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ANESTHESIA > 21 – Pathophysiology: Respiratory System > Flashcards

21 – Pathophysiology: Respiratory System Flashcards

1
Q

What are the 3 body systems that sustain life min-by-min?

A
  • CNS
  • Respiratory system
  • CV system
  • *if stop working=life threatening!
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2
Q

Upper airways include

A
  • Nose, nasal cavity and sinuses, nasopharynx
  • Mouth, oropharynx, larynx
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3
Q

Lower airways (lungs) zones

A
  1. Conducing zone
    a. Trachea, bronchi, bronchioles, tertiary bronchi
  2. Respiratory zone
    a. Tertiary bronchi, alveoli
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4
Q

Upper airway functions

A
  • Thermoregulation
  • Filtration
  • Humidification
  • Olfactory
  • Air conduction
  • Phonation
  • Swallowing (airway protection)
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5
Q

What are the 2 main functions of the lower airways?

A
  1. Non-respiratory
  2. Respiratory
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6
Q

Non-respiratory functions of the lower airways

A
  • Immunological (mucociliary)
  • Acid-base regulation
  • Vascular, metabolic, endocrine, etc.
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7
Q

Respiratory functions of the lower airways

A
  • GAS EXCHANGE
    o Works closely with CV system
  • Surfactant synthesis
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8
Q

What is ventilation primarily controlled by?

A
  • CO2
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9
Q

Respiratory center provides

A
  • Slow, steady ventilation control
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10
Q

2 areas of the respiratory center

A
  • Medulla oblongata
  • Pons
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11
Q

Medulla oblongata (respiratory centre)

A
  • Dorsal and ventral respiratory groups
    o Control inspiration and expiration
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12
Q

Pons (respiratory center)

A
  • Pneumotaxic center and apneustic center
    o Adjust ventilation controlled by medulla oblongata respiratory groups
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13
Q

Central chemoreceptors

A
  • Min-by-min changes in ventilation
  • Floor of ventral medulla
  • Dissolved CO2 passed through semipermeable membrane (BBB) and enters CSF
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14
Q

What is the normal CSF pH and what happens if it changes?

A
  • 7.32
  • If changes=control breathing
  • Increased CO2=decrease pH=STIMULATE breathing
  • *less buffering capacity than blood=greater changes in pH based on PCO2
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15
Q

Peripheral chemoreceptors

A
  • Rapid, fine-tunning ventilation
  • Aortic and carotid bodies!
  • Sense PaCO2, PaO2, pH and perfusion of carotid/aortic bodies
  • *overrides ventilation controlled by respiratory center
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16
Q

When do you get an increased ventilation from the peripheral chemoreceptors in response?

A
  • Increased PaCO2
  • Decreased blood pH
  • Decreased PaO2
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17
Q

What are the positives of endotracheal intubation?

A
  • Prevent aspiration of gastric contents
  • Prevent upper airway obstruction (due to muscle relaxation of laryngeal muscles=sedatives and tranquilizers)
  • Ability to manually ventilate for patient experiencing hypoventilation or apnea
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18
Q

What are the negatives of endotracheal intubation?

A
  • Bypass humidification and heating mechanisms of upper airways
  • Increased resistance to breathing
    o if too small tube, connectors or one-way valves in breathing circuit
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19
Q

What are ways to treat for heat and water losses with endotracheal intubation?

A
  1. Passive: COMMON
  2. Active
  3. Active warming
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20
Q

Passive ways to treat heat and water losses with endotracheal intubation?

A
  • Implement low fresh gas flow rates
  • Use HME filters
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21
Q

Active ways to treat heat and water losses with endotracheal intubation?

A
  • Humidifiers/nebulizers
  • Heated anesthesia breathing circuits
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22
Q

How can you treat for increased resistance to breathing with endotracheal intubation?

A
  • Choose largest tube possible
    o *Poiseuille’s’ law: airway resistance through a tube is INVERSELY proportional to radius to the power of 4
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23
Q

What is the normal PaCO2?

A
  • 35-45 mmHg
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24
Q

When awake, alveolar ventilation changes _______with changes in PaCO2

A
  • LINEARLY
    o Max response at PaCO2=100mmHg
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25
Q

What is involved with hypoventilation?

A
  • Inadequate CO2 elimination detected by increased PaCO2 or ETCO2
  • *PaCO2 is MORE THAN 45mmHg
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26
Q

Anesthesia effects: progressive dose-dependent decrease in spontaneous ventilation leads to

A
  • Blunted peripheral and central chemoreceptor responses to increased PaCO2
  • Muscle relaxation (respiratory muscles)
27
Q

What is the normal PaO2?

A
  • 80-100mHg on room air (=21% of inspired O2)
  • 5x inspired O2
28
Q

What does hypoxemia trigger?

A
  • Peripheral chemoreceptors to cause a STEEP INCREASE in ventilation
    o NON-LINEAR response of alveolar ventilation to changing PaO2
  • *when less than 60mmHg
29
Q

What is ‘hypoxic drive’?

A
  • Overrides normal CO2 driven ventilation
30
Q

Inhalant anesthetics have dose-dependent inhibition of peripheral chemoreceptor response, causing a

A
  • DECREASED ventilation response to hypoxemia
31
Q

Apnea

A
  • Complete absence of breathing
    o Extreme end point of respiratory depression
32
Q

When is the most common stage of anesthesia for apnea?

A
  • Induction (75% incidence)
    o Potent IV anesthetics (propofol/alfaxalone) agent used with high respiratory depressant effects
33
Q

What can induction apnea lead to?

