Regulation of Respiration

Pneumotaxic Center Controls

Switch off Point of the DRG inspiratory RAMP The pneumatic center then through this mechanism can control rate and increase the RR to 30-40 BPM or as little as 3-5 BPM.

Ventral Respiratory Group

§ Does NOT fire During NORMAL quiet breathing only when Respiratory Drive Increases

Hering-Breuer reflex Definition

A protective mechanism that terminates inhalation, thus preventing overexpansion of the lungs.

Pneumotaxic and Apneustic Center Location

Pons

DRG occupation and innervation

§ Extends the Length of the Medulla o In/Near the nucleus of the Tractus Solitarius. § VAGUS and GLOSSOPHARENGEAL nerves transmit signals into the respiratory center from: peripheral chemoreceptors, Baroreceptors, Other Lung Receptors

VRG Activated

§ When Respiratory Drive signals from the DRG spill over into VRG § VRG acts as a Contributor to DRG § Stimulation May lead to INSPIRATION or EXPIRATION § Powerful Signal to abdominal muscles with heavy Breathing (Exhalation)

•Volatile anesthetics:

Right Shift Dose dependent reduction in the slope of the carbon dioxide response curve or limiting hypercapnic drive.

DRG Ramp UP

· Not with one quick burst but: ramping up over 2 seconds then shutting down. o The ramp up time can be shortened during heavy breathing or exercise and the expiratory phase can also be shortened. · This allows for diaphragmatic stimulation and an even inspiration o Versus short gasps to gradually increase the lung volume). · Shutting down Importance: allows time for elastic passive lung recoil

Changes in Blood C02 impact on Respiratory System

· Oxygen does not directly impact the central medullary respiratory center. · High levels of PaCO2 increase the minute ventilation

Why does CO2 only last for a Couple Days?

1. Bicarbonate ions build, they recombine with hydrogen 2. Kidneys react to the lower pH by RETAINING bicarbonate. 3. Elevation Of CO2 is Strong stimulus for a Couple Days: Then Decreases (COPD) § Take home: · An acute change in PaCO2 is more potent than a chronic PaCO2 change.

Peripheral Chemoreceptor Activation

1. When the Pa02 falls to < 70mmHg, the peripheral chemoreceptors are stimulated. 2. Signals are sent through the Hering's Nerve (also called the pharyngeal branch) of the GLOSSOPHARYNGEAL nerve from the carotid bodies AND the VAGUS nerve from the aortic bodies.

Peripheral Chemoreceptors (Location)

1. bifurcation of the carotid arteries (carotid bodies) 2. aortic root

Overstretch results in 3 Possible Outcomesf

1. vagal stimulation which transmits to the DRG switching off the "ramp up" 2. increase in ventilation elicited when lungs are deflated abnormally (pneumo) 3. block the Vagus nerve to further deep inspiration (thought to be why babies take first breath)

Respiratory Center Is Made up of 3 Major Neuron Groups

1.The dorsal respiratory group (DRG) which mainly deals with inspiration. 2.The ventral respiratory group (VRG) which mainly deals with expiration. 3.Pneumotaxic center (located in the pons) which controls rate and depth of respiration.

PaO2 Falls between:

30-60 mmHg Peripheral Chemo Receptors become especially important

Juxtaposition Receptors (J-Receptors)

C Fibers Enervate J Receptors > Afferent 1. Pathway from the J Receptors is the SLOW conducting non-Myelinated C fibers IN the VAGUS nerve 2. Chemical/Mechanical Airway irritation may illicit a cough, sneeze, hyperpnea, bronchoconstriction and increase BP EVEN in a deeply SEDATED and PARALYZED patient. 3. "shortness of breath" or dyspnea encountered during pulmonary congestion and edema due to LV failure.

How long does C02 Effect the central Chemoreceptors?

CARBON DIOXIDE DRIVEN STIMULATION OF THE CENTRAL CHEMORECEPTORS ONLY LASTS FOR A COUPLE OF DAYS.

Peripheral Chemoreceptors are Especially Important in Which Disease State:

COPD, due to hypoxic respiratory drive

How Does Co2 effect the Central Chemoreceptors Then?

Combines with water to form carbonic acid which then dissociated into bicarbonate ions an hydrogen ions. This is how the hydrogen ion stimulates the chemoreceptors.

Effect of Volatile Anesthetics

Depressed hypoxic ventilatory responses · Depressing carotid body responses to hypoxemia. · Response to hypoxemia is not normal. o Ventilation impacts PaO2 to some Degree

Carbon Dioxide Response Curve

Linear Relationship between PaCo2 and MV Response Curves vary: Generally, increase of 1 mmHg Paco2 results in a MV increase of 1-4 liters/min

VRG Location

Located in Medulla near DRG

Central Chemoreceptors

Located in the Medulla and In the BLOOD BRAIN BARRIER Most sensitive to Hydrogen Ions CO2 doesn't stimulate the central chemoreceptors but QUICKLY crosses membranes

J receptors are stimulated by

Pulmonary Vascular Congestion or in interstitial Fluid Leading to Tachypnea § Engorgement of Pulmonary Capillaries § Pulmonary Edema Micro-Emboli in Lungs

Anesthesia: Opioids

RIGHT SHIFT Dampen the carbon dioxide response curve o Opioids impact respiratory rate > volume

Ventilation Maneuvers for Pao2 and PaCo2

^ FiO2 is much more effective! · Changing MV is Not helpful in ^ PaO2 · Changing MV is Very Helpful in Decreasing PaCO2

In anesthesia, the carbon dioxide response curve is subject to:

drastic changes that lead to left and right shifts.

Responses from the DRG

impulses are sent from the DRG to motor nerves of the diaphragm and external intercostal muscles.

Anesthesia: Benzos and Propofol

o Dampen Carbon Dioxide Response Curve o Right Shift

Apneustic Center

o Interfaces with the DRG and VRG Stimulates the inspiratory neurons of the DRG and VRG. § Inhibited by stretch Receptors § Inhibited by pneumotaxic Center

In anesthesia •Hypoxemia (PaO2 < 60 torr):

o LEFT shift Amplifies respiratory drive and minute ventilation

Dorsal Respiratory Group

o •Controls rhythmicity (pacemaker) o •Ramping is important o •Signals are sent to the diaphragm and external intercostal muscles

Hering-Breuer reflex How it works

stretch occurs signal is sent afferently via VAGUS nerve.