ICU Map

ICU Physiology Library

Cross-cutting physiology concepts that multiple topics depend on, kept in one place and cross-linked to each other instead of being re-explained inside every topic that touches them. Several include a lightweight, deterministic interactive visualization.

Respiratory

The pressure needed to hold the lung and chest wall at end-inspiratory volume, once flow has stopped.

Interactive visual

Plateau pressure minus PEEP — the cyclic stress the tidal volume itself imposes on the aerated lung.

Interactive visual

How much the lung and chest wall expand for a given change in pressure.

The pressure needed to drive flow through the airways, separate from the pressure needed to inflate the lung.

Trapped air pressure left in the alveoli at end-expiration when a breath doesn't fully exhale before the next one starts.

The pressure that actually stretches the lung itself, once chest wall and pleural pressure are accounted for.

Ventilated lung that isn't perfused, so it doesn't participate in gas exchange.

Interactive visual

Blood that bypasses ventilated alveoli entirely, producing hypoxemia that resists supplemental oxygen.

Interactive visual

The mechanical effort the respiratory muscles expend to move air in and out of the lungs.

Why inflamed, fluid-filled alveoli cause hypoxemia that often resists supplemental oxygen alone.

Interactive visual

How dynamic hyperinflation from insufficient expiratory time builds intrinsic PEEP that raises mean intrathoracic pressure, obstructs venous return, and can precipitate cardiovascular collapse — and why ventilator disconnection is both diagnostic and therapeutic.

Interactive visual

Diffuse alveolar-capillary barrier disruption leading to non-cardiogenic pulmonary edema, severe intrapulmonary shunt, and the protective mechanics of positive end-expiratory pressure (PEEP).

Interactive visual

How differentiating peak inspiratory pressure (Ppeak) and plateau pressure (Pplat) localizes respiratory compromise to resistive versus elastic components.

Interactive visual

Why driving pressure (ΔP = Pplat - PEEP = Vt / Crs) is the primary ventilator variable correlated with ARDS survival, indexing tidal volume to functional baby lung size.

Interactive visual

Physiologic differentiation of low V/Q (responsive to oxygen), pure intrapulmonary shunt (V/Q = 0, refractory to FiO2), and dead space (V/Q = ∞, causing hypercapnia and ventilatory inefficiency).

Interactive visual

The mechanics of expiratory flow limitation, breath-stacking (auto-PEEP), and ventilator management in severe obstructive airway disease.

Interactive visual

Cardiovascular

How cardiac output and arterial oxygen content combine to determine tissue oxygen delivery.

Interactive visual

The rate at which the tissues actually use oxygen, as opposed to how much is delivered to them.

Why oxygen consumption stays independent of delivery over a wide range — until it doesn't.

The stretch on the ventricle at end-diastole, just before it contracts.

Interactive visual

The resistance the ventricle must overcome to eject blood.

The intrinsic force the heart generates independent of preload and afterload.

Interactive visual

The volume of blood the heart pumps per minute — the product of heart rate and stroke volume.

Interactive visual

The resistance the arterial tree offers to blood flow — the main determinant of left ventricular afterload.

The flow of blood back to the right heart, driven by the pressure gradient between the venous system and the right atrium.

Why the thin-walled right ventricle is disproportionately vulnerable to rises in afterload.

How pathogen recognition triggers a cytokine storm that causes profound vasodilation, capillary leak, and distributive shock despite a high cardiac output.

Interactive visual

How left ventricular contractile failure creates a lethal cycle of falling cardiac output, rising filling pressures, pulmonary oedema, and ischaemia that worsens the very heart it originates from.

Interactive visual

Why the right ventricle fails at acutely elevated afterloads, how interventricular interdependence propagates that failure to the left heart, and why standard resuscitation manoeuvres — fluid, high PEEP, intubation — can be catastrophic.

Interactive visual

How mechanical ventilation simultaneously reduces preload (harmful in hypovolaemia and RV failure) and reduces LV afterload (beneficial in LV failure) — the same intervention can save or kill depending on what is failing.

