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ACUTE DECOMPENSATED HEART FAILURE : 2010 HFSA GUIDELINES BART COX, M.D., FACC ASSOCIATE PROFESSOR OF MEDICINE UNIVERSITY OF NEW MEXICO SCHOOL OF MEDICINE.

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Presentation on theme: "ACUTE DECOMPENSATED HEART FAILURE : 2010 HFSA GUIDELINES BART COX, M.D., FACC ASSOCIATE PROFESSOR OF MEDICINE UNIVERSITY OF NEW MEXICO SCHOOL OF MEDICINE."— Presentation transcript:

1 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

2 DISCLOSURES NONE

3 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

4 2010 HEART FAILURE SOCIETY OF AMERICA GUIDELINES JOURNAL OF CARDIAC FAILURE 2010; 16: (EXECUTIVE SUMMARY) JOURNAL OF CARDIAC FAILURE 2010; 16: e1- e194 (COMPLETE GUIDELINE)

5 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.

6 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%

7 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

8 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%

9 HFSA GUIDELINES: WHO SHOULD BE HOSPITALIZED WITH ADHF? EVIDENCE OF SEVELY DECOMPENSATED HF – ALTERED MENTATION – HYPOTENSION – WORSENING RENAL FUNCTION DYSPNEA AT REST (RESTING 02 SAT <90% OR TACHYPNEA) HEMODYNAMICALLY SIGNIFICANT ARRHYTHMIAS (INCLUDING NEW ONSET AF WITH RVR) ACUTE CORONARY SYNDROME

10 HFSA GUIDELINES:WHEN SHOULD HOSPITALIZATION FOR ADHF BE CONSIDERED? WORSENED SIGNS/SX OF CONGESTION MAJOR ELECTROLYTE DISTURBANCE REPEATED ICD FIRINGS PREVIOUSLY UNDIAGNOSED HF WITH SIGNS/ SX OF CONGESTION ASSOCIATED COMORBID CONDITIONS (PE, PNEUMONIA, TIA, CVA, DKA)

11 HFSA GUIDELINES:TREATMENT GOALS FOR HOSPITALIZED ADHF PATIENTS SYMPTOMS ABATED (IMPROVE SX OF CONGESTION AND LOW OUTPUT) DEHYDRATED (OPTIMIZE VOLUME STATUS) OXYGENATED ( RESTORE NORMAL 02 SAT) ANTICOAGULATED (INDICATION PRESENT?) MEDICATED (OPTIMIZE PO MEDS, MINIMIZE SIDE EFFECTS) EDUCATED (SELF MANAGEMENT, MEDS) OPERATED (NEED F0R REVASCULARIZATION?)

12 ONCE ADMITTED WITH ADHF, WHAT ARE THE TREATMENT GOALS? DIAGNOSED (ETIOLOGY AND PRECIPITATING FACTORS) DEVICED (CANDIDATE FOR ICD OR CRT?) DISEASE MANAGED (NEED DM PROGRAM?)

13 HFSA GUIDELINES: MINIMUM DAILY MONITORING OF ADHF PATIENTS WEIGHT + INTAKE/OUTPUT VITAL SIGNS, INCLUDING ORTHOSTATIC & 02 SATURATION (UNTIL STABLE) SIGNS (EDEMA, ASCITES, JVD, HJR, RALES, HEPATOMEGALY/ LIVER TENDERNESS) SX (FATIGUE/ LIGHTHEADEDNESS, PND, DYSPNEA, NOCTURNAL COUGH, ORTHOPNEA) LABS (Na, K, Mg, BUN, Cr)

14 6 SLIDES OF BAD MEMORIES

15 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

16 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

17 FILLING PRESSURE IS THE PRESSURE AT THE END OF DIASTOLE

18 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

19 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)

20 INTRODUCTION TO PERFUSION IIN ADHF CARDIAC INDEX = CARDIAC OUPUT / BSA TO IMPROVE PERFUSION, IMPROVE CARDIAC OUTPUT (OR INDEX)

21 THE FOUR HEMODYNAMIC PROFILES

22 INITIAL CLINICAL ASSESSMENT FIRST HOSPITALIZATION PRIORITY: ASSESS THE LEVEL OF HEMODYNAMIC COMPROMISE – CONGESTION (PCWP AND RA PRESSURE) – PERFUSION (CARDIAC INDEX)

23 RECOGNIZING THE FOUR HEMODYNAMIC PROFILES NO CONGESTION = DRY CONGESTION= WET NORMAL PERFUSION=WARM DIMINISHED PERFUSION=COLD

24 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

25 RECOGNIZING THE FOUR HEMODYNAMIC PROFILES 2 COMPONENTS OF DECOMPENSATED HEART FAILURE – ELEVATED FILLING PRESSURES (MOST COMMON) – REDUCED CARDIAC INDEX (RARE)

26 2 MINUTE ASSESSMENT AND THE 4 HEMODYNAMIC PROFILES

27 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!!!!

