Normal Variations of the Respiratory System Notes

NOTES NOTES NORMAL VARIATIONS PULMONARY CHANGES DURING EXERCISE osms.it/pulmonary_changes_during_exercise RESPIRATORY RESPONSE TO EXERCISE ▪ Exercise → muscle workload increase → consumption of significant O2 amounts, above baseline production of CO2, lactic acid ▪ Increased O2 demand → hyperpnea (ventilation increases 10–20x to compensate) ▪ Hyperpnea vs. hyperventilation ▫ Hyperpnea: aims to maintain homeostasis → blood O2 ,CO2 levels remain relatively constant ▫ Hyperventilation: excessive ventilation, blowing off too much CO2 → low PCO2, respiratory alkalosis ▪ Exercise-induced ventilation not initially prompted by alterations in blood gases (rising PCO2 , declining PO2, pH) ▪ Ventilation increases abruptly as exercise begins due to neural factors ▫ Psychological stimuli (conscious exercise anticipation) ▫ Simultaneous cortical motor activation of skeletal muscle, respiratory centers ▫ Proprioceptors moving muscles, tendons, joints → stimulate respiratory centers ▫ Initial neural regulation → early compensation to exercise as opposed to waiting for change in blood values ▪ Initial abrupt increase in ventilation is followed by gradual increase (reflective of lung CO2 delivery rate) → eventually, steady state of ventilation appropriate for intensity achieved ▪ Exercise cessation → initial small abrupt decline in ventilation (higher neurological stimulation ends) → followed by gradual decrease to pre-exercise respiratory rate (gradual decrease in CO2 flow to lungs) PULMONARY CIRCULATORY RESPONSE ▪ Cardiac output increases to meet tissue O2 demand → increased right heart output → increased blood flow through pulmonary circulation → increased blood return to left heart → increased output to systemic circulation → increased O2 tissue delivery ▪ Exercise → pulmonary resistance decrease → perfusion of more pulmonary capillary beds → more even distribution of pulmonary perfusion, ventilation → improved V/Q ratio (decreased physiological dead space) → increased gas exchange efficiency HEMATOLOGICAL RESPONSE Bohr effect ▪ Hemoglobin’s oxygen binding affinity is inversely related to acidity, carbon dioxide concentration ▫ Exercise → increased tissue PCO2, decreased tissue pH, increased temperature → right shift of O2hemoglobin dissociation curve → decreased affinity of hemoglobin for O2 → greater unloading of oxygen to exercising muscle OSMOSIS.ORG 625

Regulation of blood gases during exercise ▪ Arterial PCO2, PO2 remain nearly constant during exercise ▪ Venous PCO2, PO2 may change significantly during exercise ▫ Ventilation increases sufficiently to blow off all excess CO2, maintain arterial homeostasis Anaerobic respiration ▪ Leads to rise in lactic acid levels ▪ Not due to inadequate respiratory function ▪ Alveolar ventilation, pulmonary perfusion remain well matched during exercise → hemoglobin fully saturated ▪ Cardiac output limitation/limits of skeletal muscle to utilize oxygen → rising lactic acid 626 OSMOSIS.ORG

