Cardiac Failure

Definition:
State where the heart is unable to maintain an adequate cardiac output, or is only able to do so at the expense of an elevated filling pressure. Diagnosed whenever PT with heart disease devts S/S of low CO, pul. congestion or systemic venous congestion. Refers to a clinical syndrome rather than a specific Dx. May be caused by many heart diseases. Mx requires Rx of underlying aetiology. Poor Px: many patients die suddenly due to malignant ventricular arrhythmias or MI.

Compensatory changes in Heart Failure: Local changes

Chamber enlargement Myocardial hypertrophy Increased heart rate

Systemic changes

Sympathetic activation RAAS activation ADH release Release of natriuretic peptides

Precipitating / Aggravating factors in Heart failure:

Cardiac Myocardial infarction Arrhythmias tachy/ brady Infective endocarditis Noncompliance with therapy Drug noncompliance Fluid restriction noncompliance Over-strenuous exercises Extracardiac Anemia e.g. secondary to GI bleed Hyperthyroidism Sepsis Pregnancy Drugs fluid-retaining e.g. NSAIDs, negatively inotropic drugs (beta-blockers)

Pathophysiology:
Starlings Law: Cardiac output depends on preload (end-diastolic vol. & pressure), afterload (arterial resistance) & myocardial contractility. Angiotensinog Renin Angiotensin I ACE Angiotensin II Direct vasoconstriction Aldosterone Salt & H20 retention Preload Afterload K loss
+

Afterload Contractility

Cardiac output

Types of Heart failure:

Left-sided HF LV output LA or pul. venous pressure o Acute : Pulmonary oedema o Gradual : reflex pul. vasoconstriction and pulmonary HPT RV output Causes: Cor pulmonale, multiple Pul. emboli, pulmonary stenosis Disease affecting both ventricles, or left heart dz leads to subsequent right heart failure Causes: dilated CMP, IHD Causes: large AV shunt, beri-beri, severe anaemia, thyrotoxicosis Impaired myocardial contraction May be a/w diastolic dysfunction as well More likely in younger PTs, hx of MI, displaced apex beat, S3 gallop, cardiomegaly on CXR Defective diastolic filling due to decreased LV compliance results in impaired LV filling, elevated Lt atrial and pul venous pressures, and decreased ability to increase stroke volume Causes: LVH due to HPT or IHD Findings: LVH, dilated Lt atrium, normal ejection fraction, reversal of flow velocity across the mitral valve More likely in hx of HPT, older PTs, sustained apex beat, S4 gallop, LVH on ECG, lack of cardiomegaly on CXR

Preload

Right sided HF Biventricular HF High output failure Systolic dysf(x)

CO= SV x HR
ADH release

Contractility

Sympathetic activation Neurohormonal changes: o activates RAAS and sympathetic nervous system o Initially optimizes CO by change in afterload, preload and contractility. o Later, reduces CO by excessive increase in peripheral vascular resistance vicious cycle established. Causes of pulmonary and peripheral oedema: o High atrial pressures o Impaired renal perfusion causing salt and water retention (heart failure causes increased venous pressure which transmit to renal venous system. Decr pressure gradient btwn renal arterial and venous gradient results in decreased renal perfusion) o Secondary aldosteronism

Diastolic dysf(x)

Causes of Heart Failure:

Pump failure Heart muscle disease Ischemic HD / CAD (cause of up to 75% of cases of heart failure) Cardiomyopathy Myocarditis Restricted filling Pericarditis/ effusion Drugs Negative inotropes beta-blockers Valve disease MR, AR Fluid Retention NSAIDS, steroids Excessive afterload High output CF AS nd Systemic hypertension (2 most frequent cause) Thyrotoxicosis Anemia

