S5: respiratory failure & pulmonary embolism

Question 1

Define hypoxia, hypoxaemia and the difference between the two terms

Answer 1

Hypoxia = reduced oxygen at the tissue level
-abnormalities occurring at any point on the oxygen supply chain can result in hypoxia
Hypoxaemia = decrease in the partial pressure of oxygen
-pO2 of the blood is determined by gas exchange in the lung

Question 2

Define type 1 respiratory failure

Answer 2

Low PaO2 < 8kPa or O2 saturation < 90%
pCO2 normal or low
Gas exchange is impaired at the level of alveolar-capillary membrane
Type 1 RF can progress to type 2

Question 3

Define type 2 respiratory failure

Answer 3

Low PaO2 and high PaCO2 > 6.5 kPa

Reduced ventilatory effort (pump failure) or inability to overcome increased resistance to ventilation of entire lung

Question 4

List the effects of hypoxaemia

Answer 4

Impaired CNS function, confusion, irritability & agitation
Tachypnoea
Tachycardia
Cardiac arrhythmias & cardiac ischaemia
Hypoxic vasoconstriction of pulmonary vessels
Central cyanosis

Question 5

Explain the difference between central cyanosis and peripheral cyanosis

Answer 5

Central cyanosis – seen in oral mucosa, tongue & lips
-indicates hypoxaemia
Peripheral cyanosis – seen in fingers and toes
-poor local circulation
If central cyanosis is present, peripheral cyanosis will also be present

Question 6

List causes of hypoxaemia

Answer 6

Low inspired O2 
Ventilation:perfusion mismatch 
Diffusion defect 
Intra-lung shunt: ARDS
Hypoventilation 
Congenital heart defects

Question 7

Describe the response to chronic hypoxaemia

Answer 7

Increased EPO secreted by kidney -> raised Hb
Increased 2,3 DPG – shifts Hb saturation curve to the right so oxygen is released more freely
Increased capillary density
Chronic hypoxic vasoconstriction of pulmonary vessels results in: pulmonary hypertension & right heart failure

Question 8

List disorders where there is ventilation:perfusion mismatch

Answer 8

Asthma 
COPD
Pneumonia
RDS
Pulmonary oedema
Pulmonary embolism 
Will significantly improve with oxygen administration, but will not completely correct hypoxaemia until underlying pathology corrected

Question 9

What is shunt?

Answer 9

Perfusing an unventilated alveolus -> that bit of blood is wasted as no gas exchange will occur

Question 10

Explain what acute respiratory distress syndrome is

Answer 10

Result of acute alveolar injury caused by different insults & probably initiated by different mechanisms
Diffuse loss of surfactant resulting in alveolar atelectasis
Lungs become stiff and less compliant
Loss of hypoxic pulmonary vasoconstriction mechanism
Shunting occurs

Question 11

Describe hypoventilation

Answer 11

Entire lung is poorly ventilated – inadequate RR/volume of alveolar ventilation
Alveolar ventilation is reduced
Always causes hypercapnia = type 2 respiratory failure

Question 12

Compare acute and chronic hypoventilation

Answer 12

Acute – needs urgent treatment (artificial ventilation)
-causes: opiate overdose, head injury & very severe acute asthma
Chronic – slow onset and progression, time for compensation & therefore better tolerated
-causes: severe COPD

Question 13

List chest wall abnormalities which can cause hypoventilation

Answer 13

Scoliosis: sideways curvature of the spine
Kyphosis: spinal disorder in which an excessive outward curve of the spine results in an abnormal rounding of the upper back
Kyphoscoliosis = both -> causes disordered movement of the chest wall & respiratory system compliance reduced

Question 14

List the acute and chronic effects of hypercapnia

Answer 14

Acute: respiratory acidosis, impaired CNS function, peripheral vasodilation & cerebral vasodilation
Chronic: compensated respiratory acidosis, vasodilation mild but may still be present (‘pink puffers’)

Question 15

Describe why treatment of hypoxaemia may worse hypercapnia

Answer 15

1) Correction of hypoxia removes pulmonary arteriole hypoxic vasoconstriction -> increased perfusion of poorly ventilated alveoli
2) Haldane mechanism – oxygenated Hb can’t carry as much CO2, dissociates into blood
Treatment: give controlled oxygen therapy with a target saturation of 88-92% (if oxygen therapy causes a rise in pCO2 -> need ventilatory support)

Question 16

Describe the pathophysiology of pulmonary embolism

Answer 16

Obstruction of blood vessel by foreign substance or blood clot that travels through bloodstream, lodging in blood vessels, plugging the vessel
Thrombus, tumour, air, fat & amniotic fluid can all embolise
90% of PE arise from a deep vein thrombosis in the legs (particularly the popliteal vein)

Question 17

List risk factors for thromboembolism

Answer 17

Pregnancy
Prolonged immobilisation 
Previous VTE
Contraceptive pill 
Long haul travel
Cancer 
Heart failure
Obesity

Question 18

Describe how PE leads to acute right ventricular overload and the body’s response to this

Answer 18

Pulmonary artery pressure increases
Leads to acute right ventricular dilation and strain
Positive inotropes released by the body in attempt to maintain systemic BP -> increases pulmonary artery vasoconstriction -> further exacerbates situation
1/3 patients have a patent foramen ovale (increased risk of paradoxical embolization and stroke)

Question 19

Describe how PE leads to respiratory failure

Answer 19

Areas of ventilation perfusion mismatch
Low right ventricle output
Shunt with patent foramen ovale

Question 20

Describe how PE leads to pulmonary infarction

Answer 20

Small distal emboli may create areas of alveolar haemorrhage
Can result in haemoptysis, pleuritis & small pleural effusion -> this clinical presentation is known as pulmonary infarction

Question 21

List symptoms of PE

Answer 21

Dyspnoea 
Pleuritic chest pain
Cough
Substernal chest pain 
Haemoptysis

Question 22

List signs of PE

Answer 22

Tachypnoea 
Decreased breath sounds
Accentuated second heart sound
Tachycardia 
Fever 
Diaphoresis

Question 23

List investigations for PE

Answer 23

Blood gases – may show hypoxaemia and hypocapnia
CXR – commonest finding in PE is normal CXR -> done to exclude other diagnoses
ECG – may show signs of right ventricular strain (classic finding = SI, QIII, TIII)
D-dimer – normal D-dimer effectively rules out PE in those at low likelihood of having a PE
Imaging – CT pulmonary angiography (CONFIRMS DIAGNOSIS)

Question 24

Describe treatment for PE

Answer 24

Oxygen
Immediate heparinisation (stops thrombus propagation) - low molecular weight heparin (side effect: heparin-induced thrombocytopenia)
Haemodynamic support
Respiratory support

Question 25

Describe prevention of PE

Answer 25

Recognise and address risk factors

DVT prophylaxis after surgery & patients with malignancy

Question 26

Explain how V/Q mismatch due to PE leads to hypoxaemia

Answer 26

V/Q mismatch occurs due to redistribution of blood from occluded pulmonary arteries to the non-occluded vessels
This results in V/Q > 1 in the embolised area due to reduced blood flow
A V/Q < 1 in the non-embolised area due to overperfusion
Overperfusion of non-embolised regions, leads to development of hypoxaemia