Cardiogenic shock
(Redirected from Cardiogenic Shock)
Background
- Leading cause of death in patients with ACS who reach the hospital alive
Etiologies
- Myocardial infarction
- Pump failure
- Mechanical complications
- Acute mitral regurgitation (papillary muscle rupture)
- VSD
- Free-wall rupture
- RV infarction
- Decreased forward flow
- Mechanical obstruction to forward flow
- LV regurgitation
- Chordal rupture
- Aortic Insufficiency
- Toxic/metabolic
- Severe acidosis, severe hypoxemia
Clinical Features
Physical Exam
- Assess for signs of CHF
- elevated JVD, pulmonary edema, S3
- Assess for valvular disease (mitral regurgitation, critical aortic stenosis, or aortic regurgitation)
- Assess for end-organ hypoperfusion
- cool/mottled extremities, weak pulses, altered mental status, decreased UOP
- Assess for pulsus paradoxus (cardiac tamponade)
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)
Evaluation
Workup
- Labs
- ECG
- CXR
- TTE
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
Management
General
Aim for MAP >65
- Consider etiologies (see above) and treat specific one, if present
- Consider small fluid challenge (250-500cc normal saline IV) or fluid removal, depending on estimation of patient's point on Starling curve
- Increase inotropy
- Dobutamine +/- norepinephrine OR dopamine
- Dobutamine may initially drop pressures, so may need to use second agent to maintain BP
- Consider milrinone or beta-blocker reversal if patient is on a beta-blocker
- Consider calcium chloride 1 g if hypocalcemic or normocalcemic through good PIV or central line
- Dobutamine +/- norepinephrine OR dopamine
- Consider transfusion if hemoglobin < 10 (be aware of added fluid)
- Consider intubation
- Decreases O2 demand BUT may worsen preload
Specific Situations
Mitral Regurgitation
Increase forward flow
- Dobutamine (contractility) + nitroprusside (afterload reduction)
ACS
- PCI or thrombolysis
Aortic stenosis
Decrease afterload (with extreme caution in very small, carefully-titrated doses)
- Agents:
- Do not give preload reducers such as nitro
- Patients are flow dependent over stenotic value. Flow proportional to degree of stenosis and afterload.
Toxins
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. | 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 |
Disposition
- Admission, frequently to intensive or higher-level of care
See Also
External Links
References
- ↑ 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.
- ↑ 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
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ https://www.ncbi.nlm.nih.gov/pubmed/8449087
- ↑ Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine
- ↑ 8.0 8.1 De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789
- ↑ https://www.ncbi.nlm.nih.gov/pubmed/15542956
- ↑ Pasin L et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013 Mar;15(1):42-8.