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SRNAAnatomy II > Exam 4 Review New > Flashcards

Exam 4 Review New Flashcards

1
Q

Alveolar PO2 alveolar

A

104 mmHg

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2
Q

Alveolar PCO2 alveolar

A

40 mmHg

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3
Q

Inspired Air PO2

A

159 mmHg

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4
Q

Inspired Air CO2

A

0.3 mmhg

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5
Q

Expired Air PO2

A

127 mmHg

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6
Q

Expired Air PCO2

A

28 mmHg

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7
Q

Tissues PO2

A

40 mmHg

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8
Q

Tissue PCO2

A

46 mmHg

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9
Q

From Heart and systemic Circulation PO2

A

40 mmHg

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10
Q

From Heart and systemic Circulation CO2

A

46 mmHg

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11
Q

To Heart and systemic Circulation PO2

A

100 mmHg

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12
Q

To Heart and systemic Circulation CO2

A

40 mmHg

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13
Q

Calculating VE = minute ventilation (volume per minute) Example:

A

VE = vT x f = 500 x 10 = 5000 ml/min.

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14
Q

VE=

A

tidal volume (volume per breath) x frequency or RR (Respiratory Rate)

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15
Q

VA =Alveolar ventilation

A

VA= (VT – vDS) x RR

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16
Q

VDS = and Example

A

physiologic dead space ~ 1ml per pound ideal body wgt 150 lbs patient VA = (VT–vDS ) x RR = (500 – 150) x 10 = 3500 ml/min.

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17
Q

Tests of Ventilatory Capacity: • DLCO –

A

tests diffusing capacity of the alveolar-capillary membrane

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18
Q

FEV

A

(Forced Expiratory Volume)

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19
Q

FVC (Forced Vital Capacity) –

A

Assesses progression of lung disease – Assesses efficacy of bronchodilators

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20
Q

FEF (Forced Expiratory Flow) –

A

Assesses average flow rate

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21
Q

Single-breath Nitrogen Test –

A

Assess dead space & presence of small airway disease

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22
Q

FRC (functional residual capacity) is the

A

volume remaining in the lungs at the end of a normal tidal expiration

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23
Q

Forced Expiratory Volume – • Written as FEV1

A

The vol. of gas exhaled in 1 sec. by a forced expiration from full inspiration.

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24
Q

Normal ratio of FEV1 to FVC =

A

80% (decreases w/age)

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25
Q

FEF25-75%

A

• The middle half (by volume) of total expiration

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26
Q

Single-breath Nitrogen Test • Can be used to calculate

A

deadspace and assess for early lung disease in the small airways.

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27
Q

Explain single breath nitrogen Test

A

• Pt. takes a vital capacity breath of 100% O2, then exhales slowly through mouthpiece w/ N2 sensor.

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28
Q

Single-breath Nitrogen Test: Phase 1:

A

Pure O2 exhaled, [N]=0

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29
Q

Single-breath Nitrogen Test Phase 2

A

Phase 2: [N]↑ as deadspace washed out by alveloar air.

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30
Q

Single-breath Nitrogen Test Phase 3:

A

alveolar plateau – nearly flat in normal patients; steeper slope in lung disease.

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31
Q

Single-breath Nitrogen Test Phase 4:

A

↑ as least ventilated areas of lungs empty (more N b/c little or none of the 100% O2 reached these areas in the previous inspiration, Little dilution)

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32
Q

Single-breath Nitrogen Test

A

Slopes in Phase 3 and 4 are steeper in uneven ventilation 2o to disease (and age).

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33
Q

3 possible mechanisms of uneven ventilation:

A

Partial obstruction “parallel” ex. asthma

Dilation (↓diffusion) “series” ex. ex. emphysema

Complete obstruction “collateral” ex. COPD

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34
Q

Emphysema

A

• Destruction of alveolar walls and lung elastin by neutrophil elastase, with dilation of airways distal to terminal bronchioles.

