Michels Phys

Question 1

Tidal volume

Answer 1

(VT): amount of air that enter or leaves the lung in a single cycle ~500 ml (normal breath)

Question 2

Functional residual capacity

Answer 2

(FRC): volume of gas that remains in the lung at then end of a passive expiration (equilibrium point for lung)

Question 3

Inspiratory capacity

Answer 3

(IC): maximal volume of air that can be inhaled from FRC

Question 4

Inspiratory reserve volume

Answer 4

(IRV): volume of air that can be inhaled after a normal inspiration

Question 5

Expiratory reserve volume

Answer 5

(ERV): volume that can be exhaled after a normal expiration

Question 6

Residual volume

Answer 6

(RV): volume of air that remains in the lungs after maximal expiration (cannot be measured by spirometry)

Question 7

Vital capacity

Answer 7

(VC): maximal volume that can be expired after maximal inspiration

Question 8

Total lung capacity

Answer 8

(TLC): amount of air in the lung after maximal inspiration

Question 9

PIgas

Answer 9

Fgas(Patm-Ph20)

For PIO2=150mmHg

Question 10

Method to determine FRC

Answer 10

Helium Dilution
- helium allowed to diffuse into lungs once valve is open
Body Plethysmography
- airtight box, subject inside,close mouthpiece valve at FRC
- subject tries to inhale against closed valve, changing lung by changing volume and box by - changing volume and lowering/raising pressure in lung box

Question 11

Anatomical dead space

Answer 11

volume of conducting airways (about 150ml)

- define conducting airways

Question 12

Alveolar dead space

Answer 12

alveoli containing air but not participating in gas exchange

Question 13

Physiologic dead space

Answer 13

total dead space for the system (1/3 total)

Question 14

alveolar ventilation

Answer 14

room air delivered to the respiratory zone per minute
VA = (VT – VD)f

VT = tidal volume		VD = dead space
f   = respiratory rate

Question 15

total ventilation is

Answer 15

tidal volume x respiratory frequency

Question 16

How can alveolar ventilation be increased

Answer 16

by increasing tidal volume or respiratory volume

Question 17

Where is expired CO2 derived from

Answer 17

all expired CO2 derives from the alveolar space and none from the dead space.

Question 18

What is the relationship between CO2 concentration and alveolar ventilation

Answer 18

CO2 concentration is inversely related to alveolar ventilation

Question 19

Where is ventilation highest

Answer 19

Ventilation is highest at the base of the lung due to gravitational effects.

Question 20

What factors influence diffusion rate

Answer 20

Pressure gradient
Thickness or diffusion distance
Area of barrier
Diffusion constant

Question 21

Perfusion limited

Answer 21

: amount of gas transported is limited by blood flow (partial pressure gradient is not maintained)

O2 is perfusion limited

Question 22

Diffusion limited

Answer 22

: amount of gas that is transported depends on the diffusion process (diffusion will continue as long as the partial pressure gradient is maintained

CO is diffusion limited

Question 23

Normal uptake of O2 in the Pulmonary Capillary

Answer 23

PVO2 = 40 mm Hg

Under normal conditions, the PaO2 nearly equals the PAO2 by the time the RBC is 1/3 through the capillary bed

Question 24

Abnormal uptake of O2 in Pulmonary Capillary

Answer 24

Decreasing the PIO2 will result in increased time to equilibrate PAO2 and PaO2 (diffusion equilibrium)

Question 25

CO2 Transfer

Answer 25

The diffusion for CO2 is approximately 20X higher than O2. However, the concentration gradient for CO2 is lower than O2 and the reaction of CO2 with blood is complex. Generally, hypercapnia is rare but there is a potential for elevated levels of CO2 due to thickening of the blood-gas barrier.

Question 26

Diffusion Capacity

Answer 26

Diffusing capacity of the lung includes the distance that a gas travels across membranes into the blood and the time it takes to react with hemoglobin Diffusing capacity is measured by the uptake of CO in the lung measured in mL•min-1•mm Hg-1 (assays lung structural features) Normal diffusing capacity for CO is 25 mL•min-1•mm Hg-1

