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

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

3 Hypotension 4 types of shock Hypovolemic - inadequate circulating volume hemorrhage fluid depletion

4 Hypotension 4 types of shock Cardiogenic – inadequate cardiac pump function arrhythmia MI, dilated CM, decreased output from sepsis mechanical – VSD, aortic stenosis

5 Hypotension 4 types of shock Obstructive – extra cardiac obstruction to blood flow pericardial tamponade pulmonary embolism severe pulmonary hypertension

6 Hypotension 4 types of shock Distributive – 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

Pathophysiology

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

Definitions

JNC-VI, 1997 –O–Optimal: <120 / and <80 –N–Normal: <130 / and <85 –H–High-Normal: / or –S–Stage I: / or –S–Stage II: / or –S–Stage III: ≥180 / or ≥110 Definitions

Definitions thankfully simplified JNC-VII, 2003 NORMAL: <120/ and <80 Pre-Hypertension: / or Stage I: / or Stage II: >160 / or ≥

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 > –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 essential –Irreversible end organ damage or death within hours

Approach 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 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 ?

Cerebral Autoregulation Lancet, Hpertensive Emergencies, 2000; 356(9227): Strandgaard, et al. BMJ: 1973

Cerebral Autoregulation Strandgaard, et al. BMJ: 1973 Cerebral blood flow MAP 60 mmHg 160 mmHg 120 mmHg Adapted from: Chest, 2000; 118:

Goals of Treatment Within 1-2 hrs Lower MAP 20-25% –CONTROLLED IV titratable meds Sublingual Nifedipine –Too effective Hydralazine –Not titratable –Eclampsia

Pharmacotherapy

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  1 -blocker –Rapidly metabolized by plasma esterase –Negative chronotropy/inotropy –Kinetics Onset: 1-5 min Duration: min

Pharmacotherapy Labetolol –Selective Post-synaptic  blockade –Non-selective  blockade  :  = 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  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  1 or  1 activation –Increases renal blood flow 10 times more potent renal vasodilator than dopamine –Increases Na excretion –Kinetics Onset: <5 min Peak: 15 min Duration: min

Specific 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 O 2 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  blockade Esmolol, metoprolol Labetolol –Goal: SBP ~100 mmHg Monitor patient closely

Acute Aortic Dissection  -block FIRST!  -block 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 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: / or –Stage II: >160 / or ≥100 –“Higher”: ≥180 / ≥110 The discharged patient Follow-up 2 Months < 1 week 1 Months

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