17.2 Applied Anatomy & Physiology Across Body Systems and the Lifespan

17.2 Applied Anatomy & Physiology Across Body Systems and the Lifespan

CPCF Appendix A foundational knowledge #2 is the single largest item in the framework: human anatomy, neuroanatomy, and physiology applied to all body systems across the lifespan, including pregnancy and aging. This section is a consolidation and reference, organized around the question the examination actually asks — what does this structure do, and what happens to the patient when it stops doing it?

Respiratory

Structure and function: the upper airway warms, humidifies, and filters; the lower airway conducts; the alveolar-capillary membrane exchanges. Defence mechanisms — the cough reflex, mucociliary escalator, and gag reflex — are what a decreased level of consciousness removes, which is why unprotected airways aspirate.

Mechanics of respiration: contraction of the diaphragm and external intercostals expands the thorax, generating negative intrapleural pressure and drawing gas in. Expiration is normally passive elastic recoil. Anything that removes negative pressure — an open chest wound — or restricts expansion — circumferential burns, ascites, obesity, late pregnancy — impairs ventilation mechanically.

Control of ventilation: central chemoreceptors in the medulla respond principally to CO2 (via cerebrospinal fluid pH); peripheral chemoreceptors in the carotid and aortic bodies respond to severe hypoxaemia. In chronic CO2 retention, the hypoxic drive becomes relatively more important — which is why oxygen is titrated to a target saturation in COPD rather than withheld or given without limit.

Gas transport: oxygen is carried almost entirely bound to haemoglobin; CO2 is carried mostly as bicarbonate. The oxyhaemoglobin dissociation curve shifts right (releasing oxygen more readily to tissue) with acidosis, hypercapnia, fever, and raised 2,3-DPG, and left with alkalosis, hypocapnia, hypothermia, and carbon monoxide.

Lung volumes: tidal volume is roughly 6 to 8 mL/kg; anatomical dead space is roughly 2 mL/kg. Shallow, rapid breathing ventilates dead space preferentially and is far less effective than the respiratory rate alone suggests.

Cardiovascular

Mechanical function: cardiac output equals heart rate multiplied by stroke volume; stroke volume depends on preload, afterload, and contractility. The Frank-Starling relationship means that, up to a point, greater ventricular filling produces a stronger contraction.

Blood pressure regulation: mean arterial pressure is the product of cardiac output and systemic vascular resistance. Baroreceptors in the carotid sinus and aortic arch trigger sympathetic compensation within seconds; the renin-angiotensin-aldosterone system and antidiuretic hormone act over minutes to hours.

Electrical activity: the sinoatrial node (60–100/min) is the normal pacemaker, with the atrioventricular node (40–60/min) and ventricular foci (20–40/min) as escapes. Automaticity, excitability, conductivity, and contractility are the four properties every dysrhythmia disturbs.

Circulation: coronary perfusion occurs almost entirely during diastole, which is why tachycardia is doubly harmful in ischaemia — it raises demand and shortens supply. Cerebral blood flow is autoregulated across a wide range of mean arterial pressures, and that autoregulation is lost in brain injury.

Neurological

Central and peripheral nervous systems; the cranial nerves most relevant prehospitally are III (pupil constriction — the uncal herniation sign), VII (facial droop — upper face spared in stroke, involved in Bell's palsy), IX and X (gag and swallow), and XII (tongue deviation).

The brain is roughly 2% of body mass and consumes about 20% of resting oxygen and glucose, with essentially no stored substrate — which is why hypoglycaemia and hypoxia produce neurological signs within minutes. The blood-brain barrier limits drug entry and fails in inflammation.

Gastrointestinal and Hepatobiliary

Motility, digestion, absorption, and elimination; the liver synthesizes clotting factors, albumin, cholesterol, and glycogen, metabolizes drugs, and detoxifies blood. The clinical consequences of failure are covered in Section 14.5.

Genitourinary

Blood filtration, waste elimination, fluid and electrolyte balance, acid-base regulation, erythropoietin production, and vitamin D activation. Consequences of failure are covered in Section 14.6.

Endocrine

Hormone mechanisms of action, metabolism, growth and development, and regulation of sleep, blood pressure, emotions, and mood. Prehospitally: insulin and glucagon (glucose homeostasis), cortisol (stress response — its absence causes adrenal crisis), thyroid hormone (metabolic rate — storm and myxoedema coma), aldosterone and ADH (sodium, water, potassium), and catecholamines (fight or flight; phaeochromocytoma).

Musculoskeletal, Integumentary, Haematologic, Immunologic, EENT

• Musculoskeletal: posture, balance, mobility, and gait; bone as a reservoir of calcium and the site of haematopoiesis. Long bones can sequester large volumes of blood — a femoral shaft fracture can hold 1 to 1.5 L.
• Integumentary: protection, thermoregulation, sensation, fluid balance, and vitamin D synthesis. Losing skin loses all five (Section 13.6).
• Haematologic: red cells carry oxygen, white cells defend, platelets and the coagulation cascade seal. Fetal haematology transitions at birth.
• Immunologic: innate barriers and inflammatory response; adaptive antibody and cell-mediated responses.
• EENT: hearing, balance and the vestibular system; nasopharyngeal air filtration and voice production; the shared passage of air, food, and liquid — the anatomical reason aspiration and choking are possible at all; vision and pupillary response.

Reproductive and Obstetric

Sexual differentiation, fertility, sexually transmitted infections; the menstrual cycle, fertilization, fetal development, labour and delivery, lactation, the endocrinology of pregnancy, and postpartum changes (Chapter 15).

Maternal physiological adaptations that change your assessment: plasma volume rises by roughly 40% to 50% producing a dilutional anaemia; heart rate rises by 10 to 20 beats per minute; blood pressure falls in the second trimester and returns toward baseline at term; tidal volume rises; functional residual capacity falls, so desaturation is fast; gastric emptying slows, increasing aspiration risk; and from about 20 weeks the gravid uterus compresses the inferior vena cava when supine — hence left lateral tilt or manual uterine displacement. A pregnant patient can lose 30% to 35% of blood volume before her blood pressure falls, and the fetus is compromised long before that point.

The Lifespan: Where Physiology Differs

[!IMPORTANT] The single most examined paediatric physiological fact is that hypoxia causes bradycardia in infants and children. A bradycardic child is hypoxic until proven otherwise, and the treatment is oxygen and ventilation — not atropine and not pacing. Paediatric cardiac arrest is overwhelmingly respiratory in origin, which is also why the JumpSTART algorithm includes rescue breaths before an apnoeic child with a pulse is tagged expectant.