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Cardiopulmonary I > Test 2 (Control of Breathing and Respiratory Mechanics) > Flashcards

Test 2 (Control of Breathing and Respiratory Mechanics) Flashcards

1
Q

Breathing

A
  • The brain controls both the FREQUENCY of Breathing and the PATTERN:

VE = f x VT

1) Sensor ——–>
2) Medullary Centers —->
3) Effector —–>
4) Controlled Variable —–>
1) Sensor

**PHRENIC NERVE innervates the Diaphragm, and arises from C3-5!!!!!!!

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2
Q

Medullary Response Centers

A

1) DRG: Dorsal Respiratory Group (Medial and Front)
- Medullary
- Depth of Breathing (Tidal Volume)

2) VRG: Ventral Respiratory Group (Lateral and back)
- Medullary
- Inspiration and Expiration
- Depth

3) PRG: Pontine Respiratory Group
- Pons
- Modifies Inspiratory Timing (Activity —> Turn Off Inspiration)
* ***Known as the PNEUMOTAXIC CENTER!!!!!!!

4) Botzinger Complex
- Medullary
- Generates ‘Core’ Rhythm

5) Pre-Botzinger Complex

***The PHYSIOLOGIC portions covered by these groups are LARGER than the ANATOMIC portions covered

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3
Q

Breathing Frequency to Motoneurons

A

1) Determine Timing (f) —->
2) Determine Depth (Vt) —->
3) To Motorneurons

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4
Q

Pre- Botzinger Complex

A
  • Believed to be the site which GENERATES the TIMING (FREQUENCY) of the Respiratory Rhythm

***Very important in babies because in Utero they cant breath

**But the Pre-Botzinger Complex is not the ONLY region to play a role in Determining Respiratory Timing (f)

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5
Q

Respiratory Frequency

A
  • Part of deterring the Respiratory Frequency is deciding HOW LONG Inspiration and Expiration are!!!
  • So the transition from Inspiration to Expiration (and vice versa) is IMPORTANT in the Frequency
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6
Q

Apneusis

A
  • The FAILURE to turn INSPIRATION OFF (Stuck in Inspiration)!!!!!

**When the PRG is LESIONED, we lose the ability to turn INSPIRATION OFF without additional Sensory Information from the VAGUS NERVE!!!!

  • The PRG is therefore considered part of the network that CONTROLS the LENGTH of Inspiration under NORMAL CIRCUMSTANCES
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7
Q

Dorsal Respiratory Group (DRG)

A
  • 95% PREMOTOR to PHRENIC NERVE!!!!!
  • Receives lots of SENSORY INFORMATION

***A collection of mainly INSPIRATORY NEURONS!!!!

***Corresponds anatomically to Caudal Regions of the NUCLEUS TRACTS SOLITAOUS (NTS)!!!!!!!!!!!!!!

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8
Q

Ventral Respiratory Group (VRG)

A

1) ROSTAL:
- Premotor to Phrenic, other INSPIRATORY MUSCLES!!!!

2) CAUDAL:
- Premotor to Upper Airway, other muscles of EXPIRATION!!!!

***VRG uses the Phrenic Nerves pus a lot of other muscles to help out!

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9
Q

Breathing Map

A

1) Determine Timing:
a) Pre-Bot
b) PRG

2) Determine Pattern:
a) DRG
b) VRG

3) To Motorneurons

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10
Q

Apneusis

A

Appearance:
- Maintained Inspiratory Discharge

Results from:
- PONTINE DAMAGE

Effects:
- Slight DELAY, but the INCREASE in CO2, and DECREASE in O2, death is not supported

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11
Q

Apnea

A

Appearance:
- ABSENCE of Respiratory effort (NO INSPIRATION)

Results from:
- Medullary or Spinal Damage!!!

Effects:
- INCREASE in CO2, DECREASE in O2, Death if not supported

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12
Q

The Chemoreceptors

A

1) Chemoreceptors —->
2) Medullary Centers —>
3) Respiratory Muscles —>
4) CO2, O2, and pH —–>
1) Chemoreceptors

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13
Q

Chemoreceptors description

A
  • A Chemoreceptor is a NEURON that is SENSITIVE to Specific Chemicals. In the Respiratory System, these Chemicals at CO2, O2, and Hydrogen Ion
  • Changes in the concentration of these chemicals will change the FIRING RATE of a CHEMORECEPTOR
    1) Increase in CO2 —-> INCREASE Firing
    2) Decrease in O2 —-> INCREASE Firing
    3) Increase in H+ —-> INCREASE FIRING

***Hypoxia and Hypercapnia cause for Respiratory sensors to Shut Down which then DECREASES VENTILATION!!!

***Chemoreceptors don’t allow these Respiratory Receptors to SHUT DOWN by have an OPPOSITE Response to Hypoxia and Hypercapnia

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14
Q

What is the response of a Respiratory Neuron (or any Neuron) to an INCREASE in CO2, or a DECREASE in O2?

