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REGULATION OF

VENTILATION
Physiology Department

Universidad Autónoma de Guadalajara A.C.© 2017


RESPIRATORY CONTROL SYSTEM

West. Respiratory Physiology. 2008

Universidad Autónoma de Guadalajara A.C.© 2017


ORGANIZATION OF THE
RESPIRATORY CENTER

▪M e d u l l a r y
respiratory center

▪Apneustic center

▪P n e u m o t a x i c
center

Universidad Autónoma de Guadalajara A.C.© 2017


APNEUSTIC CENTER
▪In the lower pons
▪Slower respiration and larger tidal volume
▪When the vagi is cut there are prolonged inspiratory spasm
(apneusis)
▪ By sustained discharge of medullary inspiratory neurons

Universidad Autónoma de Guadalajara A.C.© 2017


PNEUMOTAXIC CENTER
▪ Located in the upper ponds
▪ Transmits signals to the inspiratory area.
▪ Inhibits inspiration, regulate inspiratory volume, and secondarily
respiratory rate. “fine tuning”
▪ Normal rhythm can exist in the absence of this center

Universidad Autónoma de Guadalajara A.C.© 2017


OBJECTIVES
▪List the anatomical locations of chemoreceptors
sensitive to changes in arterial PO2, PCO2, and
pH that participate in the control of ventilation.

▪Identify which chemoreceptor population is most


important in sensing short-term (acute) and long-
term (chronic) alterations in blood gases.

Universidad Autónoma de Guadalajara A.C.© 2017


SENSORS
Central
▪CHEMORECEPTORS
Peripheral

Pulmonary stretch
▪LUNG RECEPTORS Irritant Receptors
“J” Receptors

Upper airway Receptors


Gamma Receptors
▪ OTHERS Joint & muscle
Arterial Baroreceptors
Pain & temperature

Universidad Autónoma de Guadalajara A.C.© 2017


CENTRAL CHEMORECEPTORS
▪ Near ventral surface of
medulla

▪ Surrounded by brain ECF


▪ Local blood
▪ Cerebrospinal fluid (CSF)

▪ Blood and CSF separated


by Blood Brain Barrier

■ Sensitive to [H+] West. Respiratory Physiology. 2008

■ An ↑ [H+] ! Stimulates ventilation

■ A ↓ [H+] ! Inhibits ventilation

Universidad Autónoma de Guadalajara A.C.© 2017


CENTRAL CHEMORECEPTORS

▪High sensitivity to CO2


and H+
▪ CO2 levels in blood
regulates ventilation
chiefly by its effect on pH
of the CSF

▪Also … The cerebral


vasodilation with
increased PCO2
enhances diffusion

Universidad Autónoma de Guadalajara A.C.© 2017


PERIPHERAL CHEMORECEPTORS

▪Location:
▪Carotid bodies (high blood flow)
▪Aortic bodies

▪Respond to:
▪↓ arterial PO2 & pH
▪↑ arterial PCO2

Universidad Autónoma de Guadalajara A.C.© 2017


PERIPHERAL CHEMORECEPTORS

▪Very high sensitivity


to changes in
arterial PO2

▪Responsible for all


the increase of
ventilation in
response to
hypoxemia***

Universidad Autónoma de Guadalajara A.C.© 2017


PERIPHERAL CHEMORECEPTORS

Universidad Autónoma de Guadalajara A.C.© 2017


“HERING BREUER REFLEX”
HB Inflation Reflex
▪Activation by Stretch receptors located in bronchi
and bronchioles.
▪Transmit signals through the vagi into dorsal
respiratory group.
▪When lung over-inflates, stretch receptors activates
and switches off the inspiration preventing over
inflation.
▪Obtained with tidal volumes 3 times above normal
(1500 ml)
Universidad Autónoma de Guadalajara A.C.© 2017
IRRITANT RECEPTORS
▪Location: Airway epithelial cells
▪Rapidly adapting receptors

▪Stimulated by noxious gases

▪Impulses travel up vagus myelinated fibers

▪Reflex: Bronchoconstriction

Universidad Autónoma de Guadalajara A.C.© 2017


J RECEPTORS
▪“Juxta pulmonary–capillary”
▪Location: Alveolar walls close to capillaries
▪Respond to chemicals into pulmonary circulation
▪Impulses pass up vagus by non myelinated fibers
■ Respond to engorgement of capillaries and
increased interstitial fluid volume of alveolar walls
■ Rapid, shallow breathing ! dyspnea
■ Responsible of the dyspnea of LVF and onset of
exercise

Universidad Autónoma de Guadalajara A.C.© 2017


OBJECTIVES

▪Describe the interaction of hypoxia and


hypercapnia in the control of alveolar
ventilation.

