Systemic Hypertension

Question 1

Fenoldopam class and MOA

Answer 1

• selective dopamine-1 receptor agonist

Question 2

Labetalol class and MOA

Answer 2

• combined selective alpha-1-adrenergic and nonselective beta-adrenergic receptor blocker
• it maintains CO and decreases SVR without affecting total peripheral blood flow
• renal vasodilation does not occur

Question 3

Hydralazine class and MOA

Answer 3

• vasodilator that acts directly on the vascular smooth muscle to reduce peripheral resistance and BP
• renal vasodilation does not occur
• reflex tachycardia and fluid retention have been reported, so concurrent use of a beta-blocker may be required

Question 4

Esmolol MOA

Answer 4

• ultrashort-acting, cardio selective beta blocker
• most useful for severe postoperative hypertension or in situations when CO, HR and BP are all increased

Question 5

Sodium Nitroprusside MOA

Answer 5

• arterial and venous vasodilator, sodium nitroprusside decreases preload and afterload
• used more often in emergency tx. of heart failure rather than hypertension
• renal vasodilation does not occur
• avoid use in hypertensive encephalopathy because nitroprusside decreases cerebral blood flow and increases intracranial pressure
• onset immediate, DOA 1-2minutes

Question 6

Phentolamine MOA

Answer 6

• short acting, alpha-adrenergic blocker that has been used anecdotally to manage intraoperative hypertension during pheochromocytoma removal

Question 7

Amlodipine MOA and dose

Answer 7

calcium channel blocker; reduces BP by lowering peripheral vascular resistance through vasodilation and by lowering CO through negative chronotropic and inotropic effects

0.1-0.25mg/kg PO q24h

Question 8

Enalapril class and MOA

Answer 8

• ACE inhibitor; lowers peripheral vascular resistance and SV by blocking conversion of angiotensin I to angiotensin II
• cleared by the kidneys

Question 9

Why is benazepril preferred to enalapril in treatment of systemic hypertension secondary to CKD?

Answer 9

• benazepril is cleared by both the liver and kidneys, whilst enalapril is cleared by the kidneys

Question 10

Calcium channel blockers MOA

Answer 10

Reduces BP by lowering peripheral vascular resistance through vasodilation and by lowering CO through negative chronotropic and inotropic effects.
Calcium channel blockers preferentially dilate the renal afferent arteriole instead of the renal efferent arteriole.
This effect can expose the glomerulus to damage through increased glomerular capillary hydrostatic pressure.
Therefore it is not recommended to use calcium channel blockers as monotherapy for dogs with hypertension – best combined with ACE inhibitors or ARB.

Question 11

ARBs MOA

Answer 11

• selectively antagonizes the angiotensin II subtype-1 receptor. Theoretical benefits of ARB over calcium channel blockers include decreased aldosterone release and decreased proteinuria.
• ie. Telmisartan

Question 12

Spironolactone MOA

Answer 12

• aldosterone antagonist

Question 13

diseases associated with systemic hypertension

Answer 13

• renal disease (acute/chronic KD, PLN)
• endocrine (DM, hyperA, hyperaldosteronism, pheochromocytoma, hyperT, thyroid carcinoma)
• hyperviscosity disorders (polycythemia, multiple myeloma)
• medications (gluco/mineralo-corticoids, erythropoietin, phenylpropanolamine, ephedrine)

Question 14

BP =

Answer 14

CO x SVR

CO = HR x SV

Question 15

List ‘target’ organs of systemic hypertension

Answer 15

• CNS
• Ocular
• Renal
• CDV

Question 16

List the hypertension risk categories as classed based on risk of TOD

Answer 16

1) Normotensive; systolic BP <140mmHg
2) Prehypertensive: systolic BP 140-159 mmHg
3) Hypertensive: systolic BP 160-179 mmHg
4) Severely hypertensive: systolic BP >180mmHg

Question 17

explain the pathophysiology of cardiovascular damage secondary to systemic hypertension

Answer 17

• increased workload for the heart –> compensatory left ventricular hypertrophy
• hypertrophy = increased O2 demand by the myocardium and myocardial remodelling w/ XS collagen –> myocardial ischaemia, infarction, arrhythmias, heart failure
• fibrosis –> loss of compliance

Question 18

explain the pathophysiology of renal damage secondary to systemic hypertension

Answer 18

• renal afferent arteriole damage - making arterioles less responsive to changes in systemic BP
  —> glomerular hypertension (decreased renal function, proteinuria)

Question 19

explain the pathophysiology of ocular damage secondary to systemic hypertension

Answer 19

• retinal haemorrhage and arteriolar constriction and/or tortuosity
• damage to choroidal vasculature –> necrosis and atrophy of retinal pigmented epithelium
• leakage of blood and plasma from vessels results in retinal oedema, haemorrhage, retinal detachment (most commonly), or papilloedema, vitreal haemorrhage, hyphema, retinal aneurysms, secondary retinal degeneration, glaucoma

Question 20

explain the pathophysiology of CNS damage secondary to systemic hypertension

Answer 20

persistent vasoconstriction of arteriolar beds leads to ischaemia, decreased blood flow, thrombosis, haemorrhage, edema, infarction
–> CS; seizures, altered mentation, vestibular signs, head tilt, nystagmus, cervical ventroflexion, paresis, stupor, disorientation, facial nerve paralysis, focal neurologic deficits