Shock: Types & Management

Shock is acute circulatory failure causing inadequate tissue oxygen delivery relative to demand, leading to cellular hypoxia and, if unchecked, multi-organ failure and death. NEET PG loves the haemodynamic-profile table (CVP, cardiac output, SVR, SvO₂) and the drug-of-choice question — get those cold and this topic is high-yield gold.

Definition and core concept

Shock is not synonymous with hypotension. It is a state of cellular and tissue hypoxia due to reduced oxygen delivery, increased oxygen consumption, or inadequate oxygen utilisation. Hypotension is a late, unreliable sign — young patients compensate via tachycardia and vasoconstriction and can lose 30% of blood volume before systolic BP falls.

Oxygen delivery is the master equation:

$$DO_2 = CO \times CaO_2 = (HR \times SV) \times (1.34 \times Hb \times SaO_2 + 0.003 \times PaO_2)$$

Every shock state attacks one of these terms: preload (hypovolaemic), pump (cardiogenic), afterload/tone (distributive), or flow obstruction (obstructive).

High-yield: The earliest reliable clinical signs of shock are tachycardia, tachypnoea, narrowed pulse pressure, and altered mental status — not a low systolic BP. Lactate and base deficit are the best early biochemical markers of tissue hypoperfusion.

Classification — the four types

The Weil–Shubin classification recognises four mechanistic categories. Memorise their haemodynamic fingerprints.

Type	Mechanism	Examples	Key bedside clue
Hypovolaemic	Loss of intravascular volume	Haemorrhage, burns, vomiting/diarrhoea, DKA	Dry, cold, collapsed veins
Cardiogenic	Pump failure	Massive MI, arrhythmia, myocarditis, valve rupture	Raised JVP, pulmonary oedema, S3
Distributive	Pathological vasodilatation	Septic, anaphylactic, neurogenic	Warm peripheries (early), bounding pulse
Obstructive	Mechanical impedance to flow	Tension pneumothorax, cardiac tamponade, massive PE	Raised JVP + clear/quiet circulation

Haemodynamic profiles — the table examiners adore

This single table answers a huge share of MCQs. Learn the directions cold.

Parameter	Hypovolaemic	Cardiogenic	Distributive (septic)	Obstructive
CVP / preload	↓	↑	↓ or normal	↑
PCWP	↓	↑	↓ / normal	↓ (PE) / ↑ (tamponade)
Cardiac output	↓	↓	↑ (early "warm")	↓
SVR (afterload)	↑	↑	↓↓	↑
SvO₂ / ScvO₂	↓	↓	↑ (poor extraction)	↓
Skin	Cold, clammy	Cold, mottled	Warm (early) → cold (late)	Cold

High-yield: Distributive (septic) shock is the only type with a HIGH cardiac output and LOW SVR in its early "warm" phase, and a paradoxically HIGH mixed venous oxygen saturation (SvO₂) due to impaired peripheral oxygen extraction (cytopathic/mitochondrial dysfunction).

Mnemonic for cold vs warm shock: Cold = pump or tank problem (cardiogenic, hypovolaemic, obstructive → low CO, high SVR). Warm = pipe problem (distributive → high CO, low SVR, at least early).

Etiology and pathophysiology

Regardless of cause, shock progresses through recognisable stages:

1. Compensated (pre-shock) → baroreceptor-driven sympathetic surge: tachycardia, vasoconstriction, renin–angiotensin–aldosterone activation. BP maintained.
2. Decompensated (progressive) → compensation fails; hypotension, oliguria, lactic acidosis, confusion.
3. Irreversible (refractory) → cellular death, capillary leak, vasoplegia unresponsive to pressors; multi-organ dysfunction syndrome (MODS).

At the cell, oxygen lack forces a switch to anaerobic glycolysis → lactate accumulation → metabolic (high anion-gap) acidosis. The Na⁺/K⁺-ATPase pump fails, cells swell, lysosomes rupture, and inflammatory mediators (TNF-α, IL-1, IL-6, nitric oxide) flood the circulation, especially in sepsis. NO-driven vasoplegia explains pressor resistance in late septic shock.

