King Faisal Specialist Hospital and Research Center (2007-1428)
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Transcript of King Faisal Specialist Hospital and Research Center (2007-1428)
King Faisal Specialist Hospital and Research
Center(2007-1428)
ICU Case Presentation
Manar Lashkar
Samah Al-shehri
Pharm.D candidates
Supervised by:Dr. Mazen Kadri
• Hypertension affects > 65 million people in the United States and is one of the leading causes of death
• One to two percent of patients with hypertension have acute elevations of BP that require urgent medical treatment
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Hypertensive Crisis
Degree of BP
elevation
Presence of end-organ
damage
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Outline
Difference between hypertensive emergency and urgency
Management of hypertensive crisis
Special conditions of hypertensive crisis
Case Scenario
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• End Stage Renal Disease (ESRD)
• Hypertension (HTN)
• Systemic Lupus Erythrematosus (SLE)
24 years old single female with a history of
Not compliant to restricted Na intake
methyldopa stopped 2 months ago because of the SLE like side effect
BP was controlled on the medication
8 years on steroid therapyLupus nephritis Multiple viral wartsLeukopeniaAs complication of lupus nephritis
Hemodialysis (HD) 3 times a week for the past 6 months
Planned for renal transplant
SLE:• Prednisolone 5 mg PO OD
ESRD:• Epoeitin 8000 units SC 3 times a week• Sevelamer 800 mg PO TID• One a 0.25 mcg PO OD• Multivitamin 1 tab PO OD
HTN:• Metoprolol 100 mg PO TID• Clonidine 200 mcg PO TID• Nifedipine LA 60 mg PO TID
She was on
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Previous Investigations
Ejection fraction = 55% (on 12/2007)
ANA was positive (on 12/2007)
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On 14/3/2008Came to the hospital ER with
Shortness of breath (orthopnea) for one day Blood pressure 230/120 mmHg Chest x-ray reveled pulmonary interstitial infiltration
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No history of :Cough
Palpitation Chest pain Convulsion
Visual disturbance
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The patient received 40mg IV furosemide
Sent to RDU for emergency HD UF 3 kg was removed
The patient blood pressure was still uncontrolled
Medical Intervensions
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In the ward
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• SLE and ESRD: same medications
• HTN:
Furosemide 40 mg IV BID
Metoprolol 100 mg PO TID Clonidine 200 mcg PO TIDNifedipine LA 60 mg PO TID
Labetalol 200 mg PO QID
14-16/3/2008BP: 180-186/106-114 mmHg
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• SLE and ESRD: same medications
• HTN:Labetalol 200 mg PO QID Clonidine 200 mcg PO TIDNifedipine LA 60 mg PO TIDFurosemide 40 mg IV BID
Labetalol 400 mg PO QID
17/3/2008
Plan: transfer to ICU forIV medications
BP: 210/110 mmHg
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ICU
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ECG
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• SLE and ESRD: same medications • HTN:
Enalapril 20 mg PO BID
Nitroglycerin 200 mcg/ml IV infusion
Labetalol 400 mg PO QID Clonidine 200 mcg PO TIDNifedipine LA 60 mg PO TIDFurosemide 40 mg IV BID
Clonidine 300 mcg PO TID
17/3/2008 ICUHTN
Urgency
>180/120mmHg
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• SLE and ESRD: same medications • HTN:
Labetalol 400 mg PO QID Clonidine 300 mcg PO TIDNifedipine LA 60 mg PO TIDFurosemide 40 mg IV BIDEnalapril 20 mg PO BIDNitroglycerin 200 mcg/ml IV infusion
Nifedipine LA 90 mg PO TID
18/3/2008 ICU
Plan: transfer to the floor
BP: 130-155/80-95 mmHg
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18/3/2008 ICU
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19/3/2008BP: 134/92 mmHg
The patient BP was controlled so the patient discharged on the same
medications
Labetalol 400 mg PO QID Clonidine 300 mcg PO TIDNifedipine LA 90 mg PO TIDEnalapril 20 mg PO BID
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Labetalol 400 mg PO QID
Clonidine 300 mcg PO TID
Enalapril 20 mg PO BID
Nifedipine LA 90 mg PO TID
Metoprolol 100 mg PO TID
Clonidine 200 mcg PO TID
Nifedipine LA 60 mg PO TID
Past medications vs
Discharged medications
Past medicationsDischarged medications
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Hypertensive Crisis
Systolic BP (SBP) > 179 mm Hg or a diastolic BP (DBP) >109 mm Hg “HYPERTENSIVE CRISIS”
Absence of acute target-organ involvement
Presence of acute end-organ damage
“Hypertensive Urgencies”“Hypertensive Emergencies”
Important in formulating a therapeutic plan
BP should be lowered immediately, although not to “normal” levels
BP should be reduced within 24 to 48 h
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End Organ Damage
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• Hypertensive encephalopathy
• Acute aortic dissection
• Acute coronary syndrome
• Pulmonary edema with respiratory failure
• Severe pre-eclampsia, HELLP syndrome,
eclampsia
• Acute renal failure
• Microangiopathic hemolytic anemia
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Development of HypertensiveEmergency
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• The failure to adhere to prescribed antihypertensive regimens
• Inadequate control of BP
• The lack of a primary care physician
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Autoregulation is a specific form of homeostasis used to describe the tendency of the body to keep blood flow constant when blood pressure varies
Normotensive
Hypertensive
Org
an B
lood
Flo
w
Mean Arterial Blood Pressure (mmHg)
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• The preferred agents include labetalol, esmolol, nicardipine, and fenoldopam
• Oral and sublingual nifedipine are potentially dangerous in patients with hypertensive emergencies and are not recommended
• Clonidine and angiotensin-converting enzyme (ACE) inhibitors are long acting and poorly titratable
Managment
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The onset of action within 2-5 min Duration of action 2-4 hours
