Control of Ventilation - lecture 12-1 Flashcards by Stephen Schaffner

What is hyperventilation?

Hyperventilation: breathing that is beyond that required to meet the metabolic needs of the body (i.e. the PaCO2 decreases)

How well did you know this?

Not at all

Perfectly

What is hypoventilation?

Hypoventilation: Breathing that is less than that required for metabolic needs (i.e. the PaCO2 increases)

How well did you know this?

Not at all

Perfectly

What is hyperpnea?

Hyperpnea: increased breathing that meets the metabolic needs

How well did you know this?

Not at all

Perfectly

What is tachypnea?

Tachypnea: increase in the respiratory rate above the normal range (>20 breaths per minute)

How well did you know this?

Not at all

Perfectly

What is bradypnea?

Bradypnea: decrease in the respiratory rate below normal range (<10 breaths per minute

How well did you know this?

Not at all

Perfectly

What is the origin and nature of the respiratory rhythm?

Origin: brain stem
Nature: gas exchange

How well did you know this?

Not at all

Perfectly

What are the neural components involved in the drive to breathe?

Central neural activity
Peripheral sensory neural feedback
Chemical status of blood and CSF

Feedback control helps as well

How well did you know this?

Not at all

Perfectly

What are the central controllers of ventilation?

Pons, medulla, other parts of brain

brainstem: automatic
Cortex: volitional

How well did you know this?

Not at all

Perfectly

Where does the output from the central controllers of ventilation go?

Effectors - respiratory muscles

How well did you know this?

Not at all

Perfectly

Do respiratory muscles feed back on sensors that help control ventilation?

Yes - sensors help determine appropriateness of respiratory effort

How well did you know this?

Not at all

Perfectly

What are the sensors involved with control of ventilation?

Chemoreceptors - central and peripheral
Upper airway receptors
Pulmonary receptors

How well did you know this?

Not at all

Perfectly

What do medullary centers do?

Medullary centers are essential and sufficient for automatic rhythmic respiration

How well did you know this?

Not at all

Perfectly

What is the dorsal respiratory group? What does it do and how does it provide innervation?

Dorsal respiratory group (DRG):

medullary center that provides automatic rhythmic respiration

primarily inspiratory,

provides rhythmic drive to contralateral phrenic motor neurons

How well did you know this?

Not at all

Perfectly

What is the ventral respiratory group? What does it do and what does it affect?

Ventral respiratory group (VRG):

medullary center that provides automatic rhythmic respiration

primarily expiratory,

provides rhythmic drive to intercostals and abdominal muscles,

regulates the diameter of the upper airway

How well did you know this?

Not at all

Perfectly

What is the effect of the pontine centers?

Pontine centers exert a major influence on the medullary oscillator, which is erratic and unstable

How well did you know this?

Not at all

Perfectly

What are 2 examples of pontine centers?

Apneustic center

Pneumotaxic center

How well did you know this?

Not at all

Perfectly

What does the apneustic center do?

Apneustic center: keeps inspiration in the “on” position

How well did you know this?

Not at all

Perfectly

What does the pneumotaxic center do?

Pneumotaxic center: facilitates inspiratory off-switching

Why is there a burst of inspiratory activity during the expiration phase?

Thought to help smooth and control expiratory effort

- could be accentuated in asthma

What are the respiratory vagal afferents?

Pulmonary stretch receptors
Rapidly adapting receptors
J receptors
Lung C fibers

What do the pulmonary stretch receptors do?

Slowly adapting pulmonary stretch receptors (PSR) increase activity with increased lung inflation

terminating I, prolonging E

Where are the pulmonary stretch receptors located?

Located between smooth muscle cells in the airways

What mediates the Hering-Breuer inflation reflex?

Slowly adapting pulmonary stretch receptors (PSR) increase activity with increased lung inflation - increased firing at large lung volumes will stop inspiration and start expiration to prevent barotrauma

terminating I, prolonging E

What do the rapidly adapting receptors do?

Rapidly adapting receptors (RAR) respond to the rate of change of inflation, and chemical stimuli

increases resp rate
stimulated by pneumothorax

promoting I

Where are the rapidly adapting receptors located?

Located between airway epithelial cells

What reflex is mediated by the rapidly adapting receptors?

Lung deflation hyperpnea reflex

What do J receptors do?

J receptors respond quickly to chemicals in the pulmonary circulation and to changes in interstitial fluid volume - i.e. CHF Tends to promote rapid shallow breathing

Where are J receptors located?

Located in the alveolar walls, close to capillaries

What are the lung c fibers? What do they respond to? What do they do?

Lung C fibers are chemoreceptors that respond to histamine , prostaglandins; influence HR, BP, and respiratory rate

Where are the lung c fibers located?

Located in the larger (bronchial) airways

What are the respiratory mechanical afferents?

Muscle and chest wall afferents | Airflow flow receptors

What are the muscle and chest wall afferents? What kind of info do they provide?

1. Muscle spindles provide length info and influence load compensation 2. Tendon organs provide muscle tension info 3. Joint receptors found in the costal-vertebral joint provide information related to rib joint motion

What kind of information do the airway flow receptors provide? Where are they found?

Airway flow receptors Found in the upper airway These are essentially temperature receptors, and the body assesses flow by a decrease in temperature (wind chill) during inspiration.

What are the 2 types of respiratory chemoreceptor afferents?

Central | Peripheral

Where are the central respiratory chemoreceptor afferents located?

Near ventral surface of medulla

What do the central respiratory chemoreceptor afferents respond to? How fast? What is the result?

Respond to changes in PCO2 and pH in the CSF, but stimulation depends on direct interaction with H+ - important Rapid detection Stimulation results in increasing tidal volume

Where are the peripheral respiratory chemoreceptor afferents located?

Carotid and aortic bodies

What do the peripheral respiratory chemoreceptor afferents respond to? What is the result?

Respond to changes in decreased PaO2 and pH, increased PaCO2 - response increases ventilation Very weak O2 response until PO2 falls below 60 mmHg, then respiration is increased primarily by increasing f 40% of ventilatory response

Why are central chemoreceptors so sensitive to changes in pH? What are central chemoreceptors NOT sensitive to?

Central chemoreceptors respond to changes in [H+] The blood-brain barrier is permeable to CO2 CSF has it’s own carbonic anhydrase (normal pH 7.32) CSF has a lower protein concentration and therefore a lowered buffering capacity (response and change in pH is quicker) Not sensitive to PO2 levels

Generally, what is the ventilatory response to hypercapnia?

Proportional increases in ventilation to 'blow off' CO2 | - slope of linear line depicting response will be smaller with higher PaO2

Generally, what is the ventilatory response to hypoxemia?

Quick decline in ventilation after PaO2 passes 40 mm Hg PaO2 threshold Increased PaCO2 will lead to ventilation being elevated for longer, but ventilation will still decline

What can alter the magnitude of the ventilatory response to hypercapnia?

Being asleep (slight blunting) Narcotics (blunts) Anesthesia

What contributes to increased PaCO2 in acute on chronic respiratory failure?

1. Loss of stimulation of the peripheral chemoreceptors leading to reduced ventilation - Hypoxemia is partly responsible for driving respiratory rate 2. Worsening of ventilation-perfusion mismatch - Loss of hypoxic vasoconstriction upon administration of 100% O2 3. Haldane effect Administration of 100% O2 results in a higher release of CO2 from hemoglobin and subsequently higher PaCO2 levels

Where I left off

slide 22, 23