“management of heart failure in the hospitalized patient” witteles.pdfwhat is the solution? ......
TRANSCRIPT
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“Management of Heart Failure in the Hospitalized Patient”
Ronald Witteles, M.D.Stanford University School of Medicine
October 27, 2012
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DisclosuresI have nothing to disclose
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What is Heart Failure?• Not as simple as it may sound…• What does it mean?
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What is Heart Failure?• Not as simple as it may sound…• What does it mean?
• Edema
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What is Heart Failure?• Not as simple as it may sound…• What does it mean?
• Edema• Low cardiac output
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What is Heart Failure?• Not as simple as it may sound…• What does it mean?
• Edema• Low cardiac output• Lack of end-organ perfusion
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What is Heart Failure?• Not as simple as it may sound…• What does it mean?
• Edema• Low cardiac output• Lack of end-organ perfusion• Something else???
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An Interrogatory• What are my PA catheterization numbers?
• RA: • RV: • PA:• PCWP:• CO:• CI:
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An Interrogatory• What are my PA catheterization numbers?
• RA: 3 mmHg• RV: 18/3 mmHg• PA: 18/7/11 mmHg• PCWP: 7 mmHg• CO: 5.2 L/min• CI: 2.8 L/min/m2
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An Interrogatory• What are my PA catheterization numbers?
• RA: 3 mmHg• RV: 18/3 mmHg• PA: 18/7/11 mmHg• PCWP: 7 mmHg• CO: 5.2 L/min• CI: 2.8 L/min/m2
• So what are the PA catheteriztion numbers on my heart failure clinic outpatient with dilated cardiomyopathy and a 35% LVEF?
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The Answer• My clinic patient’s catheterization numbers…
• RA: • RV: • PA:• PCWP:• CO:• CI:
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The Answer• My clinic patient’s catheterization numbers…
• RA: 9 mmHg• RV:• PA:• PCWP:• CO:• CI:
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The Answer• My clinic patient’s catheterization numbers…
• RA: 9 mmHg• RV: 35/9 mmHg• PA:• PCWP:• CO:• CI:
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The Answer• My clinic patient’s catheterization numbers…
• RA: 9 mmHg• RV: 35/9 mmHg• PA: 35/15/22 mmHg• PCWP:• CO:• CI:
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The Answer• My clinic patient’s catheterization numbers…
• RA: 9 mmHg• RV: 35/9 mmHg• PA: 35/15/22 mmHg• PCWP: 14 mmHg• CO:• CI:
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The Answer• My clinic patient’s catheterization numbers…
• RA: 9 mmHg• RV: 35/9 mmHg• PA: 35/15/22 mmHg• PCWP: 14 mmHg• CO: 5.0 L/min• CI: 2.7 L/min
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The Answer• My clinic patient’s catheterization numbers…
• RA: 9 mmHg• RV: 35/9 mmHg• PA: 35/15/22 mmHg• PCWP: 14 mmHg• CO: 5.0 L/min• CI: 2.7 L/min
• So…• His resting cardiac output is preserved,• But at the expense of higher filling pressures
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A Definition We Can Agree On?• Heart failure is a syndrome
characterized by:• The need for elevated filling pressures
to maintain an acceptable cardiac output.
• Inability to achieve an adequate cardiac output for organ perfusion in response to a stressor (e.g. exercise, infection, surgery)
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A Problem of Semantics…
• Three different patients with 3 unique pathophysiologic problems – three different treatments!
• The term “heart failure exacerbation” (or “acute decompensated heart failure”) leads to incorrect treatment much of the time.
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Admission 1• 68 y.o. African-American man with ischemic
cardiomyopathy.• Baseline echo: Moderate LV dilatation, LVEF 25-
35%, 1+ MR.• Comes to ER for worsening LE edema• Baseline meds: Carvedilol 25 mg bid, lisinopril 20
mg bid, ASA 325 mg qd, furosemide 40 mg bid, digoxin 0.125 mg qd.
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Admission 1• PE: Wt 90 kg (up from 85 kg 1 month ago) BP
115/65, HR 65, SaO2 94% RA, scant bibasilar crackles, no significant murmurs/gallops, 3+ LE edema.
• Labs: Na 137, K 4.1, Cr 1.3 (baseline 1.4), BNP 1100, troponin I <0.1.
• CXR: Cardiomegaly, mild pulmonary edema• ECG: Sinus rhythm at 65 bpm, old LBBB
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What Do You Do?What about the carvedilol?
