An understanding of the mechanics of blood pressure is vital in management of canine hypertension. Arterial blood pressure (BP) is defined as the force exerted by flowing blood on the vessel walls. Determinants of BP reflect the relation to the cardiovascular system, as described by the equation:
- BP = CO x PR
where CO is cardiac output and PR is the peripheral vascular resistance. Cardiac output can be described as the product between heart rate and stroke volume. Stroke volume, or the amount of blood ejected with each ventricular contraction, is influenced by cardiac contractility, preload, and after-load. Although cardiac output plays an important role in BP during exercise, peripheral resistance is the major determinant at rest. Arterial resistance is controlled by many factors, including sympathetic stimulation, the renin-angiotensin system, and renal regulation of blood volume. BP is tightly controlled because the cardiovascular system maintains adequate BP at all costs.
In situations of decreased BP, compensatory attempts to maintain BP include vasoconstriction and tachycardia. The baroreceptors located in the walls of the carotid sinus and aortic arch send signals to the vasomotor centre in the brain stem. A fall in BP leads to sympathetic efferent impulses (from carotid and aortic sinuses to the brain stem), causing vasoconstriction, increased heart rate and ultimately, increased BP. Sympathetic stimulation (fight of flight responses) results in direct vasoconstriction and subsequent increases in systemic BP. In additional, hormonal mechanisms are important in long-term (days to weeks) BP control.
Hormonal regulation of blood pressure is regulated by the renin-angiotensin-aldosterone system.
Hypotension can be defined as a mean arterial pressure less than 60 mmHg, which is the minimum pressure required to maintain adequate perfusion to the brain and kidneys. Causes of hypotension include hypovolaemia secondary to blood loss or dehydration, sepsis, bradycardia or other arrhythmias, or cardiovascular depression caused by anaesthetic medications. If hypotension persists in spite of correcting the original cause(s), therapy with a vasopressor or positive inotrope may be considered (e.g. dopamine, dobutamine). If untreated, hypotension results in death.
Clinical hypertension is defined as a systolic BP > 160 mmHg. It may be triggered by hyperthyroidism, renal disease, or neoplasia as well as a variety of other causes, such as the 'white coat' effect when an animal is inside a veterinary clinic. Primary essential hypertension is rare in cats (and dogs). Common causes of hypertension in cats are hyperthyroidism, hypertrophic cardiomyopathy and renal disease. Hypertensive animals usually present with retinopathy and blindness, but similar changes in the brain can lead to focal haemorrhage and atherosclerotic changes. Almost half of the cats in one study had other neurological signs in addition to blindness. Seizures, ataxia, nystagmus, sudden collapse and paraparesis have been reported. Diagnosis is based upon documentation of repeatable hypertension and elucidation of the underlying cause of the elevation. Therapy is aimed at reversing the hypertension using oral antihypertensive drugs and treating the underlying cause. Certain antihypertensive drugs (nitroglycerin) can cause cerebral vasodilation, which can worsen the encephalopathy. Permanent seizure foci may be a sequela to the effects of hypertension, and long-term use of antiepileptic drugs may be necessary.
1) Low sodium diet - a diet moderately restricted in sodium should be offered
2) Antihypertensive agents
- Furosemide 1 - 2 mg/kg q 12-24 hrs
- ACE inhibitors
- Enalapril 0.35 - 0.5 mg/kg q 24-48 hrs
- Benazepril 0.25 - 0.5 mg/kg q 24 hrs
- Imidopril 0.5 mg/kg q 24hrs
- Atenolol 6.25 - 12.5 mg/kg q 24hrs
- Calcium channel blockers
- Diltiazem 1.5 - 2.5 mg/kg q 8 hrs
- Amlodipine besylate 0.625 mg/5 kg q 24 hrs