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This document discusses acute and chronic left ventricular failure. It describes the classification, aetiologies, clinical presentation, investigations and management of acute LV failure, which can occur de novo or in the setting of chronic cardiac failure. The main causes of acute de novo LV failure are acute myocardial infarction, valve failure, myocarditis, and hypertensive crisis. Acute-on-chronic cardiac failure can be precipitated by non-compliance with medications, drugs that cause sodium retention or myocardial depression, or an intercurrent illness in a patient with chronic cardiac failure. Chronic cardiac failure is a major health problem associated with ischaemic heart disease, hypertension, and other conditions.
This document discusses acute and chronic left ventricular failure. It describes the classification, aetiologies, clinical presentation, investigations and management of acute LV failure, which can occur de novo or in the setting of chronic cardiac failure. The main causes of acute de novo LV failure are acute myocardial infarction, valve failure, myocarditis, and hypertensive crisis. Acute-on-chronic cardiac failure can be precipitated by non-compliance with medications, drugs that cause sodium retention or myocardial depression, or an intercurrent illness in a patient with chronic cardiac failure. Chronic cardiac failure is a major health problem associated with ischaemic heart disease, hypertension, and other conditions.
This document discusses acute and chronic left ventricular failure. It describes the classification, aetiologies, clinical presentation, investigations and management of acute LV failure, which can occur de novo or in the setting of chronic cardiac failure. The main causes of acute de novo LV failure are acute myocardial infarction, valve failure, myocarditis, and hypertensive crisis. Acute-on-chronic cardiac failure can be precipitated by non-compliance with medications, drugs that cause sodium retention or myocardial depression, or an intercurrent illness in a patient with chronic cardiac failure. Chronic cardiac failure is a major health problem associated with ischaemic heart disease, hypertension, and other conditions.
ACUTE LEFT VENTRICULAR FAILURE Acute LV failure can either occur de novo or on a background of chronic cardiac failure, i.e. acute-on-chronic cardiac failure. This is important because the aetiologies, clinical presentation and management are quite distinct. CLASSIFICATION Most cases of cardiac failure are associated with reduced systolic function and sometimes a low-output state. Diastolic dysfunction may also contribute to cardiac failure in patients with large infarct zones, cardiomyopathies, pericardial disease or mitral stenosis. AETIOLOGY Acute de novo cardiac failure Acute MI Acute native valve failure (e.g.chordal rupture, endocarditis) or acute VSD Acute myocarditis Hypertensive crisis accelerated hypertension with background essential hypertension renovascular disease (e.g.renal artery stenosis) phaeochromocytoma
Cardiac tamponade Profound bradycardia or tachycardia Myocardial depression due to drug toxicity tricyclic antidepressants blockers calcium channel antagonists
Acute-on-chronic cardiac failure
Non compliance with or reduction in cardiac failure drug therapy (e.g.diuretic, ACE inhibitor) a common precipitant
Myocardial depressant drug or drugs that promote sodium / water retention (e.g.corticosteroids, NSAIDs) Intercurrent non-cardiac illness in a patients with chronic cardiac failure
CLINICAL PRESENTATION Acute de novo LV failure usually presents with rapidly worsening fatigue, dyspnoea and limitation of effort tolerance. Orthopnoea, paroxysmal nocturnal dyspnoea and acute respiratory distress may supervene. There may also be prodormal symptoms which suggest an underlying aetiology, e.g.chest pain or palpitation. Physical signs of cardiac failure and underlying cardiac diseases are described more comprehensively.
