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Cardiovascular and Pulmonary > Pulmonary Physiology 4 > Flashcards

Pulmonary Physiology 4 Flashcards

1
Q

SNS stimulation (via epi or norepi), histamine, alveolar hypoxia, alveolar hypercapnia, and decreased pH of venous blood all have what affect on PVR?

A

Increase PVR

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2
Q

Appear to exert much more control over pulmonary vasoconstriction than the SNS

A

Local mediators

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3
Q

What decreases PVR?

A

Upregulation of PNS tone, ACh, selective B2-adrenergic agonists, NO, and bradykinin

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4
Q

Shunts mixed venous blood from poorly ventilated sectors of the lung to those which are better ventilated

A

Hypoxic Vasoconstriction

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5
Q

Can result from alveolar hypoxia, atelectasis, or can be a local response that is controlled by vasoactive mediators

A

Hypoxic vasoconstriction

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6
Q

Decreased or absent air in all or parts of the lung

A

Atelectasis

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7
Q

Hypoxic vasoconstriction can be a local response controlled by vasoactive mediators such as

A

Histamine, catelcholamines, and certain prostaglandins

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8
Q

Hypoxia sets forth a cellular response, whereby outward K+ current is impeded in

A

Pulmonary vascular smooth muscle

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9
Q

This induces depolarization of vascular smooth muscle cells which causes subsequent

A

Ca2+ influx leading to contraction

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10
Q

In order for alveolar O2-CO2 exchange to meet metabolic demands, what must be matched?

A

Perfusion and ventilation

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11
Q

PaO2 and PaCO2 are dependent on

A

PAO2 and PACO2

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12
Q

PAO2 and PACO2 are influenced by the

A

V/Q ratio

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13
Q

An elevated V/Q (i.e. more ventilation than perfusion) in an alveolar capillary unit causes

A

Increased PAO2 and decreased PACO2

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14
Q

Elevated V/Q causes increased PAO2 and decreased PACO2. All other things equal, this would enable elevated

A

Oxygenation of blood

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15
Q

A lower V/Q will result in

A
  1. ) Decreased PAO2
  2. ) PACO2 close to that of mixed venous blood
  3. ) Reduced oxygenation of bloo
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16
Q

If severe enough, V/Q mismatching can result in the development of a

A

Shunt-like state

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17
Q

Approximately 2-5% of cardiac output returns to the left heart without encountering alveoli (via bronchial, pleural, or thesbian veins). This accounts for the

A

Normal anatomic shunt

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18
Q

Intrapulmonary shunts occur when there are V/Q mismatches. These include

A

Absolute shunts and shunt-like states

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19
Q

An ABSOLUTE shunt develops when there are

-no blood oxygenation occurs in these regions

A

Perfused but non-ventilated alveoli

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20
Q

In extreme cases, V/Q in non-ventilated regions equals

A

Zero

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21
Q

This can result from complete airway obstruction resulting in the equilibration of alveolar pressure with that of

A

Mixed venous blood

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22
Q

Result from alveolar-capillary units which have some degree of ventilation and perfusion that is below normal

A

Shunt-like states

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23
Q

Lead to a low V/Q

A

Shunt-like states

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24
Q

A High V/Q will form in regions with

A

Some ventilation but no perfusion

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25
Q

Non-perfused regions are referred to as

A

Alveolar dead space

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26
Q

In non-perfused but ventilated alveolar capillary units

  1. ) PAO2 is
  2. ) PACO2 is
A
  1. ) greater than 100 mmHg

2. ) 0

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27
Q

If sufficient shunting occurs, PaO2 and thus PaCO2 will be

A

Decreased

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28
Q

In the case of very poorly or non-ventilated alveoli, increasing FiO2 does not significantly impro the decreased

A

PaO2

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29
Q

What is better perfused and ventilated, the base of the lung or the apex?

A

Base

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30
Q

Blood pressure is greater at the lung base due to

A

Local mediators and gravity

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31
Q

Alveoli are smaller at the base of the lung, however, they are more

A

Compliant

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32
Q

Is the V/Q higher at the lung apex or the lung base?

A

Apex

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33
Q

Therefore, the apex has what characteristics?

