Author(s): Louis D’Alecy, 2009 License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution–Non-commercial–Share.

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Author(s): Louis D’Alecy, 2009 License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution–Non-commercial–Share Alike 3.0 License: 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 this material. Copyright holders of content included in this material should contact with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician 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.

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3 Respiratory Control, Ventilation, and Regulation of P a CO 2 M1 – Cardiovascular/Respiratory Sequence Louis D’Alecy, Ph.D. Fall 2008

Tuesday 11/18/08, 10:00 Respiratory Control vs. Control of Breathing (Ventilation) vs. Regulation of P a CO 2 (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

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

7 Control of Respiration Voluntary Source Undetermined

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

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

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

11 Alveolar Ventilation V A = V E - V D V T = V E V A = V T - V D or Minute Ventilation Alveolar Ventilation Dead Space Ventilation

12 Ventilation on PA CO2 Hypoventilation Normal Hyperventilation Source Undetermined

13 PERIPHERAL CHEMORECEPTORS carotid sinus common carotid artery Stimulated by  arterial P O2  arterial pH ( = H + )  arterial P CO2 Please see: ysio/resp-web/Figures/Figtt20.jpg Image of peripheral chemoreceptor location removed

14 PaO 2 leads to CO 2 Response mmHg Normal slope. Small Increases in PaCO2 markedly increase ventilation. Increased slope Hypoxia increases ventilatory response to CO 2. Alveolar Ventilation L/min Source Undetermined

15 ACIDOSIS = an increase in the [ H + ] concentration of blood Respiratory Acidosis - accumulation of CO 2 (hence H + ) due to hypoventilation. Metabolic Acidosis - Any accumulation of acid (H+) that does not come from retained CO 2. 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.

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

ventilation L /min PERIPHERAL CHEMORECEPTORS Response to Acid & CO [H ] nmol/ L pH P + CO 2

18 Arterial Acidosis CSF Alkalosis Partial respiratory compensation for acidosis by increased ventilation (2 arrows to 1 arrow) The decrease in CSF CO 2 causes CSF alkalosis. Fig 9-3 Source Undetermined

19 Arterial CO 2 is major determinant of ventilation BUT this CO 2 response can be altered significantly. mmHg VAVA Source Undetermined

20 Hyperventilation: PaCO 2 breathing CO 2 ventilation mmHg The higher the ventilation the lower the PaCO 2. Breathing CO 2 increases ventilation. Levitzky. Pulmonary Physiology. McGraw-Hill, th ed.

21 O 2 Response* Interacts with CO 2 Insensitive at normal PO 2 O 2 *response all peripheral P a O 2 not content  Low PO 2 response "fail safe". Does giving 100% O 2 to a hypercapnic patient suppress ventilation? Let’s ask Dr. Sisson. Source Undetermined

22 What about central chemoreceptors ? Source Undetermined

23 H+H+ CO 2 Central -No O 2 response. -Slower. Brain No direct effect of blood H + and HCO 3 - Weak buffer Source Undetermined

24 cerebral blood flow CO 2 CO 2 + H 2 O H + + HCO 3 - central chemoreceptors in medulla H+H+ blood-brain barrier Cerebrospinal fluid central chemoreceptors respond to  blood CO 2 and CSF H + insensitive to blood H + or O 2 D’Alecy

Summary: Control of the respiratory system is based on responses to peripheral chemoreceptor stimulation resulting in tight regulation of arterial CO 2 (P a CO 2 ).

Slide 6: D’Alecy Slide 7: Source Undetermined Slide 8: D’Alecy Slide 12: Source Undetermined Slide 13: Please see: Slide 14: Source Undetermined Slide 16: Source Undetermined Slide 18: Source Undetermined Slide 19: Source Undetermined Slide 20: Levitzky. Pulmonary Physiology. McGraw-Hill, th ed. Slide 21: Source Undetermined Slide 22: Source Undetermined Slide 23: Source Undetermined Slide 24: D’Alecy Additional Source Information for more information see: