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APEX > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

Inspiration Muscles

A

Diaphragm & external intercostals

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2
Q

Inspiration ACCESSORY Muscles

A

Sternocleidomastoid
Anterior/middle/posterior scalenes

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3
Q

What law applies to breathing & inspiration?

A

Boyle P1V1 = P2V2

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4
Q

Expiration Muscles

A

PASSIVE
Driven by chest wall recoil

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5
Q

Active Expiration Muscles

A

Transverse abdominis
Internal & external oblique
Internal intercostals

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6
Q

How many functional airway divisions are present?

A

23 divisions/generations

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7
Q

What are the 3 respiratory zones?

A

Conducting
Transitional
Respiratory (gas exchange)

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8
Q

Conducting Zone

A

Trachea, bronchi, & bronchioles
Ends w/ terminal bronchioles
Function to facilitate bulk gas movement
DEAD SPACE 150 mL or 2 mL/kg

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9
Q

Trachea

A

Conducting zone
Generation 0
Cilia present
Smooth muscle present
Cartilage present

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10
Q

Bronchi

A

Conducting zone
Generation 1-3
Cilia present
Smooth muscle present
Cartilage patchy

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11
Q

Bronchioles

A

Conducting zone
Generation 4
Cilia present
Smooth muscle present
NO cartilage

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12
Q

Transitional zone

A

Respiratory bronchioles
Duel function - air conduit & gas exchange

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13
Q

Respiratory Bronchioles

A

Transitional zone (sometimes noted as respiratory zone)
Generation 17
Some cilia & smooth muscle present
NO cartilage

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14
Q

Respiratory Zone

A

Gas exchange
Alveolar ducts & sacs

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15
Q

How does gas exchange occur?

A

Gas exchange occurs across the flat epithelium (type 1 pneumocytes) via diffusion

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16
Q

Alveolar Ducts

A

Generation 20
Some smooth muscle
NO cilia or cartilage

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17
Q

Alveolar Sacs

A

Generation 23
NO cilia, smooth muscle, or cartilage

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18
Q

What airway structures are susceptible to external compression?

A

Bronchioles & alveolar ducts
Do NOT contain cartilage

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19
Q

What keeps the airways open?

A

Positive (+) transpulmonary pressure Ptp

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20
Q

Minute ventilation

A

VE = Tidal volume (VT) x RR
Volume gas patient inhales & exhales over 1 minute
Inversely r/t PaCO2
Reference adult value = 4 L/min

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21
Q

Alveolar ventilation

A

VA = (Tidal volume - dead space) x RR
OR
= CO2 production / PaCO2

1° determinant CO2 elimination
Only measures VE available to participate in gas exchange

Directly proportional to CO2 production
Inversely proportional to PaCO2

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22
Q

Anatomic Dead Space

A

Air confined to the conducting airways

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23
Q

Alveolar Dead Space

A

Alveoli that are ventilated, but not perfused

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24
Q

Physiologic Dead Space

A

= Anatomic Vd + Alveolar Vd

Calculated w/ Bohr equation
Vd/Vt = (PaCO2 - PeCO2) / PaCO2

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25
Q

Apparatus Dead Space

A

Vd added by equipment
Facemask or HME
Circle system

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26
Q

Dead Space to Tidal Volume Ratio

A

= Vd/Vt %
Fraction tidal volume that contributes to dead space
Reference adult value 33% during spontaneous ventilation
Normal 150 mL / 450 mL = 0.33

50% during mechanical ventilation

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27
Q

↑Dead Space

A

Facemask, HME, PPV
Atropine (anticholinergic) bronchodilation ↑conducting airway volume
Old age
Neck extension opens the hypopharynx
HoTN, ↓CO, COPD, PE (thrombus, air, amniotic fluid) ↓pulmonary blood flow

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28
Q

↓Dead Space

A
  • ETT, LMA, trach
  • Neck flexion
  • ↑CO
  • Position (supine or Trendelenburg)
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29
Q