INVESTIGATION Laboratory tests U & Es - renal failure (predisposes to fluid retention) - High or low K + predisposes to arrhythmias ABGs - systemic hypoxia - Acidosis (may be metabolic due to poor tissue perfusion, or mixed due to additional CO 2 retention) Virology - If viral myocarditis suspected(e.g.antecedent H x of flu-like illness), serology may help identify the culprit organism TFTs FBC - anaemia (exacerbates cardiac failure), WCC(infection) ECG acute or previous MI ischaemic features arrhythmia, e.g.atrial fibrillation CXR pulmonary oedema Pleural effusions, fluid in horizontal fissure Septal (Kerley B) lines Pulmonary pathology Cardiac size Echo - LV function - LVH (suggests hypertension, aortic stenosis or hypertrophic cardiomyopathy)-associated with diastolic dysfunction - valve disease, e.g.mitral regurgitation, aortic stenosis - pericardial effusion - endocarditis Right heart catheterization
Key points : examination General - usually distressed or agitated - tachypnoea - semiconscious or unconscious in severe/protracted cases - signs of sympathetic activation/low cardiac output pallor sweating Cool peripheries Peripheral cyanosis - Cutaneous stigmata of endocarditis - Signs of non-cardiac ilness clinical anaemia Fever Thyroid signs Pulse - usually tachycardic. Relative bradycardia can worsen cardiac failure by limiting cardiac output - may be irregular; suggests atrial fibrillation - may be low ( output) or normal pulse volume
Blood pressure - hypotension heralds poor prognosis - hypertension may aggravate cardiac failure - check for pulsus paradoxus
JVP - often elevated, but not invariably so
Precordium - apex usually not displaced in de novo cardiac failure; may be dyskinetic in anterior MI - apex often displaced in chronic heart failure - murmur (may suggest valve pathology or acute VSD) - gallop rhythm :S 3 S 4
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inspiratory crepitations - pleural effusions in chronic cardiac failure
Other - peripheral/sacral oedema, pulsatile hepatomegaly, ascites, right parasternal lift most often accompany chronic right-sided cardiac failure, but are uncommon in de novo cardiac failure
MANAGEMENT
Acute cardiac failure should be managed in a high- dependency or coronary care unit. Patients who are unable to maintain adequate systemic oxygenation or acid-base balance despite initial therapy need to be managed in an intensive care unit with ventilation facilities. ECG, blood pressure and O 2 saturation monitoring are mandatory.
Initial management IV access High-low O 2 (60-100%) Nitrates - this is at least as important as diuretic R X . - buccal GTN 2-5 mg OR - IVI GTN 0.6-12 mg min -1 OR - IVI isosorbide dinitrate 2-10 mg h -1 - IVI sodium nitroprusside 10-200 g min -1 Opiate - IV morphine 5-20 mg Loop - IV frusemide 50-100 mg bolus OR diuretic - IVI frusemide 5-20 mg h -1
The acute effect of loop diuretic is venodilation;intravascular volume reduction occurs later
Digoxin - useful for rate control in atrial fibrillation; role in cardiac failure in sinus rhythm controversial - oral dose:0.5 mg, repeated after 6 hours - IVI:0.5 mg over 20 min, repeated after 6 hours
Treat identifiable triggers, e.g.aspirin and thrombolysis for acute MI.
An additional agent (e.g. ACE inhibitor) may be needed if nitrate therapy fails to control hypertension. Arrhythmias are often poorly tolerated. Atrial fibrillation can cause catastrophic haemodynamic collapse because of the loss of atrial contribution to ventricular filling. In these cases DC cardioversion IVI amiodarone via a central venous catheter (300 mg over 30 min, followed by 900 mg over 24 h) may be needed. Management of resistant cardiac failure Advanced haemodynamic support Hypotensive patients with cardiac failure may benefit from inotropes Dobutamine 5-20 g kg -1 min -1 Dopamine 2.5-5 g kg -1 min -1 Adrenaline 1-12 g min -1 Noradrenaline 1-12 g min -1 Intra-aortic balloon pumping
Renal failure Patients with fluid overload in whom diuresis is not achieved may require extracorporeal haemofiltration.
Respiratory failure If, despite medical management, the patients remains in a state of repiratory compromise, mechanical ventilation should be considered. Intubation, paralysis and intermittent positive- pressure ventilation Mask continuous positive airway pressure ventilation
CHRONIC CARDIAC FAILURE Chronic cardiac failure is a major public health problem in the UK, affecting between 1 and 2% of the general population. It is associated with acute high morbidity and mortality and is a major cause of recurrent hospitalization. Chronic cardiac failure is characterized by diminished cardiac reserve and a complex series of maladaptive neurohumoral responses, principally involving the sympathetic and renin-angiotensin axes. The resultant increased peripheral vascular resistance and sodium and water retention serve to increase cardiac workload and worsen LV failure. Current drug therapies in chronic cardiac failure are directed at preventing sodium and water retention and antagonizing the humoral responses that cause peripheral vasoconstriction. CLASSIFICATION Cardiac failure is classified in several ways : acute and chronic, left and right, high output and low output and sytolic and diastolic dysfunction. Cardia failure symptoms are graded using the New York Heart Association System.