Septic shock specifics

Sepsis = life-threatening organ dysfunction due to a dysregulated host response to infection. The Sepsis-3 definitions are heavily tested:

• Sepsis = suspected/confirmed infection + acute rise in SOFA ≥ 2.
• Septic shock = sepsis + need for vasopressors to keep MAP ≥ 65 mmHg AND lactate > 2 mmol/L despite adequate fluid resuscitation.
• qSOFA (bedside screen, ≥2 of 3): RR ≥ 22, altered mentation (GCS <15), SBP ≤ 100 mmHg.

High-yield: Septic shock by Sepsis-3 needs BOTH vasopressor-dependent hypotension and lactate >2 mmol/L after fluids. Lactate >2 alone or hypotension alone is not enough.

Anaphylactic shock

Type I IgE-mediated hypersensitivity → mast cell/basophil degranulation → histamine, tryptase, leukotrienes → massive vasodilatation, capillary leak, bronchospasm, angioedema. Common triggers: drugs (penicillins, NSAIDs, neuromuscular blockers — the commonest cause under anaesthesia), foods (nuts, shellfish), insect stings, latex, contrast.

Neurogenic shock

Spinal cord injury above T6 disrupts sympathetic outflow → unopposed vagal tone → hypotension WITH bradycardia (the giveaway) and warm, dry skin. Distinguish from spinal shock, which is a neurological phenomenon (transient flaccid areflexia below the lesion), not a circulatory one — a classic NEET trap.

High-yield: Hypotension + bradycardia + warm peripheries after trauma = neurogenic shock. Hypotension + tachycardia + cold peripheries after trauma = haemorrhagic (hypovolaemic) shock — always exclude bleeding first.

Clinical features

• General: tachycardia, hypotension (late), tachypnoea, oliguria (<0.5 mL/kg/hr), altered sensorium, prolonged capillary refill (>2 s), cool mottled skin (except warm distributive).
• Hypovolaemic/haemorrhagic graded by ATLS (see below).
• Cardiogenic: raised JVP, basal crepitations, gallop rhythm, cold sweaty skin, signs of underlying MI.
• Obstructive: raised JVP, pulsus paradoxus and muffled heart sounds (tamponade — Beck's triad: hypotension + raised JVP + muffled sounds); tracheal deviation, absent breath sounds, hyperresonance (tension pneumothorax).
• Anaphylactic: urticaria, angioedema, stridor, wheeze, abdominal cramps, often within minutes of exposure.

ATLS haemorrhage classes — high-yield numbers

Class	Blood loss	Blood loss %	Heart rate	BP	Mental state	Key marker
I	<750 mL	<15%	<100	Normal	Mildly anxious	Normal
II	750–1500 mL	15–30%	100–120	Normal (↓ pulse pressure)	Mildly anxious	Tachycardia + narrow PP
III	1500–2000 mL	30–40%	120–140	↓	Confused	First fall in SBP
IV	>2000 mL	>40%	>140	↓↓	Lethargic	Negligible urine

High-yield: The earliest change in haemorrhage is a narrowed pulse pressure (Class II) from a rising diastolic BP, not a drop in systolic. Systolic BP falls only in Class III (≥30% loss).

Diagnosis and investigations

Shock is a clinical diagnosis; investigations identify cause and guide therapy.

• Serum lactate — best marker of global hypoperfusion; trend it. Lactate clearance >10% guides resuscitation.
• ABG — high anion-gap metabolic acidosis, base deficit (severity marker).
• ScvO₂/SvO₂ — low in low-flow states; high in septic/cytopathic shock.
• POCUS/echocardiography — investigation of choice for rapidly distinguishing causes at the bedside: collapsed IVC (hypovolaemia), poor LV function (cardiogenic), pericardial effusion (tamponade), RV strain/dilatation (massive PE), hyperdynamic empty heart (distributive). The RUSH protocol ("pump, tank, pipes") is the structured approach.
• Cause-specific: ECG + troponin (cardiogenic/MI), cultures + procalcitonin + source imaging (septic), serum tryptase (anaphylaxis — peaks 1–2 h, mast-cell confirmation), CT pulmonary angiogram (PE), CXR/FAST (trauma).

