Hypertensive Crisis 2
Terms
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- Define Hypertensive Crisis
- Critical elevation of blood pressure usually SBP >160 and DBP >100
- Define Hypertensive URGENCY
- HTN crisis w/o acute target organ damage
- Define Hypertensive EMERGENCY
- HTN crisis with acute target organ dammage
- Describe the pathophysiology of hypertensive crisis
-
The increased BP results in arterial fibrinoid necrosis. Endothelial damage leads to activation of the clotting cascade and release of vasoconstrictor substances.
The RAS system and catecholamine release are triggered.
Pre-existing HTN actually lowers probability of hypertensive emergency through adaptive methanisms.
You also get increased release of cytokines due to mechanical stretching of vessel - Describe Autoregulation
- A protective mechanism by which cerebral blood flow maintains a constant cerebral perfusion over a large range of MAP. Chronically hypertensive patients have a right shift in the autoregulatory curve, so that cerebral blood flow is not maintained at low MAP avlues compared to non-hypertensives. Hypertensives require higher MAP to maintain adequate cerebral blood flow.
- Describe the Target End-organ damage in hypertensive emergency
-
1.Hypertensive Encephalopathy
2.Acute aortic dissection
3.Acute pulmonary edema with respiratory failure
4.Acute MI/Unstable angina
5.Eclampsia
6.Acute renal failure
7.Microangiopathic hemolytic anemia - Describe Hypertensive encephalopathy
-
HA, altered level of consciousness, advanced retinopathy with arteriololar changes, hemorrhage sand exudates.
Papilledema seen on examination of fundi - Describe Acute Aortic Dissection
- Dependent not only on elevation of BP but also on velocity of left ventricular ejection
- Describe Eclampsia
- Visual defects, severe headaches, seizures, cerebrovascular accidents, severe right upper quadrant abdominal pain, congestive heart failure and angina
- Describe acute renal failure
- Hematuria, proteinuria and increased SCr
- Describe Perioperative hypertension
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SBP >20% pre operative reading for 15 minutes or >50% increase from original value.
Incidence is 50% depending on surgery
Antihypertensive treatment reduces myocardial ischemia, neurological ischemia, neurologicla deficits and mortality. - Describe Postoperative Hypertension
-
Generally lasts 2-6 hours post surgery.
Requires rapid control of BP: Control bleeding at suture sites, neurology checks, myocardial ischemia develops due to increased oxygen needs.
Higher associaion with ICU admissions and mortality. - How does one calculate MAP
- 2/3DBP + 1/3SBP
- cPP=
- MAP-ICP
- Describe BP in Mild preeclampsia
- 130/80 to 140/95
- Describe Proteinuria in Mild preeclampsia
- 300mg/24 hours
- Describe platelets in Mild preeclampsia
- Normal
- Descibe Liver function in Mild preeclampsia
- normal
- Describe Clotting studies in Mild preeclampsia
- Normal
- Describe bilirubin in Mild preeclampsia
- Normal
- Describe BP in Moderate Preeclampsia
- >160/110
- Describe proteinuria in Moderate Preeclampsia
- >5 gm/24 hours
- Describe Platelets in Moderate Preeclampsia
- <150,000
- Describe liver function in Moderate Preeclampsia
- Elevated AST/ALT
- Describe clotting studies in Moderate Preeclampsia
- May be prolonged
- Describe bilirubin in Moderate Preeclampsia
- May be elevated
- Describe the HELLP syndrome
- Hemolysis, elevated liver enzymes and low platelet count reflect patients with greatest risk of mortality and morbidity
- What are the ideal pharmacologic considerations for Hypertensive crisis?
-
1.Easy transition to PO
2.No increase in ICP
3.Absence of coronoary or cerebreal steal phenomenon
4.Minimal ADR
5.Low number of dose adjustments
6.Maintenance of BP control
7.Rapid onset
8.Administration/cost - Goals of Therapy for Hypertensive crisis
-
TREAT THE PATIENT, NOT THE BP READING
-To lower BP or DBP over an ceeptable time frame based on severity of the crisis and individual tolerance without provoking cerebral or cardiac hypoperfusion, stroke or MI - Describe Goals of therapy for Hypertensive Emergency
- Decrease MAP by 20-30% over 30-60 minutes or decrease DBP by 5-10mmHg q 5-10 min to a diastolic pressure of 100
- Describe goals of therapy for Hypertensive urgency
- Reduce DBP gradually over a period of 12-24 hours.
- Hypertensive emergency requires _____ therapy
- IV
- Hypertensive urgency requires ______ therapy
- PO or IV
- Sodium Nitroprusside MOA
- Arterial and venous vasodilator which decreases preload and afterload
- Sodium Nitroprusside Dose
- 0.5-1mcg/kg/min to max of 10
- Sodium Nitroprusside effect on renal blood flow and myocardial oxygen demand
- Minimal
- Under what conditions is Sodium Nitroprusside unstable?
- Alkaline conditions and light
- Sodium Nitroprusside Onset
- 30 seconds to 2 minutes
- Sodium Nitroprusside, under what conditions is cyanide toxicity most likely?
- high dose for 48 hours
- Sodium Nitroprusside ADR
-
Hypotension with rapid infusion rates
Thiocyanate and cyanide toxicity - Labetolol MOA
- Selective Alpha and non-selective beta blocker with alpha:beta ratio of 1:7
- Labetolol Dose
- 20mg bolus then 0.5-2mg/min with max of 5mg/min
- Labetolol Onset
- 5-15 minutes, lasts up to 2-12 hours after cessation
- Labetolol PK
- Extensive first pass metabolism therefore oral is only 20-40% bioavailable
- Labetolol ADR
-
Heart Block
Orthostatic hypotension - Esmolol MOA
- Cardioselective beta blocker, decreases sympathetic tone
- Esmolol Dose
- 500mcg/kg over 1 min then 50mcg/kg/min with max 300mcg/kg/min (titrate every 5 minutes)
- Esmolol PK
- Very short duration, thus common in ICU
- Esmolol Onset
- Seconds and duration of 10-20 minutes after cessation
- Describe esmolol metabolism
- Occurs in erythrocytes by esterases and has metabolite (1/500th) activity eliminated in urine
- Esmolol ADR
-
Hypotension
Nausea - Fenoldopam MOA
- DA1 agonist through dilation of coronary, renal (afferent/efferent) arteries
- Fenoldopam Dose
- 1mcg/kg/min and increase by 0.05-0.02mcg/kg/min and then taper by 12% every 15-30 min
- Fenoldopam Onset
- 5-15 minutes with duration of up to 30-60 minutes after cessation
- Fenoldopam Metabolism
- Hepatic w/ Cyp450
- Fenoldopam ADR
-
Tachycardia
Nausea
Flushing - Nicardipine MOA
- 2nd Gen DHP CCB that is selective for cerebral and coronary vessels
- Nicardipine DOSE
- 5mg/hr titrate to max of 15mg/hr every 5 min by 2.5mg and oblus dosing not FDA approved
- Nicardipine Onset
- 1-5 minutes and duration is 2-6 hours after cessation
- Nicardipine binding
- >95% bound
- Does nicardipine have an effect on contractility?
- No, its a DHP CCB
- Nicardipine ADR
-
Reflex tachycardia
HA - Nitroglycerin MOA
- Potent vasodilator that decreases BP by decreasing preload and CO
- Nitroglycerin Dose
- 5-100mcg/min, prime the tubing
- Nitroglycerin Onset
- 2-5 minutes and DOA of 5 minutes
- Nitroglycerin ADR
-
HA
Tachycardia
Hypotension
Tolerance - Hydralazine MOA
- vasodilator that reduces TPR by direct action on vascular smooth muscle
- Hydralazine Dose
- 10-20 mg IV q 6-8 hour
- Hydralazine Onset
- Initially slower onset 5-15 minutes then precipitous fall in BP lasting 12 hours
- Problem with Hydralazine
- Unpredictable effects on BP and is difficult to titrate
- Hydralazine ADR
-
Tachycardia
HA
Aggravation of Angina - Enalapril MOA
- Reduces serum aldosterone, reduce in TPR and afterload. ONLY IV ACEI
- Dose Enalapril
- 0.625-5mg IV q 6 hours
- Enalapril onset
- 15-30 minutes and DOA of 6 hours
- Enalapril ADR
- Precipitous fall in BP in high-renin states, variable response
- 1st line agent in hypertensive EMERGENCY
- Nitroprusside