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Module 3: CPR > Physiology II > Flashcards

Physiology II Flashcards

1
Q

What parts of the nervous sytem are involved in respiratory control?

A
  • CNS
  • Phrenic nerve - innervates diaphragm
  • Sensory nerves - receptors that sense flow, pressure changes
  • Vagus nerve
  • Sympathetic nerves terminate near airways - control bronchodilation
  • Parasympathetic nerves - control bronchoconstriction
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2
Q

What muscles are involved in Quiet Inspiration?

A
  • Diaphragm
  • External Intercostals
  • Scalene
  • Sternocleidomastoid
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3
Q

What is quiet inspiration and quiet expiration?

A

Quiet Inspiration: unlabored inspiration

  • *Quiet Expiration:** unlabored expiration
  • Passive process with no active muscle movement
  • Elastic recoild and surface tension in alveoli pulls inward
  • Alveolar pressure increases and air is pushed out
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4
Q

What muscles are involved in forced expiration?

A
  • Internal Intercostals
  • External oblique
  • Internal oblique
  • Rectus Abdominis
  • Transversus Abdominis
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5
Q

What is the definition of an elastic structure?

A

Structure whos volume is directly proportional to the pressure difference across the wall of the structure

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6
Q

How is the Transmural pressure (Ptm) of the lung calculated?

A

Ptm = Pint - Pex

Pint = Internal surface pressure
Pex = External surface pressure

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7
Q

What is the relationship between transmural pressure and volume (in an ideal situation)?

How does this describe an elastic structure?

A

The relationship btwn Ptm and Volume is a positive, linear relationship (where slope = compliance)
- until it hits the elastic limit, which is the point at which the structure is no longer compliant (slope = 0)

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8
Q

How is compliance depicted on a Pressure/Volume curve?

A

Slope = Compliance
The less Pressure it takes to increase the volume (i.e. the higher the slope) the more compliant the structure is

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9
Q

How are alveoli connected?

A

Through bronchioles as well as pores of Kohn

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10
Q

What are pores of Kohn?

A

Openings in the interalveolar septa that allow circulation of the air from one alveolus to another

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11
Q

If pressure is higher in smaller alveoli (due to Law of LaPlace), why don’t alveoli collapse in on themselves?

**reminder, Law of LaPlace: P = 2T/r
==> smaller radius = higher pressure

A

Surfactant secreted by Type II pneumocytes decreases surface tension produced by water

  • As surface area decreases, surfactant becomes more concentrated
  • Part of the sufactant molecules dissolves in th water in the lungs, while the remainder spreads over the surface.
  • Surfactance-treated surface tension is from 1/12 - 1/2 the surface tension of pure water
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12
Q

How is PTranspulmonary calculated?

A

PTranspulmonary = Palveoli - PPleura

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13
Q

What is the importance of pleura and pleural space?

A
  • Maintains pressure differential
  • Fluid lubricates for respiration
  • Fluid helps maintain connetion between visceral and parietal pleura
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14
Q

What is the relationship of Pressure and Volume in the lung?

A
  • Relationship is curvilinear
  • Low volume = More compliance
  • high volume = less compliant
  • Respiratory muscles change the compliance of the chest wall, such that the curve shifts right during inspiration
    and left during expiration
    *Note, tidal breathing is depicted by small oval in curve
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15
Q

How does gravity affect lung space?

A
  • At the apex: Alveoli are stretched out = decreased compliance
  • At the base: lung mass pushes outward and compresses pleura = increased compliance
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16
Q

How does emphysema affect lung capacity?

A
  • Tissue is distensible (has lost elasticity)
  • Increased compliance
  • But it is difficult to expel air from the alveoli

Therefore, Total Lung Capacity has increased, but elasticity and ability to exhale has decreased

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17
Q

How does Fibrosis affect lung capacity?

A
  • Tissue is stiff = decreased compliance
  • increased elastic recoil
  • lung collapses and it is difficult to force air into the alveoli

Therefore, Total Lung Capacity has decreased, while the elasticity of the lung has increased and the ability to inhale has decreased

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18
Q

What is the definition of Total Lung Capacity?

A

Lung volume at which a static balance has been achieved btwn Maximal Inspiratory Force (resp. muscles) and Expiratory Force (elastic coils)

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19
Q

What is the definition of Functional Residual Capacity?

A

Relaxed Equilibrium Point:
Volume at which elastic recoild of lung and chest wall are equal, but opposite

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20
Q

What is the definition of Residual Volume?

A

Lung volume at which static balance has been achieved between Maximal expiratory force (resp. muscles + elastic recoi) and force generated by outward-directed elastic recoils of lung+chest wall

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21
Q

What is the difference btwn:

Anatomic Dead Space

and

Physiologic Dead Space

A

Anatomic Dead Space = Volume of the conducting airways where there is no gas exchange (i.e. respiratory passageway)

Physiologic Dead Space = Volume of the lungs that is not participating in gas exchange due to lack of perfustion (i.e. apex or V/Q mismatch)

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22
Q

How does pleural pressure drive air flow?

