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57 Cards in this Set

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What is the definition of hypertensive crisis?
SBC >160 and DBP >100
What is the definition of hypertensive urgency?
HTN crisis w/o acute target organ damage
hypertensive emergency
HTN crisis with acute target organ damage
pathophysiology of hypertensive crisis
1)endothelial damage
-clotting cascade
-vasoconstrictor release
2)renin-angio activation
3)catecholamine release
4)mechanical stretching of vessel
-cytokine release
target end-organ damage in hypertensive emergency
1)brain
-stroke, encephalopathy, mental status changes
2)retina
-papilledema, hemorrhages
3)kidney
-hematuria, proteinuria, inc.SCr
4)heart
-AMI/UA, dissecting AA
5)pulm edema, eclampsia, hemolytic anemia
perioperative hypertension definition
SBP >20% pre-operative reading for 15 mins or >50% increase from original value
perioperative hypertension etiology
1)vasoconstriction (catecholamines, baroreceptor)
2)intravascular hypovolemia
how long does postoperative hypertension last?
2-6 hours
formula for cerebral perfusion pressure
CPP = MAP - ICP
preeclampsia criteria (mild)
BP, proteinuria, platelets, liver function, clotting studies, bilirubin
-BP 130/80 - 140/95
-proteinuria 300mg/24 hours
-platelets, LF, clotting studies, bilirubin = normal
preeclampsia criteria (moderate)
BP, proteinuria, platelets, liver function, clotting studies, bilirubin
-BP = >160/110
-proteinuria = >5gm/24 hours
-platelets = <150,000
-liver function = elev AST/ALT
-clotting studies = may be prolonged
-bilirubin = may be elevated
What criteria reflect patients with the greatest risk for mortality and morbidity?
HELLP
-hemolysis
-elevated liver enzymes
-low platelets
goals of therapy
lower MAP or DBP over an acceptable time frame based on severity of crisis and individual patient tolerance w/o provoking cerebral or cardiac hypoperfusion, stroke, or MI
hypertensive emergency goal
decrease MAP by 20-30% over 30-60 mins or decrease DBP by 5-1- every 5-10 mins to a diastolic pressure of 100
hypertensive urgency goal
reduce DBP gradually over a period of 12-24 hours
route of administration for hypertensive emergency and hypertensive urgency
-IV
-oral or parenteral
What variables effect SVR?
-circulating vasoconstrictors
-circulating catecholamines
What variables effect CO?
-circulating catecholamines
Treatment options for SVR
-Calcium channel blockers
-nitrovasodilators
-dopamine agonists
-ACE inhbitors
Treatment options for CO
beta blockers
Sodium nitroprusside MOA
1)arterial and venous vasodilation which decreases both preload and afterload
-metabolized by blood vessels to NO leading to cGMP and vasodilation
sodium nitroprusside onset of action
30 seconds to 2 minutes
sodium nitroprusside metabolization
smooth muscle metabolizes nitroprusside to NO and cyanide, cyanide further metabolized by rhodanase to thiiocyanate which is elimated in urine
sodium nitroprusside toxicity
1)hypotension
2)infusion >4mcg/kg/min for >24 hours can lead to cyanide toxicity (cardiac arrest, encephalopathy, seizures, coma)
Labetalol MOA
1)selective alpha and non-selective beta adrenergic receptor blocker with alpha: beta ratio of 1:7
labetalol onset of action
5-15 mins and lasts up to 2-12 hours
labetalol adverse effects
1)heart block
2)orthostatic hypotension
Esmolol MOA
1)cardioselective beta adrenergic blocker, decreases sympathetic tone
esmolol onset of action
seconds and duration of action up to 10-20 mins (ideal in ICU)
esmolol metabolization
occurs in erythroctes by esterases and has a metabolite 1/500 activity eliminated in urine
esmolol adverse effects
1)hypotension
2)nausea
esmolol hepatic and renal considerations
don't need to adjust in hepatic or renal failure and useful in patients w/ AMI
Fenoldopam MOA
dopamine agonist (DA1 agonist) through dilation of coronary, renal (afferent/efferent) arteries
Fenoldopam onset of action
5-15 minutes w/ duration of action up to 30-60 mins
Fenoldopam metabolism
via hepatic pathway w/ involvement of P450 system
fenoldopam adverse effects
1)tachycardia
2)nausea
3)flushing
fenoldopam vs. dopamine
5-10x more potent than dopamine for renal vasodilator
Nicardipine MOA
2nd gen dihydropyridine CCB particularily selective for cerebral and coronary vessels
nicardipine onset of acction
1-5 mins and duration of action 2-6 hours
nicardipine adverse effects
1)tachycardia
2)headache
nitroglycerin MOA
-potent vasodilator that decreases blood pressure by decreasing preload and cardiac output
-compromises cerebral and renal perfusion due to decreased preload and CO
nitroglycerin onset of actio\n
2-5 mins and duration of action is 5 mins
nitroglycerin adverse effects
1)hypotension
2)tachycardia
3)headache
4)tolerance
hydralazine MOA
vasodilator that reduces peripheral resistance by direct action on vascular smooth muscle
hydralazine onset of action
5-15mins then preciptous fall in BP lasting 12 hours
hydralazine adverse effects
1)angina aggravation
2)tachycardia
3)headaches
4)unpredictable effects on BP and difficult to titrate
enalaprilat MOA
-reduces serum aldosterone, reduction in total peripheral resistance and afterload
-only IV ACE inhibitor
enalaprilat onset of action
15-30 mins and duration of action up to 6 hours
enalaprilat adverse effects
preciptous fall in BP in high-renin states, variable response
1st line treatment for hypertensive emergency
nitroprusside
severe renal or hepatic insufficiency and MI
nitroglycerin
preeclampsia or eclampsia
hydralazine
preoperative patients w/ aortic dissection
esmolol
renal insufficiency w/ risk of cyanide toxicity
fenoldopam
coronary, cerebral, or peripheral artery disease and surgical patients
nicardipine
patients with HF and at risk for cerebral hypotension
enalapril
syndromes of coronary insufficiency (avoid in CHF, COPD, decreased HR)
labetolol