Download ACUTE DECOMPENSATED HEART FAILURE

Document related concepts

Remote ischemic conditioning wikipedia , lookup

Electrocardiography wikipedia , lookup

Coronary artery disease wikipedia , lookup

Cardiac surgery wikipedia , lookup

Heart failure wikipedia , lookup

Myocardial infarction wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Transcript
ACUTE DECOMPENSATED HEART
FAILURE : 2010 HFSA GUIDELINES
BART COX, M.D., FACC
ASSOCIATE PROFESSOR OF MEDICINE
UNIVERSITY OF NEW MEXICO SCHOOL OF MEDICINE
DIRECTOR, ADVANCED HEART FAILURE PROGRAM
DISCLOSURES
NONE
OBJECTIVES
• UNDERSTAND THE DEFINITION OF ADHF
• UNDERSTAND THE 4 HEMODYNAMIC
PROFILES AND HOW TO CORRELATE THERAPY
TO EACH PROFILE
• UNDERSTAND METHODS OF DECONGESTION
• UNDERSTAND THE USE OF IV VASODILATORS
2010 HEART FAILURE SOCIETY OF
AMERICA GUIDELINES
• JOURNAL OF CARDIAC FAILURE 2010; 16:475539 (EXECUTIVE SUMMARY)
• JOURNAL OF CARDIAC FAILURE 2010; 16: e1e194 (COMPLETE GUIDELINE)
ACUTE DECOMPENSATED HEART
FAILURE (ADHF): DEFINITION
• JACOBELLIS V. OHIO (1964) AND SUPREME
COURT JUSTICE POTTER STEWART
• NEW ONSET OR GRADUAL OR RAPIDLY
WORSENING HEART FAILURE SIGNS OR
SYMPTOMS REQUIRING URGENT THERAPY.
HEART FAILURE STATISTICS
• >5.5 MILLION HF PATIENTS IN USA
• >650,000 NEW HF CASES ANNUALLY
• ANNUAL US COST OF HF IN 2010 (DIRECT AND
INDIRECT): $39.2 BILLION
• 1 YEAR MORTALITY IS 20%
• 5 YEAR MOTALITY IS HIGH AND WORSE FOR
MALES
– MALES: 59%
– FEMALE: 45%
ADHF STATISTICS
• 1 MILLION ADHF HOSPTIAL ADMISSIONS
ANNUALLY
• ANOTHER 2 MILLION ANNUAL ADMISSIONS IN
WHICH HF COMPLICATED THE PRIMARY
DIAGNOSIS
• 30-50% OF PATIENTS DISCHARGED WITH ADHF
WILL BE READMITTED WITHIN 3-6 MONTHS
ADHF STATISTICS
• 50% OF ADHF ADMISSIONS HAVE LVEF > 40%
• 50% OF ADHF ADMISSIONS HAVE LVEF < 40%
• AVERAGE PATIENT ADMITTED WITH ADHF IS
75 YEARS OF AGE WITH SUBSTANTIAL
COMORBIDITIES
• MOST COMMON CAUSE OF ADHF
HOSPITALIZATION IS EXACERBATION OF
CHRONIC HEART FAILURE
• IN HOSPITAL MORTALITY: 4%
6 SLIDES OF BAD MEMORIES
INTRODUCTION TO FILLING
PRESSURES
• VENTRICULAR FILLING PRESSURE: THE
PRESSURE IN THE VENTRICLE AT THE END OF
DIASTOLE
