Acute Respiratory Distress Syndrome Flashcards
What is ARDS?
An acute lung injury defined as respiratory distress, stiff lung with reduced lung compliance.
It may be caused by direct lung injury or secondary to severe systemic illness.
Pathophysiology of ARDS.
Non-cardiogenic pulmonary oedema is the first and clinically most evident sign of a generalised increase in vascular permeability.
Pulmonary hypertension sometimes leading to pulmonary hypertension.
Haemorrhagic intra-alveolar exudate
Resolution, fibrosis and repair
Physiological changes where there is shunt and dead space increase, compliance falls and there is airflow limitation.
What causes the non-cardiogenic pulmonary oedema in ARDS?
Microcirculatory changes and release of immune mediators.
Activated neutrophils as well.
Pulmonary epithelium is also damaged in the early stages, reducing surfactant production and predisposing to alveolar collapse.
Causes of ARDS.
Pneumonia
Aspiration of gastric contents
Sepsis
Severe traum with shock and multiple transfusions
Pulmonary contusion
Fat embolism
Acute pancreatitis
Pulmonary vasculitis
Eclampsia
Malaria
Burns
Drugs
Clinical features of ARDS.
Cyanosis
SOB
Tachypnoea
Tachycardia
Peripheral vasodilation
Bilateral fine inspiratory crackles
Investigations done in ARDS.
FBC, U&Es, LFT, Amylase, Clotting, CRP, Blood cultures, ABGs.
CXR
Pulmonary artery catheter to measure pulmonary capillary wedge pressure might be done.
CXR findings in ARDS.
Bilateral diffuse shadowing, interstitial at first but subsequently with an alveolar pattern and air bronchograms.
Diagnostic criteria of ARDS.
All 4.
1 - Acute onset
2 - Bilateral infiltrates on CXR
3 - PCWP < 19 mmHg or a lack of clinical congestive heart failure
4 - Refractory hypoxaemia with PaO2:FiO2 < 200.
Management of ARDS.
Admit to ITU, give supportive therapy and treat underlying cause.
Resp support - CPAP with 40-60% O2. However most patients will need mechanical ventilation. - Indications such as PaO2 < 8.3 kPa despite 60% O2 and PaCO2 > 6 kPa.
Circulatory support - Invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter aids the diagnoiss and may be helpful in monitoring PCWP and cardiac output. Conservative fluid management. Inotropes and blood transufions.
Inhaled Nitric oxide as a vasodilator to treat pulmonary HTN.
Diuretics to treat oedema or possible haemofiltration if not enough.