Critical Care Fundamentals: The Basics of Shock

Shock is one of the most important problems with which physicians will contend with. The magnitude of the problem is illustrated by the high mortality associated with shock. Assessment of perfusion is independent of arterial pressure, in that hypotension does not always need to be present to define shock. Emphasis in defining shock is based on tissue perfusion in relation to cellular function. In this post, the basics of shock, we will define shock, discuss the causes of lactate elevation, and review the main categories of shock.

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Shock occurs when supply does not meet demands and NOT defined by a blood pressure (patients may be normotensive, or even hypertensive in shock)

Lactate: Usually elevated in shock, but the classic belief that lactate is elevated because of anaerobic metabolism and tissue hypoxia is not the main reason. Lactate is produced in shock under aerobic conditions due to B2 adrenergic stimulation from elevated epinephrine levels. Lactate elevation doesn’t always mean a patient is in shock or has sepsis (although lactate is elevated in these conditions), but you must have a broad differential as lactate can be elevated for many additional reasons.

Cold Shock: Low SV state

Systolic Blood Pressure correlates with stroke volume

↓ SBP=↓SV

Determinants of SV: Preload, Contractility, and Afterload

Characterized by:

Tachycardia

Narrow Pulse Pressure (compensation by vasoconstriction and ↑SVR)

Cold to touch

↓peripheral pulses (later stages,↓ central pulses)

Delayed capillary refill

Categories of Cold Shock:

Cardiogenic Hypovolemic Obstructive

Warm Shock:↓Systemic vascular Resistance (ie Vasodilatory Shock)

↓ DBP=↓SVR

Characterized by:

Tachycardia

Wide Pulse Pressure

Warm to touch

Bounding peripheral pulses

Brisk capillary refill

Categories of Warm Shock: Just 1 Distributive Shock, but 5 main causes of Distributive Shock

Sepsis: Sepsis is unique and patients have components of hypovolemic shock and cardiogenic shock (Myocardial depression from circulating cytokines) Adrenal Insufficiency:↓Cortisol (up-regulates vascular tone ↓ catecholamine release) Anaphylaxis Hepatic failure: ↑ endogenous Nitric Oxide which is a potent vasodilator Neurogenic:↓ sympathetic output, and may have bradycardia due to unopposed vagal tone

Critical Care Education Curriculum

Basics of Shock – Educational Reinforcement Material

Basics of Shock – Supplemental Educational Material

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)