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N542 Physiology > Respiratory > Flashcards

Respiratory Flashcards

0
Q

What forms the anatomic dead space? Why is it called this?

A

“Conducting Airways” generation 1-16, consisting of the trachea, bronchi, and non-respiratory bronchioles. This area holds 150mL (1/3 of normal tidal volume) in volume (30% of the breath) and does not participate in gas exchange, only transports oxygen “bulk movers”

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1
Q

How much volume can the lungs hold? What is the surface area?

A

4L

82 m^2 (most of this is alveolar space)

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2
Q

What is going on in the respiratory zone/unit? What is it made up of?

A

Generation 17-23, consists of respiratory bronchioles, alveolar ducts, and alveloar sacs. This is where diffusion occurs, there is little forward movement of air

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3
Q

Type 1 vs. Type 2 alveolar cells?

A

Type 1: takes up most of the surface area (98%), site for gas exchange and diffusion (type 1 cells’ membranes are fused with capillary endothelium)
Type 2: found in the corners of the alveolus, occupies a small surface area, main function is secreting/synthesizing SURFACTANT

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4
Q

What is the function of surfactant in the lungs?

A

Surfactant is synthesized by type 2 alveolar cells, it reduces surface tension and can help regenerate alveoli after injury. Surfactant is the reason that the alveoli are never COMPLETELY closed

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5
Q

Moving from trachea to alveoli, what occurs with surface area, pressure gradient, and flow/velocity?

A

As cross sectional area increases, pressure gradient and velocity of flow decreases so that gas exchange can occur
Flow = Volume / Time
Pressure = Force / Area

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6
Q

What is the function of the upper airway (nose to larynx)?

A

humidity, warm, and filter

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7
Q

What are the major and accessory muscles of inspiration?

A

Major is diaphragm, allows for expansion of the lung downwards
Accessory are external intercostals, allowing for anterior and posterior expansion, and the scalenes, picking up the first and second rib, allowing for expansion upwards, and SCM moves sternum forward

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8
Q

What area of the lung is a potential space? What does this mean?

A

Parietal layer, if air were to go here it would be a pneumothorax

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9
Q

Is exhalation active or passive? What muscles are involved?

A

Exhalation is PASSIVE

Rectus abdominis, other abdominal muscles, oblique muscles, as well as internal intercostals

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10
Q

How is the work of breathing related to pressure and change in volume?

A

Work = pressure x change in volume

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11
Q

Restrictive vs. Obstructive lung disease

A

Restrictive: example is obese, this person has decreased compliance
Obstructive: example is COPD, this person has good compliance

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12
Q

What are collagen and elastin?

A

Collagen: major structural component of lung that limits lung distensibility
Elastin: major contributor to elastic recoil of the lung

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13
Q

Which 2 forces want to pull lungs to collapse?

A

alveolar surface tension and lung elasticity

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14
Q

During inspiration and expiration, when is the lowest and highest intrapulmonary pressure reached?

A

Lowest pressure reached halfway into inspiration

Highest pressure reached halfway into expiration

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15
Q

TLC, VC, RV?

A

TLC: total lung capacity, total volume that can be in a lung
VC: vital capacity, total exhaled from max inhale to max exhale
RV: residual volume, air remaining/”trapped” in the lung after VC
TLC = VC + RV

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16
Q

FRC, ERV?

A

FRC: functional residual capacity, volume of air in the lung at the end of exhalation during quiet breathing (resting volume of the lung)
ERV: expiratory reserve volume, volume of air that can be exhaled from resting exhale to max exhale
FRC = ERV + RV

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17
Q

RV:TLC ratio tells us what?

A

How much air is trapped, normal is 25%
In patients with obstructive diseases, RV increases
In patients with restrictive lung diseases, TLC decreases

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18
Q

What value is effected during preoxygenation?

A

FRC

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19
Q

Which values are static and measured by spirometry?

A

Tital volume and vital capacity (VC)

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20
Q

Which values are non-static, measured by a gas dilution technique such as helium spirometer or plethysmography?

A

TLC (total lung capacity), FRC (functional residual), RV (residual volume)

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21
Q

Boyle’s Law: What is happening during inspiration and expiration?

