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Respiratory Physiology Flashcards

1
Q

What are the muscles of inspiration

A

Diaphragm and external intercostals

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2
Q

The reduction in thoracic pressure and the increase in thoracic volume is an example of what law?

A

Boyles law

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3
Q

What is boyles law?

A

Pressure is inversely proportional to 1/volume

(I.e. an increase in volume results in a DECREASE in pressure)

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4
Q

What muscles are activate during exhalation?

A

Exhalation is PASSIVE!

Active exhalation is carried out by the abdominal musculature (abs, internal oblique, external oblique)

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5
Q

Why vital capacity is required for an effective cough?

A

15 mL/kg

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6
Q

What are the three divisions of the airway?

A

Conducting zone, transitional zone, respiratory zone

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7
Q

What is the conducting zone? Where does it begin/end?

A

Begins at the nares and ends with the terminal bronchioles

This is anatomical dead space

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8
Q

What is the transitional zone?

A

Respiratory bronchioles

Dual function of gas exchange and air conduit

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9
Q

What is the respiratory zone? Where is it?

A

Begins at the alveolar ducts and ends in the alveolar sacs

This is where gas takes place

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10
Q

What is alveolar pressure?

A

Pressure inside the airway

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11
Q

what is intrapleural pressure?

A

The pressure outside the airway

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12
Q

What is transpulmonary pulmonary pressure (TPP)?

A

This is the difference between the pressure inside the airway and the pressure outside of the airway.

Alveolar pressure - Intrapleural pressure

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13
Q

What happens if Transpulmonary Pulmonary Pressure (TPP) is positive?

A

Airways stay open

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14
Q

What happens if transpulmonary pulmonary pressure is negative?

A

The airways collapse

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15
Q

What is a normal tidal volume?

A

6-8 mL/kg

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16
Q

What is normal dead space?

A

2 mL/kg or about 150

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17
Q

What causes an increase in the PaCO2-EtCO2 gradient?

A

And increase in dead space

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18
Q

What is Minute Ventilation?

A

Tidal volume x respiratory rate

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19
Q

What is alveolar ventilation?

A

(Tidal volume - dead space) x respiratory rate

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20
Q

What conditions increase dead space

A

Conditions that increase the volume of the conducting zone OR decrease pulmonary blood flow

(Ex: hypotension, positive pressure ventilation, atropine)

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21
Q

The fraction of tidal volume that contributes to dead space is called what?

A

Vd/Vt ration

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22
Q

What is the most common cause of increased Vd/Vt under general anesthesia?

A

Reduction in cardiac output (rule out hypotension)

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23
Q

Name some things that increase Vd

A

Face mask
HME
Positive pressure Ventilation
Atropine
Old age
Extension
COPD
PE
Decreased CO
Sitting

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24
Q

Name some things that decrease Vd

A

ETT
LMA
Trach
Flexion
Supine
T-berg

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25
Q

In the circle ventilators system, where does dead space begin?

A

At the y-piece

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26
Q

In the textbook patient, what is ventilation and perfusion?

A

Ventilation is 4 L/min
Perfusion is 5 L/min

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27
Q

In the textbook patient, a normal V/Q ratio would be what?

A

0.8
(4L/5L)

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28
Q

Where is ventilation the greatest? And why?

A

It is highest at the lung base due to higher alveolar compliance

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29
Q

Where is perfusion the greatest? And why?

A

Perfusion is the greatest at the lung base due to gravity.

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30
Q

What is ventilation and perfusion like in the NON-dependent lung?

A

Decreased alveolar ventilation
Decreased alveolar compliance
Decreased PACO2
Increased PAO2

Decreased blood flow
Decrease vascular pressure
Increased vascular resistance

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31
Q

What is ventilation and perfusion like on the dependent lung?

A

Increased alveolar ventilation
Increased alveolar compliance
Increased PACO2
Decreased PAO2

Increased blood flow
Increased vascular pressure
Decreased vascular resistance

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32
Q

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

A

V/Q mismatch (specifically atelectasis)

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33
Q

What does the body do to combat dead space (aka zone 1 of the lungs)

A

Constriction of bronchioles to minimize of poorly perfused alveoli

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34
Q

What does the body do to combat shunt (aka zone 3)

A

Hypoxic vasoconstriction reduced pulmonary blood flow to poorly ventilated alveoli

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35
Q

What is the Law of Laplace

A

Decrives the relationship b/t pressure, radius, and tension

Tension = pressure x radius (cylinder ~ blood vessels)

Tension = pressure x radius / 2 (spherical ~ alveoli)

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36
Q

what is surfactant

A

This is a substance produced by type 2 pneumocytes to modulate surface tension and prevent alveolar collapse.

