Resp Review Flashcards
(239 cards)
1
Q
4 stages of pulmonary consolidation in pneumonia
A
1) Congestion (exudate enters alveoli) 2) Red hepatization (RBCs, fibrin) 3) Grey hepatization (RBC breakdown) 4) Resolution (sputum)
2
Q
Basic pathophys of pneumonia
A
Bacterial toxins/PAMPs –> histamine release, vascular permeability –> alveolar edema
3
Q
Community acquired pneumonia most common pathogen
A
Streptococcus pneumoniae
4
Q
Pneumonia caused by a pre-existing condition
A
Secondary pneumonia
5
Q
Hospital-aquired pneumonia happens when?
A
>48 hours after admission
6
Q
3 main types of pneumonia based on locations in lungs
A
1) Lobar (consolidation of 1 lobe) 2) Bronchopneumonia (bronchioles + adjacent alveoli, patchy) 3) Interstitial (inflamm/fibrosis of interstitium - bilateral opacities, may be indolent)
7
Q
Percussion in pneumonia
A
Dull
8
Q
Why does alcohol increase pneumonia risk? (3)
A
1) Impairs activity of macrophages/mucociliary/NK cells/other WBCs 2) Aspiration 3) Alters normal URT flora
9
Q
What might you see on palpation in lobar pneumonia?
A
Unilateral expansion
10
Q
In pneumonia you might hear what breath sounds in the parenchyma (auscultation)
A
Bronchial
11
Q
CO2 and O2 in pneumonia?
A
Hypoxemic Not necessarily hypercapnic, may be hypocapnic due to hyperventilation
12
Q
CXR signs for the 3 pneumonia types
A
1) Lobar –> lobar opacity, air bronchograms 2) Bronchopneumonia –> patchy reticular/reticulonodular infiltrates, bilateral, base of lungs 3) Interstitial - reticular opacities (diffuse lines) mostly around hila
13
Q
What are the 2 scoring systems for pneumonia (one in detail)
A
1) CURB-65: confusion, high serum urea, RR >=30, BP syst <=90 or diast <=60; >=65 years old; 2+ = hospitalize, 3+ = consider ICU Also pneumonia severity index ^mortality risk
14
Q
In Fick’s law, rate of diffusion depends on… (4)
A
Surface area Membrane thickness Diffusivity of the gas Partial Pressure gradient
15
Q
2 ways that endotracheal tube increase infection risk
A
Prevent closure of glottis May act as a fomite
16
Q
Viral RTIs make susceptible to bacterial 2o infection via…
A
1) Impairing mucociliarty escalator 2) Upregulating adhesion proteings 3) Paralyzing macrophages
17
Q
Biggest risk factor for COPD?
A
Smoking
18
Q
Drugs that reduce fever (acetaminophen, ibuprofen) inhibit what?
A
Cyclooxygenase
19
Q
Bleeding from upper GI tract
A
Hematemesis
20
Q
Blood from lower GI tract
A
Hematochezia
21
Q
Blood from airway (lungs, nose)
A
Hemoptysis
22
Q
Nosebleed proper term
A
Epistaxis
23
Q
Pneumothoax vs atelectasis
A
Atelectasis = collapse of lung tissue w/ loss of volume Pneumothorax = air in IP space –> loss of neg pressure b/w pleural membranes –> partial or complete lung collapse
24
Q
Resp distress vs failure vs arrest?
A
Distress = struggling to breath Failure = inability to regulate blood parameters through breathing (ABG-diagnosed!) Arrest = cessation of breathing
25
What test is used for clubbing?
Schamroth's test
26
Clubbing occurs in what diseases?
ILD, CF, cancer, congenital heart disease, cardiac shunting NOT COPD
27
Most dependent part of pleural cavity when upright = ? What is this called on radiograph?
Costadiaphragmatic recess (parietal pleura at base of lung b/w diaphragm and ribs) Costaphrenic angle
28
Bronchioles are composed almost entirely of
Smooth muscle
29
Without cartilage, how are the bronchioles and alveoli kept open?
Transpulmonary pressure
30
In normal conditions, most airway resistance is in the...
Larger bronchioles/bronchi near trachea (few vs terminal bronchioles)
31
Distribution of receptors for nervous control of airway diameter
BR ARs in periphery, MAch in central airways
32
Control of airway diameter mainly regulated by... (SNS or PSNS)
PSNS (SNS weak)
33
B2 ARs bind which catecholamine more strongly?
Epinephrine
34
B2 agonist
Salbutamol (ventolin)
35
PSNS fibres that release acetylcholine to lung parenchyma are derived from ___ nerve
Vagus
36
Microembolism occluding small pulmonary arteries triggers...
