Peripheral oedema is associated with a range of medicines which act on the cardiovascular system, including:^5,13,14,15

·     - calcium channel blockers (CCBs), particularly the dihydropyridine type such as amlodipine or nifedipine;

·     - vasodilators – minoxidil or hydralazine;

·     - alpha-1 blockers;

·     - alpha-2 adrenoceptor agonists;

·     - beta blockers.

Oedema can occur due to vascular dilation just before or after the capillaries, or by impairing vascular reflexes to pressure changes.¹⁵

Beta blocker effects reducing heart contractility may build up venous blood volume causing a back pressure on the capillaries, in turn forcing fluid into interstitial space. In addition, labetalol, carvedilol, and nebivolol may cause arteriole dilation, again increasing capillary pressure.¹³

Vasodilator, alpha-1 blocker and alpha-2 agonist effects in the kidneys may also cause oedema through sodium retention due to increasing reabsorption in the proximal tubules either by reduced perfusion rates or by stimulating the renin-angiotensin-aldosterone system (RAAS).¹⁵

Oedema (as well as pulmonary effusion, where fluid builds up in the lungs) can occur with drugs opening potassium channels, such as diazoxide or minoxidil, potentially due to changes in vascular tone and possibly reducing lymphatic drainage.^13,16

Drugs such as diltiazem, verapamil and minoxidil can additionally reduce lymph contractility reducing fluid drainage. CCBs are also associated with an increased risk of lymphoedema in breast cancer.¹³