Compliance

A

Compliance = ∆V / ∆P

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30
Q

Alveolar Compliance Curve
Normal Upright Awake Adult

A

Non-dependent APEX
↑PAO2
↓PACO2
↑V/Q ratio (V>Q)
↓compliance ↓alveolar ventilation
↓pulmonary blood flow ↓alveolar perfusion

Dependent BASE
↓PAO2
↑PACO2
↓V/Q ratio (V<Q)
↑compliance ↑alveolar ventilation
↑pulmonary blood flow ↑alveolar perfusion

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31
Q

Normal Va/Q Ratio

A

= 0.8

Ventilation = 4 L/min
Perfusion = 5 L/min

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32
Q

Ventilation / Perfusion Mismatch

A

↑A-a gradient
Bronchioles constrict to minimize zone 1
HPV minimizes shunt
Blood passing through under ventilated alveoli tends to retain CO2

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33
Q

What is the most common cause of hypoxemia in the PACU?

A

Atelectasis

Shunt V/Q = 0
Blood retains CO2 ↑PaCO2

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34
Q

What indicates severe V/Q mismatch?

A

Retained CO2 ↑PaCO2

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35
Q

Dead Space

A

Vd
V/Q = ꝏ
Ventilation but no perfusion
Overventilated alveoli give off an excessive amount CO2
CO2 diffuses 20x faster than oxygen

Apex V > Q Zone 1

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36
Q

Shunt

A

Shunt or venous admixture
V/Q = 0
Perfusion but no ventilation
Under-ventilated alveoli retains CO2 and unable to take in enough oxygen

Base V < Q Zone 3

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37
Q

What law applies to alveolar surface tension?

A

Law of LaPlace
P = (2 x T) / r

P = pressure
T = tension
r = radius

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38
Q

What equalizes surface tension effects?

A

Surfactant
↓radius ↑surfactant concentration

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39
Q

When does surfactant production begin & peak?

A

Begins at 22-26 weeks gestation
Peaks at 35-36 weeks

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40
Q

West Zones

A
  1. Dead space
  2. Ventilation matched to perfusion V/Q = 1
  3. Shunt
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41
Q

West Zone 1

A

Alveolar pressure PA > arterial pressure Pa > venous pressure Pv

Bronchioles constrict to minimize ventilation to poorly perfused alveoli

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42
Q

West Zone 1
Causes

A

HoTN, PE, excessive airway pressure (PPV or PEEP)

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43
Q

West Zone 2

A

Pa > PA > Pv
Blood flow directly proportional to Pa-PA difference

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44
Q

West Zone 3

A

Pa > Pv > PA
Any venous blood that empties directly into L side heart or bypasses the lungs

HPV ↓pulmonary blood flow to poorly ventilated alveoli

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45
Q

Where to place the PA catheter tip?

A

West zone 3

Capillary pressure > alveolus
Vessel always open & blood moving through

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46
Q

What are 3 anatomic shunt sites?

A

Thesbian, bronchiolar, & pleural veins

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47
Q

West Zone 4

A

Pa > Pis > Pv > PA

Pulmonary edema

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48
Q

West Zone 4
Causes

A

↑capillary hydrostatic pressure
- Fluid overload, mitral stenosis, and sever pulmonary vasoconstriction

Profound reduction in pleural pressure
- Laryngospasm or inhalation against closed glottis → negative pressure pulmonary edema

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49
Q

Alveolar Gas Equation

A

Used to estimate partial pressure O2 in the alveoli
PAO2 = FiO2 x (PB − PH2O) − (PaCO2 / RQ)

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50
Q

Respiratory Quotient

A

= CO2 production / O2 consumption
= 200 mL/min / 250 mL/min
= 0.8

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51
Q

Hypoxemia

A

Low O2 concentration in the blood
PaO2 < 80 mmHg

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52
Q

Hypoxia

A

Insufficient O2 to support the tissues

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53
Q

Hypoxemia Causes

A
  1. Hypoxic mixture
  2. Hypoventilation
  3. Diffusion limitation
  4. V/Q mismatch
  5. Shunt
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54
Q

