Cardiogenic shock: Difference between revisions

Line 34: Line 34:
*Assess for end-organ hypoperfusion
*Assess for end-organ hypoperfusion
**cool/mottled extremities, weak pulses, AMS, decreased UOP
**cool/mottled extremities, weak pulses, AMS, decreased UOP
*Assess for pulsus paradoxus ([[cardiac tamponade]])
*Assess for [[pulsus paradoxus]] ([[cardiac tamponade]])


==Differential Diagnosis==
==Differential Diagnosis==

Revision as of 20:49, 5 October 2015

Background

  • Leading cause of death in pts w/ MI who reach the hospital alive

Etiologies

Clinical Features

Physical Exam

Differential Diagnosis

Shock

Diagnosis

Workup

Brain natriuretic peptide (BNP)[1]

  • 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%)
    • Combination of BNP with clinician judgment 94% sensitive 70% specific (compared to 49% sn and 96% spec clinical judgement alone) [2]

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

  • <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

Treatment

  • General
    • Intubation
      • Decreases O2 demand BUT may worsen preload
  • Coronary perfusion
  1. Small Fluid challenge
  2. Increase inotropy
    1. Titrate to clinical effect
      • Dobutamine or Milrinone:
      1. Use milrinone if pt is on BB
      2. CaCl 1gm
        1. Give if pt is hypocalcemic
  3. Achieve MAP >65

Vasopressors

Pressor Initial Dose Max Dose Cardiac Effect BP Effect Arrhythmias Special Notes
Dobutamine 3-5 mcg/kg/min 5-15 mcg/kg/min (as high as 200) [6] Strong ß1 agonist +inotrope +chronotrope, Weak ß2 agonist +weak vasodilatation ) alpha effect minimal HR variable effects Cite error: Invalid <ref> tag; refs with no name must have content. Also Increase SA and AV node fx indicated in decompensated systolic HF, Debut Research 1979[7] 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[8]
Epinepherine 0.1-1 mcg/kg/min + inotropy, + chronotropy
Norepinephrine 0.2 mcg/kg/min 0.2-1.3 mcg/kg/min (5mcg/kg/min) [9] mild β1 direct effect β1 and strong α1,2 effects Less arrhythmias than Dopamine[8] First line for sepsis. Increases MAP with vasoconstriction, increases 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 0.01 to 0.04 U/min unknown increases via ADH peptide should not be titrated due to ischemic effects
Methylene blue[10] 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

Other Therapies

  • Transfusion
    • Consider if Hb < 10

Specific Situations

Mitral Regurgitation

ACS

Aortic stenosis

  • Do not give preload reducers such as Nitro
  • Patients are flow dependent over stenotic value. Flow proportional to degree of stenosis and afterload.
  • Maintain flow by decreasing afterload (use with extreme caution and in very small carefuly titrated doses)

Toxins

Disposition

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

See Also

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. McCullough et al. B-Type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from breathing not properly (BNP) multinational study. Circulation. 2002:DOI: 10.1161/01.CIR.0000025242.79963.4
  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. https://www.ncbi.nlm.nih.gov/pubmed/8449087
  7. Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine
  8. 8.0 8.1 De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789
  9. https://www.ncbi.nlm.nih.gov/pubmed/15542956
  10. Pasin L et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013 Mar;15(1):42-8.