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53 Cards in this Set

  • Front
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Tidal volume (TV)

Is the volume inspired or expired with each normal breath




500 mL

Inspiratory reserve volume (IRV)

Is the volume that can be inspired over and above the tidal volume




3100 mL

Expiratory reserve volume (ERV)

Is the volume that can be expired after the expiration of a tidal volume




1200 mL

Residual volume (RV)

Is the volume that remains in the lungs after a maximal expiration




Cannot be measured by spirometry




1200 mL

Dead space

150 mL

Minute ventilation

Minute ventilation=tidal volume x breaths/min

Alveolar ventilation

Alveolar ventilation=


(tidal V-physiological dead space) x breaths/min

Inspiratory capacity (IC)

Is the sum of tidal volume and inspiratory reserve volume




IC = TV + IRV

Functional residual capacity (FRC)

Is the sum of expiratory reserve volume and residual volume; 2400 mL




FRC = ERV + RV




Cannot be measured by spirometry



Vital capacity (VC)

Is the sum of tidal volume, inspiratory reserve volume and expiratory reserve volume; 4800 mL




VC = TV + IRV + ERV




Is the volume that can be forcibly expired after a maximal inspiration

Total lung capacity (TLC)

Is the sum of all four lung volumes and is the volume in the lunds after a maximal inspiration; 6000 mL




TLC = TV + IRV + ERV + RV




Cannot be measured by spirometry

Forced expiratory volume (FEV1)

Is the volume of air that can be expired in the first second of a forced maximal expiration




FEV1 / FVC = 0.8

Obstructive lung diseases

E.g. asthma and chronic obstructive pulmonary disease; expiration is impaired




Both FEV1 and FVC are reduced, but FEV1 is reduced more than FVC;




FEV1 / FVC is decreased

Restrictive lund diseases

E.g. fibrosis; inspiration is impaired




Both FEV1 and FVC are reduced, but FEV1 is reduced less than FVC;




FEV1 / FVC is increased

Compliance

Describes the distensibility of the lungs and chest wall and is inversely related to elastance and stiffness




C = delta V / delta P

Transmural pressure

Transmural pressure =


alveolar pressure - intraplural pressure

Emphysema

Increased; lung compliance




Decreased; tendency of the lungs to collapse




Result; higher FRC

Fibrosis

Increased; tendency of the lungs to collapse




Decreased; lung compliance




Result; lower FRC

Surface tension of the alveoli



Creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius (Laplace's law)



Surfactant

- Reduce surface tension (increases compliance)


- Present as early as gestational week 24

Airflow

Is inversely proportional to airway resistance; thus, the higher the airway resistance, the lower the airflow

Resistance of the airways

Is described by Poiseuille's law

Is described by Poiseuille's law



Which factors change airway resistance?

- Contraction or relaxation of bronchial smooth muscle




- Lung volume




- Viscosity or density of inspired gas

Describe the pressures and airflows at rest

Alveolar pressure (=0) equals atmospheric pressure




Intraplural pressure is negative




Lung volume is the FRC

Describe the pressures and airflows during inspiration

Alveolar pressure (=negative) decreases to less than atmospheric pressure




Intraplural pressure becomes more negative




Lung volume increases; FRC + TV

Describe the pressures and airflows during expiration

Alveolar pressure (=positive) becomes greater than atmospheric pressure




Intrapleural pressure returns to its resting value during a normal expiration




Lung volume returns to FRC

Perfusion-limited exchange

E.g. N2O and O2 under normal conditions




The gas equilibrates early along the length or the pulmonary capillary. The partial pressure of the gas in the arterial blood becomes equal to the partial pressure in alveolar air. Thus, the perfusion-limited process, diffusion of the gas can be increased only if blood flow increases.

Diffusion-limited exchange

E.g. Co and O2 during strenuous exercise




The gas does not equilibrates by the time blood reaches the end of the pulmonary capillary. The partial pressure difference of the gas between alveolar air and pulmonary capillary blood is maintained. Diffusion continues as long as the partial pressure gradient is maintained.

