W2L5 Respiratory Failure

Question 1

Define respiratory failure (type 1 and 2)

Answer 1

-Impairment of gas exchange between ambient air and circulating blood, occurring in intrapulmonary gas exchange (type 1) or in the movement of gases in and out of the lungs (type 2)

Question 2

Clinical features of patients with respiratory failure (5)

Answer 2

• SOB, drowsy, confusion, headache (particularly morning headache), inicreased resp rate, low O2 saturation

Question 3

Principles of treating respiratory failure (3 key components) (2 bonus)

Answer 3

-Maintain adequate O2delivery
(But remember, too much oxygen can be detrimental to
some patients with chronic lung disease)

-Reduce respiratory workload
– Provide rest for the respiratory muscles

• Maximise ventilation

(also maintain stable pH/ electrolytes and try and target the cause)

Question 4

What do pulse oximetry vs ABGs measure?

Answer 4

The pulse oximeter measures the hemoglobin oxygen saturation, while the arterial blood gas measures the pressure of oxygen gas dissolved in the blood (oxygen not bound to hemoglobin).

Question 5

What conditions may increase the drive to breathe (4) ?

Answer 5

Hypoxaemia, anxiety, exercise, metabolic acidosis

Question 6

What conditions may decrease the drive to breathe (4) ?

Answer 6

Metabolic alkylosis (not by much), narcotic overdose, breath holding (hypercapnia), sedatives

Question 7

What is elastic WOB? When is it increased?

Answer 7

Work required to inflate the lungs: related to lung compliance–> increased in pulmonary oedema and pulmonary fibrosis

Question 8

What is resistive WOB? When is it increased?

Answer 8

Force needed to push air through the airways–> increased in asthma where pipes are smaller (bronchoconstriction)

Question 9

What are the 3 problems that can occur in a conducting airways?

Answer 9

Obstruction/narrowing
• Bronchospasm
• Secretions/sputum verryy common problem in the hospital.
• Collapse
– Lack of elastic support eg emphysema
– Endoluminal (carcinoma, sputum)

Question 10

When is expiration active?

Answer 10

During periods of high activity

Question 11

Normal values of ABGs:
pH
PaCO2
PaO2
HCO3
SaO2

Answer 11

• pH= 7.40 (7.35-7.45, 2 SDs)
• PaCO2= 40 (35-45) mmHg
• PaO2= 100 (>85) mmHg
• HCO3= 24 (22-30)
• SaO2 95-100%

Question 12

What is the Aa gradient?
How do you calculate the Aa gradient?
What is a normal Aa gradient?

Answer 12

It is the difference between the arterial (a) and
alveolar (A) concentration of oxygen
– If elevated it suggests a problem with diffusion or a V/Q mismatch (less commonly shunt)

• On room air at sea level (150= pO2)
– A-a = (150 – (1.25· PaCO2)) – PaO2
– 7-14 in young adults, higher in the elderly

Question 13

What does impaired gas exchange (type 1 failure) primarily cause?

Answer 13

hypoxaemia (PaO2<60mmHg)

Question 14

What does hypoventilation primarily cause?

Answer 14

hypercapnia (PaCO2>50mmHg) (O2 will also fall)

Question 15

What conditions/ states result in hypoxaemia? (5)

Answer 15

• Reduced inspired O2 – Altitude, fires

• Ventilation-perfusion mismatch
– Pneumonia, pulmonary embolus, pulmonary oedema

• Impaired diffusion
- pulmonary fibrosis, COPD (less AC memb, dissolved by proteases–> in this example also airflow obstruction), any interstitial lung disease

– Shunt (extreme VQ mismatch)

– hypoventilation

Question 16

What conditions cause hypercapnic resp failure? (type II failure) (7)

Answer 16

• occasionally compensated metabolic alkylosis

• Central depression
– Narcotic overdose, sedation

• Completely blocked upper airway

• Primary “ pump” failure
– Neuromuscular disease eg GuillainBarreSyndrome, MND

• muscle fatigue as a result of increased WOB
• intrinsic lung disease eg severe COPD
• chest wall abnormailties: obesity and kyphosis

Question 17

How do we assess patients with possible respiratory failure and establish a diagnosis?

Answer 17

ABGs

Question 18

What is ARDS and why does it cause resp failure?

Answer 18

Acute respiratory distress syndrome: Following an acute inflammatory state such as multiple fracture trauma, multi-organ failure, sepsis.

ARDS is associated with diffuse alveolar damage (DAD) and lung capillary endothelial injury. The early phase is described as being exudative (increase in the permeability of the alveolar-capillary barrier, leading to an influx of fluid into the alveoli), whereas the later phase is fibroproliferative in character.

The main site of injury may be focused on either the vascular endothelium (eg, sepsis) or the alveolar epithelium (eg, aspiration of gastric contents). Injury to the endothelium results in increased capillary permeability and the influx of protein-rich fluid into the alveolar space.

2 KEY POINTS:
Increased pulmonary capillary permeability causing:

1. Gas exchange defect low V/Q units
   shunt
2. Mechanical defect
   increased elastic work of breathing

Question 19

How will ARDS present?

Answer 19

• multiple trauma
• agitation, resp distress and high RR
• high pulse and BP, bilateral basal creps
• ABG pH 7.48, PaO2 50, PaCO2 30, HCO3 26 (type 1 resp failure)
• CXR: fluid on lungs

Question 20

Management of ARDS (4):

Answer 20

= Management of respiratory failure
– High flow humidified oxygen
– Careful monitoring (clinical, SpO2, ABG)
– CPAP/ BiPAP
– Invasive ventilation if unable to sustain adequate PaO2 or if type II ventilatory failure develops

Question 21

How are O2 saturation and ABGs related?

Answer 21

O2 saturation curve: This curve shows that the percent of hemoglobin saturated with oxygen is directly related to the arterial partial pressure of oxygen. The higher the PaO2, the more oxygen is bound to hemoglobin and the higher the saturation (until the limit of 100% saturation is reached).

Notice that the oxyhemoglobin dissociation curve is sigmoidal. As the curve is flat at the high PaO2 values, changes in the PaO2 at this range have little effect on the oxygen saturation. On the other hand, at the steep part of the curve, small changes in the PaO2 produce large differences in oxygen saturation.

For instance, once the PaO2 is above 60 mm Hg, the curve is almost flat, indicating there is little change in saturation above this point. As the PaO2 increases from 60 mm Hg to 100 mm Hg, the oxygen saturation only increases from 90 to 98%. On the other hand, if the PaO2 were to drop the same amount, from 60 mm Hg to 20 mm Hg, the oxygen saturation would decrease from 90% to 33%.

Question 22

What would be the ABGs in a patient with motor neurone disease chronic resp failure?

Answer 22

Normal pH, High paCO2, low paO2= hypoventilation due to pump failure.

Question 23

What are the ABGs in an acute asthma attack?

Answer 23

High pH, low PaO2, low PaCO2, big Aa gradient

Question 24

What are the AGBs 2 hours after an acute asthma attack when the patient is undergoing type II failure?

Answer 24

Low pH, Low O2, High CO2