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37
Q

When do type 2 pneumocytes begin producing surfactant?

A

22-23 weeks

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38
Q

When does surfactant production peak?!

A

35-36 weeks

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39
Q

Zone 1 (of the West Zones)

A

PA (alveolar) > Pa > Pv

Ventilation, but no perfusion
(I.e PE, hypotension)

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40
Q

Zone 2 (of the West Zones)

A

Pa > PA > Pv

V/Q = 1
Directly proportional to the difference between Pa - PA

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41
Q

Zone 3 (West zones)

A

Pa > Pv > PA
V/Q = 0

Shunt
Blood flow is a function of arteriovenous pressure (Pa - Pv)

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42
Q

Zone 4 (West Zones of the lung)

A

Pulmonary edema
Pa > Pist > Pv > PA

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43
Q

What is the alveolar gas equation?

A

Alveolar Oxygen = FiO2 x (atmospheric pressure - 47) - PaCO2/RQ (0.8)

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44
Q

What is the respiratory Quotient?

A

Carbon Dioxide Production/oxygen concentration

200 mL/250 mL = 0.8

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45
Q

What are the 5 causes of hypoxemia

A

Hypoxic mixture, hypoventilation, diffusion limitation, V/Q mismatch, and shunt

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46
Q

What are the 3 causes of an increased A-a gradient?

A

V/Q mismatch l
Diffusion impairment
Shunt

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47
Q

What is hypoxemia

A

A low state of oxygen in the blood (PaO2 <80)

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48
Q

What is hypoxia

A

Insufficient oxygen to support the tissues

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49
Q

What are examples of an increase A-a gradient in hypoxemia

A

V/Q mismatch
Diffusion impairment
Shunt

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50
Q

What are examples of a normal A-a gradient in hypoxemia

A

Hypoventilation
Reduced FiO2 (think high altitudes)

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51
Q

What are examples of a V/Q mismatch?

A

COPD
Impaired Hypoxic Pulmonary Vasoconstriction
One-lung ventilation
Embolism

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52
Q

What are examples of impaired diffusion?

A

Pulmonary fibrosis
Emphysema
Interstitial lung disease

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53
Q

What are examples of Shunt?

A

Pneumonia
Atelectasis
Bronchial intubation
Intracardiac shunt

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54
Q

What are examples of reduced FiO2?

A

High altitude
Oxygen pipeline failure
Hypoxic mixture

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55
Q

What are examples of Hypoventilation?

A

Opioid overdose
Residual neuromuscular blockers
Residual anesthetic
Neuromuscular disease
Obesity hypoventilation

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56
Q

What is the normal A-a gradient?

A

Less than 15 mmHg

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57
Q

How do you estimate the percentage of shunt using the A-a gradient?

A

Shunt increases 1% for every 20 mmHg of A-a gradient

For example, if the A-a gradient is 218, the shunt would be about 11% (218/20 = 11)

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58
Q

What is a normal inspiratory reserve volume?

A

3,000 mL

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59
Q

What is a normal tidal volume?

A

500 mL

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60
Q

What is a normal expiratory reserve volume?

A

1,100 mL

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61
Q

What is a normal residual volume?

A

1,200 mL

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62
Q

What is a normal total lung capacity?

A

5,800 mL

IRV, TV, ERV, RV

63
Q

What is a normal vital capacity?

A

4,500 mL

IRV, TV, ERV

64
Q

What is a normal inspiratory capacity volume?

A

3,500 mL

IRV, TV

65
Q

What is a normal functional residual capacity?

A

2,300 mL

ERV, RV

66
Q

What is tidal volume in mL/kg?

A

6-9 mL/kg

67
Q

What is vital capacity in mL/kg?

A

65-75 mL/kg

68
Q

What is functional residual capacity in mL/kg?

A

35 mL/kg

69
Q

Obstructive lung diseases ( asthma, emphysema, and bronchitis) have an increased what?

A

Residual volume
Closing capacity
And total lung capacity

70
Q

What conditions reduce FRC

A

General anesthesia
Obesity
Pulmonary edema
Pregnancy
Neonates
High FiO2s
Light anesthesia

71
Q

What conditions increased FRC?

A

Advanced age
COPD
PEEP
Sigh breaths

72
Q

What is the volume of air at end expiration?

