Pulm Physio Flashcards

1
Q

What distiguishes V/Q mismatch from shunt?

A

Supplemental O2 correct the hypoxemia by raising the PO2 in blood coming from regions with a V/Q ratio

(supplemental O2 does not correct / improve conditions from a shunt)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the consequences of V/Q Mismatch?

A
  • Low PaO2 (hypoxemia)
  • Increased A-a Gradient
  • Hypoxemia is corrected with supplemental O2,
  • Also, any state of PaCO2:
    • Normal PaCO2 (eucapnia)
    • Increased PaCO2 (hypercapnia) or
    • decreased PaCO2 (hypocapnia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain Shunt and Dead Space Ventilation

A
  • Blood Goes to Parts of the lung that do not have O2 to give it
  • Blood does not go to parts of the lung that have oxygen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain Anatomical and Physiological Shunts

A

Physiological Shunt:

  • Situation within lungs
  • due to diffusion defect or obstruction to alveolus
  • Seen in Acute Respiratory Distress Syndrome (ARDS)
  • Pulm cap see no O2 and remain deoxygenated bc alveolus has diffusion defect
  • No amount of O2 will correct shunting!

Anatomical Shunt:

  • Shunt due to cadiac defects: cyanotic heart diseases
  • Deoxygenated blood never saw the lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a shunt?

A
  • desaturated blood bypasses oxygenation at the alveolar-capillary level
  • increased PAO2 - PaO2 (A-a gradient)
  • Refractory to supplemental O2
  • Ex: intracardiac R–> shunt, ARDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the consequences of a shunt?

A
  • Low PaO2 (Hypoxemia)
  • Increase A-a Gradient
  • Low PaCO2 (Hypocapnia)
  • Refractory to oxygen therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dead Space Ventilation

A

Dead Space Ventilation (VD): Volume of air per minute that enters the conducting airways and does not participate in gas exchange

  • VD: results in hypercapnia and hypoxia

Alveolar Ventilation (VA): Volume of air per minute that enters or exits the alveoli of the lung and participates in gas exchange

NB: if you don’t have perfusion CO2 cannot be perfused so you always have hypercapnia with Dead Space Ventiltation

Total Ventilation (VE): sum of alveolar and dead space ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the changes in echocardiogram in RV overload

A
  • Dilated RV
    • Compressed D-shaped LV
  • Flattended septum
  • Increased pericardial constraint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the effect of Gravity on perfusion

A
  • gravity is a passvie factor that affects relative perfusion of different regions of the lung
  • pressures are greater in the more gravity dependent regions of the lung, and resistnace to blood flow is lower in lower regions owing to more recruitment and distention of vessels in these regions
  • perfusion ceases when alveolar pressure is equal to pulmonary arterial pressure
    • so when alveolar pressure > pulmonary arterial pressure, ther eis on blood in that region (zone 1)
    • Zone 1 is ventilated but not perfused = ALVEOLAR DEAD SPACE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

If Pa (pressure of alveoli) > PA (pressure of arteriole), what would happen?

A

Alveolar pressure would theoretically collapse the alveoli so you would no longer have efficient blood flow to that region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Zones of the Lung

A

Pressures in the pulm circulation relative to pressures in the surrounding alveoli

  • Blood flow is greatest in the dependent regions of the lung
  • Therefore the pressures in the dependent circulation relative to each other are greatest in the dependent regions: Zone 3
  • Distension of the alveoli is greatest at the apicies
  • Perfusion is least at that point –> zone 1
  • Physiologic boundaries*
  • *If you increase alveolar pressures in any region of the lung, that region would function as if it were in zone 1 (as if it has more alveolar perfusion than pulmonary distension)*
  • With alveolar distension (where pressures are higher than pressures in capillaries) you will not have functional gas exchange, that is dead space.*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the effect of exercise on cardiac output and pulmonary artery pressure?

A

During exercise, cardiac output and pulmonary artery pressure increase anda ny exisiting zone 1 should be recruited to zone 3.

(true of situtations of incrase Cardiac output and increased pressures in zone 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypoxic Pulmonary Vasoconstriction

A
  • alveolar hypoxia or atelectasis causes an active vasoconstriction inthe pulmonary circulation at that level
  • occurs locally in the area of alveolar hypoxia
  • diverts mixed venous blood flow away from poorly ventilated ares of the lung by locally increasing vascular resistance
  • not a very strong response because ther eis so little smooth muscle in the pulmonary vasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What conditions may lead to pulmonary edema?