• LEFT VENTRICULAR FILLING PRESSURE =
PCWP, MEAN LA PRESSURE, LVEDP
• RIGHT VENTRICULAR FILLING PRESSURE= CVP,
MEAN RA PRESSURE, RVEDP
INTRODUCTION TO FILLING
PRESSURES
• CONGESTION= SALT AND WATER RETENTION;
FLUID OVERLOAD;
• TO RELIEVE CONGESTION IN ADHF PATIENTS,
DECREASE FILLING PRESSURES
• TO DECREASE FILLING PRESSURES, DIURESE
(OR ULTRAFILTRATE) AND VASODILATE
FILLING PRESSURE IS THE PRESSURE AT
THE END OF DIASTOLE
INTRODUCTION TO PERFUSION IN
ADHF
• IN ADHF, PERFUSION IS A FUNCTION OF CARDIAC
OUTPUT
• CARDIAC OUTPUT= HR X STROKE VOLUME (SV)
• STROKE VOLUME IS DEPENDENT UPON:
– PRELOAD: THE AMOUNT OF BLOOD IN THE VENTRICLE
AT THE END OF DIASTOLE
– CONTRACTILITY OF THE VENTRICLE
– AFTERLOAD: RESISTANCE TO VENTRICULAR EMPTYING
INTRODUCTION TO PERFUSION IN
ADHF
• TO IMPROVE CARDIAC OUTPUT:
– OPTIMIZE RATE AND RHYTHM (ELIMINATE
BRADYCARDIA, TACHYCARDIA, AV DISSOCIATION)
– OPTIMIZE PRELOAD (VENTRICLE NEITHER TOO
FULL NOR TOO EMPTY)
– IMPROVE CONTRACTILITY
– DECREASE AFTERLOAD (DILATE RESISTANCE
VESSELS)
INTRODUCTION TO PERFUSION IIN
ADHF
• CARDIAC INDEX = CARDIAC OUPUT / BSA
• TO IMPROVE PERFUSION, IMPROVE CARDIAC
OUTPUT (OR INDEX)
THE FOUR HEMODYNAMIC PROFILES
RECOGNIZING THE FOUR
HEMODYNAMIC PROFILES
•
•
•
•
NO CONGESTION = DRY
CONGESTION= WET
NORMAL PERFUSION=WARM
DIMINISHED PERFUSION=COLD
PROFILES AND HEMODYNAMICS
•
•
•
•
DRY=
WET =
WARM=
COLD=
PCWP < 18 AND RA PRESSURE < 8
PCWP > 18 OR RA PRESSURE > 8
CARDIAC INDEX> 2.2
CARDIAC INDEX < 2.2
RECOGNIZING THE FOUR
HEMODYNAMIC PROFILES
• 2 COMPONENTS OF DECOMPENSATED HEART
FAILURE
– ELEVATED FILLING PRESSURES (MOST COMMON)
– REDUCED CARDIAC INDEX (RARE)
2 MINUTE ASSESSMENT AND THE 4
HEMODYNAMIC PROFILES
PRINCIPLES OF THERAPY IN A
CONGESTED PATIENT: DECREASE THE
FILLING PRESSURES
• RELIEVE CONGESTION BY REDUCING FILLING
PRESSURES
• ABSENT CRITICAL ORGAN HYPOPERFUSION
THAT LIMITS REDUCING THE FILLNG
PRESURES, IMPROVING CARDIAC INDEX DOES
NOT WORK!!!!
PRINCIPLES OF THERAPY: THE
OPTIMAL FILLING PRESSURE
• OPTIMAL PCWP IS < 15-16 mm Hg; RA <8
– LOWERING FILLNG PRESSURES -> IMPROVED SV
• WHAT’S WRONG WITH ELEVATED
FILLNGPRESSURES?