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35
Q

Partial capillary bed destruction =

A

V/Q mismatch =dead space & pulmonary HTN

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36
Q

↓ surface area =

A

↓diffusing capacity, ↓ gas exchange

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37
Q

Pink puffers ” • Non productive cough

A

PO2 normal ∴“pink” no cyanosis

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38
Q

PInk puffers lung

A

• Have decreased lung elastic recoil

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39
Q

Pink puffers: What causes air trapping?

A

Air trapping is caused by loss of normal dynamic compression ∴ pursed lips as patients learn that prolonging expiration phase keeps the airways open slightly longer

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40
Q

Pink puffers: Tachypnea gives appears of a

A

“puffing”

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41
Q

Pink puffers Complications of emphysema: –

A

Pneumothorax 2o to ruptured bullae – Weight loss 2o to ↑ work of breathing

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42
Q

Emphysema Signs/Symptoms: Lung Decreased values

A

• FEV1 , FVC, FEV/FVC%, FEF25-75% all decreased

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43
Q

Emphysema Signs/Symptoms:

A

• Barrel chest , dyspnea, weight loss, ↓breath sounds

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44
Q

CXR –> with EMPHYSEMA there is

A

CXR: Hyperinflation Hyperlucency Low set flat diaphragm Vertical heart

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45
Q

Lateral CXR What do you see ?

A

Normal vs. Emphysema • Increased retrosternal clear space & kyphosis

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46
Q

Chronic Bronchitis

A

• Too much mucus 2o to↑ irritants – Smoking/Pollution/coal/asbestos/allergens/genetic – Smoking also destroys cilia, compromising mucociliary escalator

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47
Q

Chronic Bronchitis there is

A

↑ airway resistance

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48
Q

• Air trapping

A

↑TLC secondary to mucus plugs

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49
Q

In chronic bronchitis there is ↑ barrier thickening =

A

↓ gas exchange

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50
Q

Chronic Bronchitis and Smooth muscle bronchospasm

A

Smooth muscle bronchospasm 2o to inflammation

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51
Q

Diagnosis of Bronchitis

A

• Dx: 3 mo. x 2 yrs.

52
Q

In Chronic bronchitis, Bronchial lumen narrowed 2o to: –

A

Excessive mucus (infection can occur behind mucus plugs) – Thickened wall • smooth muscle spasm • Hypertrophy & hyperplasia of mucus glands

53
Q

Chronic Bronchitis and– Reid index

A

Reid index = ratio of mucus glands to thickness of wall • Normal < 40% in CB >40%

54
Q

“Blue Bloater” (Type B COPD) • Frequently obese

A

• Cyanosis “blue” discoloration • Hypoxia/Hypercapnia/Dyspnea • JVD

55
Q

Blue Bloater cough

A

• Chronic productive cough • Purulent sputum

56
Q

Complications of CB:

A

– Polycythemia 2o to hypoxemia – Plumonary HTN 2o to hypoxic vasoconstriction – Cor pulmonale 2o to chronic pulm. HTN

57
Q

Chronic Bronchitis

A

• FEV1 , FVC, FEV/FVC%, FEF25-75% all decreased

58
Q

Sign/Symptoms Chronic Bronchitis

A

• Cyanosis, hypoxia, dyspnea • Rales & ronchi • Chronic productive cough 3mo. x 2yrs.

59
Q

Chronic Bronchitis • Other tests:

A

– PFT – HRCT – Sputum exam

60
Q

Pulmonary Fibrosis there is ______Resulting in _______compliance

A

• Thickening of alveolar wall = ↓ compliance

61
Q

Exact cause of Pulmonary Fibrosis

A

Unknown

62
Q

Pulmonary Fibrosis is due to repeated ________causing______

A

• Repeated exposure to irritant causes abnormal repair response with scarring

63
Q

Can cause pulmonary Fibrosis (SEGIV)

A

– Smoking – Environmental dust exposure – GERD – Industrial oxidants – Viral infections

64
Q

Pulmonary Fibrosis, alveolar cells • • Uncontrolled, dysregulated deposition of extracellular matrix = thickened, stiffened fibrosis