Bronchiolar constriction reflex
37
Acetylcholine leads to broncho...
constriction
38
Give an example of a local secretory factor that leads to bronchoconstriction
Histamine
39
Define asthma (3 things)
1) Bronchial hyperresponsiveness (inflamm + narrowing)
2) Episodic exacerbations
3) Reversible airway obstruction
40
**Genetic** predisposition to immune hyperresponsiveness may manifest in what combination of disorders?
Atopic triad: atopic dermatitis (eczema), asthma, allergic rhinitis
41
Genetic predisposition to hypersensitivity/allergy
Atopy
42
What is AERD?
Aspirin-Exacerbated Respiratory Disease (Samter's Triad)
1. Asthma
2. Nasal polyps
3. ASA sensitivity
43
What causes ASA sensitivity?
COX-1 inhibition
Arachadonic acid metabolized by lipooxygenase instead --\> leukotrienes (instead of prostaglandins)
--\> bronchospasm, vascular permeability, mucus production
Submucosal edema + airway obstruction!
"Pseudoallergic reaction" - like type 1 hypersensitivity but not IgE-mediated
44
Why do beta blockers trigger asthma?
Inhibit E/NE binding of B2ARs
45
2 main categories of asthma
1. Allergic (extrinsic) - atopy; environmental allergens
2. Nonallergic (intrinsic) - neutrophil-mediated; cold, stress, GERD, chemicals, meds, RTIs
46
Endobronchial obstruction in asthma mainly due to:
Bronchospasm
Submucosal edema
Mucus production
Hypertrophy of SM
47
Allergic (extrinsic asthma) primarily mediated by
IgE --\> FcERI binding, mast cell degranulation, histamine release
(Type I hypersensitivity)
48
Nonallergic (intrinsic) asthma primarily mediated by
Neutrophils (--\>submucosal edema + obstruction)
e.g. aspirin-induced asthma
49
Chronic asthma can lead to...
Fibrosis (scarring, BM thickening, irreversible obstruction --\> COPD)
50
Summary of pathophys of asthma
Allergen phagocytosed by APC
Presented on MHCII to CD4+ T cells (differentiate into TFH and TH2)
IL4/IL5 release
IL4 --\> IgE --\> mast cell degranulation --\> histamines + leukotrienes
IL5 --\> eosinophils --\> leukotrienes/cytokines, proteases
51
How to histamines impact the bronchioles?
Histamines --\> SM constriciton in bronchioles!
Vascular permeability, inflammation, mucus production
(submucosal edema)
52
What are the 2 phases of the asthmatic immune response?
1. Mast cells recognize cross-linked IgE --\> rapid degranulation/bronchoconstriction, mucus production
2. Eospinophil/neutrophil recruitment takes time, they are part of later phase
53
Percussion in asthma
HYPERresonance (air traipping!)
54
Auscultation in asthma
Prolonged exp + exp wheeze, decreased breath sounds
| (quiet chest = badbadbad!)
55
Mucus/epithelial cells clogging bronchioles in asthma that can be coughed up
Curschmann spirals
56
Charcot-Leyden crystals
Pigments of broken-down eosinophils, seen in sputum analysis in asthma
57
FEV1 increase after bronchodilator required for asthma diagnosis
12%
58
If asthma patient asymptomatic what test could you do (instead of bronchodilator test)
Broncho*provocation* test = Methacholine challenge (muscarinic agonist)
Positive = 20% drop in FEV1
59
FEV loop in asthma appears
Concave on top
60
PFT result in asthma
Decreased FEV1/FVC (FVC may decrease due to gas trapping)
Reversible 12% post bronchodilator test
61
Initial ABG for asthma
Severe late-stage ABG for asthma
Initial: hypoxemic, hypocapnic, alkalotic (Type 1 RF)
Final: hypoxemic, hypercapnic, acidosis (Type 2 RF)
62
CXR in asthma
*If severe:* Hyperinflation - flat diaphragm, increased intercostal space, barrel chest
(but in most asthma mainly used to exclude differentials)
63
3 main categories of asthma treatment
1) Causal
2) Relievers (treat symptoms) - SABA/LABA, SAMA/LAMA
3) Controllers (treat underlying inflammation) - e.g. ICS
64
Emergency asthma med (IV)
IV magnesium sulfate (blocks Ca channels to relax SM)
65
SAMA and LAMA examples
SAMA = ipratropium bromide
LAMA = tiotropium bromide
66
What is a test that can be done during acute exacerbation of asthma, and as a way for patients to monitor if their meds are working before symptoms increase?