–
–
–
–
–
–
RESPONSIBLE FOR CONGESTIVE SYMPTOMS
ACTIVATE NEUROHORMONES (RAS, SNS)
INCREASE VALVULAR REGURGITATION
RESPONSIBLE FOR PULMONARY HTN
CAUSES RIGHT VENTRICULAR DYSFUNCTION
CAUSES ABNORMAL LV FILLNG PATTERNS
FILLING PRESSURES AND STROKE
VOLUME (SV)
STROKE VOLUME IMPROVED BY
DECREASING MITRAL REGURGITATION
Warm and dry
Warm and wet
PROFILE B: WET AND WARM
• MOST PATIENTS PRESENTING WITH ADHF ARE
PROFILE B
• GOAL OF TX: SX IMPROVEMENT BY
REDUCTION OF FILLING PRESSURES
• FOR MAJORITY, IV DIURETIC TX IS THE MAIN
INTERVENTION
– MAY NEED TO ADD 2.5-10 mg METOLAZONE PO
OR CHLORTHIAZIDE 500-1000 mg IV
PROFILE B: ROLE FOR ADJUNCTIVE
AGENTS
• USE OF ADJUNCTIVE THERAPIES BEYOND
DIURETICS HAS NOT BEEN DEMONSTRATED
TO IMPROVE OUTCOMES IN HOSPITALIZED
ADHF PATIENTS WITH PROFILE B
– INOTROPES: ISCHEMIA/ARRHYTHMIAS/ DEATH
– NESIRITIDE: EXPENSIVE PLACEBO
– ENDOTHELIN ANTAGONIST: NO IMPROVEMENT
– VASOPRESSIN ANTAGONIST: NO SUSTAINED
BENEFIT
PROFILE B: VERY HIGH OR VERY LOW
SYSTEMIC VASCULAR RESISTANCE
(SVR)
• VERY HIGH SVR= > 1500 dyne/sec/cm-5
• HOW TO RECOGNIZE HIGH SVR:
– HIGH BP
– VERY NARROW PULSE PRESSURE
– PA CATHETER MEASUREMENT
• VERY LOW SVR (WITHOUT MEDS)= LOW BP +
REASONABLE PULSE PRESSURE + WARM
EXTREMITIES
PROFILE C: COLD AND WET
PROFILE C: COLD AND WET
• < 3% OF PATIENTS PRESENT WITH CARDIOGENIC
SHOCK
• WET = CONGESTION (PCWP>18)
• COLD = INADEQUATE PERFUSION (CI<2.2)
• TX: YOU MAY NEED TO WARM THEM UP BEFORE
DRYING THEM OUT
– DIURESIS WILL IMPROVE CARDIAC OUTPUT
– DIURESIS MAY NOT BE POSSIBLE IF RENAL PERFUSION
IS SEVERELY IMPAIRED
– WHAT TO USE: VASODILATOR OR INOTROPE?
• CHECK THE SVR AND LOOK AT THE BLOOD PRESSURE
PROFILE C: IV VASODILATORS OR
INOTROPES?
• CHOICE OF THERAPY DEPENDS ON SYSTEMIC
VASCULAR RESISTANCE AND BP
• IF SVR IS HIGH, CHECK THE SBP
– SBP>85mm Hg: VASODILATOR
– SBP<85 mm Hg: INOTROPE + IABP (INTRAORTIC
BALLOON PUMP)
PROFILE L: COLD AND DRY
PROFILE L: COLD AND DRY
• EXTREMELY RARE PRESENTATION
• REQUIRES PA CATHETER PLACEMENT TO
EVALUATE FILLING PRESSURE
– PCWP<12 AND RA<6: DC DIURETICS, PO FLUIDS
– PCWP >16: PROFILE C
– PCWP 12-16 + RA PRESSURE NORMAL:
• VASODILATORS , IABP, AND INOTROPE ARE
TEMPORARY FIX
• NEEDS VAD/ TRANSPLANT EVALUATION
DIURETICS
HFSA GUIDELINE: HOW TO DIURESE
• DIURESE WITH IV LOOP DIURETIC
• ULTRAFILTRATION MY BE USED IN LIEU OF IV
DIURETICS
• DIURESE UNTIL DRY
• DIURESE AT THE CORRECT RATE
THE DOSE TRIAL: BOLUS OR
INFUSION, LOW DOSE OR HIGH
DOSE?
