Respiratory Failure (Week 8)

Question 1

Type I Hypoxic Failure

Answer 1

Intrinsic lung problem

PaO2 < 60 mmHg

Normal/low PaCO2

A-a gradient increased

Example: V/Q mismatch, shunt, diffusion impairment

Question 2

Type II Ventilatory Failure (Hypercapnic Respiratory Failure)

Answer 2

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

Question 3

Causes of hypoxic respiratory failure

Answer 3

V/Q mismatch

Shunt

Hypoventilation

Diffusion impairment

Low FiO2 (altitude)

Reduced mixed venous blood

Combinations of the above

Question 4

Does giving O2 help all causes of hypoxic respiratory failure?

Answer 4

V/Q mismatch (O2 helps)

Shunt (No!)

Diffusion impairment (O2 helps)

Hypoventilation

Low FiO2 (altitude)

Reduced mixed venous blood

Question 5

Diffusion impairment

Answer 5

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)

Question 6

Low mixed venous blood

Answer 6

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)

Question 7

Hypoventilation

Answer 7

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

Question 8

Normal A-a gradient

Answer 8

(Age + 10)/4

Cooper says Age/3

Question 9

What happens when you get hypoxemic?

Answer 9

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

Question 10

What can cause pulmonary edema?

Answer 10

1) Increased venous hydrostatic pressure (cardiogenic–CHF)
2) Decreased lymphatic drainage
3) Decreased colloid osmotic pressure
4) Increased vascular/epithelial permeability

Question 11

Peri-bronchial cuffing

Answer 11

Lymphatics upregulate to remove more fluid that has entered interstitum

Question 12

Interstitial edema

Answer 12

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

Question 13

Alveolar edema

Answer 13

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!

Question 14

How does ARDS cause pulmonary edema?

Answer 14

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

Question 15

Sequence of events for ARDS

Answer 15

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

Question 16

Is ALI the same as ARDS?

Answer 16

No, ARDS is a severe form of ALI

ARDS always has diffuse alveolar damage (DAD) that you can see under microscope

Question 17

Definition of ALI (and ARDS)

Answer 17

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

Question 18

What direct injury to the endothelium/epithelium causes ARDS?

Answer 18

1) Pulmonary infection (bacterial, viral, fungal)
2) Aspiration (chemical insult from gastric content)
3) Inhalation of toxins (Cl gas, NO2)

Question 19

What indirect injury to the endothelium/epithelium causes ARDS?

Answer 19

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

Question 20

Three microscopic phases of ARDS

Answer 20

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

Question 21

What happens macroscopically in ARDS?

Answer 21

“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

Question 22

How do you treat ARDS?

Answer 22

1) Supplemental O2
2) Intubation and mechanical ventilation (lungs pooped out from too much work of breathing)
3) Positive end-expiratory pressure (PEEP)

Question 23

Pros and cons of PEEP

Answer 23

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

Question 24

PEEP prevents de-recruitment–why is this good?

Answer 24

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

Question 25

3 ways the “lung-pump” can fail

Answer 25

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)

Question 26

How does increased PaCO2 affect PAO2?

Answer 26

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

Question 27

Equation for PaCO2 using dead space volume fraction

Answer 27

PaCO2 = K (VdotCO2/(VdotE(1 - (VD/Vt)))

Because VdotA = VdotE(1 - (VD/Vt))

Question 28

Use the equation for PaCO2 to explain why rapid shallow breathing worsens hypercapnia (raises PaCO2)

Answer 28

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

Question 29

What causes increased CO2 production in the body? (thus increasing R = CO2 production/O2 consumption)

Answer 29

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)

Question 30

Why can’t people with COPD get rid of CO2 as well as normal people can?

Answer 30

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

Question 31

What kinds of stress can add to difficulty breathing in patients with COPD?

Answer 31

Bronchitis, secretions, bronchospasms make it difficult to breathe out

Note: breathing in is fine because you actually pull the airway outward during inspiration

Question 32

3 mechanisms by which you’ll cause hypercapnia if you give a COPD patient O2

Answer 32

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)

Question 33

Things that cause hypoventilation

Answer 33

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)

Question 34

What factors can contribute to respiratory muscle failure and inability to maintain the work of breathing?

Answer 34

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)

Question 35

What happens if you get hypercapnia?

Answer 35

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

Question 36

How do you treat hypercapnia?

Answer 36

1) Identify and treat the cause!
2) Take over the work of breathing by ventilator (mask, inspiratory pressure, or PEEP)

Question 37

Pulmonary Function Testing–Simple Spirometry

(Big 3, and other 3)

Answer 37

Big 3, very helpful: FVC, FEV1, FEV1/FVC

Other 3, also helpful: TLC, RV, DLCO (diffusing capacity)

Question 38

Determining how severe an obstruction is

Answer 38

Look at FEV1/FVC %:

Mild: 65 - 80%

Moderately severe: 40 - 65%

Severe: < 40%

Question 39

Determining how severe a restriction is

Answer 39

Look at TLC (% of normal)

Mild: 65 - 80%

Moderately severe: 40 - 65%

Severe: < 40%

Question 40

What is the threshold for determining that there IS a difference between 2 FVC or FEV1 measurements?

Answer 40

FVC differences have to be greater than 11%

FEV1 differences have to be greater than 13%

Question 41

Conditions that have normal versus abnormal DLCO

Answer 41

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)

Question 42

What is DLCO?

Answer 42

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

Question 43

Diseases classified as pulmonary shunt

Answer 43

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)

Question 44

Diseases classified as hypoventilation

Answer 44

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)

Question 45

Diseases classified as V/Q mismatch

Answer 45

Pneumonia (has some areas of shunt too)

Pulmonary edema (has some areas of shunt too)

ARDS (has some areas of shunt too)

Question 46

Diseases classified as diffusion impairment

Answer 46

Liver cirrhosis because vasodilation

Interstitial lung disease (ILD)

Question 47

How does a pulse oximeter work?

Answer 47

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

Question 48

How does a capnometer work?

Answer 48

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

Question 49

What are the two categories of pulmonary edema?

Answer 49

Cardiogenic (CHF)

Non-cardiogenic (ARDS)

Question 50

What causes diffusion impairment (and thus an A - a gradient)?

Answer 50

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?

Question 51

Things that affect DLCO (diffusing capacity of the lung)

Answer 51

1) Cross-sectional area (emphysema has less)
2) Thickless (ILD)
3) Hemoglobin (anemia)

Question 52

Diseases classified as increased dead space ventilation

Answer 52

Pulmonary embolism

(Increased dead space ventilation means alveolar ventilation goes down and you can get hypoxemic)