Cardiogenic shock

(Redirected from Cardiovascular shock)

Background

  • Leading cause of death in patients with ACS who reach the hospital alive[1]

Etiologies

Clinical Features

Physical Exam

Differential Diagnosis

Shock

Evaluation

Workup


Brain natriuretic peptide (BNP)[3]

  • 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) [4]


NT-proBNP[5][6][7]

  • <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
  • 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

ACS

Aortic stenosis

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

Toxins

Vasopressors

Vasopressors may be initiated peripherally while central access is being obtained — do not delay for central line placement (SSC 2021).[8]

Pressor Initial Dose Max Dose Cardiac Effect BP Effect Arrhythmias Special Notes
Dobutamine 2-5 mcg/kg/min 20 mcg/kg/min (up to 40 in refractory cases)[9] Strong β₁ agonist (+inotrope, +chronotrope); weak β₂ agonist (+vasodilation) Minimal α effect; may decrease BP due to β₂ vasodilation Variable HR effects; can cause tachycardia Indicated in decompensated systolic CHF and cardiogenic shock with adequate BP. Not a vasopressor — it is an inotrope. Must be used with a vasopressor if hypotensive.
Dopamine 2-5 mcg/kg/min 20 mcg/kg/min β₁ and endogenous norepinephrine release Mixed α and β effects at all doses; α effects predominate at higher doses Arrhythmogenic from β₁ effects More adverse events (especially arrhythmia) when used in shock compared to norepinephrine[10]. SSC 2021 suggests against dopamine as first-line except in select patients with bradycardia and low risk of tachyarrhythmia.
Epinephrine 1-10 mcg/min (0.01-0.1 mcg/kg/min) 0.5 mcg/kg/min +Inotropy, +chronotropy (β₁) Low dose: β₂ vasodilation may predominate; high dose: α₁ vasoconstriction predominates Significant — tachycardia, SVT, VT. Increases myocardial O₂ demand. 2nd or 3rd line for septic shock (SSC 2021: add after norepinephrine ± vasopressin). 1st line for anaphylaxis (0.3-0.5 mg IM) and cardiac arrest. May cause splanchnic vasoconstriction, lactic acidosis, and hyperglycemia.
Norepinephrine 2-5 mcg/min (0.01-0.03 mcg/kg/min) 0.5-1 mcg/kg/min (some sources up to 3.3 mcg/kg/min)[11] Mild β₁ direct effect (+inotropy) Strong α₁ and α₂ vasoconstriction; β₁ effect Less arrhythmogenic than dopamine[10] 1st line for septic shock (SSC 2021)[8]. Increases MAP primarily via vasoconstriction. Increases coronary perfusion pressure. Minimal β₂ effect.
Milrinone 50 mcg/kg IV over 10 min (loading dose often omitted in acute illness due to hypotension risk) 0.375-0.75 mcg/kg/min PDE-3 inhibitor → ↑intracellular cAMP → ↑Ca²⁺ influx → +inotropy Arteriolar and venous vasodilator (reduces preload AND afterload) Less arrhythmogenic than dobutamine Inodilator — useful in decompensated HF with elevated afterload, RV failure, or pulmonary hypertension. Causes hypotension — not a vasopressor; use with a vasopressor if MAP is low. Renally cleared — dose-reduce in CKD.
Phenylephrine 100-180 mcg/min, then 40-60 mcg/min 0.4-9.1 mcg/kg/min No direct cardiac effect Pure α₁ agonist → vasoconstriction May cause reflex bradycardia Short duration of action (5-20 min IV). Use in septic shock only if: NE causes arrhythmias, cardiac output is high with persistent hypotension, or as salvage when NE + vasopressin have failed.[8]
Vasopressin 0.03 U/min (fixed dose) 0.04 U/min No direct inotropic or chronotropic effect; possible reflex bradycardia V₁ receptor agonist → vascular smooth muscle constriction Minimal 2nd line in septic shock — add to NE rather than escalating NE (SSC 2021 suggests adding before epinephrine)[8]. Fixed dose — generally not titrated. May reduce the risk of atrial fibrillation vs. catecholamine-only regimens.[12] Avoid dose >0.04 U/min → risk of cardiac and mesenteric ischemia.
Methylene blue[13] IV bolus 1-2 mg/kg over 15 min 1-2 mg/kg/hour (limited data on max duration) Possible increased inotropy; improves cardiac ATP utilization Inhibits NO-mediated peripheral vasodilation → increases SVR Minimal reported Salvage therapy for refractory vasodilatory shock unresponsive to catecholamines. Contraindicated in G6PD deficiency (hemolytic anemia), ARDS, severe pulmonary hypertension. Interferes with pulse oximetry readings (falsely low SpO₂). Avoid with serotonergic drugs (risk of serotonin syndrome).
Angiotensin II (Giapreza) 20 ng/kg/min 40-80 ng/kg/min (max 200 ng/kg/min per label) No direct cardiac effect AT₁ receptor agonist → potent arteriolar vasoconstriction; also stimulates aldosterone secretion Minimal Salvage therapy for refractory vasodilatory shock (ATHOS-3 trial)[14]. May be particularly useful in patients on ACEi/ARB or with high renin states. Monitor for thrombosis (increased risk reported).
Medication IV Dose (mcg/kg/min) Standard Concentration Final Concentration
Norepinephrine (Levophed) 0.01-2 mcg/kg/min 8 mg in 500 mL D5W 16 mcg/mL
Dopamine 2-20 mcg/kg/min 400 mg in 250 mL D5W 1,600 mcg/mL
Dobutamine 2-20 mcg/kg/min 250 mg in 250 mL D5W 1,000 mcg/mL
Epinephrine 0.01-1 mcg/kg/min 1 mg in 250 mL D5W 4 mcg/mL