Peak Expiratory Flow Rate (hsould be \>70% of expected)
67
Describe some treatment modalities for asthma
68
The mucous membrane in the bronchial tree changes from _______ in the main bronchi, lobar bronchi, and segmental bronchi to _______ with some _____ in larger bronchioles, to mostly ________ with no _____ in smaller bronchioles, to mostly\_\_\_\_\_ in terminal/respiratory bronchioles. ______ lines the alveoli (\_\_\_\_\_)
The mucous membrane in the bronchial tree changes from ciliated pseudostratified columnar epithelium in the main bronchi, lobar bronchi, and segmental bronchi to ciliated simple columnar epithelium with some goblet cells in larger bronchioles, to mostly ciliated simple cuboidal epithelium with no goblet cells in smaller bronchioles, to mostly nonciliated simple cuboidal epithelium in terminal/respiratory bronchioles. Simple squamous epithelium lines the alveoli (pneumocytes)
69
4 layers of tracheal tissue (lumen to outer)
1. I**nnermost mucosa:** resp epithlium (PSCC w/ goblet/basal cells) + BM
2. **Submucosa:** mixed seromucous glands
3. **Hyaline cartilage** anteriorly, **trachealis muscle** fibres posteriorly
4. **Adventicia**: areolar CT w/ small BVs/nerves
70
SM in bronchi vs trachea?
Complete encircles the lumen in bronchi
71
Basement membrane connects ____ to \_\_\_\_. What are the 2 parts?
Epithelial cells to CT
1. Basal lamina (secreted by epi cells, attach them to BM)
2. Reticular lamina (close to CT, contains collagen)
72
What's measured in an ABG? (8)
1. PaO2
2. PaCO2
3. SaO2
4. HCO3-
5. pH
6. Base excess
7. Anion gap
8. Other: Hb, electrolytes, glucose, etc...
73
ABG normal range for...
PaO2
80-100 mmHg
74
ABG normal range for...
## Footnote
**PaCO2**
35-45 mmHg
75
ABG normal range for...
## Footnote
**pH**
7.35-7.45
76
ABG normal range for...
## Footnote
**HCO3-**
21-27 mEg/L
77
ABG normal **anion gap**
12 mEq/L
78
Test to perform before ABG
Modified Allen's test (compress both wrist arteries, release from ulnar artery --\> colour should rapidly return if collateral circulation present)
79
ABG usually performed from which artery?
Radial
80
Anion gap and non-anion gap apply to which AB disorder subtype?
Metabolic acidosis
81
Steps of ABG interpretation
1. Look at O2 for hypoxemia
2. Alkalosis vs acidosis
3. Resp or metabolic
4. Metability acidosis --\> check anion gap
5. Check for other **primary** metabolic disorders by checking AG/bicarb ratio
6. Check for other **primary** resp disorders using CO2 Winters Formula (bicarb x 1.5+8 +/-2)
82
Describe interpretation of AG/bicarb ratio
**\< 1** --\> concurrent **primary** **metabolic** **non-AG** **acidosis**
**\>2** --\> concurrent **primary** **metabolic alkalosis**
83
2 types of restrictive lung diseases + examples
1. Intrinsict (ILD)
2. Extrinsic (pleura/pleural cavity, chest wall, resp muscles/NM disease)
84
Examples of obstructive lung diseases (4)
COPD, CF, asthma, bronchiectasis
85
Obstructive lung diseases are issues with \_\_\_\_
Restrictive lung diseases are issues with \_\_\_\_\_
Obstructive = **resistance**
Restrictive = **compliance**
86
An extra big expiratory scoop on a flow-volume curve indicates what disease and why?
Emphysema --\> airways collapse during expiration
87
What does a restrictive lung disease look like on a flow-volume loop?
Compressed bc air comes out faster all at once (think of tight elastic band snapping back)
88
3 main steps of interpreting PFT
1. Spirometry
2. Lung volumes
3. DLCO
89
Summary of spirometry interpretation
1. **Flow-volume loop** (obstructive fixed/variable, intra/extra; restrictive)
2. **FEV1/FVC ratio** --\> obstruction (\<0.7 actual value, or
3. FEV1 --> severity of obstruction (<70 = moderate, <50 = severe)
4. If ratio normal, low FVC --> restriction
5. Post-bronchodilator measurements (reversibility)
90
What are things to look for in lung volumes of PFT?
TLC --\> restriction (low), hyperinflation (high)
RV --\> obsety/restriction (low), gas-trapping (high)
91
DLCO interpretation
Intraparenchymal vs extraparenchymal restriction
If only abnormal thing --\> blood issue (anemia, PE...)