Question 27

Pathological Changes that Reduce DL

Answer 27

``` Diffuse interstitial pulmonary fibrosis - Thickening of the interstitium, alveolar wall and destruction of capillaries Chronic obstructive pulmonary disease - Loss of lung elastic tissue and pulmonary capillaries (decreases surface area and total Hb content) Loss of functional lung tissue - Decreases surface area and Hb content Anemia - Fall in Hb content ```

Question 28

Diffusion of gas across a barrier

Answer 28

is proportional to the area of the barrier and the partial pressure difference, and inversely proportional to the thickness

Question 29

Muscles of Inspiration

Answer 29

Diaphragm External intercostals Accessory muscles of inspiration include the scalenus and sternomastoids and the pectoralis

Question 30

Muscles of Expiration

Answer 30

Passive during rest | Forced expiration can involve the internal intercostals and abdominal muscles

Question 31

Transmural pressure

Answer 31

Transmural pressure is the pressure measured from inside to out.

Question 32

Movement of Lung and Chest wall as result of pneumothrax

Answer 32

When intrapleural pressure is equal to atmospheric: | lung wants to recoil and chest wall wants to expand

Question 33

Lung compliance

Answer 33

Relates to transmural pressure change required to achieve a given change in volume.

Question 34

How is compliance determined

Answer 34

Compliance is determined by elastic recoil and surface tension. - elastic recoil of the lung is determined by elastic tissue (elastin and collagen - geometry of meshwork conveys elasticity) - surface tension is reduced by surfactants

Question 35

What changes compliance

Answer 35

Obstructive (problems with exhalation) increases compliance. | Restrictive (problems with inhalation, ie fibrosis) reduces compliance.

Question 36

What are the functions of surfactants

Answer 36

1. Lowers surface tension 2. Increases alveolar stability 3. Keeps alveoli dry

Question 37

What happens in a diseased state where surfactant is absent

Answer 37

- Compliance is reduced - Collapsed region of lungs - Wet regions

Question 38

Characteristic of lung apex during ventilation

Answer 38

Intrapleural pressure more negative Greater transmural pressure gradient Alveoli larger, less compliant Less ventilation

Question 39

Characteristics of lung base during ventilation

Answer 39

Intrapleural pressure less negative Smaller transmural pressure gradient Alveoli smaller, more compliant More ventilation

Question 40

Driving pressure

Answer 40

Is the pressure change from one end of the tube to the other: P = flow x resistance For the same flow, pressure of laminar flow > turbulent

Question 41

Laminar flow

Answer 41

resistance is constant irrespective of flow

Question 42

Turbulent flow

Answer 42

resistance increases w/flow rate

Question 43

Velocity of gas in the lung

Answer 43

Increase airway in parallel with increase cross sectional area as move down tree - resistance drops Increasing velocity as move up tree to maintain flow - turbulent pattern

Question 44

Types of resistance in lung

Answer 44

Airway and Tissue Tissue resistance must be overcome for lung to inflate Over 85% of total resistance is airway

Question 45

Factors that determine cross-sectional area of airways

Answer 45

1. Lung volume - holds airways open 2. Lung elasticity - contributes to tethering effect 3. Bronchial smooth muscle tone

Question 46

Airway resistance and lung volume

Answer 46

As lung volume increases, resistance decreases. | Patients with obstructive disease breathe at higher lung volumes to decrease airway resistance

Question 47

Chemical factors that Affect Airway Resistance

Answer 47

All act by affecting smooth muscle tone of bronchioles (medium sized airways). Smooth muscle tone is the greatest determinant of resistance of the medium-sized airways.

Question 48

Bronchoconstrictors

Answer 48

Cause constriction of SM. Parasymp nervous system (acetylcholine and methacholine). histamine irritants (i.e. cigarette smoke)

Question 49

Bronchodilators

Answer 49

Cause relaxation of SM. Symp nervous system (NE via B2 receptors). Agonsists for B2 receptors (i.e. isoproteronol, albuterol). Increases PCO2 in bronchioles

Question 50

Transmural pressure during quiet respiration

Answer 50

transmural pressure remains positive during exhalation

Question 51

Transmural pressure during forced expiration

Answer 51

Engagement of expiratory respiratory muscles raises intrapleural pressure which is often positive - If intrapleural pressure exceeds airway pressure the transmural pressure becomes negative and the airway will collapse unless supported by SM or cart - Where ad if airway collapse during a forced expiration depends on the loss of pressure along the airway. - Pressure lost as resistance is overcome - Pressure is lost as velocity increases and flow becomes turbulent

Question 52

Dynamic Airway Compression Upon Forced Expiration

Answer 52

Loss of pressure occurs as gas moves from the alveolus to the mouth - Increase resistance - Increase velocity - Transition from laminar to turbulent flow

Question 53

Elastic Forces and Airway Compression

Answer 53

Quiet resp: driving force is diff btwn alveolar and mouth pressure. Airway compression: driving force is diff btwn alveolar pressure and pleural pressure. Elastic recoil pressure is the diff btwn alveolar and pleural pressure.

Question 54

FEV/FVC

Answer 54

Normally around 80% Obstructive (increased airflow resistance): drops as FEV decreases Restrictive (increase elastic resistance): increases as both FEV and FVC decrease disproportionately

Question 55

Pulmonary pressure

Answer 55

Can be altered by 1. Recruitment 2. Distension Recall pulmonary arteries contain relatively little smooth muscle- ensures arteries are highly compliant

Question 56

Behavior of Alveolar and Extra-alveolar Vessels

Answer 56

Pulmonary capillaries- exposed to alveolar pressures and have the propensity to collapse when alveolar pressure exceeds capillary pressure Extra-alveolar vessels- Include pulmonary arteries and veins; diameter increases when lung tissue expands Do contain some smooth muscle- tone can be effected by pharmacologic agents Vasodilation of pulmonary capillaries- acetylcholine, isoproterenol, NO, prostacyclins Vasoconstriction of pulmonary capillaires- serotonin, histamine, norepinephrine

Question 57

Pulmonary Vascular Resistance (PRV)

Answer 57

Pulmonary Vascular Resistance- normally very low 1. Recruitment and distension of pulmonary capillaries can lower the pulmonary vascular resistance - Exercise - Increased pressure - gravity 2. PVR Increases at high and low lung volumes 3. Increases with alveolar hypoxia due to hypoxic pulmonary vasoconstriction

Question 58

Chemicals and PRV

Answer 58

nitric oxide (NO) and prostacyclins cause vasodilation Viagra: a selective inhibitor of cGMP-specific phosphodiesterase type 5 (PDE5)

Question 59

Capillary recruitment and distension

Answer 59

Recruit in parallel Distension increases capillary diameter Both recruitment and distension usually occur at the same time

Question 60

Changes in pulmonary resistance with changes in lung volume

Answer 60

Resistance increases at high lung volumes due to increased alveolar pressure, and stretching of the capillary wall. Diameter increases with expanding lung tissue and decreases at low lung volume.

Question 61

Hypoxic Vasoconstriction

Answer 61

Note it is alveolar PO2 that controls hypoxic vasoconstriction. An example of hypoxic vasoconstriction is travel to high altitude where the PIO2 is less.

Question 62

Mechanical influences that increase PVR

Answer 62

