Effects of anesthetics on control of respiration

1. DR TR SHRESTHA, KMCTH

2. Contents
▪ Respiratory control system
▪ Central controller
▪ Chemoreceptors
▪ Effectors
▪ Effect of anesthetics on ventilation
▪ Effect of anesthetics on gas exchange

3. Respiratory control system
Basic elements of the respiratory control system

4. Central controller

5. Medullary respiratory center
Medullary Centers
▪ Pre-Botzinger Complex
▪ generates respiratory rhythm
▪ Dorsal respiratory group
▪ chiefly a/w inspiration
▪ Ventral respiratory group
▪ a/w expiration
Pontine Centers
▪ Pneumotaxic center
▪ Inhibit/limit inspiration thus
regulate inspiratory volume and RR
(increase RR)
▪ fine tuning of respiratory rhythm
▪ Apneustic center
▪ excitatory effect on inspiratory area

6. Effectors
▪ Muscles of respiration
▪ Diaphragm
▪ Intercostal muscles
▪ Abdominal muscles
▪ Accessory muscles
▪ Nasopharyngeal muscles
▪ maintain patency of upper airways

7. Central chemoreceptors
▪ Near ventral surface of
medulla in vicinity of exit
of 9th and 10th CN
▪ Surrounded by brain ECF
▪ Respond to changes in [H+]
▪ Increase [H+] stimulates
ventilation and vice versa
▪ Sensitive to PaCO2

8. Peripheral chemoreceptors
▪ Carotid bodies
▪ Aortic bodies
▪ Glomus cells
▪ Respond to ↓PaO2
→Increase ventilation

9. Hypoxic ventilatory drive

10. Lung receptors
▪ Pulmonary stretch receptors
▪ Irritant receptors
▪ J receptors

11. Alveolar ventilation and PaCO2
▪ Predominant factor controlling ventilation-
PaCO2
▪ Linear increase in ventilation
▪ Increase in 2L/min for each 1mmHg ↑ in PaCO2
▪ Acidemia and hypoxia stimulates ventilation
via peripheral chemoreceptors

12. Effects of increased arterial blood PCO2 and decreased
arterial pH (increased hydrogen ion concentration) on
the rate of alveolar ventilation.

13. CO2 response curve

14. How anesthesia affects ventilation?

15. Airway obstruction
▪ Loss of airway patency
▪ d/t relaxation of pharyngeal muscles
▪ posterior displacement of tongue
▪ Loss of cough reflex
▪ secretions on vocal cords or enter trachea
▪ airway spasm and infection

16. Reduced ventilation
▪ Reduction in ventilatory minute volume
▪ Reduction in RR (opioids)
▪ Reduction in TV (volatile anesthetics)
▪ Both (propofol)
▪ As reduced alveolar ventilation->PaCO2 inc.
▪ Increased PACO2-> displaces O2 from alveoli
and exacerbate hypoxia

17. ▪ Ventilatory response to CO2 reduced->
anesthetised pt become hypercapnic
▪ Threshold at which PaCO2 stimulates return
of spontaneous ventilation is increased->
delayed return of spontaneous ventilation
▪ Ventilatory response to acidosis blunted->
reduces ability to compensate

18. ▪ Reduce ventilatory response to hypoxia
▪ Even at concentrations as low as 0.1 MAC
▪ Post op period→ risk of hypoxemia

19. How anesthesia affect gas exchange

20. Changes in FRC
Oxygen content of FRC
▪ O2 in FRC-> lung’s store of O2
▪ Increasing [O2] of inspired gas increases
proportion of O2 in FRC-> increase time taken for
pt to become hypoxic when ventilation stops
▪ Preoxygenation -> prevent hypoxia for upto 3min

21. Volume of FRC
▪ Upright: 3000ml, supine: 2200ml
▪ GA relaxes diaphragm and intercostal muscles ->
further fall in FRC by 15-20%(approx.450ml)
▪ Dependent dorsal part of diaphragm in supine
moves cephalad
▪ This reduction in store of O2 reduce time taken to
become hypoxic after ventilation ceases

22. Relationship to closing capacity
▪ FRC exceeds CC and prevents collapse during
normal expiration
▪ GA-> CC approaches FRC producing small airway
collapse in normal expiration with resultant
atelectasis
▪ Increased intrapulmonary shunting
▪ Increased venous admixture to 5-10%