Kaplan–Meier Curves for the Clinical Composite End Point of Death, Rehospitalization, or
Emergency Department Visit .
Felker GM et al. N Engl J Med 2011;364:797-805
HFSA GUIDELINES: WHAT TO
MONITOR DAILY DURING IV DIURESIS
• MONITORING OF INTAKE & OUTPUT AND DAILY
WEIGHT IS RECOMMENDED TO ASSESS CLINICAL
EFFICACY OF DIURETIC THERAPY
– ROUTINE USE OF A FOLEY CATHETER IS NOT
RECOMMENDED FOR MONITORING VOLUME STATUS
• OBSERVE FOR DEVELOPMENT OF DIURETICINDUCED SIDE EFFECTS
• DAILY Na, K, Mg, RENAL FUNCTION, AND
ORTHOSTATIC VITALS
HEISENBERG’S UNCERTAINTY
PRINCIPLE
• REGARDING SUBATOMIC PARTICLES, YOU MAY
KNOW THE EXACT POSITION OR THE EXACT
VELOCITY BUT YOU CAN NEVER KNOW
SIMULTANEOUSLY THE EXACT
POSITION AND THE EXACT VELOCITY
COX’S UNCERTAINTY PRINCIPLE
• YOU MAY HAVE AN ACCURATE DAILY WEIGHT,
OR YOU CAN HAVE AN ACCURATE DAILY
INTAKE AND OUTPUT, BUT YOU WILL NEVER
SIMULTANEOUSLY HAVE AN
ACCURATE INTAKE AND OUTPUT AND WEIGHT
DIURETIC SIDE EFFECTS
• ELECTROLYTE ABNORMALITEIS
– HYPOKALEMIA
– HYPOMAGNESEMIA
– HYPONATREMIA
•
•
•
•
•
•
HYPOTENSION
GOUT EXACERBATION
HEARING LOSS (RARE)
INCREASED INCIDENCE OF DIGOXIN TOXICITY
RENAL INSUFFICIENCY
MUSCLE CRAMPS ARE USUALLY DUE TO OVERLY RAPID
DIURESIS
HFSA GUIDELINES: VOLUME
OVERLOAD, RENAL DYSFUNCTION,
AND DIURETIC USE
• PATIENTS WITH MODERATE – SEVERE RENAL
DYSFUNCTION AND EVIDENCE OF FLUID
RETENTION SHOULD CONTINUE TO BE
TREATED WITH DIURETICS
CARDIORENAL SYNDROME: OUTDATED
AND INCOMPLETE EXPLANATION
CARDIORENAL SYNDROME: THE
CURRENT EXPLANATION
HFSA GUIDELINES: DESTROYING
DIURETIC RESISTANCE
•
•
•
•
•
DIAGNOSE IT: ARE THEY TRULY WET?
DECREASE THE Na AND FLUID INTAKE
DOSE IT: INCREASE DOSE OF DIURETIC
DRIP IT: FUROSEMIDE DRIP AT 5-20 mg/hr
DOUBLE THE SITE OF ACTION : ADD 5-10 mg
po METOLAZONE OR IV CHLORTHIAZIDE 5001000 mg
• DEVICE IT: AQUAPHERESIS/ ULTRAFILTRATION
THE DIET AND FLUID RESTRICTION
• 2 GRAM SODIUM DIET
• 2 LITER/DAY FLUID RESTRICTON
WHAT ABOUT HYPONATREMIA
• SODIUM < 137 mEq/L ASSOCIATED WITH
PROLONGED HOSPITALIZATION AND
INCREASED IN-HOSPITAL MORTALITY
– IN GENERAL, HYPONATREMIA IS ASSOICIATED
WITH DEATH, HIGH REHOSPITALIZATION, LONGER
HOSPITAL STAYS, NEUROCOGNITIVE CHANGES,
AND RENAL/HEPATIC DYSFUNCTION
• MOST HYPONATREMIC PATEIENTS WITH ADHF
ARE VOLUME OVERLOADED
WHAT ABOUT HYPONATREMIA?
