Shock is DO2/VO2 mismatch | Shock ≠ Hypotension, although hypotension is often present during shock
Shock = inadequate oxygen delivery (DO₂) or utilisation (VO₂) relative to cellular metabolic demand, leading to cellular energy failure. MAP may be low, normal, or high at presentation. A normal or elevated BP does not exclude shock. Tissue hypoperfusion must be sought independently of haemodynamics.
Shock = inadequate oxygen delivery (DO₂) or utilisation (VO₂) relative to cellular metabolic demand, leading to cellular energy failure. MAP may be low, normal, or high at presentation. A normal or elevated BP does not exclude shock. Tissue hypoperfusion must be sought independently of haemodynamics.
IS SHOCK PRESENT?
Shock is confirmed when any 2 of the following 3 categories are positive. Category A (clinical hypoperfusion) + Category B (metabolic evidence) = cryptic / compensated shock — requires intervention even when Category C (haemodynamics) is normal. The classic teaching that shock = hypotension is a harmful oversimplification.
CATEGORY A — Clinical Hypoperfusion (any 1)
- CRT > 2 s (central sternum preferred)
- Core–periphery gradient > 4°C
- Mottling score ≥ 2 (Ait-Oufella)
- Altered consciousness (agitation, confusion, obtundation)
- Oliguria < 0.5 mL/kg/hr
- Cold, pale, clammy skin (vasoconstricted phenotype)
- Small SpO₂ waveform / ↓PPI
CATEGORY B — Metabolic Evidence (any 1)
- Lactate > 2 mmol/L (regardless of BP)
- Lactate > 4 mmol/L = overt shock; same mortality as hypotensive shock
- Base excess < −4 mEq/L
- ScvO₂ < 65% (CVC, not PA catheter)
- Rising lactate trend despite resuscitation (clearance <10%/2h)
- pH < 7.35 + metabolic component
CATEGORY C — Haemodynamic Instability (any 1)
- MAP < 65 mmHg (absolute)
- MAP fall > 15–20% from patient baseline (relative hypotension)
- HR > 100 bpm (sustained, unexplained)
- Pulse pressure < 25 mmHg
- ETCO₂ < 30 mmHg (intubated, no resp alkalosis)
- Vasopressor dependence to maintain MAP ≥ 65
THE SHOCK SPECTRUM — Normal or High BP does NOT exclude shock
Pre-shock
Normal vitals
Mild ↑lactate
Normal vitals
Mild ↑lactate
Compensated
Normal MAP
↑SVR, ↑HR
Normal MAP
↑SVR, ↑HR
Cryptic
Normal MAP
Lactate >4
Normal MAP
Lactate >4
Decompensated
↓MAP, organ failure
↑↑lactate
↓MAP, organ failure
↑↑lactate
Irreversible
Refractory
Cardiac arrest
Refractory
Cardiac arrest
Why MAP can be normal or high in shock:
① Compensated: Young patient with ↑SVR + ↑HR maintaining BP while CO falls; Class II haemorrhage (750–1500 mL) — normal BP, tachycardia only.
② Relative hypotension: Hypertensive patient (baseline MAP 100 mmHg) with MAP 72 — clinically hypotensive despite "normal" value.
③ Cryptic septic shock: Seymour et al. (2012): ~28% of septic shock patients had initial MAP ≥ 65. Lactate > 4 with normal BP = identical 28-day mortality to hypotensive sepsis (Jones et al., 2010).
④ Early distributive: High CO with ↓SVR + ↓viscosity can maintain MAP until compensation exhausted; lactate rises before MAP falls.
⑤ Pressor-dependent normotension: Normal MAP exists only because of vasopressors — vasopressor requirement = shock by definition.
① Compensated: Young patient with ↑SVR + ↑HR maintaining BP while CO falls; Class II haemorrhage (750–1500 mL) — normal BP, tachycardia only.
② Relative hypotension: Hypertensive patient (baseline MAP 100 mmHg) with MAP 72 — clinically hypotensive despite "normal" value.
③ Cryptic septic shock: Seymour et al. (2012): ~28% of septic shock patients had initial MAP ≥ 65. Lactate > 4 with normal BP = identical 28-day mortality to hypotensive sepsis (Jones et al., 2010).
④ Early distributive: High CO with ↓SVR + ↓viscosity can maintain MAP until compensation exhausted; lactate rises before MAP falls.
⑤ Pressor-dependent normotension: Normal MAP exists only because of vasopressors — vasopressor requirement = shock by definition.
PARAMETERS REVIEW
Parameters
✓ History & Context
Surgical, cardiac, septic, anaphylactic, neuraxial, PE risk, spine injury triggers
✓ CRT (Capillary Refill Time)
Central (sternal) preferred. >2 s = abnormal. ANDROMEDA-SHOCK endpoint.
✓ SpO₂ Waveform / PPI
Plethysmograph amplitude and variability; reflects perfusion index and SV
✓ MAP Trend
Absolute value AND trend from patient baseline; relative hypotension matters
✓ Core–Periphery Temperature Gradient
>4°C = vasoconstricted; <2°C = vasodilated. Forehead vs fingertip.
✓ POCUS
RUSH exam (Pump / Tank / Pipes) — see Tab 04 for full protocol
✓ ABG (incl. lactate, pH, BE, Hb, PaO₂, PaCO₂)
Metabolic evidence of shock; lactate is primary. Hb for rheological ↓SVR.
✓ PPV (when criteria met)
Valid only under strict conditions — see Fluids tab checklist
✓ Passive Leg Raise (PLR) ★ MOST IMPORTANT ADDITION
Superior to PPV: valid in spontaneous breathing, arrhythmias, ARDS. AUC 0.95. Reversible. Assess at 60–90 s.
✓ Lactate / Lactate Clearance (explicit)
Cornerstone of shock identification. >2 = occult shock. Clearance <10%/2h = failure to resuscitate.
✓ Mottling Score (distinct from CRT)
Grade 0–5. Score ≥3 = independent predictor of 14-day mortality (Ait-Oufella, CCM 2011).
✓ ECG
Essential for cardiogenic differentiation: STEMI, RV strain (S1Q3T3/new RBBB in PE), bradyarrhythmia (neurogenic).
✓ Urine Output
Renal end-organ perfusion. <0.5 mL/kg/hr = oliguria. <0.2 = severe. Part of SOFA organ failure scoring.
✓ ETCO₂ (if ventilated)
Low ETCO₂ (esp. sudden fall) reflects ↓pulmonary blood flow (↓CO or massive PE). Inversely correlates with dead space.
✓ ScvO₂ (if CVC — no SwanGanz needed)
<65% = ↑O₂ extraction (↓DO₂ or ↑VO₂). >75% = ↓O₂ utilisation (distributive/septic). ~5% higher than mixed SvO₂.
✓ Auscultation (S3/S4, bilateral crepitations, absent BS)
S3 = cardiogenic. Bilateral crepitations = pulmonary oedema. Absent unilateral breath sounds = tension PTX.
Phenotype Prediction: Select the clinical finding most closely matching your patient for each parameter. The calculator applies a weighted evidence-based scoring matrix to estimate phenotype likelihood. Mixed shock is common — scores within 4 points of the leader are flagged. Clinical gestalt always supersedes.
Phenotype Probability
Interpretation
Select findings to generate phenotype prediction.