A

pressure and volume are inversely proportional
Inspiration: air coming in expands the alveoli, volume increases (inspiration muscles are active), pressure decreases
During expiration, elastic recoil causes volume to decrease, therefore pressure increases

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22
Q

What are examples of expiration becoming active?

A

Asthma, hyperventilation, playing a wind instrument

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23
Q

What happens to the flow volume loop in restrictive and obstructive lung disease?

A

Restrictive: smaller area of loop
Obstructive: bottom of the loop is normal (inhale is normal), top of the loop is decreased (exhale abnormal)

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24
Q

When comparing the base and apex of the lung, during ventilation, which has a higher volume, where is the pressure more negative?

A

At the apex, intrapleural pressure is more negative, and there is more volume (bc gravity and Boyle’s law, the base is compressed)
Normally, base ventilation per unit volume is BETTER (base pressure is high, base volume is low)

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25
Q

Where in the airway is flow laminar vs. turbulent? What is the equation?

A

laminar in the distal bronchioles, further down the airway
turbulent in the trachea and large airways (conducting airway)
Reynold’s number = (density x diameter x velocity) / viscocity
Less than 2000 is laminar

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26
Q

In cases with increased airway resistance, such as asthma, what happens to velocity of flow and pressure?

A

More pressure is needed to keep up flow, but velocity/flow is ultimately reduced
Flow= change in P / R

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27
Q

Where is resistance the highest in the airway? What does breathing a dense gas do to resistance?

A

Medium sized bronchi

Breathing a dense gas increases resistance

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28
Q

What is the equation for Poiseuille’s Law? V=

A

V = (Pi x Pressure x r^4) / (8 x viscocity x length)

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29
Q

What do forced expiration, beta2 blockers, acetylcholine, and histamine all do to resistance of the airway?

A

INCREASE resistance

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30
Q

How is compliance measured using volume and pressure?

A

Compliance = change in volume / change in pressure

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31
Q

What are examples of increased and decreased compliance?

A

Increased: aging, obstructive lung disease, asthma, emphysema
Decreased: restrictive lung disease, pulm fibrosis, alveolar edema, atelectasis, hypoventilated lungs, increased pulmonary venous pressure

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32
Q

In emphysema and aging, what happens to the alveoli regarding compliance and recoil?

A

INCREASED compliance (overstretched), DECREASED recoil (this makes expiration ACTIVE instead of passive)

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33
Q

Surfactant: what secretes it, what does it do, and what is it composed of?

A

Secreted by Type 2 alveolar cells, it reduces surface tension and is most effective in low lung volumes (hysteresis), it increases compliance
It is composed of phospholipid/fats, acid, protein

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34
Q

What law/equation is used to measure surface tension?

A

LaPlace’s Law, shows that surfactant lowers surface tension

Pressure = (4 x surface tension) / radius

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35
Q

What are the three main goals of respiration?

A
  1. minimize workload (pressure x volume)
  2. maintain gas exchange
  3. regulate CO2
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36
Q

Where are the DRG (dorsal resp group) and VRG (ventral resp group) located and what do they do?

A

DRG: dorsomedial medulla, specifically the NTS (nucleus of tractus solitarius), signals received from CN 9 and 10 to control INSPIRATION
VRG: ventrolateral medulla, specifically in the nucleus retroambiguus, EXPIRATION (and some inspiration). Note: this area is usually quiet bc expiration should be passive

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37
Q

Pneumotaxic center: where is it located and what is its job?

A

Part of the respiratory control center, located in the pons, responsible for the rate and depth of ventilation

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38
Q

What is the Hering Bauer Reflex?

A

It is an example of the VRG, so it is located in the ventral medulla, it is a inspiratory inhibitory reflex responding to stretch receptors to stop inspiration and cause early exhalation (this is a way to increase respiratory rate)

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39
Q

How do the phases of ventilation include “ramp-up”?

A

Inspiratory neuron firing increases in “ramp-up” matter, then expiration begins as inspiration neuron firing starts to slow down. This system allows for steady volume increase and decrease.

40
Q

How does the central chemoreceptor work? What is the one equation we have to memorize (CO2 + H2O…)?

A

It detects changes in CO2 and H
When the CO2 increases, it crosses the blood brain barrier to the CSF (H doesn’t cross easily) where it undergoes that equation.. CO2 + H2O -> H2CO3 -> H + HCO3 .. When the H is liberated, the respiratory center will increase signals to breathe faster (H works more potently, CO2 works more indirectly)

41
Q

Where is the central chemoreceptor located?

A

In the ventral medulla, near CN 9&10

42
Q

Are central chemoreceptors sensitive to changes in O2?

A

NO.. They are sensitive to changes in H and CO2

Peripheral chemoreceptors are sensitive to O2 changes

43
Q

At what levels of PCO2 do the central chemoreceptors have the best compensation response to hypercarbia?

A

When PCO2 is 45-75 (this is the steep part of the curve), this is when alveolar ventilation increases linearly

44
Q

The curve showing PCO2 and alveolar ventilation that is linear: What are some things that shift this curve to the right or left? (These will increase/decrease respiratory drive)

A

Shift to the left (increased resp drive): metabolic acidosis
Shift to the right (decreased resp drive): narcotics, obstruction (COPD), deep anesthesia, and sleep (slight shift)
With patients that are shifted to the right already, they should receive less pain meds bc they are already shifted

45
Q

CSF compared to blood: which is more acidotic?

A

CSF is slightly more acidotic (7.33 vs. 7.40), slightly higher PCO2, slightly lower bicarb

46
Q

What are peripheral chemoreceptors?

A

They detect changes in O2 and transmit signals to regulate respiratory activity

47
Q

Where are peripheral chemoreceptors located?

A 
Carotid bodies (more sensitive, pass through CN 9, DRG)
Aortic bodies (pass through CN 10, VRG)
48
Q

At what level of pO2 do the peripheral receptors fire at an increased rate?

A

When pO2 drops below 100, there is a huge spike on the curve of the peripheral receptors firing

49
Q

When CO2 is increased, how does this change the normal response of alveolar ventilation to decreased O2?

A

The response is much quicker, it will start to compensate at higher levels of O2 (higher than the normal 100)

50
Q

What are the three sensory peripheral receptors in the tracheobronchial tree that effect lung mechanics?

A

J receptors, Irritant receptors, Stretch receptors

51
Q

How do irritant receptors work, specifically? Where are they found?

A

They are found in the epithelium of trachea, bronchi, and bronchioles, transmitted through myelinated CN 10 sensory fibers, rapidly adapting, results in coughing, sneezing, and bronchoconstriction (asthma, COPD)

52
Q

How do pulmonary stretch receptors work specifically? How does this relate to COPD?

A

Lung inflation activates myelinated CN 10 sensory fibers, slow adapting
In COPD, the receptors will cause a delay in the next inspiration (I:E 1:3, normal is 1:2)

53
Q

What are J receptors, specifically?

A

Juxta-alveolar receptors are stimulated when pulm capillaries become full of fluid (blood/edema), transmitted through unmylinated CN 10 C fibers, responsible for dyspnea, SOB, the shallow ventilation that comes with edema.

54
Q

What causes Cheyne Stokes breathing?

A

An abnormality in the brainstem will cause a period of apnea to be followed by hyperventilation (the respiratory centers become excited, but it is a delayed response)

55
Q

hypoxia vs hypoxemia?

A

hypoxia: low O2 in the tissues
hypoxemia: low O2 in the blood, low PaO2 levels, peripheral chemoreceptors will sense this and kick in

56
Q

What is the equation for the A-a gradient?

A

PAO2 = FiO2 x (Pb - Ph2o) - PaCO2 / R
Room Air FiO2 = 0.21
Pb = 760 (barometric pressure), Ph2o = 47 (vapor pressure)
Pb-Ph2o= 713 R = 0.8

57
Q

What is Dalton’s Law?

A

Law of partial pressures
Ex: Oxygen is 21% of air, so 21/100 x 760 = the partial pressure of oxygen (160)
Pressure is directly proportional to the concentration of gas molecule

58
Q

What happens to end title CO2 with COPD?

A

They aren’t able to completely exhale back to baseline, therefore they have a higher end title CO2

59
Q

How does PO2 and PCO2 differ in the pulmonary artery and pulmonary vein? Why is this important?

A 
Pulm artery (before lung): PO2= 40, PCO2= 46
Pulm vein (after lung.. normal values): PO2= 100, PCO2= 40
This creates a concentration gradient, O2 moves from alveoli to blood, CO2 moves from blood to alveoli
60
Q

How fast is gas exchange? How long does it take for a RBC to pick up the oxygen?