92
2 main components of interstitial lung disease
1) Alveolitis (inflammation, usually first step)
2) Fibrosis (primary process in IPF)
93
Steps leading to fibrosis in ILD
Tissues damage or Ag
Inflammation, cytokines
Proteases/oxidants (more damage! Degrading CT)
Fibroblasts recruited (building CT)
--\> abberant CT formation
94
Explain what happens with fibroblasts in ILD
Type II pneumocytes stimulate fibroblasts to differentiate into myofibroblasts --\> secrete collagen
Overproliferation, too many myofibrocytes that aren't properly apoptosing
--\> thick IL layer
95
Most common type of ILD
Idiopathic pulmonary fibrosis
96
ILD is triggered by ____ exposures/stimuli
Chronic! Long-term
97
Pneumoconioses
ILDs caused by inhalation of inorganic dusts
98
Auscultation for ILD
Inspiratory dry/fine crackles/rales
Elevated diaphragm (restriction)
Egophony will stay as EEE (differentiate from alveolar filling which would cause wet crackles)
99
PFT changes in ILD
FEV1/FVC - high/normal (elastic recoil)
FVC - low
TLC - low
FRC - low (reduced compliance, increased recoil)
DLCO - low
100
Radiological sign of ILD
Reticular opacities (fibrosis)
Honeycombing (air-filled fibrotic cysts)
101
ABG in ILD
Increased A-a gradient
Hypoxemia
Hypocapnia/resp alkalsos at first
Most of type: **hypocapnia + neutral pH** (metabolic compensation!)
Late stage - hypercapnic
102
Treatment for ILD
Treat underlying cause (AB, steroids)
Lung transplants
Generally irreversible :(
103
Acute Respiratory Distress Syndrome
Severe inflammatory reaction of lungs
**Hypoxemia** + **bilateral pulmonary infiltrates** not accounted for by heart failure/fluid overload
104
Main differential for ARDS
Cardiogenic pulmonary edema
(both call alveolar edema - different causes, similar outcomes)
105
Is ARDS always initiated with lung injury?
NO. **Systemic inflammatory response**, which is why opacities are always **bilateral**
106
Most common cause of ARDS?
Sepsis
107
Berlin criteria for ARDS
MUST MEET **ALL 4** CONDITIONS
1. **Acute onset** (resp failure \<1 week after potential trigger)
2. **Bilateral opacities** not explained by pleural effusions
3. **Hypoxemia**: **PaO2/FiO2 \<300 mmHg** (mod \<200, severe\<100, normal = 500)
4. Resp failure *not fully accounted for* by **heart failure** or **fluid overload**
108
Pathophys of ARDS
Damage --\> inflammatory cascade
1. **Exudative phase:** excess fluid in interstitium and on alveolar surface
2. **Hyaline membrane formation**: neutrophils/protein rich exudate in alveolar space --\> hyaline membranes form (fibrin + debris + RBCs), impair gas exchange, hypoxemia
Damage to pneumocytes --\> less surfactant --\> alveolar collapse, reduced compliance, shunting
Vascular occlusions --\> dead space
3. **Organizing phase:** type II pneumocyte prolif, fibroblasts infiltrate --\> IL fibrosis can occur
109
Edema in ARDS is caused by destruction/failure of what?
**Alveolar-capillary membrane**
* Endothelium* - activated, swelling/leaking
* Epithelium* - flooding, decreased surfactant/resorption (both type II pneums)
110
Is the disease in ARDS gravity-dependent?
The opacities are NOT but atelectasis is!
111
Primary imaging test for ARDS
How to distinguish from cardiac issue?
CXR: peripheral bilateral opacities
Distinguish from CHF: no (or small) pleural effusions, no cardiomegally, no pulmonary edema (septal lines)
112
ABG in ARDS
PaO2: low
pH: high; pCO2: low (initially resp alkalosis)
Increased A-a gradient
PaO2/FiO2 \<300 mmHg
...Eventual resp exhaustion (hypercapnia/acidosis)
113
Major physiological changes in ARDS:
^ A-a gradient
Lower: compliance, FRC
^WOB
R-L shunting + Dead space
Hypoxemia
^pulmonary vascular resistance (fibrin, vasoconstriction, edema)
114
Ventilation strategy for ARDS?
Lung-protective ventilation (low TV & plateau pressure, lowest FiO2 possible)
115
Severe bilateral opacities in ARDS can lead to what appearance on x-ray?
"White out"
116
Prognosis in ARDS?
Usually full resolution if patient recovers, improvement starts after 1-3 weeks
If complicated by interstitial pulmonary fibrosis --\> prolonged ventilator dependence
40% mortality if simultaneous organ failure
117
Infant respiratory distress syndrome is what?