PHENOTYPE RAPID REFERENCE TABLE — All parameters by phenotype
| Parameter | Hypovolaemic | Cardiogenic | Distributive | Obstructive | Neurogenic |
|---|---|---|---|---|---|
| Heart Rate | ↑↑ | ↑/N/↓* | ↑↑ | ↑↑ | ↓↓ (bradycardia) |
| MAP | ↓↓ | ↓↓ | N → ↓ | ↓↓ | ↓ |
| Pulse Pressure | ↓↓ (narrow) | ↓↓ | ↑↑ (wide) | ↓ | Wide (NE absent) |
| CRT | >3 s | >3 s | <2 s (warm) | >3 s | <2 s (warm) |
| Skin temp | Cold, pale, clammy | Cold, clammy | Warm, flushed | Cold (PE) / varies | Warm, dry |
| Core–periph gradient | >6°C | >6°C | <2°C | >4°C (PE) | <2°C |
| Mottling score | 2–5 | 2–5 | 0–1 | 1–3 | 0–1 |
| SpO₂ waveform / PPI | Small, low amp | Small, low amp | Large, bounding | Variable | Normal/large |
| PPV (if valid) | >13% (responsive) | <9% | Often >13% early | <9% (PE/tampo) | Variable |
| PLR response | Positive (>10%) | Negative | Often positive | Negative | Variable |
| POCUS LV | Small, hyperdynamic | Dilated, ↓↓ EF | Normal/hyperdynamic | Normal / compressed (tampo) | Normal |
| POCUS RV | Normal/small | N / dilated (RV MI) | Normal | Dilated (>1.0 RV:LV) McConnell | Normal |
| POCUS IVC | Collapsed, >50% var | Distended, flat | Collapsible (early) | Distended flat (PE/tampo) | Variable |
| POCUS Lung | A-lines | B-lines bilateral | A-lines (sepsis) | Absent sliding (PTX) / A-lines (PE) | A-lines |
| POCUS FAST | +ve (haemorrhage) | Negative | Negative | Pericardial effusion (tampo) | Negative |
| Lactate | ↑↑ (Type A) | ↑↑ (Type A) | ↑ (A+B) | ↑ (Type A) | N initially |
| Base excess | <–6 | <–6 | –4 to –8 | <–6 | Normal |
| ScvO₂ | <65% | <65% | >75% | <65% | Normal |
| ETCO₂ (ventilated) | ↓ (↓CO) | ↓ (↓CO) | N / ↑ (↑CO) | ↓↓ sudden fall (PE) | Normal |
| ECG | Sinus tachy | STEMI/new LBBB/STdep | Sinus tachy | S1Q3T3/RBBB (PE) | Brady/AV block |
| Urine output | Oliguria/anuria | Oliguria/anuria | Oliguria (late) | Oliguria | Often preserved |
| JVP / CVP | ↓↓ Flat | ↑↑ Elevated | N / ↓ | ↑↑ Elevated | Normal/↓ |
| Auscultation | Clear / quiet | S3, bilateral creps | Clear or focally infected | Absent BS (PTX) / normal (PE/tampo) | Clear |
* ↓HR in cardiogenic = RV infarction + high neuraxial block / associated bradyarrhythmia. BS = breath sounds. Tampo = tamponade. PTX = pneumothorax.
Core principle: Fluid responsiveness = ↑CO >10–15% in response to ↑preload. ~50% of haemodynamically unstable ICU patients are NOT fluid-responsive. Indiscriminate fluid loading in non-responsive patients causes harm (lung oedema, abdominal hypertension, dilutional coagulopathy). Always assess responsiveness before giving fluid.
PPV — VALIDITY CRITERIA CHECKLIST (ALL must be met)
PPV measures respiratory variation in arterial pulse pressure. It is only valid as a fluid responsiveness predictor when all 8 criteria are satisfied. Even one unmet criterion invalidates the measurement. When criteria are not met, use PLR instead.
⚠ PPV INVALID — Not all criteria met. Use Passive Leg Raise.
PPV Thresholds (when valid): <9% = non-responsive | 9–13% = grey zone | >13% = fluid-responsive (Sens 88%, Spec 90%; Marik et al. meta-analysis, CCM 2009)
PASSIVE LEG RAISE (PLR) — Preferred universally applicable test
PLR recruits ~300 mL of venous blood from the lower limbs — a reversible autotransfusion. Unlike PPV, it is valid in spontaneous breathing, arrhythmias, low Vt ventilation (ARDS), and right heart failure. Superiority: AUC 0.95 (Monnet et al. meta-analysis, CCM 2016). Measure CO response (LVOT VTI by POCUS or pulse pressure) at 60–90 seconds — the effect is maximal and transient.
01
Starting position: Patient semi-recumbent at 45°
Note baseline: measure LVOT VTI (POCUS), or pulse pressure on arterial line, or MAP. Record all three if available.
02
Manoeuvre: Lower head to flat + raise legs to 45°
Do this in one smooth movement (tilt the bed or manually). Both components are necessary. Head-down alone is insufficient. Start timer
03
Measure at 60–90 secondsPeak effect
Reassess LVOT VTI by POCUS (preferred), or pulse pressure (arterial line), or MAP. Real-time continuous CO monitoring ideal but not required.
04
Interpret: Positive = ↑CO or ↑PP > 10%
Positive PLR → fluid-responsive → consider fluid challenge 250 mL crystalloid with reassessment. Negative → fluid loading unlikely to improve CO; consider vasopressors / inotropes.
05
Return to semi-recumbent position
Haemodynamic effect is fully reversible — no fluid commitment. This is the critical advantage over a fixed fluid challenge.
PLR Limitations: Intra-abdominal hypertension (IAP >12) impairs venous return augmentation from legs. Lower limb compartment syndrome / vascular obstruction. Active haemorrhage (legs may be exsanguinated). Head trauma (avoid head-flat position).
| PPV | PLR | |
|---|---|---|
| Spontaneous breathing | ❌ Invalidates | ✓ Valid |
| Cardiac arrhythmia (AF/ectopics) | ❌ Invalidates | ✓ Valid |
| Low Vt ventilation (ARDS, ≤6 mL/kg) | ❌ Invalidates | ✓ Valid |
| Right heart failure | ❌ Invalidates | ✓ Valid |
| Open chest / sternotomy | ❌ Invalidates | ✓ Valid |
| No arterial line | ❌ Not measurable | ✓ POCUS VTI or PP |
| Fluid commitment required | None | None (reversible) |
| Equipment | Arterial line required | POCUS (preferred) or CW Doppler |
| Evidence AUC | 0.94 (when valid) | 0.95 (universal) |
RUSH Exam: Rapid Ultrasound in Shock and Hypotension (Perera et al., J Emerg Med 2010). Systematic 3-domain assessment — Pump, Tank, Pipes — integrates cardiac, volume, and vascular findings to narrow phenotype. Target completion <3 minutes at bedside.
PUMP — Cardiac
Views: Subcostal 4-chamber (quickest in ICU/OT), Parasternal long/short, Apical 4-chamber. Assess pericardium, LV size/function, RV size/function.
Pericardial effusion + RA/RV diastolic collapse O
Tamponade. Confirm IVC distension (flat IVC). RA collapse first (sensitive), RV collapse specific. Pulsus paradoxus >10 mmHg.
LV small, hypercontractile — "kissing walls" H
Hypovolaemia. Severely underfilled LV. EF appears very high. IVC collapsed. Correlates with ↓LVEDV.
LV dilated, globally reduced function (EF <30%) C
Cardiogenic shock. Regional wall motion abnormality → ischaemic aetiology. Global = dilated CMP or myocarditis. IVC distended.
LV hyperdynamic (EF >65-70%), normal size D
Distributive / high-output (sepsis, anaphylaxis, early distributive). High CO, low SVR. LV ejecting vigorously with ↓afterload.
RV dilation (RV:LV ratio >1.0 in apical 4C) O
Acute cor pulmonale. PE (most common cause), tension PTX, ARDS. Septal D-sign in PLAX: LV compressed. ↑RV:LV = severe.
McConnell sign (RV free wall hypokinesis, apex contracts) O
Highly specific for acute PE (Sp ~94%). RCA perfusion cut off by obstructed RV outflow → free wall ischaemia. Apex spared (LV dragging effect).
TANK — Volume Status
IVC view (subcostal long axis), Lung zones (2–4 per side: anterior, lateral), FAST (Morrison's, splenorenal, suprapubic, subxiphoid).
IVC collapsed <1.5 cm + >50% inspiratory variation HD
Low RAP / hypovolaemia. Fluid-responsive state likely. Note: spontaneous breathing increases IVC variation (sniff test) — less reliable than PPV on controlled MV.
