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Heart Failure

Heart Failure



Heart Failure medical lecture 4th year medical college students.

Heart Failure medical lecture 4th year medical college students.



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    Heart Failure Heart Failure Presentation Transcript

    • HEART FAILURE Dr.Abdulla Sherif. Find this lecture on: www.slideshare.net/shaikhani/heart failure .
    • HF:
      • The state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of an elevated filling pressure.
      • In the mildest forms, cardiac output is adequate at rest but becomes inadequate only when the metabolic demand increases during exercise or some other form of stress .
      • Diagnosed whenever a patient with significant heart disease develops the signs or symptoms of a low cardiac output, pulmonary congestion or systemic venous congestion .
      • It is a clinical syndrome rather than a specific diagnosis.
      • Good management depends on an accurate aetiological diagnosis, because in some situations a specific remedy may be available, but mainly because the nature of the pathophysiology guides logical drug therapy.
    • HF:
      • Is frequently due to CAD, affects elderly people& often leads to prolonged disability.
      • The prevalence rises from 1% in 50-59 years to 5 -10% of 80-89 years.
      • It carries a very poor prognosis; 50% with severe HF due to LVD will die within 2 years, many die suddenly from malignant ventricular arrhythmias or MI.
    • Features Examples Cause In coronary artery disease, 'akinetic' or 'dyskinetic' segments contract poorly and may impede the function of the normal segments by distorting their contraction and relaxation patterns MI (segmental dysfunction) Red V contractility Progressive ventricular dilatation Myocarditis/CMP (global dysfunction)   Initially concentric ventricular hypertrophy allows the ventricle to maintain a normal output by generating a high systolic pressure. However, secondary changes in the myocardium and increasing obstruction eventually lead to failure with ventricular dilatation and rapid clinical deterioration HT, AS (LHF) Pulm HT, PVS(RHF) V outflow obstr (pressure overload) Small vigorous ventricle, dilated hypertrophied atrium. Atrial fibrillation is common and often causes marked deterioration because ventricular filling depends heavily on atrial contraction MS, TS V inflow obstruction Dilatation and hypertrophy allow the ventricle to generate a high stroke volume and help to maintain a normal cardiac output. However, secondary changes in the myocardium eventually lead to impaired contractility and worsening heart failure LV volume overload (e.g. Ml or AR, AVF) VSD,RV volume overload (e.g. ASD) Increased metabolic demand (high output) V volume overload Tachycardia does not allow for adequate filling of the heart, resulting in reduced cardiac output and back pressure Atrial fibrillation Arrhythmia Incessant tachycardia causes myocardial fatigue Tachycardia CMP   Bradycardia limits cardiac output even if stroke volume is normal CHB  
    • Marked fluid retention and peripheral oedema, ascites, pleural effusions and elevated jugular veins Constrictive pericarditis Diastolic dysfunction Bi-atrial enlargement (restrictive filling pattern and high atrial pressures). Atrial fibrillation may cause deterioration Restrictive cardiomyopathy   Good systolic function but poor diastolic filling Left ventricular hypertrophy and fibrosis   Hypotension, elevated jugular veins, pulsus paradoxus, poor urine output Cardiac tamponade   Features Examples Cause
    • Pathophysiology:
      • Cardiac output is a function of the preload (the volume &pressure of blood in the ventricle at the end of diastole), the afterload (the volume & pressure of blood in the ventricle during systole) & myocardial contractility.
      • The interaction of these variables is shown is based on Starling's Law of the heart
      • . In patients without valvular disease, the primary abnormality is impairment of ventricular function leading to a fall in cardiac output. This activates counter-regulatory neurohormonal mechanisms that in normal physiological circumstances would support cardiac function, but in the setting of impaired ventricular function can lead to a deleterious increase in both afterload / preloa
      • ). A vicious circle is established as any additional fall in cardiac output will cause further neurohormonal activation & increasing peripheral peripheral vascular resistance.
