Exam 4 Review New Flashcards
(126 cards)
1
Q
Alveolar PO2 alveolar
A
104 mmHg
2
Q
Alveolar PCO2 alveolar
A
40 mmHg
3
Q
Inspired Air PO2
A
159 mmHg
4
Q
Inspired Air CO2
A
0.3 mmhg
5
Q
Expired Air PO2
A
127 mmHg
6
Q
Expired Air PCO2
A
28 mmHg
7
Q
Tissues PO2
A
40 mmHg
8
Q
Tissue PCO2
A
46 mmHg
9
Q
From Heart and systemic Circulation PO2
A
40 mmHg
10
Q
From Heart and systemic Circulation CO2
A
46 mmHg
11
Q
To Heart and systemic Circulation PO2
A
100 mmHg
12
Q
To Heart and systemic Circulation CO2
A
40 mmHg
13
Q
Calculating VE = minute ventilation (volume per minute) Example:
A
VE = vT x f = 500 x 10 = 5000 ml/min.
14
Q
VE=
A
tidal volume (volume per breath) x frequency or RR (Respiratory Rate)
15
Q
VA =Alveolar ventilation
A
VA= (VT – vDS) x RR
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.
17
Q
Tests of Ventilatory Capacity: • DLCO –
A
tests diffusing capacity of the alveolar-capillary membrane
18
Q
FEV
A
(Forced Expiratory Volume)
19
Q
FVC (Forced Vital Capacity) –
A
Assesses progression of lung disease – Assesses efficacy of bronchodilators
20
Q
FEF (Forced Expiratory Flow) –
A
Assesses average flow rate
21
Q
Single-breath Nitrogen Test –
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Assess dead space & presence of small airway disease
22
Q
FRC (functional residual capacity) is the
A
volume remaining in the lungs at the end of a normal tidal expiration
23
Q
Forced Expiratory Volume – • Written as FEV1
A
The vol. of gas exhaled in 1 sec. by a forced expiration from full inspiration.
24
Q
Normal ratio of FEV1 to FVC =
A
80% (decreases w/age)
25
FEF25-75%
• The middle half (by volume) of total expiration
26
Single-breath Nitrogen Test • Can be used to calculate
deadspace and assess for early lung disease in the small airways.
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Explain single breath nitrogen Test
• Pt. takes a vital capacity breath of 100% O2, then exhales slowly through mouthpiece w/ N2 sensor.
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Single-breath Nitrogen Test: Phase 1:
Pure O2 exhaled, [N]=0
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Single-breath Nitrogen Test Phase 2
Phase 2: [N]↑ as deadspace washed out by alveloar air.
30
Single-breath Nitrogen Test Phase 3:
alveolar plateau – nearly flat in normal patients; steeper slope in lung disease.
31
Single-breath Nitrogen Test Phase 4:
↑ 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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Single-breath Nitrogen Test
Slopes in Phase 3 and 4 are steeper in uneven ventilation 2o to disease (and age).
33
3 possible mechanisms of uneven ventilation:
Partial obstruction “parallel” ex. asthma
Dilation (↓diffusion) “series” ex. ex. emphysema
Complete obstruction “collateral” ex. COPD
34
Emphysema
• Destruction of alveolar walls and lung elastin by neutrophil elastase, with dilation of airways distal to terminal bronchioles.
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Partial capillary bed destruction =
V/Q mismatch =dead space & pulmonary HTN
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↓ surface area =
↓diffusing capacity, ↓ gas exchange
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Pink puffers ” • Non productive cough
PO2 normal ∴“pink” no cyanosis
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PInk puffers lung
• Have decreased lung elastic recoil
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Pink puffers: What causes air trapping?
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
40
Pink puffers: Tachypnea gives appears of a
“puffing”
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Pink puffers Complications of emphysema: –
Pneumothorax 2o to ruptured bullae – Weight loss 2o to ↑ work of breathing
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Emphysema Signs/Symptoms: Lung Decreased values
• FEV1 , FVC, FEV/FVC%, FEF25-75% all decreased
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Emphysema Signs/Symptoms:
• Barrel chest , dyspnea, weight loss, ↓breath sounds
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CXR --\> with EMPHYSEMA there is
CXR: Hyperinflation Hyperlucency Low set flat diaphragm Vertical heart
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Lateral CXR What do you see ?
Normal vs. Emphysema • Increased retrosternal clear space & kyphosis
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Chronic Bronchitis
• Too much mucus 2o to↑ irritants – Smoking/Pollution/coal/asbestos/allergens/genetic – Smoking also destroys cilia, compromising mucociliary escalator
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Chronic Bronchitis there is
↑ airway resistance
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• Air trapping
↑TLC secondary to mucus plugs
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In chronic bronchitis there is ↑ barrier thickening =
↓ gas exchange
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Chronic Bronchitis and Smooth muscle bronchospasm
Smooth muscle bronchospasm 2o to inflammation
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Diagnosis of Bronchitis
• Dx: 3 mo. x 2 yrs.
