Pathophysiology of Anesthesia: Respiratory System

Question 1

Which 3 body systems sustain life minute-by-minute?

Answer 1

• CNS
• respiratory system
• cardiovascular system

Question 2

If the 3 body systems that sustain life stop working, what happens?

Answer 2

• this can be life threatening
• all other systems are supported by good function of these!

Question 3

What are the upper airways of the respiratory system?

Answer 3

• nose, nasal cavity & sinuses, nasopharynx
• mouth, oropharynx, larynx

Question 4

What two zones are there in the lower airways?

Answer 4

• conducting zone
• respiratory zone

Question 5

what is the conducting zone?

Answer 5

• trachea, bronchi, bronchioles, tertiary bronchi

Question 6

What is the respiratory zone?

Answer 6

• tertiary bronchi, alveoli

Question 7

What are the functions of the upper airways?

Answer 7

• thermoregulation
• filtration
• humidification
• olfactory
• air conduction
• phonation
• swallowing (airway protection)

Question 8

What are the respiratory & non respiratory functions of the lower airways?

Answer 8

1. non-respiratory: immunological (mucocilliary, etc.; acid-base regulation; vascular, metabolic, endocrine, etc.)
2. respiratory: GAS EXCHANGE (O2 & CO2 movement - works closely w/ cardiovascular system); surfactant synthesis

Question 9

How is ventilation controlled?

Answer 9

primarily by CO2

Question 10

What is the respiratory center?

Answer 10

for slow, steady ventilation control
- medulla oblongata = dorsal & ventral respiratory groups (control inspiration & expiration)
- pons = pneumotaxic center & apneustic center (adjust ventilation controlled by medulla oblongata respiratory groups)

Question 11

what are central chemoreceptors?

Answer 11

minute by minute changes in ventilation
- floor of ventral medulla
- dissolved CO2 passes through semipermeable membrane (BBB) & enters CSF
- CSF pH = 7.32 (changes in pH = control breathing; increased CO2 = decreased pH -> stimulates breathing
- less buffering capacity than blood = greater changes in pH based on PCO2

Question 12

what are peripheral chemoreceptors?

Answer 12

rapid, fine-tuning ventilation
- sense PaCO2, PaO2, pH, & perfusion of carotid/aortic bodies (increase ventilation in response to increased PaCO2, decreased blood pH, and decreased PaO2)
- overrides ventilation controlled by respiratory center (rapid, breath-by-breath control of ventilation)
- GOAL: maintain normal CO2 & O2 levels in blood (PaCO2 = 35-45 mmHg, PaO2 = 80-100 mm Hg)

Question 13

What is good about endotracheal intubation?

Answer 13

• prevent aspiration of gastric contents
• prevent upper airway obstruction (sedatives & tranquilizers cause muscle relaxation of laryngeal muscles -> predispose to AIRWAY OBSTRUCTION)
• able to manually ventilate for patient experiencing hypoventilation or apnea

Question 14

What is potentially bad about endotracheal intubation?

Answer 14

• bypass humidification & heating mechanisms of upper airways
• increased resistance to breathing if using too small of an ET tube, connectors, & one-way valves in breathing circuit

Question 15

How do your treat for heat and water loss with endotracheal intubation?

Answer 15

• passive: implement low fresh gas flow rates & use HME filters
• active: humidifiers/nebulizers, heated anesthetic breathing circuits
• active warming (ex: Bair Hugger, HotDog)

Question 16

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

Answer 16

• choose largest endotracheal tube possible: Poiseuille’s Law: airway resistance through a tube is INVERSELY proportional to its radius, to the power of 4; ex: halving diameter -> 16- FOLD INCREASE in airflow resistance through the tube

Question 17

What is general respiratory depression?

Answer 17

• Normal PaCO2 = 35-45 mmHg
• awake: alveolar ventilation changes LINEARLY w/ changes in PaCO2 (max response at PaCO2 100mmHg)
• hypoventilation: inadequate CO2 elimination detected by increased PaCO2 or ETCO2
• HYPOVENTILATION: PaCO2 > 45 mm Hg

Question 18

Anesthetics and general respiratory depression?