1) Continue 25 mg po bid2) Cut to 12.5 mg po bid3) Stop for now with plans to reinitiate at 3.125 mg bid4) Stop for now with plans to reinitiate at 25 mg bid
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What Do You Do?What about the carvedilol?
1) Continue 25 mg po bid2) Cut to 12.5 mg po bid3) Stop for now with plans to reinitiate at 3.125 mg bid4) Stop for now with plans to reinitiate at 25 mg bid
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What Do You Do?What about the digoxin?
1) Stop digoxin (no mortality benefit anyway)2) Continue digoxin at 0.125 mg qd3) Increase to 0.25 mg qd4) Check a digoxin level & adjust dose accordingly
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What Do You Do?What about the digoxin?
1) Stop digoxin (no mortality benefit anyway)2) Continue digoxin at 0.125 mg qd3) Increase to 0.25 mg qd4) Check a digoxin level & adjust dose accordingly
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Question 1: What is the Problem?• In this patient, the problem is
volume overload• Nothing actually happened
acutely…• Are ‘heart failure exacerbation’ or
“acute decompensated heart failure” really the best terms?
• Biggest risk to the patient iatrogenesis.• “First, do no harm.”
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A Potential Complication…• Patient gets aggressive diuresis & is feeling
better, but then develops 15 second run of VT
• Electrolyte panel shows K 3.1• Potassium is repleted, but patient still has
runs of NSVT• Team decides to start patient on
amiodarone to suppress VT (a separate talk…)
• Putting the issue of whether or not to start amiodarone aside… is there anything else that needs to be done upon amiodarone initiation?
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A Potential Complication…• Patient gets aggressive diuresis & is feeling
better, but then develops 15 second run of VT
• Electrolyte panel shows K 3.1• Potassium is repleted, but patient still has
runs of NSVT• Team decides to start patient on
amiodarone to suppress VT (a separate talk…)
• Putting the issue of whether or not to start amiodarone aside… is there anything else that needs to be done upon amiodarone initiation?
• Halve the digoxin dose!
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How to Manage this Patient• 1) Loop diuretics, paying attention to electrolytes
• Goal is to get patient back to “dry weight”• Sending out too early only means he will be back
soon!• 2) Continue carvedilol/digoxin at present doses• 3) Determine why the patient developed volume
overload (sodium intake, medication noncompliance/confusion, underdosed diuretics)
• 4) Make sure patient has appropriate close outpatient follow-up (ideally in HF clinic)
• 5) Consider additional therapies that may help him long-term…
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Potential Long-Term Therapies• 1) Medical therapies
• Aldosterone antagonist with close electrolyte f/u
• Hydralazine/nitrates
• 2) Device therapy• If EF is chronically this low ICD indicated• Given LBBB & Class III sx, biventricular
pacing indicated
• 3) Statin?
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Potential Long-Term Therapies• 1) Medical therapies
• Aldosterone antagonist with close electrolyte f/u
• Hydralazine/nitrates
• 2) Device therapy• If EF is chronically this low ICD indicated• Given LBBB & Class III sx, biventricular
pacing indicated
• 3) Statin?
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How About Sodium/Fluid Intake?
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How About Sodium/Fluid Intake?• Problem is too much sodium, not too
much water!• Do not waste time/energy on fluid
restricting unless patient is hyponatremic• Patient’s non-restricted water intake is
based on maintaining sodium concentration… if he takes in less salt, he will take in less water.
• Best advice (in normonatremic patient): Drink to quench thirst – not more, not less.
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How About Sodium/Fluid Intake?• Low sodium diet is critical
• Most patients think low fat/sugar diet is most important for them.
• Multiple techniques to do low sodium
• Best diet – freshmeat/fruits/vegetables
• Nothing prepackaged/nothing that anyone has had the opportunity to add salt to.
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Trial of Free-Fluid vs. Fluid-Restriction in Treatment of Patients Admitted with ADHF
Adapted from Travers et al. J Card Fail. 2007;13:128-132.
* Time to clinical stability = symptomatic improvement with no evidence of fluid overload, stable weight x 48h, off IV therapies x 48h, no change in cardiac medications
for 48h.