• ETIOLOGY: INABILITY TO EXCRETE FREE H20
PRIMARILY DUE TO NEUROHORMONAL
ACTIVATION
– NOREPI, ANGIOTENSIN II, AVP
• HYPONATREMIA IS A MARKER FOR POOR
CARDIAC OUTPUT AND NEUROHORMONAL
ACTIVATION
TREATING HYPONATREMIA IN ADHF
• WATER RESTRICTION< 2 L/DAY
• MAXIMIZE ACEI OR ARB
• VASOPRESSIN ANTAGONIST (TOLVAPTAN)
RESERVED FOR ADHF WITH HYPONATREMIA
CAUSING SIGNIFICANT COGNITIVE
SYMPTOMS
VASODILATORS
IV VASODILATORS USED IN ADHF
• NITROGLYCERIN
• NITROPRUSSIDE
WHAT HAPPENED TO NESIRITDE?
IV VASODILATORS: NESERITIDE AND
THE ASCEND TRIAL
HFSA GUIDELINES: TREATING ADHF
PATIENTS WITH ACUTE PULMONARY
EDEMA OR SEVERE HYPERTENSION
• IV NITROGLYCERIN OR NITROPRUSSIDE ARE
RECOMMENDED FOR RAPID SYMPTOM RELIEF
IN PATIENTS WITH ACUTE PULMONARY
EDEMA OR SEVERE HYPERTENSION
HF GUIDELINES: USING IV
VASODILATORS IN ADHF
• IN THE ABSENCE OF SYMPTOMATIC
HYPOTENSION, IV NITROGLYCERIN OR
NITROPRUSSIDE MAY BE CONSIDERED AS AN
ADDITION TO DIURETIC THERAPY FOR RAPID
IMPROVEMENT OF CONGESTIVE SYMPTOMS
IN PATIENTS ADMITTTED WITH ADHF
HFSA GUIDELINES: OTHER USES OF IV
VASODILATORS
• IV NITROGLYCERIN OR NITROPRUSSIDE MAY
BE CONSIDERED IN PATIENTS WITH ADHF
WHO HAVE PERSISTENT SEVERE HF DESPITE
AGGRESSIVE TREATMENT WITH DIURETICS
AND STANDARD ORAL THERAPIES
IV NITROGLYCERIN
• HEMODYNAMIC EFFECTS
– VENODILATOR; ARTERIAL VASODILATOR AT HIGH DOSES
– DECREASES FILLING PRESSURE AT LOW DOSE; AT HIGH
DOSES, DECREASES SVR AND INCREASES CARDIAC
OUTPUT
– INCREASED CORONARY BLOOD FLOW
• DOSE RANGE
–
–
–
–
INITIAL DOSE 20 mcg/min
INCREASE DOSE 20 mcg/min q 20 MINUTES
EFFECTIVE DOSE RANGE 40-400 mcg/min
KEEP SBP> 80, DECREASE SVR<1200, REDUCE PCWP < 16
IV NITROGLYCERIN
• MAJOR LIMITATIONS
– HEADACHE
– HYPOTENSION (ESPECIALLY IF FILLNG PRESSURES
ARE LOW)
– PROLONGED PROFOUND HYPOTENSION AND
BRADYCARDIA (RARE)
– TACHYPHYLAXIS
– 20% ARE NONRESPONDERS
NITROPRUSSIDE
• HEMODYNAMIC EFFECTS
– BALANCED VASODILATOR (BOTH VEINS AND
ARTERIOLES)
– DECREASES FILLING PRESSURES, SVR, PVR, AND
INCREASES CI
• DOSE RANGE
–
–
–
–
INITIAL DOSE: 10 mcg/min
INCREASE DOSE 10-20 mcg/min q 10-20 MINUTES
EFFECTIVE DOSE RANGE: 30-350 mcg/min
KEEP SBP > 80 mm Hg, DECREASE SVR <1200, REDUCE
PCWP < 16
NITROPRUSSIDE
• MAJOR LIMITATIONS
– CYANIDE TOXICITY
• MANIFESTED BY NAUSEA AND “FEELING WEIRD”
• MOST LIKELY TO DEVELOP WITH DOSE > 250 mcg/min x
>2 days
• OCCURS IN SETTING OF LOW HEPATIC PERFUSION DUE
TO LOW CARDIAC OUTPUT
– ACCUMULATION OF THIOCYANATE
• CAN OCCUR OVER DAYS DURING CHRONIC USE,
PARTICULARLY WITH IMPARIED RENAL FUNCTION
INOTROPES: BEATING A DEAD HORSE
RANDOMIZED CONTROLLED
TRIALS SUPPORTING USE OF
INOTROPES IN ADHF:
WHAT’S WRONG WITH INOTROPES IN
ADHF?