Surfactant deficiency disorder
118
Diseases that can be classified as COPD
Mainly: chronic bronchitis + emphysema
Also: CF, bronchiectasis, asthma (irreversible)
119
Common etiologies of COPD
**_SMOKING_**
Environmental exposures
Genetics: alpha-1 antitrypsin deficiency
120
Why does alpha-1 antitrypsin deficiency beget COPD?
It is an protease inhbitor that inhibits **elastase** (secreted by neutrophils)
Without it --\> unopposed elasteolysis in alveoli
121
In COPD, lung inflammation and proteases lead to proteolytic destruction of the lung parenchyma. What are the effects of this?
1. Reduced elastic recoil --\> air trapping
2. Reduced airway patency --\> narrowing/collapse
3. Enlargement of alveoli --\> hyperinflation, bullae
Result = **emphysema**
122
Why is hypoxemia not observed as early in emphysema as in chronic bronchitis?
Matched V/Q defect (both terminal bronchioles/alveoli and capillary bed are destroyed!)
123
2 main types of emphysema
1. Centriacinar Emphysema - destruction of *respiratory bronchiole* (central acinus, alveoli ok), usually upper lobe - associated with smoking
2. Panacinar Emphysema - destruction of entire acini (incld alveoli); usually lower lobe/lung bases but can be entire lung - associated with a1-antitrypsin deficiency
124
R heart failure due to respiratory system failure
Cor pulmonale
125
How would A-a gradient be impacted by COPD or during asthma exacerbation?
Incraesed due to shunting, V/Q mismatching
126
In COPD, inflammation leads to chronic bronchitis through what pathological changes?
1. Airway fibrosis/narrowing
2. Hypertrophy/hyperplasia of mucus glands + goblet cells --\> mucus production
3. Death of airway epithelium cilia cells (mucus plugs --\> air trapping!)
4. SM hypertrophy
5. Pulmonary hypertention (V/Q mismatch, hypoxemic vasoconstriction)
127
Diagnostic criteria for chronic bronchitis
**Productive** cough on most days in 3 consecutive months for 2 consecutive years
128
Does COPD cause more issues with inspiration or expiration?
Expiration (for both CB and E)
129
How does pursed-lip breathing help patients with emphysema?
Prolongs expiration
Maintains PEEP to keep airways open
130
Auscultation in COPD
Expiratory wheeze
Inspiratory crackles/rales (airways "popping" open)
Emphysema: decreased breath sounds (alveolar hyperinflation/destruction)
Chronic Bronchitis: Rhonchi (gurgling due to mucus)l
131
Percussion in COPD
Hyperresonant (gas trapping)
132
Change in chest appearance in COPD
Barrel-chested
(^ant-post diameter due to hyperinflation caused by collapsed airways)
133
PFT changes in COPD
**Decreased:** FEV1, FVC (or normal), FEV1/FVC (\<70%), DLCO (emphysema)
Irreversible (\<12% recovery)
**Increased:** TLC, RV (gas trapping)
134
ABG in COPD
Increased: PCO2
Decreased: PO2, pH
135
COPD Radiography
Evidence of air trapping: hyperinflation, barrel chest, flat diaphragm, ^AP diameter; air pockets visible in emphysema
136
Best treatment for COPD
Smoking cessation!
Doesn't improve lung *structural* damage but reduces mucus/hyperrresponsiveness, normalizes FEV1
137
Giving too much O2 in COPD patient can lead to...
CO2 narcosis
138
List some COPD treatment modalities (other than smoking cessation and vaccines) (6-8)
Long-term **oxygen** therapy (LTOT) - aim for sats 88-92%
**Bronchodilators** (SAMA + SABA or LAMA + LABA)
**Steroids**: ICS (maintenance), IV/PO (acute exacerbations)
**PDE inhibitors** (SM relaxation) - theophylline
**ABs**
**Pulmonary rehab**
**(Lung resection)**
**(Mucolytics)**
139
Complications of COPD (8)
1. **AECOPD** (mucus trapping)
2. **Pneumonia** (mucus trapping)
3. **Macro-nutrient deficiency** (inflammation --\> hypermetabolism)
4. **Wasting/muscle atrophy** (inactivity/deconditioning, nutrient deficiency)
5. Secondary **polycythemia** (hypoxemia --\> kidney EPO --\> erythropoiesis)
6. **Pulmonary hypertension** + **cor pulmonale** (hypoxic pulmonary vasoconstriction)
7. **Depression**
8. **Pneumothorax** (bullae rupture, creating leak into pleural space)
140
Define Acinus
*Distal* to terminal bronchiole, comprised of **resp bronchiole + alveolar ducts + alveoli**
141
DIfference between acinus, primary lobule, secondary lobule?