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In Chronic bronchitis, Bronchial lumen narrowed 2o to: –
Excessive mucus (infection can occur behind mucus plugs) – Thickened wall • smooth muscle spasm • Hypertrophy & hyperplasia of mucus glands
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Chronic Bronchitis and– Reid index
Reid index = ratio of mucus glands to thickness of wall • Normal \< 40% in CB \>40%
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“Blue Bloater” (Type B COPD) • Frequently obese
• Cyanosis “blue” discoloration • Hypoxia/Hypercapnia/Dyspnea • JVD
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Blue Bloater cough
• Chronic productive cough • Purulent sputum
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Complications of CB:
– Polycythemia 2o to hypoxemia – Plumonary HTN 2o to hypoxic vasoconstriction – Cor pulmonale 2o to chronic pulm. HTN
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Chronic Bronchitis
• FEV1 , FVC, FEV/FVC%, FEF25-75% all decreased
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Sign/Symptoms Chronic Bronchitis
• Cyanosis, hypoxia, dyspnea • Rales & ronchi • Chronic productive cough 3mo. x 2yrs.
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Chronic Bronchitis • Other tests:
– PFT – HRCT – Sputum exam
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Pulmonary Fibrosis there is \_\_\_\_\_\_Resulting in \_\_\_\_\_\_\_compliance
• Thickening of alveolar wall = ↓ compliance
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Exact cause of Pulmonary Fibrosis
Unknown
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Pulmonary Fibrosis is due to repeated \_\_\_\_\_\_\_\_causing\_\_\_\_\_\_
• Repeated exposure to irritant causes abnormal repair response with scarring
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Can cause pulmonary Fibrosis (SEGIV)
– Smoking – Environmental dust exposure – GERD – Industrial oxidants – Viral infections
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Pulmonary Fibrosis, alveolar cells • • Uncontrolled, dysregulated deposition of extracellular matrix = thickened, stiffened fibrosis
• Alveolar cells injured
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Release profibrotic & inflammatory mediators:– TNF-α
– recruit inflammatory cells
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Release profibrotic & inflammatory mediators– TGF-β
stim. migration & proliferation of . migration & proliferation of fibroblasts
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Release profibrotic & inflammatory mediators–
Growth factors stim. migration of myofibroblasts
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Mediators Organize into
clusters called fibroblastic foci
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Uncontrolled, dysregulated
deposition of extracellular matrix = thickened, stiffened fibrosis
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Pulmonary Fibrosis: airway
• Excessive radial traction increases airway caliber
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Pulmonary Fibrosis Clinical Manifestations
Clinical Manifestations • Affects adults 50s-60s • Dyspnea on exertion • Tachypnea with small TVs • Nonproductive cough
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Lung Volumes changes in Pulmonary FIbrosis
• FVC ↓↓↓ • FEV1 normal to low • FEV/FVC%↑ • TLC & FRC ↓↓↓
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Pulmonary Fibrosis • CXR: RHL
Reticulonodular pattern, especially at the bases Honeycomb appearance in late ds. Lungs typically small, w/ raised diaphragms
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Pneumothorax
Penetrating chest wound or ruptured bleb allows air in P.C. = passive recoil of lung away from chest wall
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Spontaneous Pneumothorax: common
Most common form
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Spontaneous Pneumothorax: small bleb
Rupture of small bleb on surface near apex
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Spontaneous pneumothorax typically occurs in
Typically occurs in young males
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Spontaneous pneumothorax related to
Related to high mechanical stresses in upper zone of upright lung – Presents with sudden pain & dyspnea
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Tension Pneumothorax
• Occurs when the defect acts as a one-way valve • Air enters pleural space on inspiration but cannot be expelled on expiration
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What happens in spontaneous pneumothorax
Air entrained with each breath –Increasing pressure causes compression of contralateral lung and Decrease venous return
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Tension Pneumothorax occurs
↓ ↓ venous return – Surgical Emergency
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Pulmonary Edema: Pathogenesis
• Increased Capillary Permeability • High Permeability Edema (High K) • High Protein & RBCs
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Pulmonary Edema Caused by
– Inhalation injury – toxins, oxygen poisoning – Circulating factors – inflammatory mediators, endotoxins – ARDS
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Pulmonary Edema: Pathogenesis Intersitital Hydrostatic pressure
