Board Review-Respiratory-Physiology

Front 1

What is Surfactant, chemically?

Back 1

Lecithin = dipalmitoyl phosphatidylcholine

Front 2

4 other important Lung Products?

Back 2

Prostaglandins
Histamine
ACE
Kallikrein

Front 3

Fxn of Histamine in lungs?

Back 3

--> bronchoconstriction

Front 4

Fxn of ACE?

Back 4

Ang I ---> Ang II

Inactivates Bradykinin

Front 5

Fxn of Kallikrein?

Back 5

Activates Bradykinin

Front 6

What is Physiological Dead Space?

Back 6

Anatomical dead space of conducting airways
+
Functional Dead Space of alveoli
=
Volume of inspired air that doesn't take part in gas exchange

Front 7

What is the largest contributor of Functional Dead Space?

Back 7

Apex of healthy lung

Front 8

Typical makeup of Hemoglobin?

Back 8

2 alpha subunits
2 beta subunits

Front 9

2 forms of hemoglobin?

Back 9

Taut (T) w/ low O2 affinity
Relaxed (R) w/ high affinity

Front 10

Difference between fetal Hb and adult?

Back 10

Fetal = 2 alphas and 2 gamma subunits

Lower affinity for 2,3-BPG--->thus higher affinity for O2 (pulls it out of mom's blood)

Front 11

5 things that favor the T over R form? so?

Back 11

Inc Cl
Inc H
Inc CO2
Inc 2,3 BPG
Inc Temperature

shifts the dissociation curve to the right---> inc O2 unloading

Front 12

How is the majority of CO2 transported?

Back 12

In the blood
As Bicarbonate if not bound to Hb

Front 13

How can CO2 bind to Hb?

Back 13

Binds to AA's in globin chain at N terminus, but not to heme

Front 14

How does CO2 binding affect Hb?

Back 14

Favors T form, promoting O2 unloading

Front 15

2 modified forms of Hb?

Back 15

Methemoglobin
Carboxyhemoglobin

Front 16

What is Methemoglobin?

Back 16

Oxidized form of Hb (Fe3+ instead of 2+)
Doesn't bind O2 as well, but doesn love CN-

Front 17

So how can you treat Cyanide poisoning?

Back 17

Use nitrites to oxidize Hb--->metHb
This binds CN, allowing cytochrome oxidase to fxn
Then give Thiosulfate to bind this cyanide, forming thiocyanate, which is renally excreted

Front 18

What is CarboxyHb? significance?

Back 18

Hb bound to CO instead of O2
causes dec O2 binding capacity w/ left shift of dissociation curve-->dec O2 unloading

Front 19

CO vs O2 affinity for Hb?

Back 19

CO has a 200X's greater affinity than O2 does

Front 20

Factors affecting oxygen dissociation curve? significance?

Back 20

P50
Metabolic Needs
PCO2
Temperature
H+
pH
2,3-DPG

An inc in any of the factors (besides pH) shifts the curve to the right

A dec in any of the factors (except pH) shifts it left

Front 21

What happens to Pulmonary Circulation if PAO2 decreases?

Back 21

Hypoxic Vasoconstriction occurs to shift blood to well-ventilated regions of lung

Front 22

Two types of Pulmonary Capillary circulation limitations?

Back 22

Perfusion Limited
Diffusion Limited

Front 23

What is Perfusion Limited?

Back 23

Normal
Seen w/ O2, CO2, N2O
Gas equilibrates early along length of capillary

only way to change diffusion is to change perfusion (i.e. change blood flow)

Front 24

What is Diffusion Limited?

Back 24

Seen with O2 in emphysema, fibrosis
Also seen w/ CO
Gas doesn't equilibrate by time blood reaches the end of the capillary

Front 25

Normal Pulmonary Artery Pressure?

Back 25

10-14 mmHg

Front 26

Pulmonary HTN is?

Back 26

Pressure > 25 mmHg or > 35 mmHg during exercise

Front 27

Results of pulmonary HTN?

Back 27

Athersclerosis
Medial Hypertrophy
Intimal Fibrosis of pulm. arteries

Front 28

Cause of Primary Pulm. HTN?

