S5: respiratory failure & pulmonary embolism Flashcards
Define hypoxia, hypoxaemia and the difference between the two terms
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
Define type 1 respiratory failure
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
Define type 2 respiratory failure
Low PaO2 and high PaCO2 > 6.5 kPa
Reduced ventilatory effort (pump failure) or inability to overcome increased resistance to ventilation of entire lung
List the effects of hypoxaemia
Impaired CNS function, confusion, irritability & agitation
Tachypnoea
Tachycardia
Cardiac arrhythmias & cardiac ischaemia
Hypoxic vasoconstriction of pulmonary vessels
Central cyanosis
Explain the difference between central cyanosis and peripheral cyanosis
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
List causes of hypoxaemia
Low inspired O2 Ventilation:perfusion mismatch Diffusion defect Intra-lung shunt: ARDS Hypoventilation Congenital heart defects
Describe the response to chronic hypoxaemia
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
List disorders where there is ventilation:perfusion mismatch
Asthma COPD Pneumonia RDS Pulmonary oedema Pulmonary embolism Will significantly improve with oxygen administration, but will not completely correct hypoxaemia until underlying pathology corrected
What is shunt?
Perfusing an unventilated alveolus -> that bit of blood is wasted as no gas exchange will occur
Explain what acute respiratory distress syndrome is
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
Describe hypoventilation
Entire lung is poorly ventilated – inadequate RR/volume of alveolar ventilation
Alveolar ventilation is reduced
Always causes hypercapnia = type 2 respiratory failure
Compare acute and chronic hypoventilation
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
List chest wall abnormalities which can cause hypoventilation
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
List the acute and chronic effects of hypercapnia
Acute: respiratory acidosis, impaired CNS function, peripheral vasodilation & cerebral vasodilation
Chronic: compensated respiratory acidosis, vasodilation mild but may still be present (‘pink puffers’)
Describe why treatment of hypoxaemia may worse hypercapnia
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)
Describe the pathophysiology of pulmonary embolism
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)
List risk factors for thromboembolism
Pregnancy Prolonged immobilisation Previous VTE Contraceptive pill Long haul travel Cancer Heart failure Obesity
Describe how PE leads to acute right ventricular overload and the body’s response to this
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)
Describe how PE leads to respiratory failure
Areas of ventilation perfusion mismatch
Low right ventricle output
Shunt with patent foramen ovale
Describe how PE leads to pulmonary infarction
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
List symptoms of PE
Dyspnoea Pleuritic chest pain Cough Substernal chest pain Haemoptysis
List signs of PE
Tachypnoea Decreased breath sounds Accentuated second heart sound Tachycardia Fever Diaphoresis
List investigations for PE
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)
Describe treatment for PE
Oxygen
Immediate heparinisation (stops thrombus propagation) - low molecular weight heparin (side effect: heparin-induced thrombocytopenia)
Haemodynamic support
Respiratory support
Describe prevention of PE
Recognise and address risk factors
DVT prophylaxis after surgery & patients with malignancy
Explain how V/Q mismatch due to PE leads to hypoxaemia
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
