Cardiogenic shock: Difference between revisions

Line 92: Line 92:
*[[Calcium Channel Blocker Toxicity|Calcium Channel Blocker]]
*[[Calcium Channel Blocker Toxicity|Calcium Channel Blocker]]
*[[Digoxin Toxicity | Digoxin]]
*[[Digoxin Toxicity | Digoxin]]
==Disposition==
*Admission, frequently to intensive or higher-level of care


==See Also==
==See Also==

Revision as of 20:44, 5 October 2015

Background

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

Etiologies

Clinical Features

Physical Exam

  • Assess for signs of CHF
    • elevated JVD, pulmonary edema, S3
  • Assess for valvular disease (MR, critical AS, or aortic regurgitation)
  • Assess for end-organ hypoperfusion
    • cool/mottled extremities, weak pulses, AMS, decreased UOP
  • Assess for pulsus paradoxus (cardiac tamponade)

Differential Diagnosis

Shock

Diagnosis

  • Labs
    • Troponin
    • Lactate
    • CBC
    • Chem
    • BNP
      • <100 may rule-out cardiogenic shock
  • ECG
  • CXR
  • TTE

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) [1] Strong ß1 agonist +inotrope +chronotrope, Weak ß2 agonist +weak vasodilatation ) alpha effect minimal HR variable effects. indicated in decompensated systolic HF, Debut Research 1979[2] 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[3]
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) [4] mild β1 direct effect β1 and strong α1,2 effects Less arrhythmias than Dopamine[3] 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[5] 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. https://www.ncbi.nlm.nih.gov/pubmed/8449087
  2. Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine
  3. 3.0 3.1 De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789
  4. https://www.ncbi.nlm.nih.gov/pubmed/15542956
  5. Pasin L et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013 Mar;15(1):42-8.