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  • 1. Samir Rafla: Principles of Cardiology pages 62-86 HEART FAILUREHeart Failure means that the heart cannot pump sufficient blood for body needs.Classification of heart failure:A: 1. Left-sided heart failure.2. Right-sided heart failure.3. Combined left and right sided heart failure.B: 1. Systolic heart failure.2. Diastolic heart failure (heart failure with preserved systolic function.C: 1. Forward failure (eg cardiogenic shock).2. Backward failure (pulmonary congestion and pulmonary edema).D: 1. Low output failure.2. High output failure (eg in hyperthyroidism, anemia...) The pathophysiology heart of heart failureThe causes of heart failure: The heart fails either because it is subjected to anoverwhelming load, or because the heart muscle is disordered: A volume load is imposed by disorders which demand that the ventricle expelsmore blood per minute than is normal. Examples include thyrotoxicosis and anemia, inwhich the total cardiac output is increased; and mitral regurgitation and aorticregurgitation, in which the left ventricle has to expel not only the normal forward flowinto the aorta but also the large volume of regurgitated blood as well. A pressure load is imposed by disorders which increase resistance to outflowfrom the ventricles (eg systemic hypertension and by aortic stenosis). Disorders of myocardial function result not only from diminished contractility butalso from loss of contractile tissue, as occurs in myocardial infarction. This is thecommonest cause of heart failure. An additional factor in this condition is aparadoxical movement of infarcted muscle which further increases the work of theremaining myocardium. 62
  • 2. Dilatation of the heart - increase in end-diastolic volumeIn response to a volume load, the heart dilates, i.e. the ventricular volume is increased.Up to a point, dilatation is a normal and efficient response.Hypertrophy of the heartWhen the ventricle has to face a chronic increase of pressure load, such as thatimposed by arterial hypertension, aortic stenosis or pulmonary hypertension, themyocardium hypertrophies, i.e. it increases in weight as a result of an enlargement ofindividual muscle fibres.Cellular changes in heart failure: Changes include:Abnormal calcium metabolism: Heart failure results in changes in excitationcontraction coupling.• Changes in myocardial gene expression.In some types of heart failure, a process of cell self-destruction may be initiated,resulting in further loss of myocytes and progressive impairment of ventricularfunction. The process of ‘programmed cell death’ is termed apoptosis.Neuroendocrine response to heart failureCardiac failure activates several components of the neuroendocrine system, whichplay an important intermediary role in its clinical manifestations: Sympathetic nervous system. Activation of the sympathetic nervous system resultsin an increase in myocardial contractility, heart rate, and vasoconstriction of arteriesand veins. Although this may be beneficial in maintaining blood pressure, it is adversein so far as it increases preload, afterload, and myocardial oxygen requirement. Thereis also an increased plasma noradrenaline (norepinephrine), but myocardialcatecholamines are reduced. Renin-angiotensin-aldosterone systems. Both the fall in cardiac output itself andthe increase in sympathetic tone reduce effective blood flow to the kidney and,consequently, increase renin secretion. As a result, there is a rise in angiotensin IIlevels, which leads directly to vasoconstriction and indirectly, by stimulating 63
  • 3. aldosterone secretion, to sodium retention and the expansion of blood volume. This isadvantageous in so far as increasing preload helps to maintain stroke volume by theStarling mechanism, but it does so at the expense of circulatory congestion. Fig: some of the neuroendocrine and renal responses to cardiac failure Atrial natriuretic peptide (ANP). Distension of the atria leads to the release of thispeptide which has natriuretic and vasodilator properties. Levels of ANP are elevated inpatients with heart failure and correlate with functional class. In addition, ANP hasbeen suggested as a screening test to aid in the diagnosis of heart failure. Heart failure results in local vasoconstriction. This is partly a result of a reducedresponsiveness to local vasodilators (endothelial derived relaxing factor = nitric oxide)and to increased levels of the local vasoconstrictor, endothelin. A role for endothelinantagonists in the treatment of heart failure has been suggested.Regional circulations in cardiac failureThere is a redistribution of blood flow to different organs and tissues in cardiac failure.Salt and water retention 64
