Nisarg Shah, M.D. May, 2005 Hypotension and Hypertension.
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Transcript of Nisarg Shah, M.D. May, 2005 Hypotension and Hypertension.
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Nisarg Shah, M.D.Nisarg Shah, M.D.
May, 2005May, 2005
Hypotension and
Hypertension
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Hypotension
Inadequacy of tissue oxygen supply versus demand resulting in global tissue hypoperfusion
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Hypotension4 types of
shockHypovolemic - inadequate circulating volume
• hemorrhage
• fluid depletion
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Hypotension4 types of
shockCardiogenic – inadequate cardiac pump function
• arrhythmia
• MI, dilated CM, decreased output from sepsis
• mechanical – VSD, aortic stenosis
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Hypotension4 types of
shockObstructive – extra cardiac obstruction to blood flow
• pericardial tamponade
• pulmonary embolism
• severe pulmonary hypertension
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Hypotension4 types of
shockDistributive – peripheral vasodilation and maldistribution of blood flow
• sepsis
• drug overdose
• anaphylaxis
• neurogenic
• endocrinologic
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Hypotension
Find the type and treat cause
• history – vomiting, bleeding, CP, fever, medication use
• physical – temp, heart rate, skin color, jugular veins, respiratory rate
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Hypertension
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Overview
• History
• Pathophysiology
• Definitions– Hypertension
– Hypertensive Urgency
– Hypertensive Emergency
• Approach to patients– Urgency vs Emergency
• ED Management– Goals of ED treatment – Pharmacotherapy– Specific Treatments– The Discharged Patient
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• 1816– Rene Laennec invents the stethoscope
History• 1628
– William Harvey describes blood circulation• 1733
– Stephen Hales first measures blood pressure
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History• Measuring blood pressure…
– Sphygmograph, 1863
– Sphygmomanometer, 1898
– Karotkoff, 1905
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History• Hypertension…
– Osler, 1912• Simple HTN without disease• Atherosclerosis with associated
hypertension• Chronic nephritis with secondary
hypertension
– Framingham and VA studies, 1970’s– Joint National Committee on
Detection, Evaluation, and Management of High Blood Pressure
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PathophysiologyPathophysiology
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Pathophysiology• Essential Hypertension [~94%]
– Prevalence >50%• Unknown cause
• Secondary Hypertension [~6%]– Prevalence ~6%
• Renal• Endocrine• Miscellaneous
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Pathophysiology• Prevalence increases with
• Age
• Male gender
• Obesity
• African American race
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Pathophysiology
• Interestingly…
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Pathophysiology• The old renin-angiotensin-aldosterone
system...
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Aside• Leading cause of office visits and the leading
use of prescription drugs (aside from vicoden) in the U.S.
• Over 100,000,000 office visits in 1997
• HOWEVER
• - only 2/3 of Americans with HTN are aware of dx
• - almost 75% of known HTNsives are not controlling BP under 140/90
• - only 50% of known HTNsives are taking their meds as prescribed
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DefinitionsDefinitions
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•JNC-VI, 1997–Optimal: <120 / and <80–Normal: <130 / and <85–High-Normal: 130-139 / or 85-89–Stage I: 140-159 / or 90-99–Stage II: 160-179 / or 100-109–Stage III: ≥180 / or ≥110
Definitions
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Definitions thankfully simplified
JNC-VII, 2003JNC-VII, 2003NORMAL: <120/ and <80Pre-Hypertension: 120-139/
or 80-89Stage I: 140-159 / or 90-99Stage II: >160 / or ≥100-109
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Definitions
• Hypertensive Urgency
• Hypertensive Emergency– Accelerated Hypertension– Malignant Hypertension– Accelerated-Malignant Hypertension
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Definitions
• Hypertensive Crisis– Urgency or Emergency
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Hypertensive Urgency
• “Severe elevation of blood pressure”– Generally DBP >115-130– No progressive end organ damage
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Hypertensive Emergency• “Severe elevation of blood
pressure”– Generally occurs with DBP >130– WITH significant or progressive end organ
damage• Hypertensive Encephalopathy• CVA – Ischemic versus hemorrhagic• Acute Aortic Dissection• Acute LVF with Pulmonary Edema• Acute MI / Unstable Angina• Acute Renal Failure• Eclampsia
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Urgency vs. Emergency• Urgency
– No need to acutely lower blood pressure
– May be harmful to rapidly lower blood pressure
– Death not imminent
• Emergency– Immediate control of BP essentialImmediate control of BP essential– Irreversible end organ damage or Irreversible end organ damage or
death within hoursdeath within hours
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Approach to PatientsApproach to Patients
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Approach to patients• Recheck blood pressure!
