Acute Left Ventricular Failure (LVF)
SummaryHeart failure is described as an inability of the heart to deliver blood at a rate commensurate with the requirements of metabolising tissues despite normal filling pressures.
Cardiac Output (CO) is the volume of blood ejected by the ventricles in one minute. This will normally be 5 – 7 litres although in LVF this will be reduced. Cardiac Index is often used a sit relates CO to body mass.
There are a number of factors that determine cardiac ouput:
Preload: the more the myocardium is stretched in the diastolic phase the greater the force of contraction in the systolic phase. However this is true to a point as the hearts performance will decline if myocardial stretch is excessive.
Afterload: is the resistance the ventricles must overcome in order to move blood into the pulmonary artery and aorta. Systemic Vascular Resistance (SVR) reflects left ventricular afterload and is greater than Pulmonary Vascular Resistance (PVR) that reflects right ventricular afterload.
Contractility: refers to the muscular pumping ability of the ventricles.
CAUSES OF ACUTE LVF
Acute LVF may be caused or exacerbated by the following conditions:
- Ischaemic Heat Disease / Myocardial Infarction
- Aortic Stenosis
- Volume overload
- Drugs e.g. beta blockers, cocaine
- Infection e.g. Myocarditis
In LVF the cardiac output is reduced e.g. secondary to an acute Myocardial Infarction. Failure of the ventricles to eject blood results in increased intracardiac pressures and pulmonary capillary pressure.
- Fatigue / reduced exercise tolerance
- Frank pulmonary oedema
- Paroxysmal nocturnal dyspnoea
- Crepitations - after coughing
- Hypoxia & cyanosis
Chest x-ray appearances
The chest x-ray will typically demonstrate:
- Cardiomegaly i.e. an enlarged heart
- Pulmonary oedema: the lungs will appear whiter often with a typical ‘bats wing’ distribution of oedema
- Dilated pulmonary capillaries and upper lobe diversion
MANAGEMENT OF ACUTE LVF
Immediate management consists of :
Morphine IV as required – this will help allay the terror and anxiety but may also reduce preload and afterload Oxygen
Diuretics: help by reducing circulatory volume and thereby reducing preload. An intravenous loop diuretic such as Frusemide is administered in the first instance
Venodilators: an intravenous infusion of Glceryl Trinitrate may be useful in reducing preload and afterload and may also improve coronary blood flow. Caution must be exercised in patients who are hypotensive
Inotropic drugs: these drugs are used to increase myocardial contractility and output. They are often classified according to their activity at alpha and beta receptors.
Drugs with mainly alpha activity will:
- increase afterload
- increase blood pressure
- slow pulse rate
Drugs with mainly beta activity will:
- reduce afterload
- increase pulse rate and cardiac output
Exerts its effects on beta1 and beta 2 receptors and thereby Increases myocardial contractility and output. It has no renal (dopaminergic) effects.
The standard dose is 2.5 - 20 micrograms per KG per minute by continuous intravenous infusion
Dobutamine does exert chronotropic effects and it may increase myocardial oxygen consumption and aggravate angina
Side effects include:
- ventricular arrhythmias tachycardia
Exerts its effects on dopaminergic, beta1 and beta2 receptors. At low dose (0.5 - 2 mcgs/Kg/min) it has mainly dopaminergic effects ~ increased renal blood flow and diuresis. Higher doses result in vasoconstriction and contractility, afterload and systemic Blood Pressure all increase
Dopamine can be very irritant to tissue and the infusuion site should be regularly inspected for signs of local site necrosis ~ midline administration may be preferable ACE inhibitors e.g. Ramipril may be used in the long term management of heart failure. These drugs work by preventing angiotensin II formation.
Possible side effects include:
- Renal deterioration
- Taste disturbance