Respiratory Failure (Week 8) Flashcards
Type I Hypoxic Failure
Intrinsic lung problem
PaO2 < 60 mmHg
Normal/low PaCO2
A-a gradient increased
Example: V/Q mismatch, shunt, diffusion impairment
Type II Ventilatory Failure (Hypercapnic Respiratory Failure)
PaCO2 > 50 mmHg
Respiratory acidosis (acidemic pH < 7.4)
All about the diaphragm
High PaCO2, low PaO2 (more than PaCo2)
A-a gradient normal
Example: hypoventilation
Causes of hypoxic respiratory failure
V/Q mismatch
Shunt
Hypoventilation
Diffusion impairment
Low FiO2 (altitude)
Reduced mixed venous blood
Combinations of the above
Does giving O2 help all causes of hypoxic respiratory failure?
V/Q mismatch (O2 helps)
Shunt (No!)
Diffusion impairment (O2 helps)
Hypoventilation
Low FiO2 (altitude)
Reduced mixed venous blood
Diffusion impairment
1) Thick alveolar-capillary membrane (ILDs)
2) Blood moving too fast to pick up O2 (HR too high)
3) Vasodilation so O2 can’t reach RBCs (microvascular dilatation in cirrhosis)
Low mixed venous blood
Have low PaO2 and high PaCO2
Happens when you have CHF (super good gas exchange gets you down to low PaO2 and high PaCO2) and abnormal lung (bad oxygenation so low PAO2 and high-ish PACO2)
Hypoventilation
Extreme case is holding your breath
Don’t let any more air in, so get no new O2 in, and build up CO2 from metabolism of body that you can’t get out (PaCO2 increases a lot–70 mmHg)
No A-a gradient because there is equilibration
Normal A-a gradient
(Age + 10)/4
Cooper says Age/3
What happens when you get hypoxemic?
Respiratory: PaO2 < 60 mmHg causes hyperventilation
Cardiac: stress response, pulmonary hypoxic vasoconstriction, bradycardia, hypotension
Blood: polycythemia (too many RBCs)
CNS: poor night vision, decreased mental performance, confusion, restlessness, brain damage
What can cause pulmonary edema?
1) Increased venous hydrostatic pressure (cardiogenic–CHF)
2) Decreased lymphatic drainage
3) Decreased colloid osmotic pressure
4) Increased vascular/epithelial permeability
Peri-bronchial cuffing
Lymphatics upregulate to remove more fluid that has entered interstitum
Interstitial edema
Edema but still have normal gas exchange
Reduced compliance (heavy lung) and small airways
J receptors sense increased fluid and cause dyspnea/tachypnea/SOB
Wheezing
Alveolar edema
Edema and have V/Q mismatch as a result
More reduced compliance (very very heavy lung)
Surfactant gone/neutralized
Lung can collapse
Rales, hypoxemia and hypocapnia
Can respond by giving O2 until you get shunt!
How does ARDS cause pulmonary edema?
Trauma –> hypotension (reduced O2 delivery) and inflammatory mediators to endothelial cells –> endothelial cells shrivel up and cause gaps –> epithelial cells shrivel up –> edema
Pneumonia –> damage to type I pneumocytes of epithelium –> gaps between type I pneumocytes –> endothelial cells shrivel up –> edema
Sequence of events for ARDS
1) Damage to alveolar-capillary membrane (either endothelium or type I pneumocytes of epithelium)
2) Increased permeability of membranes
3) Interstitial then alveolar edema
4) Surfactant neutralized
5) Alveolar filling/collapse –> airway closure
6) Reduced lung volumes, intrapulmonary shunting
Is ALI the same as ARDS?
No, ARDS is a severe form of ALI
ARDS always has diffuse alveolar damage (DAD) that you can see under microscope
Definition of ALI (and ARDS)
1) Oxygenation abnormality with PaO2/FiO2 ratio < 300 (< 200 in ARDS)
2) Bilateral opacities on chest X-ray (interstitial then alveolar edema)
3) Pulmonary capillary wedge pressure (PCWP) < 18
4) Acute onset
What direct injury to the endothelium/epithelium causes ARDS?
1) Pulmonary infection (bacterial, viral, fungal)
2) Aspiration (chemical insult from gastric content)
3) Inhalation of toxins (Cl gas, NO2)
What indirect injury to the endothelium/epithelium causes ARDS?