A

Diaphragm and other respiratory muscles manipulat pleural pressure, producing a negative alveolar pressure gradient with environmental pressures, allowing for air to flow into the lungs

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23
Q

Name the lung function occuring at each pressure value:

A

A = Pressures at Functional residual capacity (exhale and hold)

B = pressures during inspiration

C = Pressures at peak inspiration (inhale and hold)

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24
Q

What are the two main factors moving O2 inside the lungs?

A

Combination of:

Mass Airflow

and

Molecular Diffusion
(becomes more important in periphery)

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25
Q

Where is airway resistance greatest in the lungs?

A

Resistance = change in pressure/flow

It is greatest in the mid-sized bronchi and decreases to almost nothing in terminal bronchi

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26
Q

What is the relationship between airway resistance and lung volume?

A

Resistance increases rapidly with lung volumes < functional residual capacity

Decreases with lung volumes > FRC

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27
Q

What is the relationship between airflow and volume?

A
  • *Inspiration:**
  • Markedly negative pleural pressure with large transmural pressure
  • Flow high at low Volume
  • Remains high through most of VC despite decreased inspiratory force
  • *Expiration:**
  • Airflow reaches peak near TLC
  • Flow rate falls progressively after TLC due to intrathoracic airway narrowing and increasing resistance
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28
Q

What does O2 have to move through to get from enironmental air to the target tissue?

A
  1. atmospheric air to lung alveoli by pulmonary ventilation
  2. through layers of respiratory membrane (pneumocytes –> interstitial fluid –> capillary lumen –> RBC) to hemoglobin of RBC by simple diffusion
  3. from pulmonary capillaries to tissue capillaries by circulation
  4. from hemoglobin to interstitial fluid and tissue cells via simple diffusion
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29
Q

What is simple diffusion?

A

net movement from a region of high concentration to a region of low concentration

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30
Q

What is the driving force of simple diffusion for O2 and CO2 in respiratory physiology?

A

Partial Pressures:
PO2

PCO2

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31
Q

What is partial pressure?

A

Partial pressure = (Total Pressure)*(fractional gas concentration)

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32
Q

Why is alveolar air different in composition from atmospheric air?

A
  1. Dry air is moistened by air passages
  2. Alveolar air is not completely replaced with each breath
  3. CO2 is constantly entering alveolar air
  4. O2 is constantly exiting alveolar air
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33
Q

What factors affect diffusion rate proportionally?

A
  1. Solubility of the gas in fluid (a constant)
  2. Difference in partial pressure btwn compartments
    (increase gradient = increased diffusion rate)
  3. Surface area for diffusion
  4. Temperature
    (biologically constant)
34
Q

What factors affect diffusion rate inversely?

A
  1. Square root of molecular weight of gas (a constant)
  2. Distance of diffusion
    (increase distance = decreased diffusion rate)
35
Q

What is a main factor in the lungs that allows for rapid diffusion?

A

Surface Area of diffusion

  • Between alveoli is a solid network of interconnecting capillaries described as a “sheet” of flowing blood
  • High surface area to volume ratio = high O2 diffusion rate into blood and high CO2 diffusion rate into alveoli
36
Q

How is blood oxygenation affected during exercise?

A
  • In normal/resting rate, PO2 becomes almost equal to alveolus PO2 before passing through 1/3 of the capillary length due to rapid diffusion
  • During exercise, blood is moving faster, but even though blood flow increases and duration of time the blood is in the capillaries decreases, blood is still oxygenated before it hits the veinous end due to rapid diffusion
37
Q

How is oxygen carried in blood?

A

O2 has a lower solubility in fluids compared to CO2:

97% is bound to hemoglobin

3% is dissolved in plasma or RBC cytoplasm

Each hemoglobin can has 2a and 2ß chains, each with one heme group –> each hemoglobin can bind 4 O2 molecules

95% of proteins in RBCs is hemoglobin

38
Q

How does binding of O2 affect hemoglobin?

A

Binding is allosteric and cooperative

Binding causes a conformational change to allow for easier binding of the next oxygen molecule to a different, unoccupied heme group

39
Q

What is the significance of the Oxygen/Hemoglobin dissociation curve?

A

Oxygen/Hemoglobing Dissociation Curve shows O2 saturation of hemoglobin changes more rapidly over the physiological range with changes in PO2 than if the O2-bindign sites were independent of each other

40
Q

What can cause changes in the O2 hemoglobin dissociation curve?

