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63 Cards in this Set

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Calculate partial pressure of humid air




Water vapor pp [47mm Hg]


atm pp of 760mm Hg


oxygen is .21

P (gas in humid air) = (p[atm] - P[h2o]) x % of gas




(760 - 47) x .21 = 150mmHg --> Bronchial Air (Pio2) @ normal body temps water vapor pressure is 47

Functional residual capacity

ERV + RV

Vital capacity

ERV + TV + IRV

Inspiratory capacity

TV + IRV

Compliance

delta V / Delta P

Decreased compliance diseases

surfactant and fibrotic lung diseases

alveolar ventilation

VR x ( TV - dead space)




normal is 4.2 L/min

total pulmonary ventilation aka minute volume

VR X TV




normal is 6L/min

VRG (ventral respiratory group)

includes the botzinger complex with its apparent pacemakers as well as inspiration and active expiration

Peripheral chemoreceptors on PO2

monitor anything below 60mm Hg triggers an increase in ventilation




(in carotid and aortic bodies)

Reynold's number determined by?

larger number more likely to be turbulent




2 (radius of tube) (density of gas) (Velocity)


--------------------------------------------------------------


(viscosity of gas)

Resistance of airway is proportional to what and inversely proportional to what?

(n * L)/ r^4




I: length of tube


IP: radius or tube





Emphysema

causes abnormal forced expiration by normal maximal inspiration

Maximum voluntary ventilation

125-170 L/min

V/Q ratio




and normal?

V= volume of air that reaches the alveoli per unit of time


Q= volume of blood that reaches the alveoli per unit of time




Normal is .8

V/Q mismatch with emphysema and bronchitis

emphysema - poorly perfused regions of the lung due to loss of capillaries




bronchitis - poorly ventilated due to airway constriction

4 causes of hypoxemia

reduced partial p. of O2 in inspired air


alveolar hypoventilation


abnormal gas exchange


very low cardiac output



normal A-a gradient

(age + 10)/4

A-a gradient used to




low vs high

differentiate between hypoventilation and abnormal gas exchange.




low = hypoventilation


high = gas exchange problem

Alveolar gas equation


Alveolar PO2

PAO2 = PIO2 ( is 150mmHg) - [PACO2/R]




R= .8


If not given PaCO2 normally is 40 mmHg if no lung pathology

Diffusion =

surface area X barrier permeability/distance^2

Will low or high V/Q ration improve with supplemental oxygen

high V/Q (or dead space)

Compensatory mechanisms for High and Low V/Q

High V/Q can be compensated for by increased alveolar ventilation




Low V/Q can be compensated for by hypoxic vasoconstriction

Mixed venous blood in systemic capillaries (PO2)




In alveolar arterial capillaries (PO2)




P02 at mmHg and % saturation

40 mmHg and 75% saturated to Hb




100 mmHg and 97.5% saturated to Hb

CO2 transportation

70% is in the form of bicarbonate


23% in proteins (carbaminohemoglobin)


7% in the form of plasma

Haldane effect

shift in curve upon binding to oxygen from alveolus, goes right




High PO2 in alveolus allows release of CO2 (delivery of CO2 to the lungs)

Hypercapnia physiological causes

decreased minute ventilation


decreased alveolar ventilation caused by rapid shallow breathing


V/Q mismatch


*unable to compensate due to suppression of drug or abnormality of the ventilatory pump (emphysema)

Acidosis and Alkalosis


what mmHg causes change?

7.35 and 7.45




.08 pH change for 10mmHg

Respiratory acidosis




Primary disturbance and compensation

PaCO2 increases




metabolic alkalosis by increasing serum bicarb

Respiratory alkalosis




Primary disturbance and compensation



Decrease PaCO2




Metabolic acidosis decrease serum bicarb

Metabolic acidosis




Primary disturbance and compensation

Decreasing serum bicarb




Respiratory alkalosis decrease PaCO2

Metabolic alkalosis




Primary disturbance and compensation

increasing serum bicarb




Respiratory acidosis increasing PaCO2

Ventilatory response to hypoxemia

minute ventilation increases as PaO2 falls below 60mmHg




*when combined with hypercapnia the ventilation response is increased

Ventilatory response to hypercapnia

ventilation increases linearly with acute increases in PaCO2

COPD

patients with this have trouble eliminating CO2 since elastic recoil is destroyed or airways become thick and inflamed.




