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77 Cards in this Set

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Tidal volume
Volume of air that enters and leaves the lung in a single cycle. 500ml
Functional residual capacity
Amount of air in the lungs after passive expiration. 2,700ml
Inspiratory capacity
Maximal volume of gas inspired from FRC. 4,000ml
Inspiratory reserve volume
Air that can be inhaled after normal inspiration. 3,500ml
Expiratory reserve volume
Air that can be expired after a normal expiration. 1,500ml
Residual volume
Air in the lungs after maximal expiration. 1,200ml
Vital capacity
Maximal air that can expired after maximal inspiration. 5,500ml
Total lung capacity
Air in the lungs after maximal inspiration. 6,700ml
Total ventilation
Total ventilation = Tidal volume X respiratory rate.
Dead space
Regions that contain air but do not exchange O2 and CO2
Anatomic dead space
Conducting zones. Approximately equal to person't weight in pounds.
Alveolar dead space
Alveoli with air but without blood flow
Physiologic dead space
Anatomic dead space plus alveolar dead space
Alveolar ventilation
Tidal volume - anatomic dead space X respiratory rate.
Lung recoil
Force that collapses the lung. As the lung enlarges, recoil increases and vice versa.
Intrapleural pressure
Normally -5 cmH2O. Force that expands the lung. The more negative, the more lung expansion.
Lung mechanics before inspiration
Glotis is open but no air is flowing - alveolar pressure = 0. Intrapleural pressure and lung recoil are equal but opposite. Gravity decreases intrapleural pressure at the apex and increases it at the bases. Apex alveoli are more distended.
Lung mechanics during inspiration
Diaphragm contracts, intrapleural pressure becomes more negative. Expansion of alveoli makes alveolar pressure negative causing air to flow into the lungs.
Lung mechanics at the end of inspiration
Intrapleural pressure and recoil are the same but opposite. Alveolar pressure returns to zero and air stops flowing in.
Lung mechanics during expiration
Diaphragm relaxes, intrapleural pressure increases, lung recoil collpases the lung. Alveoli compress tha air and alveolar pressure becomes positive and air flows out of the lungs until alveolar pressure is back to zero. Lung recoil and intrapleural pressure become equal but opposite.
Assisted control mode ventilation
Inspiration is initiated by the patient or the machine if no signal is detected.
Positive end-expiratory pressure
Does not allow intraalveolar pressure to return to zero at the end of expiration. The larger lung volume prevents atelectasis.
What is lung compliacnce?
It's the change in volume with a change in pressure. Increased compliance means more air flows in with a given change in pressure. Decreased compliance means the opposite. The steeper the slope of the lung inflation curve, the greater the compliance. Emphysema = very compliant; fibrosis = not compliant.
Components of lung recoil
1) the tissue's collagen and elastin fibers and 2) the surface tension (greatest component)
Functions of surfactant
Lowers lung recoil and increases compliance (↓ surface tension) more in small alveoli than large alveoli; reduces capillary filtration forces reducing tendency to develop edema.
Pathophysiology of respiratory distress syndrome
Low surfactant --> ↑ recoil, ↓ compliance (a greater change in intrapleural pressure is necessary to inflate the lungs); alveoli collapse (atelectasis); more negative intrapleural pressures promote capillary filtration (pulmonary edema)
Airway resistance
R = 1/r4; first and second bronchi have less radius than alveoli, therefore more resistance. Ach increases resistance (bronchoconstriction), catecholamines decrease resistance (bronchodilation)
Effect of lung volume on airway resistance
↑ lung volume --> ↑ radius --> ↓ resistance. The more negative the intrapleural pressure, the less resistance
Lung volumes in obstructive disease
↑ TLC, ↑ RV, ↑ FRC, ↓ FEV1, ↓ FVC, ↓ FEV1/FVC
Lung volumes in restrictive disease
↓ TLC, ↓ RV, ↓ FRC, ↓ FEV1, ↓ FEV, ↑ FEV1/FVC
Pressure of alveolar O2 and CO2
PAO2 = 100mmHg; PACO2 = 40mmHg
Pressure of venous pulmonary capillary O2 and CO2
PvO2 = 40mmHg; PvCO2 = 47mmHg
Pressure of arterial pulmonary capillary O2 and CO2
PO2 = 100mmHg; PCO2 = 40mmHg
Which factors affect PCO2?
Metabolic CO2 production and alveolar ventilation
Relationship between alveolar ventilation and PACO2
Inversely proportional. Hyperventilation decreases PACO2; hypoventilation increases PACO2.
Relationship between PAO2 and PACO2
↓ PACO2 --> ↑ PAO2 (hyperventilation); ↑ PACO2 --> ↓ PAO2 (hypoventilation)
Which factors affect PAO2?
Atmospheric pressure, oxygen concentration of inspired air and PACO2
What determines oxygen content?
Hemoglobin concentration. 1.34ml O2 combines with each gram of hemoglobin.
Amount of dissolved oxygen in the blood
0.3 volumes %; 0.3ml per 100ml of blood. Determines PO2 which acts to keep oxygen bound to Hb
What determines oxygen attachment to hemoglobin?
PO2 and the affinity of the individual attachment sites. The higher the affinity, the less PO2 is needed to keep it attached
What determines PO2?
