The methods for measuring blood pressure and reported normal blood pressure measurements in small animals are extremely variable. Blood pressure should be measured with the animal unsedated, relaxed and minimally restrained. Heart rate should be within normal resting limits (an increased heart rate tends to increase the diastolic blood pressure measurement). Direct measurements can be performed by percutaneous puncture of the femoral artery connected to pressure sensing and recording equipment. Non-invasive indirect measurements can be obtained using Doppler ultrasound or, in dogs, oscillometric techniques. Normal direct and indirect measurements for dogs and cats are given in site.
In dogs, hypertension should be suspected if systolic and diastolic measurements greater than 180 mm Hg and 100 mm Hg respectively, are obtained using an indirect Doppler ultrasound technique. In cats, hypertension is defined as sustained systolic and diastolic pressures greater than 170 mm Hg and 100 mm Hg, respectively, using a Doppler technique (Morgan, 1986); systolic / diastolic pressures greater than 200 / 145 should certainly be regarded as abnormal.
Hypertension can be classified as primary (essential) or secondary. Most cases of hypertension in small animals are secondary to other diseases. Regulation of arterial blood pressure depends on the interaction of a number of neural, cardiac, renal and humoral factors which affect cardiac output, plasma volume and vascular tone. Deregulation of these pressor and volume homeostatic mechanisms may initiate a hypertensive state. Activation of the renin-angiotensin-aldosterone system, altered adrenergic activity, and the release of vasopressor substances by the kidney and antidiuretic hormone from the neurohypophysis (the latter in response to increased angiotensin II levels) act together to increase peripheral vascular resistance and retain sodium and water. Increased vascular ‘stiffness’ associated with atherosclerosis and arteriosclerosis may also play a role in creating a hypertensive state.
Primary (essential) hypertension
Spontaneous hypertension has been reported in dogs, including a colony of primary hypertensive dogs bred from two naturally occurring cases. Diagnosis of primary hypertension essentially involves ruling out secondary causes. Since spontaneous hypertension can result in secondary renal changes (glomeruloscterosis) and renal insufficiency, identification of the primary disease process is often extremely difficult. High sodium diets have been implicated in the pathogenesis of primary hypertension. A high sodium diet may be expected to accelerate the disease process if fed to an animal with pre-existing hypertension; it is not clear, however, if a high sodium load alone can result in hypertension.
In the cat, renal disease and hyperthyroidism are both common causes of hypertension. Primary renal disease is the most common cause of hypertension in dogs. Hypertension may also be associated with hypothyroidism, hyperadrenocorticism, diabetes mellitus, phaeochromocytoma, primary hyperaldosteronism, hyperparathyroidism (resulting in hypercaleaemia), acromegaly and hyperoestrogenism. Other potential, but less well documented, causes include polycythaemia, anaemia, renin-producing tumours, coarctation of the aorta, obesity and ageing).
Hypertension leads to glomerulosclerosis and a loss of functional nephrons. If renal function is already compromised hypertension may accelerate progression towards end-stage renal failure. Hypertension also results in concentric hypertrophy of the left ventricle which predisposes the myocardium to ischaemia and the development of arrhythmias. Hypertensive retinopathy is characterized by choroidal haemorrhage and focal retinal detachments. Some animals present with sudden onset blindness due to complete retinal detachment, papilloedema, intraocular haemorrhage or glaucoma. Neurological signs are usually attributed to cerebral haemorrhage; cerebral infarction associated with atherosclerosis of the cerebral arteries is occasionally seen in dogs with hypothyroidism.
The main objective is to identify and treat appropriately the underlying disease (for example renal failure). When a specific disease cannot be identified and primary hypertension is suspected, therapy should be directed against the mechanism responsible for the hypertension, that is an attempt should be made to reduce the circulating blood volume, decrease sympathetic tone and / or inhibit the renin-angiotensin-aldosterone pathway. Suitable therapeutic strategies are summarized below.
Reduce sodium intake to 0.1-0.3% of the diet (10-40 mg kg-1 dry matter). Sodium restriction potentiates the action of antihypertensive drug therapy. Prescription diets are available which fulfil these requirements.
Diuretics. Frusemide has a natriuretic action and can be used in the face of renal failure. Spironolactone is a more appropriate drug for treating hyperaldosteronism.
Beta-adrenergic blocking drugs decrease cardiac output and decrease renin release by blocking the beta receptors on the juxtaglomerular apparatus. Their use is indicated in feline hyperthyroidism where hypertension is due to excessive adrenergic stimulation.
Hydralazine is an arterial vasodilator. It lowers blood pressure but does not protect the kidney against glomerulosclerosis. Hydralazine may result in reflex sympathetic stimulation and renin release and therefore may have to be given with beta blockers.
Calcium channel blockers such as verapamil and diltiazem cause vasodilation. Verapamil is a renal vasodilator and may transiently increase glomerular filtration rate.
Angiotensin converting enzyme inhibitors are balanced vasodilators. The decreased production of aldosterone results in increased salt and water excretion. These drugs are nephrotoxic so care should be taken if there is evidence of renal dysfunction.