Guide — Critical Care
Shock Recognition & Management
Shock is failed oxygen delivery, not a single blood pressure number. This guide sorts the four categories — hypovolemic, cardiogenic, distributive, and obstructive — by their hemodynamic fingerprints, then frames where the respiratory therapist protects oxygenation and where positive-pressure ventilation can make things worse.
9 min read · Critical Care
Written by Apex Respiratory Editorial Team
Educational use only. This material supports respiratory therapy education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional protocols, or physician orders. Always follow facility policies and current provider orders, and verify calculations independently before clinical use.
Overview
Shock is inadequate tissue perfusion — oxygen delivery (DO₂) that falls short of metabolic demand — producing cellular hypoxia, anaerobic metabolism, and a rising lactate. It is a delivery problem at heart, and the delivery equation makes the failure modes explicit: DO₂ = CaO₂ × CO × 10, where the arterial oxygen content CaO₂ = (1.34 × Hb × SaO₂) + (0.003 × PaO₂).
Read that equation and the categories of shock organize themselves. Delivery can fail because flow collapses (low cardiac output in hypovolemic, cardiogenic, and obstructive shock) or because the blood that is delivered cannot be used (impaired extraction in distributive shock). For the respiratory therapist, the levers are on the content side — SaO₂ and, to a small degree, PaO₂ — and on the airway, where the same ventilation that supports the patient can undercut the flow side of the equation.
Key Concepts
Shock sorts into four categories by mechanism. Naming the mechanism points toward the cause — and, critically, toward whether fluids will help or harm.
| Category | Mechanism | Typical Causes |
|---|---|---|
| Hypovolemic | Loss of intravascular volume | Hemorrhage, GI/burn losses |
| Cardiogenic | Pump failure | MI, arrhythmia, decompensated heart failure |
| Distributive | Pathologic vasodilation | Sepsis, anaphylaxis, neurogenic |
| Obstructive | Mechanical obstruction to flow | Tension pneumothorax, cardiac tamponade, massive PE |
Each category carries a distinct hemodynamic profile across preload (CVP/PCWP), cardiac output, systemic vascular resistance (SVR), and mixed venous saturation (SvO₂). The single most useful discriminator is SVR paired with the skin exam: distributive shock is the warm, vasodilated, low-SVR state, while the other three are cold and vasoconstricted.
| Category | Preload (CVP/PCWP) | Cardiac Output | SVR | SvO₂ |
|---|---|---|---|---|
| Hypovolemic | ↓ | ↓ | ↑ | ↓ |
| Cardiogenic | ↑ | ↓ | ↑ | ↓ |
| Distributive | ↓ or normal | ↑ or normal | ↓ | ↑ early (impaired extraction) |
| Obstructive | ↑ (often) | ↓ | ↑ | ↓ |
Assessment & Findings
- Hypotension and a low MAP. A mean arterial pressure below 65 mmHg is the usual perfusion threshold, typically with tachycardia as the body defends cardiac output.
- Pulse pressure tells a story. A narrow pulse pressure points to a low-output, vasoconstricted state, while a wide pulse pressure fits the vasodilated distributive picture.
- End-organ signs. Altered mentation, oliguria, and prolonged capillary refill mark perfusion that has fallen below what the organs need.
- Skin temperature splits the categories. Cool, clammy skin accompanies hypovolemic, cardiogenic, and obstructive shock; warm skin in early distributive shock is the outlier worth noticing.
- Lactate and SvO₂. A rising lactate signals anaerobic metabolism, and a low SvO₂/ScvO₂ reflects high extraction from inadequate delivery — though SvO₂ runs high early in septic shock from impaired extraction.
- A falling EtCO₂. On capnography, end-tidal CO₂ tracks pulmonary blood flow, so a dropping EtCO₂ can be an early flag of falling cardiac output and perfusion.
RT Priorities / Interventions
The respiratory therapist defends the content side of oxygen delivery and the airway — and is positioned to catch the obstructive causes and the ventilation pitfalls that turn shock into arrest.
- Secure airway and oxygenation. Maximize SaO₂ to raise CaO₂ and therefore DO₂; oxygenation is the lever the RT most directly controls in a failing-delivery state.
- Respect positive-pressure physiology. Positive-pressure ventilation reduces venous return and can precipitate collapse in hypovolemic or obstructive shock; when time allows, volume-load and optimize hemodynamics before intubating.