A
  • A DECREASE IN ACTIVITY, which would Decrease Ventilation, Decreasing Gas Exchange and making the Problem Worse
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15
Q

Chemoreceptors are designed the exact opposite of Respiratory Neurons

A
  • They will INCREASE their rate of activity when hypoxia or Hypercapnia occur
  • The Chemoreceptors will then ACTIVATE the Respiratory Centers and INCREASE RESPIRATION

There are two sets of Chemoreceptors:
1) CENTRAL CHEMORECEPTORS (In Brain)

2) PERIPHERAL CHEMORECEPTORS (In Carotid and Aorta)

** They each have a different role in the Control of Ventilation!!!

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16
Q

Central Chemoreceptors

A
  • Located on VENTRAL SURFACE of MEDULLA!!!!

Sensitive (INDIRECTLY) to CO2 in Blood:
1) CO2 Crosses Blood Brain Barrier

2) CO2 reacts with Water (Carbonic Anhydrase)
- CO2 + H2O —> H2CO3 —> (H+) + HCO3

**Central Chemoreceptors respons to the H+ in the CSF (not in Blood). This H+ Ion was created when CO2 crossed from the Arterial Blood to the CSF (Arterial CO2)!!!

***DRIVE TO BREATHE: Make you BREATHE REGULARLY!!!

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17
Q

Peripheral Chemoreceptors

A

Located in:
1) Aortic Arch

2) Carotid Body
* DOPAMINE*
- The Peripheral Chemoreceptos in the Carotid Body use DOPAMINE!!!

Sensitive to:

1) O2
2) CO2
3) H+

***FIRING RATE INCREASES in response to LOW Levels of O2, HIGH Levels of CO2, and HIGH levels of H+

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18
Q

Peripheral Chemoreceptors

A
  • INCREASED FIRING RATE of AFFERENTS from Carotid Body/ Aortic Arch
  • CO2 and pH also STIMULATE:
    a) Same Response
    b) QUICKER than CENTRAL

***INCREASED FIRING RIGHT; VT!!!!!!!!!!

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19
Q

Compare and Contrast the Central and Peripheral Chemoreceptors

A

CENTRAL CHEMORECEPTORS:

1) Location:
- Ventral surface of Brainstem

2) What are they sensitive to:
- DIRECTLY: pH of CSF
- INDIRECTLY: CO2 in Plasma

3) Influence:
- “RESPIRATORY DRIVE” or drive to Breathe

4) Effects:
- INCREASE Respiratory Rate/ DEPTH in response to HYPERCAPNIA (SLOWER than Peripheral)

PERIPHERAL CHEMORECEPTORS:

1) Location:
- Aortic Arch

2) What are they sensitive to:
- DIRECTLY: O2, CO2, and H+ (pH)

3) Influence:
- ACUTE Changes in Blood Gases

4) Effects:
- INCREASE Respiratory Rate/ DEPTH in response to HYPERCAPNIA, HYPOXIA, or ACIDOSIS

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20
Q

Mechanoreceptors

A

1) Pulmonary Stretch Receptors —->
2) Medullary Centers —–>
3) Respiratory Muscles —->
4) Lung Volume —->
1) Pulmonary Stretch Receptors

VE = f x VT

***AFFECTS VT!!!!!!!!!

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21
Q

Slow Adapting Pulmonary Stretch Receptors

A
  • Located in AIRWAYS
    1) SENSITIVE to: STRETCH of AIRWAYS (Directly Proportional to LUNG VOLUME)
  • FIBERS travel to Brain in VAGUS NERVE!!!!