A

Hydrogen Ions

Carbon Dioxide

Temperature

2,3 bisphosphoglycerate

–> An increase in any of these factors results in a decrease of hemoglobin affinity for O2, so the curve shifts to the right

*Note all factors increase during exercise

41
Q

How can fires affect O2 supply?

A
  • Oxygen is consumed by the fire
  • CO is produced, which has a higher affinity for hemoglobin than O2
42
Q

How does anemia affect O2 supply?

A
  • No change in Pa O2
  • No change in O2 Saturation
  • Change in O2 carrying capacity
  • May be compensated by cardiac output
43
Q

Why is carbon monoxide so poisonous?

A

CO binds to HgB with 200x more affinity than O2

  • CO changes O2 carrying capacity, and HbB adds plasma dissolved O2
  • CO-HgB at one subunit of HbB causes other subunits to increase O2 affinity –> O2-HgB curve shifts left

- Also affects O2 delivery

44
Q

What are some significant differences between O2 and CO2 transport?

A
  • Diffusion rates
  • minimal pressure differences
  • lack of dedicated carrier for CO2
45
Q

How is CO2 transported in the body?

A
  1. Dissolved CO2
  2. As bicarbonate anions (HCO2-)
  3. As Carbamino Compounds (amine-bound CO2)

–> no dedicated carrier

46
Q

How is CO2 able to travel through the body as bicarbonate anions?

A

*Majority of CO2 is transported in this form*

  • CO2 reacts with water to form carbonic acid which dissociates into bicarbonate and hydrogen ions:

CO2 +H2O => H2CO3 => H+ + HCO3-
Rxn1 Enzyme: Carbonic Anhydrase
Rxn2: spontaneous

47
Q

Why does so much more CO2 form HCO 3- in RBCs than Plasma?

A
  1. RBCs contain high concentrations of Carbonic Anhydrase - the enzyme that makes CO2 => H2CO3
  2. Cl-/HCO3- exchanger removes HCO3- from RBC and promotes formation of new HCO3-
  3. Intracellular buffers (Hb) buffer the H+ produced during HCO3- formation
48
Q

Why do venous RBCs have high intracellular Cl- concentrations than arterial RBCs?

A
  • Bicarbonate is made inside the RBC by carbonic anhydrase
  • Bicarbonate leaves the cell via bicarbonate-chloride exchanger protein –> aids in further dissociation of carbonic acid
  • Cl- is exchanged with HCO3- in order to maintain electroneutrality

Short answer: Venous RBCs have more CO2

49
Q

How does hemoglobin buffer bicarbonate formation?

A

Deoxyhemoglobin accepts hydrogen ions more readily than oxyhemoglobin.

(Association of Hb with H+ lowers Hb’s O2 affiinity, thus driving further O2 dissociation in blood with higher PCO2)

50
Q

Why does so much more CO2 form carbamino compounds inside RBCs than plasma?

A
  1. CO2 reacts slowly with proteins to produce carbamino compounds. High [Hb] in RBCs promotes this
  2. Hb forms carbamino compounds more easily than the major proteins in plasma
  3. Hb is a buffer for the H+ that is produced during carbaminio formation
  4. Hb is better at #2 and #3 in tissue capillaries as it loses its bound O2
51
Q

What does the CO2/blood dissociation curve represent?

A
  • For a given PCO2, what is the CO2 blood content?
  • The sum of these CO2 forms in blood and the relationship to PCO2 can be depicted by this curve
  • Note the normal range of CO2 curve function is narrow
52
Q

What is the Haldane effect? How does it work?

A

O2 binding to hemoglobin causes CO2 to be released from the blood more effectively.

Mechanism:

  1. O2 bidning to Hb makes it a stronger acid. Released H+ ions bidn with bicarbonate and form carbonic acid, which dissociates into CO2 and H2O
  2. O2 binding to carbamino-Hb displaces the CO2 from it directly
  3. Both of these mechanisms increase CO2 release from blood to diffuse into alveolar space
53
Q

How is blood pH calculated?

A

The Rxn is:

CO2 + H2O –> H2CO3 –> H+ HCO3-
Enzyme: Carbonic Anhydrase

The Eqn is:

pH = pK + log([HCO3-]/[CO2+H2CO3])

(Henderson Hasselbalch eqn)

54
Q

How is blood pH controlled?

A

Blood pH is determined by CO2 and bicarbonate concentrations

Respiratory system controls the amount of CO2 in the blood

Renal system controls the amount of bicarbonate in the blood

55
Q

What is the Davenport Diagram?

A

Graphical tool for interpreting bicarbonated concentrations from blood pH

Respiratory control (control of CO2) is depicted along the buffer lines (horizontal-ish lines)

Renal control (control of HCO3- and H+) is depicted along the isopleths (vertical-ish lines)

56
Q

What is respiratory acidosis? How does the body compensate for this?

