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Management of Hypertension in Critical Illness
 

Management of Hypertension in Critical Illness

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Management of Hypertension in Critical Illness Management of Hypertension in Critical Illness Presentation Transcript

  • How to Manage Hypertension 2008 PJ PAPADAKOS MD Director of Critical Care Medicine Professor of Anesthesiology, Surgery And Neurosurgery University of Rochester
  • University of Rochester Medical Center
  • Learning Objectives
    • Outline the prevalence and pathophysiology of hypertension in the inpatient setting
    • Identify treatment goals and treatment options for the severely hypertensive patient
    • Discuss the pharmacologic profile and potential benefits of different agents used in these cases
  • Hypertension
    • Common clinical problem
      • 1 billion people worldwide
      • 60 million Americans
    • At least 15% of African-Americans
    • Increases with age
    • Male +/- higher than females?
    • 30% undiagnosed
    • 15%-30% adequate BP control
  • The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure JAMA . 2003;289:2560-2572. The JNC 7 Report  100  160 Stage 2 90-99 140-159 Stage 1 80-89 120-139 Prehypertension < 80 < 120 Normal Diastolic BP mm Hg Systolic BP mm Hg BP Classification
  • Severe or Accelerated Hypertension
    • Stage III?
    • Systolic  180 mmHg or
    • Diastolic  110 mmHg
    Hypertensive Urgency Hypertensive Emergency VS
    • Hypertensive Emergency
    • Acute severe elevation of blood pressure
    • Acute end-organ damage
    • Hypertensive Urgency
    • Sub-acute to chronic severe elevation of blood pressure
    • NO acute end-organ damage
  • Hypertensive Emergencies
    • Hypertensive encephalopathy
    • Acute aortic dissection
    • Acute pulmonary edema with respiratory failure
    • Acute myocardial infarction/angina
    • Eclampsia
    • Acute renal failure
    • Microangiopathic hemolytic anemia
  • “Malignant HTN”
    • Commonly used term since 1928
    • 3rd Report of Joint National Committee*
    • Increased blood pressure
      • Encephalopathy
      • Acute nephropathy
    • Removed from recent JNC definitions
    *Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure: the 1984 Report. Arch Intern Med . 1984;114:1045-1057.
  • Historical Perspective
    • Hypertensive emergency first described by Volhard and Fahn in 1914*
      • Severe HTN with renal disease and signs of vascular injury to the heart, brain, retina, and kidneys; and characterized by a rapidly fatal course ending in heart attack, renal failure, or stroke
    • In 1939 Keith et al published first study on the natural history of “malignant hypertension” †
      • 1 year mortality of 79%
      • Median survival of 10.5 mo
    *Volhard F, Fahr T. Die brightsche Nierenkranbeit: Klinik, Pathologie und Atlas. Berlin: Springer; 1914. † Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: their course and prognosis. Am J Med Sci . 1939;197;332.
  • Epidemiology of Hypertensive Emergencies
    • 1% of hypertensives will develop a hypertensive emergency during their life
    • Prior to use of antihypertensive agents, occurred in up to 7% of hypertensives
    • In USA, - hospital admission tripled from 1980 -1990
      • 25,000 to 75,000/y
    • Epidemiology parallels that of essential hypertension (except males 2x females)
      • Higher in African-Americans and elderly
    • Risk factors*
      • Lack of primary care physician
      • Poor compliance: only 50% of patients with essential hypertension had taken medications in preceding week
      • Illicit drug use
    *Shea S, et al. Predisposing factors for severe, uncontrolled hypertension in an inner city minority population. N Engl J Med . 1992;327:776.