2) EFFECT: INHIBITION of INSPIRATION (Inspiratory Termination) and PROLONGATION of EXPIRATION!!!!
- Important in adults when TIDAL VOLUME is INCREASED

***Their Effect can be overrides by the CHEMORECEPTORS!!!

***Involved in Controlling Respiration on a Breath - to - Breath BASIS!!!!

***BARE NERVE ENDINGS!!!!!!!!!!

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22
Q

Slow- adapting Pulmonary Stretch Receptors are important for Controlling Respiration in:

A

1) INFANTS
2) ADULTS during EXERCISE

***They are probably NOT CRUCIAL in Controlling Tidal Volume in adults AT REST!!!!

23
Q

Two Sets of Mechanoreceptors involved in PROTECTING the Gas Exchange Surfaces

A

1) Rapidly Adapting Pulmonary Stretch Receptors
2) J Receptors

***They are PROTECTIVE REFLEXES that OVERRIDE the Normal Respiratory Control System (IMPORTANT FOR SURVIVAL!!!!!!!)

24
Q

Rapidly Adapting Pulmonary Stretch Receptors

A
  • Located in AIRWAYS
    1) SENSITIVE to: IRRITATION, foreign bodies in Airway; STRETCH
  • FIBERS travel to Brain in VAGUS NERVE

EFFECT: COUGH!!!!!

**Cough is also elicited by Receptors at the LARYNX

**Their FIRING RATE returns to NORMAL very rapidly. SO they detect acute changes int he airways but the response is NOT MAINTAINED!!!

25
Q

J Receptors

A
  • Located near BLOOD VESSELS in ALVEOLI

SENSITIVE to: PULMONARY EDEMA

  • FIBERS travel to Brain in VAGUS NERVE

EFFECT: COUGH, TACHYPNEA (Rapid Breathing)
- The cough is not often productive

26
Q

Compare and Contrast the Mechanoreceptor Inputs that INFLUENCE respiration

A

SLOWLY ADAPTING PSR (SARs)

1) Location:
- Airways

2) Adequate Stimulus:
- Stretch of Lung

3) Effect:
- Inhibition Inspiration/ Promote EXPIRATION

4) Role:
- IN INFANTS: Every Breath
- IN ADULTS: Exercise or other High VT times

RAPIDLY ADAPTING (RARs)

1) Location:
- Airways

2) Adequate Stimulus:
- IRRITANTS

3) Effect:
- COUGH to Clear Airway

4) Role:
- Protective (Not Every Breath)

J RECEPTORS:

1) Location:
- Near CAPILLARIES in ALVEOLI

2) Adequate Stimulus:
- PULMONARY EDEMA

3) Effect:
- Cough, TACHYPNEA

4) Role:
- Protective (Not every breath)

27
Q

Cortical Influences on Breathing

A
  • CORTICAL INFLUENCES do control breathing as well (Ex: Talking, Holding your breath)
  • In these cases, the CORTEX appears to be BYPASSING the MEDULLARY CENTERS COMPLETELY and sending input DIRECTLY to the MUSCLES of RESPIRATION!!!!!
  • **So it can BYPASS the DRG and VRG and innervate the Diaphragm DIRECTLY!!!
28
Q

Pressure/ Volume Relationships in Lungs

A

1) As “Intrapleural” Pressure becomes MORE NEGATIVE, air flows into the Lung and LUNG VOLUME INCREASES
- Note: The CHANGE in VOLUME for a Given Change of Pressure is NOT CONSTANT. If it were the line would be straight
2) At LOW LUNG VOLUMES, it takes a fairly BIG PRESSURE CHANGE to make a SMALL INCREASE in VOLUME
3) Once there is a little air in the Lungs, a LITTLE PRESSURE CHANGE produces a LARGE VOLUME CHANGE, in other words, it becomes EASY TO STRETCH THE LUNGS
4) When the Lung gets close to the TLC, it again becomes DIFFICULT to INFLATE, so a LARGE PRESSURE produces a SMALL CHANGE in VOLUME

29
Q

Compliance

A
  • The COMPLIANCE of the Lungs is a measure of the “STRETCHABILITY” of the Lungs
  • To measure the COMPLIANCE, you just take the SLOPE of the LINE (Change in Volume/ Change in Pressure)
    1) The Compliance of the Lungs is HIGHEST in the NORMAL BREATHING RANGE (Middle of the Graph). So we don’t have to work hard to get a decent VT!!!
    2) At either Extreme (Too Small or too Large), the Lung Compliance is LOW (The lines are pretty flat). So we have to WORK HARDER to INFLATE the Lungs at Low or High LUNG VOLUMES
30
Q

At birth, a baby must Inflate its lungs for the first time.
1) What is the Compliance of the Lungs for the first Breath?

2) How hard doe the baby have to work?

