Gas Exchange

Question 1

Causes of hypercapnia

Answer 1

1. Hypoventilation
2. V/Q mismatch (may be hidden by hyperventilation adaptation)
3. Increase in dead space ventilation from shallow breaths (restrictive lung disease)
4. Increase of CO₂ production in context of inability to increase ventilation (due to abnormality in ventilatory pump or respiratory controller)

Question 2

Why is hypercapnia so rare of a finding?

Answer 2

1. Individuals can adapt by hyperventilating
2. Hemoglobin buffers PaCO₂ in the same way it buffers PaO₂

Question 3

V_E total

Answer 3

V_E = V_A + V_D

Question 4

Total dead space is. . .

Answer 4

. . . the sum of anatomic dead space (normal) and alveolar dead space (pathological)

Question 5

Anatomic dead space in an individual

Answer 5

~ 1 mL per pound of body weight

Question 6

V_D / V_T

Answer 6

One way to assess dead space. This expression shows dead space as a percentage of tidal volume.

Question 7

Respitatory failure

Answer 7

Inability of the respiratory system to sustain the metabolic needs of the organism

Question 8

PCO₂ over the course of an expiration

Answer 8

Question 9

How can one estimate anatomic dead space experimentally?

Answer 9

By measuring the amount of gas exhaled that contains effectively no CO₂. The usual cutoff is the volume halfway through the ‘transition zone’.

Question 10

Mixed Expired Gas test (aka Bohr test)

Answer 10

F_ECO₂ x V_T = F_ICO₂ x V_DCO₂ + F_ACO₂ x V_A

With some simplification. . .

V_D / V_T = ( P_ACO₂ - P_ECO₂ ) / P_ACO₂

Question 11

In a normal person, the P_ACO₂ can be approximated as. . .

Answer 11

. . . the end-tidal CO₂, taken from a CO₂ exhalation test.

Question 12

In an individual with lung disease, why might P_ACO₂ not be effectively approximated by end-tidal CO₂?

Answer 12

Abnormalities in ventilation and perfusion result in loss of the clear plateau on the carbon dioxide expiration curve. For these individuals, P_aCO₂ is a reasonable substitute.

Question 13

P_aCO₂ in a healthy individual

Answer 13

38 - 42 mmHg

Question 14

Relationship representing the lungs ability to expire carbon dioxide

Answer 14

V_A = k x ( V_^CO2 / Pa_^CO2 )

Where k is a constant

Question 15

The greater the production of carbon dioxide in the individual, . . .

Answer 15

. . . the greater the ventilation must be in order to maintain a constant level.

This is a direct relationship.

Question 16

Why does air prefferentially go to the base of the lungs when an individual is standing upright?

Answer 16

Question 17

Main factors that affect pulmonary bloodflow

Answer 17

• Pulmonary arterial pressure
• Pulmonary venous pressure
• Alveolar pressure

Question 18

Starling resistors

Answer 18

Alternate between open and closed states due to the hydrostatic/hydrodynamic pressure relationships

Question 19

John West’s three ‘regions’ of lung

Answer 19

1. Arterial pressure cannot overcome gravity, and so the upper region is not perfused
2. Arterial pressure > alveolar pressure > venous pressure, so some blood gets through, but in this region the alveoli are Starling resistors
3. Arterial pressure > venous pressure > alveolar pressure, so the pressure of the vessels are always greater than the alveoli and thus the alveoli do not act as Starling resistors

Question 20

NO mechanism of regulating vessel tone by flow

Answer 20

Increased flow → Increased shear stress → Mechanical stimulation of eNOS → vasodilation

Question 21

The major regulators of pulmonary vasculature tone

Answer 21

1. Oxygenation of alveolar blood (on a per-alveolar basis)
2. NO
3. Prostacyclin

Question 22

The relationship between CO₂ content and P_aCO₂ is ____ over the physiological range.

This makes it possible for the body to . . .

Answer 22

The relationship between CO₂ content and P_aCO₂ is linear over the physiological range.