IVC distended >2.1 cm + <50% variation (flat IVC) CO
Elevated RAP (cardiogenic, tamponade, PE, tension PTX). Fluid loading will not improve CO; likely harmful. Tamponade: also see pericardial effusion + RA collapse.
Bilateral B-lines ≥3 per zone in ≥2 bilateral zones C
Interstitial-alveolar pulmonary oedema (cardiogenic most common). B-lines arise from thickened subpleural septa (Kerley B equivalent). Bilateral = high LV filling pressure.
Absent lung sliding (with A-lines) O
Pneumothorax until proven otherwise. Confirm with absent "seashore sign" on M-mode ("barcode sign"). Check contralateral for comparison. Tension PTX = haemodynamic collapse + absent sliding.
Free fluid in FAST windows H
Haemoperitoneum (abdominal trauma, ruptured viscus, surgical bleeding) or haemothorax. Positive FAST in haemodynamic instability = immediate surgical consult. Hepatorenal space most sensitive (Morrison's pouch).
Bilateral pleural effusions C
Cardiogenic oedema (often bilateral, dependent). Distinguish from haemothorax by homogeneous vs complex appearance and clinical context.
PIPES — Vascular
Aorta (parasternal long, mid/lower abdominal), DVT (femoral + popliteal compression), carotid/jugular if needed.
Abdominal aortic aneurysm (AAA) >3 cm H
Ruptured AAA: haemodynamic collapse + pulsatile mass + AAA on POCUS. Do not delay surgical transfer for formal CT in haemodynamically unstable patient.
Non-compressible femoral / popliteal vein O
DVT — raises PE probability in context of acute haemodynamic collapse. Leg vein compression (2-point) adds significantly to POCUS PE diagnosis. Absence of DVT does not exclude PE.
LVOT VTI assessment for PLR / fluid challenge response
Apical 5-chamber view + PW Doppler at LVOT. VTI = velocity-time integral = stroke volume surrogate. ↑VTI >10-15% with PLR = fluid-responsive. Requires practice but no SwanGanz.
Distended, non-pulsatile jugular veins CO
Elevated venous pressure → cardiogenic or obstructive (PE, tamponade, tension PTX). Combined with low MAP, elevated JVP = obstructive phenotype until proven otherwise.
POCUS PHENOTYPE DECISION PATHWAY
Hypovolaemic pattern:
LV small + hyperdynamic · IVC collapsed · A-lines · FAST+ or negative · No effusion · Cold skin
LV small + hyperdynamic · IVC collapsed · A-lines · FAST+ or negative · No effusion · Cold skin
Cardiogenic pattern:
LV dilated + ↓EF · IVC flat · Bilateral B-lines · ± Bilateral pleural effusion · Elevated JVP · Cold skin
LV dilated + ↓EF · IVC flat · Bilateral B-lines · ± Bilateral pleural effusion · Elevated JVP · Cold skin
Distributive pattern:
LV hyperdynamic · IVC variable/collapsible · A-lines · Warm skin · Wide PP · ↑ScvO₂
LV hyperdynamic · IVC variable/collapsible · A-lines · Warm skin · Wide PP · ↑ScvO₂
Obstructive pattern:
RV dilated (McConnell for PE) · IVC flat · Pericardial effusion + RA collapse (tamponade) · Absent sliding (PTX) · Elevated JVP
RV dilated (McConnell for PE) · IVC flat · Pericardial effusion + RA collapse (tamponade) · Absent sliding (PTX) · Elevated JVP
Neurogenic pattern:
Normal POCUS · Bradycardia + warm skin · Low MAP · Normal IVC variability · History of spinal / high neuraxial block
Normal POCUS · Bradycardia + warm skin · Low MAP · Normal IVC variability · History of spinal / high neuraxial block
Evidence basis: All diagnostic parameters, thresholds, and management recommendations in this tool are referenced to landmark trials and systematic reviews. Key trials are listed below. Where evidence is inferential or extrapolated, this is noted.
LANDMARK TRIALS & EVIDENCE
| Trial / Study | Finding | Clinical Implication |
|---|---|---|
| ANDROMEDA-SHOCKHernandez et al. JAMA 2019;321:654 | CRT-guided resuscitation non-inferior to lactate-guided for 28-day mortality in septic shock. CRT arm: fewer organ dysfunction events. | CRT is a validated resuscitation endpoint. CRT normalisation ≤2 s is a clinically meaningful target, not merely a triage sign. |
| Cryptic Septic ShockSeymour et al. Crit Care Med 2012;40:2012 | ~28% of septic shock patients had initial MAP ≥65 mmHg. Lactate >4 with normal BP had similar 28-day mortality to hypotensive septic shock. | Normal BP does not exclude septic shock. Lactate must be checked in all suspected shock patients regardless of MAP. |
| Jones et al. (Lactate)Jones AE et al. JAMA 2010;303:739 | Lactate clearance ≥10% over 2 hours non-inferior to ScvO₂-guided resuscitation as a resuscitation target. | Serial lactate measurement is the primary metabolic resuscitation endpoint. Single value less important than trend. |
| PLR Meta-analysisMonnet X et al. CCM 2016;44:981 | PLR AUC 0.95 for predicting fluid responsiveness across all ventilation modes and arrhythmias. Sensitivity 85%, specificity 91%. | PLR is the most universally applicable fluid responsiveness test. Preferred over PPV in most perioperative settings. |
| PPV Meta-analysisMarik PE et al. CCM 2009;37:2642 | PPV >13%: Sensitivity 88%, Specificity 90% for fluid responsiveness when strict criteria met. AUC 0.94. | PPV is highly accurate only when all validity criteria are satisfied. Below-threshold Vt, spontaneous breathing, or arrhythmia invalidates it. |
| Mottling ScoreAit-Oufella H et al. CCM 2011;39:1563 | Mottling score ≥3 at 6 h was an independent predictor of 14-day ICU mortality in septic shock (OR 4.1, p<0.001). | Mottling score is a validated prognostic marker distinct from CRT. Serial assessment reflects peripheral perfusion trajectory. |
| RUSH Exam ValidationPerera P et al. J Emerg Med 2010;38:100 | Systematic RUSH exam (Pump/Tank/Pipes) narrows shock aetiology in <3 minutes at bedside with high inter-rater reliability after brief training. | POCUS is the most information-dense single investigation at the bedside for shock phenotyping without invasive monitoring. |
| McConnell SignMcConnell MV et al. Am J Cardiol 1996;78:469 | RV free wall hypokinesis with apical sparing (McConnell sign): Specificity 94%, PPV 71% for acute PE. | McConnell sign is the most specific POCUS finding for acute PE-mediated RV failure. Absent in chronic cor pulmonale. |
| IVC CollapsibilityFeissel M et al. Chest 2004;125:1562 | IVC collapsibility index >18% in MV patients predicted fluid responsiveness (AUC 0.93) when Vt ≥8 mL/kg. Less reliable in spontaneous breathing. | IVC collapsibility supplements but does not replace PPV/PLR. Limitations identical to PPV regarding ventilation mode. |
| BCIS ClassificationDonaldson AJ et al. BJA 2009;102:12 | Bone Cement Implantation Syndrome Grade 3 (cardiac arrest) mortality 15-fold higher than Grade 1. Mechanism: fat/monomer embolism → acute ↑PVR + ↓SVR. | BCIS is a recognisable obstructive-distributive mixed shock phenotype with specific intraoperative triggers and risk mitigation strategies. |
| Viscosity & SVR (HP)Messmer K et al. Eur Surg Res 1972;4:56 & Hagen-Poiseuille law | SVR ∝ η (blood viscosity) per Hagen-Poiseuille. Isovolaemic haemodilution to Hct 20-25% measurably reduces SVR and PVR; compensatory CO rise may be insufficient → high-output hypotension. | Severe anaemia (Hb <7 g/dL) causes rheological ↓SVR → hypotension despite normal/high CO. Red cell transfusion, not vasopressors, corrects the mechanism. |
| Surviving Sepsis Campaign 2026Prescott HC et al. CCM 2026;54(4):725-812. | Defined septic shock as sepsis + vasopressor requirement to maintain MAP ≥65 + lactate >2 despite adequate fluid resuscitation. MAP-alone criterion explicitly insufficient. | Lactate + vasopressor requirement = formal definition of septic shock. Supports BP-independent shock recognition framework. |
Mechanistic Model — MAP = CO × SVR | CO = HR × SV | SV = f(Preload, Contractility, Afterload)
Every cause of hypotension and shock reduces MAP through one or more of 11 physiological determinants listed below — common to rare, intraoperative and postoperative. Each section is collapsible.
