Resp 212 Beachy chapter 11 Control of ventilation Flashcards

1
Q

Where do the neural Impulses responsible for breathing originate?

A

Medula Oblongata of the Brainstem

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2
Q

What Does the Dorsal Respiratory Group Do? 3 points, include nerves involved with signals etc.

A
  1. Consists mainly of** inspiratory** neurons
  2. the neurons send impulses to the phrenic and external intercostal motor nerves in the spinal chord, providing the main stimulus for inspiration.
  3. Vagus and Glossopharyngeal nerves transmit impulses to the DRG from the lungs, airways, peripheral chemoreceptors and joint proprioceptors, MODIFYING THE BASIC BREATHING PATTERN GENERATED IN THE MEDULLA
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3
Q

Describe the two neuron populations of the DRG

A

The DRG consists of 2 neuron populations,

  1. Inhibited by deep lung inflation (causing cessation of inspiratory effort)
  2. Excited by lung inflation (causing continued inspiratory effort)

These neurons are involved in the HERING-BREUER AND HEAD REFLEXES

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4
Q

What Does the Ventral Respiratory Group do? 3 points

A
  1. Contains both inspiratory and expriatory neurons.
  2. Nuceus Ambiguus- contains inspiratory neurons that innervate the laryngeal and pharyngeal muscles through the vagus nerve.
  3. Their impulses abduct the vocal chords of the larynx , increasing the diameter of the glottis and decreasing the inspiratory airways resistance.
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5
Q

Nucleus Retroambiguous 2 parts, what are they, what they contain, and what they do.

A
  1. Caudal area: mostly expiratory stimuli, drive the internal intercostal and abdonminal expiratory muscles. These muscles are normally active only at high ventilatory rates when expiratory muscle activity is required.
  2. Rostral: Mostly inspiratory discharge patterns.
    a. they help DRG neurons drive the diaphragm and external intercostal muscles
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6
Q

Botzingers Complex

A
  1. The most rostral (toward the head) part of the **VRG **
  2. Contains the only expiratory neurons known to inhibit the **inspiratory **VRG and DRG impulses.
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7
Q

Botzinger Complex, and Pre-Botzinger complex

2 major theories of rythm generation

A
  1. May have a role in the rythmic breathing pattern
  2. Pacemaker hypothesis
  • cells with intrinsic self-exciting pacemaker properties
    1. Network hypothesis
  • Rythm is a result of interconnections pattern between I and E neurons: assumed that neurons inhibit one another and that after initial firing, neuron impulses die down
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8
Q

Inspiratory Ramp Signal

A

Gradual firing of impulses after expiration ends

  • progressively stronger contraction of inspiratory muscles
  • Gradual inflation of the lung

During Exercise

  • Peripheral receptors and reflexes send impulses that create a steeper inspiratory ramp signal
  • more rapid lung filling

I time shortened (inspiration time) = increased respiration rate.

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9
Q

Inspiratory ramp signal

A

Dorsal and ventral inspiratory neurons do not send an abrupt burst of impulses to the inspiratory muscles.

RATHER

their firing rate increases gradually after expiration ceases.

CREATING

a smoothly increasing ramp signal

LEADING to

progressively stronger contraction of inspiratory muscles

SMOOTHLY and GRADUALLY

INFLATING the lungs instead of filling them in an abrupt inspiratory gasp.

During exercise, this happens more rapidly

as the INSPIRATORY RAMP SIGNAL STRENGTHENS, inhibitory neruons begin to fire with increasing frequency.

after about 2 seconds these respiratory signals become strong enough to abruptly switch off the inspiratory signal.

Expiration then occurs for 3 seconds

as expiration begins, inspiratory neruons fire briefly, braking the early phase of expiration by maintaining some inspiratory muscle tone

Inspiratory neruonal activity completely stops in the last phase of expiration.

Inhibitory Neurons that switch off the inspiratory ramp arise from the pneumotaxic center and pulmonary strech receptors.

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10
Q

Pontine Centers

A
  1. Apneustic center
  2. Pneumotaxic center
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11
Q

What does the Apneustic Center do?

