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APEX-CV & Respiratory > RESPIRATORY PHYSIOLOGY > Flashcards

RESPIRATORY PHYSIOLOGY Flashcards

1
Q

Laryngospasm treatment

A
  1. 100% Fi O2
  2. Remove noxious stimuli
  3. Deepen anesthetic
  4. CPAP 15 - 20 cmH2O
  5. Open airway (head extension, chin lift)
  6. Larson’s maneuver
  7. Succinylcholine (or roc if pt can’t have sux, can be given IM)
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2
Q

Describe how the respiratory muscles function during the breathing cycle

A

Contraction of the inspiratory muscles reduces thoracic pressure and increases thoracic volume.

Example of Boyles Law (Pressure and Volume are inversely proportional)

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3
Q

Describe how respiratory muscles function during inspiration

A
  1. Diaphragm and external intercostals contract during tidal breathing
  2. Diaphragm increases the superior-inferior dimension of the chest
  3. External intercostals increase the anterior-posterior diameter
  4. accessory muscles include the sternocleidomastoid and scalene muscles
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4
Q

Describe how respiratory muscles function during expiration

A

Exhalation is usually passive, driven by chest wall recoil

Abdominal musculature (rectus abdominis, transverse abdominis, internal obliques, and external obliques) assist in ACTIVE exhalation

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5
Q

What is minute ventilation

A

Ve is the amount of air (Vt) in a single breath multiplied by the number of breaths per minute

Ve = Vt x RR

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6
Q

What is alveolar ventilation

A

VA only measures the fraction of Va available for gas exchange.

VA = (Vt - anatomic dead space) x RR

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7
Q

What is the difference between minute ventilation and alveolar ventilation

A

Alveolar ventilation measures the fraction of Ve available for gas exchange. It removes anatomic dead space gas from the minute ventilation equation.

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8
Q

How is alveolar ventilation related CO2 & PaCO2

A

VA is DIRECTLY proportional to CO2 production

VA is INDIRECTLY proportional to PaCO2

VA = (CO2 production)/PaCO2

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9
Q

What are 4 types of deadspace

A

Anatomic
Alveolar
Physiologic
Apparatus

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10
Q

Define the 4 types of deadspace

A

ANATOMIC = air in conducting airway

ALVEOLAR = alveoli that are ventilated but NOT perfused

PHYSIOLOGIC = Anatomic Vd + alveolar Vd

APPARATUS = Vd added by equipment

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11
Q

Give an example for each type of deadspace (4)

A

ANATOMIC = nose/mouth to terminal bronchioles

ALVEOLAR = DEC pulmonary BF (i.e. DEC CO)

PHYSIOLOGIC = anything that increases anatomic or alveolar Vd

APPARATUS = facemask, HME, limb of circle system w/ incompetent valve

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12
Q

What does the alveolar compliance curve tell you?

A

Alveolar ventilation is a function of alveolar size and its position on the alveolar compliance curve.

  • Best ventilated alveoli are the MOST compliant (steep slope)
  • Poorest ventilated alveoli are the LEAST compliant (flat slope)
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13
Q

State the alveolar gas equation?

A

Alveolar Oxygen = FiO2 x (Pb - PH2O) - (PaCO2/RQ)

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14
Q

What variables are included in the alveolar gas equation?

A 
FiO2
Pb=Barometric pressure
PH2O = humidity of inhaled gas (47 mmHg)
PaCO2
RQ = Respiratory quotient (0.8)
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15
Q

What is the purpose of the alveolar gas equation?

A

To estimate the partial pressure of O2 in the alveoli

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16
Q

How is the alveolar gas equation useful

A

It can tell us the maximal PAO2 that can be achieved at a given FiO2

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17
Q

Define Henry’s Law.

A

The solubility of a gas in a liquid is directly proportional to the partial pressure of the gas above the liquid

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18
Q

How is oxygen content calculated.

A

CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)

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19
Q

What is the difference between CaO2 & DO2

A

CaO2 is how much O2 is in the blood

DO2 is how much O2 is delivered to tissue per minute

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20
Q

How is DO2 calculated?

A

DO2 = CaO2 x CO x 10

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21
Q

What does CaO2 measure

A

Oxygen content in 1 deciliter (100 mL) of blood

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22
Q

How is O2 consumption calculated?

