ACUTE DECOMPENSATED HEART FAILURE : 2010 HFSA GUIDELINES

BART COX, M.D., FACCASSOCIATE PROFESSOR OF MEDICINE

UNIVERSITY OF NEW MEXICO SCHOOL OF MEDICINEDIRECTOR, 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; 16:475-539 (EXECUTIVE SUMMARY)

• JOURNAL OF CARDIAC FAILURE 2010; 16: e1-e194 (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= PCWP < 18 AND RA PRESSURE < 8• WET = PCWP > 18 OR RA PRESSURE > 8• WARM= CARDIAC INDEX> 2.2• COLD= 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 DIURETIC-INDUCED 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 500-1000 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 ORVASODILATORS EITHER INEFFECTIVE OR

CONTRAINDICATED ORFLUID 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 END-

ORGAN 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