    • Pathophysiology:
      • Stimulation of the renin-angiotensin-aldosterone system leads to vasoconstriction, salt and water retention& sympathetic activation mediated by angiotensin II, which is a potent constrictor of arterioles both in the kidney& systemic circulation .
      • Activation of the sympathetic nervous system may initially maintain cardiac output through an increase in myocardial contractility, heart rate& peripheral vasoconstriction,but prolonged sympathetic stimulation leads to cardiac myocyte apoptosis, hypertrophy& focal myocardial necrosis.
      • Salt /water retention is promoted by the release of aldosterone, endothelin (a potent vasoconstrictor peptide with marked effects on the renal vasculature)& in severe HF, (ADH).
      • Natriuretic peptides are released from the atria in response to atrial stretch& act as physiological antagonists to the fluid-conserving effect of aldosterone
    • Pathophysiology:
      • After MI, cardiac contractility is impaired & neurohormonal activation may lead to hypertrophy of non-infarcted segments, with thinning, dilatation & expansion of the infarcted segment (remodellin , )
      • This may lead to further deterioration in ventricular function&worsening heart failure .
      • The onset of pulmonary and/or peripheral oedema is due to high atrial pressures compounded by salt and water retention caused by impaired renal perfusion & secondary hyperaldosteronism
      • Left-sided heart failure. There is a reduction in the left ventricular output and/or an increase in the left atrial or pulmonary venous pressure.
      • An acute increase in left atrial pressure may cause pulmonary congestion or pulmonary oedema; a more gradual increase in left atrial pressure, as occurs with mitral stenosis, may lead to reflex pulmonary vasoconstriction, which protects the patient from pulmonary oedema at the cost of increasing pulmonary hypertension.
      • Right-sided heart failure.
      • There is a reduction in right ventricular output for any given right atrial pressure. Causes of isolated right heart failure include chronic lung disease (cor pulmonale), multiple pulmonary emboli & pulmonary valvular stenosis.
      • Biventricular heart failure.
      • Failure of the left and right heart may develop because the disease process (e.g. dilated cardiomyopathy or ischaemic heart disease) affects both ventricles, or because disease of the left heart leads to chronic elevation of the left atrial pressure, pulmonary hypertension and right heart failure.
      • Forward HF: 
      • In some patients with heart failure the predominant problem is an inadequate cardiac output
      • Backward HF:
      • In other patients may have a normal or near-normal cardiac output with marked salt and water retention causing pulmonary and systemic venous congestion ().  
      • Systolic HF:
      • Heart failure may develop as a result of impaired myocardial contraction (systolic dysfunction)
      • Diastolic HF:
      • Due to poor ventricular filling& high filling pressures caused by abnormal ventricular relaxation ,commonly found in patients with LVH&occurs in many forms of heart disease, HT/IHD.
      • Systolic / diastolic dysfunction often coexist, particularly in patients with CAD.  
      • High-output failure
      • Conditions that are associated with a very high cardiac output (e.g. a large arteriovenous shunt, beri-beri, severe anaemia or thyrotoxicosis) can occasionally cause HF.
      • In such cases, additional causes of heart failure are often present .
      • Acute and chronic HF:
      • Heart failure may develop suddenly, as in myocardial infarction, or gradually, as in progressive valvular heart disease. When there is gradual impairment of cardiac function, a variety of compensatory changes may take place.
      • ‘ Compensated HF:
      • A patient with impaired cardiac function in whom adaptive changes have prevented the development of overt heart failure.
      • A minor event, such as an intercurrent infection or development of atrial fibrillation, may precipitate overt or acute.
      • Acute left heart failure occurs either de novo or as an acute decompensated episode on a background of chronic heart failure, i.e. acute-on-chronic HF.
      • Usually presents with a sudden onset of dyspnoea at rest that rapidly progresses to acute respiratory distress, orthopnoea & prostration. The precipitant, such as AMI, is often apparent from the patient's history.  
      • The patient appears agitated, pale & clammy.
      • The peripheries are cool to the touch & the pulse is rapid.
      • Inappropriate bradycardia or excessive tachycardia should be identified promptly as this may be the precipitant for the acute episode of heart failure.