Answer 18

• all anesthetics cause respiratory depression which can lead to hypoventilation (inhalant anesthetics: decrease tidal volume at low dosage & respiratory rate at high doses; IV anesthetics: decrease tidal volume and respiratory rate; tranquilizers, sedatives, & hypnotics: decrease respiratory rate; opioids: change CO2 response trigger to a higher value)
• anesthesia effects: progressive dose-dependent decrease in spontaneous ventilation (esp. when drugs are used in combination): blunted peripheral & central chemoreceptor responses to increase PaCO2; muscle relaxation (respiratory muscles)

Question 19

Oxygen, inhalant anesthetics, and general respiratory depression:

Answer 19

• normal PaO2 = 80-100 mmHg in room air (FiO2 21%)
• hypoxemia: triggers peripheral chemoreceptors to cause a STEEP increase in ventilation (NON-LINEAR response of alveolar ventilation to changing PaO2 levels; “hypoxic drive” = overrides normal CO2 driven ventilation)
• inhalant anesthetics: dose-dependent inhibition of peripheral chemoreceptor response -> DECREASED VENTILATORY RESPONSE TO HYPOXEMIA

Question 20

what is apnea?

Answer 20

• apnea = complete absence of breathing (extreme end-point of respiratory depression)
• most common stage of anesthesia for apnea = induction (75% incidence): potent IV anesthetic (propofol/alfaxalone) agent used w/ high respiratory depressant effects

Question 21

What can induction apnea lead to?

Answer 21

HYPOXEMIA

Question 22

Which patients are at high risk for apnea?

Answer 22

those w/ reduced functional residual capacity (FRC):
- increased intra-abdominal pressure (Ex: GDV, pregnancy)
- lung disease (Ex: pneumonia, asthma)
- obesity
- age (pediatrics & geriatrics)
- anesthesia (decreases FRC by 15% in NORMAL patients)

Question 23

How can you prevent induction apnea?

Answer 23

titrate the induction agent (use lowest dose possible to allow intubation)

Question 24

how can you prevent hypoxemia?

Answer 24

pre-oxygenate for 3-7 mins prior to induction:
- increases PaO2 & oxygen reserve
- de-nitrogenizes system
- provides extra time (~3 mins) before patient will desaturate after becoming apneic

Question 25

what are other causes of apnea?

Answer 25

- equipment failure = incompetent one-way valves on rebreathing system leading to excessive CO2 - deep anesthesia levels w/ inhalant anesthetics

Question 26

what is the maximum response of chemoreceptors to apnea?

Answer 26

PaCO2 100 mmHg, then ventilation starts to DECLINE - can become apneic & may not restart breathing at deep planes of anesthesia

Question 27

What is the anesthetic index?

Answer 27

= ratio of end-tidal anesthetic where animal becomes apneic, divided by minimum alveolar concentration (MAC) - INVERSE RELATIONSHIP: lower apneic index means drug is MORE respiratory depressant - cant compare respiratory depression to potency of inhalation anesthetics - SEVOFLURANE (3.45) < HALOTHANE (2.9) < ISOFLURANE (2.51) - as anesthetic depth increases, so does the agent's respiratory depressant effects - 1.5 - 3.0 x MAC = RESPIRATORY ARREST

Question 28

What is positive pressure ventilation?

Answer 28

- normal breathing: creates NEGATIVE intra-thoracic pressure (expands lungs; expands vascular structures (improves venous return)) - mechanical/ manual ventilation: creates POSITIVE intra-thoracic pressure (used to support patient ventilation & to assess airway patency/security; expands lungs; COMPRESSES vascular structures (reduces venous return))

Question 29

what are the effects of positive pressure ventilation?

Answer 29

- reduced venous return (preload) -> reduced stroke volume- > reduced cardiac output - RESULT = LOWER BP & POSSIBLE HYPOTENSION - can be seen as increased pulse pressure variation on arterial waveform

Question 30

How do you fix positive pressure induced hypotension?

