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heart Failure

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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 :
    • 1- Left cardiac failure :
    • - 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 :-
    • 1- HT.
    • 2- Ischemic heart disease.
    • 3- Ao stenosis & regurgitation.
    • 4- Mitral regurgitation.
    • 5- Cardiomyopathy.
    • 6- Myocarditis. 7- arrhythmias.
    • 8- High output states (anemia , A-V fistula, thyrotoxicosis, PDA, pagets disease of bone, beri-beri & gram negative septicemia.)
  • 7.
    • 2- Right cardiac failure :
    • - 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
    • 1- Lt heart failure
    • 2- Chronic lung disease (core pulmonale)
    • 3- Pulm embolism
    • 4- Pulm HT
    • 5- Tricuspid valve dis.
    • 6- Pulm valve dis
    • 7- Lt to Rt shunts ( ASD , VSD) 8- isolated Rt. Vent. Cardiomyopathy
  • 11.
    • 9- IHD.
    • 10- Constrictive pericarditis & cardiac tamponade.
    • 11- High output states .
    • 3 - CCF: C ombines both Lt & Rt HF.
  • 12.
    • Acute heart failure
    • 1- Extensive acute MI.
    • 2- Rupture of IVS producing VSD.
    • 3- Papillary or chordal rupture in endocarditis producing MR 4- Sudden Ao valve rupture in endocarditis 5- Acute 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.
    • 1- Increased salt intake.
    • 2- Uncontrolled HT.
    • 3- Anaemia & pregnancy.
    • 4- Fluid overload.
    • 5- MI.
    • 6- Arrhythmias specially AF.
    • 7- Pulm. Embolism.
  • 15.
    • 8- Infections sp. chest infections causing hyperdynamic circulation. 9-Thyrotoxicosis.
    • 10- Drug non compliance .
    • 11- Renal failure secondary to diuretic induced volium depletion or due to intrinsic renal disease.
  • 16.
    • Investigations in HF
    • This is to confirm HF & to establish the underlying cause.
    • 1- CXR : Shows cardiac size & evidence of pulmonary congestion (upper lobe venous diversion; bat win appearance
    • in pulm oedema)
    • 2- ECG : Shows arrhythmias, ischemia , chamber hypertrophy etc.
    • 3- Echo : (2- dimentional & doppler echo) show valves, chambers size, ejection fraction, intracardiac thrombi.
    Establish evidence of systolic & diastolic impairment 0f z ventricles, etiology, intracardiac
  • 17. CXR with right apical fibrosis
  • 18. Electrocardiogram
  • 19. Echocardiography
  • 20.
    • 4- CBC, LFT & blood urea & electrolytes .
    • 5- Cardiac enzymes in acute MI
    • 6- Cardiac catherization .
    • 7- Ambulatory ECG monitoring in suspected arrhythmias.
    • 8- Stress ECG .
  • 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.
    • 1- General TR :
    • - 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.
    • 2- Drug TR Of HF( Pharmacotherapy)
    • - Diuretics
    • - Vasodilators
    • - Digoxin
    • - Antiarrhythics
    • - Anticoagulants
    • - Inotropic drugs
    • - B B
    • - Statins
  • 26.
    • 2- Drug TR Of HF( Pharmacotherapy)
    • 1 - Diuretics :
    • 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.
    • 2- Vasodilater therapy :
    • 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.
    • 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.
    • 4- Inotropic drugs :
    • - Digoxin - Sympathomimetic
  • 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:
    • 1- elderly 2- renal failure
    • 3- hyperthyroidism 4- quinine therapy
    • 5- electrolyte disturbance e.g. Hypokal & hypo Mg. IV Ca is dangerous in digitalized pts.
  • 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 4- 10 mcg/kg/min. increases HR & cardiac contractility. Higher doses increase BP at the expense of tissue perfusion.
    • Noradr . Raise BP by peripheral vasoconstriction.
  • 38.
    • 5 - Anticoagulants to prevent thromboembolism in pts. with AF , endocardial thrombus & PH of thromboembolism.
    • 6 - Antiarrhythmic agents :
    • - Drugs - DC shock
    • - Implantable cardiovertor - defibrillator
    • (ICD)
    • 7 - Statins
    • BB, ACE-I, statins & spironolactone may reduce sudden death in pts. with MI and HF.
  • 39.
    • Non-pharmacological Tr. of HF : 1- Revascularization .
    • 2- Pacemaker or ICD .
    • 3- Valvular surgery & correction of other causes of HF.
    • 4- Cardiac transplantation.
    • 5- Ultra-filtration.
    • 6- Intra-aortic balloon pump .
  • 40. Pace maker
  • 41.
    • In summary : 1- All pts. with clinical HF should receive diuretics & ACE-I. 2- Patients with AF should be digitalized.
    • 3- Pts. in SR improve with addition of Digoxin or BB.
    • 4- Pts. with asymptomatic LV dysfunction benefit from prophylactic ACE- I therapy or ARB
  • 42.
    • 5- Pts. with ischemic HF & intolerant to ACE-I or in whom it is CI may benefit from nitrate/ hydralazine therapy.
    • 6- Spironolactone should be added .
  • 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.).

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