Look out also for the precipitating factors, and screen for depression Diagnosis Boston Criteria for Diagnosing Heart Failure
(Sensitivity 50%, specificity 78%) Criterion Category I: History Rest dyspnoea Orthopnea PND Dyspnoea while walking on level area Dyspnoea while climbing Category II: Examination Heart rate JVP Point value 4 4 3 2 1 1 (if HR 91-110bpm); 2 (if >110bpm) 2 (if JVP >6cm H2O); 3 (if JVP >6cm H2O + hepatomegaly or edema) 1 (if basilar); 2 (if more than basilar) 3 3

Excessive preload

Clinical Features
Low CO Fatigue / altered mental state Listlessness Poor effort tolerance Cold peripheries Low BP Pulsus alternans Cachexia Function MR / TR Tachycardia

Ventricular dysfunction Poor renal perfusion Pul. oedema

Right HF / fluid retention

Chronic HF

Displace left apex beat RV heave S3 / S4 Oliguria Uraemia SOB Inspiratory basal crepitations Orthopnea Cheyne-Stokes resp Cough (usually nocturnal) (periodic breathing) PND Raised JVP Hepatic congestion progresses to cirrhosis due to venous congestion Peripheral oedema / ascites / Pleural effusion / nocturia LOW due to anorexia and impaired absorption due to GI congestion Poor tissue perfusion Skeletal muscle atrophy due to immobility

Lung crackles Wheezing Third heart sound Category III: CXR Alveolar pulmonary edema 4 Interstitial pulmonary edema 3 Bilateral pleural effusion 3 Cardiothoracic ratio >0.5 3 Upper zone flow redistribution 2 Scoring Max 4 points per category, scored upon a max of 12 points: 8-12 points: definite 5-7 points: possible <5 points: unlikely

Complications
Depression (in 15-40% of patients) HypoK+ Hypo Na+ Impaired liver function Thromboembolism Arrhythmias In the past 2 weeks, have you: Often been bothered by feeling down/ depressed/ hopeless? Have you had little interest in doing things which previously interested you? Due to K+ losing diuretics, hyperaldosteronism (due to RAAS activation) & impaired aldosterone metab due to hepatic congestion Due to diuretics, inappropriate water retention, failure of cell membrane ion pump Hepatic venous congestion and poor arterial perfusion causes jaundice and abN LFTs and reduced clotting factor synthesis DVT & PE due to low CO, immobility, arrhythmias, AF, intracardiac thrombus due to MS or LV aneurysms Common, and due to electrolyte changes, structural heart dz, pro-arrhythmic effects of increased catecholamines and drugs

eg digoxin. Sudden death common and usually due to VF Ventricular ectopic beats and vent. Tachycardias common and a/w poor Px. Px is not changed by using anti-arrhythmic drugs

NYHA classification of Heart Failure

I II III IV No undue dyspnoea from ordinary activity Comfortable at rest, dyspnoea on ordinary activities Less than ordinary activities causes dyspnoea, which is limiting Dyspnoea at rest, all activities cases discomfort

Investigations: to confirm diagnosis of CF and exclude other differentials to look for precipitating causes of CF to look for complications of CF
Bloods FBC U/E/Cr Cardiac enzymes BNP TFT LFT ECG Radiological CXR Anemia Sepsis Electrolyte abnormalities esp. K+, Na+ MI

Management: Concise summary

Acute ABCs + monitoring Oxygen 100% if no COPD Investigations o ECG o CXR o U/E o Cardiac enzymes o +/- ABG Drug management o Frusemide 40mg IV slowly o GTN S/L or disc (if sys BP>90) o Diamorphine + antiemetic o If systolic BP>90 give IV GTN If systolic BP<90 treat as cardiogenic shock If systolic BP>180 treat as hypertensive LVF Chronic Non pharm Weight loss if obese Fluid restriction + daily weight monitoring (Avoid gain of >2kg in 1 week) Dietary salt restriction (2-3g daily) Exercise Regular low-moderate intensity aerobic exercise Avoid lifting heavy weights >10kg Cut down other risk factors Smoking Hyperlipidemia Learn to monitor symptoms of deterioration Pharm Diuretics st Spironolactone 1 choice, shown to reduce mortality Loop Thiazide ACE-I/ A2RB Beta-blockers started with low doses, up-titrated slowly Digoxin may not reduce mortality but reduces hospitalization