Hypoxic Mixture
Causes

A

O2 pipeline failure
High altitude

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55
Q

Hypoxic Mixture
Presentation & Treatment

A

Normal A − a gradient

Administer supplemental FiO2

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56
Q

Hypoventilation
Causes

A

Opioid overdose
Residual anesthetic agent
Residual NMB
Neuromuscular disease
Obesity hypoventilation

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57
Q

Hypoventilation
Presentation & Treatment

A

Normal A − a gradient

Fix underlying cause
- Narcan
- Adequate NMB reversal
Supportive ventilation CPAP/BiPAP

Administer supplemental FiO2

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58
Q

V/Q Mismatch
Causes

A

COPD
One-lung ventilation
Impaired HPV
Embolism - air, gas, amniotic fluid

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59
Q

V/Q Mismatch
Presentation & Treatment

A

↑A − a gradient

Resume 2-lung ventilation
Decrease/discontinue drugs that inhibit HPV
Identify & treat embolism

Administer supplemental FiO2

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60
Q

Diffusion Impairment
Causes

A

Pulmonary fibrosis
Emphysema
Interstitial lung disease

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61
Q

Diffusion Impairment
Presentation & Treatment

A

↑A − a gradient

Administer supplemental FiO2

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62
Q

Shunt Causes

A

R→L shunt
Atelectasis
Pneumonia
Bronchial intubation
Intracardiac shunt

63
Q

Shunt
Presentation & Treatment

A

↑A − a gradient

Supplemental FiO2 does NOT help

64
Q

A − a Gradient

A

PAO2 − PaO2
Normal < 15 mmHg (physiologic shunt)

65
Q

How much does shunt increase A − a gradient?

A

↑1% every 20 mmHg

66
Q

Lung Volumes

A

IRV
Vt
ERV
RV

*Based on healthy 70 kg male

67
Q

Lung Capacities

A

2+ lung volumes

IC
VC
FRC
TLC

*Based on healthy 70 kg male

68
Q

What are lung volumes & capacities based on?

A

IBW
Healthy 70 kg male

69
Q

How do lung volumes & capacities differ in females?

A

↓25%

70
Q

IRV mL

A

3,000 mL

71
Q

Tidal Volume mL

A

Vt = 500 mL
OR
6-8 mL/kg IBW

72
Q

ERV mL

A

1,100 mL

73
Q

RV mL

A

Unable to measure
1,200 mL

74
Q

Closing Volume

A

Variable
Lung volume above RV when small airways begin to close/collapse

75
Q

Closing Volume % TLC

A

30% TLC at 20 yo
55% TLC at 70 yo

76
Q

IC mL

A

Inspiratory capacity
IRV + Vt = 3,500 mL

77
Q

Lung Capacities

A

2+ lung volumes = capacity

78
Q

VC mL

A

Vital capacity
IRV + Vt + ERV = 4,600 mL
OR
65-75 mL/kg

79
Q

FRC mL

A

Functional residual capacity
ERV + RV = 2,300 mL
OR
35 mL/kg

Volume at end-expiration

80
Q

TLC mL

A

IRV + Vt + ERV + RV = 5,800 mL

81
Q

Closing Capacity

A

RV + CV = variable
Absolute lung volume when small airways begin to close/collapse

82
Q

What patients & scenarios does CC = FRC?

A

Neonate
30 yo under GA
Supine 40 yo adult
Standing or sitting 65 yo

83
Q

What happens when CC ≥ FRC?

A

Airway closure during normal tidal volume breaths → intrapulmonary shunting & hypoxemia ↑WOB

Unable to measure w/ spirometry

84
Q

How to measure CV or CC?