  • 4. An almost invariable feature of cardiac failure is the retention of sodium and water.This leads to a substantial increase in extracellular and plasma volume and plays alarge part in the production of the clinical features of cardiac failure.Raised venous pressure in cardiac failureWhen the left ventricle fails the pulmonary venous pressure rises, and when the rightventricle fails the pressure rises in the systemic veins. The increased blood volumeresulting from sodium and water retention contributes to the venous return and is thusa factor in producing the raised venous pressure, as is venoconstriction.The effect of Left ventricular failure on the LungsWhen the left ventricle fails, the diastolic pressure in the left ventricle rises and with itthe left atrial pressure. Since the pulmonary veins and capillaries are in continuity withthe left atrium, the pressures in these vessels rise concomitantly. As failure advances,the left atrial pressure progressively increases from its normal level of 5—10 mmHg to25—30 mmHg. The hydrostatic pressure in the capillaries may lead to an exudation offluid from the capillaries into the alveolar walls and alveoli. The pulmonarycongestion caused by the high pulmonary venous pressure and by the changes in thealveolar walls makes the lung more rigid (less compliant). As a result of this, morework must be done by the respiratory muscles to move a given volume of air.Arrhythmias in heart failurePatients with heart failure have a high incidence of sudden death. The majority ofdeaths are thought to be due to ventricular tachycardia or ventricular fibrillation.Arrhythmia prevention in patients with heart failure is a particular problem. Theefficacy of antiarrhythmic drugs is reduced and there is, moreover, an increasedincidence of proarrhythmic side-effects. In addition, most antiarrhythmic drugs havenegative inotropic effects. 65
  • 5. CLINICAL SYNDROMES OF HEART FAILURELeft heart failureAetiologyThe features of left heart failure develop when there is a major obstruction to outflowfrom the left atrium (e.g. mitral stenosis) or when the left ventricle can no longer copewith the demands upon it. The common causes of left ventricular failure are:• myocardial infarction• systemic hypertension• valvular heart disease• Cardiomyopathy.Clinical features: The clinical features of left-sided cardiac failure are largely theconsequence of pulmonary congestion. The symptoms are:• dyspnoea on exertion• orthopnoea and paroxysmal nocturnal dyspnoea• acute pulmonary oedema.The physical signs of left ventricular failure may include:• pulmonary crepitations• third heart sound• pleural effusion• pulsus alternans — alternate large and low volume indication of severe leftventricular failure.Investigations• The chest radiograph may show features of pulmonary venous congestion,particularly of the upper lobe, interstitial oedema and alveolar oedema.• The electrocardiogram (ECG) may be of value although it does not provide directevidence of left heart failure. For example, it is unusual for hypertension or aorticvalve disease to lead to the symptoms of left heart failure without producing ECG 66
  • 6. evidence of left ventricular hypertrophy first. Again, it is unusual for coronary arterydisease to lead to left heart failure if the ECG is normal. This is not, however, true ofmitral regurgitation.• Echocardiography: To assess left ventricular end-diastolic and end-systolicdimensions; systolic function (Ejection Fraction). Echocardiography is alsoimportant in the exclusion of other potentially treatable causes of heart failure such asaortic stenosis or mitral regurgitation. Atrial natriuretic peptide (ANP) levels and the closely related brain natriureticpeptide (BNP) are elevated in patients with heart failure.Differential diagnosisThe dyspnoea of left heart failure is more likely to be provoked by lying down flat.Patients with dyspnoea due to pulmonary disease usually have a history of asthmaticattacks or of chronic cough and sputum.Paroxysmal nocturnal dyspnoea and acute pulmonary oedema may be difficult todifferentiate from acute respiratory attacks. The latter are commonly associated withbronchospasm and purulent sputum. In contrast, the patient with acute pulmonaryoedema is usually free of pulmonary infection, has fine crepitations rather thanrhonchi and is liable to cough up pink frothy sputum. Furthermore, examinationusually reveals the signs of left-sided heart disease. Correct diagnosis is of greatimportance because the therapy of the two conditions is different. For example,morphine may be lethal in respiratory failure, but invaluable in acute pulmonaryoedema. The chest radiograph is also helpful in showing signs of oedema or infection.In cases of doubt, estimation of the arterial CO2 tension is of value because this isusually low in acute pulmonary oedema.Right heart failureAetiology- left ventricular failure with its consequent effects upon the pulmonary circulation. 67