Primary lobule = distale to resp bronchiole (alvelar ducts + sacs + alveoli)
Acinus = distal to terminal bronchiole (inclds resp bronchiole); 4-5 primary lobules
Secondary lobule = 3-25 acini
142
Branching of bronchial tree in the *conducting zone*
Trachea --\> mainstem (1o) bronchi --\> lobar (2o) bronchi --\> segmental (3o) bronchi --\> bronchioles (no cartilage!) --\> terminal bronchioles
143
Internal ridge at bronchial junciton = ?
Chalk-full of what?
Carina
Irritant receptors (cough reflex)
144
Which lung are we more likely to aspirate into and why?
R (bronchus is wider/more vertical)
145
How is a bronchopulmonary segment defined?
Supplied by a tertiary bronchi; structurally/functionall indepdendent
146
Adam's apple = ?
Describe
Laryngeal prominance (2 sides of thyroid cartilage come together)
147
What fully closes the airway during swallowing?
**Vocal ligaments** (vocal chords) close the glottis
**Vestibular ligaments** (false vocal chords) keep the remainder of the glottis closed
148
Costale cartilage and cartilage in the airways is what type?
Hyaline (weak cartilage, flexible/resilient gel)
149
What are the false ribs
5 ribs total
Ribs 8-10 connect to sternum indirectly via costal cartilate of 7th rib
Ribs 11-12 are "floating ribs"
150
Main anatomy of sternum
Manubrium --\> manubriosternal joint (sternal angle, angle of Louis) --\> body --\> xiphisternal joint --\> xiphoid progess
151
Which costal cartilage articulates with the sternal angle?
2nd
152
Describe locations of superior and inferior mediastinum
**Superior** = **T1-4**, just behind manubrium
**Inferior** = **T4-12** (ends at diaphragm)
153
Inferior mediastinum is divided into anterior, middle, and posterior. The heart/pericardium are in which compartment?
**Middle** inferior mediastinum
154
Superior thoracic aperature
T1 + 1st rib + upper manubrium
Passage of vasculature/nerves into thoracic cavity
155
Inferior thoracic aperature
T12, 11th/12th ribs, 7th-10th costal cartilages
Where structures exit thorax into abdominal cavity; closed by diaphragm
156
What nerve supplies the diaphragm, and what cervical segments does it come from?
Phrenic nerve
"C3, 4, and 5 keep the diaphragm alive!"
157
Describe paradoxical movement of diaphragm
If one side paralyzed, moves *up* with inspiration due to decrease in intrathoracic pressure
158
How are external intercostals oriented?
Hands-in-pockets
159
External intercostals supplied by what nerves?
Intercostal nerves, come off spine @ same level
160
Accessory muscles of *inspiration*
**Scalenes** (elevate first 2 ribs)
**Sternocleidomastoids** (elevate sternum)
**Pectoral girdle** (pectoralis minor, serratus anterior, trapezius)
161
Accessory muscles of *expiration*
**Internal intercostals**
**Abs:** rectus abdominus, internal/external obliques, transversus abdominis
162
What are the _main_ muscles in forced inspiration?
STILL DIAPHRAGM AND EXTERNAL INTERCOSTALS!
163
Origin and insertion of external intercostals
Origin = upper rib
Insertion = lower rib
(Pull insertion toward origin!)
164
Diaphragm insertion
Central tendon
165
Describe locations of the VAN and the collateral branch
VAN is in costal groove on inferior upper rib
Collateral branch on upper part of lower rib
166
What is the point of tripoding when in resp distress?
Fixes the upper shoulder girdle --\> allows better activation of accessory muscles for deeper inspiration
167
Intercostal veins drain posteriorly into what? What is this system for?
Azygous/hemiazygous veins
Alternative route for inferior vena cava (which can be compressed during pregnancy e.g.)
168
Blood supply to VAN comes from ___ posteriorly, ___ anteriorly
**Aorta** posteriorly
I**nternal thoracic arteries** anterioly
169
What is pulmonary arterial pressure?
What is pulmonary venous pressure?
PAP = Pressure generated by R ventricle
PVP ~ L atrial pressure
(very small gradient compaire to systemic!)
170
Describe the path of the pulmonary circulation
R atrium
Pulmonary trunk
R/L pulmonary arteries --\> arterioles --\> capillaries
Pulmonary venules/veins
4 pulmonary veins (2R/2L return blood to L atrium)
171
In the bronchial circulation, what is unique about circulation to the bronchioles?
Bronchioles don't have veins but they do have arteries
Blood enters *pulmonary veins* = **anatomical shunt**
172
What's the difference between thoracic aorta and abdominal aorta?
Same struction but name changes when passes through diaphragm
173
Intrapleural pressure is always...
