Pulmonology Flashcards

1
Q

Where does surfactant come from

A
  • type II pneumocytes synthesize pulmonary surfactant
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2
Q

What is tidal volume?

A
  • Tidal volume (Vt) is about 500mL and includes the volume of air that fills the alveoli plus the volume of air that fills the airways
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3
Q

What is residual volume?

A

the volume of gas remaining in lungs after maximal forced expiration. about 1200mL. Can’t be measured by spirometer.

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4
Q

What is inspirational capacity (IC)?

A

tidal volume plus inspiratory reserve volume - about 500mL plus 3000mL for 3500mL total

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5
Q

What is the functional residual capacity (FRC)?

A

expiratory reserve volume (1200mL) plus residual volume (1200mL) for 2400mL total. FRC is the volume remaining in the lungs after a normal tidal volume is expired. Called the equilibrium volume of lungs

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6
Q

What is vital capacity (VC)?

A

inspiratory capacity plus expiratory reserve volume. approx 4700mL (3500+1200). VC is the volume that can be expired after maximal inspiration. Value increases with body size, male gender, and physical conditioning. Decreases w age.

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7
Q

What is total lung capactiy (TLC)?

A

all lung volumes - vital capacity plus residual volume for about 5900mL (4700+1200). Includes residual volume, so can’t be measured by spirometry.

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8
Q

How do we measure FRC?

A

helium dilution or body plethysmograph

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9
Q

How do you sample alveolar air?

A

sample end expiratory air. First air exhaled is dead space air that has not undergone gas exchange

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10
Q

What is anatomical dead space?

A

volume of conducting airways that don’t participate in gas exchange - nose, mouth, trachea, bronchi, bronchioles (does not include respiratory bronchioles or alveoli)

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11
Q

What is physiologic dead space?

A

total volume of lungs that doesn’t participate in gas exchange. includes anatomic dead space plus any functional dead space of alveoli. In normal people, physiological and anatomical dead space are about equal.

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12
Q

What is a ventilation/perfusion defect?

A

cause of functional dead space. mismatch of ventilation and perfusion where ventilated alveoli are no perfused by pulmonary capillary blood. In healthy people, functional dead space is minimal.

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13
Q

What are elastic forces?

A

Lungs & chest wall are elastic structures that resist stretch
They passively return to state of equilibrium after they are expanded or compressed
Elastic properties of the lungs or chest wall determine elastance

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14
Q

What are resistive forces?

A
Viscosity of inhaled air
Airway diameter (flow-dependent)
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15
Q

What forces combine to create net negative intrapleural pressure?

A

Lungs tending to collapse inward and chest wall springing outward - opposing elastic forces.

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16
Q

What is compliance?

A

A measure of stiffness. A change in volume per unit change in pressure (delta V/delta P). Inversely correlated with elastance.

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17
Q

What is hysteresis?

A

A feature of the PV loop for an air filled lung where the slope is different for expiration vs. inspiration due to difference in compliance. The lung is more compliant on expiration than inspiration. Surface tension at liquid-air interface of lung causes hysteresis
Surface tension = Force of attraction between liquid molecules at the surface > force between liquid and air

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18
Q

What is the Law of Laplace?

A

P=2T/r where T is surface tension and r is radius. Describes collapsing pressure on alveolus. Small alveolus will have high collapsing pressure/inward force

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19
Q

Why surfactant?

A

Breaks up surface tension so we can keep alveoli small, reduces collapsing pressure, and improves compliance. AMPHIPATHIC

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20
Q

When is surfactant first produced?

A

after 24 weeks gestation

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21
Q

How can you change functional rsidual capacity?

A

By exhaling forcefully. Can change FRC, can’t change residual volume.

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22
Q

how does emphysema change lung compliance? how about fibrosis?

A

Emphysema: increase in lung compliance: due to loss of elastic fibers (decrease in lung elastance)

Fibrosis: decrease in lung compliance: due to excessive stiffness of fibrotic tissue

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23
Q

Where in the respiratory tract is resistance the highest?

A

medium sized bronchi

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24
Q

How does airways resistance change with disease?

