Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Pulmonary Physiology (38, 40, 42) > Flashcards

Pulmonary Physiology (38, 40, 42) Flashcards

1
Q

Pulmonary circulation is in (series/parallel) with systemic circulation

A

Series. It is the only place in the body to receive the entire CO

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

Pulmonary blood pressures are (high/low) because pulmonary vascular resistance (PVR) is (high/low).

A

BPs are low (20/7). PVR is low. Vessels have minimal basal tone thus they passively distend with increased flow

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

Do lung vessels autoregulate?

A

Not really

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

What is the difference between an anatomic and a pathological shunt?

A

Anatomic is left-to-left. It comes off the aorta, provides the lung tissues with nutrients and empties into the pulmonary vein. A pathological shunt is left-to-right and bypasses gas exchange. Pathological isn’t supposed to exist in the body

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

What are some consequences of the anatomical shunt?

A

PP O2 in arterial blood drops from 100 to 95 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define: physiological shunt

A

the sum of the normal shunt + pathological shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lung vessels are (thick/thin) walled and of (high/low) compliance.

A

Thin walled with high distensibility so low compliance

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

A mean pulmonary artery pressure of ___ indicates pulmonary hypertension. A mean pressure of ____ indicates pulmonary edema.

A

20- hypertension

25- pulm edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does one calculate PVR?

A

PVR= (P pulm a - P (LA)) x CO
Can measure CO, P of pulm a with a transducer and P of LA using a balloon. You inflate the balloon and occlude a small vessel so no flow exists. Thus the pressure will equal LA pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

During inspiration, how do pulmonary arteries change? Capillaries? Pulmonary veins?

A

Arteries and veins increase in volume b/c negative intrapleural pressure allows them to expand. Capillaries decrease in volume b/c positive alveolar pressure squishes them

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

As the lung inflates from RV to TLC, what happens to capillary resistance? Pulm a and v resistance? Total PVR?

A

Cap resistance increases, pulm a and v resistance decreases so the PVR curve is a parabola. The lowest point is at FRC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name some pulmonary vasodilators? Vasoconstrictors?

A

Vasodilators- histamine, NO, prostacyclin, Ca channel blockers
Vasoconstrictors- increased CO2, decreased pH, ang II, norepi, hypoxic vasoconstriction

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

Where is pulmonary blood flow greatest? Why?

A

At the base of the lung. B/c of gravity. And flow distends the vessels, decreasing R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the 3 zones of flow in the lung

A

1- alveolar pressure > arterial pressure (> venous pressure). Capillaries occluded. Flow stops. Not normally present in healthy lungs
2- arterial P> alveolar P> venous P. Alveolar pressure causes partial collapse of capillaries on the venous side, creating a waterfall effect.
3- arterial P> venous P> alv P. Capillaries open, flow is fine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some physiologic and pathologic causes of pulmonary edema?

A

Increased hydrostatic pressure (pulm hypertension)
Increased cap permeability (O2 toxicity)
Decreased oncotic pressure (proteinuria)
Decreased interstitial pressure (drain pneumothorax too fast)
Insufficient lymph drainage (obstruction/tumor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How would you calculate how much blood flows through a pathological shunt?

A

Normal cap flow x cap O2 + shunt flow x venous O2= total flow x arterial O2
so Q shunt/Q total= (capillary O2-arterial O2)/(cap O2- venous 2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a blood gas consequence of a shunt? Why does this occur?

A

More hypoxia than hypercapnea. The PO2 v. % vol O2 curve has a plateau so a small reduction in % vol O2 in the arteries results in a big drop in partial pressure O2. The CO2 curve doesn’t have a plateau.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Will oxygen treatment help someone with a pathological shunt?

A

No. The shunt blood is not oxygenated so increased O2 partial pressure won’t help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Q shunt in a normal person? What are the physiological consequences of a longer shunt?

A

Normal people don’t have this shunt so Q= 0

Longer shunt- blood gas composition will look more like venous blood than arterial blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Is respiration a myogenic or neurogenic process?

A

Neurogenic

21
Q

What areas in the brain are important in controlling respiration? Where are they located?

A

The central pattern generator (in the medulla)- comprising the dorsal respiratory group and the ventral respiratory group (includes the Botzinger complex)
The pontine respiratory group and the apneustic center in the pons

22
Q

What areas control inspiration? Expiration? Via which nerves to what muscles?

A

Inspriation- DRG and VRG. Phrenic nerve to the diaphragm and spinal nerves to external intercostals
Expiration- VRG. Spinal nerves to the internal intercostals and abdominal muscles

23
Q

What do action potential frequencies look like in eupnea? Hyperpnea?

A

Eupnea- inspiration is active so AP frequency increases and peaks at end-inspiration. Only a few APs occur during expiration b/c it’s a passive process
Hyperpnea- APs increase in frequency up to end-inspiration and up to end-expiration b/c both are active processes

24
Q

What is the Hering-Breuer inflation reflex? What is it’s role in breathing?

A

Deep inspirations activate stretch receptors in the lung. Vagal afferents convey this to the CPG which activates phrenic efferents to stop inflation. Only comes into play with big TVs (not during eupnea)

25
Q

What does the CPG do in breathing? The apneustic center? The PRG? The vagal nerves?

A

CPG- initiates breathing
Apneustic center- makes breathing smoother; is the inspiratory cut off switch
PRG- fine-tunes breathing by regulating the frequency and TV
Vagi- bring sensory info from peripheral chemoreceptors and stretch receptors so can modulate breathing/make it rhythmic

26
Q

What is characteristic of Cheyne-stokes respiration? When does it occur?

