Undifferentiated shock: Difference between revisions
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{{Adult top}} [[undifferentiated shock]].''
{{AdultPage|undifferentiated shock}}
==Overview==
==Overview==
*Inadequate perfusion of the tissues
*Inadequate perfusion of the tissues

Revision as of 00:43, 16 January 2026

This page is for adult patients. For pediatric patients, see: undifferentiated shock

Overview

  • Inadequate perfusion of the tissues
  • Goal to increase the flow of oxygenated blood to the tissues
  • MAP<50 in dog studies brain will become ischemic and patients might presents as an altered mental status [1]

Undifferentiated Hypotension Algorithm[2]

Check/manage the following in order:

Algorithm for the Evaluation of Hypotension(By Dr. Ravi Morchi)
  • Pulse (assess based on patient's age)
    • Too slow or too fast (to the point where CO is affected)?
      • If so, HR is likely primary etiology of hypotension
      • Pace or cardiovert
  • Volume status
  • Contractility
  • Systemic Vascular Resistance
    • Pathologic vasodilation (decreased SVR) suggested by:
      • Warm extremities
      • Bounding pulse
    • Treated based on likely etiology of distributive shock (see below)

Differential Diagnosis

Shock

Evaluation

Shock index (SI)[3]

SI = HR / SBP

  • Used when HR and SBP do not predict severity of hypovolemia in early stages
  • May be used as secondary triage tool in mass casualty incidents[4]
  • 0.5-0.7 is normal
  • >0.70-0.75 for occult shock or requirement of life-saving intervention

Simple Shock Index (sSI) was recently proposed. Subtracting SBP from HR is a good SI substitute. Working with integers is easier than dividing them, improving value availability.[5]

Consider RUSH to CVS

Management

  • Treat underlying type

Vasopressors

Vasopressors may be initiated peripherally while central access is being obtained — do not delay for central line placement (SSC 2021).[6]

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)[7] 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[8]. 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)[9] Mild β₁ direct effect (+inotropy) Strong α₁ and α₂ vasoconstriction; β₁ effect Less arrhythmogenic than dopamine[8] 1st line for septic shock (SSC 2021)[6]. 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.[6]
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)[6]. Fixed dose — generally not titrated. May reduce the risk of atrial fibrillation vs. catecholamine-only regimens.[10] Avoid dose >0.04 U/min → risk of cardiac and mesenteric ischemia.
Methylene blue[11] 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)[12]. 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)

Causes of non-response to vasopressors[13]

See Also

External Links

References

  1. ↑ Plöchl, W, D J Cook, T A Orszulak, and R C Daly. 1998. Critical cerebral perfusion pressure during tepid heart operations in dogs. The Annals of thoracic surgery, no. 1. http://www.ncbi.nlm.nih.gov/pubmed/9692450
  2. ↑ Morchi R. Diagnosis Deconstructed: Solving Hypotensionin 30 Seconds. Emergency Medicine News. 2015.
  3. ↑ Levitan, Richard M. Fundamentals of Airway Management. 3rd ed. Irving, TX: Emergency Medicine Residents' Association, 2015.
  4. ↑ Vassallo J et al. Usefulness of the Shock Index as a secondary triage tool. J R Army Med Corps. 2015 Mar;161(1):53-7.
  5. ↑ Kamikawa Y, Hayashi H. Equivalency between the shock index and subtracting the systolic blood pressure from the heart rate: an observational cohort study. BMC Emergency Medicine. 2020 Dec;20:1-8.
  6. ↑ 6.0 6.1 6.2 6.3 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.
  7. ↑ 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.
  8. ↑ 8.0 8.1 De Backer D, et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM. 2010;363(9):779-789.
  9. ↑ Martin C, Papazian L, Perrin G, et al. Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? Chest. 1993;103(6):1826-31.
  10. ↑ 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.
  11. ↑ Pasin L, et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013;15(1):42-8.
  12. ↑ Khanna A, et al. Angiotensin II for the Treatment of Vasodilatory Shock. N Engl J Med. 2017;377(5):419-430.
  13. ↑ Anand Swaminathan, "Occult Causes of Non-Response to Vasopressors", REBEL EM blog, July 13, 2017. Available at: https://rebelem.com/occult-causes-of-non-response-to-vasopressors/.

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