A

FRC

73
Q

What prevents hypoxia during apnea?

A

FRC

74
Q

What is the time until a patient desaturates?

A

FRC/VO2 (oxygen consumption)

75
Q

If patient is breathing 100% O2, how long with their O2 supply last

A

2300 (volume of a fully oxygenated FRC)/ 250 mL/min (normal oxygen consumption)

76
Q

If patient is breathing 21% O2, what is the FRC?

A

Apply Dalton’s law to determine oxygen in FRC (2300 x .21). Next divide FRC by VO2? (483/250) this patient only has 1.9 minutes!!!

77
Q

What is closing capacity?

A

The sum of closing volume and residual volume.

78
Q

What is closing volume?

A

The volume absolve residual volume where the small airways begin to close

79
Q

what factors increase closing volume?

A

COPD
Extremes of age
Pregnancy
Obesity
LV failure
Surgery

80
Q

CC~FRC when under general anesthesia by what age?

A

30

81
Q

CC~FRC when supine by what age?

A

44

82
Q

CC~FRC when standing at what age?

A

66

83
Q

What is the oxygen content (CaO2) equation?

A

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

84
Q

CaO2 equals what?

A

How much O2 is in the blood

85
Q

What does DO2 measure?

A

The amount of oxygen delivered to the tissues per minute

86
Q

What is the DO2 equation?

A

DO2= CaO2 x CO x 10

87
Q

What is the P50?

A

The P50 is the PaO2 where 50% of the hgb is saturated with oxygen. A LOWER P50 reflects a LEFT shift. A HIGHER P50 reflects a RIGHT shift

88
Q

What things will cause a left shift on the oxyhemoglobin curve?

A

Hypothermia
Decreased 2,3-DPG
Decreased CO2
Decreased H+
Increased pH (alkalosis)
HgbMet
HgbCO
HgbF

89
Q

What will cause a right shift in the oxyhemoglobin curve?

A

Hyperthermia
Increased 2,3 -DPG
Increased CO
Increased H+
Decreased pH

90
Q

What is the Bohr effect?

A

An increased partial pressure of CO2 and decreased pH cause Hbg to release oxygen

91
Q

What is 2,3-DPG?

A

It is produced during by RBC glycolysis; hypoxia increases 2,3-DPG production and facilitates O2 offloading.

92
Q

What are the 3 key processes involved in aerobic glucose metabolism?

A

Glycolysis, Krebs, and electron transport

93
Q

What is the primary goal of glycolysis?

A

To convert 1 glucose to 2 pyruvic acid molecules.

94
Q

In the absence of oxygen, pyruvic acid is converted to what?

A

Lactate in the cytoplasm

95
Q

If oxygen is available, pyruvic acid is transported where?

A

Mitochondria and then converted into 2 molecules of Acetyl Coenzyme A

96
Q

What is the primary goal of the Krebs cycle?

A

To produce a large quantity of H+ ions in the form of NADH. These are them used in the electron transport chain. Net gain is 2 ATP

97
Q

What is the primary goal of oxidative phosphorylation?

A

Split NADH into NAD+, H+, and two electrons

A proton gradient is generated which drives ATP synthesis

Oxygen serves as the final electron acceptor

End product is 34 molecules of ATP and water.

98
Q

What is the primary by-product of aerobic metabolism

A

Carbon dioxide

99
Q

What are the three ways CO2 is buffered?

A

As bicarbonate
Bound to hemoglobin as carbamino compounds
Dissolved in the plasma

100
Q

What is the main equation to create bicarbonate?

A

H2O + CO2 <> H2CO3 <> H+ + HCO3

101
Q

What Enzyme is required for the carbonic acid buffer (bicarb)

A

Carbonic anhydrase

102
Q

During the creation of carbonic acid/bicarb, what is transported into the erythrocyte to maintain electro neutrality? And what is this shift called?

A

Chloride; chloride shift/hamburger shift

103
Q

How many more times is CO2 more soluble in the blood than oxygen?

A

20!

104
Q

What does the haldane effect say?

A

That at a given PaCO2, deoxygenated hemoglobin can carry more CO2. This allows hemoglobin to load more carbon dioxide at the tissue level and release more CO2 in the lungs. The CO2 dissociation curve shifts to the left. Note the CO2 dissociation curve. Not the oxygen.

105
Q

Bohr effect = __________ carriage
Haldane effect = __________ carriage

A

Bohr = oxygen
Haldane = CO2

106
Q

What is the equation for PaCO2?

