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Anesthesia > Pathophysiology of anesthesia > Flashcards

Pathophysiology of anesthesia Flashcards

1
Q

Body systems sustaining life

A

-CNS
-respiratory system
-Cardiovascular system

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2
Q

Upper airways

A

-nose, nasal cavity and sinus, nasopharynx
-mouth, oropharynx, larynx

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3
Q

Lower airways

A

Conducting zone
-trachea, bronchi, bronchioles, tertiary bronchi

Respiratory zone
-tertiary bronchi and 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

Lower airway functions

A
  1. Non resp
    -immunological
    -acid-base regulation
    -vascular, metabolic, endocrine
  2. Resp
    -gas exchange: O2 and CO2 movement working close with CV system
    -surfactant synthesis
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6
Q

Control of Ventilation

A

**CO2 controls resp

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7
Q

Respiratory center

A

-slow steady ventilation control

1.Medulla oblongata= dorsal and ventral respiratory groups which control inspiration and expiration

  1. Pons= pneumotaxic center and apneustic center which adjusts ventilation controlled by medulla oblongata respiratory groups
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8
Q

Central chemoreceptors

A

-located at floor of ventral medulla
-minute by minute changes in ventilation
-dissolved CO2 passes through semipermeable membrane (BBB) and enters CSF

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9
Q

CSF pH

A

=7.32

-changes in pH=control breathing

Increased CO2, decreases pH to stimulate breathing

Note: less buffering capacity than blood= greater changes in pH based on CO2

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10
Q

Peripheral chemoreceptors

A

-rapid fine tuning ventilation
-sense CO2, O2, pH and perfusion of carotid/aortic bodies and results in an increase in ventilation in response to increased CO2, decreased blood pH and O2

Overrides ventilation controlled by resp center= rapid breath by breath control of ventilation

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11
Q

Normal CO2 and O2 levels

A

CO2: 35-45 mmHg

O2: 80-100mmHg

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12
Q

Pros of endotracheal intubation

A

-prevent aspiration of gastric contents
-prevent upper airway obstruction
-able to manually ventilate for patient experiencing hypoventilation or apnea

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13
Q

Why does upper airway obstruction occur during anesthesia?

A

Sedatives and tranquilizers cause muscle relaxation of laryngeal muscles predisposing to airway obstruction

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14
Q

Cons to endotracheal intubation

A

-bypass humidification and heating mechanisms of upper airways

-increased resistance to breathing if using too small endotracheal tube, connectors and one way valves in breathing circuit

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15
Q

Treatment for heat and water losses

A

-Passive: implement low fresh gas flow rates; use HME filters

-Active: humidifiers/nebulizers; heated anesthesia breathing circuits

-Active warming (bair huggers)

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16
Q

Treatment for increased resistance to breathing

A

Choose largest endotracheal tube possible

**Poiseuille’s Law= airway resistance is inversely proportional to radius (to power of 4)

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17
Q

Respiratory depression when awake

A

Alveolar ventilation changes linearly with changes in PaCO2
*max response at CO2 1000mmHg

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18
Q

Respiratory depression in hypoventilation

A

Inadequate CO2 elimination detected by increased CO2

**Hypoventilation: CO2> 45mmHg

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19
Q

Anethetics=hypoventilation

A

Inhalant anesthetics= decrease in tidal volume at low doses, and resp rate at high doses

IV anesthetics: decrease tidal volume and RR

Tranquilizers, sedatives, hypnotics: decrease RR

Opioids: change in CO2 response trigger to a higher value

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20
Q

Anesthesia effects

A

Progressive dose dependent decreased spontaneous ventilation
**especially when drugs used in combination

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21
Q

What causes anesthesia effects?

A

-blunted peripheral and central chemoreceptor responses to increased CO2

-muscle relaxation

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22
Q

Hypoxemia

A

Triggers peripheral chemoreceptors to cause a steep increased ventilation
-non linear response of alveolar ventilation to changing O2 levels

**Hypoxic drive= overrides normal CO2 driven ventilation

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23
Q

Inhalant anesthetics

A

-dose dependent inhibition of peripheral chemoreceptor response results in decrease in ventilatory response to hypoxemia

24
Q

Apnea

A

complete absence of breathing

**extreme end point of respiratory depression

25
Q

What does apnea result in?

A

Can lead to hypoxemia

26
Q

What is the most common stage of anesthetic apnea?

A

Induction (75% incidence)

-Potent IV anesthetic agent such as propofol or alfaxalone= high respiratory depressant effects

27
Q

Who are considered high risk patients to apnea/hypoxemia?

A

-increased intra abdominal pressure (pregnancy)
-lung disease
-obesity
-age (pediatrics and geriatrics)
-anesthesia (decreases FRC by 15% in normal patients)

28
Q

How to prevent apnea?

A

Titrate induction agent
-use lowest possible dose possible to allow intubation

29
Q

Prevention of hypoxemia?

