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Med-Surg > Determinants and Assessment of Pulmonary Function > Flashcards

Determinants and Assessment of Pulmonary Function Flashcards

1
Q

What does the surfactant layer consist of and what does it do?

A

Type 2 cells secrete surfactant which is a lipoprotein that lines the inner wall of alveoli, reducing surface tension to precent alveolar collapse. SURFACTANT KEEPS ALVEOLI OPEN

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2
Q

What is anaerobic metabolism?

A

The making of energy (glucose) in an environment absent of O2

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3
Q

What happens to our muscles when anaerobic metabolism occurs?

A

Our muscles get sore because there is not enough air which leads to lactic acid build up

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4
Q

Define Ventillation

A

It is the actual work of breathing and movement of air from outside to inside the lung tissues. (the amount go gas reaching alveoli)

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5
Q

Define Diffusion

A

Exchange of gases at the alveolar membrane

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6
Q

Define Perfusion

A

Pumping of blood to organs and tissues, systemic and pulmonary systems. (the blood flow in pulmonary capillaries)

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7
Q

What are the 3 determinants of O2 status?

A

PaO2, SaO2, Hemoglobin

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8
Q

What is PAO2

A

partial pressure of oxygen in alveoli
normal range 100-105 mmHg

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9
Q

What is PaO2

A

partial pressure of O2 dissolved in arterial blood
normal range 75-100 mmHg

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10
Q

What is PvO2

A

partial pressure of O2 dissolved in venous blood
normal range 40 mmHg

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11
Q

What is tidal volume

A

amount of air that moves in and out of lungs with each normal breath

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12
Q

What is vital capacity

A

maximum amount of air expired after a maximal inspiration

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13
Q

What is SaO2

A

O2 saturation; the measure of the % of O2 combined with hemoglobin

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14
Q

Why is SaO2 important

A

degree of saturation is important in determining amount of O2 available for delivery to tissues

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15
Q

What is hemoglobin

A

major carrier of O2 in blood and an important factor in tissue oxygenation - composed of protein and heme and a major component of RBC

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16
Q

What is the normal range for hemoglobin?

A

females 12-15 g/dL
males 13.5-17 g/dL

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17
Q

What does abnormally low hemoglobin indicate?

A

that tissue perfusion is also low

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18
Q

In the oxyhemoglobin dissociation curve what is a left shift?

A
  • alkalosis; increase pH, decrease PaCO2 (hypocapnia)
  • increased affinity to hmg in O2; in lungs hmg binds to O2
  • at tissues hmg does not readily release O2
  • ABG increased SaO2, O2 sat increased, increased SvO2
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19
Q

In the oxyhemoglobin dissociation curve what is a right shift?

A
  • acidosis; decrease pH, increased PaCo2 (hypercapnia)
  • decreased affinity of hmg for O2; in lungs hmg does not easily bind with O2
  • at tissues hmg readily releases O2
  • ABG decreased SaO2, decreased SpO2, decreased SvO2
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20
Q

Pulmonary Vascular Resistance

A

measures the resistance to blood flow in pulmonary vascular system, a low-resistance system

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21
Q

What 3 main factors determine pulmonary resistance

A

length of vessels
radius of vessels
viscosity

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22
Q

Cor Pulmonae

A

R ventricular hypertrophy and dilation secondary to pulmonary disease - is a complication of both restrictive and obstructive pulmonary diseases

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23
Q

Oxygenation occurs as a result of what 3 processes

A

O2 intake
O2 delivery
use of O2 for metabolic processes

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24
Q

what is the VQ ratio

A

ventilation (v) must match perfusion (Q)

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25
Q

What happens when VQ ratio is mismatched

A

impaired gas exchange

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26
Q

Why is nutritional history important when assessing respiratory system

A

malnutrition can contribute to developing respiratory failure

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27
Q

where do you hear vesicular sounds on auscultation

A

peripheral fields

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28
Q

where do you hear bronchial sounds on auscultation

A

trachea and larynx

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29
Q

where do you hear bronchovesicular sounds on auscultation

A

all lobes near major airways

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30
Q

What is orthopnea

A

state in which pt assumes a head up position to relieve dyspnea

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31
Q

Difference between cardiogenic pain and pleuritic chest pain

A

Cardiogenic pain is unaffected by breathing, pleuritic pain is sharp pains on inhalation