A

PaCO2 = CO2 production/ alveolar ventilation

107
Q

What are some causes of increased CO2 production?

A

MH
Thyroid storm
Fever
Sepsis
Burns
Overfeeding
Shivering
Seizure activity

108
Q

What are some causes of decreased CO2 elimination?

A

COPD
Airway obstruction
Drug overdose
ARDS
Increased dead space (I.e. PE)
Inadequate neuromuscular block reversal

109
Q

What are some causes of rebreathing CO2

A

Inadequate fresh gas flow
Exhausted soda lime
Incompetent unidirectional valve

110
Q

What does hypercapnia do to the P50?

A

Oxyhemoglobin curve shifts to the right ~ this release more oxygen to the tissues

Partially compensates for hypoxemia

111
Q

What does hypercapnia do to the cardiac and smooth muscle?

A

Although CO2 is a myocardial depressant and vasodilator, it also activates the SNS (unless severe)

So think:
Tachycardia
Dysrhythmias
Prolonged QT
Oculocardiac reflex is more common following a precipitating event

112
Q

What does hypercapnia do in the pulmonary vasculature?

A

Increases vascular resistance ~> increasing the workload of the right heart.

113
Q

What does hypercapnia do to alveolar ventilation?

A

Stimulates it. Minute ventilation increases.

114
Q

What does hypercapnia do to potassium?

A

Activated the H+/K+ pump; releases K+ I to the plasma to house H+

115
Q

What does hypercapnia do to calcium?

A

Increased Ca+ competes with H+ for binding sites in proteins

This:
Acidosis ~ plasma proteins buffer H+ and release Ca, this increases inotropy and helps offset myocardial depression

Alkalosis ~ plasma proteins buffer Ca+ and release H+, decreases inotropy

116
Q

What does hypercapnia do to ICP

A

Increases blood flow and volume

117
Q

What does hypercapnia do to level of consciousness?

A

CO2 narcosis when > 90 mmHg

118
Q

In acute respiratory acidosis, how much does pH decrease in response to an increase in CO2?

A

For every 10 mmHg increase above 40 mmHg, pH decreases by 0.08

119
Q

In chronic respiratory acidosis, how much does pH change in response to CO2?

A

For every 10 mmHg above 40 mmHg, pH decreases 0.03 (due to HCO3 retention)

120
Q

What is the central chemoreceptor in the medulla the primary monitor of? And where is it located?

A

PaCO2
The central chemoreceptor is located in the VENTRAL surface of the medial

121
Q

What is the apneic threshold?

A

It is the highest PaCO2 at which a person will not breath. On the PaCO2 exceeds the apneic threshold, the patient will begin to breathe.

122
Q

Where is the respiratory center located?

A

Reticular activating system in the medulla and the pons

123
Q

What is the primary respiratory pacemaker?

A

So old teachings say Dorsal Respiratory Group

However, new evidence says DRG and the pre-Botzinger complex (VRG)

124
Q

When is the dorsal respiratory group active?

A

During inspiration

125
Q

What primarily regulates expiration?

A

Ventral respiratory group

126
Q

When is the ventral respiratory group active?

A

Expiration

127
Q

What does the pneumotaxic center do?

A

Inhibits DRG (pacemaker)

Strong stimulus ~ rapid shallow breathing

Weak stimulus ~ slow and deep breathing

128
Q

What does the apneustic center do?

A

Stimulates the DRG (stimulates the pacemaker)

It’s action is inhibited by pulmonary stretch receptors (j receptors)

129
Q

What is the most important stimulus for the control of ventilation?

A

The hydrogen ion concentration

130
Q

What drives the respiratory pacemaker in the DRG!

A

H+

131
Q

Where are the peripheral chemoreceptors located?

A

Carotid bodies at the bifurcation

Transverse aortic arch

132
Q

What is the chief responsibility of the carotid body?

A

To monitor for hypoxemia (PaO2 < 60 mmHg)

133
Q

What is the Hypoxic ventilators response?

A

PAO2 < 60 closes oxygen sensitive k+ channels in Type 1 Glomus cells —> increase K = increased resting membrane potential —> opens Ca channels and increases neurotransmitter release —> an action potential is propagated along Hering’s nerve (which is a branch of the glossopharyngeal) —> this terminates at the inspiratory center in the medulla —> minute ventilation increases.

134
Q

What conditions impair the Hypoxic ventilation response?

