5 Pearls on Inpatient Heart Failure

Heart Failure (HF) exacerbation is a clinical syndrome (collection of signs and symptoms) due to elevated intracardiac filling pressures leading to vasoconstriction and/or volume retention. 

Pearl 1: Initial clinical assessment

• Blood pressure: 
  • Hypotension is more common among HFrEF patients, and can be a sign of poor perfusion and even shock. 
  • Hypertension can cause someone to go into a heart failure exacerbation. Improve BP control with vasodilation/afterload reduction.
  • Narrow Pulse pressure is a sign of low output state:
    • Lower pulse pressure is associated with increased mortality in HFrEF patients
• Heart Rate: 
  • Tachycardia could be a sign of shock. However, the prevalence of beta-blockers can prevent the tachycardic response, so a normal heart rate does not rule out shock in a heart failure patient. 
• Jugular venous distention/pulsation
  • Used to determine the central venous pressure, which is a marker for LV preload
  • 2 ways to check it. 
    • One way is to sit them upright at 90 degrees and check if you can see their JVD above the clavicle
    • Sit the side of the bed at 45 degrees and assess how high the JVD is. 
    • Tricuspid regurgitation can cause JVD to be elevated in the absence of elevated cardiac filling pressures
  • Need to differentiate between atrial and venous when assessing JVD
    • Check the radial pulse. If it correlates it may be arterial. 
    • JVP: Should have increased fullness of the pulsation when applying abdominal pressure
• Dry v Wet and Cold v Warm: This information helps determine need for volume removal and/or ionotropic support. 
  • Ideal HF patient is warm and dry. 
  • A “Wet” patient needs volume removal. 
  • A “Cold” patient is having poor perfusion and needs additional perfusion support. 

Pearl 2: Initial lab workup

• BPN
  • Elevated BNP (>1000) supports HF diagnosis, and <100 makes CHF less likely
  • BNP of 350 has a likelihood ratio of 1 in one study
  • Assess the trend
    • BNP levels are usually lower in obese patients with heart failure
    • Patients with chronic kidney disease tend to have elevated BNP levels
    • Neprilysin inhibitors (e.g. sacubitil-valsartan)can cause elevated BNPs, so we generally check a pro-BNP instead of BNP in patients on neprolysin inhibitors 
• Troponins
  • In patients with an acute MI who developed cardiogenic shock, 6 month mortality is lower in patients who are revascularized early
• Sodium:
  • Low Na on admission is a predictor of both all-cause mortality and cardiovascular mortality for patients admitted with a heart failure exacerbation. 
  • A drop in sodium levels of >3 mEq/L was associated with increased mortality 
  • Risk of death was particularly  worse for Na <125 in heart failure exacerbations
• Creatine
  • Elevation compared to baseline on admission is usually a sign of cardiorenal syndrome from elevated renal venous congestion
    • Management of cardiorenal syndrome is with diuresis
  • If the elevation occurs during diuresis, may not be due to renal injury so much as elevation in creatinine without true kidney injury
  • Small elevations secondary to diuresis in a patient who is clinically improving, the best course of management may be continuing diuresis if no other cause of the elevated creatinine is found

  Pearl 3: Home meds

  • Beta-blockers: 
    • In heart failure exacerbations, beta-blockers should be continued unless the patient is in cardiogenic shock (i.e. in a low output state)
      • Consider somnolence, cool and/or clammy extremities, livedo reticularis, low pulse pressure or thready pulse can all suggest cardiogenic shock
    • Decreasing or discontinuing beta blockers is associated with increased mortality
    • If a patient’s beta-blocker is discontinued during a heart failure exacerbation, it is hard to get them back on it. 
    • Observational data suggests improved outcomes in HF patients discharged on beta-blockers compared to those who are not. 
  • Angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), Mineralocorticoid receptor antagonists (MRA), and angiotensin receptor–neprilysin inhibitors (ARNI) 
    • These are often held due to elevated creatinine on admission or during diuresis, then patients are discharged without them. 
    • Continuation of these medications as able, and certainly resumption prior to discharge, are important for improving lifetime morbidity and mortality
    • It may be reasonable to consider continuing the ACE/ARB or decreasing dose in patients who have only a mild AKI