A

Increased arterial PCO2 –> Increased H+ and HCO3- –> lower blood pH

Renal compensatory mechanisms will increase HCO3- to return blood pH to normal levels

57
Q

What is respiratory alkalosis? How does the body compensate for this?

A

Decreased arterial PCO2 –> Decreased H+ and HCO3- –> higher pH

Renal system compensatory mechanisms will decrease HCO3- to return blood pH to normal levels

58
Q

What is hyperventilation?

A

Breathing increased more than required

Results in lower PaCO2 than normal

59
Q

What is Hypoventilation?

A

Breathing decreased more than required

results in higher PaCO2 than normal

60
Q

What is Hyperpnea?

A

Increased breathing that matches metabolic needs (i.e during exercise)

61
Q

What is Hypoxemia and how does it differ from hypoxia?

A

Hypoxemia is an inadequate level of O2 in the blood

Hypoxemia can lead to hypoxia, which is a deficiency in the amount of blood delivered to the organs

62
Q

What are some reasons for hypoxemia?

A
  • V/Q mismatch*
  • Shunt*
  • Diffusion Abnormality*
  • Low inspired O2 content
  • Hypoventilation

* = most common reasons

63
Q

What is the alveolar gas equation?

A

PAO2 = FiO2(PB-PH2O)-PaCO2/RQ

PAO2 = Alveolar partial pressure of O2
FiO2 = Fraction of inspired gas that is O2
PB = Atmospheric pressure
PH2O = saturated vapor pressure of H2O at body temp
PaCO2 = arterial pressure of CO2
RQ = respiratory quotient

64
Q

What is the importance of the ventilation/perfusion relationship?

A

It is the attempt to perfectly match pulmonary blood flow and ventilation

Overall V/Q for lung = 0.8

65
Q

What is considered “dead space”?

A

More ventilation than blood flow

V/Q = infinity

66
Q

What is considered a shunt?

A

More blood flow than ventilation

V/Q = 0

67
Q

What is the difference between alveolar dead space and anatomic dead space?

A

Alveolar = Recruitable
Body is able to create a blood flow to match ventilation
(i.e. apex of the lung)

Anatomic = NOT Recruitable
Body is not able to create blood flow to match ventilation
(i.e. bronchus, trachea)

68
Q

How do you assess for a shunt?

A

Place patient on 100% O2 and obtain blood gas

PO2 should increase to approximately 700

For every 100mmHg below 700, estimate 5% shunt

69
Q

What is respiratory failure? What are the two types?

A

When the lung fails to oxygenate the arterial blood adequately and/or fails to preevnt CO2 retention

  1. Type 1 Failure = Hypoxemic Respiratory failure
  2. Type 2 failure = Hypercapnic Respiratory Failure
70
Q

What are the pressure differences for Zone 1 in the lungs?

A

Apex:

PA > Pa > Pv

71
Q

What are the pressure differences for Zone 2 of the lungs?

A

Mid lung:

Pa > PA > Pv

72
Q

What are the pressure differences for Zone 3 of the lungs?

A

Base of lung:

Pa > Pv > PA

73
Q

What is Hypoxemic respiratory failure?

A

Defined by low O2 tension in blood (PaO2)

  • inability to transfer adequate O2 from alveolar space to pulmonary capillary blood
  • Does not account for decrements in O2 deliver (i.e. anemia)
74
Q

What is hypercapnic respiratory failure?

A

Increased PCO2 in the blood

75
Q

What may be the cause of hypoxia?

A
  • Hypoxemia

OR

  • Poor O2 delivery (i.e. anemia/heart disease)
76
Q

What are possible mechanisms of Hypoxemia that are unaffected by lung function?

A
  • Low fraction of inspired O2 (FiO2)
    (i. e. fires)
  • Low barometric pressure (PiO2)
    (i. e. altitude)
77
Q

What is an A-a gradient? What are normal and abnormal levels?

A

Alveolar O2 - arterial O2
(PAO2 - PaO2)

Used to determine source of hypoxemia

  • *Normal (<20)**:
  • Normal O2 transfer to blood
  • Or Low O2 available (altitude/fire/CO2)
  • *Elevated (>20)**:
  • Shunt, V/Q mismatch, diffusion impairments
78
Q

What are some pulmonary causes of shunts?

A

Pneumonia

ARDS

Near drowning

All alveolar filling processes
(blood, pus, or cells in alveolar spaces)

79
Q

What are some cardiac causes of shunts?

A

Atrial septal defects

Ventricular septal defects

80
Q

What are some causes of V/Q mismatch?

A

Pulmonary Embolism

Asthma

COPD

Congestive Heart Failure

81
Q

What can cause increased CO2 production (and thus lead to Hypercapnic respiratory failure)?

A

Fever

Sepsis

Malignant Hyperthermia

Overfeeding

Module 3: CPR (10 decks)

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