Cardiogenic shock: Difference between revisions
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==Background== | ==Background== | ||
*Leading cause of death in | *Leading cause of death in patients with [[ACS]] who reach the hospital alive | ||
=== | ===Etiologies=== | ||
*[[Myocardial infarction]] | *[[Myocardial infarction]] | ||
**Pump failure | **Pump failure | ||
**Mechanical complications | **Mechanical complications | ||
**Acute | **Acute [[mitral regurgitation]] (papillary muscle rupture) | ||
**VSD | **[[VSD]] | ||
**Free-wall rupture | **[[cardiac rupture|Free-wall rupture]] | ||
*RV infarction | *RV infarction | ||
*Decreased forward flow | *Decreased forward flow | ||
**[[Sepsis]] | **[[Sepsis]] | ||
**Rate-related | **Rate-related | ||
***Bradycardia | ***[[Bradycardia]] | ||
***Tachycardia | ***[[Tachycardia]] | ||
**[[Myocarditis]] | **[[Myocarditis]] | ||
**[[Myocardial contusion]] | **[[Myocardial contusion]] | ||
**Cardiomyopathy | **[[Cardiomyopathy]] | ||
*Mechanical obstruction to forward flow | *Mechanical obstruction to forward flow | ||
**[[Aortic stenosis]] | **[[Aortic stenosis]] | ||
**[[HOCM]] | **[[HOCM]] | ||
**[[Mitral stenosis]] | **[[Mitral stenosis]] | ||
**Pericardial | **[[pericardial effusion|Pericardial]] | ||
*LV regurgitation | *LV regurgitation | ||
**Chordal rupture | **Chordal rupture | ||
**Aortic | **[[Aortic Insufficiency]] | ||
*Toxic/metabolic | |||
**Severe [[acidosis]], severe hypoxemia | |||
==Clinical | ==Clinical Features== | ||
===Physical Exam=== | ===Physical Exam=== | ||
*Assess for signs of CHF | *Assess for signs of [[CHF]] | ||
**elevated JVD, pulmonary edema, S3 | **elevated JVD, pulmonary edema, S3 | ||
*Assess for valvular disease ( | *Assess for [[valvular disease]] ([[mitral regurgitation]], critical [[aortic stenosis]], or [[aortic regurgitation]]) | ||
*Assess | *Assess for end-organ hypoperfusion | ||
**cool/mottled extremities, weak pulses, | **cool/mottled extremities, weak pulses, [[altered mental status]], decreased UOP | ||
*Assess for pulsus paradoxus (cardiac tamponade) | *Assess for [[pulsus paradoxus]] ([[cardiac tamponade]]) | ||
== | ==Differential Diagnosis== | ||
{{Shock DDX}} | |||
==Evaluation== | |||
===Workup=== | |||
*Labs | *Labs | ||
**Troponin | **[[Troponin]] | ||
**Lactate | **Lactate | ||
**CBC | **CBC | ||
***WBC elevated with a left shift | |||
**Chem | **Chem | ||
** | **LFTs | ||
*** | ***elevated due to liver hypoperfusion | ||
*ECG | **[[ABG]] | ||
*CXR | ***[[anion gap acidosis]] | ||
*TTE | **[[BNP]] | ||
*[[ECG]] | |||
*[[CXR]] | |||
*[[Echocardiography|TTE]] | |||
== | {{BNP value}} | ||
==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 toxicity|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 | |||
*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: | |||
**[[Nitroprusside]] | |||
**[[Dobutamine]] | |||
**[[Hydralazine]] | |||
*Do not give preload reducers such as [[nitro]] | |||
*Patients are flow dependent over stenotic value. Flow proportional to degree of stenosis and afterload. | |||
====[[Toxins]]==== | |||
*[[Beta-Blocker Toxicity]] | |||
*[[Calcium Channel Blocker Toxicity|Calcium Channel Blocker]] | |||
*[[Digoxin Toxicity | Digoxin]] | |||
| | |||
| | |||
{{Vasopressor table}} | |||
== | ==Disposition== | ||
*Admission, frequently to intensive or higher-level of care | |||
==See Also== | ==See Also== | ||
Line 111: | Line 105: | ||
*[[Ultrasound in Shock and Hypotension]] | *[[Ultrasound in Shock and Hypotension]] | ||
== | ==External Links== | ||
*[http://emcrit.org/podcasts/cardiogenic-shock/ EMCrit Podcast – Cardiogenic Shock] | |||
*[http://www.emdocs.net/diagnosing-cardiogenic-shock-in-the-ed/ emDocs - Diagnosing Cardiogenic Shock in the ED] | |||
==Video== | |||
{{#widget:YouTube|id=GTZ8Zh8jPxA}} | |||
==References== | |||
<references /> | <references /> | ||
[[Category: | [[Category:Cardiology]] | ||
[[Category:Critical Care]] | [[Category:Critical Care]] |
Revision as of 12:03, 8 September 2021
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
Video
{{#widget:YouTube|id=GTZ8Zh8jPxA}}
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.