This makes it possible for the body to maintain a normal P_aCO₂ even in the presence of poorly ventilated alveoli by increasing ventilation rate.

Question 23

For any given CO₂ content, the P_aCO₂ is higher in the presence of ___.

Answer 23

For any given CO₂ content, the P_aCO₂ is higher in the presence of a high level of oxygen.

The Haldane Effect (oxygen has a higher affinity for hemoglobin)

Question 24

Visualization of Haldane effect

Answer 24

Question 26

Endogenous carbon monoxide production

Answer 26

There is some background endogenous carbon monoxide production from hemoglobin catabolism. Blood carboxyhemoglobin is 1-3% of nonsmokers

Question 27

Blood carboxyhemoglobin in smokers

Answer 27

Commonly reaches ~10%, may reach as high as ~15%

Question 28

Lethal concentrations of carboxyhemoglobin can be achieved within ___ in the confines of a closed garage.

Answer 28

Lethal concentrations of carboxyhemoglobin can be achieved within 10 minutes in the confines of a closed garage.

Question 29

Methylene chloride

Answer 29

Another chemical capable of causing carbon monoxide poisoning. Common component of paint remover and other solvents. Readily absorbed through the skin and lungs as a vapor and circulates to the liver, where its metabolism results in the generation of carbon monoxide.

Question 30

Determinants of inhaled CO

Answer 30

The amount of gas absorbed is dependent on the minute ventilation, the duration of exposure, and the relative concentrations of carbon monoxide and oxygen in the environment

Question 31

Non-hemoglobin aspects of CO poisoning

Answer 31

1. ROS production
2. Lipid peroxidation leading to reversible demyelination of neurons

Question 32

Clinical signs and symptoms of CO poisoning

Answer 32

• Peak during winter
• Tachycardia/tachypnia and SOB
• Headache, nausea, vomitting
• Presyncope, syncope, seizures
• Angina and arrhythmias
• Necrosis of sweat glands
• Visual changes
• Abdominal pain

Question 33

Delayed carbo-monoxide neuropathic syndrome

Answer 33

3 to 240 days after exposure. 10-30% of CO poisoning victims. Cognitive and personality changes, parkinsonism, incontinence, dementia, and psychosis have been described. 50-75% recover within 1 year.

Question 34

Diagnosing CO poisoning

Answer 34

• Elevated exhalatory CO
• Increased blood carboxyhemoglobin via spectrophotometry (NOT a pulse oximeter, these are not sensitive enough to distinguish oxy- from carboxy-Hb)
• A full neurological workup should also be done to assess for neuropathic syndrome (The Carbon Monoxide Neuropsychological Screening Battery is a frequently used tool)

Question 35

Treating CO poisoning

Answer 35

1. Remove from CO source
2. High-flow, normobaric, 100% oxygen should be administered immediately
3. Oxygen should be administered until the carboxyhemoglobin level has become normal.

Question 36

The half-life of carboxyhemoglobin on room air

Answer 36

4-6 hours

Question 37

The half-life of carboxyhemoglobin on normobaric 100% oxygen

Answer 37

40-80 minutes

Question 38

The half-life of carboxyhemoglobin on hyperbaric 100% oxygen

Answer 38

15-30 minutes

Question 39

___ is an undisputed indication for hyperbaric-oxygen therapy.

Answer 39

Coma is an undisputed indication for hyperbaric-oxygen therapy.

Question 40

____ are the hallmark sign of CO poisoning

Answer 40

Cherry red lips are the hallmark sign of CO poisoning

Question 41

A patient has a disorder of mitochondria that decreases the amount of oxygen that can be processed to produce ATP. In this case, the problem is primarily affecting skeletal muscle. What findings would you expect to see on exercise testing for this patient?

Answer 41

Patients with mitochondrial dysfunction are unable to sustain aerobic metabolism normally during exercise, and quickly develop lactic acidosis. The ventilatory threshold, therefore, occurs at a lower level of O2 consumption than normal. The acute metabolic acidosis stimulates the respiratory controller and ventilation increases faster than one would expect during mild to moderate exercise.