Interactive visual

Acute mechanical pulmonary vascular occlusion, abrupt RV afterload spike, interventricular dependence, and systemic circulatory collapse.

Interactive visual

Fluid accumulation in a fixed pericardial space causing diastolic chamber compression, equalization of end-diastolic pressures, and pulsus paradoxus.

Interactive visual

Cardiac resting membrane potential dynamics and the three-pillar therapeutic strategy: Stabilize the membrane, Shift K+ intracellularly, and Eliminate K+ from the body.

Interactive visual

The biophysics of aortic intimal tearing, the critical role of ventricular contractility (dP/dt), and why beta-blockers must precede vasodilators.

Interactive visual

The biophysical determinant of cerebral blood flow in acute brain injury, autoregulatory limits, and Brain Trauma Foundation management targets.

Interactive visual

The definitive oxygen delivery equation (DO2 = CO × CaO2), arterial oxygen content determinants, and the three distinct physiological modes of circulatory delivery failure.

Interactive visual

How mean systemic filling pressure (MSFP) and right atrial pressure (RAP) establish the driving gradient for venous return and cardiac output.

Interactive visual

How the thin-walled right ventricle responds to acute increases in pulmonary vascular resistance and how right coronary perfusion pressure governs RV survival.

Interactive visual

How tissues increase oxygen extraction ratio (O2ER) during hypoperfusion, and the critical DO2 threshold where supply-dependence and anaerobic dysoxia begin.

Interactive visual

Differentiating Type A anaerobic dysoxia from Type B adrenergic surges and impaired hepatic clearance during critical illness resuscitation.

Interactive visual

Renal

How the glomerulus separates plasma water and small solutes from blood cells and large proteins.

The rate at which the kidneys filter plasma across the glomerulus — the single best overall measure of kidney function.

How the renal tubules reclaim and fine-tune the vast majority of what the glomerulus filters.

How the kidney adjusts sodium reabsorption to match intake and maintain effective circulating volume.

How the kidney's distal nephron controls potassium excretion, and why AKI so readily produces hyperkalemia.

How the kidney reclaims filtered bicarbonate and generates new bicarbonate to excrete the body's daily acid load.

Inhibition of the Na+/K+/2Cl- cotransporter in the thick ascending limb of Henle, disruption of the medullary concentration gradient, and contraction alkalosis.

Interactive visual

How hypothalamic osmoreceptors, non-osmotic baroreceptors, and renal V2-aquaporin-2 channels regulate serum sodium concentration and water balance.

Interactive visual

How to distinguish water diuresis (central/nephrogenic DI, Uosm < 200) from solute diuresis (hyperglycemia, mannitol, urea, Uosm > 300) in polyuric ICU patients.

Interactive visual

Acid-Base

The equation linking pH to the ratio of bicarbonate to dissolved CO2 — the mathematical foundation of clinical acid-base interpretation.

Interactive visual

The calculated gap between measured cations and anions, used to narrow the differential for a metabolic acidosis.

Interactive visual

Compares the rise in anion gap to the fall in bicarbonate, to detect a second metabolic process hiding behind a high-anion-gap acidosis.

The difference between measured and calculated serum osmolality, used to screen for unmeasured osmotically active substances such as toxic alcohols.

How the respiratory and renal systems each partially correct for a primary acid-base disturbance originating in the other.

The expected respiratory compensation for a primary metabolic acidosis, used to detect a second, independent disorder.

Interactive visual

When more than one primary acid-base process is present at once, and why pH alone can hide them.

Severe absolute or relative insulin deficiency driving lipolysis, hepatic ketogenesis, profound osmotic diuresis, and whole-body potassium depletion.

Interactive visual

Systematic physiology of Metabolic Acidosis, Metabolic Alkalosis, Respiratory Acidosis, and Respiratory Alkalosis with exact compensation formulas.

Interactive visual