. Initial doses should be low. </li></ul><ul><li>4- Inotropic drugs : </li></ul><ul><li>- Digoxin - Sympathomimetic </li></ul>
  33. 33. <ul><li>Digoxin : - cardiac glycoside, It blocks AV node and increases myocardial contractility. - used in severe HF with conventional therapy, AF, atrial flutter & SVT. - 90% is excreted unchanged in urine and accumulation can occur in renal failure. Digitoxin is used In renal failure. - Usual dose is 0.125-0.25 mg/d. with dose of 1mg in emergency </li></ul>
  34. 34. <ul><li>Dose is reduced in: </li></ul><ul><li>1- elderly 2- renal failure </li></ul><ul><li>3- hyperthyroidism 4- quinine therapy </li></ul><ul><li>5- electrolyte disturbance e.g. Hypokal & hypo Mg. IV Ca is dangerous in digitalized pts. </li></ul>
  35. 35. <ul><li>- SE of Digoxin include: HA, fatigue, muscle weakness, abd. Pain, N, V, Wt. loss & gynaecomastia. </li></ul><ul><li>- Digoxin toxicity include: anorexia, N, V, coloured vision with halo around objects (xanopsia), arrhythmias & fits. - TR of digoxin toxicity : By stopping the drug, restoration of ser. K and management of arrhythmias. Digoxin abs. in life threatening toxicity. </li></ul>
  36. 36. <ul><li>Adr., dobutamine, dopexopamine & dopamine are IV adrenergic agonist. They increase CO & improve perfusion but increase myocardial O2 requirements & aggravate cardiac ischemia. Volume depletion should be corrected before their use. Main use in pts. with acute LVF, following cardiac surgery & in pts. with end stage HF as a bridge to transplantation. </li></ul><ul><li>Dobutamine is a B2 agonist increasing cardiac contraction & has vasodil. effect by alpha blocker effect. Dose 2.5-10 mcg/kg/minute . </li></ul>
  37. 37. <ul><li>Dopexamine is B2 agonist with additional action on peripheral dopamine receptors improving renal perfusion. </li></ul><ul><li>Dopamine in low dose (2-4 mcg/kg/min.) improves renal perfusion. In dose of 4- 10 mcg/kg/min. increases HR & cardiac contractility. Higher doses increase BP at the expense of tissue perfusion. </li></ul><ul><li>Noradr . Raise BP by peripheral vasoconstriction. </li></ul>
  38. 38. <ul><li>5 - Anticoagulants to prevent thromboembolism in pts. with AF , endocardial thrombus & PH of thromboembolism. </li></ul><ul><li>6 - Antiarrhythmic agents : </li></ul><ul><li>- Drugs - DC shock </li></ul><ul><li>- Implantable cardiovertor - defibrillator </li></ul><ul><li>(ICD) </li></ul><ul><li>7 - Statins </li></ul><ul><li>BB, ACE-I, statins & spironolactone may reduce sudden death in pts. with MI and HF. </li></ul>
  39. 39. <ul><li>Non-pharmacological Tr. of HF : 1- Revascularization . </li></ul><ul><li>2- Pacemaker or ICD . </li></ul><ul><li>3- Valvular surgery & correction of other causes of HF. </li></ul><ul><li>4- Cardiac transplantation. </li></ul><ul><li>5- Ultra-filtration. </li></ul><ul><li>6- Intra-aortic balloon pump . </li></ul>
  40. 40. Pace maker
  41. 41. <ul><li>In summary : 1- All pts. with clinical HF should receive diuretics & ACE-I. 2- Patients with AF should be digitalized. </li></ul><ul><li>3- Pts. in SR improve with addition of Digoxin or BB. </li></ul><ul><li>4- Pts. with asymptomatic LV dysfunction benefit from prophylactic ACE- I therapy or ARB </li></ul>
  42. 42. <ul><li>5- Pts. with ischemic HF & intolerant to ACE-I or in whom it is CI may benefit from nitrate/ hydralazine therapy. </li></ul><ul><li>6- Spironolactone should be added . </li></ul>
  43. 43. <ul><li>Pulmonary edema </li></ul><ul><li>- Life-threatening emergency. </li></ul><ul><li>- Usually preceded by PND. </li></ul><ul><li>- Interstitial edema usually occurs with capillary pressure of 20 mmHg. </li></ul><ul><li>- Alveolar edema occurs with pressure of 25-30 mmHg. </li></ul><ul><li>- Causes are those of LVF, MS & increased pulmonary capillary permeability (Adult RDS). </li></ul>
  44. 44. Pulmonary oedema
  45. 45. <ul><li>Clinical features include: </li></ul><ul><li>- Extreme SOB - Wheezing. </li></ul><ul><li>- Anxiety & sweating. </li></ul><ul><li>- Cough with frothy blood tinged sputum. </li></ul><ul><li>- Tachypnea, cyanosis, tachycardia and </li></ul><ul><li>gallop rhythm. </li></ul><ul><li>- Crackles & wheeze in z chest. </li></ul><ul><li>- Low arterial PO2. </li></ul><ul><li>- CXR shows diffuse haziness & bat wing appearance. </li></ul>
  46. 46. <ul><li>Treatment Include: </li></ul><ul><li>- Admission in CCU. - Cardiac bed. </li></ul><ul><li>- Continuous flow high O2 conc and in </li></ul><ul><li>severe cases pt. is ventilated. </li></ul><ul><li>- IV morphine 10-15 mg( + antemetic). </li></ul><ul><li>Avoided if SBP < 90 </li></ul><ul><li>- IV loop diuretic which produces immediate vasodilt. In addition to more delayed diuresis. </li></ul><ul><li>- Venodilt. & arterial vasodilators to decrease pre-load & after load. </li></ul>
  47. 47. <ul><li>- Aminophylline 5 mg/kg IV ( 250-500) slowly to avoid the risk of precipitating ventricular arrhythmias. It is bronchodilator., vasodilt. & increases cardiac contractility. Usually used when bronchospasm is present. </li></ul><ul><li>- Monitor rhythm, O2 saturation. </li></ul><ul><li>- Venesection & mechanical methods of reducing venous return are ineffective and rarely used. </li></ul><ul><li>- Treat precipitating factors (arrhythmias, chest infection, etc.) </li></ul>
  48. 48. <ul><li>- Correct the underlying cause of increased pulmonary capillary permeability (toxins, hypoxia, infections, DIC, etc.). </li></ul>