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220  Section 3  Cardiovascular Disease

            Pathophysiology of Target Organ Damage            protein‐losing renal disease, hyperadrenocorticism,
  VetBooks.ir  Arterial blood flow is maintained at relatively constant   adrenal tumors, including  pheochromocytomas and
                                                              aldosterone‐secreting tumors, and diabetes mellitus.
            levels in the brain, kidneys, and eyes through a process of
            vascular autoregulation, wherein small resistance vessels   The most common diseases associated with feline HT
                                                              include chronic renal disease, feline hyperthyroidism,
            constrict when BP is elevated and dilate when BP is   hyperaldosteronism, and diabetes mellitus. In both spe-
            decreased to maintain flow. Hypertensive damage in   cies, the suspected association (medical or age group
            these organs occurs when these autoregulatory mecha-  related) between subclinical renal dysfunction and both
            nisms fail. Elevated BP without adequate resistance ves-  diabetes mellitus and hyperthyroidism may partially
            sel constriction causes overdistension of vessels, which   account for the occurrence of HT in affected animals.
            leads to damage to endothelial tight junctions and allows   Ten to 15% of hyperthyroid cats that are normotensive at
            protein and plasma leakage into interstitial tissue in   the  time  of  diagnosis  may  become  hypertensive  after
            affected tissue beds (i.e., tissue edema). If excessive vas-  successful therapy for hyperthyroidism, indicating other
            cular resistance vessel constriction occurs, ischemia of   mechanisms of HT at work in these patients. The preva-
            local tissues may result in focal hemorrhage and necro-  lence of idiopathic and situational HT remains unclear
            sis. Permanent structural changes such as arteriosclero-  for both species.
            sis may develop, decreasing vascular distensibility. Any
            combination of these mechanisms may result in clinical
            signs of TOD (Table 22.1).                          Signalment

                                                              Systemic hypertension is associated with many diseases
              Epidemiology                                    that are more common in older animals, but aging itself
                                                              is not a cause of HT. In the case of secondary HT, the
            The most common diseases associated with HT in    signalment of affected animals reflects groups at risk for
            dogs  include acute or chronic renal disease, especially   the underlying disease. In cats, because two common


            Table 22.1  Evidence of target organ damage. Clinical signs of target organ damage and additional recommended testing

             Organ system affected  Associated clinical findings     Recommended diagnostic testing

             Eyes              Acute blindness due to retinal detachment or   Fundoscopic examination
                               severe hyphema                        Coagulation/platelet assessment if hyphema or retinal
                               Retinal hemorrhage                    hemorrhage
                               Retinal vascular narrowing or tortuosity
                               Focal retinal transudates
                               Focal retinal ischemic degeneration
                               Partial or complete retinal detachment
                               Papilledema
             Brain             Seizures (focal facial or grand mal)  Complete neurologic examination
                               “Stroke‐like” intracranial neurologic deficits  Additional imaging (e.g., MRI)
                               Decreased mentation/obtundation
                               Photophobia
                               Nystagmus
             Kidneys           Proteinuria                           Serum BUN and creatinine
                               Microalbuminuria                      Complete urinalysis
                               Progressive decrease in renal function  Urine culture
                                                                     Quantitation of proteinuria or albuminuria
                                                                     Advanced renal testing (e.g., GFR)
             Heart             Left ventricular concentric hypertrophy  Auscultation
                               Arrhythmia                            Thoracic radiographs
                               Gallop rhythm                         Echocardiography
                               Systolic heart murmur                 Doppler echocardiography may be required to rule out
                               Increased sensitivity to fluid loading (unexpected   other causes of LV hypertrophy (e.g., subaortic stenosis)
                               acute heart failure after fluid administration)  Assessment for coagulation/platelet abnormalities if
                               Epistaxis                             epistaxis
            Note: recommended testing list is not exhaustive, additional testing may be indicated in individual patients.
            BUN, blood urea nitrogen; GFR, glomerular filtration rate; LV, left ventricle; MRI, magnetic resonance imaging.
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