A

Nitrogen or Xenon

85
Q

Define FRC

A

Lung volume when inward elastic recoil (lung) balanced by the outward recoil (chest wall) = static equilibrium
O2 reserve that prevents hypoxemia during apnea

86
Q

What formula represents the time until an apneic patient desaturates?

A

= FRC / VO2

VO2 = oxygen consumption

87
Q

↑FRC

A

COPD
Advanced age elasticity ↑air trapping
PEEP
Position:
- Sitting
- Lateral
- Prone

88
Q

↓FRC

A

General anesthesia 50% reduction
NMBs
Obesity, pregnancy, and neonates
Fluid overload or pulmonary edema
↑FiO2 → absorption atelectasis
Position:
- Supine
- Lithotomy
- Trendelenburg

89
Q

Oxygen Content

A

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

O2 forms reversible bond w/ Hgb 97%
O2 dissolved in the blood plasma 3%

90
Q

Normal Hgb/Hct

A

Hgb 13-15 g/dL
Hct 39-45%

91
Q

What law applies to O2 dissolved in the blood plasma?

A

Henry’s law = gas concentration in a solution α gas partial pressure above the solution
Oxygen 20x less soluble than CO2

92
Q

Normal CaO2

A

20.4 mL O2 per dL

93
Q

Oxygen Delivery

A

DO2 = CaO2 x CO x 10

How fast O2 delivered to the tissues

94
Q

What mechanism/factor drives O2 delivery?

A

Cardiac output

95
Q

What converts dL → L?

A

Conversion factor = 10

96
Q

Normal DO2

A

1,000 mL O2 per minute

97
Q

Oxygen Consumption

A

VO2 = CO x (CaO2 − CvO2) x 10

Difference b/w O2 that leaves the lungs & O2 amount that returns

98
Q

What law/principle applies to O2 consumption?

A

Fick

99
Q

Normal VO2

A

250 mL/min
OR
3.5 mL/kg

100
Q

How does temperature affect VO2?

A

↓core body temp ↓O2 consumption
VO2 ↓5-7% every 1°C

101
Q

FICK PRINCIPLE

A

Vgas = [Diffision coefficient x (P1 − P2) x Surface area] / Membrane thickness
Vgas = (D ∗ ∆P ∗ SA) / T

ΔP = partial pressure gradient

102
Q

Oxyhemoglobin Dissociation Curve
P50

A

PaO2 when Hgb 50% saturated by O2
P50 = 26.5 mmHg

103
Q

SpO2 90% : PaO2

A

90% = PaO2 60 mmHg
80% = PaO2 50 mmHg
75% = PaO2 40 mmHg
60% = PaO2 30 mmHg

104
Q

What causes the carboxyhemoglobin dissociation curve to shift to the LEFT?

A

LEFT = LOVES
- Alkalosis ↑pH ↓H+
- Hypocarbia ↓CO2
- Hypothermia
- ↓2,3 DPG
- Fetal hemoglobin FHgb α + γ
- Benzocaine overdose → methemoglobin MetHgb
- Carboyxhemoglobin (smoke inhalation) COHgb
- Normal physiology = lungs

105
Q

What causes the carboxyhemoglobin dissociation curve to shift to the RIGHT?

A

RIGHT = RELEASE
- Acidosis ↓pH ↑H+
- Hypercarbia ↑CO2
- Hyperthermia (MH, neuroleptic malignant syndrome, or serotonin syndrome)
- ↑2,3 DPG
- Normal physiology = tissue level

106
Q

Cellular Energy Currency

A

ATP
Adenosine triphosphate

107
Q

What is the 1° substrate used for ATP synthesis?