– Appropriate size cuff.– Cuff not over clothing– Check in all limbs
• History– Prior crises– Renal disease– Medications
• Compliance• MAO inhibitors• Recreational drugs
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Approach to patients
• Physical Exam– What do you see?– Signs of end organ damage?
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End organ damage
• Neuro• Cardiac• Renal
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Neuro• Hypertensive encephalopathy
– Severe Headache– AMS– Nausea/Vomiting– Papilledema– Visual Changes– Seizures
• Focal Neurological Deficits– Ischemic vs hemorrhagic CVA
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Fundoscopy
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Fundoscopy/ Neuro
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Fundoscopy/ Vascular
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Fundoscopy/ Vascular
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Cardiac• Cardiac ischemia
– Chest pain– EKG for ischemic changes
• Acute left ventricular failure– Pulmonary edema
• Rales
– Hypoxia• SpO2
– EKG for left ventricular strain pattern• Aortic regurge murmur
– CXR?
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Renal• Electrolytes• BUN/Cr
– Chronic failure/insufficiency vs acute failure
– Cause vs effect
• UA with micro– Protein– Blood– Casts
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Goals of TreatmentGoals of Treatment
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Goals of Treatment• Prevent end organ damage
– NOT normalize BP• Exceptions??
• IV fluids– Forced natriuresis– Saline may help blunt renin-
angiotensin response
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Goals of Treatment• Harington, et al, BMJ: 1959
– 94 cases over 7 years– Immediate normalization of BP
• 12 not included in study• 30 / 82 with significant neurologic
sequelae
• Ledingham, et al, QJM: 1979– Case series of 10 patients
• All with papilledema• All with neurologic sequelae
– 3 deaths during treatment
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Goals of Treatment
WHY ?WHY ?
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Cerebral Autoregulation
Lancet, Hpertensive Emergencies, 2000; 356(9227):411-417
• Strandgaard, et al. BMJ: 1973
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Cerebral Autoregulation• Strandgaard, et al. BMJ: 1973
Cer
ebra
l blo
od f
low
MAP
60mmHg
160mmHg
120mmHg
Adapted from: Chest, 2000; 118:214-227
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Goals of Treatment• Within 1-2 hrs • Lower MAP 20-25%
– CONTROLLED• IV titratable meds
• Sublingual Nifedipine– Too effective
• Hydralazine– Not titratable– Eclampsia
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PharmacotherapyPharmacotherapy
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Pharmacotherapy• Nitroprusside
– Arterial & venous dilator• Decreases afterload and preload
– No direct negative inotropy or chronotropy
– Kinetics• Onset: seconds• Duration: 1-2 min• 1/2 life: 3-4 min
– Increased ICP (?)– Toxic metabolites
• Takes days to accumulate
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Pharmacotherapy• Nitroglycerine
– Weak anti-hypertensive– Vasodilator
• At high doses dilates arteriolar smooth muscle
• Better dilation of coronary conductance arteries
– Kinetics• Onset: 1-2 min• Duration: 3-4 min
– Tolerance– Headache, Tachycardia, Nausea,
Vomiting, Hypotension
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Pharmacotherapy• Enalaprilat
– IV ACE inhibitor– Improves cardiac index and stroke
volume without affecting HR– Degree BP reduction associated with
pretreatment plasma renin activity– Kinetics
• Onset: 15 min• Duration: 6 hours
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Pharmacotherapy• Esmolol
– Ultra-short acting
– Cardioselective β1-blocker
– Rapidly metabolized by plasma esterase
– Negative chronotropy/inotropy– Kinetics
• Onset: 1-5 min• Duration: 10-20 min
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Pharmacotherapy• Labetolol
– Selective Post-synaptic α blockade– Non-selective β blockade
•α: β = 1:7
– Maintains cardiac output– Decreased PVR without reflex tachycardia
• Maintains cerebral, renal & coronary blood flow
• Kinetics• Onset: 2-5 min• Peak: 5-15 min• Duration: 4-8 hrs
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Pharmacotherapy• Nicardipine
– Dihydropyridine Ca++ channel blocker– Decreases afterload
• Maintains cardiac output• No reflex tachycardia
– Kinetics• Onset: 5-15 min• Duration: 4-6 hrs
– May increase ICP
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Pharmacotherapy• Phentolamine