• Decreased Interstitial Hydrostatic Pressure • (Low Pi) “Negative Pressure Pulmonary Edema”
85
Pulmonary Edema Caused by:
-reexpansion injury: may also damage capillaries
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Pulmonary Edema Caused by: Oncotic
• Decreased Plasma Oncotic Pressure • (Low πc) • Caused by: overtransfusion leading to hypoalbuminemia
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Pulmonary Edema: Pathogenesis
• Reduced Lymphatic Drainage • Normally handles ~ 20ml/hr
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Reduce lymphatic drainage Caused by:
Obstruction, Tumor, Iatrogenic, Increased CVP • Interferes with drainage of thoracic duct
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Pulmonary Edema Pathogenesis
Increased Capillary Permeability Decreased Interstitial Hydrostatic Pressure Decreased Plasma Oncotic Pressure Reduced Lymphatic Drainage
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Pulmonary Edema : LVEDP
• Increased LV EDP – HF
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Most common cause of pulmonary HTN
Pulmonary HTN • Increased Pulmonary Vascular Resistance • Most common cause
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Three categories of pulmonary HTN Vasoconstrictive
Three categories: – • Ex. Hypoxia @ high altitude – Obstructive • Ex. thromboembolism – Obliterative • Ex. Destroyed capillary bed in emphysema
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Three categories of pulmonary HTN:Obstructive
• Ex. thromboembolism
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Three categories of pulmonary HTN: Obliterative
• Ex. Destroyed capillary bed in emphysema
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CO (carbon monoxide) – Binds to Hb =
with 200x the affinity of O2
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CO– Increases O2 affinity of remaining Hb
does not release O2 readily to the tissues – dissociation curve shifted to the Left
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CO no change
– No change in PaO2
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CO poisoning and O2 partial pressure
Oxygen partial pressure in the blood remains unchanged by CO poisoning (No cyanosis, no tachypnea)
99
CO is Dx by
measuring carboxyhemoglobin levels AND index of suspicion
100
Tx of CO
– Tx: 100% FiO2
101
Cigarette Smoking • Impaction
– Largest particles strike mucus surfaces, become trapped
102
Cigarette Smoking • Sedimentation
– Smoke particles settle in terminal & respiratory bronchioles, unlike gases, cannot diffuse to alvolar wall
103
Deposition of Particle Inhalation: Inhaled particles deposited in airways, mechanism based on
particle size
104
Impaction
large particles \> 5 microns filtered by nasopharynx
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Sedimentation
particles 1 to 5 microns deposit in terminal and respiratory bronchioles as laminar flow ceases
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Diffusion –
particles \< 0.1 micron, behave almost like gas. Most exhaled, but some deposits in alveoli, may be cleared by alveolar macrophages.
107
Clearance of Deposited Particles Two mechanisms:
• Particles deposited in conducting airways cleared by MCE (mucocilliary escalator) & swallowed
108
Particles deposited in gas exchange units cleared by
alveolar macrophages (“dust cells”)
109
Clearance of Deposited Particles inhibited By:
• Inhibited by: pollution, tobacco, steroids, radiation
110
MCE
• Seromucus glands & goblet cells secrete mucus 5-10 microns thick. (Gel top layer more viscous) IgA
111
Cilia sweeps mucus
~ 1mm/min in bronchioles; 2cm/min in trachea. Total clearance q 24 hrs.
112
ResFailure - Hypoxemia • “Normal” PaO2 calculation on
102 - 0.33 × age
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RF Signs/Symptoms:
– ↓ PaO2 – Cyanosis – Tachycardia – Mental confusion
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Tissue Hypoxia – vulnerability depends –
on tissue
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Most vulnerable
CNS & Myocardium
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Cessation of blood flow to cerebral cortex: • 4-6 sec
loss of function
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Cessation of blood flow to cerebral cortex: 10-20 sec. =
l.o.c.
118
Cessation of blood flow to cerebral cortex 3-5 min. =
irreversible damage
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Hypercapnia
• ⇑Work of breathing
120
Hypercapnia CNS receptor desensitization,
permissive hypercapnia
121
Hypercapnia renal compensation
( for ↑ H2CO3 - )
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CNS desensitization from chronic hypercapnia →
dependency on hypoxic respiratory drive
123
Hypercapnia Treatment with O2 could suppress
hypoxic drive and increase CO2 retention/acidosis
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Hypercapnia Answer is to give\_\_\_\_\_\_\_\_\_\_
low concentration (24-48% O2)
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Hypercapnia, monitor this
monitor ABGs frequently to determine whether depression of ventilation is occurring.
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The mucous film consists of a
superficial gel layer that traps inhaled particles and a deeper layer so it is propelled by cilia