  • 7. - right ventricular infarction .- pulmonary disease, particularly chronic bronchitis and emphysema pulmonary hypertension .- pulmonary valve disease- tricuspid regurgitation.- Right sided venous congestion can result from tricuspid stenosis.Clinical features: The characteristic features of right heart failure are:• Elevated jugular venous pressure. In the normal individual, the venous pressure inthe internal jugular veins does not exceed 2 cm vertically above the sternal angle whenthe patient is reclining at 45° In right heart failure this figure is exceeded. Even ifnormal at rest, it rises on exercise.• Hepatomegaly. If chronic, this may result in cirrhosis.• Oedema. This is of the dependent type and usually most evident in the pretibialand ankle regions.• Ascites. This may occasionally occur in patients with severe right heart failure.• Tricuspid regurgitation. This can occur in patients with severe or long-standingright heart failure, when right ventricular dilatation results in a functionalincompetence of the tricuspid valve. A prominent V wave may be seen in venouspulse and a pulsatile liver edge may be palpable.Differential diagnosis: In patients presenting with isolated signs of right heart failure,the possibility of pericardial constriction or tamponade should be considered as analternative diagnosis.Other clinical features of cardiac failureThere are a number of common but less specific features of cardiac failure:• Fatigue is a frequent symptom which is difficult to evaluate.• The nutrition of patients with cardiac failure is often good in the early stages, butcachexia sets in as disability increases. 68
  • 8. • In the very advanced case, cerebral symptoms may develop with dulling ofconsciousness, confusion or changes in personality.• Patients with cardiac failure are prone to develop venous thrombosis andpulmonary emboli are common.• Mild jaundice, due to hepatic congestion or cirrhosis, is quite frequent in right-sided heart failure.• Proteinuria due to renal congestion is often present.General management of cardiac failureThe principles of treating cardiac failure may be enumerated as follows:• the correction or amelioration of the underlying disease• the control of precipitating factors• the reduction of demands on the heart by weight loss and the restriction of physicalactivity• pharmacological therapy to modify the heart failure state and, particularly, toreverse the adverse consequences of neuroendocrine and renal responses to heartfailure.The objectives of therapy are twofold: to alleviate the symptoms caused by heartfailure and to improve the prognosis.The correction or amelioration of the underlying causeWhen heart disease is due to such causes as thyrotoxicosis or hypertension, correctivetreatment can be started immediately. In congenital and rheumatic heart disease,surgical management is usually required.In the case of ischaemic heart disease, the cause of heart failure is generally previousmyocardial infarction rather than ongoing ischemia. Coronary revascularizationprocedures may be considered.The control of complicating factors 69
  • 9. Cardiac failure is often precipitated or exacerbated by factors superimposed on theunderlying heart disease. Amongst these are:• arrhythmias• infections• pulmonary embolism• anemia• excessive sodium intake• over-exertion.The recognition of precipitating factors is of great management of heart failure,because the correction of conditions will often result in the abolition of symptoms.ExerciseRest reduces the demands on the heart and leads to a fall in venous pressure and areduction in pulmonary congestion. It allows a relative increase in renal blood flowand often leads to a diuresis. However, bed rest also encourages the development ofvenous thrombosis and pulmonary embolism.The degree of physical restriction necessary depends upon the severity of the cardiacfailure. When there is severe pulmonary congestion or peripheral oedema, a period ofcomplete rest may be required. Complete bed rest is seldom necessary for more than afew days, after which a gradual increase in activity should be encouraged, dependingupon the response.In patients with lesser degrees of heart failure, regular exercise should be encouraged.Typical exercise would be to recommend 20 to 30 mm walking three times per week.Management of salt and water retentionLow salt diets effectively counteract cardiac failure. However, with the availability ofpotent diuretic drugs, no extreme limitation of sodium intake is usually necessary. PHARMACOLOGICAL THERAPYDiuretics: The loop diuretics: furosemide (frusemide), bumetanide 70
