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

WHATS 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?

KaplanMeier 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

HEISENBERGS 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

COXS 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:

WHATS 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