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Ashraf Roshdy, Nadia Francisco, Alejandro Rendon, Stuart Gillon and David Walker

The use of echocardiography, whilst well established in cardiology, is a relatively new concept in critical care medicine. However, in recent years echocardiography's potential as both a diagnostic tool and a form of advanced monitoring in the critically ill patient has been increasingly recognised. In this series of Critical Care Echo Rounds, we explore the role of echocardiography in critical illness, beginning here with haemodynamic instability. We discuss the pathophysiology of the shock state, the techniques available to manage haemodynamic compromise, and the unique role which echocardiography plays in this complex process.


A 69-year-old female presents to the emergency department with a fever, confusion and pain on urinating. Her blood pressure on arrival was 70/40, with heart rate of 117 bpm Despite 3 l of i.v. fluid she remained hypotensive. A central venous catheter was inserted and noradrenaline infusion commenced, and she was admitted to the intensive care unit for management of her shock state. At 6 h post admission, she was on high dose of noradrenaline (0.7 μg/kg per min) but blood pressure remained problematic. An echocardiogram was requested to better determine her haemodynamic state.

Open access

Andreas Zafiropoulos, Kaleab Asrress, Simon Redwood, Stuart Gillon and David Walker

Management of medical cardiac arrest is challenging. The internationally agreed approach is highly protocolised with therapy and diagnosis occurring in parallel. Early identification of the precipitating cause increases the likelihood of favourable outcome. Echocardiography provides an invaluable diagnostic tool in this context. Acquisition of echo images can be challenging in cardiac arrest and should occur in a way that minimises disruption to cardiopulmonary resuscitation (CPR). In this article, the reversible causes of cardiac arrest are reviewed with associated echocardiography findings.


A 71-year-old patient underwent right upper lobectomy for lung adenocarcinoma. On the 2nd post-operative day, he developed respiratory failure with rising oxygen requirement and right middle and lower lobe collapse and consolidation on chest X-ray. He was commenced on high-flow oxygen therapy and antibiotics. His condition continued to deteriorate and on the 3rd post-operative day he was intubated and mechanically ventilated. Six hours after intubation, he became suddenly hypotensive with a blood pressure of 50 systolic and then lost cardiac output. ECG monitoring showed pulseless electrical activity. CPR was commenced and return of circulation occurred after injection of 1 mg of adrenaline. Focused echocardiography was performed, which demonstrated signs of massive pulmonary embolism. Thrombolytic therapy with tissue plasminogen activator was given and his condition stabilised.