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HD 1 > Respiratory pathophys. Part 1 > Flashcards

Respiratory pathophys. Part 1 Flashcards

0
Q

timeframe of Acute Respiratory Failure

A

in minutes to days,
failure to provide adequate gas exchange
–> low O2 &/or high CO2

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1
Q

A-a gradient

equation and purpose

A

–> to quantify (in)efficiency of gas exchange
A-a = P(Alv)O2 - P(art)O2

P(Alv)O2 = (Pbarometric - 47)0.21 - (PartCO21.25)

* (Pbarometric - 47)*0.21 = 150 @ sea level* * ** change 0.21 if not at room air! ***
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2
Q

PaO2 cut-off for adequate oxygen supply to tissues

A

hypoxia begins at PaO2 = 40 mm Hg

–> 75% O2 Saturation

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3
Q

pH and PaCO2 changes in ACUTE acidosis (vs. chronic)

A

Acute: pH drops 0.08 for every increase by 10 in PaCO2

Chronic: pH drops 0.03 for every increase by 10 in PaCO2
“acute on chronic” = btwn acute and chronic changes

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4
Q

Respiratory V/Q mismatch (Low V/Q)

A

when less (but some) air is getting to the problem alveoli,
–> lower PaO2 (rest of lung can’t compensate on own)
Correction: CAN increase PaO2 & PaCO2 if increase amt of O2 in air (FiO2)
ie: COPD or asthma

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5
Q

Respiratory Shunt

A

NO air gets to problem alveoli.
–> low PaO2, high PaCO2, rest of lung can’t compensate on own.
Correction: can ONLY correct PaCO2, (not PaO2)
ie: pulmonary edema

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6
Q

Bellows failure

A

failure of respiratory muscles or internal drive to breath.
* normal A-a gradient (nothing wrong w/ lungs or vasculature!)
Tx: intubation/mechanical ventilation

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7
Q

Causes of Bellows failure (4 types)

A
  1. No effort
    • depressant drugs, head trauma/hypoperfusion
  2. Impaired nerves or muscles
    • polio, curare, neurodeg. diseases
  3. Muscle fatigue –> obesity, pulmonary fibrosis
  4. Insufficiency –> flat diaphragm, low tidal volume
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8
Q

Diffuse Lung Disease (effect on A-a gradient)

A

some air into lungs, but not enough.
–> V/Q mismatch (LOW) w/ wide A-a gradient
* often acute on chronic (bc some compensation)*
From: Air trapping & hyperinflation (COPD, Asthma)
Tx: non-invasive ventilation

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9
Q

pulmonary edema (effect on A-a gradient)

A

blood flow w/ NO ventilation of problem alveoli;

–> intrapulmonary shunt & A-a gradient >15

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10
Q

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)

A
  1. pulmonary insult (surgery/trauma, etc.)
    • lag period -
  2. Capillary injury (leaky, increased coagulation)
  3. exudative phase: edema
  4. Fibroproliferative phase: stiff lungs
    ==> hypoxemia!
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11
Q

Causes & risk factors for ARDS

A

Causes (4):
pneumonia, sepsis, aspiration, trauma

Risk factors: smoking, liver cirrhosis

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12
Q

ARDS treatment

A
  1. PEEP ventilation
    * but not too high P or [O2] –> could damage lungs
  2. flipping (to prone position) –> changes air distribution in lungs
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13
Q

Causes of hypoxemia (5)

A
  1. Bellows failure – failure to ventilate (low V/Q)
    2, 3. COPD/Asthma (Diffuse lung disease) –> low V/Q
  2. Pulmonary Edema –> Shunt
  3. ARDS –> Shunt
    ** NOT high V/Q or Dead space **
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14
Q

Why use PEEP

A

PEEP = mechanical ventilation,
forcibly opens airways that are closed (atelectic)
–> relieves hypoxemia by reducing/eliminating shunt!

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15
Q

causes of aerosolized pneumonia infection

A

=> person to person, rapid infection…
Most common: viruses, mycoplasma, TB
less common: legionella, fungi

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16
Q

diseases causing TRANSudative pleural effusions

A

Increased hydrostatic P: CHF, pulmonary edema, Liver cirrhosis
Decreased oncotic P: Nephrotic syndrome, dialysis
Decreased Parietal pleura P: trapped lung

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17
Q

diseases causing EXudative pleural effusions

A

Infectious: Parapneumonic, TB, pancreatitis

Other damage: cancer, hemothorax, chylothorax (blocked lymphatic duct)

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18
Q

pleural effusion

A

Sx: dyspnea, pleuritic pain, non-productive cough
Dx: CXR (sloping diaphragm - obliterated costophrenic angle), dull to percussion, restrictive PFT (FEV1 & FVC low, normal ratio)
* may be exudate or transudate depending on cause.*
Tx: thoracentesis, + drainage

19
Q

characteristics of Parietal pleura

A

(outer layer of pleural lining)
blood supply: systemic only
lymphatic drainage: yes, w/ large stoma
Innervation: yes!

20
Q

characteristics of visceral pleura

A

(inner layer of pleural linings)
Blood supply: systemic AND bronchial
Lymphatic drainage: yes, no stoma
Innervation: NO direct nerve endings

21
Q

normal pleural pressure

A

determined by elastic pressures between chest wall (out) & lungs (in).
* primary determinant of lung volumes!
normal pleural P = -5, more negative @ top of lungs

22
Q

transudate

A

non-inflammatory process causing movement of whole fluid into pleural space.
bc of: 1. decreased capillary oncotic P, 2. Increased hydrostatic P, 3. decreased pleural P (more negative)
“whole fluid” –> meets NORMAL pleural levels for protein & LDH

23
Q

Exudate

A

inflammatory process resulting in escape of fluid into pleural space;
due to increased pleural surface permeability and capillary damage (ie: infection, neoplasm).
–> meets Light’s Criteria for abnormal protein or LDH levels

24
Q

Light’s Criteria

A

Exudate is defined as meeting 1 or more of the criteria (abnormal levels):

  1. pleural protein/cap. protein > 50%
  2. pleural LDH/cap. LDH > 60%
  3. pleural LDH > 2/3 upper limit of normal (for pleural LDH)
25
Q

Parapneumonic effusion

A

pleural effusion caused by bacterial infection.

