Surgery chapters
Shock: types, assessment and resuscitation
What shock is, the five types and how to tell them apart, the stages of severity and their signs, and how to resuscitate and monitor a shocked surgical patient.
- Shock is inadequate tissue perfusion for normal cell respiration; cells switch to anaerobic metabolism and make lactic acid.
- Five types: hypovolaemic (commonest), cardiogenic, obstructive, distributive (sepsis, anaphylaxis, neurogenic) and endocrine.
- Treat hypovolaemia first (fluid challenge), give vasopressors for distributive and inotropes for cardiogenic shock; guide by urine output, lactate and base deficit.
On this page
Overview
Shock is a body-wide state of tissue perfusion too low to support normal cellular respiration. Without enough oxygen and glucose, cells switch to anaerobic metabolism; if flow is not restored they die. Shock is the commonest and most important cause of death in surgical patients, either quickly from profound shock or later from organ failure after ischaemia–reperfusion injury.
This chapter covers the types, recognition and resuscitation of shock. Bleeding, haemorrhage classes and blood products are covered in the chapter on haemorrhage and blood transfusion.
Pathophysiology
Cellular
- Anaerobic metabolism produces lactic acid, not CO2 → metabolic acidosis.
- When glucose runs out, Na+/K+ pumps fail, lysosomes release enzymes and cells lyse, releasing potassium.
Microvascular
- Hypoxia and acidosis activate complement and prime neutrophils → oxygen radicals and cytokines.
- Endothelium is damaged and becomes leaky → tissue oedema → worse hypoxia.
Systemic responses
| System | Response |
|---|---|
| Cardiovascular | Baroreceptors → sympathetic drive → tachycardia and vasoconstriction (not in sepsis) |
| Respiratory | Faster breathing to blow off CO2 (compensatory respiratory alkalosis) |
| Renal | Lower GFR and urine output; renin–angiotensin–aldosterone activation |
| Endocrine | ADH (vasoconstriction, water retention), cortisol (Na+ and water retention, sensitises to catecholamines) |
Ischaemia–reperfusion syndrome
When blood flow returns, acid, potassium, activated neutrophils, complement and micro-thrombi are washed into the circulation. This causes myocardial depression, vasodilatation, and injury to the lungs and kidneys (ARDS, acute kidney injury), leading to multiple organ failure. The only way to limit it is to shorten the period of hypoperfusion.
Classification
| Type | Mechanism | Examples |
|---|---|---|
| Hypovolaemic | Low circulating volume | Haemorrhage; vomiting, diarrhoea, burns, third-space loss (bowel obstruction, pancreatitis) |
| Cardiogenic | Pump failure | MI, arrhythmia, valve disease, blunt cardiac injury, cardiomyopathy |
| Obstructive | Mechanical block to cardiac filling | Tension pneumothorax, cardiac tamponade, massive PE, air embolism |
| Distributive | Vasodilatation, low SVR | Sepsis, anaphylaxis (histamine), neurogenic (high spinal cord injury) |
| Endocrine | Hormone failure | Adrenal insufficiency (Addison's or relative in sepsis), hypothyroidism, thyrotoxicosis |
Hypovolaemia is the commonest type and is a component of all others. If unsure of the cause, assume hypovolaemia and give fluid, then judge the response.
Haemodynamic profile
| Measure | Hypovolaemic | Cardiogenic | Obstructive | Distributive |
|---|---|---|---|---|
| Cardiac output | Low | Low | Low | High |
| Vascular resistance | High | High | High | Low |
| Venous pressure (CVP) | Low | High | High | Low |
| Mixed venous O2 saturation | Low | Low | Low | High |
| Base deficit | High | High | High | High |
Only distributive shock is "upside down": high output, low resistance, warm hands, high SvO2. CVP separates the pump and plug problems (high) from the empty tank (low).
Distributive shock in more detail
- Septic: bacterial products (endotoxin) and immune activation; microvascular shunting and cells that cannot use oxygen. Early: warm peripheries, brisk capillary refill, bounding pulse, wide pulse pressure. Late: fluid leak into tissues and myocardial depression make it look hypovolaemic and cold.
- Anaphylactic: histamine-mediated vasodilatation and capillary leak.
- Neurogenic: cervical or upper thoracic cord injury removes sympathetic tone → hypotension with bradycardia or no tachycardia, warm skin, and no narrowing of pulse pressure.
An isolated head injury does not cause shock (unless the brainstem is involved). Look for bleeding elsewhere. In a spinal injury patient, treat as hypovolaemic first; neurogenic shock is a diagnosis made after bleeding is excluded.
Severity and clinical features
About 15% of blood volume can be lost within normal compensation. Blood pressure is usually kept up until about 30–40% is lost.
| Feature | Compensated | Mild | Moderate | Severe |
|---|---|---|---|---|
| Lactic acidosis | + | ++ | ++ | +++ |
| Urine output | Normal | Normal | Reduced (below 0.5 mL/kg/h) | Anuric |
| Conscious level | Normal | Mild anxiety | Drowsy | Comatose |
| Respiratory rate | Normal | Increased | Increased | Laboured |
| Pulse | Mild increase | Increased | Increased | Markedly increased |
| Blood pressure | Normal | Normal (narrow pulse pressure) | Mild hypotension | Severe hypotension |
- Compensated shock: only tachycardia and cool peripheries, yet skin, muscle and gut are underperfused with a hidden metabolic acidosis.
- Decompensation: renal, respiratory and cardiovascular failure as losses continue.
A fall in blood pressure comes late in shock. Earliest signs are tachycardia, cool skin and a narrowing pulse pressure.
Pitfalls in recognising shock
- Capillary refill varies widely in adults; it is brisk in septic shock despite severe shock.
- No tachycardia on β-blockers or with a pacemaker; a pulse of 80 is abnormal in an athlete whose normal is 50. Penetrating injury with little tissue damage may give a paradoxical bradycardia.
- Children and fit young adults hold their BP until very late.
- Elderly hypertensives may be shocked at a "normal" BP.
Consequences
- Unresuscitatable shock: after prolonged shock the heart and vessels stop responding to fluid, inotropes or vasopressors; death follows. Recognise futility.
- Multiple organ failure (MOF): two or more failed organ systems; treatment is supportive (ventilation, circulatory support, renal replacement). Lungs (ARDS), kidneys (acute kidney injury), clotting (coagulopathy), heart.
Resuscitation
Principles
- Airway and breathing first; high-flow oxygen.
- Circulation: do not wait for a definite diagnosis.
- Bleeding patients: large fluid volumes before stopping the bleeding raise BP, increase bleeding, cool the patient and dilute clotting factors → resuscitate in parallel with surgery.
- Non-bleeding patients (e.g. bowel obstruction): resuscitate fully before surgery.
Fluids
- Access: short, wide-bore peripheral cannulas. Long narrow central lines have high resistance and are better for monitoring than rapid infusion.
- Crystalloid (0.9% saline, Hartmann's, Ringer's lactate) and colloid give similar outcomes; colloid is dearer with more side effects, so crystalloid is preferred.
- Neither crystalloid nor colloid carries oxygen: blood loss is best replaced with blood.
- Dextrose solutions expand plasma volume poorly; do not use them to treat shock.
For resuscitating a dehydrated patient with peritonitis or obstruction, choose a balanced isotonic crystalloid (Ringer's lactate/Hartmann's) or 0.9% saline, never 5% dextrose.
The fluid challenge (dynamic response)
Give 250–500 mL quickly over 5–10 minutes and watch pulse, BP and CVP. Normally the CVP climbs by 2–5 cmH2O and then drifts back over 10–20 minutes.
| Response | Meaning | Action |
|---|---|---|
| Responder (sustained improvement) | Volume depleted but no ongoing loss | Continue filling to normal |
| Transient responder (improves then worsens in 10–20 min) | Moderate ongoing loss (bleeding or fluid shift) | Find and control the source |
| Non-responder | Severe depletion with major ongoing haemorrhage | Urgent surgery or embolisation |
A large sustained CVP rise suggests overload or cardiac insufficiency. A single CVP reading has no fixed "normal" in shock; use the trend.
Vasopressors and inotropes
| Drug type | Use |
|---|---|
| Vasopressors (noradrenaline, phenylephrine) | Distributive shock (sepsis, neurogenic) with low SVR |
| Vasopressin | Vasodilatation resistant to catecholamines (e.g. steroid deficiency) |
| Inotrope: dobutamine | Cardiogenic shock or septic shock with myocardial depression |
Never give inotropes or vasopressors to an empty heart. Correct hypovolaemia first, or the myocardium uses up its oxygen, coronary filling falls and the patient becomes unresuscitatable.
Monitoring
| Minimum | Additional |
|---|---|
| ECG (continuous heart rate) | Central venous pressure |
| Pulse oximetry | Invasive arterial pressure |
| Non-invasive blood pressure | Cardiac output monitoring (Doppler, pulse waveform) |
| Hourly urine output (catheter) | Base deficit and serum lactate, mixed venous O2 saturation |
Markers of organ perfusion
- Urine output is the best routine measure of organ perfusion (adult target 0.5 mL/kg/h; children 1 mL/kg/h; infants under 1 year 2 mL/kg/h).
- Conscious level is a poor guide: brain flow is preserved until late.
- Lactate and base deficit reflect gut and muscle perfusion. A base deficit over 6 mmol/L carries much higher morbidity and mortality.
- Mixed venous O2 saturation (SvO2): normal 50–70%. Below 50% = poor delivery, high extraction (hypovolaemic or cardiogenic). Above 70% = sepsis (cells cannot use oxygen). In sepsis aim to keep it above 70%.
End points of resuscitation
Normal pulse, BP and urine output show that brain, heart and kidneys are perfused, but the gut and muscle may still be starved. This is occult hypoperfusion: normal vital signs with persisting lactic acidosis and low SvO2. Lasting more than 12 hours it is linked with two to three times the mortality. Resuscitate to normal lactate and base deficit, not just normal vital signs.
70 kg adult, target 0.5 mL/kg/h
70 × 0.5 = 35 mL per hour
Over 4 hours: 35 × 4 = 140 mL expected
Expect: the definition of shock; classifying a scenario into hypovolaemic, cardiogenic, obstructive, distributive or endocrine shock; the haemodynamic table (high output and low SVR in sepsis, high CVP in tamponade and tension pneumothorax); neurogenic shock with bradycardia; the order in which signs appear and hypotension as a late sign; choice of fluid; fluid challenge responses; when to use dobutamine versus noradrenaline; urine output targets; SvO2, lactate and base deficit; and occult hypoperfusion.
Quick revision
- Shock = inadequate tissue perfusion → anaerobic metabolism → lactic acidosis.
- Types: hypovolaemic (commonest), cardiogenic, obstructive, distributive, endocrine.
- BP falls after 30–40% loss; tachycardia, cool skin and narrow pulse pressure come first.
- Septic shock: warm, high output, low SVR, SvO2 above 70%.
- Neurogenic: hypotension without tachycardia; exclude bleeding first.
- Wide-bore short cannulas; crystalloid first; blood for blood loss; no dextrose for shock.
- Fluid bolus 250–500 mL; transient and non-responders are still bleeding.
- Fill before pressors; dobutamine for pump failure; noradrenaline for vasodilatation.
- Urine output 0.5 mL/kg/h; base deficit over 6 is bad; occult hypoperfusion over 12 h raises mortality.
Written by The House Job from standard references (Bailey & Love's Short Practice of Surgery, 27th edition; ATLS Student Course Manual, 10th edition).
FAQ
What is the commonest type of shock in surgical practice?
Hypovolaemic shock, usually from haemorrhage; some hypovolaemia is present in nearly every type of shock.
Why is blood pressure a poor early sign of shock?
Vasoconstriction and a rising heart rate keep the pressure normal until roughly a third of blood volume is lost, especially in the young.
How does septic shock differ from hypovolaemic shock at the bedside?
Early septic shock gives warm peripheries, a bounding pulse and a high cardiac output with low vascular resistance, while hypovolaemic shock gives cold, clammy peripheries and a low output.
What is a transient responder?
A patient whose vital signs improve after a fluid bolus but worsen again within 10–20 minutes, meaning ongoing loss that needs source control.
What does a mixed venous saturation above 70% suggest in shock?
Distributive shock, especially sepsis, where tissues fail to extract and use oxygen.