3.14.19 Conference Summary

GRAND ROUNDS: Acute Heart Failure: Novel Early Treatment Approaches- Dr. Sean Collins

heart failure .jpg
  • While our diagnosis of heart failure has improved dramatically, the management of heart failure has changed minimally since 1974 (i.e. oxygen, NIPPV, nitrates, morphine, diuretics)

  • Heart failure is a disease of “residual congestion”

    • 50% of patients admitted leave the hospital with congestion and this is associated with greater likelihood of readmission

  • Hemodynamic markers like BNP are good for diagnosis but less helpful at evaluating response to therapy in acute situations

  • Phenotypes of Heart Failure

    • Hypertensive type (associated with acute “flash” pulmonary edema)

      • Function of diastology and filling time (not as much of an EF issue) so vasodilators are preferred treatment

      • High dose nitroglycerin 100 mcg bolus (or isosorbide dinitrate) is reasonable treatment and allows for redistribution of fluid (instead of overall loss of fluid)

      • IV vasodilators

        • Enalapril is safe and does not cause significant AKI

        • Hydaralazine

        • Diltiazem

      • Start with SL/topical NTG; if further BP therapy or symptom control are necessary, IV boluses are preferable over drips when possible as this allows a non-ICU admission

    • Non-hypertensive type

      • Diuretic therapy is more helpful because these patients are often total body fluid elevated in acute exacerbations

        • Give 2x their home dose diuretic (i.e. 80 mg IV furosemide bolus if taking 40 mg BID)

      • Worsening renal function in acute heart failure patients more commonly represents hypervolemia/congestion and diuretics SHOULD be given as most of these patients renal function will actually improve (i.e. “pseudo-worsening renal function”)

      • Therapeutic target for volume removal?

        • Target salt in the urine (UNa and UCr/SCr) as effective diuretic therapy will increase absolute salt loss

          • UNa > 50-70 meq/L —> continue same diuretic dosing and timing

          • UNa < 50 meq/L —> double previous diuretic dose or consider different medication (i.e. bumetanide or torsemide if furosemide already given)

        • POC Lung ultrasound is very accurate at diagnosing acute heart failure

          • 2 B lines in single lung view is normal

          • The more B lines present, the worse the pulmonary edema and heart failure exacerbation

        • Dyspnea, BNP not reliable end-points for diuretic therapy

GRAND ROUNDS: Acute Heart Failure in the ED: Who Can I Discharge?- Dr. Sean Collins

  • Endpoints of therapy is the most important factor in determining who can be discharged from the ED

  • >140,000,000 ED visits in the US and ~13% overall admission rate

  • >80% of heart failure patients are admitted to the hospital from the ED with 1-4% inpatient mortality

  • 30-day mortality 8-9%

  • Inpatient stay and ED diuresis does not improve mortality in heart failure patients; long term use of ACEi and ARB and BB are mainstay to decrease mortality

  • Most common precipitating factors leading to heart failure exacerbation

    • ACS

    • Infection

    • Afib

    • HTN

    • Medication or dietary non-compliance

  • Keys to early discharge:

    • Early treatment in the ED

      • Early and aggressive diuretic therapy improves likelihood of discharging

    • Risk Assessment

      • EHMRG score for 30 day mortality risk stratification of heart failure patients

        • May be used in the future to predict lower risk patients who are safer for discharge (i.e. 3-4% 30-day mortality vs 8-9%)

      • Cardiac troponin (Tn) and outcome in acute heart failure

        • Causes: ischemia, non-ischemia, multifactorial

        • HF patients with elevated troponins have higher mortality regardless of cause of Tn elevation and even if chronically elevated; discussion with cardiology before discharging these patients is appropriate

    • Transition plan with outpatient follow-up

      • 7 day follow up and access to home medications are particularly important

    • Reasonable patients to discharge home with heart failure exacerbation

      • No ACS, SBP >100 mm Hg

      • No significant renal dysfunction or change from baseline

      • Clear cause of exacerbation (dietary/medication non-compliance, lifestyle change)