  • simple (just exudate, Tx = antibiotics)
  • empyema (pus, Tx: antibiotics + drain)
  • complex (very inflammatory, but NO pus, Tx: drain +/- antibiotics)
26
Q

hemorrhagic effusions

A
  • trauma
  • pulmonary embolism
  • neoplasm
27
Q

Tuberculous Effusion

A

small TB rupture, usually unilateral;
–> delayed type hypersensitivity & granulomatous rxn;
Dx: thoracentesis => exudative, Biopsy => necrotizing granuloma, few TB organisms
Tx: same as active TB infection (do not drain)

28
Q

Chylothorax

A

milky pleural effusion, w/ high triglyceride content,
due to thoracic duct blockage (usually from neoplasm).
* may be unilateral OR bilateral.

29
Q

mesothelioma

A

primary malignancy of the pleura, rare.

* associated w/ asbestos exposure*

30
Q

Tension Pneumothorax symptoms

A

Sx: decreased breath sounds, hyperresonance, low BP;
CXR: tracheal deviation away from affected lung
Tx: chest tube to free air from pleural space

31
Q

Pneumothorax (types, Dx)

A

= air in pleural space;
Sx: hyperresonance, decreased breath sounds,
CXR: dark + tracheal deviation.
Primary spontaneous: 20s, healthy, apical blebs on CXR
Secondary spontaneous: underlying COPD/lung disease
(higher mortality)
Trauma: hemodynamic instability!

32
Q

Atelectasis

A

Collapse of lung (alveoli), due to…
- External compression (pulm. effusion, pneumothorax)
–> peripheral
- Inadequate ventilation (mucus plug, tumor, etc.)
–> may be complete lung!
CXR: tracheal deviation TOWARD opacity

33
Q

COPD

A

PROGRESSIVE airflow limitation due to (ABNORMAL) increasing chronic inflammatory response to inflammatory triggers.
–> alveolar dilation & destruction, + remodeling.
** Not reversible.
Dx w/ spirometry (obstructive = low FEV/FVC ratio)

34
Q

Genetic factor for COPD

A

alpha-1 antitrypsin (inhibits neutrophil elastase) – increase risk panlobar emphysema in n. europeans, esp. smokers.
* replacement therapy debated – only if young @ onset.

35
Q

Effects of smoking on lungs

A
  • increase mucus production
  • decrease ciliary clearance
  • bronchiolar wall destruction, narrowing
  • proteolytic dysregulation –> alveolar destruction
36
Q

Lung inflammation in COPD vs. asthma

A

COPD: CD8 lymphocytes, macrophages & neutrophils; NOT reversible.
Asthma: CD4 lymphocytes & eosinophils; Reversible w/ Tx

37
Q

clinical features of COPD

A
  • prolonged expiration, hyperinflated chest, use of accessory muscles to breath, exertional dyspnea, non-productive cough, …
    CXR: flattened diaphragm
38
Q

Sequence of treatment for COPD

A

(1 step at a time, stop when controlled)

  1. Reduce risk factors (ie: smoking) **ONLY way to sustain lung f(x)!
  2. Pulmonary Rehab (exercise…)
  3. Bronchodilators
  4. Inhaled corticosteroids, PDE-4 inhibitors
  5. Palliative Care – O2, Surgery
39
Q

Steps of COPD pathogenesis (3)

A
  1. structural changes
    - alveolar destruction, collagen deposition/fibrosis, mucus gland hypertrophy
  2. Inflammation - unlimited proteases, CD8s., increased IL-8/TNF-a
  3. Airflow limitation
    - increased cholinergic tone (sm. m) & bronchoconstriction, loss of elastic recoil
40
Q

Pathogenesis of Asthma (4 steps)

A

(allergen triggers macrophage & mast cells –> Th2 & eosinophils…)

  1. Mucus plug (mucus hypersecretion)
  2. Edema (vasodilation –> plasma leak)
  3. Fibrosis (thickened basement membrane & epithelial shedding)
  4. bronchoconstriction (cholinergic reflex to irritants)
    • sm. muscle constriction (hyperplasia)
41
Q

Treatment options for asthma

A

1. Limit exposure to triggers + rapid inhaler for exacerbations

  1. add prophylactic inhaled glucocorticosteroids
  2. add long-acting B-agonist
  3. add leukotriene modifier
  4. add ORAL glucocoticosteroid (last resort, increase doses of other meds 1st)
42
Q

pathologic correlate of ARDS

A

= “diffuse alveolar damage”

    • hyaline membranes! ** (early exudative stage)
      also: edema (non-cardiogenic), endothelial & epithelial damage
43
Q

Equation for mean PA pressure

A

(used to Dx pulmonary HTN –> mean PA > 25 mmHg)

2/3(diastolic) + 1/3(systolic) = mean PA

44
Q

Calculating pulmonary vascular resistance

A

(mean PA pressure - PCWP)/CO = ____ Woods units

*PCWP = pulmonary capillary wedge pressure
mean PA - PCWP = “transpulmonary P”

HD 1 (9 decks)

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