11.18.08(b): Respiratory Control, Ventilation, and Regulation of PaCO2


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11.18.08(b): Respiratory Control, Ventilation, and Regulation of PaCO2

  1. 1. Author(s): Louis D’Alecy, 2009License: Unless otherwise noted, this material is made available under the terms of theCreative Commons Attribution–Non-commercial–Share Alike 3.0 License:http://creativecommons.org/licenses/by-nc-sa/3.0/We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use,share, and adapt it. The citation key on the following slide provides information about how you may share and adapt thismaterial.Copyright holders of content included in this material should contact open.michigan@umich.edu with any questions,corrections, or clarification regarding the use of content.For more information about how to cite these materials visit http://open.umich.edu/education/about/terms-of-use.Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or areplacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to yourphysician if you have questions about your medical condition.Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers.
  2. 2. Citation Key for more information see: http://open.umich.edu/wiki/CitationPolicyUse + Share + Adapt { Content the copyright holder, author, or law permits you to use, share and adapt. } Public Domain – Government: Works that are produced by the U.S. Government. (USC 17 § 105) Public Domain – Expired: Works that are no longer protected due to an expired copyright term. Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain. Creative Commons – Zero Waiver Creative Commons – Attribution License Creative Commons – Attribution Share Alike License Creative Commons – Attribution Noncommercial License Creative Commons – Attribution Noncommercial Share Alike License GNU – Free Documentation LicenseMake Your Own Assessment { Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. } Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (USC 17 § 102(b)) *laws in your jurisdiction may differ { Content Open.Michigan has used under a Fair Use determination. } Fair Use: Use of works that is determined to be Fair consistent with the U.S. Copyright Act. (USC 17 § 107) *laws in your jurisdiction may differ Our determination DOES NOT mean that all uses of this 3rd-party content are Fair Uses and we DO NOT guarantee that your use of the content is Fair. To use this content you should do your own independent analysis to determine whether or not your use will be Fair.
  3. 3. Respiratory Control, Ventilation, and Regulation of PaCO2 M1 – Cardiovascular/Respiratory Sequence Louis D’Alecy, Ph.D.Fall 2008 3
  4. 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. 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. 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. 7. Control of Respiration VoluntarySource Undetermined 7
  8. 8. CONTROL OF RESPIRATION DURING EXERCISE motor cortextemperature RESPIRATORY CENTER epinephrine skeletal Muscle muscle joint spindles receptors & Golgi ventilation tendon organs D’Alecy 8
  9. 9. Receptor Modulation of Ventilation1. 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 dyspnea2. Baroreceptors -decreased MAP increases ventilation3. Muscles and joints - movement increases ventilation4. Pain - gasp reflex 9
  10. 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. 11. VT = VE Minute Ventilation Alveolar Ventilation Alveolar Dead Space Ventilation VentilationVA = VT - VD orVA = VE - VD 11
  12. 12. Ventilation on PACO2 Source UndeterminedHypoventilation Normal Hyperventilation 12
  13. 13. PERIPHERAL CHEMORECEPTORS carotid sinus Image of common carotid artery peripheral chemoreceptor location removed Stimulated by arterial PO2Please see: http://www.medicine.mcgill.ca/physio/resp-web/Figures/Figtt20.jpg arterial pH ( = H+) arterial PCO2 13
  14. 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. 15. ACIDOSIS = an increase in the [ H+] concentration of bloodRespiratory 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. 16. Plasma Acidosis Ventilation Minor increases in [H+] markedly stimulate ventilation.pH 7.4 7.33 16 Source Undetermined
  17. 17. PERIPHERAL CHEMORECEPTORS 16 Response to Acid & CO2ventilation 12 L /min 8 4[H +] nmol/ L 40 42 44 46pH 7.4 7.33P 40 50 55 CO 2 17
  18. 18. Fig 9-3Arterial Acidosis CSF Alkalosis 18 The decrease in CSF CO2 causes CSF alkalosis. Source Undetermined
  19. 19. Arterial CO2 is major determinant of ventilation BUT this CO2 response can be altered significantly.VA Source Undetermined mmHg 19
  20. 20. Hyperventilation: PaCO2 breathing CO2 ventilation Breathing CO2 increases ventilation. mmHgThe higher the ventilation the lower the PaCO2. 20 Levitzky. Pulmonary Physiology. McGraw-Hill, 2003. 6th ed.
  21. 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 contentLow PO2 response "fail safe". 21 Source Undetermined
  22. 22. What about central chemoreceptors ? Source Undetermined 22
  23. 23. No direct effect of blood H+ and HCO3-Brain H+ Central -No O2 response. CO2 -Slower. Weak buffer Source Undetermined 23
  24. 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 O2D’Alecy 24
  25. 25. Summary:Control of the respiratory system is based on responses to peripheral chemoreceptor stimulation resulting in tight regulation of arterial CO2 (PaCO2).
  26. 26. Additional Source Information for more information see: http://open.umich.edu/wiki/CitationPolicySlide 6: D’AlecySlide 7: Source UndeterminedSlide 8: D’AlecySlide 12: Source UndeterminedSlide 13: Please see: http://www.medicine.mcgill.ca/physio/resp-web/Figures/Figtt20.jpgSlide 14: Source UndeterminedSlide 16: Source UndeterminedSlide 18: Source UndeterminedSlide 19: Source UndeterminedSlide 20: Levitzky. Pulmonary Physiology. McGraw-Hill, 2003. 6th ed.Slide 21: Source UndeterminedSlide 22: Source UndeterminedSlide 23: Source UndeterminedSlide 24: D’Alecy