  • Etiology of Hypertensive Emergencies
    • Essential HTN
      • 20%-30% white pts
      • 80% black pts
    • Secondary HTN
      • Renal parenchymal diseases
      • Renovascular
      • Endocrine
      • Drugs
        • Cocaine, amphetamines
      • Coarctation of aorta
  • Pathophysiology
  • Regulation of Blood Pressure Blood Pressure Adrenergic Tone Baroreceptor Reflexes Volume/Pressure Renin/Angiotensin Preload Cardiac Output Catecholamines Adrenal Gland CNS Veins Arteries Capacitance Resistance Heart Kidney Afterload
  • Pathophysiology
    • Abrupt increases in systemic vascular resistance (SVR)
      • Related to humoral constrictors
    • With severe elevation of BP
      • Endothelial injury
      • Fibrinoid necrosis of arterioles
      • Breakdown of normal autoregulation process
  • Pathophysiology
  • Fibrinoid Necrosis
  •  
  • CT SCANS and X-rays
  • Hypertensive Encephalopathy/Retinopathy
  • Delanty et al Neurology 1997;49:686-689 Posterior leukoencephalopathy in hypertensive encephalopathy
  •  
  • Reversible high T2 signal abnormalities in pre-eclampsia
  • Intracerebral hemorrhage
    • Hypertension is the most important risk factor for ICH in the typical locations:
      • Putamen
      • Thalamus
      • Cerebellum
      • Pons
    • Hypertension is less important in the pathogenesis of ICH in other locations, where bleeding into a lesion or a coagulation disturbance is more common
  •  
  • Clinical Symptomatology
    • Varies from patient to patient
    • Headache, confusion, focal signs
    • Dyspnea, cough
    • Chest pain
    • Oliguria/hematuria
  • Initial Evaluation
    • Targeted history and physical examination
      • Prior anti-HTN use
      • Use of MAOs, “recreational drugs”
      • BP in all limbs
        • Obese patients: proper size cuffs
    • CBC + smear, electrolytes, BUN, Cr, U/A
    • CXR, ECG
    • CT head/CT chest
  • Aortic Dissection
  • Management Principles – Hypertensive Emergency
    • Admission to ICU
      • Careful and close monitoring
      • ? Arterial line
    • Controlled reduction of BP to limit further organ damage
    • Continuous infusion of titratable, short- acting intravenous antihypertensive agent
    • NO PLACE FOR S/L or IM route
    • 10%-15% reduction in DBP or to 110 mm Hg over 1 hour (aortic dissection 10 min)
    • Volume depleted – IV crystalloids
  •  
  • A Precipitous and Uncontrolled Fall in BP Can Have Lethal Consequences Infarct …. brain, heart, kidney Cerebral Blood Flow 60 mm Hg 120 mm Hg 180 mm Hg Mean Arterial Blood Pressure Acute Chronic
  •  
  •  
  • Treatment 2008
  • Pharmacologic Approach to Hypertensive Emergencies JOB, JF ORMC 90
  • Ideal Drug:
    • Treats underlying pathophysiology
    • Rapid onset of action
    • Predictable dose response
    • Minimal dosage adjustments
    • Titratable to desired BP
    • Minimal adverse effects
    • No increase in ICP
    • Easy transition to oral agents for long- term care
    • Cheap
  • Agent Selection for Rx of Hypertensive Emergency
    • Labetalol
    • Esmolol
    • Nicardipine
    • Nitroprusside
    • Fenoldopam
  • Labetalol
    • Combined alpha and beta-blocker (1:7)
    • Onset of action within 2-5 min
    • Peak 5–15 min
    • Duration of action–2-4 h
    • Decreases SVR … but maintains cardiac output and cerebral, renal, and coronary blood flow
    • Safe pregnancy
    • 20 mg boluses (to 80 mg) or continuous infusion starting at 1-2 mg/min
  • Beta-Blocker in Patients With Decreased Cardiac Output Decreased Contractile Force
  • Esmolol
    • Ultra-short-acting (t ½ 8 min)  1 selective antagonist
    • Quick onset of action – 60 s
    • Duration of action 10–20 min
