SEPT 13 Built from the handwritten pages you uploaded on 13 September 2026.

Shock: types & haemodynamics

Hypovolaemic, cardiogenic, obstructive and distributive — the pressure, flow and SvO₂ pattern of each, and how to tell them apart at the bedside.

The haemodynamic profiles

PAOP = pulmonary artery occlusion (wedge) pressure ≈ left atrial pressure ≈ LVEDP. CVP reflects the right side.

Type	HR	CVP	PAOP	CO	SVR	SvO₂	Bedside picture
Hypovolaemic	↑	↓	↓	↓	↑	↓	Cool, pale, clammy · weak thready pulse · urine output falls
Cardiogenic — LV	↑	↑	↑	↓	↑	↓	Cool, clammy · crackles, tachypnoea · urine < 30 ml/h
Cardiogenic — RV	↑	↑	↔ / ↓	↓	↑	↓	Raised JVP with clear lungs — e.g. RV infarct
Obstructive — PE	↑	↑	↓ ★	↓	↑	↓	PAP ↑ but wedge ↓ — the clot sits between them
Obstructive — tamponade	↑	↑	↑	↓	↑	↓	Equalisation of diastolic pressures · Beck's triad
Septic — early, warm	↑	↓	↓	↑	↓	↑	Pink, warm, flushed · full bounding pulse · fever · tachypnoea
Septic — late, cold	↑	↓ / ↔	↓	↓	↑ / ↔	↓	Myocardial depression sets in — looks like cardiogenic
Anaphylactic	↑	↓	↓	↔ / ↑ early, then ↓	↓	↔ / ↓	Cough, dyspnoea, wheeze · urticaria, pruritus · restless, falling GCS
Neurogenic	↓ BRADY	↓	↓	↓	↓	↓	Warm, dry skin · hypotension with bradycardia

Only early septic shock pushes CO and SvO₂ UP. Everything else is down. SvO₂ rises because the tissues cannot extract oxygen and flow is shunted past them.
Only neurogenic shock is bradycardic. Every other type drives a tachycardia.
Warm peripheries = distributive (septic, anaphylactic, neurogenic). Cold peripheries = hypovolaemic, cardiogenic, obstructive — the high-SVR types.
CVP splits the high-SVR group: low in hypovolaemia, high in pump failure and obstruction.
PE ★: PAP up, wedge down. Tamponade: CVP and wedge both up and equal.

The sheet gives decreased CO for septic shock. That is true late; early warm sepsis is hyperdynamic with a high CO, as your handwriting says.
Anaphylaxis: CO may be normal or high in the first minutes, then falls as venous pooling and capillary leak empty the ventricle.

Two different things that often coexist after cord injury. One is haemodynamic, the other neurological.

	Neurogenic shock	Spinal shock
What it is	Loss of sympathetic tone → venous and arterial vasodilatation	Transient loss of all reflexes below the level of injury
Level	High cord injury — T6 and above. Bradycardia when the cardioaccelerator fibres (T1–T4) are cut off	Any level
Signs	Hypotension + bradycardia, warm dry skin; fluid-resistant hypotension from immediately after the injury	Flaccid paralysis, areflexia, atonic bladder below the lesion
Course	Days to weeks; needs vasopressor ± atropine	Days to weeks; the bulbocavernosus reflex returns first, then spasticity and hyperreflexia

Fluid-resistant hypotension with a history of chest wall trauma, sternal fracture, cardiac surgery or recent line insertion.
Beck's triad: hypotension · raised JVP · muffled heart sounds.
Pulsus paradoxus — systolic BP falls by more than 10 mmHg on spontaneous inspiration. Under positive-pressure ventilation the swing can reverse (reversed pulsus paradoxus).
Mechanism: fluid compresses the heart → ↓ venous return → ↓ CO → compensatory ↑ HR, yet ↓ BP.

Full: keep preload high — CVP must stay above RV end-diastolic pressure or the RV cannot fill.
Fast: CO is rate-dependent because stroke volume is fixed; avoid bradycardia.
Tight: maintain SVR and contractility.
Ketamine is the classic induction agent. Ideally drain under local anaesthesia first; IPPV cuts venous return further and can precipitate arrest.

MAP ≥ 65 mmHg and a heart rate coming down.
Oxygenation — SpO₂ and haemoglobin adequate for delivery.
Urine output ≥ 0.5 ml/kg/h.
Lactate clearing, base excess improving.
ScvO₂ / SvO₂ — low means inadequate delivery; inappropriately high in sepsis means poor extraction.

Septic only one with ↑ CO & ↑ SvO₂

Neurogenic the only bradycardia

PE PAP ↑, wedge ↓

Tamponade equal diastolic pressures

LV failure CVP ↑ wedge ↑ CO ↓

Hypovolaemia everything ↓ but SVR

T1–T4 cardioaccelerators

Beck ↓BP · ↑JVP · muffled