1) Sepsis (release of inflammatory mediators)
2) Acute pancreatitis (inflam mediators)
3) Nonthoracic trauma with hypotension (Inflam mediators)
4) Narcotic overdose pulmonary edema
5) Cardiopulmonary bypass
Three microscopic phases of ARDS
1) Exudative phase: alveolar and interstitial edema, hyaline membranes (proteinaceous precipitation)
2) Proliferative phase: type II pneumocyte proliferation, inflam mediators and PMNs infiltrate interstitum, hyaline membranes organize
3) Fibrotic phase: macrophages release inflam mediators, angiogenesis, collagen causes fibrosis of hyaline membranes, interstitum and alveolar ducts
Result: stiff noncompliant lung with atelectasis and edema
What happens macroscopically in ARDS?
“Liver-like” lungs that are airless and heavy
1) Stiff lungs with reduced compliance
2) Fall in FRC (because of alveoli collpasing)
3) V/Q mismatch and/or shunt
4) Everything leads to hypoxemia
How do you treat ARDS?
1) Supplemental O2
2) Intubation and mechanical ventilation (lungs pooped out from too much work of breathing)
3) Positive end-expiratory pressure (PEEP)
Pros and cons of PEEP
Pros: recruits collapsed/unstable alveoli and improves oxygenation, shifts edema from alveoli to interstitum (better!)
Cons: decreases CO because higher intrathoracic pressure clamps vena cava
PEEP prevents de-recruitment–why is this good?
1) Increase PaO2
2) Recruit alveoli
3) Improve V/Q matching
Push all the stuff (proteins, leukocytes, water, etc) to the side so you can get gas exchange
Changes shunt to V/Q mismatch and you can give O2 to correct problem
3 ways the “lung-pump” can fail
1) Central depression (disconnect between brain and diaphragm)
2) Respiratory muscle problem (weakness or fatigue)
3) Mechanical defects of chest wall (spine contorted so traps chest wall and can’t take deep breath)
How does increased PaCO2 affect PAO2?
If PaCO2 is increased, PAO2 will decrease
Because CO2 is high in the blood, and will be taking up spots on hemoglobin, it will unload a lot at the alveoli –> PACO2 will go up and take up space in the alveolus so that PAO2 must decrease as a result (just not enough space) –> this obviously also causes PaO2 to decrease because there’s not as much O2 in the alveolus to get into the artery
Equation for PaCO2 using dead space volume fraction
PaCO2 = K (VdotCO2/(VdotE(1 - (VD/Vt)))
Because VdotA = VdotE(1 - (VD/Vt))
Use the equation for PaCO2 to explain why rapid shallow breathing worsens hypercapnia (raises PaCO2)
PaCO2 = K (VdotCO2/(VdotE(1 - (VD/Vt)))
When you have rapid shallow breathing, you decrease tidal volume but dead space volume stays the same so VD/Vt increases and that causes VdotA (denominator) to increase and thus PaCO2 increases
What causes increased CO2 production in the body? (thus increasing R = CO2 production/O2 consumption)
1) Fever
2) Sepsis (infection, then body has to use lots of energy generating WBCs and creates CO2 because of this hypermetabolic state)
3) Burns (body has to use energy to protect burn areas with WBCs and has to make new skin)
4) Thyroidtoxicosis (hyperthyroidism, make lots of CO2)
5) Exercise
6) Over-feeding patient with bad lungs (carbs converted to fat and that causes CO2 production)
Why can’t people with COPD get rid of CO2 as well as normal people can?
1) High dead space volume (VD)
2) Near maximal alveolar ventilation (VdotA)
3) Can’t increase Vt because diaphragm is flat and contracts outward which doesn’t give them more volume
Normal people increase ventilation in order to get rid of more CO2, but because of these three things, COPD people can’t increase ventilation well
What kinds of stress can add to difficulty breathing in patients with COPD?
Bronchitis, secretions, bronchospasms make it difficult to breathe out
Note: breathing in is fine because you actually pull the airway outward during inspiration
3 mechanisms by which you’ll cause hypercapnia if you give a COPD patient O2
1) Create V/Q mismatch (normally have good hypoxic vasoconstriction to get good V/Q match, but O2 opens up blood vessels to BAD alveoli)
2) Decreased respiratory drive (PO2<60 makes you breathe faster which is good, but giving O2 takes away this mechanism; minor mechanism though)
3) Haldane effect (give O2 and that goes to the RBC and pushes off CO2)
Things that cause hypoventilation
1) Decreased respiratory drive (medulla or pons messed up by stroke or tumor, sleep apnea, drugs/sedatives, won’t breathe)
2) Reduction in respiratory muscles or chest wall function (break ribs, neuromuscular disease, kyphoscoliosis, can’t breathe)
3) Disorder of spinal cord (cervical cord around C3, 4, 5)
What factors can contribute to respiratory muscle failure and inability to maintain the work of breathing?
