Nisarg Shah, M.D.Nisarg Shah, M.D.
May, 2005May, 2005
Hypotension and
Hypertension
2
Hypotension
Inadequacy of tissue oxygen supply versus demand resulting in global tissue hypoperfusion
3
Hypotension4 types of
shockHypovolemic - inadequate circulating volume
• hemorrhage
• fluid depletion
4
Hypotension4 types of
shockCardiogenic – inadequate cardiac pump function
• arrhythmia
• MI, dilated CM, decreased output from sepsis
• mechanical – VSD, aortic stenosis
5
Hypotension4 types of
shockObstructive – extra cardiac obstruction to blood flow
• pericardial tamponade
• pulmonary embolism
• severe pulmonary hypertension
6
Hypotension4 types of
shockDistributive – peripheral vasodilation and maldistribution of blood flow
• sepsis
• drug overdose
• anaphylaxis
• neurogenic
• endocrinologic
7
Hypotension
Find the type and treat cause
• history – vomiting, bleeding, CP, fever, medication use
• physical – temp, heart rate, skin color, jugular veins, respiratory rate
8
Hypertension
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
• 1816– Rene Laennec invents the stethoscope
History• 1628
– William Harvey describes blood circulation• 1733
– Stephen Hales first measures blood pressure
History• Measuring blood pressure…
– Sphygmograph, 1863
– Sphygmomanometer, 1898
– Karotkoff, 1905
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
PathophysiologyPathophysiology
Pathophysiology• Essential Hypertension [~94%]
– Prevalence >50%• Unknown cause
• Secondary Hypertension [~6%]– Prevalence ~6%
• Renal• Endocrine• Miscellaneous
15
Pathophysiology• Prevalence increases with
• Age
• Male gender
• Obesity
• African American race
16
Pathophysiology
• Interestingly…
Pathophysiology• The old renin-angiotensin-aldosterone
system...
18
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
DefinitionsDefinitions
•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
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
Definitions
• Hypertensive Urgency
• Hypertensive Emergency– Accelerated Hypertension– Malignant Hypertension– Accelerated-Malignant Hypertension
Definitions
• Hypertensive Crisis– Urgency or Emergency
Hypertensive Urgency
• “Severe elevation of blood pressure”– Generally DBP >115-130– No progressive end organ damage
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
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
Approach to PatientsApproach to Patients
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
Approach to patients
• Physical Exam– What do you see?– Signs of end organ damage?
End organ damage
• Neuro• Cardiac• Renal
Neuro• Hypertensive encephalopathy
– Severe Headache– AMS– Nausea/Vomiting– Papilledema– Visual Changes– Seizures
• Focal Neurological Deficits– Ischemic vs hemorrhagic CVA
Fundoscopy
Fundoscopy/ Neuro
Fundoscopy/ Vascular
Fundoscopy/ Vascular
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?
Renal• Electrolytes• BUN/Cr
– Chronic failure/insufficiency vs acute failure
– Cause vs effect
• UA with micro– Protein– Blood– Casts
Goals of TreatmentGoals of Treatment
Goals of Treatment• Prevent end organ damage
– NOT normalize BP• Exceptions??
• IV fluids– Forced natriuresis– Saline may help blunt renin-
angiotensin response
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
Goals of Treatment
WHY ?WHY ?
Cerebral Autoregulation
Lancet, Hpertensive Emergencies, 2000; 356(9227):411-417
• Strandgaard, et al. BMJ: 1973
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
Goals of Treatment• Within 1-2 hrs • Lower MAP 20-25%
– CONTROLLED• IV titratable meds
• Sublingual Nifedipine– Too effective
• Hydralazine– Not titratable– Eclampsia
PharmacotherapyPharmacotherapy
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
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
48
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
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
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
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
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
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
Specific TreatmentSpecific Treatment
Hypertensive Encephalopathy
• Nitroprusside• Fenoldopam
• Nicardipine• Labetolol
–Symptoms of encephalopathy should improve with treatment
CVA• Nicardipine• Labetolol• Fenoldopam
– Decrease DBP no more than 20% in 24hrs
– Nitroprusside increases ICP• Commonly used• NOT recommended
Cardiac Ischemia• Nitroglycerine• Nitroprusside
• Fenoldopam
–Nifedipine• Reflex tachy
• Increases myocardial O2 demand
• May aggravate ischemia
Acute LVF• Nitroprusside
– Afterload reduction• Fenoldopam
• Nitroglycerine– If ischemia is suspected
• Furosemide– Loop diuretic
• Opioids
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
Acute Aortic Dissection
•ββ-block -block FIRST!FIRST!
– Esmolol– Metoprolol
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
Acute Renal Failure• Nicardipine• Nitroprusside
– “Use with caution” • toxic metabolites...
– Thiocyanate excreted via kidneys
– Fenoldopam
• Labetolol
Eclampsia• Hydralazine
– Used historically– Arterial vasodilator– Maintains placental blood flow
• Nicardipine• Labetolol
– Magnesium
The Discharged PatientThe Discharged Patient
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”...
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
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
The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• STABLE ANGINA– BB / (CCB)
• ACS (USA/AMI)– BB / ACEI
• POST-MI: – ACEI / BB / AA
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
The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• CHRONIC KIDNEY DZ– ACE / ARB
» 35% rise in Creatinine is acceptable» withhold if hyperkalemia
The discharged patient• JNC-VII Recommendations
– “Compelling Indications”
• CEREBROVASCULAR DZ– COMBINATION THERAPY
» ACEI & THIAZIDE DIURETIC» Reduces risk of recurrent stroke
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
• 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
74
Questions...
• Comments…
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