A
  • increased capillary endothelium permeability (infections, toxins)
  • increased capillary hydrostatic pressure (LV failure)
  • Decreased interstituial hydrostatic pressure (negative pressure pulmonary edema)
  • Increased reflection coefficient
  • decrease in plasma colliod pressure (hypoproteinemia)
  • increased interstitial colloid osmotic pressure
  • lymphatic insufficiency
    • any fluid that makes its way into the pulmonary interstitum must be removed by the lymphatic drainage of the lung
    • volume of lymph flow is capable of increasing 10 fold under pathologic conditions –> if overhwlemed –> pulmonary edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is ventilation normally regulated?

A
  • Vl is normally regulated by CO2 sensitive chemoreceptors in the central respiratory center to maintain PaCO2 within a normal range.
  • Changes in Vl at constant metabolic rates affects PsCO2 per the alveolar ventilation equation: [PaCO2 - k* VCO2/V]
  • An increase in PaCO2 normally increases ventilation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain hypoxic drive

A
  • Respiratory diseases which severely impair the ability to excrete CO2 (ie: severe COPD)
  • –> result in chronic CO2 retention causing a desensitization of this center
  • these patients rely on their hypoxia to drive ventilation
17
Q

What receptors are responsible for responding to respiratory drive in states of acidosis?

A

Cases of Acidosis with Brain Origin:

  • primary receptors responsible for the increase in ventilation are the peripheral chemoreceptors

Metabolic Acidosis Cases that DO have a Brain Origin:

  • CSF [H+] increases and the central chemoreceptors are stimulated to increase respiratory drive
18
Q

What are the effects of Metabolic Acidosis (Nonbrain Origin) on Peripheral and Central Chemoreceptors?

A
  • H+ does NOT cross the blood-brain-barrier so metabolic acidosis results in hyperpnea due to stimulation of the peripheral chemoreceptors
  • Hyperpnea (ventilatory compensation) decreases PaCO2 and causes a rise in pH and a reduction in peripheral chemoreceptor drive
  • The reduction in arterial blood PCO2 creates a downhill CO2 gradient from the CSF to the arterial blood => increase in CSF pH & reduction in central chemoreceptor drive
  • In cases where the metabolic acidosis is of brain origin (eg: meningitis) hyperpnea occurs due to stimulation of central chemoreceptors
19
Q

What is the effect of hypoventilation on PaO2?

A
  • At normal values of PaCO2 (38-40 mmHg) and PaO2 (76-100mmHg), VI is not stimulated by PaO2 (no hypoxic drive)
  • Hypoventilation results in a decrease in PaO2 and if severe enough to decrease PaO2 below 60 mmHg would cause a stimulation of Vl
  • Hypoxic drive is a result of stimulation of the carotid body chemoreceptors
    • aortic chemoreceptors respond to hypoxia but don’t regulate breathing as much
    • CENTRAL CHEMORECEPTORS DO NOT RESPOND TO HYPOXIA (do respond to CO2 and acid)
      *
20
Q

What happens to a “normal” person at a high altitude (ie: hypoxia alone)?

A

Increase ventilation and decrease PaCO2 (respiratory alkalosis)

21
Q

What is the nature of the response of hypoxia?

A
  • Hypoxia is detected by carotid receptors that respond to PaO2 (not CaO2 or SaO2)
  • The only types of hypoxemia that stimulates ventilation are those that actually change PO2
22
Q

What are examples of hypoxemia without actual decrease in PO2?

A
  • Carbon Monoxide
    • decrease in SaO2 but PaO2 is normal (so also have decrease in CaO2)
  • Anemia: decreases content of O2 but doesn’t affect SaO2 or PaO2 (unless there is an acidosis)
23
Q

Explain the difference between chemical drive at PaO2 levels around 100mmHg and when PaO2 levels fall below 60mmHg.