  • 10. These drugs prevent reabsorption at multiple sites including the proximal and distaltubules and the ascending limb of the loop of Henle.Thiazide diureticsThe main mechanism is the inhibition sodium reabsorption in the distal convolutedtubule. These drugs sometimes cause hyperglycaemia and hyperuricaemia, and mayprecipitate diabetes and clinical gout.Potassium-sparing diuretics:This group comprises two classes of agent:• Spironolactone. This drug is an aldosterone antagonist, providing a weak diuresiswith a potassium-sparing action.• Amiloride and triamterene. These drugs inhibit sodium—potassium exchange inthe distal tubule. They have a weak diuretic effect.Recently, spironolactone has been shown to confer an additional mortality benefit ofapproximately 30% in patients with severe heart failure.Hyperkalaemia is a potential complication, particularly in patients with impaired renalfunction. Particular caution is necessary when adding potassium retaining diuretics toACE inhibitor therapy. Spironolactone causes breast enlargement or pain inapproximately 10% of men taking the drug.Inhibitors of the renin-angiotensin systemTwo types of pharmacological agent can be used to block the renin—angiotensinsystem:• ACE inhibitors, which inhibit the conversion of angiotensin I to angiotensin II.• Angiotensin II receptor blocking agents provide an alternative approach toinhibition of the rennin-angiotensin system. They block the vasoconstrictor and otheractions of angiotensin II.ACE inhibitorsACE inhibitors are indicated both for the treatment of symptoms and to improveprognosis in patients with heart failure. In view of these benefits, ACE inhibitors 71
  • 11. should be prescribed, unless contraindicated, in patients with symptomatic heartfailure and in all patients, irrespective of symptoms, with an ejection fraction of lessthan 40%.Following myocardial infarction, ACE inhibitors are of particular value. They areindicated not only for the treatment of failure, but also for the prevention of adverseremodeling.ACE inhibitors are in general well tolerated. However, a number of problems may beencountered, including hypotension, renal impairment and cough:• First-dose hypotension can be minimized by reducing the dose of the ACEinhibitor on commencing therapy and omitting diuretics for 1—2 days beforehand.• ACE inhibitors occasionally cause deterioration of renal function. They arecontraindicated in patients with an initial creatinine level greater than 200 mmol/L (orcreatinine > 2.6 mg/dl). Renal function should be checked routinely 1—2 Weeks aftercommencing therapy.• Cough is a potentially troublesome side-effect, occurring in up to 10% of patients.Angiotensin II receptor blockersIn patients intolerant of ACE inhibitors there is evidence that angiotensin receptorblocking drugs do improve prognosis.Other vasodilatorsThe widespread applicability and indications for ACE inhibitors have reduced theimportance of other vasodilators in the management of heart failure.Nitrate vasodilators remain of value in the management of acute left ventricularfailure. Sublingual glyceryl trinitrate can be administered in the acute phase and canbe followed by an intravenous infusion. Nitrates act predominantly as venodilators.Hydralazine, by contrast, is predominantly an arterial dilator.Beta-blockers 72
  • 12. Excessive sympathetic stimulation may contribute to progression of heart failure in anumber of ways, including additional energy requirements, ventricular hypertrophyand arrhythmias. Beta-blockers result in a reduction in mortality, of the order of 30%.The reduction in mortality relates substantially to a reduction in sudden deaths, butbeta-blockers also benefit symptoms and have been shown to reduce hospitalizationsfor heart failure. Beta-blockers have been shown to benefit patients with class II andIII heart failure and to benefit selected patients with class IV heart failure. In general,the more severe the degree of heart failure and the worse the prognosis of the patient,the greater the benefit to be gained from beta-blockade.• Patient selection is crucial. Beta-blockers should not be given in new onset oruncontrolled heart failure. Patients presenting with acute heart failure or with anexacerbation of chronic heart failure should be stabilized with diuretics and ACEinhibitors before initiating a beta-blocker. Bradycardia (heart rate < 60) andhypotension (systolic blood pressure < 100) are relative contraindications and requireparticularly careful monitoring on commencement of therapy.• Low dose initiation of therapy is crucial.• Slow upward dose titration with clinical monitoring. Titration should occur atintervals of not less than 2 weeks. Dizziness, postural hypotension and worseningheart failure are all relatively common and may require dose reduction or cessation ofbeta-blocker therapy.Inotropic agentsDigitalis glycosidesMechanisms of actionThe inotropic action of digitalis is mediated through the sodium/potassium ATPase(sodium) pump, to which it binds. The inhibition of this pump leads to anaccumulation of intra-cellular sodium; because of the sodium— calcium exchangesystem, this results in an increase in the amount of calcium available to activatecontraction. Digitalis also has sympathomimetic and parasympathetic (vagal) effects.The latter is clinically important, in that it causes slowing of the sinus rate. 73
