Does the thought of managing acute decompensated heart failure (ADHF) give you paroxysmal nocturnal dyspnea? Recline for a bit while Dr. Michelle Kittleson MD, PhD @MKittlesonMD (Cedars Sinai) takes us through the Zen of jugular venous pressure (JVP) exams, how to approach diuresis, and the fine points of hospital discharge. This knowledge food is easier to swallow than an oral potassium replacement.
Listeners can claim Free CE credit through VCU Health at http://curbsiders.vcuhealth.org/ (CME goes live at 0900 ET on the episode’s release date).
The Curbsiders are partnering with VCU Health Continuing Education to offer FREE continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit. See info sheet for further directions. Note: A free VCU Health CloudCME account is required in order to seek credit.
Renal misinterpretation of decreased cardiac output as volume depletion leads to fluid retention and consequently acute decompensated heart failure (ADHF). This volume overload causes pulmonary congestion, abdominal bloating, and gravity dependent edema in the lower extremities or sacral region. While the pathophysiology of heart failure (HF) is diverse, the phenomena of ADHF occurs in both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Although diuresis has not been shown to reduce long term mortality, removing excess fluid is necessary to reverse the pulmonary edema of ADHF that leads to shortness of breath and hypoxia (Ellison and Felker 2017).
*NOTE: The discussion below pertains to HFrEF (ejection fraction <40%).
Asking the correct questions is the key to unlocking an acute heart failure diagnosis. There are innumerable reasons for a patient to be short of breath, but orthopnea, shortness of breath while laying flat, is more specific for ADHF –though the LR is only 2.2 (Wang et al 2005). Uncover a history of orthopnea by asking not just how many pillows your patient uses, but also why your patient is using multiple pillows. Additionally, instead of just asking if a patient ever wakes up in the middle of the night, clarify if when they wake up do they feel short of breath or if waking up was due to other factors. Ask about abdominal bloating and lower extremity edema, patients often know how their ADHF presents. A history of HF is a great predictor of ADHF (Wang et al 2005).
Understanding the cause of ADHF is an important component of treatment; either you can address the underlying cause of an exacerbation, or an unprovoked decompensation suggests severe disease. It is important to take a history in a non-judgemental manner. Patients may be unaware of the salt content of food that they eat in a restaurant. The FAILURES mnemonic is a great way for remembering the factors that can precipitate ADHF:
Forgetting medication (or taking beta blockers, NSAIDs, methamphetamine, or cocaine)
Arrhythmia or Anemia
Ischemia or Infarction
Lifestyle choices including dietary indiscretions.
Upregulation of cardiac demand from either pregnancy or hyperthyroidism.
Renal failure from progression of kidney disease or insufficient dialysis.
Embolus (pulmonary embolism)
Stenosis from worsening renal artery stenosis, aortic stenosis, or other valvular disease.
While the evidence of sodium restriction in hypertension is strong, the role of sodium restriction (2-3 g daily) in HF is less conclusive (HFSA Guidelines 2010). However, it is important to ask your patient what foods, high sodium or high carbohydrate, lead to fluid retention for them. For more information on this topic, our friends at the Core IM podcast have a great episode on salt restriction and HF. A 2 liter fluid restriction is “recommended” by the HFSA Guidelines 2010 for those with severe hyponatremia (sodium <130 mEq/L) and can be “considered” for those with difficult to control fluid retention despite other measures (expert consensus).
The physical exam is crucial to diagnosing ADHF and risk stratifying patients. The two profiles of ADHF are warm-and-wet or cold-and-wet; warm-and-wet refers to well perfused decompensated patients, and cold-and-wet refers to sicker patients who may need inotropic support.
The jugular venous pressure (JVP) is estimated by observing the vertical height of the jugular venous pulse above the sternal angle, >4 cm is considered abnormal. This pulse is the internal jugular vein that can be found in the triangle formed by the sternocleidomastoid and the clavicle. To assess the JVP, recline the patient at 30 or 40 degrees with their head turned gently away from you, so as to not tamponade the vein with muscle or skin tension. Become one with the neck, and observe the biphasic flicker; the a wave corresponds with atrial contraction, and the v wave is from increased venous pressure during filling. If you see a c wave, theoretically formed by the bulging of the tricuspid valve during ventricular contraction, tweet at Dr. Kittleson, and she will be very impressed and/or not believe you. If the JVP is not visible, adjust the angle of the patient to bring it into view. To distinguish between carotid and jugular pulses, press on the belly to see if increased venous return will increase the presumably venous pulsation, or press on the pulsation itself, an arterial pulse will not compress but a venous pressure will. Elevated JVP is 11% sensitive and 97% specific for ADHF, and the addition of checking for the abdominojugular reflux increases sensitivity to 24% (Wang et al 2005).
Listen for an S3 gallop. S3 is 13% sensitive and 99% specific for heart failure; LR = 11; 95% CI, 4.9-25.0 (Wang et al 2005).
While the lung exam is important for assessing other pathologies, listening to the lungs is not an effective way to evaluate ADHF. Crackles alone are not sensitive or specific for ADHF (Wang et al 2005). [#1 thing that irritates Dr. Kittleson: basing a volume assessment on a lung exam]
Dr. Kittleson urges providers to respect sinus tachycardia, because it can indicate that there is a severe underlying condition.
Lastly, bedside ultrasound is an emerging way to augment a ADHF physical exam (Marini et al 2020).
