Physiology

Cardiac output (~5 L/min at rest) is the product of rate and stroke volume, and stroke volume's three determinants organise every haemodynamic decision in theatre and intensive care. Preload — the ventricular end-diastolic volume or wall stretch — sets the starting sarcomere length: the Frank-Starling mechanism means greater diastolic filling generates greater force of contraction (length-tension optimisation of actin-myosin overlap plus length-dependent calcium sensitivity), so the heart automatically ejects what it receives, matching the two ventricles' outputs beat by beat. The curve's shape carries the clinical meaning: on its steep ascending limb, volume raises output — the fluid-responsive patient; on the plateau, further filling adds only congestion — the physiology formalised by the passive leg raise and stroke-volume-variation testing in this bank's critical care section. Afterload — the load resisting ejection, approximated by systemic vascular resistance and aortic impedance — inversely affects stroke volume, most punishingly in the failing ventricle (why vasodilators help cardiogenic failure and why cross-clamping the aorta stresses the heart). Contractility — the inotropic state at any given load, set by sympathetic drive, calcium handling and drugs (catecholamines up; acidosis, hypoxia, beta-blockade down) — shifts the whole curve up or down: the failing septic or ischaemic heart operates on a flattened, downshifted curve, the rationale for inotropes when volume and pressure are optimised but output is not.

Why the others are wrong: A, B, C and E — stroke volume matters as much as rate; Starling describes stronger contraction with (physiological) stretch; pre- and afterload are distinct loading conditions; contractility is load-independent and drug- or state-modified, not fluid-modified.

Key point: Output = rate × stroke volume; stroke volume = preload (Starling's steep limb vs plateau — the whole basis of fluid-responsiveness testing), afterload (resistance to ejection) and contractility (the curve's position) — locate the patient on the curve before choosing fluid, vasopressor or inotrope.

Oxygen delivery = cardiac output × arterial oxygen content, and content is almost all haemoglobin-bound (1.34 mL O₂ per gram at full saturation — around 200 mL/L — versus ~3 mL/L dissolved), which is why anaemia and low output starve tissues despite a perfect PaO₂. The dissociation curve's sigmoid shape comes from cooperativity: each oxygen bound increases affinity for the next, giving a flat association plateau above ~8 kPa (loading is secure across a wide PaO₂ range — but equally, saturation stays deceptively high until PaO₂ falls onto the steep part, so a falling SpO₂ is a late alarm) and a steep unloading segment at tissue tensions. Shifts encode physiology: rightward — acidosis and CO₂ (the Bohr effect: exercising, hypercapnic tissue plucks oxygen off), fever, and raised 2,3-DPG (chronic hypoxia, anaemia) — favour unloading; leftward — alkalosis, hypothermia, depleted 2,3-DPG (stored bank blood transiently unloads poorly until DPG regenerates), fetal haemoglobin (placental extraction), and carboxyhaemoglobin — favour retention. Carbon monoxide is the double poison: 200-plus-fold haemoglobin affinity displaces oxygen AND left-shifts the remaining curve, while PaO₂ — dissolved oxygen — reads normal and standard two-wavelength pulse oximetry reads carboxyhaemoglobin as if oxygenated: the burns-and-inhalation patient (Parkland scenario elsewhere) needs co-oximetry and high-flow oxygen regardless of the numbers.

Why the others are wrong: B, C, D and E — haemoglobin carries the load; right shift lowers affinity to release oxygen; stored blood is DPG-depleted and left-shifted; oximetry is blinded by COHb.

Key point: Content lives on haemoglobin, and the sigmoid curve's shifts are delivery physiology — right (acid, CO₂, heat, DPG) unloads, left (alkalosis, cold, stored blood, CO, HbF) withholds; carbon monoxide poisons with a normal PaO₂ and a lying oximeter, and the flat plateau makes SpO₂ a late warning of hypoxaemia.

Guidelines: BTS emergency oxygen guidelines 2017: oxygen delivery depends on haemoglobin saturation, not dissolved oxygen — hence target saturations 94-98% (88-92% in hypercapnic risk), and 15 L/min via reservoir mask for carbon monoxide poisoning despite a normal PaO₂.