  • 13. Indications: Digoxin is particularly indicated in patients with heart failure and atrialfibrillation, for its beneficial effects to reduce ventricular response rate. In this settingit is an appropriate first line agent. VENTRICULAR RESYNCHRONIZATION THERAPYThere is growing evidence that some individuals with severe heart failure may beimproved by biventricular pacing to provide ventricular resynchronization.In many patients with severe heart failure, left ventricular contraction becomesincoordinate. Delay in the spread of the electrical impulse to different regions of theventricle results in a dispersion of the onset of contraction. As a consequence, theregions of the ventricle activated earliest may be relaxing by the time later regionshave started to contract. This results in an additional inefficiency of pump function,responsible for an additional deterioration in ejection fraction and cardiac output.Ventricular resynchronization pacing aims at pacing the septum and lateral wall of theleft ventricle simultaneously, thereby improving the synchrony of contraction. Oneelectrode is placed in the right ventricle, as for conventional pacing, and the other atthe left free wall. Left ventricular pacing is achieved via the coronary sinus.Simultaneous pacing at the two sites results in a narrowing of QRS width and animprovement in cardiac output.Criteria of selection of patients likely to benefit most from ventricularresynchronization pacing include:• Severe heart failure, New York Heart Association class III or IV• Left bundle branch block• QRS width greater than 120 ms• Evidence of incoordinate left ventricular contraction on echocardiography. ARRHYTHMIA MANAGEMENT 74
  • 14. About 50% of patients with heart failure die from progressive heart failure. The other50% die suddenly as a result of ventricular arrhythmias.Beta-blockade has been shown to dramatically reduce sudden deaths.There is growing evidence to suggest a role for implantable defibrillators in thispatient population. Implantable defibrillators have been shown to significantlyreduce mortality in patients with an ejection fraction less than 30%.As implantable defibrillators can be combined with ventricular resynchronization,there is likely to be a growing role for device therapy in the management of patientswith severe heart failure. ACUTE LEFT VENTRICULAR FAILUREAcute pulmonary oedema is a life-threatening emergency. Characteristically, thepatient is extremely breathless and frightened. The patient is unable to lie flat andprefers to sit bolt upright. In severe cases they may cough up blood tinged, pinksputum.Causes of acute left ventricular failure:- Acute myocardial infarction.- Atrial fibrillation and other tachyarrhythmias.- Severe hypertension.- Myocarditis- Infective endocarditis with acute valve damage (incompetence).- Chordal rupture.- Cardiac tamponade- Acute exacerbation of chronic heart failure (due to increased sodium intake, non-compliance with medications (eg stopping digitalis), exacerbation of hypertension,acute arrhythmias, infection and/or fever, pulmonary embolism, anemia andhemorrhage, thyrotoxicosis, pregnancy and child birth, infective endocarditis withvalve damage, rheumatic fever, physical emotion and stress, and prolongedtachycardia or bradycardia). 75
  • 15. Causes of non-cardiac pulmonary edema:- Adult respiratory distress syndrome.- Pulmonary embolism.- Toxic gases.- Gram negative septicemia (shock-lung).- Diffuse pulmonary infections.- Aspiration.- Narcotic overdose especially parentral heroin.- Lymphatic obstruction.- Following cardio-pulmonary bypass.- Hemorrhagic pancreatitis.Clinical features• The patient is tachypnoeic and distressed.• Perspiring profusely.• Systolic pressure is frequently elevated.• A marked tachycardia is evident with a gallop rhythm on auscultation.• Crackles and wheeze are heard throughout the chest.Table: Differentiating Points Between Bronchial Asthma and Cardiac Asthma Bronchial Asthma Cardiac AsthmaHistory of allergy usually present usually absentAge usually young usually olderCardiac lesion absent present (causing left heart failure)Cough associated with viscid associated with frothy pinkish sputum sputumChest examination mainly wheezes wheezes and crepitationsEosinophilia usually present absentCirculation time normal or short prolongedInvestigations 76
  • 16. • Chest radiograph shows diffuse haziness due to alveolar fluid. Changes generallybilateral (Bat-wing appearance) but occasionally may be unilateral.• Blood gases. Arterial p02 falls. Initially pCO2 also falls due to breathing, but inthe later stages pCO2 may rise due to impaired exchange.Management: Management of acute LVF:• General. A venous line should be inserted and the patient should be monitored.• Oxygen. This should be administered in high concentrations (60%) unless thepatient has concomitant airways disease.• Diamorphine. The standard dose of diamorphine is 5 mg given intravenously.• Diuretics. The patient should be given intravenous furosemide (frusemide). Theusual dose would be 40 mg, but this may be increased in patients already on diuretictherapy.• Nitrates. Administration of a sublingual tablet of glyceryl trinitrate has animmediate effect of lowering pulmonary pressures and reducing pulmonary oedema.This may be followed, if necessary, by an infusion of the drug.