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