ARRHYTHMIAS (OPTIME-CHF)
HYPOTENSION (OPTIME CHF)
INCREASED TROPONIN RELEASE
INCREASE IN-HOSPITAL AND 6 MONTH
MORTALITY (ADHERE NATIONAL REGISTRY,
ESCAPE TRIAL)
• DOES NOT SHORTEN HOSPITALIZATION
(OPTIME-CHF)
•
•
•
•
INOTROPES USED IN ADHF AND
STARTING DOSES
•
•
•
•
DOBUTAMINE:1-10 mcg/kg/min
MILRINONE: 0.01-0.75 mcg/kg/min
DOPAMINE: 1-4 mcg/kg/min
EPINEPHRINE AND NOREPINEPHRINE: 1
mcg/min
HFSA GUIDELINES: WHEN TO USE
INOTROPES
• IV INOTROPES (MILRINONE OR DOBUTAMINE)
MAY BE CONSIDERED TO RELIEVE SYMPTOMS
AND IMPROVE END-ORGAN DYSFUNCTION IN
PATIENTS WITH ADVANCED HF WITH LOW
OUTPUT SYNDROME, ESPECIALLY WITH SBP
<90, SYMPTOMATIC HYPOTENSION WITH
NORMAL FILLING PRESSURES, OR
INTOLERANT OR UNRESPONSIVE TO
VASODILATORS AND DIURETICS
3 REQUIREMENTS FOR INOTROPE
USE:
ADVANCED SYSTOLIC HEART FAILURE
+
LOW OUTPUT SYNDROME
+
HYPOTENSION
OR
VASODILATORS EITHER INEFFECTIVE OR
CONTRAINDICATED
OR
FLUID OVERLOADED AND UNRESPONSIVIE TO DIURETICS
OR MANIFEST DETERIORATING RENAL FUNCTION
INOTROPES: WHAT IS ADVANCED
SYTOLIC HF?
• LVEF IS REDUCED AND USUALLY DILATED
• INOTROPES ARE NOT APPROPRITE FOR HEART
FAILURE WITH PRESERVED EJECTION
FRACTION
INOTROPES: WHAT IS LOW OUTPUT
SYNDROME IN ADHF?