      • The blood pressure is usually high because of sympathetic nervous system activation, but may be normal or low if the patient is in cardiogenic shock.
      • The JVPis usually elevated, particularly with associated fluid overload or RHF.
      • In acute de novo HF, there has been no time for ventricular dilatation & the apex is not displaced.
      • Auscultation occasionally identifies the murmur of a catastrophic valvular or septal rupture, or reveals a triple 'gallop' rhythm. Crepitations are heard at the lung bases, consistent with pulmonary oedema.
      • Acute-on-chronic heart failure will have additional features of long-standing heart failure.
      • Potential precipitants, such as an upper respiratory tract infection or inappropriate cessation of diuretic medication, should be identified.
    • Acute LHF: Precipitating/agravating factors .
      • Myocardial ischaemia or infarction
      • Intercurrent illness, e.g. infection
      • Arrhythmia, e.g. atrial fibrillation
      • Inappropriate reduction of therapy
      • Administration of a drug with negative inotropic properties (e.g. β-blocker) or fluid-retaining properties (e.g. non-steroidal anti-inflammatory drugs, corticosteroids)
      • Pulmonary embolism
      • Conditions associated with increased metabolic demand, e.g. pregnancy, thyrotoxicosis, anaemia
      • Intravenous fluid overload, e.g. post-operative i.v. infusion
      • Commonly experience a relapsing / remitting course, with periods of stability & episodes of decompensation leading to worsening symptoms necessitaine hospitalisation.
      • The clinical picture depends on the nature of the underlying heart disease, the type of HFd& the neural/ endocrine changes.
      • A low cardiac output causes fatigue, listlessness and a poor effort tolerance; the peripheries are cold &BP is low.
      • To maintain perfusion of vital organs, blood flow may be diverted away from skeletal muscle contributing to fatigue / weakness.
      • Poor renal perfusion may lead to oliguria/ uraemia.
      • Pulm oedema due to LHF present with breathlessness, orthopnoea, PND& inspiratory crepitations over lung bases
      • RHF produces a high JVP, with hepatic congestion& dependent peripheral oedema.
      • In ambulant patients oedema affects the ankles, whereas in bed-bound patients it collects around the thighs/sacrum.
      • Ascites or pleural effusion can occur in some.
      • Chronic HF is sometimes associated with marked weight loss (cardiac cachexia) caused by a combination of anorexia& impaired absorption due to GIT congestion; poor tissue perfusion due to a low cardiac output, skeletal muscle atrophy due to immobility&increased plasma TNF-alpha .
    • Complications:
      • Renal failure is caused by poor renal perfusion due to a low cardiac output &exacerbated by diuretic therapy, ACEIs /ARBs.
      • Hypokalaemia may be the result of treatment with potassium-losing diuretics or hyperaldosteronism caused by activation of the RAS &impaired aldosterone metabolism due to hepatic congestion. Most of the body's potassium is intracellular& there may be substantial depletion of potassium stores, even when the plasma potassium is in the normal range.
      • Hyperkalaemia may be due to drug treatment, particularly the combination of ACEIs/spironolactone &renal dysfunction.
      • Hyponatraemia is a feature of severe HF, may be caused by diuretic therapy, inappropriate water retention due to high ADH secretion, or failure of the cell membrane ion pump. It is a poor prognostic sign,
    • Complications:
      • Impaired liver function is caused by hepatic venous congestion &poor arterial perfusion, which frequently cause mild jaundice & abnormal LFTs; reduced synthesis of clotting factors may make anticoagulant control difficult.
      • Thromboembolism. DVT/PE may occur due to the effects of a low cardiac output & enforced immobility, whereas systemic emboli may be related to arrhythmias, atrial flutter or fibrillation, or intracardiac thrombus complicating MS or LV aneurysm.