28 PRINCIPLES OF THERAPY: THE OPTIMAL FILLING PRESSURE OPTIMAL PCWP IS < 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

29 FILLING PRESSURES AND STROKE VOLUME (SV)

30 STROKE VOLUME IMPROVED BY DECREASING MITRAL REGURGITATION

31 Warm and dry

32 Warm and wet

33 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 mg METOLAZONE PO OR CHLORTHIAZIDE mg IV

34 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

35 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

36 PROFILE C: COLD AND WET

37 < 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

38 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)

39 PROFILE L: COLD AND DRY

40 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 RA PRESSURE NORMAL: VASODILATORS, IABP, AND INOTROPE ARE TEMPORARY FIX NEEDS VAD/ TRANSPLANT EVALUATION

41 DIURETICS

42 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

43 THE DOSE TRIAL: BOLUS OR INFUSION, LOW DOSE OR HIGH DOSE?

44 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:

45 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

46 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

47 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

48 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

49 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

50 CARDIORENAL SYNDROME: OUTDATED AND INCOMPLETE EXPLANATION

51 CARDIORENAL SYNDROME: THE CURRENT EXPLANATION

52 HFSA GUIDELINES: D ESTROYING DIURETIC RESISTANCE D IAGNOSE IT: ARE THEY TRULY WET? D ECREASE THE Na AND FLUID INTAKE D OSE IT: INCREASE DOSE OF DIURETIC D RIP IT: FUROSEMIDE DRIP AT 5-20 mg/hr D OUBLE THE SITE OF ACTION : ADD 5-10 mg po METOLAZONE OR IV CHLORTHIAZIDE mg D EVICE IT: AQUAPHERESIS/ ULTRAFILTRATION

53 THE DIET AND FLUID RESTRICTION 2 GRAM SODIUM DIET 2 LITER/DAY FLUID RESTRICTON

54 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

55 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

56 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

57 VASODILATORS

58 IV VASODILATORS USED IN ADHF NITROGLYCERIN NITROPRUSSIDE

59 WHAT HAPPENED TO NESIRITDE?

60 IV VASODILATORS: NESERITIDE AND THE ASCEND TRIAL

61 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

62 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

63 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

64 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 mcg/min – KEEP SBP> 80, DECREASE SVR<1200, REDUCE PCWP < 16

65 IV NITROGLYCERIN MAJOR LIMITATIONS – HEADACHE – HYPOTENSION (ESPECIALLY IF FILLNG PRESSURES ARE LOW) – PROLONGED PROFOUND HYPOTENSION AND BRADYCARDIA (RARE) – TACHYPHYLAXIS – 20% ARE NONRESPONDERS

66 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 mcg/min q MINUTES – EFFECTIVE DOSE RANGE: mcg/min – KEEP SBP > 80 mm Hg, DECREASE SVR <1200, REDUCE PCWP < 16

67 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

68 INOTROPES: BEATING A DEAD HORSE

69 RANDOMIZED CONTROLLED TRIALS SUPPORTING USE OF INOTROPES IN ADHF:

70 WHAT’S WRONG WITH INOTROPES IN ADHF? INOTROPES STIMULATE cAMP AND THUS PHOSPHORYLATE Ca-HANDLING PROTEINS, PROVIDING INOTROPY BY INCREASING RELEASE OF Ca SPARKS BY COUPLONS DISTRIBUTED THROUGHOUT THE CELL

71 Goldhaber J I, Hamilton M A Circulation 2010;121: Copyright © American Heart Association

72 WHAT’S WRONG WITH INOTROPES IN ADHF? SARCOPLASMIC RETICULUM BECOMES OVERLOADED WITH CALCIUM, SPONTANEOUSLY RELEASING CALCIUM INTO THE CYTOPLASM, INDUCING: – ARRHYTHMIAS – MALADAPTIVE REMODELING – DEATH

73 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)

74 INOTROPES USED IN ADHF AND STARTING DOSES DOBUTAMINE:1-10 mcg/kg/min MILRINONE: mcg/kg/min DOPAMINE: 1-4 mcg/kg/min EPINEPHRINE AND NOREPINEPHRINE: 1 mcg/min

75 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

76 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

77 INOTROPES: WHAT IS ADVANCED SYTOLIC HF? LVEF IS REDUCED AND USUALLY DILATED INOTROPES ARE NOT APPROPRITE FOR HEART FAILURE WITH PRESERVED EJECTION FRACTION

78 INOTROPES: WHAT IS LOW OUTPUT SYNDROME IN ADHF? DILATED LV WITH REDUCED LVEF + DIMINISHED PERIPHERAL PERFUSION OR END- ORGAN DYSFUNCTION

79 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

80 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

81 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

82 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

83 CASE #1 DO YOU STOP BETA BLOCKER AND START INOTROPIC THERAPY?

84 CASE #1: SOLUTION CONTINUE BETA BLOCKER INOTROPE SHOULD NOT BE INITATED TREAT WITH IV DIURETICS AND VASODILATOR THERAPY

85 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

86 CASE #2 SHOULD YOU START AN INOTROPE?

87 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

88 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

89 CASE #3 SHOULD YOU START AN INOTROPE?

90 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


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