▪Describe the significance of the feed


forward control of ventilation (central
command) during exercise, and the effects
of exercise on arterial and mixed venous
PCO2, PO2 and pH.

Universidad Autónoma de Guadalajara A.C.© 2017


INTEGRATED RESPONSES
▪Changes in CO2

▪Changes in O2

▪Changes in pH

▪Exercise

Universidad Autónoma de Guadalajara A.C.© 2017


RESPONSE TO CO2
▪Sleep

▪Age

▪Personality factors

▪Athletes (decreased sensitivity)

▪Drugs

▪Genetic determined
Universidad Autónoma de Guadalajara A.C.© 2017
Response to CO2
▪Inputs to ventilatory control
system in establishing
breath-to-breath levels
▪CSF PCO2
▪PaCO2
▪P h y s i o l o g i c r e s p o n s e
depends on its concentration
and the PAO2
▪At normal PAO2, ventilation
increases 2-3 L/mmHg of
CO2
Universidad Autónoma de Guadalajara A.C.© 2017 West. Respiratory Physiology. 2008
RESPONSE TO O2
▪Hypoxia
▪Sensed by peripheral
chemoreceptors

▪Carotid bodies

▪Increasing the PCO2


increases the
ventilation at any
PO2

West. Respiratory Physiology. 2008


Universidad Autónoma de Guadalajara A.C.© 2017
EXERCISE
▪O2 consumption of 4L/min
▪Total ventilation of 120L/min
▪15 times greater than resting level
▪PCO2 no changes
▪PH normal/heavy exercise decreases
(lactic acid)
▪Temperature

Universidad Autónoma de Guadalajara A.C.© 2017


ABNORMAL PATTERNS OF BREATHING

A. Eupnea

B. Kussmaul breathing.
The breathing is fast and
has a high amplitude (large
VT)

Severe metabolic acidosis –


diabetic ketoacidosis --

Universidad Autónoma de Guadalajara A.C.© 2017


ABNORMAL PATTERNS OF
BREATHING

▪Cheyne – Stokes respiration


▪Caused by severe hypoxemia
▪Periods of apnea 10 – 20 sec with periods of
hyperventilation
▪High altitude during sleep
▪Severe heart disease
▪Brain damage

Universidad Autónoma de Guadalajara A.C.© 2017


Hypercapnia in Respiratory failure
Patient with COPD with severe hypoxemia
and CO2 retention over a period of months
Who is driving ventilation?
Low PO2 stimulating peripheral receptors

How is arterial and CSF pH in this patient?


Arterial pH is normal (compensated respiratory acidosis)
and pH of CSF is normal (↑ HCO3)

Universidad Autónoma de Guadalajara A.C.© 2017


Hypercapnia in Respiratory failure
▪The patient developed mild respiratory infection
and is treated with high inspired O2
▪ What can be expected?
Hypoxic ventilatory drive may be abolished and the
work of breathing increased (retained secretions &
bronchospasm)

▪ What is the consequence of this?

Ventilation is grossly depressed, high levels of


PaCO2
Universidad Autónoma de Guadalajara A.C.© 2017
How to treat this patient?
▪Give relatively low O2 concentration
24 to 28% O2

▪Monitor the arterial blood gases to


detect depression of ventilation

▪Intubation and mechanical ventilation


may become necessary

Universidad Autónoma de Guadalajara A.C.© 2017


Summary
▪Control of the respiration by the CNS
▪Brainstem & cortex
▪Apneustic center
▪Pneumotaxic center
▪Effector muscles
▪Receptors of the lungs
▪Abnormal patterns of the breathing

Universidad Autónoma de Guadalajara A.C.© 2017


Images Reference

▪Boron & Balpeaup. Medical Physiology. 2009

▪Guyton & Hall. Medical physiology. 2016

▪West. Respiratory Physiology. 2008

Universidad Autónoma de Guadalajara A.C.© 2017


Bibliography

Boron, W., Boulpaep, E. (2009). Medical Physiology. (2nd


Ed.). Philadelphia: Mosby-Elsevier.
Guyton, A., Hall, J. (2006). Textbook of Medical Physiology.
(11th Ed.). Philadelphia: Elsevier-Saunders.
Koeppen, S., Stanton, S. (2008). Berne & Levy Physiology.
(6th Ed.). Philadelphia: Mosby-Elsevier.
West. (2008). Respiratory Physiology. (8th Ed.): Lippincott.
Williams & Wilkins

Universidad Autónoma de Guadalajara A.C.© 2017

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