Diagnostic flow: Recognise hypoperfusion → assess JVP/CVP → low CVP = hypovolaemic/distributive; high CVP = cardiogenic/obstructive → bedside echo to localise → treat cause + restore perfusion.

Management — principles and drugs of choice

Universal first steps

1. A-B-C + high-flow oxygen; secure airway if obar (GCS, anaphylaxis).
2. Two large-bore IV cannulae (14–16 G); send bloods including group & crossmatch, lactate.
3. Fluid challenge (except cardiogenic): balanced crystalloid (Ringer's lactate / Plasma-Lyte preferred over normal saline to avoid hyperchloraemic acidosis) — 30 mL/kg in septic shock within the first 3 hours, reassessed with dynamic measures (passive leg raise, IVC variation, stroke volume variation).
4. Target MAP ≥ 65 mmHg and reverse the cause.
5. Monitor urine output, lactate clearance, mentation.

High-yield: Balanced crystalloids (Ringer's lactate) are preferred first-line resuscitation fluid. Albumin is reserved for sepsis needing large volumes. Starches (HES) are contraindicated in sepsis (renal injury, mortality). Colloids confer no survival benefit over crystalloids.

Vasopressors and inotropes — drugs of choice

Drug	Receptors	Main effect	First choice in
Noradrenaline	α1 ≫ β1	Vasoconstriction, modest inotropy	Septic & most undifferentiated shock
Adrenaline	α + β1 + β2	Inotrope + vasopressor + bronchodilation	Anaphylaxis; second-line in septic
Vasopressin	V1 receptors	Pure vasoconstriction (catecholamine-sparing)	Add-on in septic shock
Dobutamine	β1 ≫ β2	Inotrope, mild vasodilatation	Cardiogenic; sepsis with low CO
Dopamine	Dose-dependent D/β/α	Variable	Largely abandoned (arrhythmias)
Phenylephrine	Pure α1	Vasoconstriction, reflex bradycardia	Niche (e.g., tachyarrhythmia, obstetric spinal hypotension)

High-yield (most-tested):

• First-line vasopressor in septic shock = NORADRENALINE.
• Second-line / add-on = VASOPRESSIN (fixed 0.03 U/min) to reduce noradrenaline dose; then adrenaline.
• Inotrope when cardiac output stays low despite adequate MAP = DOBUTAMINE.
• Dopamine is no longer recommended (Surviving Sepsis) due to tachyarrhythmias and higher mortality.

Specific management

Septic shock (Surviving Sepsis "Hour-1 Bundle"):

1. Measure lactate (remeasure if >2). 2. Obtain blood cultures before antibiotics. 3. Give broad-spectrum antibiotics within 1 hour. 4. 30 mL/kg crystalloid for hypotension or lactate ≥4. 5. Start noradrenaline if MAP <65 during/after fluids. Add low-dose hydrocortisone (200 mg/day) for refractory shock.

High-yield: Each hour of delay in appropriate antibiotics in septic shock measurably increases mortality. Cultures first, but never delay antibiotics beyond 1 hour to obtain them.

Anaphylactic shock — adrenaline is life-saving:

• Adrenaline 0.5 mg (0.5 mL of 1:1000) IM into the anterolateral thigh in adults, repeat every 5 min. IM is the route of choice; IV adrenaline only by experts in monitored peri-arrest settings.
• Remove trigger, high-flow O₂, IV fluids, supine with legs raised.
• Adjuncts (second-line, not substitutes): antihistamines (chlorphenamine), corticosteroids (hydrocortisone), bronchodilators (salbutamol). Glucagon if on beta-blockers and refractory.

High-yield: In anaphylaxis the drug of choice is IM adrenaline 1:1000 into the thigh — antihistamines and steroids are adjuncts and do NOT treat the acute airway/circulatory collapse.

Cardiogenic shock: Avoid large fluid boluses (worsen pulmonary oedema); cautious small challenges only if preload-dependent. Inotrope of choice dobutamine (± noradrenaline if hypotensive). Definitive: emergency revascularisation (PCI) for MI — the single most effective intervention. Mechanical support: intra-aortic balloon pump (limited evidence), Impella/ECMO in selected cases.

Obstructive shock: Treatment is relieving the obstruction:

• Tension pneumothorax → immediate needle decompression (2nd ICS mid-clavicular, or 5th ICS anterior axillary line) then chest drain.
• Cardiac tamponade → pericardiocentesis.
• Massive PE → thrombolysis (or embolectomy).

Neurogenic shock: Fluids first; vasopressors (noradrenaline/phenylephrine) for vasoplegia; atropine for symptomatic bradycardia. Maintain MAP to protect cord perfusion.

Complications

• Acute kidney injury (acute tubular necrosis) — the kidney is an early casualty.
• ARDS from capillary leak/inflammation.
• Disseminated intravascular coagulation (DIC) — especially septic shock.
• Ischaemic hepatitis ("shock liver") with transaminases in the thousands.
• Stress ulceration and gut ischaemia → bacterial translocation.
• Lactic acidosis, myocardial depression, and ultimately MODS and death.

Key differentials

• Hypotension without shock — vasovagal syncope, drug-induced, chronic well-compensated low BP (no hypoperfusion, normal lactate).
• Distinguishing the four shocks is the real differential exercise — use CVP/JVP + bedside echo as above.
• Sepsis vs cardiogenic when both hypotensive: warm + bounding + low diastolic + high CO favours sepsis; cold + raised JVP + pulmonary oedema favours cardiogenic.
• Neurogenic vs haemorrhagic in trauma (bradycardia vs tachycardia).
• Adrenal crisis and thyroid storm/myxoedema coma as endocrine mimics of distributive shock.

Recently asked / exam angle

• Single best vasopressor in septic shock? → Noradrenaline. (Repeatedly tested.)
• Mixed venous O₂ saturation is HIGH in which shock? → Septic/distributive (impaired extraction).
• Type of shock with low CVP + low CO + high SVR? → Hypovolaemic.
• Earliest sign of haemorrhagic shock / first ATLS class with hypotension? → narrowed pulse pressure (Class II); SBP first falls in Class III.
• Hypotension + bradycardia after spinal injury? → Neurogenic shock.
• Route and concentration of adrenaline in anaphylaxis? → IM, 1:1000, 0.5 mg thigh.
• Preferred resuscitation fluid / contraindicated fluid in sepsis? → balanced crystalloid; HES contraindicated.
• Sepsis-3 definition of septic shock (vasopressor + lactate >2) and qSOFA criteria.
• Beck's triad and management of tamponade (pericardiocentesis).
• Inotrope of choice in cardiogenic shock? → Dobutamine; definitive therapy = PCI.

Rapid revision

1. Shock = tissue hypoxia from inadequate O₂ delivery; hypotension is a late sign.
2. Four types: hypovolaemic, cardiogenic, distributive, obstructive.
3. High CO + low SVR + high SvO₂ = distributive (septic) shock — the unique profile.
4. Low CVP = hypovolaemic/distributive; high CVP = cardiogenic/obstructive.
5. Serum lactate is the best early marker; bedside echo (RUSH) localises the cause.
6. Septic shock = noradrenaline first, add vasopressin, then adrenaline; dopamine abandoned.
7. Dobutamine is the inotrope for cardiogenic shock / low-CO states.
8. Anaphylaxis → IM adrenaline 1:1000, 0.5 mg in the thigh; steroids/antihistamines are adjuncts.
9. Balanced crystalloid (RL) is first-line fluid; 30 mL/kg in septic shock; HES contraindicated.
10. Trauma: tachycardia + cold = haemorrhage; bradycardia + warm = neurogenic.
11. ATLS: narrowed pulse pressure in Class II, SBP falls only in Class III (≥30% loss).
12. Obstructive shock = relieve the obstruction (needle decompression / pericardiocentesis / thrombolysis); Sepsis-3 septic shock needs vasopressor + lactate >2.