Back 28

Due to inactivating mutation in BMPR2 gene (usually fxns to inhibit vascular smooth muscle prolif)

Front 29

Px for Primary Pulm. HTN?

Back 29

POOR

Front 30

Causes of Secondary Pulm. HTN?

Back 30

COPD
Mitral Stenosis
Recurrent Thromboemboli
Autoimmune Disease (systemic sclerosis)
Left-to-Right Shunt
Sleep Apnea
Living at High Altitude

Front 31

Clinical Course of Pulm HTN?

Back 31

Severe Resp. Distress-->Cyanosis and RVH--->Death from decompensated cor pulmonale

Front 32

What is Pulm. Vascular Resistance = ?

Back 32

PVR = (pressure in pulm art - pressure in LA) / CO

Front 33

What is O2 content = ?

Back 33

(O2 binding capacity X % saturation) + dissolved O2

Front 34

How much O2 can 1 g of Hb normally bind?

Back 34

1.34 mL of O2

Front 35

Normal O2 binding capacity?

Back 35

20.1 mL O2/dL

Front 36

Oxygen delivery to tissues = ?

Back 36

CO * Oxygen content of blood

Front 37

What is the Alveolar Gas Equation?

Back 37

PAo2 = PIo2 - (PAco2/R)

PAO2 = alveolar PO2
PIO2 = PO2 in inspired air
PACO2 = alveolar PCO2
R = resp quotient = CO2 produced/O2 consumed

Front 38

What is the A-a gradient? what does it normally = ?

Back 38

PAO2 - PaO2 = 10-15 mmHg

Front 39

Difference between Hypoxemia, Hypoxia, and ischemia?

Back 39

Hypoxemia = dec PaO2
Hypoxia = dec delivery of O2 to tissue
Ischemia = Loss of blood flow

Front 40

Causes of Hypoxemia?

Back 40

High altitude (normal A-a)
Hypoventilation (normal A-a)
V/Q mismatch (inc A-a)
Diffusion Limitation (inc A-a)
Right-to-Left Shunt (inc A-a)

Front 41

Causes of Hypoxia?

Back 41

Dec CO
Hypoxemia
Anemia
CN poisoning
CO poisoning

Front 42

Causes of Ischemia?

Back 42

Impeded arterial flow
Reduced venous drainage

Front 43

What is V/Q normally = ?

Back 43

1
i.e. they're match-->adequate gas exchange

Front 44

Lung Zones and their V/Q's?

Back 44

Apex of Lung: V/Q = 3 (wasted ventilation)
Base of Lung: V/Q = 0.6 (wasted perfusion)

Front 45

Ventilation and Perfusion at the base of the lungs are...

Back 45

both Greater than at the apex

Front 46

What's going on if V/Q--> 0?

Back 46

Airway Obstruction, so no V

Front 47

What's going on if V/Q --> infinity?

Back 47

Blood Flow Obstruction, so no Q

i.e. physiological dead space

Front 48

How is CO2 transported to Lungs?

Back 48

Bicarb (90%)
Bound to Hb as carbaminoHb (5%)
Dissolved CO2 (5%)

Front 49

What is the Haldane Effect?

Back 49

In the lungs, Oxygenation of Hb---> dissociation of H+ from Hb--->shifts equilibrium toward CO2 formation and thus CO2 is released from RBC's

Front 50

What is the Bohr Effect?

Back 50

In peripheral tissue, inc H+ from tissue metabolism shifts the curve to the right, unloading O2

Front 51

Progression of Responses to high altitude?

Back 51

Acute inc in ventilation
Chronic inc in ventilation
Inc EPO--->inc Hct and Hb
Inc 2,3-DPG (binds to Hb, so Hb will release more O2)
Cellular Changes (inc mito's)
Inc renal excretion of bicarbonate to compensate for resp. alkalosis
Chronic hypoxic pulmonary vasoconstriction ---> RVH

Front 52

Response to Exercise?

Back 52

Inc CO2 production
Inc O2 consumption
Inc Ventilation rate to meet O2 demand
V/Q ratio from apex to base become more uniform
Inc Pulm blood flow from inc CO
Dec pH secondary to lactic acidosis
No change in PaO2 or PaCO2, but inc in venous CO2 content