Cardiogenic shock: Difference between revisions
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==Other Therapies== | |||
*Transfusion | *Transfusion | ||
**Consider if Hb < 10 | **Consider if Hb < 10 | ||
==Specific Situations== | |||
#Mitral Regurg | |||
##Need to increase forward flow | |||
##Dobutamine (contractility) | |||
##Nitroprusside (afterload reduction) | |||
#MI | |||
##PCI or thrombolysis | |||
#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) | |||
###Nitropruside | |||
###Dobutamine | |||
###Hydralazine | |||
#Toxins | |||
##[[Beta-Blocker Toxicity]] | |||
##[[Calcium Channel Blocker Toxicity|Calcium Channel Blocker]] | |||
##[[Digoxin Toxicity | Digoxin]] | |||
==See Also== | ==See Also== | ||
Revision as of 03:49, 8 November 2013
Background
- Leading cause of death in pts w/ MI who reach the hospital alive
Work-Up
- Labs
- Troponin
- Lactate
- CBC
- Chem
- BNP
- <100 may rule-out cardiogenic shock
- ECG
- CXR
- TTE
Etiology
- Myocardial infarction
- Pump failure
- Mechanical complications
- Acute MR (papillary muscle rupture)
- VSD
- Free-wall rupture
- RV infarction
- Decreased forward flow
- Sepsis
- Rate-related
- Bradycardia
- Tachycardia
- Myocarditis
- Myocardial contusion
- Cardiomyopathy
- Mechanical obstruction to forward flow
- AS
- HOCM
- Mitral stenosis
- Pericardial
- LV regurgitation
- Chordal rupture
- Aortic insufficiency
DDX
- MI
- PE
- COPD exacerbation
- Peri/myocarditis
- Aortic dissection
- Pericardial tamponade
- Acute valvular insufficiency
- Sepsis
- Hemorrhage
- Toxins/drugs of abuse
Treatment
- General
- Intubation
- Decreases O2 demand BUT may worsen preload
- Intubation
- Coronary perfusion
- Small Fluid challenge
- Increase inotropy
- Titrate to clinical effect
- Dobutamine or Milrinone:
- Use milrinone if pt is on BB
- CaCl 1gm
- Give if pt is hypocalcemic
- Titrate to clinical effect
- Achieve MAP >65
Pressors
| Pressor | Initial Dose | Max Dose | Cardiac Effect | BP Effect | Arrhythmias | Special Notes | |
|---|---|---|---|---|---|---|---|
| Dobutamine | 2.5mcg/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[1] Isoproterenol has most Β2 vasodilatory and Β1 HR effects | |
| Dopamine | 2mcg/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[2] | |
| Norepinephrine | 8-12mcg/min | 30 mcg/min | β1 direct effect | β1 and α1,2 effects | Less arrhythmias than Dopamine[2] | Increases MAP, coronary perfusion pressure, little β2 effects. | |
| Milrinone | 50mcg/kg x 10 min | 0.375-75mcg/kg/min | Direct influx of Ca2+ channels | Smooth muscle vasodilator | PDE Inhibitor which increases Ca2+ uptake by sarcolemma. No venodilatory activity | ||
| Phenylephrine | 100-180mcg/min then 40-60mcg/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 |
Other Therapies
- Transfusion
- Consider if Hb < 10
Specific Situations
- Mitral Regurg
- Need to increase forward flow
- Dobutamine (contractility)
- Nitroprusside (afterload reduction)
- MI
- PCI or thrombolysis
- 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)
- Nitropruside
- Dobutamine
- Hydralazine
- Toxins
See Also
Source
Tintinalli EMCrit Podcast 10