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Systemic Hypertension
Rebecca L. Stepien, DVM, MS, DACVIM (Cardiology)
Department of Medical Sciences, University of Wisconsin School of Veterinary Medicine, Madison, WI, USA
Etiology/Pathophysiology poorly understood for most diseases. Blood pressure in
health is modulated by interaction of diverse physiologic
Systemic hypertension (HT) describes a situation of systems affecting the heart, kidney, brain, and vasculature.
sustained elevation of blood pressure (BP). Systemic These systems rely on neural modulation (via the sympa-
hypertension is a clinical condition and should be con- thetic nervous system [SNS]), hormonal modulation (e.g.,
sidered a clinical complication of certain diseases rather renin‐angiotensin‐aldosterone system [RAAS], natriu-
than a disease in itself. In veterinary medicine, systolic retic peptides), vascular resistance modulation by circu-
blood pressure (SBP) is the value most often used to lating or local vasoactive mediators (e.g., endothelin,
assess BP status in the conscious clinical patient, and sys- thromboxane, prostaglandins, etc.) and any structural
temic hypertension is typically diagnosed when reliable changes (e.g., arteriosclerosis) that may be present.
measures of SBP deliver values ≥160 mmHg. Clinically Abnormalities in any of these contributing factors or the
detectable damage caused by HT may be noted in the interaction among these factors may alter arterial BP.
eyes, central nervous system, heart, and kidneys. Injury In health, increased BP typically leads to natriuresis in
related to HT in these organ systems is often collectively the normal kidney and lowering of systemic BP. No mat-
termed “target organ damage” (TOD). Target organ ter what the mechanism by which the initial elevation in
damage may be clinically obvious, especially in the ocular BP occurs (e.g., catecholamine excess or alterations in
or nervous systems. In other cases, TOD may be subtle RAAS activity), if “normalization” of elevated BP via
and result in accelerated progression of deterioration of natriuresis does not occur or is inadequate, abnormality
damaged organs (e.g., accelerated deterioration of renal in renal sodium handling is implied, and this may be the
function) rather than overt clinical signs. final common pathway for many etiologies of HT.
In veterinary patients, systemic hypertension has typi- The fact that multiple and complicated pathophysio-
cally been identified as one of three types: situational logic pathways are involved in modulation of BP and
(so‐called “white coat”) hypertension, systemic hyper- development of HT has three clinical repercussions.
tension secondary to systemic disease, and idiopathic First, HT due to different diseases is likely to respond to
systemic hypertension. Once situational hypertension different medications, based on the pathophysiologic
has been ruled out, systemic hypertension secondary to pathway of the development of HT in an individual
systemic disease is more common than idiopathic hyper- patient. Second, lack of complete understanding of these
tension. The designation of HT as “idiopathic” in a given pathways limits our ability to apply specific physiologic
patient is dependent on a thorough search for common blocks to lower BP, and nonspecific vasodilation becomes
diseases associated with HT. the treatment of choice for many cases of HT. Last,
because any decrease in BP below the individual’s cur-
rent set point (normal or abnormal) is likely to stimulate
Pathophysiology of Systemic Hypertension
reactive, BP‐increasing responses from modulating sys-
The pathophysiologic mechanism(s) of any individual’s tems like the SNS and RAAS, simultaneous blockade of
elevated BP is likely related to the cause of the HT, but the these systems may be required when direct vasodilators
specific pathways leading to sustained elevations in BP are are used in order to optimize response.
Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical