L35 - Respiratory Failure

Question 1

Define respiratory failure.

Answer 1

when lungs are unable to maintain arterial blood gases at normal levels when the subject breathes air at rest

Question 2

What processes malfunction during respiratory failure?

Answer 2

1. Failure for oxygenation
2. Failure for CO2 removal
3. Failure for both

Question 3

What are the general guide for arterial blood gases in respiratory failure?

Answer 3

 PO2 <60 mm Hg and/or

 PCO2 >50 mm Hg

Question 4

What are the 2 types of resp. failure?

Answer 4

A. Pump (Ventilatory) failure

B. Gas-exchange failure

Question 5

In ventilatory failure, what 2 main groups of defects develop?

Answer 5

1) defect along respiratory control pathway from medulla through resp. muscles
2) Defect in ventilatory apparatus

Question 6

What 3 pathology conditions cause ventilatory failure by neural failure?

Answer 6

1. Depressed central respiratory drive
2. Defect in nerves to respiratory muscles
3. Neuromuscular disease

Question 7

Name some diseases that correspond to the different neural defect mechanisms leading to ventilatory failure.

Answer 7

1. Depressed central respiratory drive: Brain tumour or hemorrhage, Narcotic drugs (morphine)
2. Defect in nerves to resp. muscles: poliomyelitis
3. Neuromuscular disease: myasthenia gravis (transmitter deficiency)

Question 8

What 4 ways can Defect in ventilatory apparatus lead to Ventilatory failure?

Answer 8

1. Thoracic cage deformities / disorder
2. Respiratory muscle weakness
3. Limitation of lung expansion
4. Airway obstruction

Question 9

Give examples of defects of resp. apparatus leading to resp. failure.

Answer 9

1. Thoracic cage deformities / disorder, e.g.:
    Kyphoscoliosis
    Morbid obesity
2. Respiratory muscle weakness, e.g. trauma
3. Limitation of lung expansion, e.g. interstitial lung diseases - pulmonary fibrosis)
4. Airway obstruction, e.g. COPD - chronic bronchitis)

Question 10

Apart from ventilatory failure, what leads to resp. failure?

Answer 10

Gas- exchange failure

Question 11

What defects arise from gas-exchange failure?

Answer 11

(i) Defective alveolocapillary membrane (increase thickness, less SA)
(ii) Mismatch of ventilation and perfusion (V/Q mismatching)

Question 12

Give examples of diseases causing defective alveolocapillary membrane?

Answer 12

 Interstitial lung diseases (e.g. fibrosis of membrane)

 Acute respiratory distress syndrome (ARDS): fluid filled lungs

Question 13

Give examples of diseases causing V/Q mismatch?

Answer 13

Uneven distribution of ventilation:
 COPD
 Interstitial lung diseases

Uneven distribution of blood flow: vascular diseases

Question 14

Difference between type I and II of respiratory failure according to pO2 and pCO2 levels?

Answer 14

Type I = gas exchange failure
LOW pO2 < 60 mmHg
NORMAL OR LOW pCO2 (50mmHg or below)

Type II= pump (ventilatory) failure
LOW pO2 < 60mmHg
HIGH pCO2 >50mmHg

Question 15

Explain how alveolar hypoventilation leads to one type of resp. failure?

Answer 15

Alveolar hypoventilation (either due to defect in ventilatory appartus or neural defect) > Pump (ventilatory) failure > Severe hypoxemia and hypercapnia > Type II resp. failure

Question 16

Explain the compensation to hypoventilation?

Answer 16

Caused by either defect in ventilatory apparatus or nerves > NO vent. compensation > further worsen

Question 17

Explain how COPD leads to one type of resp. failure? (remember types of resp. failure are different in CO2 levels)

Answer 17

COPD > obstructive airway = high Raw > ventilatory apparatus failure + V/Q mismatch (gas-exchange failure) > Severe hypoxemia and moderate hypercapnia > Type II resp. failure

Question 18

Explain the compensation to COPD?

Answer 18

Some ventilatory compensation but LIMITED by high Raw

Question 19

Explain how Interstitial lung disease leads to one type of resp. failure?

Answer 19

Interstitial lung disease e.g. severe fibrosis of alveolocapillary wall > diffusion impairment and V/Q mismatch > gas exchange failure > Severe hypoxemia, unchanged pCO2 > Type I resp. failure

Question 20

Explain the compensation to interstitial lung disease?

Answer 20

Ventilatory compensation effective for pCO2 but not pO2 due to LOW O2 SOLUBILITY

Question 21

Explain how ARDS leads to one type of resp. failure?

Answer 21

ARDS > rapid severe inflammation and fluid accumulation > gas exchange failure > Extreme hypoxemia and low arterial CO2 > Type I resp. failure

Question 22

Explain the ventilatory compensation to ARDS?

Answer 22

ARDS > rapid severe inflammation and fluid accumulation in alveoli

VERY STRONG VENTILATORY COMPENSATION > cause fall in pCO2 (CO2 washed out) but cannot correct severe hypoxemia due to Low O2 Solubility

Question 23

What are the 4 causes of hypoxemia?

Answer 23

 Hypoventilation
 Diffusion impairment
 Shunt
 V/Q mismatching

Question 24

Signs of hypoxemia?

Answer 24

 Cyanosis (most common sign)
 Tachycardia (reflex by chemoreceptors)
 Mental clouding (CNS) = direct depressant action (on central chemoreceptors)
 Low PaO2 in blood sample

Question 25

What organ systems are most susceptible to hypoxemia?

