Carlos J. Mucha, MV, MSc
Hypertension (AHT), remains one of the most common causes of morbidity and mortality in human medicine. In recent years, the diagnosis in small animals is more common, this is due to higher studies and the possibility of determining blood pressure by noninvasive methods (Doppler, oscillometric, etc.), very sensitive.
Blood Pressure: The Factors Governing
We can define the arterial pressure (AP) in a simplified way, as the product of blood volume by peripheral resistance.
AP= Volume x Resistance
Could also interpret the volume as the amount of blood ejected by the heart per minute (cardiac output). The AP is the physiological result a number of regulatory mechanisms (nervous, humoral, etc.) working in interrelated with the role of AP to maintain an appropriate, allowing adequate perfusion of the body. In the regulation of the AP, are mechanisms for fast action or short term, such as:
Vasoconstrictor mechanism mediated by epinephrine / norepinephrine.
Vasopressin or antidiuretic hormone.
Action of the endothelium: The secretion of vasodilator substances such as nitric oxide, also known as endothelium derived relaxing factor (FRDE), prostacyclin and endothelium derived factor hyperpolarizant (FHDE). It also develops property vasoconstrictive substances like endothelin (ET1).
Natriuretic atrial factor.
The renin-angiotensin-aldosterone (RAAS).
Other regulatory mechanisms are intrinsic circulation as the passage of fluid from the capillaries to the tissues and the effect of relaxation / tension of the muscles. All these mechanisms come into play during the course of seconds to minutes, but after a few days lose their ability or adapted, and thus cannot maintain the regulation of BP in the long run.
Regulatory mechanisms to slow or long-term are:
The renal system and body fluids: through regulating what is known as pressure diuresis and natriuresis.
The mechanisms governing the long-term PA during sustained periods of time, their action is more prolonged and only they can return to normal BP.
Normal Blood Pressure
In Veterinary Medicine cannot be determined a unique value for the PA as normal, since there is a variation and heterogeneity as race, age, and body size. It is also important to take into account environmental influences, such as visiting the veterinarian, fear, stress and white coat syndrome, whose influence has been demonstrated in Veterinary Medicine. In a study conducted by Dr. Bodey by oscillometry in 1782 dogs, determined average values of: Systolic BP: 133 mmHg Diastolic BP: 75.5 mmHg PA Media: 98.6 mmHg.
In the case of cats there are several studies, but taking into account the factor of the visit to the vet many authors consider a systolic BP of 150 mmHg as normal. Considering that before the discovery of hypertension, we must repeat the takes and find evidence of underlying disease or damage in target organs.
Arterial Hypertension (AHT)
AHT is called, a persistent elevation of the figures for systolic blood pressure (SBP), diastolic (DBP), or both, with respect to the values considered normal, according to characteristics of sex, race, age and other factors inherent to both the individual and environment. Normally in Veterinary medicine, unlike human medicine, is very rare presence of primary or essential hypertension, most respond to a secondary cause, therefore the primary diagnosis of hypertension should be made after ruling out the probable causes. Among them are hypothyroidism, which occurs due to hypercholesterinemia atherosclerosis and stiffness of the blood vessels and increases peripheral resistance. Chronic kidney disease can cause hypertension due to the inability to remove sodium and water, or because of the lack of production of vasodilating agents (prostaglandins, prostacyclin, etc.).
In hyperthyroidism, the thyroxine increases the number of myocardial adrenoreceptors more sensitized to the heart, the effect of catecholamines and increased heart rate, the inotropic and therefore the PA. Pheochromocytoma act in the same way due to increased production of catecholamines. In Cushing, increased cortisol and mineralocorticoids stimulate an increased production of renin, and thus the synthesis of AGII. Diabetes is also suspected of producing AHT, although the mechanisms are unclear, it is believed caused by an expansion of extracellular volume flow, or activation of renin-angiotensin system, or an alteration of the sensitivity of vasopressors or a flaw in the production of natriuretic agents or vasopressors. The consequence of a sustained hypertension, will produce a series of alterations in target organs such as: Eye abnormalities (hemorrhage, retinal detachment, hyphema, tortuous vessels, blindness, in the case of the cat choroid due to its high rate of passage of blood flow is an area very sensitive to AHT), damage to the CNS (hemorrhage, stroke), at the heart (left ventricular hypertrophy, diastolic failure, secondary valvular insufficiency), epistaxis, in the circulatory we see the proliferation of intima in arteries and arterioles, and kidney because of its high blood flow is another target organ, and here is a vicious circle: the kidney is affected due to hypoxic vasoconstriction of the afferent arteriole and that the active RAAS, due to the inability of the kidney to eliminate sodium and water increases the cardiac output and peripheral resistance, coupled with the inability of this form vasodilating agents such as prostaglandins.
The aim would be to seek the primary cause (hyperthyroidism, hypothyroidism, etc.). So restores BP to normal levels. The decision to start antihypertensive therapy, should be confirmed hypertension, this is after several repeated takes on the day and / or different days, and in established cases of diseases in target organs. We may use non-pharmacological treatments such as weight control, low sodium diet or avoid the use of agents that increase the PA such as glucocorticoids, amphetamines or drugs that affect the kidney (cyclosporine, aminoglycosides). The choice of drug treatment is based on the use of monotherapy or combination of drugs among which are:
Channel blockers calcium: Acting at vascular smooth muscle, interfering in the process of contraction (which is calcium dependent), thus reducing peripheral resistance. Such as verapamil, but it presents the problem of reducing cardiac output and depresses myocardial function. In contrast, Diltiazem, to a lesser extent the depressed cardiac function. Diltiazem dose is 0.5 to 1.5 mg / kg / 8 hrs VO. Within the new generation of channel blockers calcium, Amlodipine, a proven effective in hypertension in cats at doses of 0.625 to 1.25 mg / 24 hours / VO per cat.
Beta blockers: The β1 as Atenolol, Metoprolol, Acebutolol, Carvedilol (also α) and cardio-selective and of thus avoiding side-effects of β2 blockade. Beta blockers reduce cardiac properties, thus the fall of the minutes volume decrease sympathetic neuronal release of norepinephrine by blocking pre-synaptic beta also decreases the secretion of renin and alter the sensitivity of baroreceptors adjusting your threshold discharge to a lower level of blood pressure.
Alpha-adrenergic blockers: Hydralazine acts occurring arterial dilation without effect on the venous territory, thus reducing peripheral resistance and hence the PA. The doses is 1 mg/kg/12 hours, oral, and up to 3 mg/kg every 12hs.
Diuretics: Their choice is based on achieving lower BP by a decrease in blood volume and cardiac output. In Medicine, the combination of restriction of sodium in the diet plus the addition of diuretics is one of the first choice, but it is believed that this combination produces a poor response in dogs and cats.
Enzyme inhibitors of angiotensin Converter (ACEI): In physiological conditions, the enzyme converter of angiotensin promotes the growth of PA and retention of sodium and water, for their ability to form AG II, Aldosterone and degrade more quickly cininas (bradykinin) vasodilator.
Therefore, the inhibition of ACE results in a decrease in BP. The most commonly used ACE inhibitors in veterinary include Captopril, Enalapril and Benazepril, there is little documented work of its use in hypertension, and can be given as monotherapy or in combination. One should keep in mind that your administration may exacerbate renal failure.
References are available upon request.