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32
Q

What is capnography

A

noninvasive measurement of CO2 concentration in expired gases

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33
Q

Arterial Blood Gases

A

provide valuable information on pts acid-base and oxygenation status

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34
Q

Kidney function

A

is a slow but powerful response

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35
Q

Lung function

A

is a rapid but limited response

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36
Q

normal pH

A

7.35-7.45

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37
Q

normal PaCO2

A

35-45

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38
Q

normal HCO3

A

24-28

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39
Q

normal PaO2

A

80-100

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40
Q

normal SaO2

A

greater than 95%

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41
Q

Compensation occurs when

A

another value is outside its normal range

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42
Q

No compensation occurs when

A

other value is within normal range

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43
Q

buffer systems prevent

A

major changes in H+

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44
Q

in respiratory/metabolic acidosis increased ____ is attempt to get rid of _____

A

respiration; CO2

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45
Q

in respiratory/metabolic alkalosis decreased ___ is to retain _____

A

respirations; CO2

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46
Q

kidneys regulate ____ level in ECF

A

HCO3-

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47
Q

in respiratory/metabolic acidosis the kidneys

A

excrete hydrogen ions and conserve HCO3 to restore balance

48
Q

in respiratory/metabolic alkalosis the kidneys

A

retain hydrogen ions and excrete HCO3 ions to restore balance

49
Q

uncompensated =

A

abnormal pH with one abnormal value and one normal value

50
Q

partially compensated =

A

abnormal pH with 2 abnormal values

51
Q

compensated (chronic) =

A

normal pH with 2 abnormal values

52
Q

corrected =

A

normal pH and 2 normal values. No acid-base disturbance currently exists

53
Q

common causes of acute respiratory acidosis

A

respiratory depression, decreased ventilation, altered diffusion/ventilation/perfusion mismatch

54
Q

restrictive pulmonary disease =

A

reduced total lung capacity

55
Q

obstructive pulmonary disease

A

air moves in and out at reduced rate

56
Q

pneumonia arises from

A

micro-aspiration of colonized organisms in the upper airway

57
Q

pneumonia infection results in

A

pulmonary inflammation -> congestion

58
Q

red hepatization of pneumonia

A

blood vessels and capillaries dilate and fill with exudate and organisms

59
Q

grey hepatization of pneumonia

A

blood flow decreases and leukocytes and fibrin consolidate

60
Q

resolution of pneumonia

A

exudate becomes lysed and macrophages clean up

61
Q

consolidation in grey hepatization means

A

worsening, not a bad things but shown progression

62
Q

signs and symptoms of pneumonia

A

cough, fever, pleuritic chest pain, weight loss, muscle aches and pains, fatigue, decreased air entry, hemoptysis, night sweats, crackles/congestion on auscultation

63
Q

goals in pneumonia pt

A

improve gas exchange and improve airway patency

64
Q

clinical manifestations of restrictive pulmonary disorders

A

increased resp rate, decrease tidal volume, SOB, cough, chest pain/discomfort, fatigue, history of weight loss

65
Q

types of COPD

A

emphysema, chronic bronchitis, cystic fibrosis, asthma

66
Q

pathophysiology of obstructive disorders (COPD)

A

air is able to flow into lungs but then becomes trapped, difficult to exhale so air moves in and out at a decreased rate

67
Q

respiratory insufficiency

A

maintains oxygenation, acid base imbalance persists, normal pH + increased PaCO2 and increased HCO3 = compensated respiratory acidosis
- live with impeding respiratory failure

68
Q

COPD is characterized by

A

exacerbations caused by triggers

69
Q

clinical features of obstructive pulmonary disorders (COPD)

A

bronchospasm, bronchoconstriction, airway obstruction

70
Q

physical findings of obstructive pulmonary disorders (COPD)

A

diminished breath sounds (often related to pneumonia), increased accessory muscle use, rhonchi, wheezes, prolonged expiration, increased sputum production, pursed lip breathing, cough, crackles not cleared by coughing and deep breathing

71
Q

COPD treatment is aimed at

A

(1) improving airway obstruction
(2) providing relief of symptoms
(3) modifying or preventing exacerbations
(4) altering disease progression

72
Q

using O2 therapy in pts with COPD increases risk for

A

hypoxemia

73
Q

pharmacotherapy for pulmonary disorders

A

beta 2 agonsits, anti cholinergic bronchodilators, corticosteroids, mucolytics, pulmonary vasodilators