A

Higher PAO2 and lower PACO2 than the base

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34
Q

In the apex of the lung, the:

  1. ) O2 content is
  2. ) CO2 content is
A
  1. ) Higher

2. ) Lower

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35
Q

However, more gas exchange occures in the

A

Base

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36
Q

Intravascular pressure is lower at the

A

Apex

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37
Q

Thus, the apex undergoes less recruitment and distension of blood vessels which leads to greater resistance to

A

Blood Flow

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38
Q

Although there is a more negative intrapleural pressure at the apex, the alveoli are

A

Larger and less compliant

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39
Q

This results in less ventilation in the apex than in the

A

Base

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40
Q

TO summarize, the V/Q ratio rises dramatically from the

A

Base to the apex

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41
Q

The major difference in the V/Q ratio between the base and the apex is due to their differences in

A

Perfusion (Q)

42
Q

A healthy resting mean pulmonary arterial pressure is around

A

12-15 mmHg

43
Q

Occurs when pulmonary blood pressure rises to levels that are inappropriate for a given cardiac output

A

Pulmonary HTN

44
Q

A rare disease which occurs in the absence of other heart and lung pathologies.

-More prevalent in younger women than men

A

Idiopathic (primary) pulmonary HTN

45
Q

Idiopathic (primary) pulmonary HTN usually leads to death within

A

2-8 years

46
Q

rise from left-right intracardial shunts, increased PVR, occlusive/thromboembolic diseases, and elevated LAP

A

Secondary Pulmonary HTN

47
Q

Cause a chronic increase in pulmonary blood flow

A

Left-right intracardial shunts

48
Q

Burdened in the case of pulmonary HTN

A

Right Ventricle

49
Q

Physical forces within the lumen and intersitium that will determine which direction fluid will move

A

Starling Forces

50
Q

Shows how filtration is regulated by the relationships between hydrostatic and oncotic pressures in the capillaries and intersitium

A

Starling Equation

51
Q

What are the four main Starling forces?

A
  1. ) Capillary pressure (Pc)
  2. ) Interstitial fluid pressure (Pi)
  3. ) Plasma colloid osmotic pressure (Or Oncotic pressure PIc)
  4. ) Interstitial colloid osmotic pressure (PIi)
52
Q

Colloid osmotic pressure is caused by the concentration of proteins, namely

A

Albumin

53
Q

High colloid osmotic pressure tends to draw fluid

A

IN to the cappilaries (results in increased reabsorption of H2O)

54
Q

At the entrance to the capillary network (arterial feed), forces cause a net outward movement of fluid. This net outward movement is known as

A

Filtration

55
Q

Wht are the characteristics of the forces in the arterial feed of the capillaries?

A
  1. ) Pc is high
  2. ) Pi is negative
  3. ) PIc is robust
  4. ) PIi is modest
56
Q

Occurs primarily at the arterial feed of a capillary network

A

Filtration

57
Q

At the venous end of the capillary network, what is the characteristic of the starling forces?

A

PIc is larger than the other 3 and so reabsorption occurs

58
Q

When considering the mean net force of the capillary network, a general trend favors

A

Filtration

59
Q

This concept of net filtration over absorption is referred to as the

A

Starling equilibrium

60
Q

Designed to drain away the fluid accumulation that would occur due to the net filtration which occurs in the capillary beds

A

Lymphatic system

61
Q

The capillary endothelium is much more permeable to fluid when compared to the

A

Alveolar membrane

62
Q

First occurs in the interstitium and can migrate to the alveoli if severe enough

A

Pulmonary edema

63
Q

The presence of edema increases the diffusion barrier for O2-CO2 exchange between the

A

Pulmonary capillaries and alveoli

64
Q

Pathologic changes in 1) capillary membrane permeability, 2) capillary hydrostatic pressure, 3) interstitial hydrostatic pressure, 4) blood protein content, and 5) lymphatic vessel structure/function all an lead to

A

Pulmonary edema

65
Q

Can result from one or more pathologies inducing left heart failure; mitral and aortic valve insufficiencies

