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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