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