    • Metabolized by red blood cell esterases (not dependent on hepatic or renal function)
    • 0.5-1 mg/kg loading dose, followed by an infusion at 50-300  g/kg/min
  • Sodium Nitroprusside
    • Combined arterial and venous vasodilator
    • cGMP – NO with smooth muscle relaxation
    • Very potent – acts within seconds
    • Plasma t ½ 3-4 min
    • Duration of action 1-2 min
    • Cerebral blood flow decreases
    • Increases ICP
    • CAD – Coronary steal
  • Sodium Nitroprusside Profile
    • Advantages
      • Immediate onset
      • Short duration
      • Potent
    • Disadvantages
      • Toxicity (cyanide poisoning and death)
      • Light sensitive
      • Requires arterial line for monitoring
      • Cerebral blood flow decreases, increases ICP
      • CAD – coronary steal
  • Sodium Nitroprusside Adverse Effects
    • Excessive hypotension
    • Tachyphylaxis
    • Redistribution of flow
      • Intrapulmonary shunting
      • Conorary steal
      • Reduced cerebral and renal blood flow
    • Platelet dysfunction
    • Peroxynitrate generation – lipid peroxidation
    • CYANIDE POISONING
  • Sodium Nitroprusside
    • 4 of the 5 CN – ions are promptly released
    • 44% of fractional weight is cyanide
    2 Na + NO + CN - CN - Fe ++ CN - CN - CN -
  • Metabolism of Sodium Nitroprusside Tinker JH, Michenfelder JD. Anesthesiology . 1976;45:340-354. Inactive Cytochromes CN - TOXICITY Thiocyanate (SCN - ) Thiosulfate Renal Excretion Cytochrome Oxidases Hepatic Rhodanase Nitroprusside Nitroprusside Radical Oxyhemoglobin Methemoglobin Non-enzymatic Cyanmethemoglobin
  • Cyanide Toxicity
    • Hypotension
    • Increased mixed venous saturation
    • Metabolic acidosis
    • Altered mental status
    • Seizures
    • Death (may be very rapid)
  • Monitoring Sodium Nitroprusside Toxicity
    • Metabolic acidosis is late finding (preterminal)
    • Serum thiocyanide levels late and not specific
    • RBC cyanide
      • Levels above 200 nmol/L are associated with significant toxicity
      • Infusion > 4 ug/kg/min for 2-3 h toxic levels
  • NEJM . 1982; 306:1129. Survival Patients Rx with nitroprusside within 9 hours of AMI
  • Nitrovasodilators in Patients With Recent Stroke and Compromised Coronary Blood Flow Coronary Steal Syndrome
  • Nitrovasodilators in Patients With Decreased Cerebral Circulation and Compromised Coronary Blood Flow Decreased Cerebral Blood Flow
  • Nitrovasodilators Dilate Both Arterial and Venous Vessels NITROVASODILATORS - Hypotension - Reflex tachycardia - Exacerbated by volume depletion
  • Fenoldopam HO HO DOPAMINE NH · CH 3 SO 3 H OH HO HO Cl FENOLDOPAM MESYLATE NH 2 Highly selective DA 1 agonist
  • Physiologic Effects of Fenoldopam Systemic Vasodilation Does not cross BBB
    • Coronary Vasodilation without “steal”
    • Reflex tachycardia
    • Metabolized by conjugation
    • No P450 interaction
    •  RBF
    •  Na excretion
    •  H 2 O excretion
    • Maintains GFR during BP lowering
    • Mesenteric vasodilation
    •  Mucosal PO 2
    • (in animals)
  • Fenoldopam
    • Onset of action within 5 min
    • Max response in 15 min
    • Duration of action 30-60 min
    • No rebound once stopped
    • No bolus
    • Continuous infusion starting at 0.1  g/kg/min increased up to 0.3  g/kg/min
  • Fenoldopam Metabolism
    • Metabolism via conjugation
    • Metabolites pharmacologically inactive
    • No cytochrome P450 interactions
    • No known metabolic drug interactions
    • No dose adjustment for renal or hepatic impairment
  • Renal and Hemodynamic Effects of Intravenous Fenoldopam Versus Nitroprusside in Severe Hypertension CrCl ml/Min Circulation . 1990;81:970.
