POTD: Decompensated CHF - a deep dive

This is probably bread and butter for us at Maimo and we are roughly familiar with how to manage it.  Today, we take a deep dive into the classification and etiology of decompensated CHF to better understand the disease process. And then a short review on the basics of management just go through it systematically.


What is decompensated heart failure

  • When something structural or functional happens to the heart, leading to inability to eject and/or accommodate blood within physiological levels.

  • Leads to a functional limitation

  • Requires immediate intervention


2 different scenarios:

1) New-onset acute CHF

  • No prior history or symptoms of CHF

  • Triggered by:

    • Acute MI

    • Hypertensive crisis

    • Rupture of chordae tendineae 

  • Usually more prominent pulmonary congestion > systemic congestion

    • Usually normal blood volume

  • Treatment focused on treating underlying cause

    • High dose diuretics less helpful


2) Decompensated (chronic) CHF

  • Worsening of symptoms in existing CHF

  • Most commonly caused by:

    • Low treatment adherence - med noncompliance or poor diet (high salt)

    • Infection

    • PE

    • Tachy/bradyarrhythmias 

      • Often new-onset afib 


Factors indicating poor prognosis in DHF:

  • Pts with BUN > 90 and Cr > 2.75 on admission have a 21.9% risk of in-hospital mortality

  • Age (above 65 years)

  • Hyponatremia (sodium <130meq/L)

  • Impaired renal function

  • Anemia (hemoglobin <11g/dL)

  • Signs of peripheral hypoperfusion

  • Cachexia

  • Complete left bundle branch block

  • Atrial fibrillation

  • Restrictive pattern on Doppler

  • Persistent elevation of natriuretic peptides levels despite treatment

  • Persistent congestion

  • Persistent third heart sound

  • Sustained ventricular tachycardia or ventricular fibrillation


Classification system - Stevenson Classification (below)


Here’s another similar classification chart that’s more visually stimulating:

Forrester Classification (below)

​​

Use to guide management

  • A (dry, warm) = compensated

  • B (wet, warm) = most common

    • Vasodilators and diuretics

    • Consider inotropes especially when SBP b/w 90-120

  • C (wet, cold) = worst prognosis

    • Ionotropes and diuretics

    • IV vasodilators if BP is being intensively monitored

  • L (dry, cold) = rare

    • Volume resuscitation +/- inotropes

Causes of CHF exacerbation

Tsuyuki et al, 180 pts 

  • Most common primary cause: excessive salt intake (15%)

  • Noncardiac disorders (15%)

  • Inappropriate reductions in CHF therapy (9%)

Ghali et al, 101 pts at Cook County Hospital in Chicago

  • Lack of compliance with diet, drugs, or both (64.4%)

  • Uncontrolled HTN (43.6%)

  • Cardiac arrhythmias (28.7%)

Opasich et al, 161 pts referred to CHF service at Italian hospital

  • Arrhythmias (24%)

  • Infection (23%)

  • Poor compliance (15%)

  • Angina (14%)

My takeaway: there is wide variability in the causes of DHF and limited studies out there about the various causes. Given that poor medication / diet compliance is often at the top of the list, it seems like good patient education may go a long way in preventing CHF exacerbation. Consider taking the time to really get at why your patient is in CHF exacerbation. Do they not understand how often they’re supposed to take their diuretic? Are they in denial about junk food intake? 

You MUST understand the classification of your patient’s CHF in order to manage them appropriately. It’s not always cookie cutter diuretics. 

I also decided to touch on basics of CHF management because I thought this was a nice review by emcrit.

1. Treat the lungs

  • BIPAP - reduce preload and afterload (like ACEI)

  • Intubation - cardiogenic shock

  • Drain large pleural effusions if causing respiratory distress

  • Inhaled pulmonary bronchodilator - epoprostanol or NO


2. Optimize MAP - reduce afterload if pt can tolerate

  •  High dose nitroglycerin - up to 200-250 mcg/min

  • Transition to oral once stabilized - ACEI, ARB, hydralazine + isosorbide dinitrate 

  • Manage hypotension with pressor - NOREPINEPHRINE IS KING

    • EPI is reasonable if reduced EF, hypotensive, with poor cardiac output

    • AVOID dopamine - evidence of harm compared to NE in SOAP-II trial


3. Optimize volume status

  • Fluids?

    • End organ perfusion (AKI)

    • NO evidence of pulmonary congestion (no B lines on US)

    • Appears truly hypovolemic (no systemic congestion)

    • Give small boluses at a time and reassess

  • Diuresis?

    • SIgnificant pulmonary or systemic congestion

    • Overall appears hypervolemic


4. Inotrope for HFrEF

  • Very temporary improvement in hemodynamics and actually associated with worse outcomes in some studies

  • Inotropes should ONLY be used if:

    •  Hypoperfusion with low-normal BP (like AKI with poor UO despite above interventions)

    • Refractory cardiogenic pulmonary edema (like if the interventions above don’t work and you still need to reduce pulmonary congestion)

  • Dobutamine?

    • Shorter half life, more titratable than milrinone

    • Preferred for immediate stabilization of very ill patient, someone with marked pulmonary edema on the verge of intubation

  • Milrionone?

    • More effective vasodilation than dobutamine

    • Renally excreted so tricky to titrate dose in renal failure - half life 2.3 hours in normal kidneys

  • DIgoxin? 

    • The only positive inotrope that doesn’t correlate with increased mortality

    • Consider for patients with long standing afib and systolic HF

    • Not front line


5. Treat underlying cause

  • New onset tachyarrhythmia - convert to sinus. Beware slowing HR if it isn’t high already

  • Cardiogenic shock 2/2 MI - ASA, antiplatelet, anticoagulation

    • Revascularization is essential!!! Valuable even if delayed.

    • Thrombolysis works poorly


THINGS TO AVOID:

  • Anything nephrotoxic - NSAIDs, ACE/ARB

  • DO NOT suppress sinus tach since this is usually compensatory and keeping the patient alive

  • Avoid diltiazem in afib with DHF

  • Do NOT treat mild stable hypoNa with hypertonic or salt tablets

  • Fluid and sodium restriction actually haven’t shown benefit in RCTs once they are in decompensated HF

  • BEWARE BETA BLOCKERS - don’t start them in decompensated heart failure

    • Great for chronic compensated HF

    • Negative inotrope could impair cardiac function

    • Controversial if BB should be continued in patients who are already taking them -- in general should be held in cardiogenic shock 


References

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/649270

Acute Precipitants of Congestive Heart Failure Exacerbations | Cardiology | JAMA Internal Medicine | JAMA Network

jamanetwork.com

Background&nbsp; Few studies have prospectively and systematically explored the factors that acutely precipitate exacerbation of congestive heart failure (CHF) in patients with left ventricular dysfunction. Knowledge of such factors is important in designing measures to prevent deterioration of...


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4878602/

Decompensated heart failure

www.ncbi.nlm.nih.gov

Heart failure is a disease with high incidence and prevalence in the population. The costs with hospitalization for decompensated heart failure reach approximately 60% of the total cost with heart failure treatment, and mortality during hospitalization ...


https://emcrit.org/ibcc/chf/#hemodynamic_evaluation_&_risk_stratification



Forrester classification

Forrester classification - management

Stevenson classification

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