Management of Heart Failure in the Hospitalized Patient Ronald Witteles, M.D. Stanford University School of Medicine October 27, 2012
I have nothing to disclose Disclosures
What is Heart Failure? Not as simple as it may sound What does it mean?
What is Heart Failure? Not as simple as it may sound What does it mean? Edema
What is Heart Failure? Not as simple as it may sound What does it mean? Edema Low cardiac output
What is Heart Failure? Not as simple as it may sound What does it mean? Edema Low cardiac output Lack of end-organ perfusion
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???
An Interrogatory What are my PA catheterization numbers? RA: RV: PA: PCWP: CO: CI:
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/m 2
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/m 2 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:
The Answer My clinic patient s catheterization numbers RA: 9 mmhg RV: PA: PCWP: CO: CI:
The Answer My clinic patient s catheterization numbers RA: 9 mmhg RV: 35/9 mmhg PA: PCWP: CO: CI:
The Answer My clinic patient s catheterization numbers RA: 9 mmhg RV: 35/9 mmhg PA: 35/15/22 mmhg PCWP: CO: CI:
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:
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
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
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 bid 2) Cut to 12.5 mg po bid 3) Stop for now with plans to reinitiate at 3.125 mg bid 4) Stop for now with plans to reinitiate at 25 mg bid
What Do You Do? What about the carvedilol? 1) Continue 25 mg po bid 2) Cut to 12.5 mg po bid 3) Stop for now with plans to reinitiate at 3.125 mg bid 4) Stop for now with plans to reinitiate at 25 mg bid
What about the digoxin? What Do You Do? 1) Stop digoxin (no mortality benefit anyway) 2) Continue digoxin at 0.125 mg qd 3) Increase to 0.25 mg qd 4) Check a digoxin level & adjust dose accordingly
What about the digoxin? What Do You Do? 1) Stop digoxin (no mortality benefit anyway) 2) Continue digoxin at 0.125 mg qd 3) Increase to 0.25 mg qd 4) 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?
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 fresh meat/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 * 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. Adapted from Travers et al. J Card Fail. 2007;13:128-132.
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 4 th 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, furosemide 2) BIPAP, sublingual nitroglycerin, furosemide 3) BIPAP, nitroglycerin drip, furosemide 4) BIPAP, dobutamine, furosemide
What Do You Do? What should you do immediately? 1) Intubation, furosemide 2) BIPAP, sublingual nitroglycerin, furosemide 3) BIPAP, nitroglycerin drip, furosemide 4) 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 H 2 O 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
ECG: Sinus tach at 120, nonspecific ST-T changes (unchanged from baseline except HR) Patient 3 STAT RUQ U/S: + gallbladder wall thickening possibly c/w cholecystitis, + ascites, normal CBD
What Do You Do? 1) Consult surgery for cholecystectomy 2) Start on Abx/fluids for cholecystitis 3) Diurese 4) Diurese/afterload reduce 5) Diurese/pressors 6) Diurese/inotropes
What Do You Do? 1) Consult surgery for cholecystectomy 2) Start on Abx/fluids for cholecystitis 3) Diurese 4) Diurese/afterload reduce 5) Diurese/pressors 6) 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
Pressors: What Do the Drugs Do? 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 Vasodilatation Dobutamine/Milrinone Dopamine Epinephrine Norepinephrine Inotropy Phenylephrine/Vasopressin Vasoconstriction
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!) Minnesota Living with Heart Failure Score Adapted from Pfisterer et al. JAMA 2009;301:383-92.
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!