``` Increased lung volume (above FRC) - lengthening and compression of pulmonary caps Decreasing lung volume - compression and loss of traction of extra-alveolar vessels Increased interstitial pressure - compression of vessels Increased blood viscosity - increased resistance ```

Question 63

Mechanical influences that decrease PVR

Answer 63

Increased pulmonary artery pressure, left atrial pressure, pulmonary blood volume, cardiac output - recruitment and distension Gravity - recruitment and distension due to hydrostatic effects

Question 64

Positive-Pressure Ventilation

Answer 64

``` Impact on PVR: Increases PVR Increased alveolar pressure - compression of alveolar vessels Positive intrapleural pressure - compression of extra-alveolar vessels; decreased in pulmonary blood flow ```

Question 65

Endogenous Chemicals and Effects on Vascular SM (Extra-alveolar vessels)

Answer 65

Vasoconstrictors→ serotonin, histamine, norepinephrine - Increases vascular resistance Vasodilators→ acetylcholine - Decreases vascular resistance

Question 66

Causes of pulmonary edema

Answer 66

Increased cap hydrostatic pressure - MI, mitral stenosis, fluid overload, pulmonary veno- occlusive disease Increased cap permeability - Inhaled or circulating toxins,sepsis, radiation, O2 toxicity; ARDS Reduced lymph drainage - Increased central venous pressure, lymphangitis carcinoma Decreased interstitial pressure - Rapid removal of pleural effusion or pneumothorax, hyperinflation Decreased colloid osmotic pressure - Overtransfusion, hypoalbuminemia, renal disease Uncertain etiology - high altitude, neurogenic, overinflation, heroin

Question 67

Control of circulation

Answer 67

- Hypoxic vasoconstriction limits pulmonary blood flow with PIO2 is reduced (hypoxic vasoconstriction limits pulmonary blood flow in fetuses which is quickly reversed upon delivery) - Nitric oxide (NO) is an endothelium-derived factor that relaxes pulmonary vessels and capillaries Endothelins are endothelium-derived factors that constrict pulmonary vessels and capillaries. - Sympathetic stimulation (ex. Norepinephrine) acts as a vasoconstrictor.

Question 68

Metabolic functions of Pulmonary Circulation

Answer 68

- Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) found on the surface of capillary endothelial cells - Bradykinin is inactivated by ACE in the lung Serotonin is inactivated by uptake and storage in the lung - Prostaglandins E1, E2, and F2α are inactivated in the lung - Norepinephrine is partly taken up by the lung - Other substances such as epinephrine, prostaglandins A1 and A2, angiotensin II, and vasopressin are not metabolized by the lung