“management of heart failure in the hospitalized patient” witteles.pdfwhat is the solution? ......

“Management of Heart Failure in the Hospitalized Patient”

Ronald Witteles, M.D.Stanford University School of Medicine

October 27, 2012

DisclosuresI have nothing to disclose

What is Heart Failure?• Not as simple as it may sound…• What does it mean?


• Edema


• Edema• Low cardiac output


• Edema• Low cardiac output• Lack of end-organ perfusion


• Edema• Low cardiac output• Lack of end-organ perfusion• Something else???

An Interrogatory• What are my PA catheterization numbers?

• RA: • RV: • PA:• PCWP:• CO:• CI:


• 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


• 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?

The Answer• My clinic patient’s catheterization numbers…

• RA: • RV: • PA:• PCWP:• CO:• CI:


• RA: 9 mmHg• RV:• PA:• PCWP:• CO:• CI:


• RA: 9 mmHg• RV: 35/9 mmHg• PA:• PCWP:• CO:• CI:


• RA: 9 mmHg• RV: 35/9 mmHg• PA: 35/15/22 mmHg• PCWP:• CO:• CI:


• RA: 9 mmHg• RV: 35/9 mmHg• PA: 35/15/22 mmHg• PCWP: 14 mmHg• CO:• CI:


• 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


• 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

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)

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.

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.

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

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

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

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.”

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?

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!

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…

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?

How About Sodium/Fluid Intake?

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.

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.

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.

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.

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

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

What Do You Do?What should you do immediately?

1) Intubation, furosemide2) BIPAP, sublingual nitroglycerin, furosemide3) BIPAP, nitroglycerin drip, furosemide4) BIPAP, dobutamine, furosemide

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

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

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

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!

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)

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

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

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

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

What Do You Do?1) Consult surgery for cholecystectomy2) Start on Abx/fluids for cholecystitis3) Diurese4) Diurese/afterload reduce5) Diurese/pressors6) Diurese/inotropes

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

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!

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)

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

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

IV Drips – From Vasodilators to Pressors

NTG/Nitroprusside/Nesiritide

Dobutamine/MilrinoneDopamineEpinephrineNorepinephrine

Phenylephrine/Vasopressin

Vasodilatation

Vasoconstriction

Inotropy

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?

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)

No Difference in Hospital-Free Surivival

Adapted from Pfisterer et al. JAMA 2009;301:383-92.

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

? Slides on NE vs. DA controversy &

DOSE trial

Thank you!

“management of heart failure in the hospitalized patient” witteles.pdfwhat is the solution? ......

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