• Inotropic therapy. In cases of refractory pulmonary oedema, inotropic therapyshould be considered. Aminophylline 250 mg i.v. over 10 mm is frequently effective.Alternatively, patients may be started on a dobutamine infusion, beginning at 5µg/kg/min. CARDIOGENIC SHOCKThe terms acute circulatory failure, low output state, and shock are used to describe asyndrome comprising arterial hypotension, cold, moist and cyanosed extremities, arapid weak pulse, a low urine output and a diminished level of consciousness. Thispattern can arise as a result of impaired cardiac function, in which case, it is termedcardiogenic shock.This clinical pattern is common to a number of other disorders and cardiogenic shockmust be differentiated from other causes of shock, including: 77
  • 17. • hypovolaemic shock, eg by haemorrhage and loss of fluid from burns, vomitingand diarrhoea• septicaemic shock• anaphylactic shock• acute pancreatitis.Shock is described as cardiogenic when it is clearly cardiac in origin. This may be dueto many different causes, including myocardial infarction, massive pulmonaryembolism, dissecting aneurysm, pericardial tamponade, rupture of a valve cusp, andarrhythmias; also pulmonary embolism. In cardiogenic shock, the central venouspressure is usually raised, in contrast to hypovolaemic shock, in which it ischaracteristically low.Clinical features• In the first stage of shock, there is a fall in cardiac output and blood pressure, dueto either a diminution in venous return or to an inability of the myocardium to expel anadequate stroke volume.• As a consequence of the hypotension, there is a fall in renal blood flow, witholiguria.• Reflex tachycardia occurs.• Compensatory reflex arteriolar vasoconstriction further reduces blood flow to thekidneys, abdominal viscera, muscle and skin. Vasodilatation of the cerebral andcoronary vessels permits the maintenance of a relatively good blood flow in theseterritories. If the vasoconstriction is sufficiently great, the blood pressure may be keptat or close to normal levels but at the expense of producing tissue hypoxia withconsequent acidosis.Management of cardiogenic shockGeneral managementIf the patient is in severe pain or distress, opiates should be given intravenously(provided there is no contraindication) and high-flow oxygen administered, preferablyby a tight-fitting face mask making use of the Venturi principle, or by mechanical 78
  • 18. ventilation. Unless there is pulmonary oedema, the patient should be laid flat, with thelegs slightly raised. A catheter should be introduced to measure urinary output.Arterial blood gases and pH should be monitored. A Swan-Ganz balloon- tip cathetershould be used to obtain pulmonary artery and ‘pulmonary capillary wedge’ pressuresif a cardiac or pulmonary cause is known or suspected (recently this invasivemonitoring was considered not mandatory in some cases). As measurement of bloodpressure by a sphygmomanometer is unreliable in severe shock, direct arterial pressuremonitoring should be undertaken, when possible.Correction of hypovolaemiaAlthough left ventricular filling pressures are most commonly elevated in patients withcardiogenic shock, this is not always the case. Patients may have undergone a periodof prior diuretic therapy resulting in fluid depletion. Alternatively, in cases of rightventricular infarction the left ventricle may be under filled. A Swan—Ganz catheterenables pulmonary artery wedge pressure to be estimated to achieve an optimalpressure of between 18 and 20 mmHg. If the pressure is below this level, saline shouldbe administered to increase the wedge pressure and optimize cardiac outputInotropic agentsThese drugs enhance myocardial contractility but at the expense of increased oxygenconsumption. Dopamine and dobutamine are most frequently used.The effects of dopamine, a natural precursor of noradrenaline (norepinephrine),depend upon the dose. Administered intravenously in a dosage of 2—5 µg/kg/min, itcauses dilatation of renal and mesenteric vessels; at doses of 5—10 µg/kg/min, itincreases myocardial contractility and cardiac output. At higher doses, it causesvasoconstriction (it should not be infused directly into a peripheral vein as leakagemay cause local necrosis). Dopamine may induce nausea and vomiting, and can leadto an excessive tachycardia and arrhythmias. 79
  • 19. Dobutamine is a synthetic sympathomimetic agent whose predominant action is one ofstimulating activity. It is less likely to cause vasoconstriction or tachycardia thandopamine. It is given by intravenous infusion at a rate of 2.5—10 µg/kg/min.Mechanical supportThe intra-aortic balloon pump is of value in acute myocardial infarction if shock hasbeen caused by a surgically correctable lesion, such as a ventricular septal defect orpapillary muscle rupture. REFRACTORY HEART FAILUREHeart failure is termed refractory when it persists or deteriorates despite intensivetherapy. Causes:- Hyperthyroidism- Anemia- Recurrent pulmonary emboli- Atrial fibrillation and other arrhythmias- Multiple myocardial infarcts, multivessel coronary disease- Hypertension uncontrolled- Pneumonia, other infections, chronic obstructive pulmonary disease withexacerbations.- Infective endocarditis- Rheumatic activity- Pregnancy- Constrictive pericarditis and endomyocardial fibrosis- Left ventricular aneurysm- The myocardium reached end stage with fibrosis, scars, and multiple infarcts.Diagnosis and Treatment: according to cause. ACUTE EXACERBATION ON TOP OF CHRONIC HEART FAILURECause, diagnosis and treatment: Review above page 69. 80
