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Respiratory Volumes
Respiratory Capacities
Dead Space
Forced vital capacity (FVC)gas forcibly expelled after taking deep breath
Alveolar Ventilation
Minute ventilationtotal amount of gas flow into or out of respiratory tract in
one minute
Alveolar ventilation rate (AVR)flow of gases into and out of alveoli during a
particular time
AVR
(ml/min)
frequency
(breaths/min)
Both involve
Total pressure exerted by mixture of gases = sum of pressures exerted by each gas
Partial pressure
water
Alveoli contain more CO2 and water vapor than atmospheric air
External Respiration
Influenced by
Respiratory membranes
0.5 to 1 m thick
Large total surface area (40 times that of skin) for gas exchange
Alveolar Pco2 = 40 mm Hg
Though gradient not as steep, CO2 diffuses in equal amounts with oxygen
Ventilation-Perfusion Coupling
Perfusion
Ventilation-Perfusion Coupling
Internal Respiration
Tissue Po2 always lower than in systemic arterial blood oxygen from blood to
tissues
O2 Transport
O2 and Hemoglobin
O2
O2 and Hemoglobin
to cells
Po2
Temperature
Blood pH
Pco2
In arterial blood
Po2 = 100 mm Hg
Hb is 98% saturated
In venous blood
Po2 = 40 mm Hg
Hb is 75% saturated
Venous reserve
Oxygen remaining in venous blood
Homeostatic Imbalance
Hypoxia
CO2 Transport
In systemic capillaries
In pulmonary capillaries
HCO3 moves into RBCs (while Cl move out); binds with H+ to form H2CO3
Haldane Effect
Lower Po2 and hemoglobin saturation with O2; more CO2 carried in blood
As HbO2 releases O2, it more readily forms bonds with CO2 to form
carbaminohemoglobin
Neural controls
Its inspiratory neurons excite inspiratory muscles via phrenic (diaphragm) and
intercostal nerves (external intercostals)
VRG
Smooth out transition between inspiration and expiration and vice versa
One hypothesis
Chemical Factors
If blood Pco2 levels rise (hypercapnia), CO2 accumulates in brain
Chemical Factors
Influence of Po2
Peripheral chemoreceptors in aortic and carotid bodiesarterial O2 level sensors
When excited, cause respiratory centers to increase ventilation
Influence of arterial pH
Can modify respiratory rate and rhythm even if CO2 and O2 levels normal
depth
When arterial Po2 falls below 60 mm Hg, it becomes major stimulus for
respiration (via peripheral chemoreceptors)
Hypothalamic controls act through limbic system to modify rate and depth of
respiration
Inflation Reflex
Hyperpnea
Gradual decline to baseline because of decline in CO2 flow after exercise ends
Not from poor respiratory function; from insufficient cardiac output or skeletal
muscle inability to increase oxygen uptake
Less O2 available
Homeostatic Imbalances
Homeostatic Imbalance
Emphysema
Homeostatic Imbalance
Chronic bronchitis
Obstructed airways
Homeostatic Imbalance
Homeostatic Imbalances
Asthmareversible COPD
Homeostatic Imbalances
Tuberculosis (TB)
Lung cancer
Lung cancer
tumor
During fetal life, lungs filled with fluid and blood bypasses lungs
Cystic fibrosis
Research into
Introducing normal genes
Prodding different protein Cl- channel
Developmental Aspects
At birth, respiratory centers activated, alveoli inflate, and lungs begin to function
Lungs continue to mature and more alveoli formed until young adulthood