L4 Heart Failure PDF

Heart Failure Dr. Mohammed Ismael Dawood Associated Professor of Medicine Heart failure: ❑ The state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of elevated filling pressures. ❑ Ini...

Heart Failure Dr. Mohammed Ismael Dawood Associated Professor of Medicine Heart failure: ❑ The state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of elevated filling pressures. ❑ Initially it causes mainly exertional symptoms, but advanced heart failure may cause symptoms at rest. Classification of HF: 1. Left-sided heart failure, right-sided heart failure or biventricular. 2. Acute & chronic heart failure. 3. Systolic & diastolic failure. 4. Aetiological classification e.g., Ischaemic heart failure, CMP. 5. According to cardiac output: HFrEF & HFpEF  Pathophysiology of HF: Compensatory mechanisms: The presence of underlying heart disease leads to compensatory mechanisms which is able to prevent the appearance of manifestations of heart failure under basal conditions (compensated heart failure). Theses mechanisms include: 1. Ventricular dilatation: this occurs in cases with increased preload, and according to Starling low, this dilatation will lead to increase in CO. However, if the dilatation exceeds certain limit, the ventricular contractility will decline. 2. Ventricular hypertrophy: this occurs in cases with increased afterload. The increase in muscle mass will lead to increase in cardiac contractility and CO. However, since this hypertrophy is not associated with increase in blood supply, ischemia of the hypertrophic muscle fibers will lead to fibrosis and decline in cardiac contractility by time. 3. Tachycardia: Since CO= SV X HR, reduction in SV due to cardiac disease is compensated for by increase in HR to maintain CO. The increase in HR occurs through the following mechanism: ✓ Marry's low: HR is inversely proportionate to blood pressure. ✓ Bainbridge reflex: Increased RA pressure causes increased HR ✓ Marked tachycardia may lead to diminished CO due to decreased diastolic (filling) time. 4. Redistribution of blood flow: Activation of smypathatic nervous system due to low CO will lead to diversion of blood flow from less vital organs (e.g. skin) to more vital organs ( e.g, brain &heart). 5. Hypervolemia: ❑ Reduction in CO will lead to salt and water retention through: ✓ Reduction of GFR. ✓ Renal ischemia ➔ ↑ renin ➔ ↑ Ang II ➔ ↑ aldosterone ➔ salt & water retention. ✓ Increased ADH ➔ water retention. ❑ Increased blood volume will increase preload and cardiac contraction. ❑ If it exceeds certain limits, it will reduce cardiac contractility and lead to edema. If the compensatory mechanisms exceed their limits, or if the cardiac load or damage is increased, manifestations of heart failure will appear (decompensated heart failure). Neuro-hormonal changes: ❑ Reduction of CO will lead to activation of neuro-hormonal mechanisms aiming at maintaining perfusion pressure to body organs, however this may be on the expense of increasing cardiac load and requirements. ❑ These mechanisms include: 1. Activation of renin-Angiotensin- aldosterone system. 2. Increased catecholamine level: in chronic heart failure there is: Reduction of adrenergic receptor level (down regulation). Reduction of G-protein activity that couples -receptors to adenylcyclase system. Reduction of c-AMP → ↓ intracellular Ca → reduce contractility. Precipitating factor: ❑ These factors may cause cardiac decompensation due to overwhelming of the cardiac compensatory mechanisms. ❑ These include: ❖ Infections: as infective endocarditis, Lung infection. ❖ Myocardial Infarction. ❖ Iatrogenic: discontinuation of anti failure therapy excess salt, IV fluids, steroid, -Ve inotropic (B blocker) ❖ Physical and emotional stress. ❖ Pregnancy & labour. ❖ Pulmonary embolism. ❖ Arrhythmia e.g., marked tachycardia or bradycardia. ❖ Anemia, thyrotoxicosis ,,, hyperdynamic circulation. Clinical Picture Of HF: Complications of HF: Weight loss (cardiac cachexia) as a result of anorexia and impaired absorption because of GI congestion. Renal failure from poor renal perfusion as a result of a low cardiac output—exacerbated by diuretics, ACE inhibitors and angiotensin receptor blockers. Hypokalaemia caused by diuretics and hyperaldosteronism. Hyperkalaemia caused by the effects of drugs (particularly ACE inhibitors given with spironolactone) and renal dysfunction. Hyponatraemia caused by diuretic therapy or inappropriate water retention because of high ADH secretion—a poor prognostic sign. Thromboembolism—either DVT with pulmonary embolism or systemic emboli from cardiac thrombus in atrial fibrillation or complicating MI. Atrial and ventricular arrhythmias may be related to electrolyte changes (e.g., hypokalaemia, hypomagnesaemia), underlying cardiac disease and accompanying sympathetic activation. Sudden death occurs in up to 50% of patients, probably caused by VF. Investigations of HF: ❑ CXR: ✓ Cardiomegaly. ✓ Characteristic changes in pulmonary oedema, including distension of upper lobe pulmonary veins, Kerley B lines (horizontal lines near the costal margin indicating interstitial oedema), hazy hilar opacification (alveolar oedema) and pleural effusions. ❑ Echocardiography: consider in all patients with heart failure to determine the aetiology (e.g., valvular disease, regional wall motion defect in MI) and assess LV impairment. ❑ ECG: may reveal LV hypertrophy, evidence of previous MI. ❑ U&Es, LFTs, TFTs and FBC: may identify some of the associated causes and complications listed previously. ❑ Brain natriuretic peptide (BNP): elevated in heart failure and is a prognostic marker, as well as being useful in differentiating heart failure from other causes of breathlessness or peripheral oedema. To be continued….. Thanks a lot