  Pearl 4: Loop diuretics

  • Various clinician’s practices range from starting with 2-2.5 times the patient’s home diuretic dose to using 1mg/kg IV. If the hospital has a HF orderset, may need to change the dose
  • Thresholds and ceiling
    • Adequate 
    • Loop diuretics have a threshold dose below which they don’t have much effect. 
    • Loop diuretics also are considered to have a “ceiling” dose, above which they will not cause a significant increase in diuresis. 
  • Dose adjustment
    • A “good” dose of a loop diuretic will result in excretion of 250 mEq (~6g) of Na in about 2-3L of urine
    • IIncrease dose if not adequate response to dose
    • Increase frequency if adequate response to dose but 24h UOP is not sufficient. 
    • Can check spot urine sodium if unsure about the effectiveness of diuresis based on questionable Is/Os and inability to do accurate weights
      • If Na >100, dose was effective, if significantly lower you may need to increase dose
  • Furosemide drip
    • Per DOSE trial, it has not been proven to improve symptoms or length of stay in a typical heart failure patient.
    • Reasonable to consider for diuretic resistant patients.

  Pearl 5: Additional Volume Removal

  • Thiazide and Thiazide like Diuresis: Addition of a thiazide diuretic to a loop diuretic can lead to improved diuresis in a diuretic resistant patient.  
    • Because they act on the distal convoluted tubule, it is working downstream of furosemide, which can help augment diuresis. 
    • Hydrochlorothiazide and chlorthalidone are reasonable options. Metolazone, a thiazide like diuretic, is also commonly used. It is cheap and effective. 
      • Need caution though, as thiazides can cause significant lab abnormalities, particularly potassium and magnesium. 
      • Recommend checking electrolytes twice daily initially if used. 
      • It can be effective for a few days, so does not need to be dosed daily. 
      • Typical dose ranges from 5mg to 20mg. Typically start with 5mg and extra dose if needed. 
  • Diuresis in COPD:
    • Need to monitor bicarb levels. Can start retaining CO2 to compensate for the metabolic alkalosis that diuresis causes. Can lead to dangerously elevated PCO2s. Aggressive chloride repletion can be used to help prevent this. 
  • Chloride depletion metabolic alkalosis
    • Pendrin is a sodium bicarbonate exchanger that will remove bicarb and reabsorb chloride
    • Pendrin activity decreases with hypokalemia, elevated aldosterone, and chloride depletion
      • Aggressive diuresis will lead to more chloride depletion and hypokalema, which decrease pendrin’s ability to remove bicarbonate. Therefore, it will worsen the elevated bicarbonate and chloride depletion metabolic alkaosis
    • Can add spironolactone to help with hypokalemia and KCl to give additional chloride
  • Ultrafiltration: is another option for volume removal
    • Usually will only do after diuresis fails; however, there are a few exceptions: 
    • Emergent situations: Overload is the “O” in the AEIOU mnemonic of indications for emergent dialysis. If someone is in imminent danger from volume overload, ultrafiltration is an appropriate next step. 
    • If a patient is on a very large dose of home diuretics and are very volume up, can consider going straight to ultrafiltration. A decision to do ultrafiltration in this situation is often stylistic, and determined in conjunction with the heart failure specialist and nephrologist

Contributors

Shreya Trivedi, MD ^- Host, Show Notes

Martin Fried, MD - Host, Show Notes

Michael Dunleavy, MD - Host, Show Notes, CME Questions

Swapnil Hiremath, MD, MPH - Guest Expert

Gregory Katz, MD - Guest Expert

Michelle Kittleson, MD, PhD - Guest Expert

Ayesha Hasan, MD - Guest Expert

Reviewers

Stephen Pan, MD*

Eugene Yuriditsky, MD

* Stephen Pan reports participating in speakers’ bureaus for Pfizer and Akcea

Those named above unless otherwise indicated have no relationships with any entity producing, marketing, reselling, or distributing health care goods or services consumed by, or used on, patients.

Release Date: June 24, 2020

Expiration Date: June 24, 2023

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