A

Glucose

108
Q

Aerobic Metabolism

A
  1. Glycolysis
  2. Krebs cycle
  3. Oxidative phosphorylation
109
Q

Glycolysis

A

Convert 1 glucose to 2 pyruvic acid molecules
Net gain 2 ATP

110
Q

Krebs Cycle

A

Occurs in the mitochondria matrix
Produces H+ ions as NADH to be used in the electron transport chain
Net gain 2 ATP

111
Q

Oxidative Phosphorylation

A

Electron transport chain
Goal to produce ATP (energy)
Net gain 34 ATP

112
Q

Anaerobic Metabolism

A

Pyruvate acid → lactic acid → lactic acidosis
Anion gap metabolic acidosis

When oxygen supply reestablished intracellular lactate converted back to pyric acid inside the cell

113
Q

What clears serum lactate?

A

Liver

114
Q

CO2 Buffer System

A

H2O + CO2 ↔ H2CO3 (carbonic acid) ↔ H+ + HCO3¯
Reaction requires carbonic anhydrase enzyme

115
Q

CO2 Transportation

A

Bicarbonate HCO3¯ 70%
Hgb bound 23%
Dissolved in plasma 7%`

116
Q

Bohr Effect

A

O2 offloading from Hgb
CO2 + ↓pH ↑H+ → erythrocyte releases O2

L shift at the tissue level

117
Q

Haldane Effect

A

CO2 loading onto Hgb
↑O2 → erythrocyte releases CO2

R shift at the lungs

118
Q

Hypercapnia
Definition & Equation

A

Respiratory acidosis PaCO2 > 45 mmHg

PaCO2 = (CO2 production) / (Alveolar ventilation)

119
Q

Hypercapnia Causes

A
  1. ↑CO2 production
  2. ↓CO2 elimination
  3. Rebreathing
120
Q

What consequences are associated w/ hypercapnia?

A

↑CO2 displaces alveolar O2 → arterial hypoxemia
↓oxygen carrying capacity
Oxyhemoglobin curve shifts R ↑P50 releases more O2 to the tissues
Myocardial depressant & directly dilates the peripheral vasculature ↑HR ↑MVO2
↑Pulmonary vascular resistance PVR
Respiratory stimulant ↑minute + alveolar ventilation
Hyperkalemia H+/K+ pump activation buffers CO2
Acidosis → plasma proteins buffer H+ & release Ca2+ → ↑Ca2+
↑ICP CO2 freely diffuses across the blood-brain barrier ↓CSF pH ↓cerebrovascular resistance ↑CBF & volume

121
Q

Acute Respiratory Acidosis
Predicted pH

A

Every 10 mmHg > 40 mmHg → pH ↓0.08

122
Q

Chronic Respiratory Acidosis
Predicted pH

A

Every 10 mmHg > 40 mmHg → pH ↓0.03

123
Q

CO2 Ventilatory Response Curve

A

Describes the relationship b/w PaCO2 & minute ventilation VE

124
Q

What causes the CO2 ventilatory response curve to shift to the LEFT?

A

Respiratory center ↑sensitivity to CO2
Hypoxemia
Metabolic acidosis
Surgical stimulation
Intracranial HTN ↑ICP
Fear & anxiety
Salicylates, Aminophylline, Doxapram, & NE

125
Q

What causes the CO2 ventilatory response curve to shift to the RIGHT?

A

Respiratory center ↓sensitivity to CO2
Metabolic alkalosis
Volatile anesthetics
Opioids
NMBs
Post carotid endarterectomy
Natural sleep

126
Q

What receptors are the 1° PaCO2 monitor?

A

Central chemoreceptors in the medulla
Respond INDIRECTLY to PaCO2

127
Q

Where is the respiratory control center located?

A

Reticular activating system RAS in the medulla & pons

128
Q

Respiratory Control Center
1° Function

A

1° job to determine how fast & deep patient breathes
Regulate PaCO2 & PaO2

129
Q

Where does the respiratory control center receive inputs from?

A

Central & peripheral chemoreceptors
AND
Stretch receptors in the lungs

130
Q

Where are central chemoreceptors located?