A
  • Hypoxemia
34
Q

Who are high risk patients of induction apnea?

A
  • *those with reduced functional residual capacity (FRC)
    o Increased intra-abdominal pressure (ex. pregnancy)
    o Lung disease
    o Obesity
    o Age (pediatrics and geriatrics)
    o Anesthesia (decreases FRC by 15%)
35
Q

How can you prevent induction apnea?

A
  • Titrate induction agent
    o Use lowest does possible to allow intubation
36
Q

How can you prevent hypoxemia?

A
  • Pre-oxygenate for 3-7 mins PRIOR to induction
37
Q

What does pre-oxygenating for 3-7mins prior to induction do?

A
  • Increases PaO2 and oxygen reserve
  • De-nitrogenize system
  • Provides extra time (~3mins) before patient will DESATURATE after becoming apneic
38
Q

What are some other causes of apnea?

A
  • Equipment failure (incompetent one-way flow)
  • Deep anesthesia levels with inhalant anesthetics
39
Q

When is the max response of chemoreceptors and what happens?

A
  • PaCO2=100mH
  • Ventilation DECLINES
    o Can become apneic and may not restart breathing at deep planes of anesthesia
40
Q

Anesthetic index

A
  • Ratio of end-tidal anesthetic where animals becomes APNEIC, divided by MAC
  • *inverse relationship
  • Ex. sevoflurance (3.45) < Halothan < Isoflurane (2.5)
41
Q

What does a lower apnetic index mean?

A
  • Drug is MORE respiratory depressant
42
Q

When does/what is the equation for respiratory arrest?

A
  • Respiratory arrest = 1.5-3.0 x MAC
43
Q

Normal breathing creates a

A
  • NEGATIVE intra-thoracic pressure
    o Expands lungs
    o Expands vascular structures (improves venous return)
44
Q

What happens with mechanical/manual ventilation?

A
  • Creates POSITIVE intra-thoracic pressure
    o Used to support ventilation and assess airway patency
    o Expands lungs
    o COMPRESSES vascular structures
45
Q

What are the effects of positive pressure ventilation?

A
  • Reduced venous return (preload) leads to reduced SV=decreased CO
  • *result=lower BP and possible hypotension
  • Can be seen as increased PP variation on arterial wave form
46
Q

How do you fix positive pressure induced hypotension?

A
  • Increase venomotor tone (ephedrine: alpha1 agonist causing venoconstriction)
  • Increase venous return=IV fluid bolus OR adjust ventilatory settings to reduce pressure within the chest
47
Q

Atelectasis

A
  • Complete/partial collapse of entire or an area of a lung
    o Unable to participate in gas exchange=reduced ventilation and oxygenation
48
Q

What does atelectasis create?

A
  • R-to-L circulatory SHUNT
49
Q

R-to-L circulatory SHUNT

A
  • De-oxygenated blood bypasess lung -> re-enters arterial system=reduces PaO2
  • *can lead to hypoxia
50
Q

3 types of atelectasis

A
  1. Compression
  2. Resorption
  3. Contractions
51
Q

Compression atelectasis

A
  • Weight of internal organs on lungs
    o Affected by posture/recumbency
  • *Fasting
52
Q

How does fasting help with compression atelectasis?

A
  • Reduces intra-abdominal pressure
  • Increases functional residual capacity by 16%
53
Q

What gas is responsible for keeping alveoli open?

A
  • Nitrogen
54
Q

What is de-nitrogenization (resorption atelectasis)?

A
  • Provide 100% O2 for anesthesia=it removes all nitrogen
    o Result=small alveoli collapse
55
Q

How does airway blockage by secretions contribute to resorption atelectasis?

A
  • Reduced mucociliary action during anesthesia and NO coughing reflex=build up of secretions
  • O2 in alveoli taken up by Hgb -> collapse
56
Q

Lung zone 1

A
  • Upper lung region
  • Ventilation>perfusion=high V/Q ratio
57
Q

Lung zone 2

A
  • Middle lung region
  • Ventilation=perfusion
  • IDEAL
58
Q

Lung zone 3

A
  • Lower lung region
  • Ventilation<perfusion=low V/Q ratio
59
Q

How can you improve V/Q mismatch?

A
  • Choose best position
  • Use high fraction inspired O2 (will loose N scaffold)
  • Ventilate to maintain normal PaCO2
  • Maintain stable BP (perfusion)
  • Use bronchodilators (ex. inhaled salbutamol)
  • *Perform recruitment maneuver=open collapsed alveoli
60
Q

Choose the best position to improve V/Q mismatch

A
  • Sternal > left lateral > right lateral > dorsal > Trendelenburg (‘head stand’)
    o R. lung field is larger
  • Tilt surgical table
  • Avoid changing sides
61
Q

How can you perform recruitment maneuver=open collapse alveoli?

A
  • Manually squeeze re-breathing bag
  • Hold peak inspiratory pressure (PIP) of 20-30cm H2O (small) 40-50cm H2O (large) for 20-30s
  • WILL reduce venous return (watch BP)
  • Can repeat as needed
62
Q

What is a common anesthetic period to experience hypoxemia due to hypoventilation?

A
  • Recovery
    o Switch from 100 to 21% O2
    o Still experiencing respiratory depression from anesthesia and atelectasis
    o Most important in patients with lung disease or reduced functional residual capacity
63
Q

How can you improve hypoxemia due to hypoventilation during recovery

A
  • Provided supplemental O2 (increased FiO2)
    o Improve PaO2 until patient recovers more and stops hypoventilation
    o Monitor SpO2 with pulse oximeter

ANESTHESIA (27 decks)

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