Nisarg Shah, M.D. May, 2005 Hypotension and Hypertension.

transcript

Nisarg Shah, M.D.Nisarg Shah, M.D.

May, 2005May, 2005

Hypotension and

Hypertension

Hypotension

Inadequacy of tissue oxygen supply versus demand resulting in global tissue hypoperfusion

Hypotension4 types of

shockHypovolemic - inadequate circulating volume

• hemorrhage

• fluid depletion

shockCardiogenic – inadequate cardiac pump function

• arrhythmia

• MI, dilated CM, decreased output from sepsis

• mechanical – VSD, aortic stenosis

shockObstructive – extra cardiac obstruction to blood flow

• pericardial tamponade

• pulmonary embolism

• severe pulmonary hypertension

shockDistributive – peripheral vasodilation and maldistribution of blood flow

• sepsis

• drug overdose

• anaphylaxis

• neurogenic

• endocrinologic

Hypotension

Find the type and treat cause

• history – vomiting, bleeding, CP, fever, medication use

• physical – temp, heart rate, skin color, jugular veins, respiratory rate

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

Pathophysiology• Prevalence increases with

• Age

• Male gender

• Obesity

• African American race

Pathophysiology

• Interestingly…

Pathophysiology• The old renin-angiotensin-aldosterone

system...

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

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

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

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”...

– “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

• 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

• STABLE ANGINA– BB / (CCB)

• ACS (USA/AMI)– BB / ACEI

• POST-MI: – ACEI / BB / AA

• DIABETES– COMBINATION THERAPY

» THIAZIDE

» ACEI / ARB» slow progression of nephropathy» reduce albuminuria» ARB’s reduce progression» BB / CCB (and above)» reduce CVD & stroke

• CHRONIC KIDNEY DZ– ACE / ARB

» 35% rise in Creatinine is acceptable» withhold if hyperkalemia

• CEREBROVASCULAR DZ– COMBINATION THERAPY

» ACEI & THIAZIDE DIURETIC» Reduces risk of recurrent stroke

• 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

Questions...

• Comments…

Nisarg Shah, M.D. May, 2005 Hypotension and Hypertension.

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