- Monitor gases and lactate. Trend ABGs and lactate to gauge perfusion and the adequacy of resuscitation — interpret the gas with the ABG interpreter to keep the acid-base picture straight.
- Use capnography as a perfusion monitor. EtCO₂ tracks cardiac output and pulmonary blood flow, giving an early, continuous read on whether resuscitation is restoring perfusion.
- Assist access and resuscitation. Support vascular access and the resuscitation effort so volume and vasoactive therapy can be delivered without delay.
- Recognize RT-relevant obstructive causes. A tension pneumothorax is an obstructive shock the RT is well placed to spot — escalate immediately for decompression rather than treating the hypotension in isolation.
Common Pitfalls
- Intubating before resuscitating. Pushing positive pressure on a hypovolemic, under-resuscitated patient is the classic route to peri-intubation cardiovascular collapse. Volume first when the clock allows.
- Missing a tension pneumothorax. An obstructive shock that is reversible in seconds gets lethal when it is mistaken for another category — keep it on the differential for sudden hypotension on the ventilator.
- Over-aggressive positive pressure. High tidal volumes and pressures drop preload further; in a preload-dependent patient, gentler ventilation protects the very cardiac output you are trying to support.
- Fluids for every shock. Volume rescues hypovolemic and distributive states but worsens cardiogenic shock — flooding a failing pump is harmful, so the mechanism has to guide the resuscitation.
Board Exam Pearls
- Memorize the four categories with their CVP/CO/SVR/SvO₂ profiles — the table is the highest-yield thing to recall under stem pressure.
- The MAP target is ≥ 65 mmHg; a stem treating a MAP below that as acceptable perfusion is steering you wrong.
- Distributive shock is the warm one: high or normal cardiac output with a low SVR. If the picture is vasodilated and high-output, think distributive.
- SvO₂ runs high early in septic shock because the tissues cannot extract oxygen — a high mixed venous saturation here is impaired extraction, not good delivery.
- Know the obstructive causes — tension pneumothorax, cardiac tamponade, and massive PE — because the fix is to relieve the obstruction, not to chase the blood pressure.
FAQ
What defines shock?
Shock is inadequate tissue perfusion and oxygen delivery (DO₂) relative to metabolic demand, which produces cellular hypoxia and a rising lactate. It is a state of failed oxygen delivery, not a single blood pressure number — oxygen delivery equals the arterial oxygen content multiplied by cardiac output (DO₂ = CaO₂ × CO × 10), so it can fail through low content, low flow, or both.
How do the four shock categories differ hemodynamically?
Hypovolemic shock has low preload, low cardiac output, high systemic vascular resistance, and low mixed venous saturation. Cardiogenic shock has high preload, low cardiac output, high resistance, and low SvO₂. Distributive shock has low-to-normal preload, high-to-normal cardiac output, low resistance, and a high SvO₂ early from impaired oxygen extraction. Obstructive shock typically has high preload, low cardiac output, high resistance, and low SvO₂. The quick discriminator is resistance and skin: distributive is the warm, vasodilated, low-resistance state, while the other three are cold and vasoconstricted.
Why can intubating a patient in shock cause cardiac arrest?
Positive-pressure ventilation raises intrathoracic pressure and reduces venous return to the heart. In a patient who is already preload-dependent — hypovolemic or obstructive shock — that drop in venous return can collapse cardiac output the moment the breath is delivered, producing peri-intubation cardiovascular collapse. Volume-loading and optimizing hemodynamics before intubation, when time allows, blunts this effect.
Why is SvO₂ sometimes high in septic shock?
In early distributive shock from sepsis, the tissues cannot extract oxygen normally, so blood returns to the heart still carrying much of its oxygen and the mixed venous saturation reads high. A high SvO₂ here reflects impaired extraction at the cell, not generous delivery — it is the signature of distributive physiology rather than reassurance that perfusion is adequate.
Put it to work
Shock declares itself in the gas — a falling pH and a rising lactate with a base deficit. Run a set of values through the interpreter to read the acid-base picture behind a hypoperfused patient.
Open the ABG Interpreter →Related Resources
Sources
- Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-1734.
- Kacmarek RM, Stoller JK, Heuer AJ. Egan's Fundamentals of Respiratory Care. 12th ed. Elsevier; 2021. Hemodynamic monitoring and cardiovascular support chapters.