A

Pre oxygenate for 3-7mins prior to induction
-increases O2 and oxygen reserve
-de-nitrogenize system
-provide extra time before patient will desaturate after becoming apneic

30
Q

Other causes of apnea

A
  1. Equipment failure= incompetent one way valves on rebreathing system leading to excessive CO2
  2. Deep anesthesia levels with inhalant anesthetics
31
Q

Max response of chemoreceptors

A

CO2 100mmHg, then ventilation will start to decline

Then can become apneic and may not restart breathing at deep planes of anesthsia

32
Q

Anesthetic index

A

ratio of end tidal anesthetic where animal becomes apneic, divided by MAC

33
Q

Anesthetic index inverse relationship

A

Lower apneic index means the drug is more respiratory depressant

34
Q

Respiratory depression potency of inhalation anesthetics

A

Sevoflurane (3.45) < Halothane (2.9) < Isoflurane (2.51)

As anesthetic depth increases, so does the agents respiratory depressant effects

1.5-3.0 x MAC = respiratory arrest

35
Q

Normal breathing pressure

A

Creates negative intra-thoracic pressure
-expands lungs
-expands vascular structures (improves venous return)

36
Q

Mechanical/manual ventilation

A

Creates positive intra thoracic pressure
-used to support patient ventilation and to assess airway patency/security
-expands lungs
-compresses vascular structures (reduces venous return)

37
Q

Effects of positive pressure ventilation

A

-Reduced venous return (preload)= reduced SV= reduced CO
**results in lower BP and possible hypotension. Seen as increased pulse pressure variation on arterial waveform

38
Q

How to fix positive pressure induced hypotension?

A
  1. increase venomotor tone (ephedrine= alpha 1 agonist causing venoconstiction)
  2. Increase venous return= IV fluid bolus, adjust ventilator settings to reduce pressure within the chest
39
Q

Atelectasis

A

Complete/partial collapse of entire or area of the lung
-unable to participate in gas exchange therefore reduced ventilation and oxygenation

40
Q

Results of atelectasis

A

Creates a right to left circulatory SHUNT
-deoxygenated venous blood bypasses the lungs and re-enters arterial system leading to decreased O2=hypoxemia

41
Q

Types of atelectasis

A

-compression
-resorption
-contraction

42
Q

Compression atelectasis

A

Weight of internal organs on lungs
-affected by posture/recumbency

**Fasting= reduced intra abdominal pressure and increases functional residual capacity by 16%

43
Q

Anesthesia effects resulting in compression atelectasis

A

-general muscle relaxation includes the respiratory muscles= unable to normally expand lungs

**loss of deep sign!

44
Q

Resorption atelectasis

A

Need nitrogen to keep alveoli open. Medical gas that is 100% O2 will result in de-nitrogenization= collapse of small alveoli

Hemoglobin removes all O2 from within the alveoli resulting in little gas in the alveoli

45
Q

Airway blockage by secretions resulting in resorption atelectasis

A

Reduced mucociliary action during anesthesia and no coughing reflex= build up of secretions

O2 in alveoli taken up by Hemoglobin= collapse

46
Q

V/Q mismatch

A

Ventilation: Perfusion

Distribution of blood flow depends on gravity which promotes perfusion (Q) to dependent lung field (V/Q changes over different lung zones)

47
Q

Zone 1 V/Q

A

upper most lung region

ventilation> perfusion= high V/Q ratio

48
Q

Zone 2 V/Q

A

middle lung region

Ventilation=perfusion (ideal area)

49
Q

Zone 3 V/Q

A

Lower most lung region

Ventilation<perfusion= low V/Q ration

50
Q

How does position of animal effect V/Q mismatch?

A

Anesthesia patients often in lateral or dorsal recumbency
*changes physiological zones of the lung

51
Q

How does anesthetic drugs effect V/Q mismatch?

A

1.Reduces CO= reduced perfusion

  1. Atelectasis: ventilation preferentially goes to upper most lung region
  2. Lose spontaneous sigh reflex
52
Q

How does mechanical ventilation effect the V/Q mismatch?

A

Mechanical ventilation= reduced venous return + atelectasis worsens

53
Q

Overall result of V/Q mismatch

A

Can lead to lower O2 and higher CO2 levels

54
Q

Ways to improve V/Q mismatch

A
  1. Position (Sternal>left lateral> right lateral> dorsal> Trendelenburg)
    -tilt surgical table
    -avoid changing sides
  2. Use high fraction inspired O2
  3. Ventilate to maintain normal CO2
  4. maintain stable BP

5.Use bronchodilators

  1. Perform recruitment maneuvers
55
Q

Recruitment maneuver

A

Opens collapsed alveoli
-manually squeeze re-breathing bag
-hold peak inspiratory pressure of 20-30 cm H2O (small animal) or 40-50 cm H2O (large animal) for 20-30sec

**Results in venous return= watch BP

56
Q

Recovery

A

Common anesthetic period that will experience hypoxemia due to hypoventilation
-switch from 100% to 21% fraction inspired O2
-period where they are still experiencing depression effects from anesthesia and atelectasis

**important in patients with lung disease or reduced FRC

57
Q

How to fix hypoxemia during recovery?

A

Provide supplemental O2
-improve O2 until patient recovers more and stops hypoventilation
-monitor O2 with pulse oximeter

Anesthesia (24 decks)

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