Labetalol is a combined selective a1-adrenergic and nonselective b-adrenergic receptor blocker with an alfa to beta blocking ratio of 1:7
Labetalol
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Labetalol maintains cardiac output
Cerebral, renal, and coronary blood flow are also maintained
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The onset of action within 5-15 min Duration of action 4-6 hours
Nicardipine is a second-generation dihydropyridine derivative calcium-channel blocker with high vascular selectivity and strong cerebral and coronary vasodilatory activity
IV nicardipine has been shown to reduce both cardiac
and cerebral ischemia
Nicardipine
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The onset of action within 60 sec Duration of action 10 to 20 min
Esmolol is an ultrashort-acting b1-adrenergic blocking agent
The metabolism of esmolol is via rapid hydrolysis of ester linkages by RBC esterases and is not dependant on renal or hepatic function
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Esmolol
“ideal b–adrenergic blocker” for use in critically ill patients
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The onset of action 5 min Duration of action 30 to 60 min
No rebound hypertensionFenoldopam improves creatinine clearance in severely hypertensive patients with both normal and impaired renal function
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Fenoldopam
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It mediates peripheral vasodilation by acting on peripheral dopamine-1receptors
It is a very potent arterial and venous vasodilator that decreases both afterload and preload
• Intraarterial BP monitoring is recommended• It requires special precaution to prevent severe toxicity
and adverse events• It requires special handling to prevent its degradation
by light
The onset of action seconds Duration of action 1 to 2 min
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Nitroprusside
Factors limiting the use of nitroprusside:
Nitroprusside Nonenzymatically release
Cyanide
(toxic)Thiosulfate
Liver
Thiocyanate
(less toxic)Kid
ney
excretion
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NitroprussideContraindications:• Increased intracranial pressure• Coronary artery disease
• Hepatic or renal impairment
Nitroprusside decreases blood flow
Increased risk of cyanide
toxicity
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Precautions:• The drug should only be used when other IV
antihypertensive agents are not available and in certain circumstances and in patients with normal kidney and liver function
• The duration of treatment should be as short as possible
• infusion rate should not be > 2 mcg/kg/min
Nitroprusside
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It reduces afterload without affecting cardiac filling pressures or causing reflex tachycardia
It is third-generation dihydropyridine calcium channel blocker with an ultrashort-acting selective arteriolar vasodilator properties
Clevidipine
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It is rapidly metabolized by RBC esterases. Thus, its metabolism is not affected by renal or
hepatic function
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Nifedipine
But
Sublingual Oral
It has been widely used via oral or sublingual administration in the management of hypertensive emergencies
It is poorly soluble and is not absorbe through the buccal
mucosa
Rapidly absorbed from the GI tract after the capsule is broken or dissolved
This rout is not FDA approved
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Nitroglycerin reduces BP by reducing preload and cardiac output It causes hypotension and reflex tachycardia
It is a potent venodilator and only at high doses affects arterial tone
Nitroglycerin
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Low-dose administration (60 mg/min) may be used as an adjunct to IV antihypertensive therapy in patients with
hypertensive emergencies associated with acute coronary syndromes or acute pulmonary edema
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It is best avoided in the
management of hypertensive crises
Following IM or IV administration, there is an initial latent period of 5 to 15 min followed by a progressive and often precipitous fall in BP that can last up to 12 h
It is a direct-acting vasodilator
Hydralazine
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Special Conditions
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Treatment:
Vasodilator
AlternativeDrug of Choice
b-blocker
Nitroprusside
MetoprololEsmolol
Nicardipine fenoldopam
If vasodilator alone:reflex tachycardia
increase aortic ejection velocity promote dissection propagation
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Acute Aortic Dissection
Cerebral Ischemia
Cerebral Hemorrhage
withhold antihypertensive therapy for acute ischemic stroke unless
• planned thrombolysis• evidence of concomitant noncerebral acute organ
damage• if the BP is excessively high, a SBP 220 mm Hg or a
DBP 120 mm
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Cerebrovascular Accidents
Cerebral Hemorrhage
The controlled lowering of the BP is currently recommended only when
• SBP is > 200 mm Hg • DBP is > 110 mm Hg• MAP is > 130 mm Hg
Nicardipine has been demonstrated to be an effective agent for the
control of BP in patients with intracerebral
hemorrhage
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Cerebrovascular Accidents
Initial treatment for preeclampsia
Magnesium sulfate for seizure prophylaxis
Blood pressure control
Volume expansion
Nitroprusside and ACE inhibitors are contraindicated in pregnant patients
IV labetalol or nicardipine
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Preeclampsia / Eclampsia
• Hypertensive crisis is medical emergency that requires immediate treatment
• Target-organ damage differentiates emergency versus urgency
• Hypertensive emergency should be treated with parenteral medications of rapid onset of action and short duration
• Blood pressure should not be rapidly reduced
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Summary
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