1) High work required (resistance from COPD or stiffness from pulmonary edema)
2) V/Q mismatch makes it hard to ventilate
3) Reduced respiratory muscle mass (malnutrition)
4) Hypoxia
5) Electrolyte deficiencies (esp P needed to make ATP)
What happens if you get hypercapnia?
Respiratory acidosis
Cardiac: stress response, systemic vasodilation more than increased cardiac output, catacholamine surge causes headaches, cerebral edema, flushing, diaphoresis, pulmonary artery constriction
CNS: headache, lethargy, coma
Pulmonary: hypoxic vasoconstriction and pulmonary hypertension
How do you treat hypercapnia?
1) Identify and treat the cause!
2) Take over the work of breathing by ventilator (mask, inspiratory pressure, or PEEP)
Pulmonary Function Testing–Simple Spirometry
(Big 3, and other 3)
Big 3, very helpful: FVC, FEV1, FEV1/FVC
Other 3, also helpful: TLC, RV, DLCO (diffusing capacity)
Determining how severe an obstruction is
Look at FEV1/FVC %:
Mild: 65 - 80%
Moderately severe: 40 - 65%
Severe: < 40%
Determining how severe a restriction is
Look at TLC (% of normal)
Mild: 65 - 80%
Moderately severe: 40 - 65%
Severe: < 40%
What is the threshold for determining that there IS a difference between 2 FVC or FEV1 measurements?
FVC differences have to be greater than 11%
FEV1 differences have to be greater than 13%
Conditions that have normal versus abnormal DLCO
Normal: chest wall abnormality, neuromuscular disease
Abnormal (reduced): COPD, alpha-1 anti-trypsin, ILD, pulmonary vascular disease/hypertension, anemia
Abnormal (increased): polycythemia, pulmonary hemorrhage, left-to-right shunt, asthma (because of inflammation and thus increased blood flow, but also DLCO could be normal)
What is DLCO?
Diffusing capacity of the lung measured by having patient inspire known concentration of CO, hold for 10 seconds, then expire
We can determine how well they UPTAKE CO from alveoli into blood
Measures volume of gas transferred across alveolar-capillary membrane
Diseases classified as pulmonary shunt
Pneumonia (as well as V/Q mismatch)
Right-to-left shunt (atrial septal defect w/reversal of flow)
Pulmonary edema
Atelectasis
ARDS (as well as V/Q mismatch)
Diseases classified as hypoventilation
Hypercapnic failure (Type II respiratory failure)!
1) Not breathing because of decreased drive/control mechanisms: sleep apnea, sedative drugs
2) Not breathing because of mechanical problem: muscle diseases (polymyositis, muscular dystrophy), neurologic disease (polio, ALS), chest wall/pleural disease (kyphoscoliosis, pneumothorax)
Diseases classified as V/Q mismatch
Pneumonia (has some areas of shunt too)
Pulmonary edema (has some areas of shunt too)
ARDS (has some areas of shunt too)
Diseases classified as diffusion impairment
Liver cirrhosis because vasodilation
Interstitial lung disease (ILD)
How does a pulse oximeter work?
Relies on differences of absorption of infrared and red light based on if hemoglobin oxygenated or deoxygenated
Downside: will measure CO bound to hemoglobin as oxygenated (smokers have CO in lungs), so SpO2 of 95% in smoker is really SpO2 of 85%
Also, doesn’t give you A-a gradient
How does a capnometer work?
Measures end tidal CO2 (remember, CO2 = 0 in air), and actually traces all levels of CO2, but you can determine end tidal CO2 with a capnometer
Photodetector with infrared light source used to measure expired gas CO2
First sees no CO2 (from dead space) then a little CO2, then more (alveolar gas)
Measured CO2 from alveolar air (later in exhalation, after past dead space) gives you measure of CO2
What are the two categories of pulmonary edema?
Cardiogenic (CHF)
Non-cardiogenic (ARDS)
What causes diffusion impairment (and thus an A - a gradient)?
1) Increased blood flow (HR) so decreased transit time: exercise
2) Increased path length/thickness: pulmonary edema, ILD, interstitial fibrosis
3) Vasodilation: cirrhosis (end stage liver disease)
4) Decreased functioning of pulmonary capillaries (increases transit time for functioning area?): pulmonary embolism, pulmonary vascular disease, emphysema?
Things that affect DLCO (diffusing capacity of the lung)
1) Cross-sectional area (emphysema has less)
2) Thickless (ILD)
3) Hemoglobin (anemia)
Diseases classified as increased dead space ventilation
Pulmonary embolism
(Increased dead space ventilation means alveolar ventilation goes down and you can get hypoxemic)