  • Other Agents with Specific Indications
    • Phentolamine
    • Diazoxide
    • Trimethaphan camsylate
    • Enalaprilat
    • Metoprolol
    • Verapamil
    • Diltiazem
  • Recommended Antihypertensive Agents for Hypertensive Emergency Fenoldopam or nicardipine Acute renal failure/ microangiopathic anemia Verapamil, diltiazem, or nicardipine in combination with benzodiazepine Sympathetic crisis/cocaine Labetalol or nicardipine Eclampsia Labetalol or combination of nicardipine or fenoldopam and esmolol or nitroprusside with esmolol/metoprolol Acute aortic dissection Labetalol, nicardipine, or fenoldopam Hypertensive encephalopathy Labetalol or esmolol in combination with nitroglycerin Acute myocardial ischemia Fenoldopam or nitroprusside in combination with nitroglycerin and loop diuretic Acute pulmonary edema Preferred agent(s) Condition
  • Calcium Channel Agents
  • Nicardipine
    • 2nd generation dihydropyridine Ca++ blocker with high vascular selectivity
    • 100 times more water soluble than nifedipine; easily titratable IV formulation
    • Onset within 5-10 min; duration of action 4-6 h
    • Decreases cardiac and cerebral ischemia in hypertensive emergencies
    • No significant rebound once infusion is stopped
    • 5 mg/h up to 30 mg/h
  • Ca2+ inf lux Voltag e- Operated Ca2+ specific Receptor- O perated Ca2+ / Cation Ligand-Operated Ca2+/Cation Plasma membrane channels Ca2+ Mitochondrial Ca Uptake Sarco-/Endo-plasmic reticulum Ca Uptake Ca/Mg pump Na-Ca exchg.
  • Ca2+ I Ca Ca2+ Ca2+ Ca-pump CICR Sarcoplasmic reticulum L-type Channel Myofilament Voltage-operated Ca2+ Channel (VOCC) Electrical Impulse
  • IV Calcium Channel Blockers The relative effects are ranked from no effect (0) to most prominent (+++++). Adapted from Goodman and Gilman, 9th ed. McGraw-Hill;1996 and Massie, Am J Cardiol . 1997;80:231-321. ++++ +++++ ++ +++ Diltiazem 0 + 0 +++++ Nicardipine +++++ +++++ ++++ ++++ Verapamil Suppression of AV Node Suppression of SA Node Suppression of Cardiac Contractility Coronary Vasodilatation Compound
  • Dihydropyridine CCBs Cardene ® IV nicardipine Intravenous preparations 2nd Generation: Procardia ® , Adalat ® Cardene ® Norvasc ® DynaCirc ® Plendil ® Nimotop ® Sular ® nifedipine nicardipine amlodipine isradipine felodipine nimodipine nisoldipine Oral preparations 1st Generation: 2nd Generation: Brand Name Drug
  • “ The Routine Use of Short-acting Nifedipine Capsules in Hypertensive Emergencies Should Be Abandoned” !!!!!
    • May cause severe hypotension, acute MI, stroke and death due to:
      • Uncontrollable decrease in BP
      • Peripheral vasodilation producing steal phenomena
      • Reflex effects, including catecholamine release
      • SL absorption negligible
    1. Grossman E, Messerli FH, Grodzicki T, et al: Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies? JAMA . 1996;276:1328-1331.   In 1985, the Cardiorenal Advisory Committee of FDA concluded that the use of SL nifedipine should be abandoned, because it was neither safe nor efficacious.