A

Carotid endarectomies (it severs the afferent limb)

Anesthetic doses of inhalation

135
Q

What prevents alveolar overdistention? How?

A

The Hering-Breuer inflation reflex

Stops inhalation when lung volume is too large. When lung inflation is > 1.5L above FRC, this reflex turns off the dorsal resp center (like the pneumotaxic center, but diff)

136
Q

What reflex helps prevent atelectasis by stimulating the patient to take a deep breath?

A

Hering-Breuer Deflation reflex

137
Q

What do J receptors do?

A

J receptor stimulation cause tachypnea. They are activated by anything that JAMS traffic in the pulmonary vasculature. I.e. embolism, CHF

138
Q

What causes a newborn to take his/her first breath?

A

The paradoxical reflex of the head

139
Q

What is hypoxic pulmonary vasoconstriction?

A

It is a local reaction that occurs in response to a reduction in alveolar oxygen tension

140
Q

What does HPV (hypoxic pulmonary vasoconstriction) do?

A

It selectively constricts areas of poor ventilation to minimize shunt flow. The response begins in seconds and exerts full effect in 15 mins.

It is a protective mechanism in one-lung ventilation

141
Q

What impairs hypoxic pulmonary vasoconstriction?

A

Volatile agents (1 MAC and >)
Vasodilators (phosphodiesterase, dobutamine, calcium channel blockers)
Vasoconstrictive drugs may affect HPV by constricted well oxygenated vessels
Severe hypervolemia (LAP > 25 mmHg)
Excessive PEEP or high tidal volumes (they increase dead space~ zone 1) and reduce optimal V/Q matching

142
Q

What has the most significant contribution to airflow resistance?

A

Radius

143
Q

What systems determine airway diameter?

A

PNS
Mast cells and non-cholinergic fibers
Non-cholinergic PNS
SNS

144
Q

How does the PNS system determine airway diameter?

A

PNS —> vagus nerve —> vasoconstriction

Supplies PNS inner action to smooth muscle

M3 receptor—> Gq protein—>activates phospholipase C—>activates IP3–>stimulates Ca+ release from sarcoplasmic reticulum—> activates myosin light chain kinase—> bronchoconstriction

145
Q

How does mast cells determine airway diameter?

A

Release mediators (histamine, prostaglandins, leukatrinenes
Bradykinin) that hit receptors (histamine 1, thromboxane-specific prostanoid receptor, bradykinin-2) ~ amplifies inflammatory response

146
Q

How does the SNS system determine airway diameter?

A

SNS —> circulating catecholamines —> bronchodilation

B2 receptors—>coupled with Gs proteins—>activated adenylate cyclase —> activates cAMP—> reduces Ca+ —>reduces smooth muscle contraction—> bronchodilation

147
Q

How do non-cholinergic PNS systems affect airway diameter? (NO)

A

NO is a potent vasodilator

Non-cholinergic PNS nerves release intestinal peptide onto airway smooth muscle —> increases NO production—> NO stimulates cGMP—> smooth muscle relaxation and bronchodilation.

148
Q

How do beta-2 agonist work on the airway?

A

Beta 2 stimuation—> ^ cAmP—> decreased Ca+ = bronchodilation

(SE: tachycardia, dysrhythmias, hypokalemia, hyperglycemia, tremors)

149
Q

How do anticholinergics work on the airway?

A

M3 antagonism—> decreased IP3 —> decreased Ca+

(SE: dry mouth, tachycardia, urinary retention, blurred vision)

150
Q

How do corticosteroids steroids work on the airway?

A

Stimulate intracellular steroid receptors

Regulates inflammatory protein synthesis —> decreased airway inflammation, decreased airway hyper-responsiveness

(SE: dysphonia, oropharyngeal candidiasis, myopathy of laryngeal muscles)

151
Q

How do mast cells affect the airway?

A

Stabilizes the cell membrane of mast cells (decreased release of cytokines, leukotrienes, and histamine)

Cromolyn

152
Q

How do leukotriene modifiers affect the airway?

A

Inhibit 5-lipoxygenase enzyme

Decreased leukotriene synthesis

(Montelukast, zileuton)

153
Q

How do methylxanthines affect the airway?

A

Inhibit phosphodiesterase —> increase cAMP—> decreased Ca+

Increase endogenous catecholamine release

Inhibits adenosine receptors

(SE: N/V, diarrhea, HA, disrupted sleep ~~ > 30 mcg/mL causes seizures, tachydysrhythmias, CHF)

Theophylline

Apex (47 decks)

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