Cardiogenic shock: Difference between revisions
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Revision as of 07:20, 18 February 2015
Background
- Leading cause of death in pts w/ MI who reach the hospital alive
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
- Aortic stenosis
- HOCM
- Mitral stenosis
- Pericardial
- LV regurgitation
- Chordal rupture
- Aortic insufficiency
Clinical Presentation
Physical Exam
- Assess for signs of CHF
- elevated JVD, pulmonary edema, S3
- Assess for valvular disease (MR, critical AS, or aortic regurgitation)
- Assess e/o end-organ hypoperfusion
- cool/mottled extremities, weak pulses, AMS, decreased UOP
- Assess for pulsus paradoxus (cardiac tamponade)
Work-Up
- Labs
- Troponin
- Lactate
- CBC
- Chem
- BNP
- <100 may rule-out cardiogenic shock
- ECG
- CXR
- TTE
Differential Diagnosis
Shock
- Cardiogenic
- Acute valvular Regurgitation/VSD
- CHF
- Dysrhythmia
- ACS
- Myocardial Contusion
- Myocarditis
- Drug toxicity (e.g. beta blocker, CCB, or bupropion OD)
- Obstructive
- Distributive
- Hypovolemic
- Severe dehydration
- Hemorrhagic shock (traumatic and non-traumatic)
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