A

PaO2 at 100mmHg:

  • ventilation is regulated by the level of PCO2 primarily due to stimulation of central chemoreceptors with some contributions from the carotid body chemoreceptors

PaO2 levels below 60mmHg:

  • ventilation is regulated by both PCO2 and PO2
  • hypoxia is sensed by peripheral (primarily carotid body) chemoreceptors as O2 tension (PaO2) only!
    • NOT O2 content (CaO2)
    • NOT saturation (SaO2)
    • ie: no response to breatihing Carbon monoxide
24
Q

What do central chemoreceptors respond to vs. peripheral chemoreceptors?

A
  • Central: acid and CO2
  • Peripheral: acid, CO2, and hypoxia
25
Q

Why can ventilation with supplemental O2 lead to respiratory failure in pts with severe COPD?

A
  • Ventilation is normally regulated to maintain PaCO2 within a narrow range by the chemosensitive region of the respiratory center
  • In severe COPD, chronic CO2 retention causes a desensitization of this center and these pts rely on their hypoxic drive to breathe
  • Oxygen therapy improves hypoxia and reduces the hypoxic ventilatory drive to breathe –> thus WOSENING THE HYPERCAPNIA AND ITS NEUROLOGICAL EFFECTS

INSTEAD:

  • Start O2 therapy cautiously
  • admin O2 at levels to adjust the inhaled O2 to correct the hypoxia with careful monitoring of blood gases
  • If CO2 retention worsens, the pt may need ventilatory support
  • STILL NEED TO CORRECT HYPOXIA
26
Q

What are the lung and airway reflexes?

A
  • 3 receptor types: stretch, irritant, and J-receptors (give feedback on how much has been expanded)
  • Vagus nerve (mostly) - afferents
    • some trigem, laryngeal, glossopharyngeal
  • Pulm Stretch Recepter: lung inflation reflex
    • “slowly adapting receptors” that continue to fire with level of expansion/deflation to give volume feedback to inform level of adequacey of inflations
    • “Inspiratory off”: cause inspriation to terminate
      • breath within a breath feedback to monitor how much lung has been expanded to then terminate that expansion as needed/defined
  • Deflation reflex: if there is a strong deflation of the lung, it travels through vagus and causes hyperpnea (to increase resp if there is a deflation)
    • irritant and j-receptors
  • _Paradoxical reflex: p_artially cool the vagus nerve–> stimulates inspriation (paradoxical to lung inflation reflex, which terminates inspiration)
  • Bronchodilation: coordinate inspiration with decreasing airway resistance
  • Pharyngeal airway is very collapsable: negative pressure receptors in upper airway cause an activation of dilator muscles, so airway is splinted open during inspiratory effort
    • this reflex is depressed during sleep –> contriubtes to OSA (obstructive sleep apnea) bc airway is more susceptable to collapse during sleep
  • Diving reflex: if water/sensation around face or receptors in nasal mucosa, you get apnea so you don’t inspire water
27
Q

What are the brain centers responsible for respiratory rhythm generation?

A
  • Pontine Respiratory Neurons (PRG) in the rostral 1/3 of the pons is located in the Pneumotaxic Center - mediates smooth transition to expiration by inhibiting inspiratory activity
  • Caudal 2/3 of pons contains the apneustic center:
    • in absence of vagal feedback, the pneumotaxic center inspiratory terminating influences an apneustic breathing pattern (prolonged inspiration) emerges.
  • Medulla
    • contains neurons responsible for spontaneous rhythm generation
    • DGR: dorsal respiratory group
    • VRG: ventral respiratory group
28
Q

PRG

A
  • contains both inspirtory and expiratory neurons
  • activation leaves to rapid shallow breathing
29
Q

DRG

A

contains only inspiratory neurons

30
Q

VRG

A
  • contains both inspiratory and expiratory neurons
  • Botzinger complex is a major expiration
  • Pre-Botzinger complex is the respiratory pacemaker that can initiate rhythm generation
  • respiratory rhythm is generated through a process of recirprocal inhibition between the inspiratory and expiratory neurons
31
Q

Control Of Breathing During Exercise

A
  • Phase I:
    • abrupt increase may reflect anticipatory response
  • Phase II:
    • gradual increase invovles a variety of afferents
  • Phase III:
    • “steady-state”- reflects a precise matching of ventilation to metabolism below “anerobic threshold”
    • ie: blood gases are unaltered
32
Q
A