In COPD patient CO2 is chronically high and hypoxic drive from the peripheral chemoreceptors becomes more important in the drive to breath




Oxygen supplement reduce drive to breath

Collapse tendency of lungs

Elastic fibers (1/3)


Surface tension (2/3)






Aids in expiration



Sufactant

Reduces surface tension




Type 2 cells, have less effect at higher lung volumes.


Phospholipoprotein.

Atelectasis

areas of the lungs that are collapsed

Compliance problems indicated how?

by a change in resting intrapleural pressures




(lack of surfactant, emphysema)

Airway resistance problems are indicated how?

changes in pressures during inflow or outflow but not at rest




(asthma, aspiration of a crown)

Ventilation pressures with decreased surfactant

same intra-alveolar pressure




EVEN lower intrapleural pressure


(more subatmospheric)

Asthma ventilation pressures




Intra-avleolar pressure


Intrapleural pressure

Intra-avleolar and Intrapleural pressure - higher peaks but same resting values




the peaks are due to the flow phase/airway resistance

Ventilation pressure with increased Tidal volume

Intra-alveolar pressure --> increased peaks




Intrapleural pressure --> increased peaks but more resting subatmospheric pressure since holding inspiring more air.

Diffusion Rate factors

Solubility


-------------


Sqrt (MW)




Membrane thickness, surface area, gas pressure difference, diffusion coefficient (solubility and MW)

diffusion limited vs perfusion limited

perfusion limited - the blood PO2 is full saturated and reaches equilibration




diffusion limited - never reached equilibrium of saturation, a problem with diffusion.

Inspired air vs Alveolar air

dilution of inspired air by FRC


Addition of CO2 and water vapor


Removal of O2 by blood

At 18,000 ft altitude the barometric pressure decreases by

half

CO2 and O2 pressure gradient

CO2 is only about a 5 difference (45 --> 40)


O2 is about 60 difference (100 --> 40)





End-tidal CO2 meter is measured

Is measured at the nose or at the end of an endotracheal tube.


End tidal CO2 is 40 mmHg

base or apex receives more tidal volume?

base due to pleural pressures differences surrounding these regions. More volume change at the base then you will get at the apex. Since it operates lower on the compliance curve.

Base or apex as higher blood flow

base due to the effect of gravity, harder to push blood up into the apices.



Ventilation Perfusion Ratio


Blood Flow (slope) - dominates where?


Ventilation (slope) - dominates where?




Match where?

Blood flow has a steeper declining slope


Ventilation has a less of decline




Ventilation dominates at apex (>3)


Blood flow dominates at base ( <1)




Match at rib number 3

Where is V/Q ratio 1

at rib number 3

Arterial hypoxia is caused by

v/q mismatch

V/Q extremes are?

Shunt --> 0 V/ High Q



Alveolar Dead space --> High V/ 0 Q

Physiologic Dead Space

Anatomic dead space + alveolar dead space




Alveolar dead space from alveoli with little or no blood flow or pulmonary emboli





Dissolved oxygen formula

.003 mls O2/ 100 mls of blood / mmHg




so normally




.3 mls O2 per 100 mls of blood OR Vol. % since mmHg = 100


or 3mls per L of blood

Oxygen attached to hemoglobin formula

1.34 mls O2 / g Hemoglobin




15 g% normal Hb Concentration




[Hb] X 1.34 mls O2/ g Hb X % saturation




15 g X 1.34 mls X .97 = 19.5 vol %

20 Vol % is equal to


20 mls O2 / 100 mls blood

Bohr Effect

Right shift caused by Increased (acidity) H+ / CO2


Curve also shifts right by :


Increased temperature and 2,3 -DPG causing oxygen to decrease affinity.

CO poisoning

Binds to ferrous iron of heme group 210X more successfully than O2




--> turn cherry red




.1% compete almost equally with O2 for Hb

Cyanosis

Bluish skin color


5 g% deoxygenated hemoglobin (1/3 of hemoglobin is deoxygenated)


Reduced blood flow to tissues

Chloride shift

As bicarbonate [] increases within the RBC it begins to diffuse out into the plasma. The resulting negativity within the RBCs induces an inward diffusion of chloride ions from the plasma