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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
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