A
  1. Sends signals to the DRG
  • Prevents Inspiratory ramp signal from being switched off
  • Apneusis: prolonged inspiratory gasps interrupted by occasional expirations
      2. ***Pneumotaxic Center***
  • Controls off - switch point of DRG’s inspiratory ramp signal
  • Strong signal shortens inspiratory time: increased breathing rate.
  • Weak signal prolongs inspiratory time: increases tidal volume

Pontine impulses “fine tune” medullary rhythm

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12
Q

Pneumotaxic center Roles

A
  1. Controls off-switch point of DRG’s Inspiratory ramp signal
  2. Strong signal shortens inspiratory time: increases rate
  3. Weak signal prolongs inspiratory time: Increases tidal volume.
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13
Q

Figure 11-2 and 11-3 Beachy

A
  1. Neural inspiratory signals during ventilation.

Breathing patterns produced by transections of the brainstem at different levels

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14
Q

**Hering-Breuer **Inflation reflex

A
  • Stretch receptors in smooth muscle of large and small airways
  • Inhibit inspiration via vagal impulses to DRG
  • Stops further inspiration
  • Activated only with large tidal volumes ~0.8-1.0L
  • Regulates rate and depth during exercise
  • If decreased lung compliance
  • Increased inspiratory effort= increased mechanical stress on stretch receptor: Increases firing rate,** which shortens inspiratory time = faster breathing rate
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15
Q

Hering-Breuer Deflation Reflex

A
  • Sudden lung collapse stimulates breathing
  • Hypernea observed with pneumothorax
  • Due to decreased stretch receptor activity?
  • Due to irritant receptor stimulation?

-vagus nerve is the pathway from lung to medulla

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16
Q

Head’s paradoxical reflex 4 points

A
  • Vagus cooling** blocks** HB reflex: hyperinflation causes further inspiratory effort
  • May ** help maintain** large tidal volumes during exercise
  • responsible for deep sighs during quiet breathing?
  • Involved in first breath of newborn infant?
17
Q

Irritant receptors

A
  • Rapidly adapting irritant receptors in the epithelium of the larger conducting airways have vagal sensory nerve fibers.
  • When stimulated by inhaled irritants or mechanical factors, they cause reflex bronchoconstriction, coughing, sneezing, tachypnea, and narrowing of the glottis.
18
Q

Vagovagal reflexes

A
  • Both sensory and motor neurons:

Responsible for reflex bronchoconstriction, coughing, sneezing tachypnea, glottic narrowing, bradycardia

Instrumentation of airway elicits vagovagal response

19
Q

J-Receptors

A
  • C-fibers in the lung parenchyma near capillaries
  • Juxtacapillary receptors
20
Q

What Stimulates J-receptors? 3 points

A
  • Alveolar Inflammatory processes (pneumonia)
  • Pulmonary vascular congestion (congestive heart failure)
  • Edema
21
Q

What does J-receptor stimulation cause?

A
  • Rapid, shallow breathing
  • A sensation of dyspnea
  • expiratory narrowing of the glottis (causing grunting on expiration, especially in infants)
22
Q

What do Peripheral Proprioceptors do?

A
  • Send impulses to the medullary centers, increasing inspiratory activity and hypernea.
  • For this reason, slapping the skin, or moving the limbs of pts. with respiratory depression can stimulate respiration
23
Q

Muscle Spindles in Diaphragm and intercostal muscles.

A
  • Muscle spindles are strech-sensing elements located on intrafusal muscle fibers, which are arranged in parallel with extrafusal muscle fibers.
  • Send signals to the nervous system and help inspiratory muscle force to automatically adjust to the load imposed by decreased lung compliance, or increased airway resistance
24
Q

nucleus ambiguous

A

contains inspiratory neurons that innervate the laryngeal and pharyngeal muscles through the vagus nerve.

Their impulses abduct the vocal chords of the larynx, increasing the diameter of the glottis and decreasing the inspiratory airways resistance

25
Q

Chemical Control of Ventilation

A
  • Because Ventilation is important in maintaining proper amounts of oxygen, carbon dioxide, and hydrogen ions in the body.
  • Changes in these substances affect ventilation.
26
Q

Chemoreceptors

A
  • When stimulated they transmit impulses to the central respiratory centers in the medulla.
  • Ventilation then increases in an attempt to return oxygen, carbon dioxide, and hydrogen ion levels to normal.
27
Q

Central (medullary) chemoreceptors

A
  • Highly responsive chemosensitive nerve cells that are located in the medulla
  • Stimulated by hydrogen ions
  • HOWEVER
  • The medullarey chemoreceptors are considered to be CO2 sensitive because the Hydrogen surrounding them is dependent on the PCO2 of their environment.
28
Q

Why is the Hydrogen surrounding the medullary chemoreceptors dependent on the PCO2 in the environment?