– Non-selective α blockade– Reflex tachycardia– Kinetics
• Onset: 1-2 min• Duration: up to 15 min
– May induce angina or MI• Use mainly limited to catecholamine induced
hypertension
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Pharmacotherapy• Fenoldopam
– Dopamine DA-1 agonist• No α1 or β1 activation
– Increases renal blood flow• 10 times more potent renal vasodilator than
dopamine
– Increases Na excretion– Kinetics
• Onset: <5 min• Peak: 15 min • Duration: 30-60 min
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Specific TreatmentSpecific Treatment
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Hypertensive Encephalopathy
• Nitroprusside• Fenoldopam
• Nicardipine• Labetolol
–Symptoms of encephalopathy should improve with treatment
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CVA• Nicardipine• Labetolol• Fenoldopam
– Decrease DBP no more than 20% in 24hrs
– Nitroprusside increases ICP• Commonly used• NOT recommended
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Cardiac Ischemia• Nitroglycerine• Nitroprusside
• Fenoldopam
–Nifedipine• Reflex tachy
• Increases myocardial O2 demand
• May aggravate ischemia
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Acute LVF• Nitroprusside
– Afterload reduction• Fenoldopam
• Nitroglycerine– If ischemia is suspected
• Furosemide– Loop diuretic
• Opioids
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Acute Aortic Dissection• Nitroprusside
• Nicardipine, Fenoldopam
–Afterload reduction– Increases ventricular contraction
velocity–Requires β blockade• Esmolol, metoprolol
• Labetolol
–Goal: SBP ~100 mmHg• Monitor patient closely
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Acute Aortic Dissection
•ββ-block -block FIRST!FIRST!
– Esmolol– Metoprolol
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Sympathetic Crisis• Nicardipine• Nitroprusside• Phentolamine
– Cocaine / Amphetamines / PCP– Pheochromocytoma– MAOI with TCA’s or tyramine containing foods– Spinal cord syndromes
–Labetolol• Increases seizures in animal models• Does not alleviate cocaine induced
coronary vasospasm
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Acute Renal Failure• Nicardipine• Nitroprusside
– “Use with caution” • toxic metabolites...
– Thiocyanate excreted via kidneys
– Fenoldopam
• Labetolol
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Eclampsia• Hydralazine
– Used historically– Arterial vasodilator– Maintains placental blood flow
• Nicardipine• Labetolol
– Magnesium
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The Discharged PatientThe Discharged Patient
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The discharged patient• JNC-VII Recommendations
– Stage 1• Thiazide diuretic
– Consider: ACEI, ARB, BB, CCB
– Stage 2• Combination tx
– Thiazide + ACEI, ARB, BB, CCB
– “Compelling Indications”...
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• URGENCY: – ALL PATIENTS WITH HTN URGENCY BEING
DISCHARGED HOME SHOULD BE PLACED ON COMBINATION THERAPY AND HAVE RAPID FOLLOW UP.
– THIAZIDE– ACEI / ARB / BB / CCB
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• CHF: – Asymptomatic with ventricular dysfunction
» ACE / BB– Symptomatic ventricular dysfunction / end-
stage dz» ACEI / BB / ARB with loop diuretic
– Regression of LVH with aggressive management
» Not seen with direct vasodilators» Hydralazine / minoxidil
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• STABLE ANGINA– BB / (CCB)
• ACS (USA/AMI)– BB / ACEI
• POST-MI: – ACEI / BB / AA
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• DIABETES– COMBINATION THERAPY
» THIAZIDE
» ACEI / ARB» slow progression of nephropathy» reduce albuminuria» ARB’s reduce progression» BB / CCB (and above)» reduce CVD & stroke
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• CHRONIC KIDNEY DZ– ACE / ARB
» 35% rise in Creatinine is acceptable» withhold if hyperkalemia
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• CEREBROVASCULAR DZ– COMBINATION THERAPY
» ACEI & THIAZIDE DIURETIC» Reduces risk of recurrent stroke
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The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• AFRICAN AMERICANS– Monotherapy
» CCB / Diuretic– Reduced response to monotherapy
» BB / ACEI / ARB» Eliminated when combined with diuretic
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• Follow up...
– Stage I:• 140-159 / or 90-99
– Stage II:• >160 / or ≥100
– “Higher”:• ≥180 / ≥110
The discharged patient
Follow-up2 Months
< 1 week
1 Months
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Questions...
• Comments…