A

Cardiogenic pulmonary edema

66
Q

The reduction of PaO2

A

Hypoxemia

67
Q

The cellular manifestation of low O2 tensiondue to hypoxemia

A

Hypoxia

68
Q

Decreased atmospheric pressure, decreased inspired fraction of O2, alveolar hypoventilation, V/Q mismatch, shunts, and diffusion impairments all are pathologic mechanisms that can lead to

A

Hypoxemia

69
Q

Recall that in healthy lungs, complete equilibration of gas tensions between ventilated alveoli and capillary blood occurs during

A

Capillary transit time

70
Q

In the event of reduced alveolar ventilation (decreased atmospheric pressure, decreased FiO2, or alveolar hypoventilation), the A-a gradient is preserved since

A

Both PaO2 and PAO2 are low

71
Q

Whereas, the cardiopulmonary causes of hypoxemia (V/Q mismatch, shunt, and diffusion impairment) each result in abnormal

A

A-a gradients

72
Q

Two very common causes of hypoxemia due to V/Q mismatch

A

COPD and Asthma

73
Q

With increased altitude, we see a drop in

A

Ambient PO2

74
Q

The ensuing drop in PaO2 triggers activation of the

A

Peripheral hypoxic drive

75
Q

Activation of the peripheral hypoxic drive raises both

A

Tidal volume and respiratory rate

76
Q

Increased minute ventilation lowers PaCO2, resulting in a

A

Respiratory Alkalosis

77
Q

Hypocapnia in turn dampens the

A

Central ventilatory drive

78
Q

Over days, renal compensation drives the excretion of HCO3- in

A

Urine

79
Q

This moves the pH toward normal and allows the central ventilatory drive to once again turn up the ventilatory rate, thereby increasing

A

PAO2

80
Q

People who live in high altitude environments undergo a

A

Hypoxic desensitization phenomenon

81
Q

Finally, increased production of erythropoietin stimulates polycythemia. This enables

A

Increased O2 delivery to tissues

82
Q

Increased cardiac output is coupled to rise in

A

Tidal volume and alveolar ventilation

83
Q

During intense exercise, minute ventilation can increase from around 5-6 L/min to upwards of

A

150 L/min

84
Q

The limiting factor to the level of exercise a healthy individual can sustain is

A

Cardiac function (NOT pulmonary function)

85
Q

With intense exercise, increased alveolar ventilation results in

A

Lower PACO2 with increased PAO2

86
Q

This lower PACO2 and increased PAO2 results in

A

Raised PaO2, reduced PACO2

87
Q

This elevated tissue O2 uptake increases the

A

Arteriovenous O2 difference (PaO2-PvO2)

88
Q

With increased tidal volume, the work of breathing required to overcome elastic recoil of both lungs and chest wall is

A

Elevated

89
Q

More turbulent airflow and increased dynamic compression of airways also contribute to the increased work of breathing during

A

Exercise

90
Q

While exerciosing, with increased exercise intensity, there is a linear increase in

A

Pulse rate and systolic BP

91
Q

Why does diastolic blood pressure stay stable or maybe even drop during exercise?

A

Production of vasodilators in skeletal muscle

92
Q

The increase in cardiac output is relatively greater than the fall in TPR, thus there is a slight increase in

A

MAP

93
Q

Does mean pulmonary BP rise significantly during intense exercise?

A

No

94
Q

During intense exercise, increased perfusion of previously under-perfused alveolar-capillary units raises

A

DLCO (thereby elevating V/Q)

95
Q

Control of the cardiorespiratory response during exercise is complex. Important control mechanisms include

A

CNS, arterial baroreceptors, arterial chemoreceptors, central venous chemoreceptors, muscle mechanoreceptors, and muscle chemoreceptors

96
Q

Mediated largely through neurons known as class IV unmyelinated C fibers

A

Muscle chemoreceptors

97
Q

During intensive exercise, the act of increased respiratory rate may contribute substantially to the generation of

A

Lactic acid

98
Q

Lactic acid accumulation in muscles causes the release of endorphins in the CNS, which blunts the

A

Respiratory response

99
Q

Blunting the respiratory response limits unnecesary

A

O2 utilization and lactate production

100
Q

Part of a two-fold mechanism that increases venous return during exercise

A

SNS-induced vasoconstriction (especially in splanchnic beds)

Cardiovascular and Pulmonary (25 decks)

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