Physiology — Cardiovascular & Respiratory — USMLE Step 1 Notes

Cardiac output and its determinants

• CO = heart rate × stroke volume; mean arterial pressure = CO × total peripheral resistance.
• Stroke volume is set by preload, afterload and contractility. Preload rises with venous return and volume; afterload rises with arterial pressure/aortic stenosis.
• Frank-Starling: greater end-diastolic stretch → greater force of contraction, so the heart pumps out whatever it receives.
• Contractility (and stroke volume) rises with sympathetic tone, catecholamines and calcium; it falls with heart failure, beta-blockade and acidosis.

The cardiac cycle

• Systole: isovolumetric contraction → ejection. Diastole: isovolumetric relaxation → filling.
• S1 = mitral/tricuspid closure (start of systole); S2 = aortic/pulmonary closure (start of diastole).
• S3 = rapid ventricular filling (volume overload, heart failure); S4 = atrial kick into a stiff ventricle.

Cardiac electrophysiology

• Pacemaker (SA/AV) cells: unstable phase-4 depolarisation (funny Na current) sets rate; upstroke is calcium-driven.
• Ventricular myocyte: phase 0 Na influx, phase 2 plateau (Ca influx balances K efflux), phase 3 repolarisation (K efflux).
• Conduction: SA node → AV node (delay allows filling) → His → bundle branches → Purkinje fibres.

Vascular control & reflexes

• Baroreceptor reflex: carotid sinus/aortic arch sense stretch; a fall in pressure reduces firing → sympathetic surge (raises HR, contractility, vasoconstriction).
• Resistance is dominated by arterioles; capillaries have the largest total cross-sectional area and slowest flow (exchange).
• Starling forces govern capillary fluid movement; oedema results from raised hydrostatic or lowered oncotic pressure, or lymphatic blockage.

Respiratory mechanics

• Compliance = change in volume per change in pressure; surfactant (type II pneumocytes) lowers surface tension and prevents alveolar collapse.
• Lung volumes: tidal, IRV, ERV, residual (cannot be measured by spirometry); FRC is the resting balance of lung recoil inward and chest-wall recoil outward.
• Obstructive disease lowers FEV1/FVC; restrictive disease lowers volumes with a preserved or raised ratio.

Gas exchange & transport

• V/Q matching: ventilation and perfusion are highest at the lung base. High V/Q = dead space; low V/Q → 0 = shunt (does not correct with oxygen).
• Oxygen-haemoglobin curve is sigmoid (cooperative binding). A right shift (more O2 unloading) comes from raised CO2, H+, temperature and 2,3-BPG (Bohr effect); a left shift holds oxygen tighter (fetal Hb, CO, alkalosis).
• CO2 is carried mostly as bicarbonate (via carbonic anhydrase in red cells), plus carbaminohaemoglobin and dissolved; the Haldane effect lets deoxygenated blood carry more CO2.

Control of ventilation

• The medulla sets the rhythm. Central chemoreceptors respond to CSF H+/CO2 (the main minute-to-minute driver); peripheral chemoreceptors (carotid/aortic bodies) respond mainly to low PaO2.
• In chronic CO2 retention the hypoxic drive matters more — why uncontrolled oxygen can blunt ventilation.

Written by StepSherpa in our own words, grounded in Human Physiology (Wikibooks), used under CC BY-SA 3.0.