A

• Alveolar cells injured

65
Q

Release profibrotic & inflammatory mediators:– TNF-α

A

– recruit inflammatory cells

66
Q

Release profibrotic & inflammatory mediators– TGF-β

A

stim. migration & proliferation of . migration & proliferation of fibroblasts

67
Q

Release profibrotic & inflammatory mediators–

A

Growth factors stim. migration of myofibroblasts

68
Q

Mediators Organize into

A

clusters called fibroblastic foci

69
Q

Uncontrolled, dysregulated

A

deposition of extracellular matrix = thickened, stiffened fibrosis

70
Q

Pulmonary Fibrosis: airway

A

• Excessive radial traction increases airway caliber

71
Q

Pulmonary Fibrosis Clinical Manifestations

A

Clinical Manifestations • Affects adults 50s-60s • Dyspnea on exertion • Tachypnea with small TVs • Nonproductive cough

72
Q

Lung Volumes changes in Pulmonary FIbrosis

A

• FVC ↓↓↓ • FEV1 normal to low • FEV/FVC%↑ • TLC & FRC ↓↓↓

73
Q

Pulmonary Fibrosis • CXR: RHL

A

Reticulonodular pattern, especially at the bases Honeycomb appearance in late ds. Lungs typically small, w/ raised diaphragms

74
Q

Pneumothorax

A

Penetrating chest wound or ruptured bleb allows air in P.C. = passive recoil of lung away from chest wall

75
Q

Spontaneous Pneumothorax: common

A

Most common form

76
Q

Spontaneous Pneumothorax: small bleb

A

Rupture of small bleb on surface near apex

77
Q

Spontaneous pneumothorax typically occurs in

A

Typically occurs in young males

78
Q

Spontaneous pneumothorax related to

A

Related to high mechanical stresses in upper zone of upright lung – Presents with sudden pain & dyspnea

79
Q

Tension Pneumothorax

A

• Occurs when the defect acts as a one-way valve • Air enters pleural space on inspiration but cannot be expelled on expiration

80
Q

What happens in spontaneous pneumothorax

A

Air entrained with each breath –Increasing pressure causes compression of contralateral lung and Decrease venous return

81
Q

Tension Pneumothorax occurs

A

↓ ↓ venous return – Surgical Emergency

82
Q

Pulmonary Edema: Pathogenesis

A

• Increased Capillary Permeability • High Permeability Edema (High K) • High Protein & RBCs

83
Q

Pulmonary Edema Caused by

A

– Inhalation injury – toxins, oxygen poisoning – Circulating factors – inflammatory mediators, endotoxins – ARDS

84
Q

Pulmonary Edema: Pathogenesis Intersitital Hydrostatic pressure

A

• Decreased Interstitial Hydrostatic Pressure • (Low Pi) “Negative Pressure Pulmonary Edema”

85
Q

Pulmonary Edema Caused by:

A

-reexpansion injury: may also damage capillaries

86
Q

Pulmonary Edema Caused by: Oncotic

A

• Decreased Plasma Oncotic Pressure • (Low πc) • Caused by: overtransfusion leading to hypoalbuminemia

87
Q

Pulmonary Edema: Pathogenesis

A

• Reduced Lymphatic Drainage • Normally handles ~ 20ml/hr

88
Q

Reduce lymphatic drainage Caused by:

A

Obstruction, Tumor, Iatrogenic, Increased CVP • Interferes with drainage of thoracic duct

89
Q

Pulmonary Edema Pathogenesis

A

Increased Capillary Permeability Decreased Interstitial Hydrostatic Pressure Decreased Plasma Oncotic Pressure Reduced Lymphatic Drainage

90
Q

Pulmonary Edema : LVEDP

A

• Increased LV EDP – HF

91
Q

Most common cause of pulmonary HTN

A

Pulmonary HTN • Increased Pulmonary Vascular Resistance • Most common cause

92
Q

Three categories of pulmonary HTN Vasoconstrictive

A

Three categories: – • Ex. Hypoxia @ high altitude – Obstructive • Ex. thromboembolism – Obliterative • Ex. Destroyed capillary bed in emphysema