  • Cardene ® IV (nicardipine HCl)
    • Arterial vasodilator
    • More selective for vascular smooth muscle than cardiac muscle
    • Produces significant decreases in systemic vascular resistance
    • Only intravenous CCB indicated for treatment of hypertension
    • Not associated with coronary steal
  • Nicardipine vs Nitrovasodilators +++ ++ ++++ Ease of Administration 0 ++++ 0 Cyanide Toxicity +++ ++ + Hypotension ++ ++ + Tachycardia ++++ + +++ Coronary vasodilation 0 + 0 Coronary Steal ++++ ++ 0 Preload Reduction + ++++ ++++ Afterload Reduction ++++ ++++ ++++ Rapid Onset Vasodilator Vasodilator CCB Drug Class Nitrobid IV ® Nipride ® Nitropress ® Cardene ® IV Brand Name Nitroglycerin Nitroprusside Nicardipine
  • Nicardipine vs Adrenergic Blockers +/- Decreased Minimal increase HR Slower Rapid Rapid Offset Positive Positive Positive Myocardial O 2 Balance Labetalol (Normodyne) ® Esmolol (Brevibloc) ® Nicardipine (Cardene ® IV) Bolus Continuous infusion Bolus Continuous infusion Continuous infusion* Administration Rapid Rapid Rapid Onset Decreased 0 Decreased SVR +/- Decreased Increased Cardiac Output Severe bradycardia Heart block >1° Overt heart failure Cardiogenic shock Sinus bradycardia Heart block >1° Overt heart failure Cardiogenic shock Advanced aortic stenosis Contraindications
  • New For 2008 Including work of Dr Eaton at SMH
  • Clevidipine: Metabolized by Plasma and Tissue Esterases
    • Clevidipine is rapidly metabolized by esterases in blood and extravascular tissue to an inactive carboxylic acid metabolite
    *The chiral center of clevidipine. Reproduced from Ericsson H, et al. Eur J Clin Pharmacol . 1999;55:61-67. Bailey JM, et al. Anesthesiology. 2002;96:1086-1094. Ericsson H, et al. Drug Metab Dispos. 1999;27:558-564. Ericsson H et al. Eur J Clin Pharmacol . 1999;55:61-67. Ericsson H, et al. Eur J Pharm Sci. 1999;8:29-37. + O H O H H O Clevidipine Cl O O O O N H Cl O O * Esterases + O O N H Cl O O Cl H Primary metabolite
  • Clevidipine: Ultrashort Half-Life
    • Clinically relevant half-life: approximately 1 minute
    Reproduced from Ericsson H, et al. Anesthesiology . 2000;92:993-1001. Arterial and venous clevidipine blood samples
  • Clevidipine: Linear Pharmacokinetics
    • At steady state, there is a linear relationship between dosage and arterial blood concentrations
    • Linear relationship maintained for dosages as high as 21.9 mcg/kg/min
    *Css = concentration at steady state; median blood concentration of clevidipine obtained during the last 10 minutes of infusion. Reproduced from Ericsson H, et al. Anesthesiology . 2000;92:993-1001. Ericsson H, et al. Anesthesiology . 2000;92:993-1001. Ericsson H, et al. Br J Clin Pharmacol. 1999;47:531-538. 120 100 80 60 40 20 0 0 5 10 15 20 35 Clevidipine Concentration at Css (nmol/L)* Dose Rate (nmol/kg/min) 25 30
  • Clevidipine: Linear Dose Response
            • Linear dose response in postoperative cardiac surgery patients
    • Effective in 95% of patients at ≤3.2 mcg/kg/min
    Responders = treatment success: >10% decrease in MAP or >20% decrease in MAP at each measured concentration. Bailey JM, et al. Anesthesiology. 2002;96:1086-1094. n=19 Infusion Rate (mcg/kg/min) 0 10 20 30 40 50 60 70 80 90 100 0 0.05 0.18 0.32 1.37 3.19 Responders (%) n=0 n=1 n=4 n=6 n=9
  • Postoperative Hypertension
  • Postoperative Hypertension
    • Occurs in up to 1/3 of patients
    • May occur in previously normotensive patients
    • More common after carotid endarterectomy and major abdominal vascular procedures 1
    • Results in higher mortality and unplanned critical care admissions 2
    • Miller: Anesthesia, 5th ed. Churchill Livingstone 2000.
    • Goldman L, Caldera DL. Anesthesiology 1979;50:285-292.
  • Postoperative Hypertension
    • Usually lasts 2-6 hours
    • Requires rapid intervention
    • Systemic vasoconstriction with intravascular hypovolemia
    • Mechanisms related to:
      • Vasoconstriction and tachycardia secondary to increased circulating catecholamines
      • Vasoconstriction secondary to activation of the renin-angiotensisn system
    1. Miller. Anesthesia . 5th ed. Churchill Livingstone; 2000. 2. Goldman L, Caldera DL. Anesthesiology . 1979;50:285-292.
  • Diagnostic Criteria for Postoperative Hypertension
    • If patient is hypertensive pre-op:
    • Post-op HTN  30 mm Hg above pre-op BP value
    • Following noncardiac surgery:
    • Post-op HTN = 190/100 mm Hg
    • Following cardiac surgery:
    • Post-op HTN = 160/100 mm Hg
    Gal TJ, Cooperman LH. Br J Anaesth . 1975;47:70-74. Viljoen JF, Estafanous FG, Tarazi RC. J Thorac Cardiovasc Surg . 1976;71:548-550.