DILATED LV WITH REDUCED LVEF
+
DIMINISHED PERIPHERAL PERFUSION OR ENDORGAN DYSFUNCTION
LOW OUTPUT SYNDROME IS USUALLY
MANIFESTED BY ONE OR MORE OF
THE FOLLOWING:
• SBP < 90 MM Hg
• SYMPTOMATIC HYPOTENSION WITH NORMAL
FILLING PRESSURES
• LACK OF RESPONSE TO VASODILATORS
• SBP TOO LOW FOR VASODILATORS
• END ORGAN DYSFUNCTION, SUCH AS ELEVATED
BUN AND/OR CREATININE AND OLIGURIA,
MENTAL STATUS CHANGES, OR ELEVATED LFTS
HFSA GUIDELINES: WHEN TO USE
INOTROPES IN ADHF
ADVANCED HF (LV DILATION AND REDUCED EF)
+
LOW OUTPUT SYNDROME
+
INTOLERANT TO VASODILATORS
OR
POOR RESPONSE TO DIURETICS
OR
WORSENING RENAL FUNCTION
2 THINGS THAT MUST BE KNOWN
BEFORE STARTING AN INOTROPE
• IV INOTROPES (MILRINONE OR DOBUTAMINE)
ARE NOT RECOMMENDED UNLESS THE PA
CATHETER READINGS OR CLEAR CLINICAL
SIGNS DEMONSTRATE:
– LEFT HEART FILLNG PRESSURES ARE ELEVATED
AND
– CARDIAC INDEX IS SEVERELY IMPAIRED
CASE #1
• 68 YEAR OLD MALE
• ISCHEMIC CM WITH LVEF 25% ON MAXIMALLY
TOLERATED DOSE OF ALL APPROPIATE HF MEDS
• HX: SEVERE DYSPNEA + ABDOMINAL SWELLING
• EXAM: BP 95/56 HR PACED AT 70
– SEVERE JVD, MODERATE ASCITES, +3 EDEMA
• LABS:
– CREAT RISE FROM BASELINE 1.3 TO 2.3
– BUN RISE FROM BASELINE 20 TO 52
CASE #1
DO YOU STOP BETA BLOCKER AND START
INOTROPIC THERAPY?
CASE #1: SOLUTION
• CONTINUE BETA BLOCKER
• INOTROPE SHOULD NOT BE INITATED
• TREAT WITH IV DIURETICS AND VASODILATOR
THERAPY
CASE #2
• 52 YEAR OLD FEMALE
• DILATED NONISCHEMIC CM, LVEF 20% +
MODERATE MR
• HX: PROGRESSIVE FATIGUE
• EXAM:
– BP 86/60 (BASELINE); HR 95
– HEMODYNAMICS: PA 65/28, , RA 14, PCWP 25, CI 1.4,
SVR 1822
• LAB:
– CREAT STABLE FROM BASELINE AT 1.4
CASE #2
SHOULD YOU START AN INOTROPE?
CASE #2: SOLUTION
• NO CLINICAL SIGNS OF HYPOPERFUSION
• SVR IS SIGNIFICANTLY ELEVATED AND SBP IS
>85
• INOTROPE IS NOT INDICATED
• TREAT WITH IV DIURETIC AND NITROPRUSSIDE
• DIURESIS + NITROPRUSIDE REDUCED MR,
DECREASED SVR, INCREASED CI, DECREASED
FILLING PRESSURS, DECREASED PA PRESSURES
CASE #3
• 70 YEAR OLD MALE WITH ADVANCED PROSTATE
CA
• ISCHEMIC CM, LVEF 18%
• HX: 2 EPISODES OF NEAR SYNCOPE.
HYPOTENSION PRECLUDES BETA BLOCKER; ON
LISINOPRIL 2.5 mg DAILY
• EXAM: SOMNULENT DURING EXAM, BP 72/55,
HR 70, NO JVD, CLEAR LUNGS, S3,COOL
EXTREMITIES, TRACE EDEMA
• LABS: Cr 1.8
CASE #3
SHOULD YOU START AN INOTROPE?
CASE #3: SOLUTION
INOTROPE SHOULD BE STARTED.
THIS IS CARDIOGENIC SHOCK.
BP TOO LOW FOR VASODILATOR
ADVANCED PROSTATE CA PRECLUDES VAD
AND TRANSPLANT
• IT IS PERFECTLY ACCETPTABLE TO START
INOTROPE IN HOSPITAL AND SEND TO
PALLIATIVE CARE OR HOSPICE WITH INOTROPE
•
•
•
•