Integrated Physiology: Exercise, Altitude and Shock
Key multi-system concepts linking cardiovascular, respiratory, renal and endocrine responses to exercise, altitude and shock.
Keyboard Shortcuts
💡 Pro tip: Use keyboard shortcuts for faster studying!
Study Smart Tips for Integrated Physiology: Exercise, Altitude and Shock
Master these concepts using proven study techniques that actually work:
Active Recall
Test yourself before flipping each card to strengthen memory retention
Spaced Repetition
Review difficult cards more frequently than easy ones
Multiple Sessions
Break study time into shorter, focused sessions
Explain Aloud
Verbalize answers to reinforce understanding
Questions Covered in This Set
12 cards to master
State the Fick principle and its use
VO₂ = CO × (CaO₂ − CvO₂). Decompose any change in O₂ delivery into cardiac output, [Hb], SaO₂ or tissue extraction.
Formula for arterial oxygen content
CaO₂ ≈ 1.34 × [Hb] × SaO₂ + 0.003 × PaO₂ — almost all O₂ is haemoglobin-bound.
What raises heart rate at the very onset of exercise?
Central command feed-forward from motor cortex to medulla causing vagal withdrawal — HR rises within one beat, before any metabolite accumulates.
What happens to TPR and MAP during exercise?
TPR falls (metabolic vasodilation in muscle, up to 20-fold flow rise) but MAP rises modestly because cardiac output rises even more (5 → 20–25 L/min).
How do PaO₂, PaCO₂ and pH change in moderate exercise?
Essentially unchanged — ventilation rises in proportion to CO₂ production. Above the anaerobic threshold, lactic acidosis drives extra ventilation so PaCO₂ falls and pH drops.
Which contributes more to increased CO in exercise: HR or SV?
Heart rate (70 → 180 bpm) dominates; stroke volume rises ~50% via increased preload (muscle/respiratory pumps, venoconstriction) and β₁ contractility.
Renal and endocrine response to exercise
Renal plasma flow falls but GFR is roughly maintained by autoregulation; ADH and aldosterone rise, urine output falls to conserve volume for sweat losses.
Alveolar gas equation
P_AO₂ = F_IO₂(P_B − 47) − PaCO₂/R. At 4,500 m (P_B ≈ 430 mmHg) P_AO₂ ≈ 50 mmHg and SaO₂ ≈ 80%.
Why is the initial hyperventilation at altitude submaximal?
Carotid body hypoxic drive (PaO₂ < 60 mmHg) causes respiratory alkalosis, which brakes ventilation via central chemoreceptors until renal bicarbonate excretion normalises CSF pH.
How does acetazolamide speed acclimatisation?
Carbonic anhydrase inhibition → bicarbonate diuresis and mild metabolic acidosis → removes the alkalotic brake, allowing ventilation to rise sooner.
Days-to-weeks adaptation to altitude
Hypoxia stabilises HIF-1α → erythropoietin release → increased haematocrit and [Hb], raising CaO₂; also 2,3-BPG changes and pulmonary vasoconstriction.
Which factors right-shift the O₂–Hb curve in exercising muscle?
Increased CO₂/H⁺ (Bohr effect), raised temperature and 2,3-BPG — improving O₂ unloading; capillary recruitment shortens diffusion distance.