A
  • Prior to the First Breath, Lung Volume is VERY LOW. COMPLIANCE is LOW and the effort to breath is HIGH
  • With Successive breaths, the baby Lungs inflate and become more Compliant so work DECREASES
31
Q

Pressure/ Volume Relationships with Exhaling

A
  • Something really interesting happens when we allow our Lung Model to “EXHALE”
  • The lung DOESNT DEFLATE the same way it INFLATED!!!!
32
Q

Pressure/ Volume Relationships with Saline

A
  • Even better, if we inflate the Lungs with Saline (Rather than air), the whole SHAPE CHANGES
  • And the lung DOES (mostly) DEFLATE the same way it INFLATED!!!
33
Q

Whats the difference between Air Inflation and Saline Inflation?

A

SURFACE TENSION!!!!

  • Air/ Water Interface
  • Air (Alveolus)
  • Water (The Tissue)
34
Q

Why Surfactant Matters: Surface Tension

A

LaPlace’s Law:

Pressure = (2T)/ r

T = Tension

SURFACTANT Changes the Surface Tension (T)
- It REDUCES T in the SMALLEST ALVEOLI More than in Larger Alveoli

35
Q

What is the difference in Inspiratory and Expiratory lines due to?

A
  • It is due largely to the presence of SURFACTANT!!!!
36
Q

Hysteresis

A
  • The difference between Inspiration and Expiration!!!!
37
Q

Pressure/ Volume Relationships with Hysteresis

A
  • The Hysteresis is due to the molecules of SURFACTANT moving ONE DIRECTION during INSPIRATION, but coming back a DIFFERENT WAY
  • The SURFACTANT is not evenly distributed on the ALVEOLAR SURFACE
  • Small droplets RANDOMLY POSITIONED
  • If the Alveolar VOLUME is SMALL, the DROPLETS are CLOSE TOGETHER and Pull APART during INSPIRATION/ FUSE during EXPIRATION!!!!!!!

***The slight Hysteresis of the Saline-filled curve is due tot he RESISTANCE of the TISSUE SLIDING OVER ONE ANOTHER!!!

38
Q

Compliance

A
  • The Change in Volume/ The Change in Pressure

LOW Compliance: LOW Stretchability; Hard to Inflate!!!

HIGH Compliance: HIGH Stretchability; Easy to Inflate!!!

**But, when there is HIGH Compliance, it is harder for the Lung to DEFLATE!!!

39
Q

Pressure/ Volume Relationships Test

A

1) The subject takes in a breath of KNOWN VOLUME
2) The line is CLOSED OFF so no AIR can ESCAPE
3) The subject RELAXES and the PRESSURE in the RESPIRATORY TRACT (the air has no where to go) is MEASURED!!!

40
Q

Pressure/ Volume Relationships with Lungs

A
  • The Lungs alone look like what we saw for INSPIRATION in the previous Graph. Their NORMAL RESTING POINT (Without the Rib Cage) is QUITE SMALL!!!!
41
Q

Pressure/ Volume Relationships with Rib Cage

A
  • The Rib Cage on its own “Wants” to be at a LARGER VOLUME (the NORMAL RESTING Point of the Rib Cage is the one that produces 0 cm H2O PRESSURE when RELAXED)!!!!!!!!!

***Rib Cage WANTS TO EXPAND!!!!!

42
Q

Pressure/ Volume Relationships with Rib Cage and Lungs Together (Mathematical Sum)

A
  • The Entire system is the Mathematical Sum of the LUNGS alone and the RIB CAGE alone
    1) The ELASTIC RECOIL of the Lungs and that of the Rib Cage exactly balance each other at the FUNCTIONAL RESIDUAL CAPACITY (FRC)

***If you have a patient who is not complaint, the lungs will be still and the FRC will MOVE DOWN!!!

** Can be seen in COPD patients as the Rib Cafe starts to WIN against the Elastic Recoil of the LUNGS!!!

2) The Lung themselves want to be SMALLER. They’ll get there when they get down to MINIMAL VOLUME!!!!
3) The balance point for the Rib Cage alone is much higher in VOLUME than the Other two, due to the EXPANDING FORCES acting on it (The joints and the Muscle)!!!

43
Q

A patient suffers an injury that results in the entrance of air into the Thorax. What is it called?

A

Pneumothorax

44
Q

Once the air has entered the Thorax, what line does the rib cage alone go to?

A
  • Line D!!!
  • Once the coupling between the Lungs and the Thorax is disrupted by air, the recoil of the Rib Cage (Thorax) causes the Rib Cafe to SPRING AWAY from the Lungs to a Larger Volume
45
Q

Once the air has entered the Thorax, what line does the Lung alone go to?

A
  • Line A

- Once free of the Rib Cage’s Pull, the Lungs COLLAPSE and go to MINIMAL VOLUME!!!!

