Respiratory Physiology Part II Bio 219 Napa Valley College Dr. Adam Ross
Gas exchange Gas exchange in the lungs (to capillaries) occurs by diffusion across respiratory membrane due to differences in partial pressure Partial Pressure: is the driving force for the diffusion of gasses (P O2 P CO2 ) Gas will diffuse from high to low partial pressure Dalton s Law: total pressure = sum of all partial pressures in a mixture Ptotal = PN2 + PO2 + PCO2 + PH2O PO2 = Ptotal x (% O2/100) = 760 x 0.21 = 160 mm Hg
Pulmonary gasses and diffusion O2 diffuses from air in alveoli to blood in pulmonary capillaries CO2 diffuses from pulmonary capillaries into alveoli - high diffusion efficiency due to: (1) high surface area of alveoli (2) thin respiratory membrane
Air and Blood Gases PO2 PCO2 O2 saturation inspired air 160 0.3 alveolar air 100 40 pulmonary veins & systemic arteries 100 40 98% arterial blood vena cava & pulmonary arteries 40 46 75% mixed venous blood
Hemoglobin (Hb) Iron containing protein found in erythrocytes Capable of binding both oxygen and CO 2 Carries oxygen to tissues Helps carry (10%) CO 2 away from tissues (85% is dissolved in blood as bicarbonate, 5% = free CO 2 in solution)
Bohr Shift When Hb is bound by CO 2 its affinity for O 2 is reduced, causing oxygen to be released at tissues that are releasing CO 2 Low ph has the same effect (remember CO 2 = H + )
Control of Ventilatory Effort Respiratory centers: Primary respiratory control located in brainstem Contains Inspiratory (I) and Expiratory (E) neurons Medulla Oblongata: central pattern generator, generates breathing rhythm Dorsal Respiratory Group: Mostly I neurons Ventral Respiratory Group: E and I neurons Pons: pontine respiratory group, smoothes out breathing rhythm
Central Chemoreceptors Medulla: Sensitive to PCO 2+ via [H + ] of cerebrospinal fluid arterial PCO2 PCO2 of CSF CO2 + H2O H2CO3 H+ + HCO3- [H+] in CSF stimulates ventilation Central chemoreceptor has the dominant role in regulating breathing at rest
Peripheral Chemoreceptors Carotid bodies - sensitive to low PO2, also PCO2 and ph of arterial blood - stimulate ventilation directly at very low PO2 (< 60 mm Hg) - increase sensitivity of central response to CO2 - contribute to increase in ventilation during exercise
Ventilation Ventilation is normally regulated to maintain constant arterial PCO2 (normal = 40 mm Hg) hypoventilation - PCO2 (> 45 mmhg) hyperventilation - PCO2 (< 35 mmhg)
Hering-Breuer Reflex Prevents over inflation of the lungs Lungs have stretch receptors that can sense fullness of lung Pulmonary stretch receptors in smooth muscle of the airways When lung inflates the send APs to the respiratory centers in the brain Inhibits the INSPIRATORY centers of the medulla and ends inspiration
Hypoventilation Decrease in ventilation leading to an increase in arterial P CO 2 (hypercapnia) Carbon dioxide will start to build up throughout the body The increase in P CO will cause a decrease in ph (respiratory acidosis) 2 This will activate chemoreceptors to increase respiratory rate
Hyperventilation Increase in ventilation by an increase in respiratory rate and/or increasing tidal volume leading to a decrease in P (hypocapnia) CO 2 Rate of ventilation is higher than what is needed to remove carbon dioxide from blood A decrease in P CO will decrease the inspiratory drive 2 (Are able to hold breath for a longer period of time) Prolonged hyperventilation will lead to respiratory alkalosis (increase in ph) which can cause arterioles in the brain to constrict -> decrease in blood flow to the brain -> dizziness
Exercise Hyperpnea : increase in ventilation matching an increase in metabolic activity (ex. Exercise) Ventilation rate matches demand for carbon dioxide removal so there is no decrease in arterial P CO that was 2 seen in hyperventilation Exercise increases demand for oxygen and produces more carbon dioxide There is an increase in perfusion of the upper lungs (that are normally closed at rest) to increase gas exchange, because the increase in CO during exercise increases pulmonary vascular pressure The mechanisms that control the respiratory response to exercise are not understood well