Answer 30

- increase venomotor tone (ephedrine = a1 agonist causing venoconstriction) - increase venous return = IV fluid bolus, adjust ventilator settings to reduce pressure w/in chest

Question 31

What is atelectasis?

Answer 31

- complete/partial collapse of entire or area (lobe) of a lung (unable to participate in gas exchange -> reduces ventilation & oxygenation) - creates right-to-left circulatory SHUNT (de-oxygenated venous blood bypasses lung -> re-enters arterial system -> reduces PaO2; can lead to hypoxemia)

Question 32

what are the 3 types of atelectasis?

Answer 32

1. COMPRESSION 2. RESORPTION 3. contraction

Question 33

What is compression atelectasis?

Answer 33

- weight of internal organs on lungs (affected by posture/recumbency; FASTING = reduces intra-abdominal pressure & increases FRC by 16%) - anesthesia effects: general muscle relaxation includes respiratory muscles (diaphragm, intercostal muscles, etc.) -> unable to normally expand lungs; loss of 'deep sigh'

Question 34

What is resorption atelectasis?

Answer 34

- gas responsible for keeping alveoli open = NITROGEN - de-nitrogenization = provides 100% O2 as medical gas for anesthesia, removes all nitrogen (result = small alveoli collapse; Hgb remove all oxygen from within the alveoli -> little gas remains in alveoli -> collapse) - airway blockage by secretions: reduced mucociliary action during anesthesia & no coughing reflex -> can build up secretions; O2 in alveoli is taken up by Hgb -> collapse

Question 35

What is V/Q mismatch?

Answer 35

- distribution of blood flow depends on GRAVITY -> promotes perfusion (Q) to dependent lung field - ventilation / perfusion (V/Q) relationship changes over different lung zones - normal ventilation distribution (standing position): zone 1: upper-most lung region (ventilation > perfusion = high V/Q ratio); zone 2: middle lung region (ventilation = perfusion (IDEAL AREA)); zone 3 = lower-most lung region (ventilation < perfusion = low V/Q ratio)

Question 36

How does position effect the V/Q mismatch?

Answer 36

anesthesia patients are usually in lateral or dorsal recumbency (changes physiological zones of the lung)

Question 37

What are the anesthetic drug effects on V/P mismatch?

Answer 37

- reduced cardiac output -> reduced perfusion - atelectasis: ventilation preferentially goes to upper-most lung region - loose spontaneous 'sigh' reflex

Question 38

how is mechanical ventilation related to V/Q mismatch?

Answer 38

mechanical ventilation = reduces venous return + atelectasis worsens

Question 39

What is the result of V/Q mismatch?

Answer 39

can lead to lower PaO2 & higher PaCO2

Question 40

How do you improve V/Q mismatch?

Answer 40

- choose best position (keep weight off diaphragm): sternal > left lateral > right lateral > dorsal > Trendelenburg; tilt the surgical table; avoid changing sides - use high FiO2 (but will loose nitrogen scaffold) - ventilate to maintain normal PaCO2 - maintain stable BP (perfusion) - use bronchodilators (ex: inhaled salbutamol) - perform recruitment maneuver: open collapsed alveoli (manually squeeze re-breathing bag; hold peak inspiratory pressure (PIP) of 20-30 cmH2O (small animal) or 40-50 cmH2O (large animal) for 20-30 seconds; WILL reduce venous return -> watch BP!; can repeat as needed

Question 41

What is recovery?

Answer 41

- common anesthetic period to experience hypoxemia due to hypoventilation: switch from 100% -> 21% FiO2 (room air); still experiencing respiratory depression effects from anesthesia & atelectasis; most important in patients w/ lung disease or reduced FRC - how to fix this: provide supplemental O2 (increase FiO2; improve PaO2 until patient recovers more & stops hypoventilation; monitor SpO2 w/ pulse oximeter)