46
Q

Air Resistance Equation

A

R = (8nL)/ r^4

R = Resistance
n = Viscosity
L = Length of the Tube
r = Radius of the Tube

***Air Resistance is also controlled by Smooth Muscle and the ANS!!!!!

***What Pressure do I have to generate to get the air to move???

47
Q

Airway Resistance with Smooth Muscle

A
  • Contraction of Bronchial (Airway) Smooth Muscle changes the radius of the airway and therefore the Resistance!!!!!
  • Decrease the Radius = INCREASE the RESISTANCE
48
Q

Airway Resistance Graph

A

1) The FORCED EXPIRATORY VOLUME is very helpful in identifying changes in the Pulmonary Mechanics. Both the FEV itself (Total Volume out) and HOW FAST AIRE can be MOVED OUT of the Lungs is IMPORTANT!!!

FVC: Forced Vital Capacity

2) The amount of air that can be exhaled in the FIRST SECOND (Abbreviated FEV1) is used as one measure of Pulmonary Functions, although the absolute number isn’t so important
3) The ratio of the FEV1 and the FVC is VERY IMPORTANT Test of Pulmonary Functions. In a NORMAL PERSON, about 80% of the FVC is EXHALED in the FIRST SECOND of a FORCED EXPIRATION

49
Q

Person with Obstructive Disease (Emphysema or Asthma)

A
  • In a person with Obstructive Disease (Emphysema or Asthma) it takes far longer to get the AIR OUT of the Lungs. The FVC is REDUCED due to AIR getting trapped in the Lungs, but FEV1 is even MORE REDUCED. The REV1/ FVC ratio is below about 70%!!!!!!!!
50
Q

Person with RESTRICTIVE DISEASE (Interstitial Fibrosis)

A
  • In a person with Restrictive Disease (interstitial Fibrosis), the absolute values of the FVC and FEV1 are BOTH REDUCED due to INABILITY of the Lungs to EXPAND, but the FEV1/ FVC Ratio is HIGHER than NORMAL (about 90%) because the ELASTIC RECOIL of the Lungs FORCES the AIR OUT MORE RAPIDLY!!!!!
51
Q

Interdependence

A

1) The ELASTIC RECOIL of the Lung would normally create a Collapse of the Small Airways and Alveoli
2) However, the SHARED WALLS of the Alveoli and Airways PREVENT that COLLAPSE because their RECOIL OPPOSES the RECOIL of the OTHER ALVEOLI

  • ** This is called INTERDEPENDENCE**
  • Each Alveoli depends on the others
52
Q

What happens to Interdependence when we lose some tissue?

A
  • If we lose some of the walls, we alter of lose the FORCES that would NORMALLY counter the Collapse. And these Alveoli can collapse DURING EXPIRATION!!!!!!!!!!

**Happens during Expiration because the Interpleural pressure is going Positive and we are squeezing down on the Lungs and DECREASING the Radius of the Alveoli and therefore INCREASING the Airway RESISTANCE!!!

53
Q

The Work of Breathing and how it Influences Normal Respiratory Process

A
  • As AIRWAY RESISTANCE INCREASES, it takes a GREATER PRESSURE CHANGE to generate FLOW INTO the Lungs!!!
  • Therefore, it takes MORE PRESSURE to generate a VOLUME CHANGE, which means an INCREASE in AIRWAY RESISTANCE CHANGES our first graph
    1) First, We adjust the axis to a somewhat more realistic Organization

2) The Work of Breathing: If i have an INCREASED AIRWAY RESISTANCE then the AREA WITHIN THE loop GETS BIGGER!!!!
- The WORK done to STRETCH the LUNGS/ THORAX is represented in the AREA between the LINES!

  • ***ELASTIC FORCES:
  • The WORK Needed to OVERCOME the ELASTIC FORCES is shown by the BLACK LINE that goes from the Y AXIS to the Center of the Loop and only works at the CENTER and not the WHOLE LOOP!!!
  • To Stretch the Lungs and Stretch the Rib Cage, we put in ELASTIC WORK!!!
    3) WHILE the Work done to OVERCOME AIRWAY RESISTANCE is in the Hatched Area (Under the black line but within the loop)
  • Expiration is PASSIVE as long as the WORK REQUIRED to move the Air Out (White Space) is SMALLER than the ORIGINAL EXPIRATION CURVE!!!
  • If this white area gets bigger than the CURVE for EXPIRATION, then we have to use our ABDOMINAL MUSCLES to PUSH the AIR OUT!!!

Cardiopulmonary I (12 decks)

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