A

Airways are tethered by the surrounding lung tissue, thus airway diameter varies with lung volume. Loss of surrounding lung parenchyma, as occurs in emphysema, will lead to loss of radial traction on the airways, narrowing them, increasing airway resistance (COPD)
. Pulmonary fibrosis increases radial traction, which may result in larger airway diameters at a given lung volume and decreased airway resistance

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25
Q

What muscles are associated with inspiration and expiration during exercise?

A

external intercostals, accessory muscles (sternocleidomastoid and scalenus) with inspiration. internal intercostals and abdominals with expiration in exercise and disease.

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26
Q

what is transmural pressure?

A

intra-alveolar pressure – intrapleural pressure. When positive, pressure is expanding and ensures alveoli stay open

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27
Q

What is normal intrapleural pressure?

A

-5 cm H2O

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28
Q

What is pulmonary vascular resistance (PVR)?

A

PVR = Pressure differential between Pulmonary Artery and Left Atrial Pressure/Flow
(mPAP - mLAP)/Cardiac Output

29
Q

What is hypoxic vasoconstriction?

A

When partial O2 pressure is low in alveolar gas, vasoconstriction occurs. Opposite of what happens in other capillary beds. This restricts blood flow away from any diseased areas of the lung.

30
Q

What is the mechanism for hypoxic vasoconstriction?

A

Reduced alveolar PAO2 < 70 mmHg
Inhibition of pulmonary arterial smooth muscle K+ channel
Depolarization then opens voltage gated Ca++ channels
Ca++ influx leads to Smooth muscle contraction

31
Q

Where is nitric oxide derived from?

A

L Arginine

32
Q

What mediates vasodilation?

A

NO, prostacyclin, O2 levels

33
Q

What mediates vasoconstriction?

A

O2 levels, thromboxane, endothelin

34
Q

What does high altitude do to PVR?

A

Reduced barometric pressure leads to decrease in inspired PO2 which leads to low alveolar PAO2
Global vasoconstriction (not just loco-regional) occurs.
Increases in PVR
Chronically over time, this causes RV pressure overload leading to hypertrophy

35
Q

What part of the lungs has the least blood flow?

A

The apex - gravity causes lower arterial pressure. pulm arterioles can be compressed by the higher alveolar pressure around them. alveolar pressure>arterial pressure>venous pressure

36
Q

What are the different pressures in zone 2?

A

blood flow driven by arterial and alveolar pressure differences. Arterial pressure>alveolar pressure>venous pressure

37
Q

What are the different pressures in zone 3?

A

blood flow driven by arterial/venous pressure difference. arterial pressure>venous pressure>alveolar pressure. blood flow highest here.

38
Q

What are physiologic shunts?

A

Bronchial blood flow – blood supply to conducting airways - drains directly into left atrium

Coronary blood flow drains directly into left ventricle through thebesian veins

This is why arterial O2 pressure is always lower than alveolar O2 pressure

39
Q

Can hypoxemia from R to L shunt be corrected with inhaled O2?

A

NO. Shunted blood will dilute normally oxygenated blood no matter how high alveolar PAO2 is
Breathing higher FIO2 (fraction of inspired O2) increases dissolved O2 in capillary blood adding very little to total O2 content of blood.

40
Q

How do chemoreceptors react to hypoxemia?

A

Very sensitive to higher CO2 pressures - leads to hyperventilation to get rid of excess CO2. Less sensitive to O2.

41
Q

What is a left to right shunt?

A

Oxygenated blood from left side of circulation enters right side
ASD, VSD, Patent Ductus Arteriosus
Oxygenated blood re-circulates through lungs
Pulmonary blood flow increases as part of left cardiac output enters right side - pulmonary HT, damage to endothelial cells from turbulent blood flow.
If you measure PO2 of right sided heart chambers, it will be abnormally elevated
Does not cause hypoxemia

42
Q

What is the conducting zone?

A

Conducting Zone: nose, nasopharynx, larynx, trachea, bronchi, terminal bronchioles
Structure: mucus-secreting glands, cilia, smooth muscle (alters airway diameter hence resistance)
Function: warm, humidify, filter

43
Q

What is the respiratory zone?

A

Respiratory Zone: respiratory bronchioles, alveolar ducts, alveolar sacs
Structure: elastic fibers, epithelial cells (type I and type II pneumocytes)
Function: gas exchange, surfactant production

44
Q

how do you measure dead space?

