Slideshow is from the University of Michigan Medical School's M1 Cardiovascular / Respiratory sequence View additional course materials on Open.Michigan: openmi.ch/med-M1Cardio

1. Author(s): Louis D’Alecy, 2009
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3. Respiratory Control, Ventilation,
and Regulation of PaCO2
M1 – Cardiovascular/Respiratory
Sequence
Louis D’Alecy, Ph.D.
Fall 2008 3

4. Tuesday 11/18/08, 10:00
Respiratory Control
vs.
Control of Breathing (Ventilation)
vs.
Regulation of PaCO2
(22 slides, 50 minutes)
Apnea, Eupnea, Tachypnea, Hyperpnea
Hyperventilation & Hypoventilation

5. Eupnea: normal quiet ventilation
• Automatic & cyclic
• Originate in CNS - medulla
• “final common pathway” via phrenic nerves
• Bursts of nerve firing cause inspiration
• Interval between groups determines rate
• Frequency and # of motor units - depth (TV)
• Diaphragm (2/3 supine)+external intercostals
5

6. All modifiers
of basic
rate
respiratory
center in medulla
RECEPTORS
1. lung and airways Ach-nicotinic
2. baroreceptors
3. muscle and joints
respiratory
4. pain muscles
5. chemoreceptors
D’Alecy 6

7. Control of Respiration
Voluntary
Source Undetermined
7

8. CONTROL OF RESPIRATION DURING EXERCISE
motor
cortex
temperature RESPIRATORY CENTER
epinephrine skeletal
Muscle muscle
joint spindles
receptors & Golgi
ventilation tendon
organs
D’Alecy 8

9. Receptor Modulation of Ventilation
1. Lung and airway receptors
A. stretch receptors - inflation inhibits inspiration
Hering-Breuer reflex
B. irritant receptors - sneeze and cough
C. juxtapulmonary receptors - stimulated by
pulmonary edema - sensation of dyspnea
2. Baroreceptors -decreased MAP increases ventilation
3. Muscles and joints - movement increases ventilation
4. Pain - gasp reflex 9

10. Altered Breathing
• Apnea: absence of breathing
• Eupnea: normal quiet breathing
• Tachypnea: rapid breathing
• Hyperpnea: increase VT + or - increased VA
• Hyperventilation: excess ventilation that
– ******* Lowers PaCO2 *******
• Hypoventilation: inadequate ventilation
10
– ******** Increases PaCO2 *******

11. VT = VE Minute Ventilation
Alveolar Ventilation
Alveolar
Dead Space Ventilation
Ventilation
VA = VT - VD or
VA = VE - VD 11

12. Ventilation on PACO2
Source Undetermined
Hypoventilation Normal Hyperventilation
12

13. PERIPHERAL CHEMORECEPTORS
carotid sinus
Image of common carotid artery
peripheral
chemoreceptor
location removed
Stimulated by
arterial PO2
Please see: http://
www.medicine.mcgill.ca/physio/
resp-web/Figures/Figtt20.jpg
arterial pH ( = H+)
arterial PCO2
13

14. PaO2 leads to CO2 Response
mmHg Hypoxia
increases
mmHg ventilatory
Alveolar Ventilation L/min
mmHg response
to
CO2.
Increased Normal slope.
slope Small Increases in PaCO2
markedly increase
ventilation.
14
Source Undetermined mmHg

15. ACIDOSIS = an increase in the [ H+] concentration of blood
Respiratory Acidosis - accumulation of CO2 (hence H+)
due to hypoventilation.
Metabolic Acidosis - Any accumulation of acid (H+) that
does not come from retained CO2.
From: a) metabolic production of organic acids such
as lactic acid or ketone bodies,
b) ingestion of acidic substances or
c) failure of kidneys to excrete acid.
15

16. Plasma Acidosis Ventilation
Minor increases in [H+]
markedly
stimulate ventilation.
pH 7.4 7.33 16
Source Undetermined

17. PERIPHERAL CHEMORECEPTORS
16 Response to Acid & CO2
ventilation 12
L /min
8
4
[H +] nmol/ L
40 42 44 46
pH 7.4 7.33
P 40 50 55
CO
2 17

18. Fig 9-3
Arterial Acidosis CSF Alkalosis
18
The decrease in CSF CO2 causes CSF alkalosis.
Source Undetermined

19. Arterial CO2 is major determinant of
ventilation BUT this CO2 response can be
altered significantly.
VA
Source Undetermined
mmHg 19

20. Hyperventilation: PaCO2
breathing CO2 ventilation
Breathing CO2
increases
ventilation.
mmHg
The higher the ventilation
the lower the PaCO2. 20
Levitzky. Pulmonary Physiology. McGraw-Hill, 2003. 6th ed.

21. O2 Response* Interacts with CO2
Does giving 100% O2
•Insensitive at normal PO2 to a hypercapnic patient
suppress ventilation?
•O2 *response all peripheral
Let s ask Dr. Sisson.
•PaO2 not content
Low PO2 response "fail safe".
21
Source Undetermined

22. What about central chemoreceptors ?
Source Undetermined
22

23. No direct effect of blood H+ and HCO3-
Brain
H+
Central
-No O2 response.
CO2
-Slower.
Weak buffer
Source Undetermined
23

24. cerebral blood flow
Cerebrospinal fluid
CO2 CO2 + H2O H+ + HCO3-
central chemoreceptors
in medulla
H+
central chemoreceptors
respond to
blood-brain blood CO2 and CSF H+
barrier
insensitive to blood
H+ or O2
D’Alecy 24

25. Summary:
Control of the respiratory system is based on
responses to peripheral chemoreceptor
stimulation resulting in tight regulation of
arterial CO2 (PaCO2).

26. Additional Source Information
for more information see: http://open.umich.edu/wiki/CitationPolicy
Slide 6: D’Alecy
Slide 7: Source Undetermined
Slide 8: D’Alecy
Slide 12: Source Undetermined
Slide 13: Please see: http://www.medicine.mcgill.ca/physio/resp-web/Figures/Figtt20.jpg
Slide 14: Source Undetermined
Slide 16: Source Undetermined
Slide 18: Source Undetermined
Slide 19: Source Undetermined
Slide 20: Levitzky. Pulmonary Physiology. McGraw-Hill, 2003. 6th ed.
Slide 21: Source Undetermined
Slide 22: Source Undetermined
Slide 23: Source Undetermined
Slide 24: D’Alecy