Every cause of hypotension and shock reduces MAP through one or more of 11 physiological determinants listed below — common to rare, intraoperative and postoperative. Each section is collapsible.
COMMON
UNCOMMON
RARE
INTRA Intraoperative
POST Postoperative
BOTH Both
ONCO Oncosurgery-specific
01 · HEART RATE
CO = HR × SV | Bradycardia (↓CO) and extreme tachycardia (↓diastolic filling → ↓SV) both cause hypotension
▾
Optimal HR for MAP is ~60–90 bpm. Bradycardia reduces CO directly. Tachycardia >130–150 bpm compresses diastole, reduces LVEDV, and in IHD reduces coronary perfusion time — precipitating ischaemia and further contractile failure.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | High neuraxial block (≥T4) — vagal predominance | INTRA | Sympathetic cardioaccelerator fibres (T1–T4) blocked → unopposed vagal tone → sinus bradycardia ± AV block |
| Common | Vasovagal / Bezold-Jarisch reflex (peritoneal traction) | INTRA | Mechanoreceptor / C-fibre activation → afferent vagal burst → cardioinhibitory centre → sinus bradycardia; BJR paradoxically triggered in hypovolaemia when compensatory tachycardia → sudden vagal surge |
| Common | Beta-blocker / CCB effect (pre-operative continuation) | BOTH | β₁ blockade or L-type Ca²⁺ channel inhibition → ↓chronotropy and ↓dromotropy |
| Common | Opioid-induced bradycardia (fentanyl, remifentanil) | INTRA | μ-opioid receptor activation → central vagomimetic → sinus rate suppression; most marked with rapid remifentanil bolus or high-dose fentanyl induction |
| Common | Dexmedetomidine bolus / high infusion rate | BOTH | α₂ agonism at locus coeruleus → ↓sympathetic outflow; presynaptic α₂ at SA node → bradycardia; direct coronary and peripheral vasoconstriction compounds hypotension |
| Common | Neostigmine (reversal agent) | INTRA | Acetylcholinesterase inhibition → ↑ACh at cardiac muscarinic (M₂) receptors → bradycardia; attenuated by glycopyrrolate/atropine co-administration |
| Uncommon | Oculocardiac reflex | INTRA | Stretch of extraocular muscles → trigeminal afferent → vagal efferent → sinus bradycardia; strabismus surgery and orbital procedures at highest risk |
| Uncommon | Reflex bradycardia from phenylephrine (baroreceptor) | INTRA | Pure α₁ agonist → ↑SVR/MAP → baroreceptor → ↑vagal tone → bradycardia; may overshoot to hypotension if HR fall is excessive |
| Uncommon | Hyperkalaemia (≥6.5 mEq/L) | BOTH | ↓Resting membrane potential gradient → slows SA/AV conduction → bradyarrhythmias; sine wave at severe levels; massive transfusion, renal failure, rhabdomyolysis |
| Uncommon | SVT / AF with rapid rate → ↓diastolic filling → ↓SV | BOTH | Paradoxical tachycardia-mediated hypotension; diastolic filling time inadequate → LVEDV falls disproportionately to HR rise → net ↓CO; worse in diastolic dysfunction |
| Uncommon | High-degree AV block (Mobitz II / CHB) | BOTH | Blocked conduction → ventricular escape 30–45 bpm insufficient for adequate CO; may emerge intraoperatively in subclinical conduction disease |
| Uncommon | Ventricular tachycardia / VF | BOTH | Disorganised or haemodynamically ineffective ventricular contraction → CO → 0 (VF) or severely depressed (haemodynamically unstable VT) |
| Rare | Cushing reflex bradycardia (raised ICP) | BOTH | Extreme sympathetic surge (ICP>CPP) → severe hypertension → baroreceptor-mediated bradycardia; bradycardia = late ominous sign; hypotension follows brainstem herniation |
| Rare | Severe hypothyroidism / myxoedema coma | POST | ↓Thyroid hormone → ↓β-adrenoceptor expression → sinus bradycardia, ↓contractility, pericardial effusion |
| Rare | Refractory bradycardia — severe hypoxia / agonal rhythm | BOTH | Progressive cellular energy failure → loss of automaticity → junctional/idioventricular escape or asystole; end-stage common pathway of any unresolved cause |
02 · LV PRELOAD (LVEDV)
Frank-Starling: ↓LVEDV → ↓SV | Governed by venous return, intrathoracic pressure, and obstruction
▾
LV preload = LVEDV. Determinants: venous return (systemic venous tone, circulating volume, posture), intrathoracic pressure (PPV reduces venous return), obstruction to filling (tamponade, pericardial constriction, tension PTX, high PVR obstructing RV output). Operates on the steep portion of the Starling curve in hypovolaemic states.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Haemorrhage — surgical / traumatic | BOTH | Absolute intravascular volume depletion → ↓MSFP → ↓venous return → ↓RVEDV → ↓LVEDV; head/neck, hepatic, pelvic tumour resections at highest risk in oncosurgery |
| Common | Perioperative interstitial sequestration — lymphatic saturation, surgical lymphatic disruption, venous tourniquet effect of compartment oedema | INTRAONCO | (1) Lymphatic kinetics saturation: Surgical inflammation ↑ capillary hydraulic conductance + ↓oncotic reflection coefficient (σ) via glycocalyx disruption → net filtration rate exceeds maximum lymphatic transport capacity (~10–20× resting); protein-rich interstitial fluid accumulates as functional plasma loss. (2) Surgical lymphatic disruption: Direct transection (neck dissection, axillary clearance, RPLND, hepatoportal dissection) abolishes local drainage; most pronounced in oncosurgical lymphadenectomy. (3) Venous tourniquet effect of compartment oedema: ↑Interstitial pressure → compresses low-pressure venules → ↑local venous hydrostatic pressure → further Starling-driven extravasation → self-amplifying cycle; most significant in confined fascial compartments. |
| Common | Open body cavity evaporative losses (peritoneal, pleural, bowel serosa) | INTRA | Convective + evaporative loss of pure water vapour from warm visceral surfaces; losses are hypotonic (not plasma-equivalent) → free-water deficit + ↑plasma osmolality. Modern evidence: ~0.5–1 mL/kg/hr (far below classical 10–15 mL/kg/hr teaching); cumulative in prolonged laparotomy/thoracotomy; contributes to hypernatraemia and ↑plasma viscosity. Mechanistically distinct from interstitial sequestration above. |
| Common | Inadequate fluid resuscitation / fasting losses | BOTH | Obligate overnight fast + bowel prep dehydration → ↓MSFP; compounded by vasodilatory effect of induction agents |
| Common | Positive pressure ventilation — high PEEP / high tidal volume | BOTH | ↑Mean intrathoracic pressure → compresses RA and intrathoracic IVC → ↓venous return gradient; PEEP ≥12 cmH₂O markedly reduces CO in hypovolaemic patients |
| Common | Vasodilatory (distributive) pooling — neuraxial / GA induction | INTRA | Sympathetic blockade or direct venodilation (propofol, volatile agents) → venous capacitance ↑ → MSFP falls → venous return ↓ → functional hypovolaemia despite unchanged total volume |