A

VO2 = CO x (CaO2 - CvO2) x 10

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23
Q

What 2 ways is O2 carried in the blood

A
  1. Reversibly binds with Hgb (97%)

2. Dissolves in plasma (3%)

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24
Q

Equation for O2 bound to Hgb

A

(1.34 x Hgb x SaO2)

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25
Q

Equation for O2 dissolved in plasma

A

PaO2 x 0.003

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26
Q

What is the Fick principle

A

Oxygen consumption is the difference in oxygenated arterial blood and returning pulmonary venous blood. Thus flow (CO) can be calculated

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27
Q

What is the Bohr effect

A

An increased partial pressure of CO2 and decreased pH causes hgb to release O2.

CO2 and hydrogen ions cause a conformational change in the hgb molecule which causes hgb to release O2

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28
Q

What does the oxyhemoglobin dissociation curve describe?

A

The tendency of hgb to bind O2

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29
Q

What is 2,3-DPG

A

It is produced during RBC glycolysis and stabilizes the deoxygenated form of hgb facilitating O2 release at tissues
(2,3 diphophoglyceric acid)

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30
Q

How is 2,3-DPG & the Oxyhemoglobin dissociation curve affected by banked blood

A

The concentration of 2,3-DPG falls and shifts the dissociation curve left, reducing the amount of O2 available at the tissues

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31
Q

How does Hgb F respond to 2,3-DPG and the associated effect on the oxyhemoglobin dissociation curve

A

Hgb F doesn’t respond to 2,3-DPG which is why there is a left shift (P50 = 19)

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32
Q

How does hypoxia affect 2,3-DPG

A

It increases 2,3-DPG production and facilitates O2 offloading (right shift)

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33
Q

What is the Hamburger shift?

A

Chloride(-) shift into the deoxygenated erythrocyte to maintain neutrality w/ H+. It replaces HCO3-

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34
Q

What is the Bohr effect?

A

Hgb-O2 binding affinity is inversely related to acidity and CO2 concentration

High acidity = low affinity = release(right)

Low acidity = high affinity = lock(left)

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35
Q

What is the Haldane effect?

A

Effect of O2 on CO2 transport

Deoxygenated blood can carry increasing amounts of CO2, whereas oxygenated blood has reduced CO2 capacity

Produces left shift (venous blood becomes more acidic)

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36
Q

How is carbonic acid produced in the RBC?

A

Carbonic anhydrase is an enzyme that facilitates formation of carbonic acid (H2CO3).
Carbonic anhydrase is only found in the erythrocyte

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37
Q

What is the result of carbonic acid

A

rapid dissociation into H+ & HCO3-

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38
Q

3 ways that CO2 is transported in the blood. From greatest to least

A 
Bicarbonate (70%)
Carbamino compounds ( (23%)
Dissolved CO2 (7%)
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39
Q

What is CO2 solubility compared to O2

A

CO2 solubility = 0.067 mL/dL/mmHg
It is 20x more soluble than O2

O2 solubility = 0.0031 mL/dL/mmHg

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40
Q

How does the CO2 dissociation curve shift in the presence of oxygenated hgb and why?

A

RIGHT SHIFT

  • blood has decreased affinity for CO2
  • facilitates CO2 unloading in lungs
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41
Q

How does the CO2 dissociation curve shift in the presence of DEOXYgenated hgb and why?

A

LEFT SHIFT

  • Blood has increased affinity for CO2
  • Facilitates CO2 loading in systemic capillaries
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42
Q

Where in the body is the CO2 dissociation curve right-shifted?

A

Lungs to facilitate CO2 offloading from Hgb

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43
Q

Where in the body is the CO2 dissociation curve left-shifted?

A

Systemic capillaries to facilitate CO loading on Hgb

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44
Q

3 categories of hypercapnia

A

Increased CO2 production
Decreased CO2 elimination
Rebreathing

45
Q

Examples of reasons for hypercapnia d/t increased CO2 production

A 
sepsis
overfeeding
MH
Intense shivering
Prolonged seizure
Thyroid storm
Burns
46
Q

Examples of reasons for hypercapnia d/t decreased CO2 elimination

A 
Airway obstruction
Increased DS
Increased Vd/Vt
ARDS
COPD
Respiratory center depression
Drug OD
Inadequate NMB reversal
47
Q

Examples of reasons for hypercapnia d/t rebreathing

A

Exhausted soda lime
incompetent unidirectional valve in circle system
inadequate FGF

48
Q

Hypercapnia effects on P50

A

RIGHT shift

Release more O2

49
Q

Hypercapnia effect on cardiac and smooth muscle depression

A

CO2 is myocardial depressant and directly dilates peripheral vasculature

It activates SNS, increasing catecholamine release from adrenal medulla

50
Q

Result of hypercapnia on cardiac rate and rhythm changes

A

Tachycardia, increasing myocardial O2 consumption and decreasing O2 delivery
Dysrhythmias
Prolonged QT interval