TTE (2D echo)

Hyper/Hypo-thyroidism if clinically suspected Cardiogenic liver cirrhosis MI, ischemia, arrhythmia Pulmonary edema upper lobe diversion blunting of costophrenic angles Bats winging Kerleys B lines (interstitial edema) alveolar shadowing Heart size (may be normal in diastolic dysfunction) Infections Ventricular dysfunction Ejection fraction Valvular lesions For those unable to exercise Dipyramidole Dobutamine Thallium scintigraphy Technitium-99m sestamibi For CAD, and KIV PCI if suitable Plasma concentration of BNP reflects ventricular pressure High negative predictive value: low BNP suggests that if patient is dyspneic, cause is highly unlikely to be CF To diagnose rare forms of CMP or infiltrative heart diseases

Special tests to diagnose underlying IHD

Exercise stress test Non-exercise stress test (pharmacologic) Radionuclide imaging Coronary Angiography Cardiac Catheterization Plasma B-type natriuretic peptide

Super-specialised tests )

Endomyocardial biopsy

episodes Treat associated comorbidities AF, hyperlipidemia, CRF etc

Detailed Summary
Presentations: 1. Acute decompensation of chronic left HF - Decreased effort tolerance / pedal oedema / wheeze (cardiac asthma) 2. Acute cardiogenic pulmonary oedema 3. Cardiogenic shock 1) Acute Mx of Acute Decompensation of Chronic HF 1. Monitoring: vital signs, pulse oximetry, continuous ECG 2. Maintain airway, supplemental O2 3. IV access 4. Blood invxs: FBC, U/E/Cr, Cardiac enzymes 5. Position patient: seated upright with legs hanging down to reduce venous return 6. ECG: concomitant MI, dysrhythmias, LVH, old MI, chronic HPT 7. CXR: cardiomegaly & features of pul. edema (eg upper lobe diversion) 8. Diuretics: IV frusemide 40-60 mg 9. Nitrodisc 5-10mg: relieve symptoms of pul. congestion 10. IV GTN: lower LV end-diastolic volume and pressure rapidly for resolution of symptoms 11. Monitor urine output to assess response to Rx. 12. Admit / discharge Admit Symptomatic dysrhythmias New MI Rapid onset of new symptoms of HF Decompensation of chronic HF Ppting factors require inpatient Mx Anasarca / severe oedema Hypotension Lack of home support D/C If patient is well and responsive to diuretics TCU 2/52 If not on medication: start Lasix 40mg om + Span K 1.2mg om If already on med, increase diuretic dose If concurrent HPT present, add ACEI Captopril 6.254-12.5mg tds or hydralazine 25mg tds Diet advice: salt restriction, fluid restriction (~1 L/day; titrate against weight gain/loss and fluid output) 2) Acute Mx of Acute Pulmonary Oedema Main pathogenic mechanism is sympathetic overdrive leading to elevated LV enddiastolic vol. & pressure 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

There is NO vol. overload per se, thus main Rx is with vasodilators End point of Rx is resolution of symp. overdrive, as indicated by pulse rate, BP, restoration of warm dry extremities & PT comfort. Features to aid clinical diagnosis: i. Severe resp distress, orthopnea ii. Cold clammy extremities iii. Thready pulse iv. SpO2 Features of impending resp failure: i. Altered mental state ii. Poor and uncoordinated respiratory effort iii. Progressive desaturation iv. PaO2 <50mmHg, PaCO2 >50mmHg Monitoring + attach defibrillator ABC assessment: intubate in impending respiratory failure 100% O2 / CPAP in alert PT, but of limited utility IV access ECG: exclude inferior/right ventricular infarct which is a CI to use of nitrates Bloods: RBC, U/E/Cr, cardiac enzymes, Troponin T ABG: baseline CXR Catheterize: assess urine output Drugs: Nitroglycerine 10-200 g/min, starting at 10g/min, increasing by 5g/min every 5 mins until MAP = 90mmHg. Continuous BP monitoring required. Nitroprusside 0.25-10g/kg/min. invasive monitoring required to prevent precipitous drop in BP. Hydralazine IV 10mg every 30 mins. Monitor PT Frusemide 40-80mg IV bolus. Onset of effects from 20min-2h Morphine 0.1mg/kg, starting with IV 3-5mg incremental boluses of 1 mg. GTN 0.5-1.5mg SL stat Captopril 6.25 or 12.5mg SL Combination regimes IV GTN + frusemide Frusemide stat dose + titrate IV GTN titratable infusion IV GTN + captopril SL Captopril stat + titrate IV GTN titratable infusion Frusemide + morphine

