Systemic Hypertension Flashcards
Fenoldopam class and MOA
- selective dopamine-1 receptor agonist
Labetalol class and MOA
- 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
Hydralazine class and MOA
- 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
Esmolol MOA
- ultrashort-acting, cardio selective beta blocker
- most useful for severe postoperative hypertension or in situations when CO, HR and BP are all increased
Sodium Nitroprusside MOA
- 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
Phentolamine MOA
- short acting, alpha-adrenergic blocker that has been used anecdotally to manage intraoperative hypertension during pheochromocytoma removal
Amlodipine MOA and dose
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
Enalapril class and MOA
- ACE inhibitor; lowers peripheral vascular resistance and SV by blocking conversion of angiotensin I to angiotensin II
- cleared by the kidneys
Why is benazepril preferred to enalapril in treatment of systemic hypertension secondary to CKD?
- benazepril is cleared by both the liver and kidneys, whilst enalapril is cleared by the kidneys
Calcium channel blockers MOA
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.
ARBs MOA
- 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
Spironolactone MOA
- aldosterone antagonist
diseases associated with systemic hypertension
- 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)
BP =
CO x SVR
CO = HR x SV
List ‘target’ organs of systemic hypertension
- CNS
- Ocular
- Renal
- CDV
List the hypertension risk categories as classed based on risk of TOD
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
explain the pathophysiology of cardiovascular damage secondary to systemic hypertension
- 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
explain the pathophysiology of renal damage secondary to systemic hypertension
- renal afferent arteriole damage - making arterioles less responsive to changes in systemic BP
—> glomerular hypertension (decreased renal function, proteinuria)
explain the pathophysiology of ocular damage secondary to systemic hypertension
- 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
explain the pathophysiology of CNS damage secondary to systemic hypertension
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
