--- module: 001-02 language: en chapter: 1 title: "Homeostasis, Cellular Energetics, and Physiological Reserve" module_title: "Control systems, energy failure, and hidden reserve" source_sha256: b19010ccf07115be061f9a03a752375a9ce52157faa84471e5bf0ccc547b0fa0 --- # Control systems, energy failure, and reserve ## Layered control ### Overlapping loops on different timescales #### Blood pressure: baroreceptors in seconds #### Sympathetic tone and hormones over minutes to hours #### Renal sodium and water over days ### Fast tachycardia, slower renal volume defence ### Layering buffers failure of one component ## Measured versus regulated quantity ### Baroreceptors sense stretch in selected arteries ### Beta cells respond to nutrient metabolism ### Brain integrates core and skin temperature ### Normal value may hide intense compensation ### Abnormal value may be adaptive ### Fever is a regulated upward shift #### Body conserves and generates heat, causing chills ### Hyperthermia: heat gain exceeds loss, no shift ## Gain, delay, and reset ### Low gain leaves residual error ### High gain plus delay causes oscillation #### Hormones, gene expression, kidneys are slow #### Correction can overshoot ### Glucose, carbon dioxide, sodium keep moving ### Persistent hypertension blunts baroreceptors ### Chronic hypercapnia shifts bicarbonate retention ### Adaptation conceals disease #### Abrupt reversal can be harmful ## Feed-forward control ### Anticipates demand before variable changes ### Exercise: central command and limb input ### Food cues start salivation and secretion ### Reduces disturbance feedback must correct ### Maladaptive when conditioned without need ## Energy supply and tissue tolerance ### ATP is not stored; continuously regenerated ### Brain: high demand, little fuel reserve ### Cardiac muscle depends on aerobic metabolism ### Skeletal muscle uses phosphocreatine and glycolysis #### Accepts lactate and lower efficiency ## Oxygen delivery and use ### Flow, haemoglobin, saturation, extraction ### Anaemia, shock, hypoxaemia, microvascular failure ### Mitochondrial toxins block use despite delivery ### Separate ventilation through cellular utilisation ## Ordered cell injury and reperfusion ### Specialised activity lost before integrity ### Ion transport fails, sodium and water enter #### Cells swell ### Calcium activates lipases, proteases, nucleases ### Reactive oxygen species damage membranes and DNA ### Early correction allows recovery ### Beyond a threshold, damage self-amplifies #### Injury becomes irreversible ### Reperfusion rescues but can add injury #### Speed, temperature, electrolytes shape recovery ## Compartments and effective osmoles ### Sodium salts outside, potassium and phosphates inside ### Water shifts until osmotic forces equalise ### Low plasma sodium usually means excess water ### Oedema with low effective arterial volume #### Kidneys sense underfilling and retain ### Urea crosses membranes, weak effective osmole ### High glucose draws water out, dilutes sodium ### Brain adapts to chronic tonicity change #### Rapid correction of hypotonicity damages myelin #### Rapid correction of hypertonicity causes oedema #### Chronic adaptation narrows safe correction rate ## Reserve, compensation, decompensation ### Resting values cannot reveal reserve #### Early cardiac dysfunction: breathless on exertion #### Creatinine normal despite lost filtration ### Compensation has costs #### Sympathetic drive raises myocardial oxygen demand #### Renin-angiotensin-aldosterone worsens congestion #### Hyperventilation increases respiratory work #### Bone buffering depletes mineral ### Decompensation: demand exceeds reserve #### Breathing work, mental state, urine, lactate #### Trends precede vital sign collapse ### Physiology is a trajectory, not a photograph ## Five clinical questions ### Which variable is defended ### Which sensors, integrators, effectors ### What compensation preserves the value ### What cost that compensation imposes ### How much reserve remains