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35 Cards in this Set

  • Front
  • Back
Central chemoreceptors
Medulla

Directly sense decreasing pH (increasing H+)

Stimulated by PCO2 via BBB diffusion and formation of H+


* COPD pts w/ chronic hypercapnia: high [CO2] stops stimulating respiratory center - hypoxia remains only remaining drive, so if supplemental O2 is admin this is dangerous because then the stimulus disappears and respiration is inhibited --> respiratory failure
Peripheral chemoreceptors
Carotid/aortic bodies

Respond to hypoxia (senses PaO2)
Right lobe aspiration
Right side because right main stem bronchus more vertical and wider than left

If aspirate while upright = inferior portion of inferior lobe

If aspirate while supine = superior portion of inferior lobe
Pulmonary artery and bronchus
RALS

Right, Anterior

Left, Superior
Diaphragm structures
Perforating diaphragm

T8 = IVC
T10 = esophagus, vagus (2 trunks)
T12 = aorta, thoracic duct, azygous vein

Diaphragm innervation: C3-5 = phrenic N.
Referred pain = shoulder and neck
Pulmonary vessel anatomical relationships
Pulmonary trunk = unox blood
- conus arteriosus from RV
- at sternal angle --> R+L pulmonary arteries (most superior vessels in hilum of each lung)

Right pulmonary artery
- passes laterally
- posterior to asc. aorta & SVC
- to R hilum of R lung

Left pulmonary artery
- anterior to descending thor. aorta
- to L hilum of L lung

Pulmonary veins = ox. blood
- 2 pulm v. / lung exit hilum anteriorly & inferiorly pulm arteries
- 4 pulm veins drain into the LA
Thoracocentesis
Miclavicular line = 5-7 ribs

Midaxillary line = 7-9 ribs

Paravertebral line = 9-11 ribs
Exercise: Muscles of respiration
Inspiration = external intercostals, scalenes, sternomastoids

Expiration = rectus abdominis, internal/external obliques, transversus abdominis, internal intercostals
Angiotensin converting enzyme (ACE)
AngioI --> Angio II cnversion

Inactivates bradykinin
(ACE-I's increase bradykinin and cause cough, angioedema)

Kallikrein - activates bradykinin
Capacity
sum of >2 volumes

Vital capacity = TV + IRV + ERV

FRC = RV + ERV
* lowest PVR

IC = IRV + TV

TLC = IRV + TV + ERV + RV
Ventilation
Minute ventilation = includes all air
Tidal vol x (breaths/min)

Alveolar ventilation = refers ONLY to air participating in gas exchg/min
Tidal vol - dead space x (breaths/min)

Dead space = vol of air that does NOT participate in gas exchg; apex of lung contributes most to this

Vd = Vt x (PaCO2- PeCO2)/PaCO2
Hb modifications
TISSUE HYPOXIA (from dec O2 sat)

Methemoglobin:
- Nitrite drugs cause Fe2+ (normal iron in Hb)-->Fe3+
- Fe3+ Hb does not bind O2 as readily but has inc affinity for CN-
- CN- also inhibit cyto c oxidase (but preferentially bonds to MetHb instead)
* Note: partial P of O2 in blood remains NORMAL b/c amt of dissolved O2 in plasma = same (O2's partial P is not related to Hb fxn)
- Tx: Thiosulfate binds CN- --> thiocyanate (renally excreted) or tx w/ methylene blue

CarboxyHb:
- CO bound instead of O2 to Hb
- Dec O2 binding --> Lshift on curve
- Dec O2 tissue unloading
O2-Hb dissociation curve
Right-shift = decreased Hb affinity for O2 = O2 tissue unloading caused by an increase in ALL factors:
- dec O2 affinity, inc P50
- inc metabolic needs
- inc PCO2
- inc temp
- inc H+/dec pH
- high altitude, inc 2,3,-DPG

Left-shift: a decrease in ALL factors:
- inc Hb-O2 affinity, dec P50
- dec met needs
- dec PCO2, dec temp
- dec H+/inc pH
- dec 2,3,-DPG
- Fetal Hb!!!