A

By comparing the partial pressure of CO2 in alveoli (PACO2) and the partial pressure of CO2 in expired air (PECO2). The calculation assumes that arterial PaCO2 is equal to alveolar PACO2 level
VD = VT x [(PaCO2 – PECO2)]/PaCO2

45
Q

What is minute ventilation?

A

=tidal volume (volume/breath) x respiratory rate (breaths/minute)

46
Q

what are normal tidal volume and RR?

A

Normal tidal volume is about 450-500 ml, and normal respiratory rate is 12-14 breaths/minute

47
Q

how do you measure alveolar ventilation?

A

minute ventilation - dead space ventilation

48
Q

What is the alveolar gas equation?

A

Describes the relationship b/w alveolar PACO2 with PAO2
PAO2 = PIO2 – PACO2 /R

ONLY DIVIDE PACO2 by R, not PIO2.

R is respiratory exchange ratio = CO2 production/O2 consumption
Normal R level is 0.8

49
Q

Where does FRC mainly reside?

A

In the lung apex

50
Q

Where is ventilation highest?

A

In the base of the lung. Weight of the lung squeezes air out from the base at end of a breath.
With next breath in: the most potential space exists in the base since apex is already full (of FRC)

51
Q

what is a normal value for V/Q?

A

.8. normal V is 4-4.8LPM and normal Q (cardiac output) is 5-6LPM

52
Q

Where is V/Q ratio highest?

A

in Apex, lowest at base

53
Q

what is boyles law

A

p1v1=p2v2 at a given temp

54
Q

How many O2s can Hb bind?

A

4, one for each subunit

55
Q

when is the dissociation curve shifted to the R?

A

Due to acidic pH or higher PCO2: BOHR effect (exercising skeletal muscles)
Higher 2,3-DPG conc: byproduct of glycolysis in RBC, under hypoxic conditions, binds Hb & reduces affinity for O2
Due to higher temp (exercise)

56
Q

when is the dissociation curve shifted to the L

A

decreased unloading of O2 to tissues, increased affinity of Hb for O2

Decrease in PCO2 & increase in pH
Decrease in temp
Decrease in 2,3-DPG conc
HbF: βchain replaced by γ chain and 2,3-DPG doesn’t bind as avidly to γchain

ALSO carbon monoxide.

57
Q

What are some causes of hypoxia?

A

hypoxemia (decreased arterial O2, dec O2 sat of hb, dec dissolved O2), dec CO, anemia, carbon monoxide poisoning, cyanide poisoning. All hypoxemia leads to hypoxia, but hypoxia can occur w/o hypoxemia

58
Q

where are the central chemoreceptors?

A

near surface of medulla. respond to CO2

59
Q

where are the peripheral chemoreceptors?

A

aortic and carotid bodies. thought to respond to O2 and changes in arterial pressure

60
Q

how is hypoxic drive mediated?

A

Mediated by peripheral chemoreceptors
Carotid bodies
Aortic body
Magnitude of response smaller than hypercapnic drive
Clinically beware: it is not uncommon to be hypoxic with little or no dyspnea
People are not necessarily aware when oxygen is low, really just Pco2

61
Q

Hering-Breuer reflex?

A

Hering-Breuer reflex: hyperinflation of the lung causes apnea (suspension of internal breathing)

62
Q

what do the juxtacapillary receptors do?

A
Respond to 
Pulmonary vascular congestion
Interstitial inflammation
Chemicals in the pulmonary circulation
Pulmonary hypertension?
Lung Deflation?
63
Q

Cheyne-Stokes Respiration?

A

Periodic breathing with central apneas
Best example: CHF with increased circulation time
Delayed thermostat

64
Q

what is FVC

A

Forced Vital Capacity (FVC) - The volume of air a subject is able to exhale after a maximal inspiration to total lung capacity

65
Q

What is FEV?

A

Forced Expiratory Volume in 1 second (FEV1) - The volume of air exhaled in the first second of expiration

66
Q

What changes in spirometry do you see with obstruction?

A

dec FEV, no change in FVC. eg bad asthma

67
Q

What changes in spirometry do you see with restriction?

A

dec FVC dec FEV. eg obesity

68
Q

what are some obstructive diseases?

A

Asthma
Emphysema
Chronic Bronchitis

69
Q

what are some restrictive diseases?

A

Interstitial Lung Disease
Neuromuscular Disease
Obesity