23. Changes in ventilation and perfusion
▪ Promote hypoventilation
▪ Central depression of chemoreceptor
▪ Depression of external intercostal muscle activity
▪ Magnitude of hypoventilation proportional to
anesthetic depth
▪ Peripheral response to hypoxemia nearly
abolished even by subanesthetic dose of most
anesthetics

24. ▪ Both V/Q mismatch and shunt increases
▪ Profound effect reducing oxygenation of
blood
▪ Suppress HPV: blood flow to under
ventilated or collapsed alveoli is not
reduced

25. Effects on respiratory pattern
▪ Light anesthesia: irregular breathing
pattern, breath holding
▪ Deeper levels: breaths become regular
▪ Inhalational agents-> rapid shallow breaths
▪ Nitrous oxide, opioids-> slow deep breaths

26. Other effects
▪ Reduce ciliary activity
▪ Dry gases result in mucus plugging
▪ Volatile drugs: irritant to airway, coughing
▪ Ketamine and neostigmine: increased
salivation and mucous production

27. Pharmacological effects of anesthetics
Inhalational
agents
Positive effects Negative effects
N2O No significant change in MV –
CO2 normal range, Non-irritant
Isoflurane Bronchodilation Reduced MV due to reduced TV
Reduced response to hypoxia & hypercarbia
Pungent – causes coughing, Increased secretions
Sevoflurane MV stable due to ↑ed RR at lower
doses
Bronchodilation, Non-irritant
Hypercarbia
Depressed response to CO2
Inhibition HPV
Halothane Bronchodilation
Non- irritant
Reduced bronchial secretions
Reduced MV due to reduced TV
Blunted response to hypoxia and hypercarbia
Inhibits HPV
Enflurane Non-irritant
Bronchodilation
No increase in secretions
Reduced MV (> other volatiles), Hypercarbia
Blunted response to hypoxia & hypercarbia
Inhibits pulmonary macrophages and mucociliary transport

28. IV inducing
agents
Positive effects Negative effects
Thiopentone Dose dependent respiratory depression
Increased bronchial smooth muscle tone with
increased bronchospasm & laryngospasm
Propofol Laryngeal relaxation – ease of LMA
insertion
Bronchodilation, May preserve HPV
Respiratory depression
Reduced response to hypoxia & hypercarbia
Etomidate Dose dependent reduction in MV
Apnoea, Coughing
Ketamine Preserved laryngeal reflexes
Maintain patent airway
Less respiratory depression
↓ bronchial smooth muscle tone
Increased saliva and mucous production
Opiates Anti-tussive Respiratory depression, Chest wall rigidity
Bronchospasm

29. Neuromuscular blocking agents
▪ d/t effect on effector muscles
▪ Expiratory abdominal m and intercostal
m>inspiratory intercostal m> diaphragm
▪ Obstuction of upper airway
▪ Upper airway resistance increased
▪ Inspiratory flow decreased
▪ Reduction of chest wall strength

30. Questions
The following are true or false:
a. Airway patency can be lost without the use of muscle
relaxants.
b. Sevoflurane causes an increase in saliva production.
c. Propofol causes a loss of the cough reflex.
d. Saliva on the vocal cords can cause laryngospasm.
e. Ketamine causes an increase in saliva production.

31. End-tidal carbon dioxide:
a. Corresponds to the arterial oxygen partial pressure.
b. Is inversely proportional to the alveolar ventilation.
c. Is raised after the administration of opioids.
d. Is reduced if the cardiac output is significantly reduced.
e. Can confirm the tracheal placement of an endotracheal
tube.

32. Ventilation:
a. Is reduced by in the presence of an acidaemia.
b. Is controlled only in the brain stem.
c. Is stimulated by hypoxia.
d. Is significantly impaired when using ether.
e. Is unaffected by the use of isoflurane.

33. Hypoxia:
a. Can always be corrected by increasing the inspired oxygen
concentration.
b. Can be caused by airway obstruction.
c. Can not be prevented when inducing anaesthesia.
d. Is caused by shunt when small airways collapse.
e. Is made worse by hypoxic pulmonary vasoconstriction.

34. The following are true or false:
a. When the airway is obstructed, the main oxygen reserve is within
arterial blood.
b. FRC is reduced by abdominal distension.
c. FRC is greater than closing capacity in an 80 year woman with COPD.
d. FRC can be filled with oxygen by breathing 50% oxygen.
e. A patient with a BMI of 35 breathing 100% oxygen will de-saturate
faster than a patient with a BMI of 22.