51
Q

Hypercapnia effect on pulmonary vascular resistance

A

Increases PVR

CO2 constricts pulmonary vasculature, increasing PVR and workload of right heart

52
Q

Hypercapnia effect on alveolar ventilation

A

Increases alveolar ventilation d/t CO2 stimulating effects and increases in Ve

53
Q

Hypercapnia effect on K+

A

INCREASES K+
d/t activation of H+/K+ pump
Buffers CO2 acid in exchange for releasing K+ into plasma

54
Q

Hypercapnia effect on Ca++

A

INCREASES Ca++

iCa++ competes w/ H+ for binding sites on plasma proteins

55
Q

Acidosis/Alkalosis effects on Ca++/H+ binding

A

Acidosis = plasma proteins buffer H+ and release Ca++ (increase inotropy)

Alkalosis = plasma proteins release H+ and bind Ca++ (decrease inotropy)

56
Q

Hypercapnia effect on ICP

A

INCREASES

Decreased CSF pH leads to decreased cerebrovascular resistance and increased CBF/volume

57
Q

Hypercapnia effect on LOC

A

CO2 narcosis

58
Q

How do the kidneys handle acidosis

A

Kidneys excrete H+ and conserve HCO3- to return pH to normal

59
Q

How much does acute respiratory acidosis decrease pH

A

For every 10 mmHg >40 mmHg, pH decreases by 0.08

60
Q

How much does chronic respiratory acidosis decrease pH, and why is this different than acute?

A

For every 10 mmHg >40 mmHg, pH decreases by 0.03.

d/t HCO3- retention by the kidneys

61
Q

What does a right shift of the CO2 response curve demonstrate?

What are contributing examples?

A

That the respiratory center is LESS sensitive to CO2

Sevoflurane
s/p CEA
Opioids 
NMBs
Metabolic alkalosis
62
Q

What does a left shift of the CO2 response curve demonstrate?

What are contributing examples?

A

That the respiratory center is MORE sensitive to CO2

Hypoxemia
Salicylates
Surgical stimulation
Intracranial HTN
Metabolic acidosis
63
Q

What does the CO2 ventilatory response curve describe?

A

The relationship between PaCO2 and minute ventilation

64
Q

Where is the primary monitor of PaCO2 and what type is it?

A

Where = Medulla

Type = central chemoreceptors

65
Q

What is the apneic threshold?

A

It is the highest PaCO2 which a person will not breathe

When PaCO2 is greater than apneic threshold, the patient will begin to breathe

66
Q

What locations play a secondary role in monitoring in monitoring PaCO2

A

Carotid bodies
Transverse aortic arch

Peripheral chemoreceptors

67
Q

What does the slope of the CO2 ventilatory response curve indicate

A

The sensitivity of the entire respiratory apparatus to PaCO2

68
Q

At what level (mmHg) does CO2 become a respiratory depressant?

A

PaCO2 >80-100 mmHg

69
Q

How is minute ventilation affect by shifts in the CO2 ventilatory response curve?

A

Left shift = Ve is higher than expected for a given PaCO2, creating respiratory alkalosis

Right shift = Ve is lower than expected for a given PaCO2, creating respiratory acidosis

70
Q

How does the CO2 ventilatory response curve impact apneic threshold

A

Left shift = apneic threshold is decreased

Right shift = apneic threshold increased

71
Q

What is the pacemaker for normal breathing?

A

Dorsal respiratory center

72
Q

What is the role of the pneumotaxic center

A

To inhibit DRC, the pacemaker for breathing

73
Q

What is the role of the apneustic center

A

To stimulate the DRC

74
Q

What does the ventral respiratory center control

A

Responsible for expiration

75
Q

Where is the respiratory center located and what is the primary job?