      • Atrial /arrhythmias are very common, may be related to electrolyte changes (e.g. hypokalaemia, hypomagnesaemia), the underlying structural heart disease& the pro-arrhythmic effects of increased circulating catecholamines& some drugs (e.g. digoxin). Sudden death occurs in up to 50% often due to a ventricular arrhythmia. Frequent ventricular ectopic beats & runs of non-sustained VT are common findings in patients with HF& are associated with an adverse prognosis.
    • Investigations:
      • Simple tests (e.g. urea, electrolytes, haemoglobin, thyroid function, ECG, chest X-ray) may help to establish the nature& severity of the underlying heart disease& detect any complications.
      • Brain natriuretic peptide (BNP) is elevated &can be used as a screening test in breathless & edematous.
      • Echocardiography is a very useful investigation considered in all patients with significant HF in order to:
      • Determine the aetiology
      • Detect hitherto unsuspected valvular heart disease (e.g. occult mitral stenosis)& other treatable condition.s
      • Identify patients who will benefit from long-term therapy with drugs such as ACEIs.
    • Investigations:
      • The chest X-ray:
      • A rise in pulmonary venous pressure from left-sided cardiac failure first shows on the chest X-ray as an abnormal distension of the upper lobe pulmonary veins (with the patient in the erect position).
      • The vascularity of the lung fields becomes more prominent& the right &left pulmonary arteries dilate.
      • Subsequently, interstitial oedema causes thickened interlobular septa and dilated lymphatics.
      • These are evident as horizontal lines in the costophrenic angles (septal or 'Kerley B' lines).
      • More advanced changes due to alveolar oedema cause a hazy opacification spreading from the hilar regions& pleural effusions .
    • APE Management:
      • This needs urgent treatment:
      • Sit the patient up in order to reduce pulmonary congestion.
      • Give oxygen (high flow, high concentration).
      • Non-invasive positive pressure ventilation (continuous positive airways pressure, CPAP, of 5-10 mmHg) by a tight-fitting face mask results in a more rapid.
      • Administer nitrates (e.g. i.v. glyceryl trinitrate 10-200 μg/min or buccal glyceryl trinitrate 2-5 mg) titrated upwards every 10 minutes, until clinical improvement occurs or systolic blood pressure falls to < 110 mmHg.
      • Administer a loop diuretic such as furosemide 50-100 mg i.v.
    • APE Management:
      • The patient should initially be kept on strict bed rest with continuous monitioring, including cardiac rhythm, blood pressure & pulse oximetry.
      • IVopiates may be cautiously used when patients are in extremis. They reduce sympathetically mediated peripheral when second vasoconstriction but run the risk of respiratory depression& exacerbation of hypoxia/ hypercapnia.
      • If these measures prove ineffective, inotropic agents may be required to augment cardiac output, particularly in hypotensive patients.
      • Insertion of an intra-aortic balloon pump can be very beneficial in patients with acute cardiogenic pulmonary oedema, especially when secondaary to myocardial ischaemia .
    • Chronic HF Management: General
      • Effective education of patients&their relatives about the causes & treatment can help adherence to a management plan.
      • Some patients may need to weigh themselves daily& adjust their diuretic therapy accordingly.
      • In patients with CAD, secondary preventative measures such as low-dose aspirin& lipid-lowering therapy are required.
    • Chronic HF Management: General
      • Education
      •   Explanation of nature of disease, treatment & self-help strategies
      • Diet
      • Good general nutrition and weight reduction for the obese
      • Avoidance of high-salt foods& added salt, especially for patients with severe congestive heart failure
      • Alcohol
      • Moderate or eliminate alcohol consumption. Alcohol-induced cardiomyopathy requires abstinence
      • Smoking : Stopping
      • Exercise
      • Regular moderate aerobic exercise within limits of symptoms
      • Vaccination
      • Influenza and pneumococcal vaccination should be considered
    • Chronic HF Management: Drugs
      • Cardiac function can be improved by increasing contractility, optimising preload or decreasing afterload.
      • Drugs that reduce preload are most appropriate in patients with high end-diastolic filling pressures&evidence of pulmonary or systemic venous congestion (backward failure); drugs that reduce afterload or increase myocardial contractility are more useful in patients with signs& symptoms of a low cardiac output (forward failure).