A

Alternating periods of hyperpnea and apnea

Brain injury or trauma (or CO poisoning)

27
Q

What is characteristic of Cluster/Biot’s breathing? When does it occur?

A

Closely grouped shallow breaths of a similar size followed by apnea
Stroke, head trauma, lower pons lesion

28
Q

What is characteristic of ataxic breathing? When does it occur?

A

Irregular inspirations and expirations with irregular pauses

Medullary lesion

29
Q

What activates central chemoreceptors? Peripheral chemoreceptors?

A

Central- increased concentration of H+ in CSF

Peripheral- mainly a decrease in arterial P O2 but also can be increased arterial P CO2 or decreased pH

30
Q

What is the major controller of respiratory rate?What happens when you increase this?

A

Arterial P CO2

Minute ventilation increases

31
Q

What makes the response to increased alveolar P CO2 more sensitive?

A

Hypoxia (decreased arterial P O2) and decreased arterial pH (increased arterial P CO2) shift the alveolar CO2 curve to the L, making alveolar ventilation greater for the same arterial PP CO2

32
Q

Do pH and arterial P O2 affect minute ventilation when arterial P CO2 is held constant?

A

Yes, decreased pH and decreased arterial P O2 increase ventilation but not as strongly as the arterial P CO2 does

33
Q

What is the ventilatory set point? How is it established?

A

It is where the sensory curve (the effect of arteriolar P CO2 on ventilation) and effector curve (the effect of ventilation on arterial P CO2) intersect. This is where the body wants arterial P CO2 and minute ventilation to be in homeostasis (i.e 40 mm Hg and 7.5 L/min)

34
Q

How does H+ concentration in the CSF increase (as detected by central chemoreceptors)?

A

Increased CO2 in the blood means more CO2 crosses the blood brain barrier. In the brain, CO2 reacts with H20 to form H+ and HCO3-. This H+ enters the CSF so the central receptors respond to it

35
Q

Where are peripheral and central chemoreceptors located?

A

Peripheral- aortic and carotid bodies

Central- near the DRG and VRG in the medulla

36
Q

What is the mechanism by which peripheral chemoreceptors tell the CPG about hypoxia?

A

Type I gloms cells sense a decreased arteriolar P O2. This causes inhibition of K+ ion channels and membrane depolarization. This opens voltage-gated Ca2+ channels. Ca2+ enters the cell and causes vesicle fusion and neurotransmitter release. The neurotransmitter binds to a neuron (Cr. IX or X) and triggers an AP which tells the CPG what’s up

37
Q

How does the body respond to hypoxia if the peripheral chemoreceptors were cut?

A

Ventilation would actually decrease, probably b/c lack of O2 is toxic for brain function (i.e. in the CPG)

38
Q

What type of a system is the chemoreceptor response?

A

A negative feedback system

39
Q

Is ventilation greater at the base or apex of the lungs? How about perfusion (blood flow)? Why?

A

Both are greater at the base of the lungs
Ventilation- Ppl is less (-) at the base so alveoli are collapsed so they have greater compliance (greater change in Vol for given change in P) and will fill with air preferentially
Flow- less resistance at the base of the lung b/c Pvenous > Palv so no collapsed capillaries

40
Q

Does gravity have a greater effect on ventilation or blood flow?

A

Flow. It’s about 6x greater at the base of the lung. Ventilation is only about 50% greater

41
Q

What pathologies lie at normal ends of the spectrum of V/Q ratios?

A

Very high V/Q- ventilation without perfusion- alveolar dead space (ADS)
Very low V/Q- perfusion without ventilation- shunt flow

42
Q

What does the blood gas composition for shunt flow resemble? What about the air gas composition for ADS?

A

Shunt- blood gasses look like venous gasses

ADS- alveolar gasses look like inspired air

43
Q

What does a V/Q scan look like in a normal subject? How does that change with age?

A

Most ventilation and perfusion occur where V/Q=1. Both V and Q curves are bell curves around V/Q=1
In older individuals, the bell curves widen b/c there is more heterogeneity in the lungs so some ADS and some shunt flow are normal. This is b/c of increased compliance of the lungs

44
Q

What is a normal A-a (alveolar-arterial) gradient? What about a normal Hb level? Normal Hb-CO?

A

Aa gradient- About 5 mm Hg
Hb- about 15%
Hb-CO- up to 1%

45
Q

Describe the blood gas composition and Aa gradient for inspiratory hypoxia such as at high altitude. Does O2 therapy help?

A

Decreased alveolar PO2 with normal Aa gradient so decreased end cap and arterial PO2. O2 therapy helps

46
Q

Describe the blood gas composition and Aa gradient for a diffusion problem such as pulmonary edema. Does O2 therapy help?

A

Alveolar PO2 is normal but the Aa gradient is increased at the level of the capillaries b/c some does not make it into the capillaries (decreased end cap and arterial PO2). O2 therapy helps

47
Q

Describe the blood gas composition and Aa gradient for a R to L shunt. Does O2 therapy help?

A

Alveolar PO2 and end capillary PO2 are normal but b/c of the shunt, the Aa gradient is increased at the level of shunt admixture and arterial PO2 is decreased. O2 therapy will not help

48
Q

Describe the blood gas composition and Aa gradient for alveolar dead space. Does O2 therapy help?

A

Dead space alveolar air has greater PO2 than normal so the functional alveoli have decreased PO2. This means that end capillary and arterial PO2 are also decreased. The Aa gradient is normal but appears increased b/c alveolar PO2 is measured via an end tidal sample (which is elevated in the pt). O2 therapy will help

49
Q

When does O2 therapy not help?

A

Shunt flow, anemia, congestive heart failure/stagnant hypoxia, histotoxic hypoxia (some tissue died)

Physiology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions