Download - 2. Current Manag. Hipertensi Crisis
Current Management of Hypertensive Crisis
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DR. Dr. H. DJOKO TRIHADI, Sp.PD, FCCPRSUD Kota Semarang – SMF Penyakit Dalam
Epidemiology of Hypertensive Emergency (HE)
First described by Volhard and Fahr (1914), who saw patients with severe hypertension accompanied by signs of vascular injury to the heart, brain, retina, and kidney.
Prior to the introduction of antihypertensive medications, ñ 7% of hypertensive pts had HE.
Currently, 1 to 2% of pts with hypertension will have a HE at some time in their life.
Marik Paul E, Varon Joseph, CHEST 2007;131:1949-62
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Definitions
Hypertensive Crisis BP > 180/120
Hypertensive Urgency Hypertensive Emergency
Markedly elevated BP Markedly elevated BP without severe symptoms or with acute or progressing
progressive target organ damage. target organ damage. BP should be reduced within hours. BP should be reduced immediate.
Oral agents. Parenteral agents.
Kaplan NM ,Hypertensive Crises in : Clinical hypertension 9 th Ed,
Lippincott Williams & Wilkins 2006:609-630
Definitions (cont'd)
Accelerated malignant hypertension represents markedly elevated BP with papiledema (grade 4 Keith-Wagener retinopathy) and/or hemorrhages and exudates (grade 3 Keith-Wagener retinopathy). The Clinical features and prognosis are similar with grade 3 or 4 retinopathy (Ahmed et al., 1986)
Hypertensive encephalopaty is a sudden, marked elevation of BP with severe headache and altered mental status, reversible reduction of BP.
Kaplan NM ,Hypertensive Crises in : Clinical hypertension 9th
Ed, Lippincott Williams & Wilkins 2006:609-630
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Keith-Wagner Classification System
Grade I: Change in ratio of arteriole-venule
diameter. Grade II : Arteriovenous nicking "copper wire"
appearance. Grade III: Focal or diffuse arteriolar spasm,
flame hemorrhages, cotton wool spots, exudate, silver wire appearance, right-angle deviation.
Grade IV: Papilledema, vessel obstruction.
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Pathophysiology: Mechanism of malignant hypertension
Critical degree of hypertension
Increase in vasoconstrictors Endothelial damage (renin-angiotensin, vasopressin,
cathecolamines) Platelet and fibrin deposition
Further BP increase
Intravascular hemolysis
Pressure natriuresis
Fibrinoid necrosis and Intimal proliferation Hypovolemia
Further release of vasoconstrictors
Increase in BP and ischemia
Etiology Essential hypertension Renal parenchymal etiologies: Glomerulonephritis,
tubulointerstitial nephritis, Systemic disorders with renal involvement: SLE,
vasculitides. Renovascular: atheroma, fibromuscular dysplasia Endocrine: pheocromocytoma, Conn's syndrome,
Cushing syndrome Drugs : cocain, amphetamine, clonidine withdrawal, etc Tumor related Coarctation of the aorta Pre-eclampsia/ eclampsia Kitiyakara C, Guzzman NJ.J Am Soc Nephrl 1998:133-42
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Clinical Presentation
30%
25% 25%
23%
20%
16%
14% 15% 12%
10%
5% 5%
2%
0% Cerebral ICH or SAH Hypertensive Acute Acute CHF AMI or UAP Aortic Infarction encephalopathy pulmonary dissection
edema Zampaglione B, Pascale C et al. Hypertension 1996;27:144-7
Initial Evaluation of Patients with a Hypertensive Emergency History :
- Prior diagnosis and treatment of HT - Intake of pressor agents : street drugs,
sympathomimetics - Symptoms of cerebral, cardiac, and visual dysfunction
Physical exam. - BP - Funduscopy - Neurologic status - Cardiopulmonary status - Body fluid volume assessment - Peripheral pulses
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Initial Evaluation of Patients with a Hypertensive Emergency
Lab. evaluation - Hematocrit and blood smear - Urine analysis - Automated chemistry : creatinine, glucose, electrolytes - Plasma renin activity and aldosterone (if primary aldosteronism
is suspected) - Plasma renin activity before and 1 h after 25 mg captopril (if
renovascular hypertension is suspected) CXR (if heart failure or aortic dissection is suspected) ECG
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Autoregulation mechanism
CBF
Normal Mean Arterial Pressure (mmHg)
Chronic Hypertension 11
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Management of Hypertensive Emergency Patients should be admitted to an ICU for
continuous monitoring of BP and parenteral administration of an appropriate agent
Initial goal therapy is to reduce MAP by no more than 25% (within min. to 1 hour).
Then if stable, to 160/100 to 110 mmHg within the next 2 to 6 hours.
Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.
Chobanian AV et al, The JNC 7 report, JAMA 2003;389-2560-70
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Management of Hypertensive Emergency (cont'd)
If this level of BP is well tolerated and the patients is clinically stable, further gradual reductions toward a normal BP can be implemented in the next 24 to 48 h.
Exceptions : 1. Ischemic stroke
2. Aortic dissection SBP should < 100 mmHg
3. Patients whom BP is lowered to enable the use of thrombolytic agents
Chobanian AV et al, The JNC 7 report, JAMA 2003;389-2560-70
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Parenteral Drugs for Treatment of Hypertensive Emergencies based on JNC 7
Dose Onset Duration of Action
Sodium Immediate 1-2 minutes after nitroprusside infusion stopped
NTG 5-500 ug/min 1-3 minutes 5-10 minutes
Labetalol HCl 20-80 mg every 10-15 min 5-10 minutes 3-6 minutes or 0.5-2 mg/min
Fenoldopam HCl 0.1-0.3 ug/kg/min <5 minutes 30-60 minutes
Nicardipine HCl 5-15 mg/h 5-10 minutes 15-90 minutes
Esmolol HCl 250-500 ug/kg/min IV 1-2 minutes 10-30 minutes bolus, then 50-100 ug/kg/min by infusion; may repeat bolus after 5 min or increase infusion to 300 ug/min
Chobanian AV et al, The JNC 7 report, JAMA 2003;389-2560-70
Parenteral Drugs for Treatment of Hypertensive Emergencies based on ASA Guideline
Drug I.V. Bolus Dose Continous Infus Rate
5 - 20 mg every 15' Labetalol 2 mg/min (max 300mg/d)
Nicardipine NA 5-15 mg/h
Esmolol 250 ug/kg IVP loading dose 25-300 ug/kg/m
Enalapril 1,25-5 mg IVP every 6 h NA 5 - 20 mg IVP every 30' Hydralazine 1,5-5 ug/kg/m
Nipride NA 0,1-10 ug/kg/m
NTG NA 20-400 ug/m
This parenteral drugs are approved for hypertensive emergency 15 in acute ischemic stroke and ICH
AHA/ASA Guideline, 2007 update. Stroke. 2 007;38: 2001-23.
Parenteral Drugs for Treatment of Hypertensive Emergencies based on CHEST 2007
Acute PE / Systolic Nicardipine, fenoldopam, or nitropruside combined with dysfunction NTG and loop diuretic
Acute PE/ Diastolic Esmolol, metoprolol, labetalol, verapamil, combined with dysfunction low dose of NTG and loop diuretics
Acute Ischemia Coroner Labetalol or esmolol combined with diuretics
Hypertensive encephalopaty Nicardipine, labetalol, fenoldopam
Acute Aorta Dissection Labetalol or combined Nicardipine and esmolol or combine nitropruside with esmolol or IV metoprolol
Preeclampsia, eclampsia Labetalol or nicardipine
ARF / microangiopathic Nicardipine or fenoldopam anemia
Sympathetic crises/ cocaine Verapamil, diltiazem, or nicardipine combined with overdose benzodiazepin
Acute postoperative Esmolol, Nicardipine, Labetalol hypertension
Acute ischemic stroke/ ICH Nicardipine, labetalol, fenoldopam
Marik Paul E, Varon Joseph, CHEST 2007;131:1949-62
Actions to increase organ blood flow Pharmacodynamic action
Nicardipine: 3 ? g/kg/min ? 20 min
( ? %) (Hypertensive patients, n = 9) Mean BP Vertebral Renal Coronary artery blood flow blood flow Blood
flow change rate
60 blood flow
Baseline value 40
103 ? 11 mmHg Mean blood pressure
20 Vertebral artery 183 ? 65 mL/min blood flow
Renal artery 563 ? 29mL/min 0 blood flow Mean
blood pressure
Coronary artery 121 ? 42 mL/min change rate blood flow -10
- 20
( ? %) (Shoji Suzuki, et al., The 20th Annual Scientific Meeting of the Japanese Society of Hypertension: 1997)
Special Condition: Stroke
To recent consensus, decreasing BP in acute phase of ischemic stroke is allowed only if : - Ischemic Stroke with BP >220/120. - Candidate of rtPA therapy : BP >185/110. - Hemorrhage stroke with BP >180/100. - Acute stroke in hypertensive patients with hypertensive
encephalopathy, aortic dissection, acute MCI, acute lung edema and ARF.
Choose parenteral antihypertensive drugs and do the BP control cautiously
Labetalol and Nicardipine has been demonstrated to be an effective agent for the control of BP in patients with Ischemic Stroke and ICH. InaSH-2009 23
Special Condition: Preeclampsia and Eclampsia Initial therapy of preeclampsia includes volume
expansion, Mg SO4 for seizure prophylaxis , and BP control.
Delivery is definite treatment for preeclampsia and eclampsia
Based on current data, suggest that hydralazine and nifedipine not be used as first line treatment of severe hypertension in pregnancy.
IV labetalol or nicardipine , which are easier to titrate and appear to be safe and effective.
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Special Condition: ARF
Elevated BP causes deterioration of renal
function, therefore lowering BP is required Therapy should reduce BP without
compromising the RBF or GF Preferred agents : Nicardipine or
fenoldopam, because of it has been show to reduce BP, but still maintain and increase blood flow to renal artery.
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Special Condition: LV failure and PE Acute heart failure occurs as a result of an acute
rise in systemic vascular resistance and reduced LV compliance.
Acute PE / Systolic dysfunction : Nicardipine,
fenoldopam, or nitropruside combined with NTG and loop diuretic
Acute PE/ Diastolic dysfunction : Esmolol,
metoprolol, labetalol, verapamil, combined with low dose of NTG and loop diuretics
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Special Condition: Post operative hypertension Acute postoperative hypertension has been
defined as a significant elevation in BP during the immediate postoperative period that may lead to serious neurologic, cardiovascular, or surgical site complications.
Pain and anxiety are common contributors to BP elevations and should be treated before administration of antihypertensive therapy.
Labetalol, esmolol, nicardipine ,and clevedipine have proven effective in the management of APH.
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Conclusion Patients with hypertensive emergencies require
the immediate reduction of the elevated BP to prevent and arrest progressive end organ damage.
The best clinical setting to achieve this control is in the ICU .
There are several antihypertensive agents available including esmolol, nicardipine , labetalol, and fenoldopam.
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