King Faisal Specialist Hospital and Research Center (2007-1428)

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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

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ICU Case Presentation. King Faisal Specialist Hospital and Research Center (2007-1428). 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 - PowerPoint PPT Presentation

Transcript of King Faisal Specialist Hospital and Research Center (2007-1428)

Page 1: 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

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• 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

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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

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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

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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:

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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

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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

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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

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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

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• 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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