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