93
Q

Three categories of pulmonary HTN:Obstructive

A

• Ex. thromboembolism

94
Q

Three categories of pulmonary HTN: Obliterative

A

• Ex. Destroyed capillary bed in emphysema

95
Q

CO (carbon monoxide) – Binds to Hb =

A

with 200x the affinity of O2

96
Q

CO– Increases O2 affinity of remaining Hb

A

does not release O2 readily to the tissues – dissociation curve shifted to the Left

97
Q

CO no change

A

– No change in PaO2

98
Q

CO poisoning and O2 partial pressure

A

Oxygen partial pressure in the blood remains unchanged by CO poisoning (No cyanosis, no tachypnea)

99
Q

CO is Dx by

A

measuring carboxyhemoglobin levels AND index of suspicion

100
Q

Tx of CO

A

– Tx: 100% FiO2

101
Q

Cigarette Smoking • Impaction

A

– Largest particles strike mucus surfaces, become trapped

102
Q

Cigarette Smoking • Sedimentation

A

– Smoke particles settle in terminal & respiratory bronchioles, unlike gases, cannot diffuse to alvolar wall

103
Q

Deposition of Particle Inhalation: Inhaled particles deposited in airways, mechanism based on

A

particle size

104
Q

Impaction

A

large particles > 5 microns filtered by nasopharynx

105
Q

Sedimentation

A

particles 1 to 5 microns deposit in terminal and respiratory bronchioles as laminar flow ceases

106
Q

Diffusion –

A

particles < 0.1 micron, behave almost like gas. Most exhaled, but some deposits in alveoli, may be cleared by alveolar macrophages.

107
Q

Clearance of Deposited Particles Two mechanisms:

A

• Particles deposited in conducting airways cleared by MCE (mucocilliary escalator) & swallowed

108
Q

Particles deposited in gas exchange units cleared by

A

alveolar macrophages (“dust cells”)

109
Q

Clearance of Deposited Particles inhibited By:

A

• Inhibited by: pollution, tobacco, steroids, radiation

110
Q

MCE

A

• Seromucus glands & goblet cells secrete mucus 5-10 microns thick. (Gel top layer more viscous) IgA

111
Q

Cilia sweeps mucus

A

~ 1mm/min in bronchioles; 2cm/min in trachea. Total clearance q 24 hrs.

112
Q

ResFailure - Hypoxemia • “Normal” PaO2 calculation on

A

102 - 0.33 × age

113
Q

RF Signs/Symptoms:

A

– ↓ PaO2 – Cyanosis – Tachycardia – Mental confusion

114
Q

Tissue Hypoxia – vulnerability depends –

A

on tissue

115
Q

Most vulnerable

A

CNS & Myocardium

116
Q

Cessation of blood flow to cerebral cortex: • 4-6 sec

A

loss of function

117
Q

Cessation of blood flow to cerebral cortex: 10-20 sec. =

A

l.o.c.

118
Q

Cessation of blood flow to cerebral cortex 3-5 min. =

A

irreversible damage

119
Q

Hypercapnia

A

• ⇑Work of breathing

120
Q

Hypercapnia CNS receptor desensitization,

A

permissive hypercapnia

121
Q

Hypercapnia renal compensation

A

( for ↑ H2CO3 - )

122
Q

CNS desensitization from chronic hypercapnia →

A

dependency on hypoxic respiratory drive

123
Q

Hypercapnia Treatment with O2 could suppress

A

hypoxic drive and increase CO2 retention/acidosis

124
Q

Hypercapnia Answer is to give__________

A

low concentration (24-48% O2)

125
Q

Hypercapnia, monitor this

A

monitor ABGs frequently to determine whether depression of ventilation is occurring.

126
Q

The mucous film consists of a

A

superficial gel layer that traps inhaled particles and a deeper layer so it is propelled by cilia

SRNAAnatomy II (16 decks)

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