Respiratory pathophys. Part 1 Flashcards
timeframe of Acute Respiratory Failure
in minutes to days,
failure to provide adequate gas exchange
–> low O2 &/or high CO2
A-a gradient
equation and purpose
–> 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! ***
PaO2 cut-off for adequate oxygen supply to tissues
hypoxia begins at PaO2 = 40 mm Hg
–> 75% O2 Saturation
pH and PaCO2 changes in ACUTE acidosis (vs. chronic)
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
Respiratory V/Q mismatch (Low V/Q)
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
Respiratory Shunt
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
Bellows failure
failure of respiratory muscles or internal drive to breath.
* normal A-a gradient (nothing wrong w/ lungs or vasculature!)
Tx: intubation/mechanical ventilation
Causes of Bellows failure (4 types)
- No effort
- depressant drugs, head trauma/hypoperfusion
- Impaired nerves or muscles
- polio, curare, neurodeg. diseases
- Muscle fatigue –> obesity, pulmonary fibrosis
- Insufficiency –> flat diaphragm, low tidal volume
Diffuse Lung Disease (effect on A-a gradient)
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
pulmonary edema (effect on A-a gradient)
blood flow w/ NO ventilation of problem alveoli;
–> intrapulmonary shunt & A-a gradient >15
Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)
- pulmonary insult (surgery/trauma, etc.)
- lag period -
- Capillary injury (leaky, increased coagulation)
- exudative phase: edema
- Fibroproliferative phase: stiff lungs
==> hypoxemia!
Causes & risk factors for ARDS
Causes (4):
pneumonia, sepsis, aspiration, trauma
Risk factors: smoking, liver cirrhosis
ARDS treatment
- PEEP ventilation
* but not too high P or [O2] –> could damage lungs - flipping (to prone position) –> changes air distribution in lungs
Causes of hypoxemia (5)
- Bellows failure – failure to ventilate (low V/Q)
2, 3. COPD/Asthma (Diffuse lung disease) –> low V/Q - Pulmonary Edema –> Shunt
- ARDS –> Shunt
** NOT high V/Q or Dead space **
Why use PEEP
PEEP = mechanical ventilation,
forcibly opens airways that are closed (atelectic)
–> relieves hypoxemia by reducing/eliminating shunt!
causes of aerosolized pneumonia infection
=> person to person, rapid infection…
Most common: viruses, mycoplasma, TB
less common: legionella, fungi
diseases causing TRANSudative pleural effusions
Increased hydrostatic P: CHF, pulmonary edema, Liver cirrhosis
Decreased oncotic P: Nephrotic syndrome, dialysis
Decreased Parietal pleura P: trapped lung
diseases causing EXudative pleural effusions
Infectious: Parapneumonic, TB, pancreatitis
Other damage: cancer, hemothorax, chylothorax (blocked lymphatic duct)
pleural effusion
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
characteristics of Parietal pleura
(outer layer of pleural lining)
blood supply: systemic only
lymphatic drainage: yes, w/ large stoma
Innervation: yes!
characteristics of visceral pleura
(inner layer of pleural linings)
Blood supply: systemic AND bronchial
Lymphatic drainage: yes, no stoma
Innervation: NO direct nerve endings
normal pleural pressure
determined by elastic pressures between chest wall (out) & lungs (in).
* primary determinant of lung volumes!
normal pleural P = -5, more negative @ top of lungs
transudate
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
Exudate
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
Light’s Criteria
Exudate is defined as meeting 1 or more of the criteria (abnormal levels):
- pleural protein/cap. protein > 50%
- pleural LDH/cap. LDH > 60%
- pleural LDH > 2/3 upper limit of normal (for pleural LDH)
Parapneumonic effusion
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)
hemorrhagic effusions
- trauma
- pulmonary embolism
- neoplasm
Tuberculous Effusion
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)
Chylothorax
milky pleural effusion, w/ high triglyceride content,
due to thoracic duct blockage (usually from neoplasm).
* may be unilateral OR bilateral.
mesothelioma
primary malignancy of the pleura, rare.
* associated w/ asbestos exposure*
Tension Pneumothorax symptoms
Sx: decreased breath sounds, hyperresonance, low BP;
CXR: tracheal deviation away from affected lung
Tx: chest tube to free air from pleural space
Pneumothorax (types, Dx)
= 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!
Atelectasis
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
COPD
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)
Genetic factor for COPD
alpha-1 antitrypsin (inhibits neutrophil elastase) – increase risk panlobar emphysema in n. europeans, esp. smokers.
* replacement therapy debated – only if young @ onset.
Effects of smoking on lungs
- increase mucus production
- decrease ciliary clearance
- bronchiolar wall destruction, narrowing
- proteolytic dysregulation –> alveolar destruction
Lung inflammation in COPD vs. asthma
COPD: CD8 lymphocytes, macrophages & neutrophils; NOT reversible.
Asthma: CD4 lymphocytes & eosinophils; Reversible w/ Tx
clinical features of COPD
- prolonged expiration, hyperinflated chest, use of accessory muscles to breath, exertional dyspnea, non-productive cough, …
CXR: flattened diaphragm
Sequence of treatment for COPD
(1 step at a time, stop when controlled)
- Reduce risk factors (ie: smoking) **ONLY way to sustain lung f(x)!
- Pulmonary Rehab (exercise…)
- Bronchodilators
- Inhaled corticosteroids, PDE-4 inhibitors
- Palliative Care – O2, Surgery
Steps of COPD pathogenesis (3)
- structural changes
- alveolar destruction, collagen deposition/fibrosis, mucus gland hypertrophy - Inflammation - unlimited proteases, CD8s., increased IL-8/TNF-a
- Airflow limitation
- increased cholinergic tone (sm. m) & bronchoconstriction, loss of elastic recoil
Pathogenesis of Asthma (4 steps)
(allergen triggers macrophage & mast cells –> Th2 & eosinophils…)
- Mucus plug (mucus hypersecretion)
- Edema (vasodilation –> plasma leak)
- Fibrosis (thickened basement membrane & epithelial shedding)
- bronchoconstriction (cholinergic reflex to irritants)
- sm. muscle constriction (hyperplasia)
Treatment options for asthma
1. Limit exposure to triggers + rapid inhaler for exacerbations
- add prophylactic inhaled glucocorticosteroids
- add long-acting B-agonist
- add leukotriene modifier
- add ORAL glucocoticosteroid (last resort, increase doses of other meds 1st)
pathologic correlate of ARDS
= “diffuse alveolar damage”
- hyaline membranes! ** (early exudative stage)
also: edema (non-cardiogenic), endothelial & epithelial damage
- hyaline membranes! ** (early exudative stage)
Equation for mean PA pressure
(used to Dx pulmonary HTN –> mean PA > 25 mmHg)
2/3(diastolic) + 1/3(systolic) = mean PA
Calculating pulmonary vascular resistance
(mean PA pressure - PCWP)/CO = ____ Woods units
*PCWP = pulmonary capillary wedge pressure
mean PA - PCWP = “transpulmonary P”
