Hypertension

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• Consistent increase in arterial blood pressure above the species normal.
• Cause: usually secondary, eg chronic renal failure, hyperthyroidism (23-87% of cases); primary (idiopathic) cases have been reported.
• Diagnosis: probably underdiagnosed in veterinary medicine.
• Treatment: address underlying cause, ACE inhibitors, beta or calcium channel blockers.
• Prognosis: early screening and identification important to prevent organ damage (particularly eyes, central nervous system, heart and kidney).

 Print the owner factsheet on hypertension  to give to your client.

• Retinopathy; decreased visual acuity followed by blindness .
• Progressive renal disease with proteinuria, polyuria, polydipsia, uremia .
• Acute heart failure , dysrhythmias , cardiac infarction.

• Neurological signs: depression, seizures , dementia, disorientation, etc.

• May be diagnosed when severe organ damage has occurred, eg blindness, stroke, cardiac failure , renal decompensation.

• Blood pressure increases with age.
• Older animals - usually with renal failure , or hyperthyroidism .

• Younger animals (primary hypertension).

• Male.

• Female.

• Some breeds have (slightly) above-average normal blood pressure ranges - this is not clinical hypertension.

• Same as congestive heart failure , or renal failure , depending on target organ damage.

• Rare; 1 colony in USA: familial hypertension.

Secondary

• Renal disease .
• Hyperthyroidism , (23-87% of cases of hypertension).
• Diabetes mellitus .
• Hyperadrenocorticism .
• Primary aldosteronism.
• Others, eg neurological disorders, polycythemia, syndrome of inappropriate ADH secretion.
• Acromegaly .
• Pheochromocytoma .

• Age (related to incidence of primary disease).

• Obesity .

• Pre-existing disease.

• Depends on cause.
• Often poorly understood.

Generally

• Arterial blood pressure = cardiac output x peripheral resistance.
• Factors affecting cardiac output and peripheral resistance:
  • Renin-angiotensin-aldosterone system.
  • Altered adrenergic activity.
  • Renal vasodepressor/vasopressor substances.
  • Sympathetic nervous system.
• All are interrelated, eg in the proposed pathophysiology of hypertension in renal disease:
  • Decreased renal blood flow renin/angiotensin release further Na retention and vasoconstriction increased renopressor substance production.
  • Anemia increased cardiac output.
  • Vascular wall stiffness, eg arteriosclerosis increased peripheral resistance.
• Proposed pathophysiology of hypertension in hyperthyroidism:
  • Increased sensitivity and numbers of beta receptors in myocardium increased sensitivity to catecholamines increased cardiac output.
  • Thyroid hormone-specific mediators increased cardiac output.
• Sustained hypertension muscular hypertrophy and necrosis of arterial walls ischemia and hemorrhage end organ damage especially eyes, kidneys, brain, heart.
• Idiopathic primary hypertension has been reported - ?familial, genetic.

• Usually chronic organ damage.
• May present acutely when organ damage occurred.

• Polyuria.
• Polydipsia.
• Blindness.
• Dementia, disorientation.
• Weakness, collapse.
• Seizures .

• History related to primary disease, eg progressive polyuria, polydipsia.

• Sudden blindness.
• Weakness, collapse.
• Dementia, disorientation, neurological deficits, etc.

• Clinical signs related to primary disease, eg anemia, pallor, dehydration.
• Bullous retinopathy (small circular donut lesions throughout fundus).
• Retinal hemorrhage .
• Hyphema , or retinal detachment, .

• Neurological deficits, depression, seizures.

• Blood pressure measurement:
  • Various definitions of hypertension; take repeated readings.
  • Consensus probably 180/100 mmHg systolic/diastolic.
  • Direct: intra-arterial, (technically difficult in unsedated cats).
  • Indirect: Doppler, oscillometric (Dinamap), photoplethysmograph.
  
   Marked 'White Coat Effect' in cats - blood pressure often elevated by stress.

Ophthalmology , .

• Hypertensive retinopathy: tortuous, dilated retinal vessels retinal hemorrhages retinal detachment , hyphema, papilledema, glaucoma .

Urinalysis

• Hypertension related to renal disease.
• Proteinuria .

Biochemistry

• Electrolyte assay, (hypertension related to renal disease).
• Uremia .
• Hypernatremia .

• Secondary left ventricular hypertrophy.

Serology

• Hormone assay.
• Thyroid , for hyperthyroidism.
• Cortisol for hyperadrenocorticism .
• For ADH, renin.

• History.
• Signs.
• Blood biochemistry.
• Hormone assay.

• Blood pressure measurement.
   May be difficult to differentiate from stress.

• Complete systematic examination required to look for primary and secondary lesions, including kidneys, adrenals, eyes, nervous system and cardiovascular system.

• Small, sclerotic end-stage kidneys.
• Ventricular wall and chamber enlargements best evaluated on transverse section one third proximally from apex. Compare with normal if unsure.

• Kidneys: fibrinoid lesions, hyalisation, myoarteritis, tubular degeneration, interstitial fibrosis.

• Cardiac and cerebral atherosclerosis/arteriosclerosis.

• Other causes of clinical signs:
  • Chronic renal failure without hypertension .
  • Primary cardiac failure .
• Other causes of retinal hemorrhage/hyphema:
  • Feline infectious peritonitis .
  • Toxoplasmosis .
  • Feline leukemia virus .
• Other causes of neurological signs.