Amount of oxygen dissolved in plasma. Normally 0.3 volumes %.
Site 4 of hemoglobin
Oxygen is attached at 100mmHg. Least affinity, last site to be saturated.
Site 3 of hemoglobin
Oxygen is attached at 40mmHg. More affinity than site 4, less affinity than site 2.
Site 2 of hemoglobin
Oxygen is attached at 26mmHg which is p50. More affinity, second site to be saturated.
Site 1 of hemoglobin
Oxygen remains attached under physiologic conditions. Highest affinity, first site to be saturated.
Factors that shift oxygen dissociation curve to the right
↑ CO2, ↑ 2,3BPG, fever, acidosis
Factors that shift oxygen dissociation curve to the left
↓ CO2, ↓ 2,3BPG, hypothermia, alkalosis, HbF, methemoglobin, carbon monoxide, stored blood
How is CO2 carried in the blood?
5% dissolved; 5% attached to Hb (carbamino compounds); 90% as bicarbonate.
Main drive for ventilation
H+ ions from dissociated H2CO3 which stimulate central chemoreceptors. H2CO3 is proportional to PCO2 of CSF
Central chemoreceptors
Sense [H+] which is proportional to PCO2 and H2CO3 of the CSF (not systemic)
Peripheral chemoreceptors
Carotid bodies (afferents via IX), aortic bodies (afferents via X). Monitor PO2 and [H+/CO2]
Main drive for ventilation in severe hypoxemia
Peripheral chemoreceptors sense PaO2 (dissolved oxygen) once PaO2 falls to 50-60mmHg.
Ventilatory response to chronic hypoventilation
Peripheral chemoreceptors are the main drive for ventilation eventhough PaCO2 is increased.
Ventilatory response to anemia
PaO2 and PACO2 are normal, therefore neither peripheral nor central chemoreceptors respond.
Central control of ventilation
Apneustic center in the caudal pons promotes prolonged inspiration. Pneumotaxic center in the rostral pons inhibits apneustic center. Efferents are from the medulla to the phrenic nerve (C1-C3) to the diaphragm
Differences in ventilation between the base and the apex of the lung
Base intrapleural pressure is -2.5, alveoli are compliant and small with a small volume of air but are underventilated due to too much blood flow; Apex pressure is -10, alveoli are large and stiff and contain a large volume of air but are overventilated due to limited blood flow
Differences in blood flow between the base and the apex of the lung
Blood vessels of the apex are less distended, have more resistance and receive less blood flow. Blood vessels of the base are more distended, have less resistance and receive more blood flow
Ventilation/perfussion relationship at the base of the lungs
Blood flow is higher than ventilation, the relationship is less than 0.8; the bases are underventilated, ↑ shunts
Ventilation/perfussion relationship at the apex of the lungs
Blood flow is lower than ventilation, the relationship is more than 0.8; the apex are overventilated, ↑ dead space
What does a ventilation/perfussion relationship under and over 0.8 mean?
Under 0.8 (at the bases) lungs are underventilated and less gas exchange takes place, therefore PACO2 and end-capillary PCO2 will be higher and PAO2 and end-capillary PO2 will be lower.
What is hypoxic vasoconstriction?
A decrease in PAO2 causes vasoconstriction and shunting of blood through that segment.
What is the effect of a thrombus in a pulmonary artery?
Blood flow decreases, therefore ↑ Va/Q --> ↓ PACO2, ↑ PAO2
What is the effect of a foreign object occluding a terminal bronchi?
Ventilation decreases, therefore ↓ Va/Q --> ↑ PACO2, ↓ PAO2
What constitutes a pulmonary shunt?
Regions of the lung where blood is not ventilated. Low Va/Q relationship.
What constitutes alveolar dead space?
Regions of the lung where there's no blood flow in spite of ventilation. High Va/Q relantionship
Va/Q > 0.8
Represents alveolar dead space. Can be reversed with supplemental O2
Va/Q < 0.8
Represents a pulmonary shunt. Cannot be reversed with supplemental O2
What is the normal A-a gradient?
5-10 mmHg
↓ PAO2 but diffusion and A-a gradient are normal. Perfusion-limited defect.
What is a perfussion-limited defect?
There's a lung problem but A-a gradient is normal
What is a diffusion-limited defect?
There's a lung problem where A-a gradient is below normal, therefore diffusion isn't normal
Diffusion impairment lung defect
Due to structural problem (↑ thickness or ↓ surface area). A-a gradient is more than normal. Supplemental oxygen compensates structural deficit but increased A-a gradient remains. Fibrosis, emphysema.
Diffusion capacity of the lung
Its measured with CO because it's a diffusion-limited gas. Structural problems decrease CO uptake. It's an index of surface area and membrane thickness.
Pulmonary right-left shunt
↓ Va/Q. Ther is an increased A-a gradient that is unresponsive to supplemental O2. Atelectasis or ARDS.
PO2 in atrial septal defect
↑ Right atrial PO2, ↑ right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary blood flow and pressure
PO2 in ventricular septal defect
No change in right atrial PO2, ↑ right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary flow and pressure
PO2 in patent ductus arteriosus
No change in right atrial PO2 nor right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary flow and pressure