Acute heart failure

Acute heart failure (AHF) occurs with the rapid onset of symptoms and signs of heart failure secondary to abnormal cardiac function, causing elevated cardiac filling pressures. This causes severe dyspnoea and fluid accumulates in the interstition and alveolar spaces of the lung (pulmonary oedema). AHF has a poor prognosis with a rate of death or rehospitalization of 35% within 60 days.

Poor prognostic indicators include a high (> 16 mmHg) pulmonary capillary wedge pressure (PCWP), low serum sodium concentration, increased left ventricular end-diastolic dimension on echo

The aetiology of AHF is similar to chronic heart failure: Patients with ischaemic heart disease present with an acute coronary syndrome or develop a complication of a myocardial infarct, e.g. papillary muscle rupture or ventricular septal defect requiring surgical intervention. Patients with valvular heart disease also present with AHF due to valvular regurgitation in endocarditis or prosthetic valve thrombosis. Patients with hypertension present with episodes of ‘flash’ pulmonary oedema despite preserved left ventricular systolic function. In both acute and chronic kidney disease fluid overload and a reduced renal excretion will produce pulmonary oedema. Atrial fibrillation is frequently associated with AHF and may require emergency cardioversion.

Diagnosis Initial investigations performed in the emergency room should include: a 12-lead ECG for acute coronary syndromes, left ventricular hypertrophy, atrial fibrillation, chamber enlargement, left bundle branch block a chest X-ray (cardiomegaly, pulmonary oedema, pleural effusion, non-cardiac disease) blood investigations (serum creatinine and electrolytes, full blood count, blood glucose, cardiac enzymes and troponin) plasma BNP or NTproBNP (BNP > 100 pg/ml or NTproBNP > 300 pg/ml) indicates heart failure transthoracic echocardiography should be performed without delay to confirm the diagnosis of heart failure and possibly identify the cause.

Treatment Patients with AHF should be managed in a high-care area with regular measurements of temperature, heart rate, blood pressure and cardiac monitoring. All patients require prophylactic anticoagulation with low molecular weigh heparin, e.g. enoxaparin 1 mg/kg s.c. daily.

Management of acute pulmonary oedema This is urgent: Sit the patient up in order to reduce pulmonary congestion. Give oxygen (high-flow, high-concentration). Noninvasive positive pressure ventilation (continuous positive airways pressure (CPAP) of 5–10 mmHg) by a tight- fitting facemask results in a more rapid improvement in the patient’s clinical state. Administer nitrates, such as 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 BP falls to < 110 mmHg. Administer a loop diuretic such as furosemide 50– 100 mg i.v. an intravenous bolus of Morphine 2.5 to 5 mg as soon as an intravenous line is inserted; the same doses can be repeated as required. Morphine should be used cautiously or avoided in the presence of hypotension, bradycardia, advanced atrioventricular block, or carbon dioxide retention

Group of drugs used for AHF Vasodilators Nitrates Sodium Nitroprusside BNP, nestiride Inotropes with Vasodilatory Properties Dopamine Dobutamine phosphodiesterase 3 inhibitor , milrinone Levosimendan is a calcium sensitizer and ATP- dependent potassium channel opener that has positive inotropic and vasodilatory effect Vasopressor Agents vasopressin antagonists , tolvaptan ? NA

Inotropic support with dobutamine, phosphodiesterase inhibitors or levosimendan can be added in patients who do not respond to the initial therapy . If blood pressure is low use noradrenaline (norepinephrine). Patients with profound hypotension may require inotropes and vasopressors to improve the haemodynamic status and alleviate symptoms, but these have not been shown to improve mortality.

Cor Pulmonale Definition Cor pulmonale, often referred to as pulmonary heart disease, is defined as dilation and hypertrophy of the right ventricle in response to diseases of the pulmonary vasculature and/or lung parenchyma.

Although chronic obstructive pulmonary disease (COPD) and chronic bronchitis are responsible for approximately 50% of the cases of cor pulmonale , any disease that affects the pulmonary vasculature or parenchyma can lead to cor pulmonale. Once patients with chronic pulmonary or pulmonary vascular disease develop cor pulmonale, the prognosis worsens.

Pathophysiology and Basic Mechanisms Although many conditions can lead to cor pulmonale, the common pathophysiologic mechanism in each case is pulmonary hypertension that is sufficient to lead to RV dilation, with or without the development of concomitant RV hypertrophy.

Clinical Manifestations Symptoms The symptoms of chronic cor pulmonale generally are related to the underlying pulmonary disorder. Dyspnea, the most common symptom Tussive or effort-related syncope may occur because of the inability of the RV to deliver blood adequately to the left side of the heart. Central chest pain Abdominal pain and ascites that occur with cor pulmonale are similar to the right-heart failure that ensues in chronic HF. Lower-extremity edema may occur secondary to neurohormonal activation, elevated RV filling pressures, or increased levels of carbon dioxide and hypoxemia, which can lead to peripheral vasodilation and edema formation.

Signs Many of the signs encountered in cor pulmonale are also present in HF patients with a depressed EF, including tachypnea, elevated jugular venous pressures, hepatomegaly, and lower-extremity edema. Patients may have prominent v waves in the jugular venous pulse as a result of tricuspid regurgitation. Other cardiovascular signs include an RV heave palpable along the left sternal border or in the epigastrium. The increase in intensity of the holosystolic murmur of tricuspid regurgitation with inspiration ("Carvallo's sign") may be lost eventually as RV failure worsens. Loud P2 which is sometimes palpable Cyanosis is a late finding in cor pulmonale and is secondary to a low cardiac output with systemic vasoconstriction and ventilation-perfusion mismatches in the lung.

Diagnosis The ECG in severe pulmonary hypertension shows P pulmonale, right axis deviation, and RV hypertrophy. Radiographic examination of the chest may show enlargement of the main pulmonary artery, the hilar vessels, and the descending right pulmonary artery. Spirometry and lung volumes can identify obstructive and/or restrictive defects indicative of parenchymal lung diseases; arterial blood gases can demonstrate hypoxemia and/or hypercapnia. Spiral computed tomography (CT) scans of the chest are useful in diagnosing acute thromboembolic disease; however, ventilation-perfusion lung scanning remains best suited for diagnosing chronic thromboembolic disease . A high-resolution CT scan of the chest can identify interstitial lung disease. Two-dimensional echocardiography is useful for measuring RV thickness and chamber dimensions as well as the anatomy of the pulmonary and tricuspid valves.

Treatment The primary treatment goal of cor pulmonale is to target the underlying pulmonary disease, since this will decrease pulmonary vascular resistance and lessen RV afterload. General principles of treatment include decreasing work of breathing by using noninvasive mechanical ventilation and bronchodilation, as well as treating any underlying infection . Adequate oxygenation (oxygen saturation 90–92%) and correcting respiratory acidosis are vital for decreasing pulmonary vascular resistance. Patients should be transfused if they are anemic, and phlebotomy may be considered in extreme cases of polycythemia. Diuretics are effective in RV failure, and indications are similar to those for chronic HF. Digoxin is of uncertain benefit in the treatment of cor pulmonale and may lead to arrhythmias in the setting of tissue hypoxemia and acidosis. Therefore, if digoxin is administered, it should be given at low doses and monitored carefully. Pulmonary vasodilators can effectively improve symptoms through modest reduction of pulmonary pressures and RV afterload when isolated pulmonary arterial hypertension is present.