Vasodilatation of the cerebral blood vessels can cause a rise in intracranial pressure due to expansion of the vessels within the confined space of the cranium. It is often throbbing in nature, due to the pulsation of the dilated meningeal arteries.
This usually settles after a few days after starting the CCB.
Cerebral vasodilatation can cause a throbbing headache
The mechanisms by which CCBs give rise to ankle oedema are not currently understood. Proposed mechanisms include an increase in capillary pressure due to arterial dilation. This results in fluid loss from the capillaries.
It typically worsens in the evening, and may resolve or improve following the patient lying down overnight.
Managing the oedema can involve measures like leg elevation or reducing the dose of CCB. Diuretics are not effective in reducing the ankle oedema associated with CCBs.
Constipation occurs in around 25% of patients taking verapamil and can occur with other CCBs.
The mechanism behind this is unknown, however one paper suggests it may be due to reduced myoelectric response to eating (see Bassotti et all, 1998)
Verapamil and diltiazem are contraindicated in heart failure due to their negative inotropic effect which would reduce cardiac output (not ideal in HF!) and potentially push a patient into cardiogenic shock.
Dihydropyridine CCBs are not contraindicated and can be used safely in patients with HF who have another indication for a CCB (see Packer et al, 1996)
Vasodilatation of capillaries means that patients can look and feel flushed when taking CCBs.
Reduction in arterial blood pressure as a result of arterial vasodilatation can cause a reflex tachycardia. This is true of dihydropyridine CCBs but not of verapamil or diltiazem as their negative chronotropic effects negate this reflex tachycardia.
Features of postural hypotension