Diagnosis of diastolic heart failure requires : Symptoms or sign of heart failure Normal or mildly abnormal LV systolic function Abnormal LV relaxation, filling or diastolic distensibility or stiffness
AETIOLOGY
The main causes of chronic cardiac failure in western countries are : Ischaemic heart disease Hypertension Valvular heart disease Toxic : alcohol, adriamycin, cobalt Viral myocarditis : Coxsackie, HIV Other cardiomyopathies : hypertrophic, restrictive, dilated (sometimes familial) Infiltrative : amyloidosis, sarcoidosis Metabolic and nutritional : haemochromatosis, thyroid dysfunction, beri-beri CLINICAL PRESENTATION The most common cause of chronic cardiac failure is IHD; cardiac failure usually follows presentation with an acute MI. In some cases myocardial ischaemia or infarction is silent and the first presentation may be with cardiac failure itself. Conversely, some patients with IHD have asymptomatic LV dysfunction. However, most patients with chronic cardiac failure present with exertional fatigue and breathlessness and/or symptoms of fluid retention (e.g.oedema), or with an episode of acute LV failure. INVESTIGATIONS Laboratory tests U & Es - may be concomitant renal failure (due to renovascular disease, low cardiac output, or to diuretics, ACE inhibitor) - K + because of diuretics - Na + an ominous sign in advanced cardiac failure glucose - prognosis for diabetics with cardiac failure very poor LFTs - may be deranged because of liver congestion TFTs - hypo- and hyperthyroidism may exacerbate failure FBC - anaemia may exacerbate failure
cardiomyopathy screen - ferritin (haemochromatosis), Ca 2+
autoantibody screen - probably disease marker rather than causitive factor; anti- - and -myosin antibodies
blood group and tissue type - if transplantation being considered ECG Rarely normal in cardiac failure. Look for : evidence of previous MI LVH (large voltages seen both with LVH and cardiac dilatation) conduction defects atrial fibrillation
CXR cardiomegaly cardiac contour (e.g.left or right enlargement) may give clue to aetiology upper lobe venous diversion, interstitial oedema, pleural effusions, Kerley B lines may present. Echo Radionuclide ventriculography Stress testing Cardiac catheterization
MANAGEMENT Drug therapy Diuretics Loop diuretics, e.g. frusemide (typically 40-120 mg d -1 )orbumetanide (typically 1-4 mg d -1 )
Nitrates Nitrates, e.g.oral isosorbide mononitrate (30-120 mg d -1 )
Vasodilators Oral ACE inhibitors, e.g.captopril 12.5-50 mg tid, enalapril 10-20 mg bd or lisinopril 10-20 mg d -1 Oral AT 1 receptor antagonists, e.g.losartan 50-100 mg d -1 In patients with renal dysfunction or intolerance of ACE inhibitors and AT 1 receptor antagonists, the combination of hydralazine, and a nitrate is a suitable alternative. The regimen used in the VeHEFT-II trial was hydralazine 75 mg qid and isosorbide dinitrate 40 mg qid, although different dosing intervals and nitrate preparations can be used to improve compliance.
Inotropes Blockers Antiarrhythmics Anticoagulants
Surgery Revascularization Valve replacement Cardiac transplantation Causes and precipitating factors in AHF 1. Decompensation of pre-existing chronic heart failure (e.g.cardiomyopathy)
2. Acute coronary syndromes a) Myocardial infarction/unstable angina with large extent of ischaemia and ischaemic dysfunction b) Mechanical complication of acute myocardial infarction c) Right ventricular infarction
3. Hypertensive crisis 4. Acute arrhythmia (ventricular tachycardia, ventricular fibrillation, atrial fibrillation or flutter, other supraventricular tachycardia) 5. Valvular regurgitation (endocarditis, rupture of chordae tendinae, worsening of pre-existing valvular regurgitation) 6. Severe aortic valve stenosis 7. Acute severe myocarditis 8. Cardiac tamponade 9. Aortic dissection
10. Post partum cardiomyopathy
11. Non-cardiovascular precipitating factors a. lack of compliance with medical treatment b. Volume overload c. Infections, particularly pneumonia or septicaemia d. Severe brain insult e. After major surgery f. Reduction in renal function g. Asthma h. Drug abuse i. Alcohol abuse j. phaeochromocytoma 12. High output syndromes a) Septicaemia b) Thyrotoxicosis crisis c) Anaemia d) Shunt syndromes