    • Chronic HF Management: Diuretics
      • These are usually the first-line treatment.
      • In heart failure, diuretics produce an increase in urinary sodium excretion, leading to a reduction in blood and plasma volume, and may also cause a small but significant degree of arterial and venous dilatation.
      • Diuretic therapy will therefore reduce preload and improve pulmonary and systemic venous congestion; it may also cause a small reduction in afterload and ventricular volume, leading to a fall in wall tension and increased cardiac efficiency.  
      • Although a fall in preload (ventricular filling pressure) tends to reduce cardiac output, the 'Starling curve' in heart failure is flat so there may be a substantial and beneficial fall in filling pressure with little change in cardiac ,but excessive diuretic therapy may cause an undesirable fall in cardiac output, with a rising blood urea, hypotension and increasing lethargy, especially in patients with a marked diastolic component to their heart failure.
    • Chronic HF Management: Diuretics
      • In some patients with severe chronic heart failure, particularly in the presence of chronic renal impairment, oedema may persist despite oral loop diuretics. In such patients an IV infusion of furosemide 10 mg/hr for example, can initiate a diuresis. Also combining a loop diuretic with a thiazide (e.g. bendroflumethiazide 5 mg daily) or a thiazide-like diuretic (e.g. metolazone 5 mg daily) may prove effective; however, such combinations can produce an excessive diuresis.
      • Aldosterone receptor antagonists such as spironolactone and eplerenone are potassium-sparing diuretics that are of particular benefit. They may cause hyperkalaemia, particularly when used with an ACE inhibitor. They improve long-term clinical outcome in patients with severe HF&those with HF following AMI.
    • Chronic HF Management: Vasodilators
      • Used in acute circulatory failure is described
      • Also valuable in chronic HF; venodilators (e.g. nitrates) reduce preload& arterial dilators (e.g. hydralazine) reduce afterload,but their use is limited by pharmacological tolerance& hypotension
    • Chronic HF Management: ACEIs
      • A major advance in the treatment of HF.
      • They interrupt the vicious circle of neurohormonal activation that is characteristic of moderate and severe heart failure by preventing the conversion of angiotensin I to angiotensin II, thereby preventing salt and water retention, peripheral arterial and venous vasoconstriction, and activation of the sympathetic nervous system& also prevent the undesirable activation of the renin-angiotensin system caused by diuretic therapy.
      • The major benefit of ACE inhibitor is a reduction in afterload; however, there may also be an advantageous reduction in preload & a modest increase in the plasma potassium.
      • Treating heart failure, with a combination of a loop diuretic & an ACEI therefore has many potential advantages.
    • Chronic HF Management: ACEIs
      • In moderate&severe HF, ACEIs can produce a substantial improvement in effort tolerance& in mortality& improve outcome& prevent the onset of overt heart failure in patients with poor residual LVF following AMI.
      • ACE inhibitors in chronic HF due to ventricular dysfunction reduce mortality & readmission rates.
      • 'ACE inhibitors can delay the development of symptomatic heart failure and reduce the frequency of cardiovascular events (death, myocardial infarction, hospitalisation) in patients with asymptomatic left ventricular systolic dysfunctio n.
    • Chronic HF Management: ACEIs S/Es
      • Profound hypotension with postural symptoms& a deterioration in renal function (especially in patients with bilateral renal artery stenosis or pre-existing renal disease).
      • Potentially catastrophic fall in blood pressure following the first dose of an ACE inhibitor, particularly if the drug is started in the presence of hypotension, hypovolaemia or hyponatraemia due to prior diuretic therapy, especially in the elderly.
      • In stable patients without hypotension (systolic BP > 100 mmHg), ACE inhibitors can usually be started in the community without problems,but in other patients it is usually advisable to withhold diuretics for 24 hours before starting treatment with a low dose, while the patient is supine & under observation.
      • If hypotension occurs, this can be counteracted by elevating the foot of the bed & giving IVsaline.
      • Renal function must be monitored &checked 1-2 weeks after starting therapy.