P50 = partial P of O2 in blood at which Hb is 50% sat (26mmHg is nl)
Perfusion limited
Rapidity with which alveolar air equilibrates with partial P of O2 + CO2 in blood depends on how quickly a given vol. of blood can course through alveolar capillaries

CO2, N2O

Gas equilibrates early along length of capillary
Diffusion can be increased only if blood flow increases
Diffusion limited
O2 (emphysema, fibrosis), CO

Gas does not equilibrate by time blood reaches end of capillary
Pulm HTN
Nl pulm artery pressure = 10-14mmHg
Pulm HTN = >25 mmHg or >35 mmHg during exercise
S2 split present

If 1* - due to inactiv mut in BMPR2 that normally functions to inhibit vascular smooth muscle proliferation; requires lung transplant
PVR
PVR = [P(pulm artery) - P(Latrium)]/CO

R = 8nl/pie(r^4)
* major site of airway R = med-sized bronchi (>2mm)
* small airways do not contribute to R as much b/c of PARALLEL arrangement

Parasymp stim = inc R
Symp stim = dec R
Total O2 content
Affected by 3 main variables:

1. [Hb]
2. O2 saturation of Hb
3. Partial P of O2 dissolved in blood
A-a gradient
PAO2 - PaO2 = 10-15 (nl)

PAO2 = 150 - PACO2/0.8

Helps determine cause of hypoxemia
Hypoxemia
Dec PaO2

If normal A-a grad:
1. High altitude
2. Hypoventilation

If inc A-a grad:
1. V/Q mismatch
2. Diffusion limitation
3. R-L shunt
Hypoxia
Dec O2 deliv to tissues

1. Dec CO
2. Hypoxemia
3. Anemia
4. CN poisoning
5. CO poisoning
Ischemia
Loss of blood flow

1. Impeded arterial flow
2. Reduced venous drainage
CO2 transport
CO2 transported from tissues --> lungs in 3 forms:

1. Bicarbonate (transported in blood) = 90%
2. CarbaminoHb (bound to Hb) = 5%
3. Dissolved CO2 (5%)
Sleep apnea
Central (no resp effort) v. Obstructive (resp effort)

Peritubular cells in renal cortex sense hypoxia and respond by releasing EPO --> 2* polycythemia
Physical lung findings: bronchial obstruction
- absent/dec breath sounds over area
- dec resonance
- dec fremitus
- trach deviation TOWARDS sign of lesion
Pleural effusion
- dec breath sounds over effusion
- dull resonance
- dec fremitus
Pneumonia
- bronchial breath sounds over lesion
- dull resonance
- inc fremitus
Tension pneumothorax
dec breath sounds
hyperresonance
absent fremitus
trach dev AWAY from side of lesion
Lung CA complications
Pancoast tumor
- may affect cervical symp plexus --> Horner's syndrome (ptosis, miosis, anhidrosis)
- can invade brachial plexus --> weakness/paresthesias of arm

SVC syndrome
- SVC has thin walls so easily compressible by mediastinal masses
- usu assoc w/ bronchogenic CA or NHL
- sx's include dyspnea, cough, facial swelling, UE/ncek swelling, tracheal compromise
Squamous Cell Carcinoma
Hilar mass central, from bronchys
Cavitation
Smoking associated
PTHrP --> hypercalcemia
Keratin pearls and intracellular bridges
Small cell Carcinoma
Central location
ACTH/ADH production
LE syndrome
NE cells w/ granules
Lobar Pneumonia
4 stages
1. Congestion
- 1st 24h
- red heavy boggy w/ vascular dilation, alveolar exudate w/ bacteria

2. Red hepatization
-2-3d; red firm lobe
- alveolar exudate 2/ erythrocytes, neutrophils, fibrin

3. Gray hepatization
- 4-6d
- gray brown firm lobe w/ RBCs disintegrated, alevolar exudate contains neutrophils + fibrin

4. Resolution
- restoration of normal architecture
- enzymatic dig of exudate
Pulmonary alveolar proteinosis
autoAbs against GM-CSF

impaired surfactant CL by alveolar macrophages
Chylothorax
Disruption of thoracic duct in posterior chest via malignant neoplasms (NH lymphoma)
Farmer's Lung
= hypersensitivity pneumonitis
Type III/IV reaction (Type IV only when chronic exposure to Ag)
Granulomas can form but dz abates when Ag exposure stops