Difference between revisions of "Cardiogenic shock"

(Treatment)
(Etiologies)
 
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==Background==
 
==Background==
*Leading cause of death in pts w/ MI who reach the hospital alive
+
*Leading cause of death in patients with [[ACS]] who reach the hospital alive
  
==Work-Up==
+
===Etiologies===
*Labs
+
*[[Myocardial infarction]]
**Troponin
 
**Lactate
 
**CBC
 
**Chem
 
**BNP
 
***<100 may rule-out cardiogenic shock
 
*ECG
 
*CXR
 
*TTE
 
 
 
==Etiology==
 
*Myocardial infarction
 
 
**Pump failure
 
**Pump failure
 
**Mechanical complications
 
**Mechanical complications
**Acute MR (papillary muscle rupture)
+
**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
**AS
+
**[[Aortic stenosis]]
**HOCM
+
**[[HOCM]]
**Mitral stenosis
+
**[[Mitral stenosis]]
**Pericardial  
+
**[[pericardial effusion|Pericardial]]
 
*LV regurgitation
 
*LV regurgitation
 
**Chordal rupture
 
**Chordal rupture
**Aortic insufficiency
+
**[[Aortic Insufficiency]]
 +
 
 +
==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 DDX}}
 +
 
 +
==Evaluation==
 +
===Workup===
 +
*Labs
 +
**[[Troponin]]
 +
**Lactate
 +
**CBC
 +
**Chem
 +
**LFTs
 +
**[[BNP]]
 +
*[[ECG]]
 +
*[[CXR]]
 +
*[[Echocardiography|TTE]]
  
==DDX==
+
{{BNP value}}
*MI
 
*PE
 
*COPD exacerbation
 
*Peri/myocarditis
 
*Aortic dissection
 
*Pericardial tamponade
 
*Acute valvular insufficiency
 
*Sepsis
 
*Hemorrhage
 
*Toxins/drugs of abuse
 
  
==Treatment==
+
==Management==
*General
+
===General===
**Intubation
+
''Aim for MAP >65''
***Decreases O2 demand BUT may worsen preload
+
#Consider etiologies (see above) and treat specific one, if present
*Coronary perfusion
+
#Consider small fluid challenge (250-500cc normal saline IV) or fluid removal, depending on estimation of patient's point on Starling curve
#Small Fluid challenge
 
 
#Increase inotropy  
 
#Increase inotropy  
***Titrate to CO (e.g. warm extremities)
+
#*[[Dobutamine]] +/- [[norepinephrine]] '''OR''' [[dopamine]]
***Dobutamine or Milrinone - if  
+
#**[[Dobutamine]] may initially drop pressures, so may need to use second agent to maintain BP
****Use milrinone if pt is on BB
+
#**Consider [[milrinone]] or [[beta-blocker toxicity|beta-blocker reversal]] if patient is on a [[beta-blocker]]
***CaCl 1gm
+
#*Consider [[calcium chloride]] 1 g if hypocalcemic or normocalcemic through good PIV or central line
****Give if pt is hypocalcemic
+
#Consider [[transfusion]] if hemoglobin < 10 (be aware of added fluid)
#Achieve MAP >65
+
#Consider [[intubation]]
 +
#*Decreases O2 demand BUT may worsen preload
  
==Pressors==
+
===Specific Situations===
 +
====[[Mitral Regurgitation]]====
 +
''Increase forward flow''
 +
*[[Dobutamine]] (contractility) + [[nitroprusside]] (afterload reduction)
  
{| class="wikitable"
+
====[[ACS]]====
|-
+
*PCI or [[thrombolysis]]
! 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<ref>Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine</ref> 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<ref name="soap2">De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789</ref>
 
|-
 
| Norepinephrine || 8-12mcg/min || 30 mcg/min || β1 direct effect || β1 and α1,2 effects || Less arrhythmias than Dopamine<ref  name="soap2"></ref>  || Increases MAP, coronary perfusion pressure, little β2 effects.
 
|-
 
|Milrinone || 50mcg/kg x 10 min || 0.375-75mcg/kg/min || Direct influx of Ca<sup>2+</sup> channels|| Smooth muscle vasodilator ||  || PDE Inhibitor which increases Ca<sup>2+</sup> 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 ||
 
|}
 
  
*Transfusion
+
====[[Aortic stenosis]]====
**Consider if Hb < 10
+
''Decrease afterload (with extreme caution in very small, carefully-titrated doses)''
*Specific
+
*Agents:
**Mitral Regurg
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**[[Nitroprusside]]
***Need to increase forward flow
+
**[[Dobutamine]]
****Dobutamine (contractility)
+
**[[Hydralazine]]
****Nitroprusside (afterload reduction)
+
*Do not give preload reducers such as [[nitro]]
**MI
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*Patients are flow dependent over stenotic value.  Flow proportional to degree of stenosis and afterload.
***PCI or thrombolysis
+
 
**Tox
+
====[[Toxins]]====
***Reverse CCB, BB, or dig toxicity
+
*[[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 100: Line 99:
 
*[[Ultrasound in Shock and Hypotension]]
 
*[[Ultrasound in Shock and Hypotension]]
  
==Source==
+
==External Links==
Tintinalli
+
*[http://emcrit.org/podcasts/cardiogenic-shock/ EMCrit Podcast – Cardiogenic Shock]
EMCrit Podcast 10
+
 
 +
==Video==
 +
{{#widget:YouTube|id=GTZ8Zh8jPxA}}
 +
 
 +
==References==
 
<references />
 
<references />
[[Category:Cards]]
+
 
 +
[[Category:Cardiology]]
 +
[[Category:Critical Care]]

Latest revision as of 15:14, 27 September 2019

Background

  • Leading cause of death in patients with ACS who reach the hospital alive

Etiologies

Clinical Features

Physical Exam

Differential Diagnosis

Shock

Evaluation

Workup

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

  1. Consider etiologies (see above) and treat specific one, if present
  2. Consider small fluid challenge (250-500cc normal saline IV) or fluid removal, depending on estimation of patient's point on Starling curve
  3. Increase inotropy
  4. Consider transfusion if hemoglobin < 10 (be aware of added fluid)
  5. Consider intubation
    • Decreases O2 demand BUT may worsen preload

Specific Situations

Mitral Regurgitation

Increase forward flow

ACS

Aortic stenosis

Decrease afterload (with extreme caution in very small, carefully-titrated doses)

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 [7]. Also Increase SA and AV node fx indicated in decompensated systolic HF, Debut Research 1979[8] 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[9]
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) [10] mild β1 direct effect β1 and strong α1,2 effects Less arrhythmias than Dopamine[9] 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 0.4 U/min unknown increases via ADH peptide should not be titrated due to ischemic effects
Methylene blue[11] 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

References

  1. 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.
  2. 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
  3. 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.
  4. 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.
  5. 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.
  6. https://www.ncbi.nlm.nih.gov/pubmed/8449087
  7. Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine
  8. 9.0 9.1 De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789
  9. https://www.ncbi.nlm.nih.gov/pubmed/15542956
  10. Pasin L et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013 Mar;15(1):42-8.