  • 20. INFECTIVE ENDOCARDITISInfective endocarditic can occur in two ways:1. When the heart valves and endocardium are damaged, organisms of lowpathogenicity (e.g. streptococcus viridans) can invade them and produce a slowlyprogressive infection, i.e. subacute bacterial (or infective) endocarditis.2. Normal valves and endocardium can be invaded by organisms of highpathogenicity (e.g. staphylococcus aureus, pneumococcus, gonococcus) in the courseof a fulminating septicemia originating in another organ. In these cases the course isusually acute, i.e. acute bacterial (or infective) endocarditis.SITE OF INVOLVEMENT:- Subacute infective endocarditis occur on top of a preexisting heart disease, e.g.chronic rheumatic heart disease, congenital heart disease, etc. or on artificial(prosthetic) valve.- It most commonly complicates mitral regurgitation, aortic stenosis, aorticregurgitation, calcific or sclerotic aortic valve, ventricular septal defect, patent ductusarteriosus, bicuspid aortic valve or artificial valves.- It is less common in cases of Fallot’s tetralogy and pure mitral stenosis. It is veryrare in cases of atrial septal defect. Endocarditis of the tricuspid valve occurs inintravenous drug abusers who inject drugs under septic conditions.- It is more common in the left side of the heart than the right side. 81
  • 21. ORGANISM:The most common causative organism is Streptococcus viridans. Less common areStaphylococcus aureus and enterococcus. Fungal endocarditis is caused by candida oraspergillus and it is common in patients receiving large doses of antibiotic, steroids orcytotoxic drugs. It is also common in drug abusers and in infections of prostheticmaterials placed in the circulation e.g. indwelling catheters, prosthetic valves, etc.SOURCE OF INFECTION:Bacteremia, by dental extraction and other dental procedures, urinary catheterization,labor, abortion, upper respiratory infection, etc. But often the source of infection isunknown.CLINICAL PICTURE:1. Onset is usually insidious with fever, sweating, arthralgia, malaise, toxic anemiclook.2. Persistent fever is usually of low grade but varies, with pallor and earthy “café aulait” facies.3. The heart may show the following:a. There is always evidence of pre-existing heart disease.b. Change or increase of existing murmurs or the development of new murmurs dueto destruction of heart valves by the infection.c. In advanced cases heart failure results from toxic myocarditis and the effects ofvalvular defects.4. The spleen is moderately enlarged and tender in most cases.5. Clubbing of the fingers occurs after 5-6 weeks.6. Involvement of the kidney may result ina. Hematuria, whether microscopic or macroscopic, and proteinuria occurs in mostcases.b. A picture of immune complex acute glomerulonephritis. 82
  • 22. c. Renal failure may complicate advanced cases.d. Renal infarction may cause pain in the loins and hematuria.7. Embolism may involve any organ, e.g. spleen, kidney, limbs, brain, retina,mesenteries. It produces variable signs and symptoms of infarction depending on thesite and size of the embolus and may cause mycotic aneurysm. Pulmonary embolismmay complicate endocarditis involving the right cardiac chambers. Retinal emboli orimmune complexes cause areas of hemorrhage with pale center (Roth spots).8. Neurologic manifestations include:a. Infective endocarditis sometimes presents as cerebral embolism. Septic infarctionmay result in cerebral abscess.b. Cerebral or subarachnoid hemorrhage may result from rupture of a mycoticaneurysm.c. A picture stimulating meningitis or encephalitis may occur.9. Skin lesions include:a. The commonest are petechial hemorrhages. They appear as crops of small brownred spots that do not disappear on pressure. They are most commonly found in thechest, neck, palate and conjunctiva.b. Osler nodules are tender intracutaneous nodules usually found in the pulps offinger and in the thenar and hypothenar eminence.c. More rarely streaks of hemorrhage under the nails (splinter hemorrhage), or flaterythematous macules in the palms and soles (Janeway lesions) may be seen.DIAGNOSIS:1. Bacterial endocarditis must always be suspected in any patient with a murmur ora known heart disease who develops an unexplained or prolonged fever.2. When bacterial endocarditis is suspected the diagnosis is confirmed by bloodculture. Culture must be done for aerobic and anaerobic bacteria and fungi and mustbe incubated for up to 3 weeks to allow slow growing organisms to emerge. When anorganism is isolated its antibiotic sensitivity must be tested. Cultures may also be 83
