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Cardiacfailure 091023124947-phpapp01


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  • 1. Cardiac failure By Dr. Osman Bukhari
  • 2. Cardiac failure : Occurs when the heart is unable to maintain sufficient cardiac output to .meet the demands of the body .Incidence increases with age .Many pts. are admitted repeatedly Despite improvement in management mortality is still high …….Pathophysiology - -
  • 3. :Manifestations of cardiac failure : Left cardiac failure - 1 Symptoms include: fatigue, exertional dyspnoea, orthopnoea & paroxysmal . nocturnal dyspnoea Signs include: Cardiomegaly with displaced & often sustained apical impulse, triple & gallop rhythm, basal lung crackles, pulsus alternans, .functional MR & pulmonary edema -
  • 4. Cardiomegaly
  • 5. LVF & pulmonary oedema
  • 6. :-Causes .HT- 1 .Ischemic heart disease- 2 .Ao stenosis & regurgitation- 3 .Mitral regurgitation- 4 .Cardiomyopathy- 5 Myocarditis. .arrhythmias High output states (anemia , A-V fistula, thyrotoxicosis, PDA, pagets disease of bone, beri-beri & gram .(negative septicemia 7- - 6 -8
  • 7. :Right cardiac failure - 2 Symptoms include: - fatigue, anorexia and nausea related to distension and fluid accumulation .in areas drained by systemic veins Rt hypochondrial pain swelling of of the LLs - -
  • 8. Signs: include: - increased JVP tender smooth hepatomegaly dependent pitting edema ascites & pleural transudates tachycardia. LPH, TR, Rt. S3 - -
  • 9. Pitting oedema of the LL
  • 10. Causes Lt heart failure- 1 ( Chronic lung disease (core pulmonale- 2 Pulm embolism- 3 Pulm HT- 4 .Tricuspid valve dis- 5 Pulm valve dis- 6 Lt to Rt shunts ( ASD , VSD( 8- isolated Rt. Vent. Cardiomyopathy -7
  • 11. .IHD- 9 Constrictive pericarditis & cardiac . tamponade .High output states- 11 - 10 .CCF: Combines both Lt & Rt HF- 3
  • 12. Acute heart failure .Extensive acute MI- 1 .Rupture of IVS producing VSD- 2 Papillary or chordal rupture in -3 endocarditis producing MR 4Sudden Ao valve rupture in endocarditis 5Acute pulmonary embolism & cardiac .tamponade In all these conditions the heart size is . relatively normal
  • 13. High output states are associated with tachycardia, gallop rhythm & patients .are often warm with distended veins
  • 14. Factors precipitating HF in controlled . patients . Increased salt intake- 1 .Uncontrolled HT- 2 .Anaemia & pregnancy- 3 .Fluid overload- 4 .MI- 5 .Arrhythmias specially AF- 6 .Pulm. Embolism- 7
  • 15. Infections sp. chest infections causing - 8 hyperdynamic circulation. 9.Thyrotoxicosis .Drug non compliance- 10 Renal failure secondary to diuretic - 11 induced volium depletion or due to . intrinsic renal disease
  • 16. Investigations in HF This is to confirm HF & to establish the .underlying cause CXR: Shows cardiac size & evidence of - 1 pulmonary congestion (upper lobe venous diversion; bat win appearance (in pulm oedema ECG: Shows arrhythmias, ischemia , - 2 . chamber hypertrophy etc Echo: (2- dimentional & doppler echo( - 3 show valves, chambers size, ejection . fraction, intracardiac thrombi
  • 17. CXR with right apical fibrosis
  • 18. Electrocardiogram
  • 19. Echocardiography
  • 20. .CBC, LFT & blood urea & electrolytes- 4 Cardiac enzymes in acute MI- 5 .Cardiac catherization- 6 Ambulatory ECG monitoring in -7 . suspected arrhythmias . Stress ECG- 8
  • 21. Coronary angiography
  • 22. Treatment of HF Preventive measures in HF include: - Cessation of smoking Control of DM Effective treatment of HT TR of hypercholesterolemia .pharmacological TR following MI
  • 23. 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 - -
  • 24. :General TR- 1 Physical activity: ranges from bed rest in severe HF to low level exercise in compensated HF . Avoid strenuous .exercise Dietary modifications: WT reduction, salt restriction, alcohol abstinence & fluid restriction in severe HF .and dilutional hyponatraemia .Education - - -
  • 25. (Drug TR Of HF( Pharmacotherapy- 2 Diuretics Vasodilators Digoxin AntiarrhythicsAnticoagulants Inotropic drugs BBStatins -
  • 26. (Drug TR Of HF( Pharmacotherapy- 2 :Diuretics- 1 Act by promoting renal excretion of salt and water reducing preload & rapidly improves dyspnoea & systemic congestion. They also cause arteriolar . vasodilatation reducing after load Loop diuretics: e.g. frusemide (lasix( have a rapid onset of action & short duration of action.They cause (hypokalaemia ( add slow-K