Answer 25

CNS, CVS

Question 26

How can hypoxemia cause metabolic acidosis?

Answer 26

Low O2 > cessation of aerobic respiration > anaerobic glycolysis > lactic acid accumulation > metabolic acidosis

Question 27

Classify the SEVERITY (not type) of hypoxemia based on PaO2 values.

Answer 27

Mild = 60mmHg Severe <40 mmHg Very severe <20mmHg

Question 28

List the 3 physiological changes under mild hypoxemia.

Answer 28

Impair mental performance Impair vision Mild hyperventilation (induced by peripheral chemoreceptors)

Question 29

List the physiological changes under severe hypoxemia. (divide into CVS and CNS)

Answer 29

CNS: Depressive effects, headache, sleepiness, confusion CVS: Tachycardia, mild hypertension + pulmonary hypertension (hypoxic global vasoconstriction)

Question 30

List the physiological changes under Very severe hypoxemia.

Answer 30

CNS: permanent damage CVS: direct depressant action on heart: bradycardia, hypotension + Severe pulmonary hypertension Retinal hemorrhages Renal: Proteinuria Convulsions

Question 31

What are some causes of hypercapnia?

Answer 31

Hypoventilation V/Q mismatch Misguided use of O2 therapy

Question 32

How can misguided use of O2 therapy for COPD patient cause hypercapnia?

Answer 32

COPD patient: low O2 = more important drive than high CO2 Drastic increase in O2 > Abolish ventilatory drive > decrease Ventilation > Hypercapnia Abolish hypoxic vasoconstriction > worsen V/Q mismatch

Question 33

What are the effects of moderate hypercapnia?

Answer 33

Control of blood flow to brain by CO2, not neural Moderate hypercapnia > cerebral vasodilatation > increase cerebral blood flow> increase intracranial pressure> headache

Question 34

What are the effects of severe hypercapnia?

Answer 34

Severe hypercapnia = direct depressant action:  Narcotic (催眠)  Clouding of consciousness

Question 35

What are the two types of acidosis caused by?

Answer 35

Respiratory acidosis = rise in volatile acid level (e.g. CO2) Metabolic acidosis = rise in non-volatile acid level (e.g. lactate)

Question 36

What are the 4 types of hypoxemia? (HASH)

Answer 36

Hypoxemic Anemic Stagnant Histotoxic

Question 37

Compare the PaO2 between types of hypoxemia.

Answer 37

``` Hypoxemic = low PaO2 Anemic = normal Stagnant = normal Histotoxic = normal ```

Question 38

What are the 4 types of hypoxemia effect?

Answer 38

1) Hypoxemic: Insufficient O2 reaching blood 2) Anemic: Reduced O2 carrying capacity of blood 3) Stagnant: Impaired blood flow = fail to transport O2 4) Histotoxic: Impaired utilization of O2 by the cell

Question 39

Causes of hypoxemic hypoxia?

Answer 39

 Low atmospheric PO2 (e.g. high altitude) |  Respiratory failure

Question 40

Causes of Stagnant hypoxia?

Answer 40

 Heart failure  Circulatory shock  Local disruption of blood flow

Question 41

Causes of Anemic hypoxia?

Answer 41

 decrease RBC  Abnormal hemoglobin  Carbon monoxide poisoning

Question 42

Causes of Histotoxic hypoxia?

Answer 42

` Cellular poisoning by cyanide |  Tissue edema

Question 43

Give examples for treating underlying disease for resp. failure e.g. infection or neuromuscular disorder

Answer 43

 Infection > antibiotic therapy |  Neuromuscular disorder > specific treatment

Question 44

What are the two ways to treat airway obstruction?

Answer 44

 Remove secretion > cough, bronchoscopy, hydration and drugs to thin sputum  Bronchoconstriction > use bronchodilators

Question 45

What are the 3 treatment options for hypoxemia?

Answer 45

O2 therapy for COPD or shock lungs Mechanical ventilation for neuromuscular disorder/ hypercapnia Mechanical ventilator with PEEP (positive end-expiratory pressure) for shock lung

Question 46

How does O2 therapy differ between COPD and SHOCK patients?

Answer 46

``` COPD = 25-30% O2 Shock = 60% O2 ```

Question 47

What treatments for cardiac failure leading to resp. failure?

Answer 47

1) Diuretics for edema, fluid retention (increase urine output) 2) Digitalis drug for heart failure (increase contractility)

Question 48

What are the three causes of cardiac failure relating to resp. failure?

Answer 48

- Hypoxic pulmonary vasoconstriction - Polycythemia - Water retention

Question 49

What are some other hazards of O2 therapy?

Answer 49

Removal of hypoxic ventilatory drive > hypercapnia, O2 toxicity & oxidative damage : - edema, - fibrosis, - absorption acelectasis (form of alveolar collapse)

Question 50

How is Retrolental fibroplasia caused by misused O2 therapy on infants with respiratory distress syndrome at birth?

Answer 50

Infant RDS > loss of surfactant > apply O2 therapy > body acclimatize to new O2 level > removal of therapy cause hypoxia > fibrous tissue grows into viscous humour > blinds baby

Question 51

Why does O2 therapy of too high O2 conc cause absorption atelectasis?

Answer 51

atelectasis = collapsed lungs Normally lung has 78% nitrogen that remains in alveolar space and maintain pressure to keep lungs inflated 100% oxygen therapy displaces nitrogen > loss of intra-alveolar pressure > all gas quickly absorbed into capillary > collapse lungs