Ch 19 Respiratory Physiology & Pathophysiology

Question 1

What is the formula for O2 content in blood?

Answer 1

CaO2 = (SaO2 x Hb x O2 combining capacity of Hb) + (O2 solubility x PaO2)
with numbers dubbed in

CaO2 = (SaO2 x Hb X1.34) + (0.003 x PaO2)

Question 2

How is Methemoglobin different from Hemoglobin?

Answer 2

MetHb is formed by the oxidation to Fe3+ (ferric) instead of the usual Fe2+ (ferrous).
-Less able to bind O2, therefore less O2 content and delivery

Question 3

What are medical causes of MetHb? What is the antidote?

Answer 3

Causes: benzocaine, dapsone, inhaled nitric oxide (in susceptible patients)
Antidote: Methylene blue

Question 4

What is the pathophysiology behind carbon monoxide poisoning?

Answer 4

CO binds to Hb with >200x more avidity than O2.
The CO-Hb has 2 main effects:
-fewer site available for O2 binding, thus reduced blood O2 content
-Formation of CO-Hb causes conformational change in Hb. Tendency to release bound O2 is decreased (LEFTward shift of Hb-O2 curve)

Question 5

What is the BOHR EFFECT as it relates to the Hb-O2 dissociation curve?

Answer 5

Shift of the Hb-O2 curve caused by changes in CO2 and pH.
E.g., in systemic capillaries, PCO2 is higher (and lower pH) b/c of local CO2 production. This shifts Hb-O2 curve to right –> increased offloading of O2 to tissues
In pulmonary capillaries, PaCO2 is lower, so curve is shifted to left to facilitate binding of O2 to Hb

Question 6

What are the three forms that CO2 is transported in the blood?

Answer 6

1. Dissolved (PaCO2 - 5%)
2. Bicarbonate ion (90%)
3. carbamino CO2 (bound to the terminal amino group in Hb molecules - 5%)

Question 7

Describe the “Haldane effect” and how it relates to O2 inducing hypercapnia

Answer 7

The difference in the amount of CO2 carried in oxygenated vs deoxygenated blood. Two mechanisms:

1. Increased PaO2 decreases ability to form carbamino compounds (less CO2 bound to Hb) - thus raised dissolved CO2 (PCO2)
2. increased PO2 increases O2 bound to Hb, which alters heme-linked histamine and reduces its H+ buffering capacity. More H+ is free and binds to HCO3-, releasing stored CO2

Question 8

Is Venous O2 saturation (SO2) higher in the IVC or SVC and why

Answer 8

Higher in IVC - possibly due to high renal and hepatic flow relative to O2 consumption

Question 9

Central venous blood enters the right ventricle and is joined by which sources to form “mixed venous blood”?

Answer 9

SVC and IVC enter RV (Central venous blood) and are joined by venous blood from coronaries (through coronary sinus) and venous drainage from myocardium (Thebesian veins)

Question 10

What is typical minute ventilation? What is typical alveolar ventilation? Why is there a difference?

Answer 10

Minute ventilation: 7-8L/min
Alveolar ventilation: 5L/min
Difference due to dead space ventilation. Alveolar ventilation closely matches cardiac out put (~5L/min)

Question 11

What is a typical dead space to tidal volume ration (VD/VT)? How does this change with a PE? With COPD?

Answer 11

VD/VT = ~0.3
With PE, more dead space so VD/VT can be up to 0.8 with a high burden. Need to increase minute ventilation significantly to maintain alveolar ventilation. Similar with COPD. Ratio can be up to 0.9.

Question 12

What is functional residual capacity (FRC)? How much is it usually?

Answer 12

The amount of air in the lungs after ordinary expiration.

Usually ~3-4L

Question 13

Why is FRC important?

Answer 13

1. Keeping lungs partially inflated results in lower surface tension at the alveoli (air-liquid interface rather than just liquid). This makes re-inflation easier.
2. Continuous perfusion through lungs, so if lung is totally collapsed, there would be virtually no O2 available to passing blood. May cause rapid desaturation. With maintenance of FRC there is some O2 available to circulating blood between breaths.

Question 14

What is transpulmonary pressure?

Answer 14

It is the “distending pressure” of the lungs. It is the difference between the (positive) airway pressure and (negative) pleural pressure

Question 15

What is compliance? How is it affected by very low or very high lung volumes?

Answer 15

Compliance is the change in volume divided by change in pressure. Normal is 0.2-0.3 L/cmH2O.
Compliance is lowest at extremely low and high lung volumes.

Question 16

What is the Alveolar Gas Equation?

Answer 16

PAO2 = FiO2 (atm pressure - pH20) - (PaCO2/RQ)

=0.21(760-47)-(PaCO2/0.8)

Question 17

What is the equation for resistance to gas flow in the lungs?
What is a normal value? How does this change with the presence of an ETT

Answer 17

Resistance = driving pressure/gas flow
Driving pressure in spontaneous breathing = pleural pressures. In PPV driving pressure = difference between pressures applied to ETT and alveolus.
Normally, ~1cmH2O/L/sec. Increases to 5 with a size 8 tube.

Question 18

Why does most (~80%) of impedance to gas flow occur in the large airways?

Answer 18

1. As bronchi branch, resistance is arranged in parallel and cross-sectional area is almost 10x trachea
2. Small airways have laminar flow, whereas large airways have turbulent. When flow is laminar: F=∆P/R. Turbulent flow = ∆P/R^2

Question 19

How does airway resistance change when lung volume approaches residual volume?

Answer 19

Airways are narrowed in parallel with compressing lung tissue and resistance increases

Question 20

How much does lung tissue resistance account for total resistance to breathing?

Answer 20

~20%.
Lung tissue resistance is the applied pressure on tissue/velocity of tissue movement
It can be increased 3-4x in chronic lung disease and reduced by panting respirations

Question 21

How is ventilation distributed between upper and lower lung regions? How does this change at rest versus with exercise?

Answer 21

More ventilation to lower lung regions, especially in low flow states (at rest). The ratio of ventilation in upper to lower lungs is more even with exercise (high flow state)

Question 22

What is closing volume and closing capacity?

Answer 22

Closing volume: volume above residual volume (RV) where expiration below FRC closes some airways
Closing Capacity: Closing volume + Residual volume (i.e., the total volume of the lung at which closing can occur)

Question 23

How does velocity of gas molecules change from large airways to fourteenth generation bronchioles and alveoli?

Answer 23

Velocity falls rapidly. This is due to a massively larger cross-sectional area and a constant number of gas molecules

Question 24

What is the average height of an adult lung? How does this affect pulmonary artery pressure at the base of the lung, at the heart and at the apex?

Answer 24

Average 25cm. Therefore, when a person is standing, base of the lung hydrostatic pressure is ~25cmH2O(18mmHg). Mean PAP at level of heart is 12mmHg, and at the apex can be almost zero. Thus, less blood flow will occur at the apex.

Question 25

Describe the relationship between Palv, Ppa, Ppv (i.e., left atrial pressure) in West zones I, II, III

Answer 25

Zone I: Palv>Ppa>Ppv
Zone II: Ppa>Palv>Ppv –> only perfusion during systole
Zone III: Ppa>Ppv>Palv –> perfusion during systole and diastole

Question 26

What is the primary driver of hypoxic pulmonary vasoconstriction?

Answer 26

PAO2 (low alveolar oxygen tension)