*Negative* compared to alveolar/atmospheric
(elastic recoils of lungs inward, chest wall outward)
174
Transpulmonary pressure =
If higher, lungs are...
alveolar - intrapleural pressure
Higher --\> lungs larger!
175
Is inspiration or expiration longer?
Expiration
176
How does IP pressure change during inspiration/expiration
Declines throughout insp (-5 --\> -8)
Lower peak at end of insp
Increases throughut exp
177
How does alveolar pressure change throughout insp/exp?
Insp: Decrease then increase back to atm
Exp: increase then decrease back to atm
178
Poiseuille Relationship and flow
179
Define lung compliance (ratio)
dV/dP
180
Define eupnea
Quiet breathing
181
In the cough reflex, afferent impulses sent to medulla via \_\_\_\_
Vagus nerve
182
What do the peripheral chemoreceptors sense?
Where are they?
What is their afferent innervation?
O2/CO2/pH
**Aortic bodies** (aortic arch) --\> **vagus** nerve (X)
**Carotid bodies** (carotid arteries) --\> **glossopharyngeal** nerve (IX)
183
Central chemoreceptors respond to what?
pH, CO2
(more robust response to H+ changes than peripheral bc less buffering proteins)
184
Describe medullary resp centre
**Dorsal respiratory group** (inspiration, diaphragm/intercostals via phrenic/intercostal nerves)
**Ventral respiratory group** (forced breathing, accessory muscles)
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What/where is the respiratory "pacemaker"
Pre-Botzinger complex in VRG
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Describe the **pontine respiratory group**
**Apneustic centre -** simulates DRG neurons to increase *_depth_* of breathing
**Pneumotaxic centre** - inhibits DRG neurons via apneustic centre
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What would happen if there was damage to your pneumotaxic resp centre?
Prolonged inspiration + short gasping expiration (bc not inhibiting the medullary centre/DRG!)
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Where is the pressure cutoff for PO2 where things start getting real bad?
60 mmHg (90% Hb sats)
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Changes in O2 that trigger chemoreceptors to induce respiration are what particular O2 in the blood?
Free O2!
So that's why you need large drop - some will release from Hb to buffer it
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Hering-Breuer reflex:
Baroreceptors in bronchi/bronchioles stretch during lung overinflation --\> vagus nerves --\> DRG inhibition
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Define the 4 types of hypoxia
1. Hypoxic (hypoxemia) hypoxia - low pO2 in arterial blood
2. Anemic hypoxia - lack of functional Hb
3. Ischemic hypoxia - lack of blood flow to tissue
4. Histotoxic hypoxia - tissues can't use O2 (e.g. cyanide)
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Define hyperpnea and hypopnea
High/low TV
*(does not refer to speed!)*
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Define hyperventilation
overall alveolar minute ventilation exceeds metabolic needs à hypocapnia/respiratory alkalosis
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Define hypoventilation
Minute volume does not meet metabolic needs (low TV or RR) --\> resp acidosis
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Define tachypnea and bradypnea
RR high or low
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Unifying factor for hypercapnia
Alveolar hypoventilation!
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# Define alveolar ventilation
AV = volume of gas reaching alveoli per min
(tidal volume - physiologic dead space) x RR
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Define minute ventialtion
Volume of air a person breaths per mind
= TV x RR
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Define the types of dead space
**Physiologic** dead space =
**Anatomical** dead space (conducting airways) +
**Alveolar** dead space (V in alveoli that don't partake in gas exchange)
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Reference blood levels for PO2 and PCO2
O2: 100 --\> 40 mmHg
CO2: 40 --\> 45 mmHg
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Majority of muscles in pharynx, soft palate, larynx have motor innervation from....
name a few actions
Vagus nerve
| (swallowing, phonation, coughing)
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Name the 4 tonsils
What are they called all together?
**Pharyngeal (adenoids)** - roof/posterior wall of nasopharynx
**Palantine** - sides of oropharynx
**Lingual** - base of tongue
**Tubal** - lateral wall of basopharynx
Together = **Waldeyer's ring**
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Main causes of platypnea-orthodeoxia syndrome
**V/Q mismatch**
Pulmonary **arteriovenous shunts**
Intracardiac shunts
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In platypnea orthodeoxia syndrome why are symptoms alleviated by lying down?
Diseased basal lung (V/Q mistmach)--\> more perfusion of apical lung!
Hepatopulmonary syndrome --\> intrapulmonary vascular dilation more at base of lung
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O2 binding to Hb involves ____ binding resulting in sigmoidal curve
Cooperative
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What is the effect of 2,3-BPG on Hb binding?