Methemoglobin

- Iron is in the Fe3+ state




- Does not bind O2

Hemoglobin S

- Causes sickle cell disease




- In the deoxygenated form, deoxyhemoglobin forms sickle-shaped rods that deform red blood cells (RBCs)

Which factors affect the hemoglobin dissociation curve to shift to the right?

Occur when the affinity of hemoglobin for O2 is decreased

- Increase in PCO2


- Decrease in pH


- Increase in temperature


- Increase in 2,3-DPG concentration



Which factors affect the hemoglobin dissociation curve to shift to the left?

Occur when the affinity of hemoglobin for O2 is increased


- Decreased PCO2


- Increased pH


- Decreased temperature


- Decreased 2,3-DPG concentration


- CO poisoning

Causes of hypoxemia

Hypoxemia is decreased arterial PO2


- High altitude


- Hypoventilation


- Diffusion defect


- V/Q defect


- Right-to-left shunt

Causes of hypoxia

Hypoxia is decreased oxygen delivery to the tissues


- Decrease in cardiac output


- Hypoxemia


- Anemia


- Carbon monoxide poisoning


- Cyanide poisoning

Erythropoietin (EPO)

A growth factor that is synthesized in the kidneys in response to hypoxia

Regulation of pulmonary blood flow

Hypoxic vasoconstriction (which is opposite than in other organs)

Right-to-left shunts

Rare




Decrease in arterial PO2 because of the admixture of venous blood with arterial blood

Left-to-right shunts

More common




Do not result in a decrease in arterial PO2

V/Q ratio

Is the ratio of alveolar ventilation (V) to pulmonary blood flow (Q); 0.8




The V/Q ratio results in an arterial PO2 of 100 mmHg and an arterial PCO2 of 40 mmHg




Perfusion is lowest at the apex and highest at the base because of gravitational effects on arterial pressure



Control of breathing

The output of the brain stem controls the respiratory muscles and the breathing cycle

Central control of breathing

Medullary respiration center


1) dorsal respiratory group


2) ventral respiratory group


Apneustic center


Pneumotaxic center


Cerebral cortex

Dorsal respiratory group

Inspiration and the basic rhythm for breathing



Ventral respiratory group

Expiration and is not active during normal, quiet breathing




Activated during exercise

Apneustic center

Lower pons




Stimulates inspiration

Pneumotaxic center

Upper pons




Inhibits inspiration

Cerebral cortex

Voluntary control; hyperventilation and hypoventilation

Chemoreceptors

CO2, H+ and O2




- Central chemoreceptors in the medulla


- Peripheral chemoreceptors in the carotid and aortic bodies

Central chemoreceptors in the medulla

Sensitive to pH of the CSF; decreased pH of CSF produce hyperventilation




Stimuli that increase breathing rate:


- High; PCO2


- Low; pH

Peripheral chemoreceptors in the carotid and aortic bodies

Decreases in arterial PO2; hyperventilation




Increases in arterial PCO2; hyperventilation




Increases in arterial H+

Metabolic acidosis

Hyperventilation because the arterial H+ concentration is increased and pH is decreased

Other types of receptors for control of breathing

- Lung stretch receptors (Hering-Breuer reflex)


- Irritant receptors


- Juxtacapillary receptors


- Joint and muscle receptors

Response to exercise

Increased;


O2 consumption, CO2 production, ventilation rate, venous PCO2, pulmonary blood flow




Decreased;


Arterial pH in strenuous exercise




No change;


Arterial PO2 and PCO2, arterial pH




V/Q ration is more evenly distributed in lung (=decrease in physiological dead space)

Response to high altitude

Increased;


Ventilation rate (hyperventilation), arterial pH (respiratory alkalosis), hemoglobin concentration (increased EPO), 2,3-DPG concentration, pulmonary vascular resistance (hypoxic vasoconstriction)




Decreased;


Alveolar PO2, Arterial PO2 (hypoxemia)




Hemoglobin-O2 curve shifts to the right