Dyregulation of contractiliy Frank Starling mechanism? Force-frequency-relationship? Catecholamine refractoriness Neuroendocrine activation Sympathetic nervous system RAAS ADH,endothelin,etc Hypertrophy Low cardiac output Remodeling Ischaemia Fibrosis Myocyte Death Apoptosis Necrosis Acidosis, radical load Coronary perfusion Peripheral perfusion? Myocardial oxygen consumption? Reduced renal blood flow Tachycardia Hypotension Filling pressure? Wall tension? Cardiac output? Blood volume ? Vascular resistance? Precipitating condition Anaemia, thyroid disease,etc. Critical LV-Deterioration Previous myocardial injury Remodeling Chronic heart failure Afterload-Chronotropy/Inotropy/Lusitropy mismatch Hypertensive crisis Arrhythmias,etc. Acute critical myocardial injury Acute myocardial infarction Suspected Acute Heart Failure Assess Symptoms & Signs Heart Disease? ECG/BNP/X-ray? Evaluate cardiac function by Echocardiography/other imaging HEART FAILURE, assess by Echocardiography Characterize type and severity Consider other diagnosis Selected tests (angio, haemodynamically monitoring, PAC) Normal Abnormal Abnormal Normal Assessment of Ventricular Function Left Ventricular Ejection Fraction Reduced LVEF Systolic LV dysfunction <40%> Preserved LVEF Error in evaluation, other causes of heart failure, Diagnostic error (no heart failure Diastolic Dysfunction Transient Systolic Dysfunction Goals of treatment of the patient with AHF Clinical symptoms (dyspnoea and/or fatigue clinical signs body weight diuresis oxygenation Laboratory Serum electrolyte normalization BUN and/or creatinine S-bilirubin Plasma BNP Blood glucose normalization
Haemodynamic pulmonary capillary wedge pressure to<18 mmHg cardiac output and/or stroke volume Outcome Length of stay in the intensive care unit Duration of hospitalization Time to hospital re-admission Mortality
Tolerability Low rate of withdrawal from therapeutic measures Low incidence of adverse effects If moribund BLS, ALS Analgesia or sedation Immediate Resuscitation Patient distressed or in pain YES NO Increase FiO 2 , consider CPAP, NIPPV NO YES Arterial oxygen saturation >95% Pacing, antiarrhythmics etc YES YES YES NO Normal Heart Rate and rhythm Vasodilators, consider diuresis if volume overload NO Mean BP >70 mmHg Fluid challenge NO Adequate preload Consider inotropes or further afterload manipulation Reassess frequently YES NO Adequate Cardiac Output: reversal of metabolic acidosis, SvO 2 >65%, clinical signs of adequate organ perfusion Invasive monitoring eg PAC may be require Definitive Treatment Diagnosis algorithm Definitive Diagnosis Acute Heart Failure Acute heart failure with systolic dysfunction Oxygen/CPAP Furosemide vasodilator Clinical evaluation (leading to mechanistic theraphy) SBP < 85 mmHg Volume Loading? Inotrope and/or dopamine > 5 g/kg/min and/or norepinephrine No response: reconsider mechanistic therapy Inotropic agents SBP 85-100 mmHg Good response Oral therapy furosemide, ACEI Vasodilator and/or inotropic (dobutamine, PDEI or levosimendan) Vasodilator (NTG, nitroprusside, BNP) SBP > 100 mmHg Immediate surgical correction Pericardiocentesis Fluids Inotropes Consider IABP DIAGNOSIS Free wall rupture Echocardiography Pericardial effusion (especially if>10 mm) Echodensities in the effusion Echo signs of tamponade Immediate surgical correction Coronary Angiography Urgent surgical correction Coronary Angiography Stable patient Medical Therapy Unstable patient Consider : IABP Mechanical ventilation PAC Echocardiography DIAGNOSIS VSR VSR Site Size Qp:Qs Diagnosis uncertain PAC Oximetry O 2 step up>5% RA-RV Immediate surgical correction Coronary Angiography Urgent Surgical Therapy Coronary Angiography Stable Patient Medical Therapy Unstable patient Consider IABP Mechanical Ventilation PAC DIAGNOSIS Acute MR If Diagnosis Uncertain Consider TEE If TEE non Diagnostic Consider PAC To exclude VSR Echocardiography Echo signs of acute severe MR +/- Visualization of ruptured papillary muscle Echocardiography akinetic apex Hyperdinamic basal IVS, SAM Discontinue positive inotropes nitrates IABP Consider -blockers -agonists
Medical therapy Consider IABP Mechanical ventilation PCI or CABG VAD Heart transplant
Cardiogenic shock fromm loss of ventricular muscle mass Low EF No signs of mechanical complication Echocardiography