Heart failure can be defined as the inability of the heart to supply sufficient oxygen to satisfy tissue oxygen demand. The primary aim of treatment is to improve cardiac output. This can be achieved by several methods and must be tailored to the individual patient.

In acute heart failure with pulmonary edema, a patient may have a decreased plasma volume and diuretics could worsen the failure and compromise coronary blood flow. A fluid challenge under guidance of cardiac filling pressures should be considered as a first-line intervention.

Improved contractility can be achieved by various agents, each of which have positive and negative aspects and must be selected according to the specific needs of the patient. Dobutamine is our inotropic agent of choice. If there is a low flow state but no cardiovascular collapse, the addition of phosphodiesterase inhibitors can be helpful to enhance the b-adrenergic effects. Digoxin has mild inotropic effects, and so its use should be reserved for rapid atrial fibrillation.

Vasodilators can effectively increase cardiac output by reducing left ventricular afterload. Intravenous agents with a short half-life, such as nitroglycerin or sodium nitroprusside, are preferred. Vasodilating therapy is prohibited in the presence of arterial hypotension. Diuretics are prescribed to reduce the sodium and water retention which aggravates the development of edema. However, diuretics should be used prudently to avoid an excessive reduction in ventricular preload.

Ventilatory support may be required in the management of severe cardiogenic pulmonary edema where hypoxemia is very severe. The increase in intrathoracic pressure can also improve ventricular function by reducing venous return. The use of CPAP by mask may be sufficient to achieve beneficial cardiorespiratory effects in patients with cardiogenic pulmonary edema.

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Sleep Apnea

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