A
  1. Blood Brain barrier is almost impermeable to hydrogen, and bicarbonate ions so the hydrogen comes in with CO2
  2. The CO2 reacts with H2O to form Hydrogen and bicarbonate ions (HCO3)
  3. THEN
  4. The Hydrogen ions stimulate the central chemoreceptors, which in turn stimulate the medullary inspiratory neurons
29
Q

What is the primary mechanism that drives ventilation in humans?

A
  1. Arterial PCO2
  2. A change in PCO2 of only 2mm Hg, causes a measurable ventillary response
30
Q

Why does the chronically high PCO2 in patients with advanced obstructive pulmonary disease (COPD) who have compensated respiratory acidosis, not stimulate the central chemoreceptors?

A
  1. The stimulatory effect of PCO2 decreases over 1-2 days because of renal compensatory responses
  2. Kidneys retain bicarbonate ions in response to respiratory acidosis
  3. this returns blood ph to normal range
  4. the increased bicarbonate ions slowly diffuse across the blood-brain barrier into the CFS, where they eventually buffer the H+ and bring the CFS pH back to normal
  5. This removes the stimulus to the chemoreceptors and ventilation decreases.
31
Q

hypercapnia

A

CO2 in the blood is too high

32
Q

What is Oxygen induced Hypercapnia?

A
  1. an acute increase in PaCO2 when O2 is given to chronically hypoxemic, hypercapnic patients (eg. COPD)
  2. Induced V/Q mismatches- Breathing O2 relieves the hypoxic vasoconstriction of underventilated regions in the lungs.
           - if **uderventilated alveoli receive additional blood flow, their capillary PCO2 rises, increasing** **PaCO2**. It's coming in, but they aren't recieving enough O2 through ventilation, so the CO2, continues to rise in concentration.

There is a potential for these patients to stop breathing, however it is very rare, and tissue oxygenation is the overriding priority. so you need to to be prepared to ventilate if O2 administration induces severe hypoventillation.

33
Q

How is breathing controlled during Chronic hypercapnia?

what is the Medullary Response to acute CO2 increase in Chronic hypercapinia

A
  • Medullary response to acute CO2 increase in chronic hypercapnia
  1. Central chemoreceptors recieve less stimulation because blood has a higher buffer content (HCO3-)
  2. eVentilatory respons to CO2 is depressed
  3. Buffering capacity is increased because of the previously existing compensated respiratory acidosis.
34
Q

Cheyne-Stokes Breathing pattern

A
  1. Cycles of gradual increase in rate and vollume followed by gradual decreases to complete apnea.
  2. when cardiac output is decreased, decreased blowd flow rate,
  • Medullary response to PCO2 lags behind hypoventilation
35
Q

Biot’s Breathing Pattern

A
  • Similar to Cheyne - Stokes, but tidal volumes have essentially the same depth.
  • occurs in patients with lesions of the pons
36
Q

what role does CO2 play in cerebral blood flow?

A
  1. Plays an important role in regulating cerebral blood flow
  2. this effect is mediated through CO2’s formation or hydrogen ions.
  3. increased PCO2 dilates cerebral vessels, raising cerebral blood flow.
  4. decreased PCO2 constricts cerebral vessels and reduces cerebral blood flow.
37
Q

What happens in patients with traumatic Brain injury?

A
  1. Increase in ICP (normal is < or = to 10mm Hg)
  2. Decrease in CPP (cerebral Profusion Pressure) (normal is > or = to 60mm Hg)
  3. CPP = MAP(mean arterial Pressure) - ICP
  4. Intercranial pressure increase of 1mm Hg=decrease in cerebral blood flow by 0.5-0.7 mL
  5. PaCO2 decrease of 1mm Hg = 3% decrease in Cerebral blood flow
  6. So use of mechanical ventilation in traumatic brain injury to lower the PaCO2 and therefore reduce cerebral blood flow and Intracranial pressure can potentially cause cerebral ischemia
38
Q

What happens if a head trauma patient with high ICP is Hypoventilated

A
  • dangerous because the resulting hypercapnia dilates cerebral vessels and elevates the ICP even more.