Heart Failure

Definition A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent

Aetiology It is a common end point for many diseases of cardiovascular system It can be caused by : -Inappropriate work load (volume or pressure overload) -Restricted filling -Myocyte loss

Causes of left ventricular  failure

Volume over load	Regurgitate valve High output status
Pressure overload	Systemic hypertension Outflow obstruction
Loss of muscles	Post MI, Chronic ischemia, Connective tissue diseases, Infection, Poisons (alcohol,cobalt,Doxorubicin)
Restricted Filling	Pericardial diseases, Restrictive cardiomyopathy, tachyarrhythmia

Pathophysiology

Hemodynamic changes	From hemodynamic stand point HF can be secondary to systolic dysfunction or    diastolic dysfunction.
Neurohormonal changes
Cellular changes	Changes in Ca+2 handling. ·  Changes in adrenergic receptors:            • Slight ↑ in α1 receptors                  • β1 receptors desensitization ® followed by down regulation  · Changes in contractile proteins  · Program cell death (Apoptosis)  · Increase amount of fibrous tissue

Presentation

Symptoms

SOB, Orthopnea, paroxysmal nocturnal dyspnea • Low cardiac output symptoms • Abdominal symptoms: Anorexia,nausea, abdominal fullness, Rt hypochondrial pain

Physical Signs

High diastolic BP & occasional decrease in systolic BP (decapitated BP) JVP Rales (Inspiratory) Displaced and sustained apical impulses Third heart sound (S3) low pitched sound that is heard              during rapid filling of ventricle Mechanism of S3 sudden deceleration of as elastic limits of the ventricles are reached Vibration of the ventricular wall by  filling Common in children Fourth heart Sound (S4) Usually at the end of diastole Exact mechanism is not known Could be due to contraction of atrium against stiff ventricle Pale, cold sweaty skin

Framingham Criteria for Diagnosis of Heart Failure

Major Criteria	PND JVP Rales Cardiomegaly Acute Pulmonary Edema S3  Gallop Positive hepatic Jugular reflex ↑ venous pressure > 16 cm H2O
Minor criteria	Lower limb edema, Night cough Dyspnea on exertion Hepatomegaly Pleural effusion ↓ vital capacity by 1/3 of normal Tachycardia 120 bpm Weight loss 4.5 kg over 5 days management

Diagnosis of CHF requires the simultaneous presence of at least 2 major criteria or 1 major criterion in conjunction with 2 minor criteria.

Forms of Heart Failure

Systolic & Diastolic High  Output Failure- Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, Pagets disease Low Output Failure Acute large MI, aortic valve dysfunction--- Chronic

	Left ventricular failure (commoner)	Right ventricular failure
Symptoms	Exertional dyspnoea orthopnoea PND nocturnal cough + pink frothy sputum tachypnoea (Cheyn-Stokes Crackles at lung bases (Pulmonary oedema) +ve abdominojugular test S3, apex displaced lateral to mid-clavicular line	Peripheral oedema abd. distention(ascites) anorexia nausea JVP ↑ Hepatomegaly

Ddx

Pericardial diseases Liver diseases Nephrotic syndrome Protein losing enteropathy

New York Classification of HF

Class I  asymptomatic Class II symptoms at routine activity Class III symptoms at less than routine activity Class IV symptoms at rest

Risk Factor

Previous MI Hx of arrhythmia, valvular/ vascular disease HTN Family hx of cardiomyopathy DM Obesity Prior exposure to cardiotoxic agents

Investigation

Initial lab	Findings: anaemia, hyperthyroid, chronic renal insufficiency, electrolytes abnormality, pre-renal azotemia, haemochromatosis
BNP	B-type Natriuretic Peptide(BNP) secreted by the heart in response to excessive stretching of heart muscle cells 100pg/ml, HF likely, sensitivity = 90%, specificity = 76% ↓ aldosterone, endothelin-1 (vasoconstrictor)&  noradrenaline, ↑diuresis, lusitropic, anti-fibrotic, anti-remodelling Caveats: lower with ↑ BMI, affected by renal fn, ↓ by ACEi, diuretics,
ECG	Usually shows abnormality (causes) – MI, arrythmia, LBBB If ECG and BNP are normal, heart failure is unlikely
Echocardiography	Not diagnostic, indicate the causes (MI, valvular disease, LV dysfunction), performed if BNP ↑. Findings: Ejection fraction: EDV-ESV > 50% + 5% valvular disease Diastolic dysfunction - ↑ wall thickness, LA dimension Wall motion abnormality that may signify CAD Intra-cardiac shunts
CXR	eg: features in LVF: Alveolar oedema – perihilar bat’s wing shadowing Kerley B lines (interstitial oedema) Cardiomegaly -cardiothoracic ratio >50% Dilated prominent upper lobe vessels Pleural Effusion
Others	Cardiac CT, MRI Coronary angiogram