    • Chronic HF Management: ARBs
      • ARBs are better tolerated with similar efficacy in reducing CV events.
      • ARBs reduce cardiovascular morbidity& mortality in patients with symptomatic heart failure who are intolerant of ACE inhibitors.
      • These drugs act by blocking the action of angiotensin II on the heart, peripheral vasculature and kidney; in heart failure, they produce beneficial haemodynamic changes that are similar to the effects of ACE inhibitors.
      • They have comparable effects on mortality and are a useful alternative for patients who cannot tolerate ACE
      • Unfortunately, they share all the more serious adverse effects of ACE inhibitors including renal dysfunction.
    • Chronic HF Management: BBs
      • These drugs may help to counteract the deleterious effects of enhanced sympathetic stimulation and reduce the risk of arrhythmias and sudden death.
      • When initiated in standard doses they may precipitate acute-on-chronic heart failure, but when given in small incremental doses (e.g. bisoprolol started at a dose of 1.25 mg daily, and increased gradually over a 12-week period to a target maintenance dose of 10 mg daily) under carefully monitored conditions, they can increase ejection fraction, improve symptoms, reduce the frequency of hospitalisation& reduce mortality.
    • Chronic HF Management: Digoxin
      • This should be used as first-line therapy in patients with heart failure & atrial fibrillation, when it usually provides adequate control of the ventricular rate together with a small positive inotropic effect.
      • The role of digoxin in the treatment of patients with heart failure and sinus rhythm is less certain&may have no effect on overall survival but did reduce the need for hospitalisation .
    • Chronic HF Management: Amiodaron
      • This is a potent anti-arrhythmic drug which has little negative inotropic effect ,valuable in patients with poor left ventricular function.
      • It is only effective in the treatment of symptomatic arrhythmias, & should not be used as a preventative agent in the asymptomatic.
    • Chronic HF Management: ICD/CRT
      • Patients with symptomatic ventricular arrhythmias &heart failure have a very poor prognosis.
      • Irrespective of their response to anti-arrhythmic drug therapy, all should be considered for implantation of a cardiac defibrillator
      • In patients with marked intraventricular conduction delay, prolonged depolarisation may lead to uncoordinated left ventricular contraction.
      • When this is associated with severe symptomatic heart failure, CRT may be considered,whwre both the left and right ventricles are paced simultaneously in an attempt to generate a more coordinated LV contraction to improve cardiac output.
      • Because of the limited supply of donor organs, ventricular assist devices (VADs) employed as a bridge to cardiac transplantation, or more recently as potential long-term or 'destination' therapy.
    • Chronic HF Management: revascularization.
      • CABG or PCI may improve function in areas of the myocardium that are 'hibernating' because of inadequate blood supply&can be used to treat carefully selected patients with HF&CAD.
      • If necessary, 'hibernating' myocardium can be identified by stress echocardiography and specialised nuclear techniques .
    • Chronic HF Management: cardiac transplant.
      • Cardiac transplantation is an established&very successful form of treatment for patients with intractable HF.
      • CAD& dilated cardiomyopathy are the most common indications.
      • The introduction of ciclosporin for immunosuppression has improved survival, which now exceeds 90% at 1 year.
      • The use of transplantation is limited by the availability of donor hearts so it is generally reserved for young patients with severe symptoms.
      • Conventional heart transplantation is contraindicated in patients with pulmonary vascular disease due to long-standing left heart failure, complex congenital heart disease (e.g. Eisenmenger's syndrome) or primary pulmonary hypertension
      • Lung transplantation has been used for primary pulmonary HT.
    • HF in elderly:
      • Incidence: rises with age affecting 5-10% of people in their 80s.
      • Common causes: CAD,HT &calcific degenerative valvular disease.
      • Diastolic dysfunction: often prominent, particularly in those with a history of HT.
      • ACE inhibitors: improve symptoms/mortality but more frequently associated with postural hypotension& renal impairment than in younger patients.
      • Loop diuretics: usually required but may be poorly tolerated in those with urinary incontinence& men with prostate enlargement.