using vasodilators for heart failure

1
USING VASODILATORS FOR HEART FAILURE The choice of vasodilator depends on the patient's symptoms and haemodynamics The use of vasodilators in the treatment of heart failure has gained much attention in recent years. Vasodilators are indicated in acute myocardial infarction where they may improve pump function, and thereby lessen pulmonary oedema and the area of ischaemic injury. Secondly, they can help patients with chronic heart failure which is refractory to digitalis and diuretics. Only those vasodilators that can be given orally are of use in chronic heart failure. Hydralazine, minoxidil and nifedipine dilate mainly the precapillary arteriolar bed, but spare venous capacitance vessels. When the chief symptoms of a heart failure patient are tiredness and fatigue, and his cardiac output is decreased and systemic vascular resistance increased, treatment with arteriolar vasodilators is appropriate. Glyceryl trinitrate (nitroglycerin) and the organic nitrates (such as isosorbide dinitrate) dilate mainly the smooth muscle of the veins, with little effect on arterioles. Venous dilation may be valuable in heart failure patients who have symptoms of pulmonary venous congestion and an increased pulmonary capillary wedge pressure. Some clinicians have argued that using vasodilators in heart failure may not always be a safe practice. Indeed, ifleft ventricular function were normal, there could be an unacceptable fall in arterial BP. However, heart failure patients have abnormal left ventricular function. Thus, vasodilation will reduce aortic impedance, thus increasing stroke volume and cardiac output and preventing unwanted BP reductions. Other clinicians fear that dilators of postcapillary venous capacitance beds may produce venous pooling. Although this fear is justified in the normal heart, it is not in patients with a compromised heart. In heart failure, a lessening of venous return reduces cardiac filling pressures, thus relieving the signs of raised pulmonary capillary pressure. Collateral blood flow is increased by vasodilators, and this may reduce segmental myocardial ischaemia. Vasodilators have produced unpredictable responses in right heart failure. Further research needs to be done to ascertain whether the effectiveness of vasodilators in heart failure is maintained on a long term basis, and whether deterioration occurs after withdrawal of vasodilator therapy. 'The choice of vasodilator is determined by the patient's symptoms and signs and by haemodynamic considerations ... In practice, the more deranged the haemo- dynamics the better seems the response to vasodilators.' Breckenridge, A.: British Medical Journal 284: 765 (13 Mar 1982) 0156-2703/82/0403-0003/0$01.00/0 © ADIS Press INPHARMA 3 Mar 1982 3

Upload: vothuy

Post on 16-Mar-2017

213 views

Category:

Documents


0 download

TRANSCRIPT

USING VASODILATORS FOR HEART FAILURE

The choice of vasodilator depends on the patient's symptoms and haemodynamics The use of vasodilators in the treatment of heart failure has gained much attention in recent years. Vasodilators are indicated in acute myocardial infarction where they may improve pump function, and thereby lessen pulmonary oedema and the area of ischaemic injury. Secondly, they can help patients with chronic heart failure which is refractory to digitalis and diuretics. Only those vasodilators that can be given orally are of use in chronic heart failure. Hydralazine, minoxidil and nifedipine dilate mainly the precapillary arteriolar bed, but spare venous capacitance vessels. When the chief symptoms of a heart failure patient are tiredness and fatigue, and his cardiac output is decreased and systemic vascular resistance increased, treatment with arteriolar vasodilators is appropriate. Glyceryl trinitrate (nitroglycerin) and the organic nitrates (such as isosorbide dinitrate) dilate mainly the smooth muscle of the veins, with little effect on arterioles. Venous dilation may be valuable in heart failure patients who have symptoms of pulmonary venous congestion and an increased pulmonary capillary wedge pressure. Some clinicians have argued that using vasodilators in heart failure may not always be a safe practice. Indeed, ifleft ventricular function were normal, there could be an unacceptable fall in arterial BP. However, heart failure patients have abnormal left ventricular function. Thus, vasodilation will reduce aortic impedance, thus increasing stroke volume and cardiac output and preventing unwanted BP reductions. Other clinicians fear that dilators of postcapillary venous capacitance beds may produce venous pooling. Although this fear is justified in the normal heart, it is not in patients with a compromised heart. In heart failure, a lessening of venous return reduces cardiac filling pressures, thus relieving the signs of raised pulmonary capillary pressure. Collateral blood flow is increased by vasodilators, and this may reduce segmental myocardial ischaemia. Vasodilators have produced unpredictable responses in right heart failure. Further research needs to be done to ascertain whether the effectiveness of vasodilators in heart failure is maintained on a long term basis, and whether deterioration occurs after withdrawal of vasodilator therapy.

'The choice of vasodilator is determined by the patient's symptoms and signs and by haemodynamic considerations ... In practice, the more deranged the haemo­dynamics the better seems the response to vasodilators.'

Breckenridge, A.: British Medical Journal 284: 765 (13 Mar 1982)

0156-2703/82/0403-0003/0$01.00/0 © ADIS Press INPHARMA 3 Mar 1982 3