| Uncommon | Sepsis-induced venous capacitance ↑ (venous component) | BOTH | iNOS-derived NO → venous and arteriolar smooth muscle relaxation → ↑venous capacitance → relative hypovolaemia; LPS-mediated vascular leak compounds true hypovolaemia |
| Uncommon | Tension pneumothorax | BOTH | Air accumulation under pressure → mediastinal shift → compression of IVC and RA → ↓venous return → ↓LVEDV; also ↑RV afterload from lung compression; PPV accelerates; needle decompression is definitive |
| Uncommon | Cardiac tamponade | BOTH | Pericardial fluid → ↑intrapericardial pressure → progressive diastolic compression of RA and RV → ↓RVEDV → ↓LVEDV; pulsus paradoxus, Beck's triad; exacerbated by hypovolaemia and PPV |
| Uncommon | Massive PE — RV failure reducing LV filling | BOTH | Acute ↑PVR → RV dilation → interventricular septal shift leftward (D-shaped LV on echo) → ↓LVEDV → ↓SV → ↓CO; obstructive shock phenotype |
| Uncommon | Aortocaval compression (gravid uterus) | INTRA | IVC compression at ≥20 weeks gestation → ↓venous return; compounded by aortic compression → ↓uteroplacental flow; lateral tilt obligatory |
| Rare | RA/IVC obstruction — intracardiac tumour (RA myxoma, RCC with IVC thrombus) | BOTH | Mechanical obstruction of RA inflow → ↓RVEDV → ↓LVEDV; position-dependent (myxoma can intermittently prolapse through tricuspid) |
| Rare | Surgical retraction compressing IVC / hepatic veins | INTRA | Manual/mechanical retraction during hepatic/retroperitoneal surgery compresses IVC → acute ↓venous return; rapid correction upon release |
| Rare | Pericardial constriction (unrecognised pre-operative) | BOTH | Fibrous/calcified pericardium limits biventricular diastolic filling → fixed low preload state; exposed by fluid challenge failure; prevalent in prior RT/TB/viral pericarditis patients |
| Rare | Pneumoperitoneum (high IAP) — laparoscopic surgery | INTRA | IAP >15 mmHg → IVC compression → ↓venous return; typically modest but important with steep Trendelenburg reversal and hypovolaemia |
03 · LV CONTRACTILITY
EF, dP/dt, SV at constant preload/afterload | Primary cardiogenic or drug/metabolic depression
▾
Inotropy depends on intracellular Ca²⁺ cycling (SERCA, NCX, RyR2), sarcomere cross-bridge kinetics, energy substrate supply (ATP, phosphocreatine), and adrenergic receptor density. Anaesthetic agents, ischaemia, and metabolic derangements intersect at multiple points. Cardiogenic shock = cardiac index <2.2 L/min/m² with PCWP >18 mmHg.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Volatile agent depression (isoflurane, sevoflurane, desflurane) | INTRA | Dose-dependent ↓L-type Ca²⁺ influx, impaired SR Ca²⁺ release, ↓myofilament Ca²⁺ sensitivity; sevoflurane at 2 MAC reduces contractility ~30%; compounded by concurrent vasodilation and bradycardia |
| Common | Propofol — negative inotropy and vasodilation | INTRA | ↓Ca²⁺ transient + ↓myofilament sensitivity + SERCA activation → ↓contractility; simultaneous ↓SVR compounds hypotension; TIVA at high rates or bolus induction most hazardous in pre-existing LV dysfunction |
| Common | Acute myocardial ischaemia / NSTEMI / STEMI intraoperative | BOTH | Supply-demand imbalance → regional wall motion abnormalities → ↓global EF; tachycardia, hypotension, and ↑LVEDP create a self-propagating ischaemia-dysfunction spiral; troponin rise 3–48 h post-op |
| Common | Pre-existing LV dysfunction decompensated by perioperative stress | BOTH | Reduced preoperative EF → narrow haemodynamic reserve; anaesthetic vasodilation, fluid shifts, tachycardia, or ischaemia tip compensated failure into decompensated low-output state |
| Uncommon | Septic cardiomyopathy | BOTH | TNF-α, IL-1β, NO → ↓contractility, Ca²⁺ desensitisation; typically biventricular; transient — EF recovery over 7–10 days with source control |
| Uncommon | Acidaemia (pH <7.2) | BOTH | H⁺ competes with Ca²⁺ at troponin C binding site → ↓myofilament Ca²⁺ sensitivity; ↓SR Ca²⁺ release; ↓β-adrenoceptor density; pH <7.1 = severe refractory contractile failure |
| Uncommon | Hypocalcaemia (ionised Ca²⁺ <1.0 mmol/L) | BOTH | ↓Trigger Ca²⁺ for CICR from SR → ↓contraction amplitude; massive transfusion (citrate chelation), post-thyroid/parathyroid surgery, pancreatitis |
| Uncommon | Myocardial stunning (post-CPB, post-ischaemia) | INTRA | Reperfusion-related Ca²⁺ overload and oxidative stress → transient contractile dysfunction despite restored flow; duration hours to days; inotropes as bridge |
| Uncommon | Hypothermia (core <34°C) | BOTH | ↓Enzymatic reaction rates → ↓Ca²⁺-ATPase activity → impaired SERCA → ↓contractility; progressive below 32°C; coagulopathy compounds haemorrhagic contribution; J waves on ECG |
| Uncommon | Local anaesthetic systemic toxicity (LAST) | INTRA | Na⁺ channel blockade → conduction abnormalities; Ca²⁺ channel inhibition → ↓contractility; mitochondrial uncoupling → ATP depletion; bupivacaine most cardiotoxic; Intralipid® is antidote |
| Uncommon | Takotsubo (stress) cardiomyopathy | BOTH | Catecholamine surge → apical ballooning with basal hyperkinesis; predominantly postmenopausal women; mimics anterior STEMI; reversible in weeks |
| Rare | Air / fat / bone cement embolism → coronary occlusion | INTRA | Air entering coronary ostia (RCA most susceptible) → acute RV+LV ischaemia; PMMA monomer causes ↑PVR and direct myocardial depression; fat emboli from long bone/spinal surgery → lipid microemboli in coronary bed |
| Rare | Acute myocarditis (viral, drug-induced) | BOTH | Direct viral cytopathic effect or immune-mediated myocyte necrosis → global LV dysfunction; giant cell myocarditis = fulminant cardiogenic shock |
| Rare | Negative inotropy — high-dose dexmedetomidine (α₂-mediated) | BOTH | Presynaptic α₂ reduces NE release; post-junctional α₂ in myocardium inhibits adenylyl cyclase → ↓cAMP → ↓PKA → ↓L-type Ca²⁺ current; clinically significant in cardiac dysfunction |
| Rare | Phosphodiesterase inhibitor overdose (milrinone infusion error) | BOTH | High milrinone concentrations → severe vasoplegia-dominant hypotension overwhelming inotropy; vasopressin or noradrenaline required |
04 · LV AFTERLOAD / SVR
MAP = CO × SVR | SVR = (MAP−CVP)/CO × 80 | SVR ∝ η (viscosity) per Hagen-Poiseuille · ↓SVR vasomotor or rheological → ↓MAP
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Per the Hagen-Poiseuille relationship (R = 8ηL / πr⁴), SVR is determined by vessel radius (dominant, r⁴ dependence), vessel length, and blood viscosity (η). Most clinical ↓SVR is vasomotor (↓r), but rheological ↓SVR from ↓η is a distinct, under-recognised mechanism. In distributive shock, profound vasodilation with preserved or elevated CO characterises early sepsis, anaphylaxis, and neuraxial block.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Neuraxial anaesthesia — sympathetic blockade | INTRA | Pre-ganglionic sympathetic fibres blocked → arteriolar vasodilation (↓SVR) + venodilation (↓preload) + bradycardia if T1–T4 affected; exacerbated by hypovolaemia |