Allosteric effector
Lowers O2 affinity to ^unloading @ tissues (stablizes reduced Hb)
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Bohr effect
Shift of O2-Hb curve right/down
* Hypoxic/acidotic area (lactic acid formation due to anaerobic metabolism)
* pH drop raising the P50 of Hb (pressure at which 50% of receptor saturated)
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What are 4 things that shift the Hb-O2 binding curve right?
1. H+ (low pH)
2. High CO2
3. High temp
4. 2,3-BPG
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At what point is the steep drop-off in the Hb-O2 dissociation curve?
60 mmHg
90% saturation
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Describe the major and minor phenomena in the Haldane effect
Minor: Hb bound to O2 has lower affinity for CO2 (but most CO2 transported as bicarb)
Major:
O2 binds Hb making it more acidic --\> H+ release --\> shifts bicarb equilibrium L generating CO2 + H2O (in the lung)
Then CO2 can diffuse into alveoli for expulsion
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What is the reciprocal of compliance?
Elastance
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If IP pressure is still negative during expiration, why do the lungs shrink?
Because it's less than the **elastic recoil pressure**, leading to net *positive* pressure in the alveoli
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If a patient's O2 sats are 100% do you know they have enough O2?
No! Other types of hypoxia, e.g. anemia
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Pressure of pulmonary circulation (R heart) vs systemic circulation (L heart)
10-20 mmHg (pulmonary)
80-100 mmHg (systemic MAP)
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If drive doesn’t lead to muscle tension =
If tension doesn’t lead to movement =
Weakness
Impedance
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Pneumothorax:
Negative IP pressure comes from recoil forces of _____ and _____ and the fact that the body gets rid of air pockets. If air enters IP space due to puncture, these forces disappear leading to...
Lung inward
Chest outward
^lung deflation and chest wall moves outward due to no more opposing recoil forces
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Describe the V/Q ratios in diff parts of the lung
**0.3-2.5** from base --\> apex
**~0.8** average
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Ventilation is ~50% greater in what part of the lung when standing and why?
Base because weight of **pleural fluid** increases intrapleural pressure at the base to a *less negative* value --\> alveoli less expanded and **more compliant** to increase V on inspiration
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All V no Q =
All Q no V =
With increasing V/Q, O2/CO2 values approach what?
Absolute dead space
Absolute shunting
Approach *inspired air*
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What does the A-a gradient say about cause of hypoxemia?
Normal --\> issue extrinsic to lungs; e.g. neuromuscular disorder, high altitude
Elevated --\> lung issue: V/Q mismatch, shunting, diffusion impariment, alveolar hypoventilation
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If PaCO2 and PaO2 are both low then what *must* you see with the A-a gradient?
Elevation!
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What are the 2 types of pulmonary shunts and how do they respond to supplemental O2?
Anatomic - alveoli bypassed, unresponsive
Physiological - non-ventilated alveoli are perfused; responsive
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Describe anatomical R-L shunts that move blood directly from pulmonary arteries --\> veins
**Arteriovenous malformations**
Dilated, high capacitance, don't regulate diameter via V/Q matching
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Define shunt fraction
% blood distributed by L ventricle that is not completely oxygenated
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Define apneusis
Protracted/deep/gasping inhalation + short exhalation (think of apneusic centre!)
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Is O2 supplementation effective for hypoventilation?
Yes for hypoxemia but not for hypercapnia
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Is O2 supplementation effective for impaired membrane diffusion
Yes (^gradient)
228
Cyanosis is caused by what? What patients would you be VERY likely to observe cyanosis in?
Deoxy-Hb
Anemic patients
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Hypercapnia seen in what 2 causes?
Hypoventilation (CO2 transfer impacted as much as O2)
Circulatory deficiency (CO2 affected much less than O2 due to ^^^ blood transport capacity)
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Does super high CO2 increase respiration?
Actually *depresses* it
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Dyspnea =
Shortness of breath, "air hunger"
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Why doesn't asthma necessarily cause hypercapnia?
* Not everyone with COPD or asthma is a CO2-retainer
* There are still parts of the lungs working well in these diseases so can compensate if the V-Q mismatch is accounted for appropriately
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Is providing O2 helpful if just parts of the lung are underventilated? (COPD, asthma, emphysema, ILD, pneumonia)
YUPPERS
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Important history considerations for ongoing dyspnea/cough
Smoking
Occupation
235
Tests if you suspect COPD?
Spirometry (to confirm)
CXR (to rule out, e.g. cancer)
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#1 predictor if someone will quit smoking
Whether or not they are personally ***motivated*** to do so (e.g. after health diagnosis, pregnancy)
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12% increase for reversibility in asthma is in what parameter?
FEV1
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What med used in bronchodilator test?
SABA (e.g. salbutamol = ventolin = albuterol)
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