Cardiogenic shock

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Background

  • Leading cause of death in patients with ACS who reach the hospital alive

Etiologies

Clinical Features

Physical Exam

Differential Diagnosis

Shock

Evaluation

Workup

Brain natriuretic peptide (BNP)[1]

  • Biologically active metabolite of proBNP (released from ventricles in response to increased volume/pressure)
  • Utility is controversial and may not affect patient centered outcomes[2]
  • May be trended to gauge treatment response in acute decompensated CHF
  • May have false negative with isolated diastolic dysfunction
  • Measurement
    • <100 pg/mL: Negative for acute CHF (Sn 90%, NPV 89%)
    • 100-500 pg/mL: Indeterminate (Consider differential diagnosis and pre-test probability)
    • >500 pg/mL: Positive for acute CHF (Sp 87%, PPV 90%)

NT-proBNP[3][4][5]

  • N-terminal proBNP (biologically inert metabolite of proBNP)
  • <300 pg/mL → CHF unlikely
  • CHF likely in:
    • >450 pg/mL in age < 50 years old
    • >900 pg/mL in 50-75 years old
    • >1800 pg/mL in > 75 years old

Differential Diagnosis (Elevated BNP)

BNP In Obese Patients

  • Visceral fat expansion leads to increased clearance of active natriuretic peptides[6]
  • Obese patients also frequently treated for hypertension or coronary artery disease which may also contribute to lower BNP levels

Interpretation

  • In one study of 204 patients with acute CHF, an inverse relationship between BMI and BNP was noted. The standard cutoff of 100pg/mL resulted in a 20% false-negative rate[7]
  • Analysis of a subgroup of patients with documented BMI from the Breathing Not Properly study showed that a lower cutoff was more appropriate to maintain 90% sensitivity in obese and morbidly obese patients (54pg/mL)[8]

Management

General

Aim for MAP >65

  1. Consider etiologies (see above) and treat specific one, if present
  2. Consider small fluid challenge (250-500cc normal saline IV) or fluid removal, depending on estimation of patient's point on Starling curve
  3. Increase inotropy
  4. Consider transfusion if hemoglobin < 10 (be aware of added fluid)
  5. Consider intubation
    • Decreases O2 demand BUT may worsen preload

Specific Situations

Mitral Regurgitation

Increase forward flow

ACS

Aortic stenosis

Decrease afterload (with extreme caution in very small, carefully-titrated doses)

Toxins

Vasopressors

Pressor Initial Dose Max Dose Cardiac Effect BP Effect Arrhythmias Special Notes
Dobutamine 2.5 mcg/kg/min 10-40 mcg/kg/min mainly inotrope (ß1) alpha effect minimal Some HR(ß1) increase. Also Increase SA and AV node fx Debut Research 1979[9] Isoproterenol has most Β2 vasodilatory and Β1 HR effects
Dopamine 2 mcg/kg/min 20-50 mcg/kg/min β1 and NorEpi release α effects if > 20mcg/kg/min Arrhythmogenic from β1 effects More adverse events when used in shock compared to Norepi[10]
Epinepherine 0.1-1 mcg/kg/min
Norepinephrine 8-12 mcg/min 30 mcg/min β1 direct effect β1 and α1,2 effects Less arrhythmias than Dopamine[10] Increases MAP, coronary perfusion pressure, little β2 effects.
Milrinone 50 mcg/kg x 10 min 0.375-75 mcg/kg/min Direct influx of Ca2+ channels Smooth muscle vasodilator PDE Inhibitor which increases Ca2+ uptake by sarcolemma. No venodilatory activity
Phenylephrine 100-180 mcg/min then 40-60 mcg/min 0.4-9 mcg/kg/min Alpha agonist Long half life
Vasopressin Fixed Dose 0.4 U/min unknown increases via ADH peptide should not be titrated due to ischemic effects
Methylene blue[11] IV bolus 2 mg/kg over 15 min 1-2 mg/kg/hour Possible increased inotropy, cardiac use of ATP Inhibits NO mediated peripheral vasodilation Don't use in G6PD deficiency, ARDS, pulmonary hypertension
Medication IV Dose (mcg/kg/min) Concentration
Norepinephrine (Levophed) 0.1-2 mcg/kg/min 8mg in 500mL D5W
Dopamine 2-20 mcg/kg/min 400mg in 250 D5W
Dobutamine 2-20 mcg/kg/min 250mg in 250 mg D5W
Epinephrine 0.1-1 mcg/kg/min 1mg in 250 D5W

Disposition

  • Admission, frequently to intensive or higher-level of care

See Also

External Links

Video

References

  1. ↑ Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347(3):161-167. doi:10.1056/NEJMoa020233.
  2. ↑ Carpenter CR et al. BRAIN NATRIURETIC PEPTIDE IN THE EVALUATION OF EMERGENCY DEPARTMENT DYSPNEA: IS THERE A ROLE? J Emerg Med. 2012 Feb; 42(2): 197–205.
  3. ↑ Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients: the International Collaborative of NT-proBNP Study. Eur Heart J. 2006 Feb. 27(3):330-7.
  4. ↑ Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med. 2005 Feb 17. 352(7):666-75.
  5. ↑ Moe GW, Howlett J, Januzzi JL, Zowall H,. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation. 2007 Jun 19. 115(24):3103-10.
  6. ↑ Clerico A, Giannoni A, Vittorini S, Emdin M. The paradox of low BNP levels in obesity. Heart Fail Rev. 2011;17(1):81-96. doi:10.1007/s10741-011-9249-z.
  7. ↑ Krauser DG, Lloyd-Jones DM, Chae CU, et al. Effect of body mass index on natriuretic peptide levels in patients with acute congestive heart failure: A ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) substudy. Am Heart J. 2005;149(4):744-750. doi:10.1016/j.ahj.2004.07.010.
  8. ↑ Daniels LB, Clopton P, Bhalla V, et al. How obesity affects the cut-points for B-type natriuretic peptide in the diagnosis of acute heart failure. Results from the Breathing Not Properly Multinational Study. Am Heart J. 2006;151(5):999-1005. doi:10.1016/j.ahj.2005.10.011.
  9. ↑ Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine
  10. ↑ 10.0 10.1 De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789
  11. ↑ Pasin L et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013 Mar;15(1):42-8.
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