• Direct-acting vasodilator may be required in emergency, eg acute neurological signs:
  Either Hydralazine , (0.5 mg/kg PO).
  Or Sodium nitroprusside , constant-rate infusion [CRI] (2.5-15 ug/kg/min IV using an infusion pump for CRI and continuous monitoring of blood pressure response).

• Where CRI and monitoring unavailable: hydralazine + frusemide , in combination + beta-blocker (see Normal Treatment), when blood pressure not normal within 12 hours.

• Treat hypertension when sustained indirect systolic blood pressure >170 mmHg.
• Therapy is stepwise; gradual addition of drugs, tailoring to suit individual case until blood pressure is controlled.
• Treat primary disease.
• Dietary sodium restriction .
• Diuretics: frusemide , (1-2 mg/kg q12-48h PO) spironolactone if primary aldosteronism (1-2 mg/kg BID PO), hydrochlorothiazide (2-4 mg/kg BID PO).
   Thiazides are not effective in renal failure - but can be used in other cases.
• Calcium channel blockers, eg verapamil , diltiazem , amlodipine (under trial in USA) shows promise (single agent, 0.625 mg/cat SID in the mornings).
• Angiotensin converting enzyme (ACE) inhibitors, eg enalapril (0.25-0.5 mg/kg BID-SID PO), benazapril (1 mg/kg SID PO).
   Monitor renal function carefully.
• Direct vasodilators, eg hydralazine (0.5-2.0 mg/kg BID PO).
• Beta-blockers: eg atenolol (6.25- 12.5 mg/cat SID PO), metoprolol (2-15 mg/cat TID PO), propanolol (2.5-5.0 mg/cat [0.4-1.2 mg/kg] TID-BID PO; 0.1 mg/cat slow IV).
• Alpha-blockers - specifically indicated in hypertension due to Pheochromocytoma, eg Prazosin (0.5-2.0 mg/cat TID-BID PO).

• Blood pressure (goal = <170 mmHg), and signs every 1-2 weeks until stabilized.

• Maintenance therapy usually continued for life unless primary condition can be cured.
• Therapy for hypertension helps to slow progression of renal failure and vice versa.
• Dietary sodium restriction + frusemide usually sufficient.

• Blood pressure measurement.
• Renal function: blood biochemistry, urinalysis, electrolytes.
• Ophthalmoscopic retinal examination.
• Signs.

• Control weight.
• Screen for hypertension, especially if renal/cardiac disease or hormonal problems.
• Once hypertension detected, treat early to prevent organ damage.

• Guarded: if renal failure will progress, but can control short-term.
• Good: if hormonal disease, eg hyperthyroidism should respond to definitive treatment.
• Poor: if primary hypertension.

• Signs.
• Sustained reduction in blood pressure measurement.
• Resolution/lack of progression of target organ damage.

• Too severe.
• Late diagnosis: target organ damage severe.
• Late decompensated primary disease, eg renal failure.
• Inappropriate/insufficient therapy, lack of response to medication.
• Standard reasons .

• Recent references from PubMed.
• Jepson R E, Elliott J, Brodbelt D & Syme H M (2007) Effect of control of systolic blood pressure on survival in cats with systemic hypertension. J Vet Intern Med 21 (3), 402-409 PubMed.
• Komaromy A M, Andrew S E, Denis H M, Brooks D E & Gelatt K N (2004) Hypertensive retinopathy and choroidopathy in a cat. Vet Ophthalmol. 7 (1), 3-9. DOI PubMed
• Forster-Van Hijfte M (2002) Feline hypertension: pathophysiology, clinical signs and treatment options. In Practice 24 (10), 590-594.
• Snyder P S, Sadel D & Jones G L (2001) Effect of amlodipine on echocardiographic variables in cats with systemic hypertension. JVIM 15, 43-46.
• Elliott J, Barber P J, Syme H M, Rawlings J M & Markwell P J (2001) Feline hypertension - clinical findings and response to antihypertensive treatment in 30 cases. JSAP 42, 122-129.
• Sparkes A H, Caney S M A, King M C A & Gruffydd-Jones T J (1999) Inter and intra individual variations in doppler ultrasonic indirect blood pressure measurements in healthy cats. JVIM 13, 314-318.
• Bodey A R & Sansom J (1998) Epidemiological study of blood pressure. JSAP 39 (12), 567-573.
• Henick R A (1997) Diagnosis and Treatment of Feline Systemic Hypertension. Comp Cont Ed 19 (2), 163-179 (very good, in depth, readable).
• Sansom et al (1994) Ocular disease associated with hypertension in 16 cats. JSAP 35, 604-611.
• Michell A R (1993) Hypertension in companion animals. Vet Annual 33, 11-23 (interesting, rather philosophical, overview).
• Dukes J (1992) Hypertension - a review of the mechanisms, manifestations and management. JSAP 33, 119-129 (very good, readable overview, especially of pathophysiology).

• Littman M P & Drobatz K J (1995) Hypertensive and hypotensive disorders. In: Textbook of Veterinary Internal Medicine. 4th edn. S J Ettinger & E C Feldman. Philadelphia: W B Saunders. pp 93-97.

• Dr Serena Brownlie BVM&S PhD CertSAC MRCVS, Broadacres, Bedford Road, Little Houghton, Northampton NN7 1AW, UK.
• Dr Phil Nicholls BVSc BSc PhD MRCVS MRCPath, Division of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, WA 6150, Australia.
• P Watson MA VetMB CertVR DSAM MRCVS, Department of Clinical Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK.
• Dr Mark Rishniw DVM DipACVIM, VRT Box 34, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.

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