Management

Acute HF (emergency)

Chronic HF

ABC Sit pt upright O2 100% if no lung disease IV access and monitor ECG, treat any arrhythmia. Investigation while treating Diamorphine 2.5-5mg IV slowly, caution in liver failure and COPD Furosemide 40-80mg IV slowly, larger doses in AKI GTN spray 2 puffs SL, don’t give if systolic BP <90mmHg Necessary investigation, hx and exam if systolic BP>100mmHg, start a nitrate infusion, isosorbide dinitrate 2-10mg/h IVI, keep systolic BP>90mmHg If worsens, further dose of furosemide 40-80-mg. Consider ventilation, eg. CPAP, get help If systolic BP< 100mmHg, treat as cardiogenic shock, ie. consider a Swan-Ganz catheter and inotropic support

Treat the cause, eg. valve disease Treat exacerbating factors, eg thyroid disease, infection, HTN Avoid exacerbating factors- NSAIDs, verapamil Stop smoking, eat less salt, maintain weight Drugs: Diuretics, ACEi, B-Blocker, Spirinolactone, Digoxin, vasodilators Intractiblable HF reassess the cause, compliance bed rest metolazone,frusemide, opiates, nitrates DVT prophylaxis: heparin and TED consider heart transplant. Jarvik thumb-sized titanium axial flow impeller pump.

Therapeutic Management

Diuretic Therapy	The most effective symptomatic relief Mild symptoms Eg HCTZ Chlorthalidone Metolazone Thiazides are ineffective with GFR < 30 --/min MoA Block Na reabsorbtion in loop of henle and distal convoluted tubules S/E Pre-renal azotemia Skin rashes Neutropenia Thrombocytopenia Hyperglycemia ↑ Uric Acid Hepatic dysfunction severe Eg Lasix (20 – 320 mg QD), Furosemide Bumex (Bumetanide 1-8mg) Torsemide (20-200mg) MoA Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis and metabolic alkalosis S/E pre-renal azotemia Hypokalemia Skin rash ototoxicity
K+ Sparing Agents	Triamterene & amiloride – acts on distal tubules to ↓ K secretion Spironolactone (Aldosterone inhibitor)    recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin-aldosterone system with subsequent effect on myocardial remodeling and fibrosis
Angiotensin Converting Enzyme Inhibitors	They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II → vasodilation and ↓ Na retention Bradykinin degradation ↑ its level → ↑ PG secretion & nitric oxide Ace Inhibitors were found to improve survival in CHF patients onset & progression of HF in pts with asymptomatic LV dysfunction cardiac remodeling S/E Angioedema Hypotension Renal insuffiency Rash cough
Angiotensin II receptor blockers	Has comparable effect to ACE I Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)
Digitalis Glycosides	(Digoxin, Digitoxin) The role of digitalis has declined somewhat because of safety concern Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant   Reduction in hospitalization Reduction in symptoms of HF Mechanism of Action +ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase → inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange Vagotonic effect Arrhythmogenic effect Digitalis Toxicity Narrow therapeutic to toxic ratio Non cardiac manifestations Anorexia, Nausea, vomiting, Headache, Xanthopsia sotoma, Disorientation Digitalis Toxicity Cardiac manifestations Sinus bradycardia and arrest A/V block (usually 2nd degree) Atrial tachycardia with A/V Block Development of junctional rhythm in patients with a fib PVC’s, VT/ V fib (bi-directional VT) Digitalis Toxicity Treatment Hold the medications Observation In case of A/V block or severe bradycardia → atropine followed by temporary PM if needed In life threatening arrhythmia → digoxin-specific fab antibodies Lidocaine and phenytoin could be used – try to avoid D/C cardioversion in non life threatening arrhythmia contraindication is severe decompensated CHF
β Blockers	Has been traditionally contraindicated in pts with CHF Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV function In addition to improved LV function multiple studies show improved survival The only contraindication is severe decompensated CHF
Vasodilator	Reduction of afterload by arteriolar vasodilatation (hydralazin)  reduce LVEDP, O2 consumption,improve myocardial perfusion, ­ stroke volume and COP Reduction of preload By venous dilation    ( Nitrate) ↓ the venous return ®↓ the load on both ventricles. Usually the maximum benefit is achieved by using agents with both action.

Prognosis Annual mortality rate depends on patients symptoms and LV function 5% in patients with mild symptoms and mild ↓ in LV function 30% to 50% in patient with advances LV dysfunction and severe symptoms 40% – 50% of death is due to SCD