11. Hypotension in Pul. oedema Indicates severe HF IV dobutamine or dopamine (5-20g/kg/min) 12. Admit: CCU: PTs with acute coronary syndrome or if intubated HDU: PTs on CPAP General Wd: the rest 3) Long term Management of CCF Bed rest

Stamina building exercise Diet: low salt diet, fluid restriction (~1L/day; monitor with weight, urine output and symptoms of pedal oedema/ascites) Pharmacotherapy o Reduce preload in backward failure (pul. or systemic congestion) o Reduce afterload and increase myocardial contractility in forward failure (low CO) o For patients with LVEF <40% ACE-I for all PTs -blockers for all PTs who are haemodynamically stable Spironolactone for all PTs with rest dyspnoea Digoxin for PTs who are symptomatic despite ACEI + diuretics + blockers, and Pts with rest dyspnoea Diuretics Reduce preload Excessive diuretic Rx may cause fall in CO. Combination of different classes of diuretics (loop, thiazides and K+ sparing) prevents hypo K+. eg Frusemide + spironolactone. Symptomatic. Does not improve survival. Reduce afterload mainly, + some reduction in preload Prevents RAAS & sympathetic activation Eg Captopril, enalapril, lisinopril. SE: postural hypotension, renal failure (therefore check renal function one mth after starting), catastrophic fall in BP on first dose of ACEI (therefore give at night before PT sleeps), hyperK+, cough, neutropenia, altered taste. Similar action to ACE-I. Blocks effect of AT II on heart, peripheral bld vsls & kidneys. Eg losartan nd Usually 2 line Rx if PT does not tolerate ACE-I Advantage: does not cause cough Reduce sympathetic stimulation to increase ejection fraction Non-cardioselective -blockers better as they do not decrease CO as much Venodilators (nitrates) reduce preload Arterial dilators (hydralazine) reduce afterload Limited by SE of hypotension For AF in HF Controls ventricular rate + small positive inotropic effect No effect on survival, but reduces hospitalisation Anti-arrhythmic drug for PTs with symptomatic arrhythmias Prevent thromboembolism

treat with ACEI (change to ARB if cough occurs, change to hydralazine + nitrate if worsening renal insufficiency or angioedema occurs) Beta blockers: for NYHA Class II or III Spironolactone: for NYHA Class III or IV Digoxin: for symptomatic NYHA Class III or IV Diuretics: for fluid overload in NYHA Class III or IV If refractory to above treatment, add dobutamine or milrinone & IV diuretic Diastolic dysfunction: treat underlying cause (eg IHD or HPT) with beta blockers, CCB, ACEI +/- diuretics

ACE-I

ARB

-blockers

Vasodilators

Digoxin

Amiodarone Anticoagulants

Systolic vs Diastolic dysfunction: Long term Mx different, therefore impt to differentiate btwn the two. However, both may be concomitant in the same patient. o Systolic dysfunction:

Digitally signed by DR WANA HLA SHWE DN: cn=DR WANA HLA SHWE, c=MY, o=UCSI University, School of Medicine, KTCampus, Terengganu, ou=Internal Medicine Group, email=wunna. hlashwe@gmail.com Reason: This document is for UCSI year 4 students. Date: 2009.02.24 10:04:48 +08'00'