Serially checking brain natriuretic protein (BNP) is not useful in managing ADHF (Desai 2013). BNP can be negative in HFpEF or obesity, if it’s high it could be due to renal failure or chronic ventricular dysfunction. [#2 thing that irritates Dr. Kittleson: getting called to the ER for a high BNP without a history or physical exam to accompany it.]
Daily sodium, potassium, and creatinine are pivotal for monitoring diuresis. Low serum sodium is a sign of poor perfusion. Potassium can drop with diuresis, and low potassium can dictate use of MRAs. Creatinine can also indicate perfusion issues.
Continue guideline directed medical therapy (GDMT) during hospitalization (Tran et al 2018). Stopping a beta-blocker may lead to worse outcomes (Prins et al 2015). However, if the patient has symptomatic hypotension or severe bradycardia, adjust anti-hypertensive medication. Additionally, if there was a recent increase in a beta blocker that could have precipitated a decompensation, reduce the dose. Prioritize medications, consider each component of GDMT as “spending blood pressure.” ARNI/ACE/ARB have an acute benefit of afterload reduction and should be prioritized over beta blockers, unless there is a compelling reason for the beta blocker like arrhythmias.
The standard of care for diuresis are loop diuretics, which block the Na+-K+-2CL– symporter in the proximal tubule leading to enhanced excretion of water along with these electrolytes. Start dosing with 2.5x outpatient dose IV twice a day (DOSE-Trial). Diurese the patient as quickly as possible, because every day that they spend in the hospital is a chance to get C. Diff. Be nice and consider the timing of diuresis to allow patients to sleep.
Check the efficacy of dose after the first few hours instead of waiting until the end of the day. If a diuretic is working, the patient will be making an obviously large volume of urine. Loop diuretics have a threshold effect. For example, if 40 mg IV is not effective, don’t give 40 mg IV more often, give 80 mg IV. Aim for a minimum target of 2 liters net negative each day, but there is no such thing as too much diuresis if labs are stable. Consider how much water a patient needs to lose, and set daily goals based on this target. Replete electrolytes as needed; keep the potassium > 4 mg and magnesium > 2 mg to allow for buffer to avoid deadly arrhythmias. Dr. Kittleson suggests that magnesium may be a wonderdrug to fix muscle aches from “furosemide-ennui”, and oral magnesium oxide is a low risk intervention.
If 80 mg IV BID is not effective at achieving diuresis goals, consider adding a furosemide drip (escalating from 10, 20, 40, to 80 mg/hr). However, turn the drip off at night (11pm to 5 am, say) to allow the patient to sleep, unless you are a sadist or your patient has a foley. If an 80 mg/hr furosemide drip is not effective, worry and add on metolazone–a thiazide diuretic that inhibits a sodium-chloride symporter in the distal convoluted tubule–for sequential blockade. It is important to figure out why this patient is so diuretic resistant, do they have severe underlying cardiac or kidney issues contributing. If creatinine is less than double baseline, a high creatinine could be a result of venous back pressure due to congestion, and it may resolve with effective diuresis.
You can start (a touch of an) inotrope empirically if creatine is moving in the wrong direction to see if that support augments diuresis. However, a right heart Swan-Gnatz catheter allows you to measure filling pressures, pulmonary artery pressure, and cardiac output. If you have volume overload and renal dysfunction or progresssive hypotension, pulmonary artery catheter can help determine your course of action. Right heart catheters are a diagnostic not a therapeutic intervention. Use diuresis and inotropes to achieve the goals of RA <10 mmHg, wedge <20 mmHg, and cardiac index >2.
The patient is ready to switch to an oral diuretic when they achieve resolution of symptoms, normalization of JVP, and an absence of edema. Less valuable therapeutic targets are clear lungs and dry weight [#3 way to irritate Dr. Kittleson is saying that the patient is diuresed to dry weight and is ready to go home].
Decide on a new outpatient dose by looking at their old outpatient diuretic dose. If they were not taking their diuretic prior to admission, the same dose will probably be sufficient. However, if they were taking their diuretic and still decompensated, an increased dose will likely be necessary. Try the home oral diuretic dose for 24 hours to gain insight into how to adjust discharge dosing. Dr. Kittleson advises that a dose resulting in 500 cc negative in hospital will likely keep them net even at home. Include the admission and discharge weight in the discharge note. While self-reported dry weights are not typically accurate, admission and discharge weights will be useful during future hospitalizations. Patients should follow up in the clinic within one week of discharge to check potassium and medication.
Use hospitalizations as an opportunity to add on medications that are included in GDMT. SGLT-2 inhibitors are newly approved for the treatment of HF in patients even in the absence of diabetes (DAPA-HF).
Listeners will learn how to manage acute decompensated heart failure.
After listening to this episode listeners will…
Dr Kittleson reports no relevant financial disclosures. The Curbsiders report no relevant financial disclosures.
Kittleson MM, Gorth DJ, Williams PN, Watto MF. “#230 Kittleson Rules Heart Failure”. The Curbsiders Internal Medicine Podcast. http://thecurbsiders.com/episode-list Final publishing date August 17, 2020.
Got feedback? Suggest a Curbsiders topic. Recommend a guest. Tell us what you think.
We love hearing from you.
Yes, you can now join our exclusive community of core faculty at Kashlak Memorial Hospital along with all the perks:
Close this notice to consent.