      • Good response to ED therapy (i.e. UNa >50 meq/L after diuretic therapy in ED)

      • Effective discharge plan of care

CPC: Dr. Luke Apisa vs. Dr. Ben Boswell

  • Presentation by Dr. Apisa

  • 61 yo M presents with frontal HA and fingertip and toes tingling

    • Day 1: initial ED visit -> neuro consult -> DC

    • Day 2: saw ortho spine -> representation to ED

      • Day 1: Frontal headache associated with phonophotbia, subjective weakness of L side, difficulty walking

      • PMH: depression, insomnia, HTN, HSV 1, chronic low back pain

      • PSH: B/L hip replacements off fluoxetine for 5 days

      • SocHx: recent trip to China for 4 weeks, then 1 week in Oregon, hiked 2x, and took 1 tab of LSD; 2 drinks daily

      • Meds: fluoxetine, stopped taking 5 days ago

      • PE: SpO2 94% otherwise WNL; PE otherwise normal with normal neuro exam

      • Neuro consult: L sided ptosis, L sided reduced muscle bulk, LUE shoulder abduction limited to 15 degrees, RLE reflexes decreased, L C5 dermatome with decreased sensation; gait narrow but not ataxic

      • Negative UA, Utox, CBC, CMP, CRP, ESR, UPEP, B12, HbA1c, TSH, CK, Mg normal

      • CXR normal

      • CT head normal

      • MRI C spine at request of neurology normal

      • Neuro impression: pt with ?hx of ETOH abuse presenting with peripheral neuropathy in setting of known chronic shoulder issues; recommended discharge home with follow up in clinic in 1 week

      • Patient discharged and saw his ortho spine doc next day

        • Difficulty with balance 3 days after migraine headache and myelopathy; told to come back to ED

      • Return ED visit; headache, difficulty walking, paresthesias now worsened; patient fell today; LEs now weaker

      • No recent diarrhea, cough, fever, rash or other infectious sx

      • Repeat PE: no ptosis, new winging of L shoulder; now ataxic gait, diffuse areflexia, decreased sensation of lower extremities, positive Romberg test

  • Rebuttal by Dr. Boswell

    • Differential: B12 deficiency, thiamine deficiency, MS, Lyme disease, GB syndrome, Multiple Myeloma, Hypercalcemia, Hypothyroidism, Acute flaccid myelitis, Polio, Lead poisoning, SSRI withdrawal, neurosyphilis, transverse myelitis, CVA, brain mass, Wernicke’s, Prion disease, Chronic inflammatory demyelinating polyneuropahty, ALS, Parsonage Turner syndrome, West Nile Virus

    • Diagnosis: Neurosyphilis (primarily because the patient had headaches as a primary symptom)

    • Diagnostic test of choice: LP with VDRL

  • Diagnosis by Dr. Apisa

    • Guillain Barre Syndrome

    • Test of choice: LP to eval for albumino-cytologic dissociation

    • Unique features of this case:

      • ?Miller Fischer variant

      • Upper extremity predominance

      • Presence of headache is rare although case reports exist

      • No identifiable infectious trigger in history (though this is not uncommon in GBS)

    • Patient admitted to NIU for 5 days

      • LP performed consistent with GBS

      • IVIG given and ambulatory difficulties and weakness improve quickly

      • Neuro exam on DC: continued diminished reflexes otherwise strength 5/5 throughout

    • UMN vs LMN disease

      • He fit the LMN disease clearly with atrophy, decreased reflexes, weakness, no spasticity, and negative Babinski

    • Guillain Barre Syndrome

      • Types

        • Acute inflammatory demyelinating disease

          • Classically, LMN disease with areflexia that typically progresses superiorly and is most commonly caused by C. Jejuni diarrheal disease

        • Miller Fischer Variant

          • Primarily UE involvement with cranial palsies and more pronounced bulbar symptoms

      • This patient was DC’d quickly (5 days after admission)

        • Had no liver dysfunction, proximal muscle weakness, or bulbar symptoms and had strong cough which is predictive of lower need of for ventilatory support

        • He responded quickly to IVIG and had rapid improvement in his weakness