| Common | General anaesthetic induction (propofol, thiopentone) | INTRA | Propofol → Ca²⁺ channel blockade in VSM + ↑NO + ↓sympathetic tone → ↓SVR ± ↓contractility; most marked in hypovolaemic/elderly patients |
| Common | Volatile agents (isoflurane > sevoflurane) — vasodilation | INTRA | K(ATP) channel activation in VSM → hyperpolarisation → vasodilation; isoflurane most vasodilatory; concentration-dependent ↓SVR with mild ↑HR (reflex) |
| Common | Sepsis / SIRS — distributive shock | BOTH | LPS/PAMPs → TLR4 → iNOS induction → ↑NO → cGMP → VSM relaxation → ↓SVR; vasopressin deficiency in prolonged septic shock (V1 receptor desensitisation) |
| Common | Anaphylaxis / anaphylactoid reaction | INTRA | IgE-mediated mast cell degranulation → histamine (H1/H2) + tryptase + LTC4/D4 → profound vasodilation (↓SVR), ↑vascular permeability (↓preload), bronchospasm; NMBAs, antibiotics, latex commonest OT triggers |
| Uncommon | Adrenal insufficiency / crisis | BOTH | Cortisol deficiency → ↓catecholamine receptor sensitivity + ↓aldosterone → refractory vasodilation + hypovolaemia; steroid withdrawal, bilateral adrenal metastases, post-adrenalectomy; hydrocortisone 100 mg IV stat |
| Uncommon | Iatrogenic vasodilators (GTN, SNP, hydralazine, ACE-I, CCB) | BOTH | Direct or NO-mediated arteriolar/venous smooth muscle relaxation; intraoperative continuation of oral antihypertensives compounds anaesthetic vasodilation |
| Uncommon | Hypercapnia — systemic vasodilatory effect | BOTH | CO₂ → carbonic acid → tissue acidosis → VSM relaxation; net effect at PaCO₂ >60 mmHg is ↓SVR and hypotension; initial catecholamine surge may temporarily mask |
| Uncommon | Hepatic failure (acute or chronic decompensation) | BOTH | ↑Glucagon, ↑NO, ↑prostacyclin → splanchnic + systemic vasodilation; bacterial translocation triggers distributive shock superimposed on hepatic shock |
| Uncommon | ↓Blood viscosity (η) — rheological ↓SVR (severe anaemia, haemodilution) | BOTHONCO | Hagen-Poiseuille: SVR ∝ η; ↓η → ↓SVR → ↓MAP independently of vasomotor tone. Viscosity values: ~4 cP at Hb 12, ~2.5 cP at Hb 7, ~2.0 cP at Hb 5 g/dL. ↓Haematocrit accounts for ~85–90% of viscosity reduction in severe haemodilution; plasma proteins (particularly fibrinogen, not albumin) contribute the remaining ~10–15%. Albumin is a minor viscosity contributor (~0.01–0.02 cP per g/dL — compact globular protein). High CO + low MAP paradox: ↓afterload → ↑SV + compensatory ↑HR → ↑CO, but when η falls steeply the ↓SVR outpaces ↑CO compensation → high-output hypotension despite normal/elevated CO. Blood is shear-thinning (Fåhræus-Lindqvist effect in microvessels <300 μm partially attenuates macrovascular rheological changes). |
| Uncommon | Thyroid storm | BOTH | Excess TH → ↑β-adrenoceptor number and sensitivity → tachycardia + ↓SVR + ↑CO; decompensation when myocardial reserve exhausted; triggered by surgical stress / iodinated contrast |
| Rare | Protamine reaction — Type I (histamine-mediated) | INTRA | Non-immunological mast cell degranulation → histamine → ↓SVR; usually mild/transient; distinct from Type II (anaphylactic IgE) and Type III (complement-mediated pulmonary vasoconstriction) |
| Rare | Neurogenic shock (high cervical SCI ≥T6) | BOTH | Loss of supraspinal sympathetic control → ↓SVR + bradycardia (unopposed vagal) + ↓cardiac inotropy; warm peripheries with bradycardia distinguishes from hypovolaemic shock |
| Rare | Systemic mastocytosis / carcinoid crisis | INTRA | Tumour manipulation → histamine (mastocytosis) or serotonin/kallikrein (carcinoid) → profound vasodilation ± bronchoconstriction; octreotide is specific antidote for carcinoid |
| Rare | Vasoplegia syndrome (post-CPB, post-LVAD, post-liver transplant) | BOTH | Refractory ↓SVR despite preserved CO; AVP depletion + iNOS upregulation + K(ATP) channel activation; vasopressin and methylene blue (guanylate cyclase inhibition) are rescue therapies |
05 · RV PRELOAD
RV fills from systemic venous return | Ventricular interdependence — RV failure → septal shift → ↓LV preload
▾
RV preload determinants largely identical to LV. Because ventricles are in series, ↓RV preload → ↓LV preload. Ventricular interdependence: RV dilation shifts septum leftward, directly reducing LVEDV independent of pulmonary flow.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Hypovolaemia (all causes — same as LV section) | BOTH | ↓Venous return → ↓RVEDV; RV more sensitive to preload as it operates on a steeper Starling slope at normal filling pressures |
| Uncommon | SVC syndrome (tumour, thrombosis, mediastinal compression) | BOTH | SVC obstruction → ↓upper body venous drainage to RA → ↓RV preload; chronic may be compensated by venous collaterals; relevant in mediastinal tumour / central catheter thrombosis |
| Uncommon | High PEEP / auto-PEEP | BOTH | ↑Intrathoracic pressure compresses intrathoracic IVC and RA → ↓venous gradient → ↓RV filling; auto-PEEP in obstructive lung disease on IPPV creates same physiology |
| Rare | Tricuspid stenosis / RA mass obstructing tricuspid inflow | INTRA | Fixed obstruction to RV filling; carcinoid heart disease produces TS/TR; may be unmasked under anaesthesia |
06 · RV CONTRACTILITY
RV is a thin-walled flow generator — poorly tolerates acute ↑afterload | RV failure → septal shift → ↓LV preload → ↓CO spiral
▾
The RV is 4–6× more sensitive to acute ↑afterload than the LV. Acute cor pulmonale from PE or severe hypoxia can collapse CO within minutes. RV dilation → D-sign on TTE → ↓LVEDV → ↓CO — broken only by treating the primary RV insult.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Acute cor pulmonale from massive PE | BOTH | Thrombus obstruction → acute ↑PVR → RV dilation → RV ischaemia (wall stress ↑, RCA perfusion ↓) → contractile failure → septal shift → ↓LV preload → ↓CO |
| Common | RV dysfunction from pre-existing PHTN decompensated by anaesthesia | INTRA | Fixed elevated PVR → RV hypertrophy limits adaptation; anaesthetic vasodilation ↓CPP to hypertrophied RV → ischaemia → acute-on-chronic RV failure; hypoxia/hypercapnia worsen PVR intraoperatively |
| Uncommon | RV ischaemia / infarction (acute — RCA territory) | BOTH | RCA occlusion → inferior wall MI with RV involvement in ~40%; triad: hypotension, elevated JVP, clear lung fields; avoid nitrates; volume load; maintain sinus rhythm |
| Uncommon | Acute ARDS / ALI → ↑PVR → RV failure | BOTH | HPV + vascular destruction + hypercapnia + high PEEP → ↑PVR → acute cor pulmonale; MV strategy must balance lung protection with RV protection (permissive hypercapnia limited by RV) |