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Potential Iatrogenic Problems• Iatrogenic problems to avoid:
• Arrhythmias due to:• Electrolyte abnormalities• Stopping beta-blocker
• Starting new medications without appropriate follow-up
• Amiodarone• Aldosterone antagonist
• Worsened renal function• Not as easy to avoid as it sounds• Should we accept some worsening of renal
function?• Nesiritide? Adenosine antagonists?
Ultrafiltration?• Answer: No, no, and no.
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Admission 2• 76 y.o. woman with HTN is taken to the ER from
her 4th of July BBQ because of sudden SOB• PE: Wt 75 kg (baseline 74 kg) BP 185/110, HR
105, SaO2 85% RA, diffuse rales, trace edema.• Baseline meds: ASA 325 mg qd, HCTZ 25 mg qd,
amlodipine 10 mg qd, lisinopril 20 mg qd• CXR: Normal cardiac silhouette, diffuse
pulmonary edema• ECG: Sinus tachycardia at 105 bpm, LVH with
repolarization abnormality
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Admission 2• Labs: Na 137, K 4.1, Cr 1.6 (baseline 1.6), BNP
450, troponin I <0.1. ABG: 7.49/28/50 on RA
• Baseline echo: Normal LV size/systolic function, moderate LVH, 2+ MR
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What Do You Do?What should you do immediately?
1) Intubation, furosemide2) BIPAP, sublingual nitroglycerin, furosemide3) BIPAP, nitroglycerin drip, furosemide4) BIPAP, dobutamine, furosemide
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What Do You Do?What should you do immediately?
1) Intubation, furosemide2) BIPAP, sublingual nitroglycerin, furosemide3) BIPAP, nitroglycerin drip, furosemide4) BIPAP, dobutamine, furosemide
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What is the Problem?• Characteristic findings in a patient who develops
“flash” pulmonary edema:• Poorly compliant ventricle (often with LVH)
• Can be worsened by ischemia
• Small weight gain, relatively unimpressive BNP• Often have significant mitral regurgitation• Almost always hypertensive at presentation
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What is the Solution?• In this patient, the main problem is increased
pressure• afterload or preload in noncompliant ventricle
LVEDP wedge pressure (especially with MR) pulmonary edema afterload
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What is the Solution?• Patient is in a vicious cycle
• Pulmonary edema/hypoxia distress/raised BP worsened pulmonary edema/hypoxia
• Pulmonary edema/hypoxia ischemia worsened pulmonary edema/hypoxia
• Time is of the essence – you are at a crossroads• Quick, decisive action rapid improvement• Delayed (or unaggressive) action
worsening of vicious cycle
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How to Treat this Patient• Vasodilator at reasonable doses
• Nitroglycerin (can start with SL)• Nitroprusside• Nesiritide
• Diuresis• Important, but not as important
• Respiratory support• Oxygen• BIPAP (also helps lower preload)• Intubation – beware sudden
hypotension!
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What to Tell this Patient Long Term• This is the patient most sensitive to sodium intake
• Literally one indiscretion flash pulmonary edema• Focus on BP control• Role of ‘conventional’ heart failure medications
not clear• No indication for device therapy (e.g. ICD,
resynchronization)
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Patient 3• 45 y.o. man with idiopathic dilated
cardiomyopathy ER for nausea/vomiting, abdominal pain
• Exam:• Vitals: AF BP 80/40 HR 120 RR 22 SaO2 95% RA• + scleral icterus/mild jaundice• JVP elevated to 20 cm H2O• Loud S3 gallop• Abd: Distended, diffusely tender but worst over RUQ,
equivocal Murphy’s sign• Ext: Clammy, 2+ bilateral edema
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Patient 3• CXR: Cardiomegaly, mild
interstitial thickening, no obvious pulmonary edema
• Baseline echo: Severe LV dilatation, LVEF 20%, 3+ MR, 2-3+ TR, RVSP = 55 mmHg
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Patient 3• Outpatient meds: Carvedilol 3.125 mg bid,
lisinopril 2.5 mg bid, furosemide 80 mg bid, digoxin 0.125 mg qd, spironolactone 25 mg qd
• Labs: Na 128, K 5.6, Cr 2.0 (baseline 1.4) Bilirubin 5.4 (baseline 1.0), Alk phos 180, INR 1.5, AST 240, ALT 300, WBC 10k, BNP 2500, Lipase 60
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Patient 3• ECG: Sinus tach at 120,
nonspecific ST-T changes (unchanged from baseline except HR)
• STAT RUQ U/S: + gallbladder wall thickening possibly c/w cholecystitis, + ascites, normal CBD
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What Do You Do?1) Consult surgery for cholecystectomy2) Start on Abx/fluids for cholecystitis3) Diurese4) Diurese/afterload reduce5) Diurese/pressors6) Diurese/inotropes
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What Do You Do?1) Consult surgery for cholecystectomy2) Start on Abx/fluids for cholecystitis3) Diurese4) Diurese/afterload reduce5) Diurese/pressors6) Diurese/inotropes
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What is the Diagnosis?• Low output heart failure (e.g. cardiogenic shock)• Keys to the diagnosis: Hypotension, elevated JVP,
S3• Frequently present differently than you might
think• GI complaints• Elevated LFTs (can be bili or transaminase pattern)• Worsened renal function• Much less common: Pulmonary edema/hypoxia
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How to Functionally Manage This Patient• Augment forward flow
• Afterload reduce if possible (cannot now due to hypotension)
• Inotrope (different from pressor!)• Diurese• Mechanical support
• IABP• LVAD
• Transplant?• Remember to look for an inciting cause!