  • 27. 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 Loop & thiazide diuretics have no proven * survival benefit. They give symptomatic relieve
  • 28. 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 Ameloride & triamterene are weak but useful when combined with loop ..diuretics
  • 29. :Vasodilater therapy- 2 a- ACE-Is 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
  • 30. ACE-I should be carefully introduced in pts. on high doses diuretics & in the presence of hyponatraemia. .Care with K- sparing diuretics -
  • 31. b- ARBs have similar effects to ACE-I but . do not affect bradykinin metabolism 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 d- Nitrates (glyceride trinitrates and isosorbide mononitrates( reduce preload and reduce pulm edema.Only
  • 32. combination with hydralazine have . proven prognostic value 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 :Inotropic drugs- 4 Digoxin - Sympathomimetic- -3
  • 33. 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
  • 34. :Dose is reduced in elderly renal failure hyperthyroidism 4- quinine therapy electrolyte disturbance e.g. Hypokal & hypo Mg. .Ca is dangerous in digitalized pts 2-- 1 -3 -5 IV
  • 35. SE of Digoxin include: HA, fatigue, muscle weakness, abd. .Pain, N, V, Wt. loss & gynaecomastia 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
  • 36. 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 Dobutamine is a B2 agonist increasing cardiac contraction & has vasodil. effect by alpha blocker effect. Dose 2.5-10 .mcg/kg/minute
  • 37. Dopexamine is B2 agonist with additional action on peripheral dopamine receptors .improving renal perfusion Dopamine in low dose (2-4 mcg/kg/min.) improves renal perfusion. In dose of 410 mcg/kg/min. increases HR & cardiac contractility. Higher doses increase BP at . the expense of tissue perfusion Noradr. Raise BP by peripheral .vasoconstriction
  • 38. Anticoagulants to prevent thromboembolism in pts. with AF , endocardial thrombus & PH of .thromboembolism -5 :Antiarrhythmic agents- 6 Drugs - DC shock Implantable cardiovertor - defibrillator )ICD ( Statins- 7 - BB, ACE-I, statins & spironolactone may .reduce sudden death in pts. with MI and HF
  • 39. Non-pharmacological Tr. of HF: .1- Revascularization .Pacemaker or ICD- 2 Valvular surgery & correction of other . causes of HF .Cardiac transplantation- 4 .Ultra-filtration- 5 .Intra-aortic balloon pump- 6 -3
  • 40. Pace maker
  • 41. In summary: 1- All pts. with clinical HF should receive diuretics & ACE-I. 2Patients with AF should be .digitalized Pts. in SR improve with addition of - 3 . Digoxin or BB Pts. with asymptomatic LV -4 dysfunction benefit from prophylactic ACE- I therapy or ARB
  • 42. Pts. with ischemic HF & intolerant to - 5 ACE-I or in whom it is CI may benefit from nitrate/ hydralazine . therapy .Spironolactone should be added- 6
  • 43. Pulmonary edema .Life-threatening emergency .Usually preceded by PND Interstitial edema usually occurs with . capillary pressure of 20 mmHg Alveolar edema occurs with pressure of . 25-30 mmHg Causes are those of LVF, MS & increased pulmonary capillary ).permeability (Adult RDS -
  • 44. Pulmonary oedema
  • 45. :Clinical features include Extreme SOB .Wheezing .Anxiety & sweating .Cough with frothy blood tinged sputum Tachypnea, cyanosis, tachycardia and . gallop rhythm .Crackles & wheeze in z chest .Low arterial PO2 CXR shows diffuse haziness & bat wing . appearance - -
  • 46. :Treatment Include Admission in CCU. - .Cardiac bed Continuous flow high O2 conc and in .severe cases pt. is ventilated ). IV morphine 10-15 mg( + antemetic Avoided if SBP < 90 IV loop diuretic which produces immediate vasodilt. In addition to . more delayed diuresis Venodilt. & arterial vasodilators to . decrease pre-load & after load
  • 47. 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 .Monitor rhythm, O2 saturation Venesection & mechanical methods of reducing venous return are ineffective . and rarely used Treat precipitating factors (arrhythmias, .) chest infection, etc
  • 48. Correct the underlying cause of increased pulmonary capillary permeability (toxins, hypoxia, .). infections, DIC, etc -