A

Medulla

131
Q

Where are peripheral chemoreceptors located?

A

Carotid bodies at the common carotid artery bifurcation
AND
Transverse aortic arch

132
Q

Outline the central respiratory center

A

Medulla
- DRG/VRG
- Central chemoreceptors
Pontine
- Pneumotaxic (upper pons)
- Apneustic (lower pons)
Cerebral cortex - conscious breathing control able to modify responses

133
Q

DRG

A

Dorsal respiratory group or center (DRC)
Located in the nucleus tractus solitarius (medulla)
Respiratory pacemaker
Dorsal = inspiration

134
Q

VRG

A

Ventral respiratory group or center (VRC)
Located in the medulla
1° responsible for expiration
Ventral = active expiration
More important during exercise or stress

135
Q

Pneumotaxic center

A

Located in the upper pons
Inhibits the DRG (pacemaker)
Triggers END inhalation

136
Q

Apneustic Center

A

Located in the lower pons
Stimulates the DRG (pacemaker)
Triggers INhalation

137
Q

Define Apneic Threshold

A

The highest PaCO2 where the patient will NOT breathe

138
Q

How do central chemoreceptors respond to PaCO2?

A

INDIRECT response to PaCO2
Sends stimulatory impulses to the DRG

139
Q

What 1° stimulates the central chemoreceptors?

A

CSF pH or H+ ion concentration

140
Q

What receptors are the 1° PaO2 monitor?

A

Peripheral chemoreceptors
Monitor hypoxemia PaO2 < 60 mmHg

141
Q

What do peripheral chemoreceptors 2° monitor?

A

1° PaO2
2° PaCO2, H+, & perfusion pressure

142
Q

What cells sense & transduce PaO2 into an AP?

A

Type 1 glomus cells
Mediate hypoxic ventilatory drive

143
Q

What serve as the peripheral chemoreceptors afferent limb?

A

Hering’s nerve & glossopharyngeal nerve IX
Terminates in the inspiratory center in the medulla

144
Q

How does carotid endarterectomy impair peripheral chemoreceptors?

A

Severs the afferent limb on the surgical side

145
Q

Pulmonary Reflexes

A
  1. Hering-Breuer inflation reflex
  2. Hering-Breuer deflation reflex
  3. J receptors
  4. Paradoxical head reflex
146
Q

What transduces pulmonary reflexes?

A

Stretch receptors in the smooth airway muscle transduce pressure conditions in the airway
Information transmits along the Vagus → DRG
Efferent response via phrenic nerve

147
Q

Hering-Breuer Reflex

A

INFLATION
- When lung inflation > 1.5 L above FRC (3x Vt) reflex turns off the DRG
- Stops further inspiration; helps to avoid overinflation
- Reflex not active during normal inspiration

DEFLATION
- Stimulates patient to take a deep breath
- Prevents atelectasis

148
Q

J Receptors

A

Pulmonary C-fiber receptors
Stimulation causes tachypnea in response to pulmonary embolism or CHF

149
Q

Paradoxical Head Reflex

A

Newborn baby stimulus to take 1st breath

150
Q

HPV

A

Hypoxic pulmonary vasoconstriction
Local response to ↓alveolar oxygen tension PAO2 → minimizes shunt

Pulmonary vascular bed the only region in the body that responds to hypoxia with vasoconstriction

151
Q

How long to initiate the HPV response?
When is the peak effect achieved?

A

Only seconds to initiate
Achieves peak effect ≈ 15 minutes

152
Q

What inhibits HPV?

A

Volatile anesthetics > 1.5 MAC
Phosphodiesterase inhibitors
Dobutamine
Hypervolemia
Excessive PEEP
↑Vt

153
Q

How do volatile agents affect HPV?

A

Impair HPV
↑shunt fraction & ↓PaO2

154
Q

What preserves HPV?

A

IV anesthetic agents
- Ketamine
- Propofol
- Opioids

APEX (18 decks)

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