| Uncommon | Venous air embolism (neurosurgical / sitting position) | INTRA | Air bolus → RV outflow obstruction (air-lock) + pulmonary gas microembolism → ↑PVR + ↓RV output → ↓CO; mill-wheel murmur; ETCO₂ fall is early sign |
| Uncommon | Septic cardiomyopathy — biventricular | BOTH | Same cytokine/NO mechanism as LV; RV failure often underappreciated; TAPSE <17 mm, S' <10 cm/s on TTE; responds to source control + noradrenaline ± dobutamine |
| Rare | Protamine reaction — Type III (complement-mediated TXA₂) | INTRA | Heparin-protamine complexes → complement → C5a → pulmonary macrophage TXA₂ → ↑PVR → acute RV failure; inhaled NO, epoprostenol, vasopressin |
| Rare | Bone cement implantation syndrome (BCIS) | INTRA | PMMA monomer + fat/marrow microemboli → acute ↑PVR + ↓SVR + ↓myocardial contractility; femoral cementing in THA; Grade 3 = cardiac arrest; high-FiO₂ and pre-emptive volume loading are preventive |
| Rare | Amniotic fluid embolism (AFE) | INTRA | Fetal debris + AF contents → acute pulmonary vasoconstriction → RV failure → cardiovascular collapse → DIC; bimodal: obstructive shock then coagulopathic haemorrhage; supportive care only |
| Rare | Acute pulmonary hypertensive crisis (post-cardiac surgery, OLT) | INTRA | Triggers in pre-sensitised pulmonary vasculature → abrupt ↑PAP → RV failure; management: inhaled NO 10–40 ppm, milrinone, iloprost nebulisation, ECMO |
07 · PULMONARY VASCULAR RESISTANCE (PVR / RV Afterload)
PVR = (mPAP − PCWP) / CO × 80 | Normal 80–240 dyne·s/cm⁵ | PVR ∝ η (viscosity) · ↑PVR → ↑RV afterload → RV failure
▾
Pulmonary vascular tone governed by alveolar PO₂ (HPV — von Euler-Liljestrand reflex), PaCO₂, pH, autonomic input, and vasoactive mediators. Additionally, PVR ∝ blood viscosity (η) per Hagen-Poiseuille — extreme haemodilution lowers PVR and is deliberately exploited during CPB. Pulmonary vessels constrict to hypoxia — adaptive in V/Q matching, maladaptive in global hypoxaemia.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Hypoxia (global / OLV) — HPV | INTRA | Alveolar PO₂ <60–70 mmHg → inhibits KATP channels in pulmonary VSM → membrane depolarisation → Ca²⁺ influx → vasoconstriction; volatile agents blunt HPV (↑shunt but ↓PVR in OLV) |
| Common | Hypercapnia / respiratory acidosis | BOTH | CO₂ and H⁺ cause pulmonary vasoconstriction (opposite to systemic effect); PaCO₂ >50 mmHg significantly ↑PVR; compounded by concurrent hypoxia |
| Common | Metabolic acidosis (pH <7.35) | BOTH | H⁺ → pulmonary vasoconstriction via Ca²⁺-dependent pathway; synergistic with hypoxia; bicarbonate correction lowers PVR |
| Common | High tidal volume / high PEEP / auto-PEEP | BOTH | Over-distension → compression of intra-alveolar capillaries; under-distension (atelectasis) → HPV; PEEP >10 cmH₂O progressively increases RV afterload, especially in ARDS |
| Uncommon | Massive PE | BOTH | Direct mechanical obstruction + reflex vasoconstriction (serotonin, TXA₂) → acute ↑PVR; RV can only generate mPAP ~40 mmHg acutely; chronic CTEPH in ~4% survivors |
| Uncommon | Pre-existing PAH (WHO Group I–V) | BOTH | Fixed elevated PVR limits RV adaptive capacity; anaesthetic triggers → acute-on-chronic ↑PVR → RV failure; perioperative mortality high in WHO FC III–IV |
| Uncommon | Protamine — thromboxane-mediated vasoconstriction (Type III) | INTRA | Complement cascade → C5a → pulmonary macrophage TXA₂ → acute severe pulmonary vasoconstriction; distinguishable from systemic anaphylaxis by ↑PAP with ↓CO |
| Uncommon | ↓Blood viscosity (η) — rheological ↓PVR (extreme haemodilution, CPB prime) | INTRA | PVR ∝ η; ↓η → ↓PVR → ↓RV afterload; physiological basis of deliberate CPB haemodilution. More commonly protective (↓RV afterload in borderline PHTN) than harmful; problematic only in extreme haemodilution + vasoplegia combination. Does not respond to inhaled NO; corrects with red cell transfusion. |
| Rare | Fat embolism syndrome (post-long bone fracture / medullary nailing) | INTRA | Marrow fat globules → mechanical obstruction + free fatty acid-mediated endothelial injury → ↑PVR + ARDS; classic triad 24–72 h post-injury |
| Rare | Nitrous oxide — ↑PVR in pre-existing PHTN | INTRA | N₂O is a sympathomimetic pulmonary vasoconstrictor; modest in normal PVR but clinically significant in pre-existing PHTN; avoided in Fontan physiology, severe PAH |
| Rare | Intracardiac air → pulmonary gas embolism (cardiac surgery) | INTRA | Air into pulmonary arteries → gas-blood interface → surfactant disruption + vasoconstriction + endothelial activation → ↑PVR + hypoxaemia; TOE de-airing protocol is preventive |
08 · pH (ACID-BASE)
Acidaemia → ↓contractility · ↓SVR (systemic) · ↑PVR (pulmonary) · ↓catecholamine responsiveness
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pH exerts direct cardiovascular effects independent of aetiology. Acidaemia below pH 7.2 causes progressive myocardial depression, vasodilation, and pulmonary vasoconstriction. Alkalemia induces coronary vasospasm, hypokalaemia, hypocalcaemia, and leftward ODC shift. Bicarbonate is temporising only — identify and treat the cause.
| Freq | Cause of Acidaemia | Context | Cardiovascular Effect |
|---|---|---|---|
| Common | Lactic acidosis — Type A (↓tissue O₂ delivery) | BOTH | Hypoperfusion → anaerobic glycolysis → H⁺ + lactate; pH fall → ↓inotropy via troponin C competition + ↓cAMP pathway + ↓β-receptor function; positive feedback: ↓CO → ↑lactate → ↓pH → ↓CO |
| Common | Respiratory acidosis (hypoventilation, airway obstruction, ARDS) | BOTH | ↑PaCO₂ → ↑H₂CO₃ → ↓pH; acute ↑PVR + ↓SVR; catecholamine release buffers initially but exhausted in prolonged hypercapnia |
| Common | Dilutional acidosis (large-volume 0.9% NaCl) | INTRA | Hyperchloraemia → ↓strong ion difference → ↑H⁺; pH typically 7.25–7.35; mild cardiovascular impact but compounds pre-existing metabolic derangement |
| Uncommon | Diabetic ketoacidosis decompensated perioperatively | BOTH | Insulin deficiency → ketone accumulation → severe high anion gap acidosis; pH <7.1 causes vasodilation, ↓inotropy, arrhythmias; osmotic diuresis → hypovolaemia compounds |
| Rare | Severe metabolic alkalosis (pH >7.55) | BOTH | ↓Ionised Ca²⁺ (alkalosis ↑ albumin binding) → ↓contractility + ↑neuromuscular excitability; hypokalaemia-mediated arrhythmias; coronary vasospasm; ↑Hb-O₂ affinity → ↓O₂ offloading; clinically under-recognised |
09 · PaCO₂
Hypercapnia → ↑sympathetic + ↓SVR (systemic) + ↑PVR (pulmonary) | Hypocapnia → alkalosis + vasoconstriction
▾
CO₂ has tissue-specific vascular effects: systemic vasodilation but pulmonary vasoconstriction. This divergence is adaptive (V/Q matching) but haemodynamically hazardous when PaCO₂ is elevated globally. Hypocapnia-induced alkalosis can paradoxically reduce DO₂ despite normal PaO₂.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Inadvertent hypoventilation during IPPV (obstructed ETT, bronchospasm, disconnect) | INTRA | ↑PaCO₂ → sympathomimetic buffering initially; sustained hypercapnia (PaCO₂ >70 mmHg) → ↓inotropy, ↑PVR, arrhythmias, ↓SVR-mediated hypotension predominates |