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Inotropes vs. Pressors• These agents do three basic things:
• Vasodilate• Vasoconstrict (“pressor”)• Inotropy
• What agent to choose = what are you trying to achieve?• Septic patient: Problem is inappropriate vasodilatation
use vasoconstrictor• Hypertensive pulmonary edema (patient 2): Problem is
inappropriate vasoconstriction use vasodilator• Cardiogenic shock patient: Problem is weak muscle/low
cardiac output use inotropic agent + vasodilator (as tolerated)
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What Do the Drugs Do?• -1: Vasoconstrict• -1: Inotropy (& chronotropy)• -2: Vasodilate• NO: Vasodilate• Natriuretic peptide: Vasodilate• Vasopressin: Vasoconstrict (‘vaso’ ‘pressin’)• Phosphodiesterase Inhibitor: Inotrope/vasodilator
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What Do the Drugs Do?• Pressors:
• Pure: Phenylephrine, Vasopressin• Mixed: Norepinephrine, Epinephrine, Ephedrine
• Vasodilators:• Nitroglycerin, Nitroprusside, Nesiritide (BNP)
• Inotropes/vasodilators:• Dobutamine, Milrinone
• Inotropes/vasodilator/vasoconstrictor:• Dopamine
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IV Drips – From Vasodilators to Pressors
NTG/Nitroprusside/Nesiritide
Dobutamine/MilrinoneDopamineEpinephrineNorepinephrine
Phenylephrine/Vasopressin
Vasodilatation
Vasoconstriction
Inotropy
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A Word on Dopamine…• Used frequently in CCU/ICU setting
• Familiarity with it• Some inotropy, some BP ‘support’/no hypotension
• Hits dopamine, -1, 1 receptors• Lowest doses: Predominantly dopamine receptor• Smaller doses: Dopamine/beta receptors• Middle-higher doses: All receptors• Remember: None of this is pure!
• Dopamine vs. Dobutamine• Do you want some vasoconstrictive action or not?
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Finally – A Word on BNP Monitoring• BNP’s use: Distinguishing HF vs. non-HF cause of
acute dyspnea• Should we be measuring regular BNPs & guiding
therapy by it?• General answer: NO!• Biggest trial: TIME-CHF trial
• 499 patients age >60 with NYHA II-IV HF• All with HF hospitalization within past year• Intervention: Symptom-guided management or NT-BNP-guided
therapy• Primary endpoints: 18-month survival free of hospitalization &
QOL at 18 months• Not blinded to physician – only patient (possible bias)
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No Difference in Hospital-Free Surivival
Adapted from Pfisterer et al. JAMA 2009;301:383-92.
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No Difference in QOL(If Anything – Better Without NT-BNP!)
Adapted from Pfisterer et al. JAMA 2009;301:383-92.
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Summary• Avoid term ‘heart failure exacerbation’• 3 patients, 3 problems, 3 treatments
• Patient 1 – Volume overload: Diurese• Patient 2 – Pressure overload: Vasodilate• Patient 3 – Low output: Inotropic/mechanical support
• Other key points to remember…• What caused the admission?• Salt restriction is key; water restriction isn’t• Avoid stopping beta-blocker (except #3)• Remember drug-interactions• Short-term f/u in clinic & electrolyte f/u
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? Slides on NE vs. DA controversy &
DOSE trial
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Thank you!