Chapter 72 Respiratory Physiology: Normal Variations PULMONARY CHANGES AT HIGH ALTITUDE & ALTITUDE SICKNESS osms.it/pulmonary_changes_high_altitude_altitude_sickness RESPIRATORY RESPONSE TO ALTITUDE ▪ Humans typically live at altitudes between sea level and 2400m/7800ft ▪ Altitudes > 2400m/7800ft → lower overall atmospheric pressure → lower PO2 → hemoglobin less saturated at baseline ▫ At rest at sea level hemoglobin typically unloads 20–25% O2 content on a single trip through the circulatory system ▫ Significant functional reserve allows for survival due to further hemoglobin unloading when poorly saturated ACCLIMATIZATION ▪ Long-term, slow steady move from sea level to higher altitude → respiratory, hematopoietic adaptation ▪ Decrease in arterial PO2 → peripheral chemoreceptors more responsive to increases in PCO2 → chemoreceptors stimulate medullary inspiratory center → increased breathing rate Initial (fast) adaptation ▪ Some changes occur immediately, others over course of days ▪ Pulmonary ▫ Minute ventilation → 2–3L/min higher than sea level ▫ Increased ventilation → decreased arterial CO2 (<40mmHg) → respiratory alkalosis → increased blood pH → inhibition of central, peripheral chemoreceptors → offset increase in ventilation rate (initial effect) ▫ As adaptation occurs → HCO3- excretion increases → HCO3- concentration in cerebrospinal fluid (CSF) decreases → CSF pH decreases toward normal → increased ventilation rate resumes ▫ Respiratory alkalosis as result of rapid ascent to high altitude managed with carbonic anhydrase inhibitors → increased HCO3- excretion → mild compensatory metabolic acidosis ▪ Hematological ▫ Increase in 2,3-bisphosphoglyceric acid (2,3-BPG) concentration → hemoglobin affinity for O2 reduced → increased unloading of O2 at tissue level (also decreases efficiency of oxygen loading in lungs) ▪ Cardiac ▫ Increased heart rate ▫ Right heart hypertrophy: low PO2 alveolar gas → pulmonary vasculature vasoconstriction → increase in pulmonary vascular resistance → increased right heart strain → right ventricular hypertrophy ▪ Oxygen conservation ▫ Non-essential body functions suppressed → reduction in food digestion efficiency (decreased circulation in favor of perfusing more important organs) Late (slow) acclimatization ▪ Occurs over weeks to months ▪ Hematological: hypoxia → kidneys produce more erythropoietin → stimulates bone marrow production of red blood cells → total O2 carrying capacity of blood increased ▫ Essential compensation for living at altitude ▫ Increases blood viscosity → greater blood flow resistance → greater heart workload ▫ Full acclimatization: increase in red blood cell plateaus ▪ Effect on complete blood count parameters ▫ Total red cells: ↑ ▫ Hemoglobin: ↑ ▫ Hematocrit: ↑ OSMOSIS.ORG 627

▫ Mean corpuscular volume: unchanged ▫ Mean corpuscular hemoglobin concentration: ↑ Exercise at altitude ▪ Adaptations normally serve to achieve homeostasis at rest → unless fully acclimatized intense physical activity → homeostasis loss → severe hypoxia ▪ This transient intentional hypoxia can be exploited by athletes → further adaptive changes to altitude → blood with greater oxygen carrying capacity → improved performance at lower altitude ▪ Late phase acclimatization of skeletal muscle includes: increased capillary concentration, increased myoglobin amount, increased mitochondria number, increased aerobic metabolism enzyme concentration ACUTE MOUNTAIN SICKNESS ▪ AKA altitude sickness ▪ Commonly associated with altitudes above 2400m/7800ft ▫ Minor symptoms may occur at as low as 1500m/5000ft ▫ Death zone: 5500m/18000ft, altitude considered incompatible with human life; acclimatization not possible ▪ Caused by sudden transition to altitude without sufficient acclimatization → low atmospheric pressure → low PO2 → hypoxia ▪ Contributing factors ▫ Rate of ascent ▫ Rate of water vapor loss from lungs ▫ Activity level ▪ Sudden increase in altitude without taking time to acclimatize Symptoms ▪ Headache, shortness of breath, nausea, dizziness, peripheral edema Complications ▪ Severe complications of high altitude can be fatal ▪ High altitude pulmonary edema (HAPE) ▫ Low atmospheric pressure → decreased oxygen partial pressures, poor oxygenation → increased pulmonary arterial, capillary pressures, idiopathic increase in permeability of vascular endothelium → fluid extravasation → pulmonary edema ▪ High altitude cerebral edema (HACE) ▫ Hypoxia → increased cerebral microvascular permeability, failure of cellular ion pumps → vasogenic, cytotoxic edema Treatment ▪ Supplemental oxygen/immediate descent 628 OSMOSIS.ORG