Norepinephrine 2-5 mcg/min (0.01-0.03 mcg/kg/min), max 0.5-1 mcg/kg/min IV drip — 1st line for septic shock (SSC 2021) Epinephrine 1-10 mcg/min (0.01-0.1 mcg/kg/min), max 0.5 mcg/kg/min IV drip — 1st line for anaphylaxis and cardiac arrest Vasopressin 0.03 U/min (fixed dose), max 0.04 U/min IV drip — Add to NE rather than escalating NE (SSC 2021) Dopamine 2-5 mcg/kg/min, max 20 mcg/kg/min IV drip — SSC 2021 suggests against as 1st line; more arrhythmogenic than NE Dobutamine 2-5 mcg/kg/min, max 20 mcg/kg/min IV drip — Inotrope, not a vasopressor; use with vasopressor if hypotensive Phenylephrine 100-180 mcg/min, then 40-60 mcg/min IV drip — Pure alpha-1 agonist; short duration 5-20 min Milrinone 0.375-0.75 mcg/kg/min (loading often omitted) IV drip — Inodilator; causes hypotension; useful in RV failure/pulmonary HTN Methylene blue 1-2 mg/kg IV bolus over 15 min IV — Salvage for refractory vasodilatory shock; contraindicated in G6PD deficiency Angiotensin II (Giapreza) 20 ng/kg/min, max 40-80 ng/kg/min IV drip — Salvage for refractory vasodilatory shock (ATHOS-3 trial)

Disposition

  • Admission, frequently to intensive or higher-level of care

See Also

External Links

References

  1. ↑ Sarma D, Jentzer JC. Cardiogenic Shock: Pathogenesis, Classification, and Management. Crit Care Clin. 2024 Jan;40(1):37-56. PMID 37973356
  2. ↑ Tehrani BN, et al. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC Heart Fail. 2020 Nov;8(11):879-891. PMID 33121700
  3. ↑ 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.
  4. ↑ 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
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 8.0 8.1 8.2 8.3 Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063-e1143.
  9. ↑ Unverferth DV, Blanford M, Kates RE, Leier CV. Tolerance to dobutamine after a 72 hour continuous infusion. Am J Med. 1980;69(2):262-6.
  10. ↑ 10.0 10.1 De Backer D, et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM. 2010;363(9):779-789.
  11. ↑ Martin C, Papazian L, Perrin G, et al. Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? Chest. 1993;103(6):1826-31.
  12. ↑ McIntyre WF, et al. Association of Vasopressin Plus Catecholamine Vasopressors vs Catecholamines Alone With Atrial Fibrillation in Patients With Distributive Shock. JAMA. 2018;319(18):1889.
  13. ↑ Pasin L, et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013;15(1):42-8.
  14. ↑ Khanna A, et al. Angiotensin II for the Treatment of Vasodilatory Shock. N Engl J Med. 2017;377(5):419-430.
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