  • 23. negative in fungal endocarditis and in infections by fastidious or slowly growingorganisms, but most commonly in those who recently received antibiotic therapy.3. Echocardiography is essential and may show vegetations on the valves, an abscesson the valve ring, and the underlying heart disease. Transesophageal echocardiographyis more sensitive than the transthoracic technique.4. Urine examination commonly shows microscopic or macroscopic5. Hematuria. Red cell casts and heavy proteinuria indicate the presence of immunecomplex glomerulonephritis.6. Blood examination shows elevated ESR, anemia and sometimes leukocytosis.Duke criteria for diagnosis of IE:I- Definite IE:A- Pathological criteria:1- Microorganisms--------culture or histology or2- Pathological lesions----vegetations, abscess confirmed by histologyb- Clinical criteria: (2 major, or 1 major +3 minor, or 5 minor)*Major criteria:1- Positive blood culture for IE.2- Evidence of endocardial involvement:Positive echo---vegetations, abscess, new dehiscence of prosthetic valve, or new orworsened valvular regurgitation.* Minor criteria:1- Predisposition: heart disease, or IV drug use.2- Fever: >38 c3- Vascular phenomena:4- Immunologic phenomena:5- Microbiological evidence:6- Echo findings:II- Possible IE: 84
  • 24. Findings consistent with IE that fall short of (definite) but not (rejected)III- Rejected: Firm alternative diagnosis for manifestations of endocarditis orResolution of manifestations of endocarditis, antibiotic for 4 days or lessCOMPLICATIONS:The most important complications are:1. Arterial emboli may cause hemiplegia, aphasia, infarction of the bowel, kidney,lung, or ischemia or gangrene of arm or leg.2. Destruction or perforation of cardiac valves. Large vegetations may interfere withprosthetic valve function.3. Congestive cardiac failure.4. Uremia.DIFFERENTIAL DIAGNOSIS:The most important differential diagnosis is:a. Rheumatic activityb. Intercurrent infections and fevers.1. Sometimes, it may be very difficult to differentiate infective endocarditis fromrheumatic activity. The presence of enlarged spleen, clubbing of the fingers, petechiae,embolic manifestations and hematuria points towards infective endocarditis. On theother hand, the appearance of fleeting arthritis, erythema marginatum, subcutaneousnodules and evidence of previous streptococcal throat infection favours the diagnosisof rheumatic activity. When in doubt, multiple blood cultures should be done and thepatient should be treated as infective endocarditis.2. Infective endocarditis must be differentiated from other causes of fever inpatients with previous heart disease, e.g. specific infections as brucella, typhoid,tuberculosis etc., connective tissue diseases, lymphomas, etc. These diseases arediagnosed by their specific signs and tests. 85
  • 25. PROPHYLAXIS:1. Amoxicillin (2 gm) prophylaxis should be given orally to all patients withrheumatic or congenital heart disease, one hour before all procedures that may resultin bacteremia. These include dental extraction, tonsillectomy, urethral catheterization,prostatic massage, delivery, abortion, etc. In cases of penicillin sensitivityclindamycin, erythromycin or vancomycin can be used.2. In patients at very high risk of developing endocarditis (e.g. those with prostheticvalves or history of previous endocarditis), more intensive prophylaxis is required.Ampicillin 2 gm IV or IM should be given 30 minutes before the procedure togetherwith gentamycin 1.5 mg/kg. This should be repeated 6 hours later.TREATMENT:- Streptococcus viridans is usually penicillin sensitive and is eradicated by giving 3million units of penicillin l.V. every 4 hours (18 million per day) for 3-4 weekstogether with gentamycin 1 mg/kg every 8 hours I.M. for the first two weeks oftreatment. For penicillin resistant streptococci and for penicillin allergic patientvancomycin is given 15 mg/kg/12 hours + gentamycin.1. Enterococcus is less sensitive and needs 20-40 million units of penicillin G I.V.plus gentamycin 3 mg/kg I.M. daily. Ampicillin in a dosage of 2 gm every 4 hoursI.M. may be substituted for penicillin. The effective dose should be maintained for atleast 6-8 weeks.2. Staphylococcus: most strains secrete penicillinase and these should be treated bypenicillinase-resistant penicillins (nafcillin or oxacillin) or cefazolin or vancomycin 15mg/kg/12 hours for 6 weeks. An aminoglycoside antibiotic and rifampicin 300 mgtwice daily may be added.3. Culture-negative endocarditis patients should be treated as enterococcalendocarditis. Surgery will also be needed if: 86
  • 26. a. Infection cannot be controlled.b. An abscess forms around the valve ring.c. Very big vegetations that may cause major emboli.d. Congestive heart failure develops due to destruction or perforation of a valve. 87

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