A

gas exchange only takes 1/4 sec, it takes 3/4 sec for RBC to pick up the oxygen

61
Q

What is the average amount of pulmonary capillary blood volume and pulmonary blood flow?

A

pulm cap blood volume: 70 mL

pulm blood flow: 5L/min (100% flow from the heart)

62
Q

What is Henry’s Law?

A

Using partial pressures (Dalton’s), but adding the solubility coefficient
partial pressure = conc gas / solubility coefficient

63
Q

What is the solubility coefficient for CO2? What does that mean?

A

0.57.. This means CO2 is EXTREMELY attracted to water and dissolves more easily in water (compared to oxygen and nitrogen)
If a molecule is attracted to water, the higher the coefficient (closer to 1) but the lower the partial pressure (coefficient and partial pressure are inverse)

64
Q

What percent of oxygen is normally carried by hemoglobin?

A

97%, so 3% of oxygen make it to the tissues without hemoglobin

65
Q

What is Fick’s Law? What is the equation? (Rate of diffusion = …)

A

As thickness increases, diffusion decreases
Rate of Diffusion = (conc gradient x surface area x diffusion coefficient) / THICKNESS of the membrane
(Diffusion coefficient = permeability / square root of molecular weight)
Remember: Thickness is INVERSE to diffusion rate

66
Q

What layers of membrane does the gas diffuse through? (What makes up the respiratory/ alveolar-capillary membrane)

A

From capillary to alveoli: capillary endothelium, capillary basement membrane, interstitial space, epithelial basement membrane of alveoli, alveolar epithelium, surfactant layer of alveoli
(note: this is the path of CO2 moving out of the blood, O2 takes the opposite path into the blood)

67
Q

What is the normal thickness and surface area of the respiratory membrane?

A

THIN: 0.3-0.6 micrometers
SA: 70 m^2

68
Q

Anatomic vs. Physiologic dead space?

A

Anatomic: 150 mL of conducting airways (washes out the nitrogen)
Physiologic: volume of gas that doesn’t participate in gas exchange and doesn’t eliminate CO2 (perfused but not ventilated)
These are normally the same (different in disease states)

69
Q

At 100% oxygen, how many mL will bind to 1 gram of hemoglobin?

A

1.34 mL

70
Q

What is the equation for arterial oxygen content (CaO2)?

A

CaO2 = (Hgb x SaO2 x 1.34) + (0.003 x PaO2)
= portion bound to hemoglobin + dissolved component
(SaO2 is sats)

71
Q

What is the equation for oxygen delivery?

A

CaO2 x CO x 10

72
Q

In a normal oxygen dissociation curve, what is PO2 when sats are 90%? What is PO2 when sats are 50%? 100%?

A

Sat of 90%, PO2 60
Sat of 50%, PO2 50
Sat of 100%, PO2 100

73
Q

What causes a shift to the left in the hemoglobin dissociation curve?

A

Left shift: INCREASED affinity for oxygen, oxygen binds more tightly to hemoglobin, inhibition of oxygen delivery to the tissues, so alkalosis, decreased CO2, decreased temp (when cold, you might turn blue bc oxygen is not being released to the tissue), and low 2,3-DPG

74
Q

What is the Bohr effect?

A

The effect of CO2 on the affinity of hemoglobin for O2
So, when someone gets acidosis or alkalosis, the O2 will be more or less tightly bound to hemoglobin (Acidosis- decreased affinity)

75
Q

What is 2,3-DPG (diphosphoglycerate)

A

It is an intermediary formed in the RBC during glycolysis
The affinity of Hgb for O2 decreases as 2,3-DPG levels increase
Note: blood-bank RBC is LOW in 2,3-DPG and can cause a shift to the left

76
Q

What happens with a shift to the right in the Oxyhemoglobin dissociation curve?

A

Decreased affinity of hemoglobin for oxygen, therefore it more easily releases oxygen to the tissues for diffusion, increased temp, increased PCO2 (acidosis), increased 2,3-DPG

77
Q

What is the respiratory exchange quotient?

A

0.8 (CO2 of 80 : O2 of 100)

This is the ratio of expired CO2 to O2 uptake

78
Q

What is the relationship between alveolar ventilation and CO2?

A

Inverse relationship

79
Q

How is CO2 transported?