  • Postoperative Hypertension: Goal of Therapy
    • Rapid control of BP
    • Prevention of:
      • Bleeding at suture sites
      • Cerebral vascular accident
      • Elevated left ventricular afterload
      • Myocardial ischemia
    ME Goldberg, GE Larijani. Pharmacotherapy . 1998.
  • Nicardipine vs Nitroprusside for Postoperative HTN
    • Trial Design
    • Multicenter, prospective, randomized, open-label trial
    • N=139 patients with postoperative HTN
    • Cardiac and noncardiac surgery
    • Randomization:
      • Nicardipine (71)
      • Nitroprusside (68)
    Halpern NA, et al. Crit Care Med . 1992.
  • Nicardipine vs Nitroprusside for Postoperative HTN
    • Dosing and Assessments
    • Nicardipine: Initial infusion rate of 10 mg/h is higher than Package Insert recommended rate of 5 mg/h.
    Halpern NA, et al. Crit Care Med . 1992.
  • Nicardipine vs Nitroprusside for Postoperative HTN
    • Efficacy Results
    • Time to BP control: significantly lower for nicardipine pts (14.0  1.0 min) vs nitroprusside pts (30.4  3.5 min) ( P =.0029)
    • Total number of dose changes: significantly less for NC (1.5  0.2) vs NP (5.1  1.4) ( P <.05)
    • HR at therapeutic response was lower in nicardipine-treated cardiac surgical patients
    • Both drugs decreased SVR but not right heart pressures, CI or SV
    Halpern NA, et al. Crit Care Med . 1992.
  • Nicardipine vs Nitroprusside for Postoperative HTN
    • Safety Results
    • Adverse events:
      • Nicardipine patients = 7%
      • Nitroprusside patients = 18%
      • Chest pain, supraventricular tachycardia, sinus tachycardia, hypotension, nausea and vomiting
    Halpern NA, et al. Crit Care Med . 1992.
  • Not for Use in Hypertensive Emergencies
    • S/L nifedipine
    • Nitroglycerin
    • Hydralazine
    • Diuretics
    • ACE Inhibitors
    • Clonidine
  • Nitroglycerin, Hydralazine, ACE, Diuretics
    • Nitroglycerin
      • Potent venodilator
      • Decreases BP by decreasing CO
        • Decreases cardiac, renal, myocardial flow
      • Reflex tachycardia
    • Hydralazine
      • Latency 5-15 min, progressive often precipitous fall in BP that can last 12 h
      • Prolonged and unpredictable effect
    • IV enalaprilat
      • Unpredictable fall in BP
    • Diuretics should be avoided
      • Most patients’ volume depleted
  • JAMA . 1996;276:1328.
  • Nifedipine
    • Not absorbed through buccal mucosa
    • Rapidly absorbed by GI tract if capsule broken
    • A rapid fall in BP 5-10 min
    • Peak effect 30-60 min
    • Sudden precipitous fall in BP
      • CVA, AMI, ARF
    • FDA: caution against use
      • Neither safe nor efficacious
  • Recommended Antihypertensive Agents for Hypertensive Emergency Fenoldopam or nicardipine Acute renal failure/ microangiopathic anemia Verapamil, diltiazem, or nicardipine in combination with benzodiazepine Sympathetic crisis/cocaine Labetalol or nicardipine Eclampsia Labetalol or combination of nicardipine or fenoldopam and esmolol or nitroprusside with esmolol/metoprolol Acute aortic dissection Labetalol, nicardipine, or fenoldopam Hypertensive encephalopathy Labetalol or esmolol in combination with nitroglycerin Acute myocardial ischemia Fenoldopam or nitroprusside in combination with nitroglycerin and loop diuretic Acute pulmonary edema Preferred agent(s) Condition
  •