A

In the reticular activating system in medulla and pons

Job = to determine how fast and deep you breath. REgulation of PaCO2 and PaO2

76
Q

Describe the afferent input, integration and modifier of the respiratory center

A

Afferent input = from central and peripheral chemoreceptors, lung stretch receptors

Integration = incoming signals w/ intrinsic respiratory pattern and sending a coordinated response to muscles of respiration

77
Q

What are the medullary respiratory centers

A

Dorsal respiratory group

Ventral respiratory group

78
Q

What are the pontine respiratory centers

A

Pneumotaxic center (UPPER pons)

Apneustic center (LOWER pons)

79
Q

What are the 4 determinants of respiratory rate and pattern

A
  1. Neural control in respiratory center - Medulla
  2. Chemical control in the central chemoreceptors - medulla
  3. Chemical control in peripheral chemoreceptors - carotid bodies, aortic arch
  4. Baroreceptors - lungs
80
Q

Where does the respiratory center receive afferent input from

A

Central and peripheral chemoreceptors

Lung stretch receptors

81
Q

What does new evidence report is the respiratory pacemaker

A

The central pattern generator, which includes:
DRG
pre-Botzinger complex (in VRG)
Other medullary structures

82
Q

What stimulates the central respiratory chemoreceptors and where is this located

A

pH changes in the CSF and PaCO2

location = ventral surface of medulla

83
Q

What byproduct freely diffuses across BBB

A

CO2

84
Q

Which ions do not freely diffuse across the BBB in relationship to respiration

A

H+ and HCO3-

85
Q

How does H+ and HCO3- enter CSF

A

CO2 dissociates into H+ and HCO3-

86
Q

How does H+ concentration in CSF affect respiration

A

Increases rate and depth of respirations until new steady state is achieved

87
Q

How long do effects of hyperventilation reduce ICP

A

a few hours to 2 days

88
Q

What substances can freely diffuse across CSF

A

Some gases and lipid soluble molecule

89
Q

The concentration of which ion in the CSF is most important for stimulating the central chemoreceptors of the respiratory center?

A

H+

90
Q

What type of relationship does H+ CSF concentration have with respiratory rate and depth

A

Direct relationship, as H+ rises so do rate and depth of respirations

91
Q

How doe ions, glucose and amino acids travel across the BBB

A

Active transport mechanisms

92
Q

What is the difference in response of central versus peripheral chemoreceptors

A

Central chemoreceptors respond to PaCO2

Peripheral chemoreceptors respond to PaO2

93
Q

What type of cells mediate peripheral chemoreceptor hypoxic ventilatory drive ?
How?

A

Type 1 Glomus cells

sense and transduce PaO2 into an action potential

94
Q

What nerve makes up the AP of the afferent limb of the peripheral chemoreceptor response

A

AP is propagated along the afferent limb of Hering’s nerve and glossopharyngeal nerve (CN 9)

95
Q

How does CEA affect peripheral chemoreceptor function?

A

It impairs function on the ipsilateral side

96
Q

What is the chief responsibility of the carotid bodies

A

To monitor hypoxemia

97
Q

Do the carotid bodies or transverse aortic arch chemoreceptors respond to SaO2 or CaO2?

A

No

98
Q

Why aren’t bilateral CAE performed simultaneously?

A

Because CEA severs the afferent limb of the hypoxic ventilatory response and takes time for recalibration

99
Q

Where are the carotid bodies located

A

at the bifurcation of the common carotid artery

100
Q

What are secondary responsibilities of the carotid bodies

A

Monitoring PaCO2, H+, perfusion pressure

101
Q

What layer are the carotid bodies located?

A

Adventitia

102
Q

Describe the hypoxic ventilatory response to hypoxemia (5)

A
  1. Decreased PaO2 closes O2-sensitive K+ channels in Type 1 glomus cells
  2. Resting membrane potentials rise d/t altered K+, Ca++ channels open and increase NT release of Ach and ATP
  3. An AP is propagated via Hering’s nerve and glossopharyngeal nerve (CN 9)
  4. The afferent path terminates in the inspiratory center of medulla (DRG)
  5. Ve increase to restore PaO2
103
Q

Conditions that impair hypoxic ventilatory response

A

CEA

Sub-anesthetic doses of inhalation and IV anesthetics

104
Q

What is the Hering-Breuer inflation reflex

A

lung hyperinflation turns off the respiratory drive to avoid overinflation

105
Q

Hering-Breuer deflation reflex

A

Activates the respiratory drive when lung volume is too small to prevent atelectasis

106
Q

What are J receptors

A

Pulmonary C-fiber receptors

Increases the respiratory rate in the setting of PE or CHF

107
Q

How is ventilation controlled in the lungs

A

Stretch receptors in the smooth airway muscles which transduce pressure conditions inside the airway

108
Q

What nerve transduces the pressure conditions inside lung smooth muscle and to where

A 
Vagus nerve (CN 10)
To the dorsal respiratory center (DRG, respiratory PM)

APEX-CV & Respiratory (8 decks)

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