A

The majority (70%) of it is transported as bicarb (HCO3)
Some of it is transported with hemoglobin (deoxygenated hemoglobin as a high affinity for CO2)
Only 7% transported as CO2

80
Q

What is the Haldane effect?

A

The effect of changes in oxygemoglobin saturation on the relationship of CO2 content to PCO2
The dissociation curve of CO2 is linear (unlike the S-shaped O2 curve)

81
Q

What does DLCO measure?

A

(Diffusion limitation) Diffusion capabilities of the alveolar-capillary membrane (it is effected by membrane thickness and surface area), it is useful in diagnosing restrictive lung disease

82
Q

What is the equation for Alveolar gas exchange? (A-a gradient)

A 
PAO2 = FiO2 x (Pb-Ph2o) - PaCO2/R
Pb = barometric pressure, 760
Ph2o= vapor pressure, 47
R= resp exchange quotient, 0.8
83
Q

How much cardiac output does the lung receive?

A

ALL of it!!

84
Q

How much blood is in the pulmonary circulation? How much is in the alveolar-capillary membrane?

A

pulm circulation: 500mL

alveolar-capillary membrane: 75 mL

85
Q

How does the pulmonary artery differ from other arteries, like the aorta?

A

It is THINNER, has a SHORTER length, and has a WIDER diameter, it lacks smooth muscle so it can’t dilate/constrict, more COMPLIANT, and LOW pressure
It carries DEOXYGENATED blood

86
Q

What are the two unique ways that pulmonary circulation can allow increased blood flow without an increase in pressure?

A
  1. With increased demand (exercise), more pulmonary vessels are recruited (they are usually closed)
  2. The vessels in pulmonary circulation are so distensible that only a small increase in pulmonary pressure can drastically increase diameter
87
Q

How do alveolar (in intra-alveolar septa, capillaries) and extra-alveolar vessels (arteries/veins) work differently related to PVR during inspiration?

A

During inspiration, PVR INCREASES in Alveolar vessels (exposed to air pressure) and PVR DECREASES in extra-alveolar vessels (more sensitive to interstitial pressures)

88
Q

How to PVR and PAP compare to systemic pressures?

A

PVR and PAP have lower pressures (less force needed to eject blood from RV to lung)

89
Q

What is hypoxic vasoconstriction?

A

When the lungs sense low pO2, blood is shunted to well ventilated portions of the lung to pick up more O2, this provides better VQ matching
hypoxia in all sections in the lung leads to pulmonary hypertension

90
Q

How does pulmonary vascular resistance relate to pressure and flow? When is PVR at its lowest?

A

PVR = change in pressure / flow
Remember, PVR is LOW compared to systemic
PRV is at its lowest during FRC (functional residual capacity)

91
Q

What causes pulmonary vasodilation: Acidosis or alkalosis?

A

Alkalosis

92
Q

What is normal V/Q of the lung, the values and the ratio?

A

V: 4 L/min (alveolar ventilation)
Q: 5 L/min (pulm blood flow)
0.8

93
Q

What are the 4 ways of getting hypoxemia?

A
  1. hypoventilation
  2. diffusion limitation (DLCO)
  3. shunt (patency or embolism)
  4. VQ mismatch (most common)
94
Q

How does V/Q differ at the base and apex of the lung?

A

Q is lowest at the apex (against gravity) and ventilation is a little lower, apex is better ventilated than perfused
Apex has a higher V/Q, base has a more normal V/Q

95
Q

What is the normal A-a gradient for O2 and CO2? What is going on if the A-a gradient is normal and the patient is hypoxic?

A

O2 A-a: 5-15
CO2 A-a: 2-10
If normal, then hypoxia is due to hypoventilation
If grossly abnormal, then it is due to V-Q abnormality

96
Q

Compare pressure gradients of pulmonary blood flow from the top of the lung (zone 1) to the bottom of the lung (zone 3) with Pa, PA, and Pv

A

Zone 1: PA > Pa > Pv
Zone 2: Pa > PA > Pv
Zone 3: Pa > Pv > PA

97
Q

What are the non-respiratory functions of the lung?

A 
Filters (macrophages), contains mast cells (they produce heparin)
Metabolizes vasoactive (produces ACE) and bronchoactive substances
Produces immunoglobulins (IgA)

N542 Physiology (9 decks)

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