74
Q

NPPV is

A

noninvasive positive pressure ventilation

75
Q

what is NPPV for

A

reduces intubation, used in exacerbations and ICU setting

76
Q

BREATH AIR acronym

A

Bronchospasm
Rales
Effusions
Airway obstruction
Thick secretions
Hemoglobin (low)

Anxiety
Interpersonal issues
Religious concerns

77
Q

external respiration

A

bulk flow of air into and out of the lungs

78
Q

internal respiration

A

capillary gas exchange in body tissues

79
Q

alveolar gas exchange

A
  1. surface area
  2. partial pressure gradient of gases
  3. matching of ventilation and perfusion
80
Q

in emphysema alveoli are ____________, surface area is _______, and ________ _________

A

gradually reduced; reduced; diffusion decreases

81
Q

gas exchange in lungs happens at the

A

alveoli-capillary membrane

82
Q

alveoli-capillary membrane has a large surface area for

A

efficient gas exchange

83
Q

ARDS is

A

acute respiratory distress syndrome aka acute lung injury

84
Q

pathophysiology of ARDS

A

widespread damage to alveolar capillary membrane causes widespread inflammatory event, can be fatal

85
Q

acute respiratory failure

A

cardiopulmonary system fails to maintain gas exchange
- oxygenation failure and ventilation failure

86
Q

ARDS can affect all organs because of

A

hypoxemia

87
Q

if ARDS is accompanied by decreased CO2 it can lead to

A

hypoperfusion and shock

88
Q

ventilatory failure can result in

A

hypercapnia and respiratory acidosis

89
Q

ARDS can be ____ stage of someone with COPD and/or penumonia

A

end stage

90
Q

clinical manifestations of pt in respiratory failure

A

cyanotic, pallor, high resps, breath sounds diminished, high BP, high pulse, increased temp (due to infection), CXR would show consolidation

91
Q

acute respiratory failure =

A

oxygenation failure

92
Q

in acute respiratory failure PO2 is less than

A

60

93
Q

CO2 can diffuse ____ times faster than O2

A

20 times

94
Q

acute respiratory failure causes

A

acute respiratory acidosis, alveolar hypoventilation, build up of CO2

95
Q

complications of respiratory failure

A

oxygenation failure and ventilation failure

96
Q

oxygenation failure

A

organ hypoxia, hypoperfusion/hypoxic organ

97
Q

ventilation failure

A

severe hypercapnia, severe respiratory acidosis

98
Q

pulmonary embolism

A

large thrombi obstructs perfusion in the pt artery or its branches

99
Q

small PE

A

may be asymptomatic

100
Q

large PE

A

lodge in main pulmonary artery - severe, immediate symptoms

101
Q

may have several ____________ cause obstruction of multiple tiny pulmonary vessels

A

micro-emboli

102
Q

blockage in pulmonary artery causes

A

increased pulmonary pressure, increased resistance to blood flow in right ventricle = increased R ventricle workload and decreased lung perfusion

103
Q

if R ventricle cannot pump against the pressure

A

right heart failure occurs

104
Q

inflammatory response is

A

increased neutrophils and increased platelet activating factors (clots)

105
Q

manifestations of pulmonary embolism

A

hypotension, hypoxemia, SOB, dyspnea, wheezing, pleuritic pain, orthopnea

106
Q

common outcome of pulmonary embolism

A

impaired gas exchange

107
Q

___% of those with a PE have pre-existing confirmed DVT

A

44%

108
Q

types of emboli

A

thromboembolism, fat embolism, amniotic, venous air embolism

109
Q

thromboembolism

A
110
Q

fat embolism

A
111
Q

amniotic

A
112
Q

venous air embolism

A
113
Q

more than 80% if PE originates as DVT in the ___ ______

A

lower extremities

114
Q

management of PE includes

A

anticoagulant therapy, vena cava filter, thromboembolytic therapy, embolectomy

115
Q

ABGs for PE would look like

A

low PaO2 and low PCO2 because no exchange of CO2 and/or O2 happens

116
Q

catheter directed thrombolysis

A

thrombolytic agent is administered directly into the pulmonary artery via a pulmonary artery catheter, the usual thrombolytic agent is full dose heparin

Med-Surg (16 decks)

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