| Common | Pneumoperitoneum CO₂ absorption (laparoscopic surgery) | INTRA | Peritoneal CO₂ absorption → ↑PaCO₂ → initial ↑HR/MAP (catecholamine surge); haemodynamically significant if ventilation not increased; PHTN makes PVR rise clinically important |
| Common | Malignant hyperthermia — hypermetabolic state | INTRA | RYR1 mutation → uncontrolled SR Ca²⁺ release → skeletal muscle hypermetabolism → ↑VO₂ + ↑VCO₂ → exponential ↑PaCO₂ and ↓pH → cardiovascular collapse; ETCO₂ >55 mmHg during GA is sentinel sign |
| Uncommon | Permissive hypercapnia in ARDS → haemodynamic compromise | POST | Deliberate ↑PaCO₂ (60–80 mmHg) → acceptable if RV preserved; RV afterload ↑ from pulmonary vasoconstriction limits PaCO₂ permissiveness to ~60 mmHg in overt RV dysfunction |
| Uncommon | Severe hypocapnia (PaCO₂ <25 mmHg) — haemodynamic effects | BOTH | Alkalosis → ↑albumin-Ca²⁺ binding → ↓ionised Ca²⁺ → ↓contractility; cerebral vasoconstriction → ↓CBF; coronary vasospasm; leftward ODC shift → ↑Hb-O₂ affinity → ↓O₂ offloading |
10 · PaO₂
Hypoxaemia → ↑sympathetic → compensated | PaO₂ <40 mmHg → ↓myocardial function + ↑PVR → decompensated
▾
Myocardial O₂ extraction is ~70–75% at rest (nearly maximal), leaving minimal reserve. Hypoxaemia-driven hypotension cannot be buffered by ↑extraction alone — ↑CO must compensate. When CO cannot rise (pre-existing dysfunction), critical DO₂ is reached rapidly.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Airway loss / failed intubation / oesophageal intubation | INTRA | Acute hypoxaemia within 3–5 min → compensatory tachycardia + ↑SVR initially; sustained hypoxia (SaO₂ <85%) → myocardial depression → bradycardia → cardiac arrest; SpO₂ decline to 70% precedes decompensation by 2–3 min |
| Common | Bronchospasm / laryngospasm — severe V/Q mismatch | INTRA | Airway obstruction → ↓alveolar ventilation → hypoxaemia; reflex ↑PVR from HPV; haemodynamic compromise when SpO₂ <90%; concurrent ↑PEEP from gas trapping → ↓venous return |
| Common | Postoperative atelectasis + hypoxaemia in ICU | POST | Lobar/segmental collapse → intrapulmonary shunting → refractory hypoxaemia; modest haemodynamic impact if isolated but synergistic with sepsis or post-surgical myocardial depression |
| Uncommon | Severe ARDS → refractory hypoxaemia → myocardial O₂ debt | POST | PaO₂ <55 mmHg despite FiO₂ 1.0 → ↓DO₂ to myocardium → anaerobic metabolism → ↑lactate → ↓contractility in context of concurrent ↑PVR from ARDS physiology |
| Uncommon | One-lung ventilation hypoxaemia (OLV) | INTRA | Shunt from non-ventilated lung (~30–40% of CO) → SpO₂ 85–90%; volatile agents blunt HPV, TIVA preserves it; limit Vt ≤6 mL/kg IBW for ventilated lung |
| Rare | Paradoxical embolism via PFO (R→L shunt from ↑RA pressure) | BOTH | PFO (~25% of adults) + ↑RA pressure (PE, PHTN, PPV) → reversal of transatrial gradient → R→L shunting → systemic hypoxaemia disproportionate to lung pathology + risk of arterial embolism |
11 · TEMPERATURE
Hypothermia → ↓HR · ↓contractility · arrhythmias · coagulopathy | Hyperthermia → ↑HR · ↓SVR · vasodilation
▾
Core temperature directly governs enzymatic kinetics, ion channel function, and coagulation cascade efficiency (each 1°C ↓ reduces clot strength ~10%). Hypothermia is the most common temperature-related cause of haemodynamic compromise. Hyperthermia signals MH, sepsis, thyroid storm, or NMS — all life-threatening.
| Freq | Cause | Context | Mechanism |
|---|---|---|---|
| Common | Perioperative hypothermia (core 34–36°C) | BOTH | ↓Enzymatic activity → ↓SERCA → ↓SR Ca²⁺ cycling → ↓inotropy; ↑blood viscosity; prolonged drug metabolism; coagulopathy → ↑bleeding → ↓preload; shivering raises O₂ demand by 400% |
| Common | Moderate hypothermia (32–34°C) in cardiac / vascular surgery | INTRA | Progressive ↓HR, ↓CO; ↑VF risk below 30°C; J (Osborn) waves on ECG; cold-induced diuresis compounds hypovolaemia; rewarming vasodilation-induced ↓SVR = post-bypass hypotension risk |
| Uncommon | Severe hypothermia (<30°C) — accidental or therapeutic | BOTH | Spontaneous VF threshold; cold myocardium unresponsive to conventional vasopressors; ECMO (VA) is definitive rewarming and haemodynamic support in cardiac arrest from hypothermia |
| Uncommon | Sepsis-induced hyperthermia → ↓SVR + vasodilation | BOTH | Pyrexia → ↑metabolic rate → ↑CO demand; cytokine-mediated vasodilation amplifies tachycardia and ↑DO₂ requirement; haemodynamic compromise is primarily distributive, not temperature-dependent |
| Rare | Malignant hyperthermia (MH) — fulminant | INTRA | RYR1 mutation + triggering agents (volatile, succinylcholine) → uncontrolled SR Ca²⁺ release → skeletal muscle hypermetabolism → hyperthermia, hypercapnia, acidosis, rhabdomyolysis, hyperkalaemia → cardiovascular collapse; dantrolene 2.5 mg/kg IV is antidote |
| Rare | Neuroleptic malignant syndrome (NMS) | BOTH | D2 receptor blockade (antipsychotics, antiemetics) → hypothalamic dysregulation → muscle rigidity + hyperthermia + autonomic instability; ↓SVR from vasodilation; bromocriptine + dantrolene |
| Rare | Thyroid storm | BOTH | Massive TH release → ↑thermogenesis + profound ↓SVR + tachyarrhythmia → high-output state; decompensation when cardiac reserve exhausted; fever >41°C + AF + haemodynamic collapse = crisis; PTU + beta-blockade + iodine + hydrocortisone |
▸ Integrative Map of Shock Phenotypes — Haemodynamic Fingerprints
HYPOVOLAEMIC
- Haemorrhage · third spacing · burns
- Adrenal crisis (salt-wasting)
- Diabetes insipidus · GI losses
- Aortocaval compression
HR ↑↑
CO ↓↓
SVR ↑↑
CVP ↓
PCWP ↓
SvO₂ ↓
CARDIOGENIC
- Acute MI · cardiomyopathy
- Volatile agent excess · Local Anaesthetic Toxicity (LAST)
- Severe acidaemia · hypothermia
- Tamponade · constrictive physiology
HR ↑/N
CO ↓↓
SVR ↑↑
CVP ↑
PCWP ↑↑
SvO₂ ↓↓
DISTRIBUTIVE / VASODILATORY
- Sepsis · SIRS · anaphylaxis
- Neuraxial / GA induction
- Adrenal crisis · hepatic failure
- ↓Viscosity (high-output hypotension)
HR ↑↑
CO ↑/N
SVR ↓↓
CVP ↓/N
PCWP ↓/N
SvO₂ ↑
OBSTRUCTIVE
- Massive PE · tension pneumothorax
- Cardiac tamponade
- Auto-PEEP · air embolism · Bone Cement Implantation Syndrome (BCIS)
- Protamine Type III
HR ↑↑
CO ↓↓
SVR ↑↑
CVP ↑↑
PCWP ↓ (PE/PTX)
PAP ↑↑ (PE)
MIXED / COMPLEX
- Sepsis + relative hypovolaemia
- PE + RV failure → ↓LV preload
- MH: distributive + metabolic
- Post-CPB: vasoplegia + stunning
HR Variable
CO Variable
SVR Variable
TTE required
NEUROGENIC
- High cervical SCI (≥T6)
- Brainstem herniation (late)
- High spinal / epidural block
HR ↓ (brady)
CO ↓
SVR ↓↓
Skin Warm/dry