Demand raises ventilation and flow
Working muscle increases oxygen use and CO₂ production; ventilation, cardiac output, extraction, and heat-fluid regulation rise together.
LUNGS / 04
Exercise and altitude recruit adaptive responses. Asthma and COPD alter airflow through different mechanisms. Pneumonia disrupts alveolar units, while pulmonary embolism obstructs perfusion.
Working muscle increases oxygen use and CO₂ production; ventilation, cardiac output, extraction, and heat-fluid regulation rise together.
Fitness, intensity, airway and lung mechanics, hemoglobin, heart function, environment, and muscle metabolism constrain performance.
Lower barometric pressure reduces inspired PO₂, stimulating ventilation and producing an early respiratory-alkalosis signal.
Bicarbonate excretion supports sustained hyperventilation; plasma-volume and erythropoietic changes occur on different timescales.
Susceptible airways can develop swelling, mucus, sensitivity, and episodic smooth-muscle constriction after diverse triggers.
Bronchodilation acts on muscle tone, while inhaled corticosteroids change inflammatory signaling over time.
Airway inflammation, mucus, loss of elastic recoil, and alveolar destruction can combine in different proportions.
Uneven ventilation, surface loss, hypoxemia, carbon-dioxide retention, and pulmonary vascular effects vary by phenotype and severity.
Infection can fill exchange units with fluid, cells, mucus, and debris, producing low ventilation despite continued perfusion.
Fever, immune activity, breathing work, dehydration, and comorbid reserve influence severity and recovery.
A clot can block pulmonary arterial flow, increasing dead space and right-ventricular afterload.
Sudden breathlessness, pleuritic chest pain, fainting, or coughing blood requires urgent evaluation rather than graph interpretation.