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The electrocardiograph (ECG) has been recognized as a valuable diagnostic tool since the end of the 19th century. The normal ECG waveform consists of P, QRS, and T waves (and sometimes U waves)—P waves result from atrial depolarization, QRS complexes from ventricular depolarization, and T waves from ventricular repolarization. The standard 12-lead ECG utilizes four limb electrodes and six precordial electrodes to generate 12 leads or ‘views’ of the heart’s electrical activity. There are six limb leads (termed I, II, III, aVR, aVL, and aVF) and six precordial leads (termed V1, V2, V3, V4, V5, and V6). Supplementary ‘views’ can be obtained by using additional leads, such as V7, V8, and V9 to assess the posterior aspect of the heart and right-sided chest leads to look for a right ventricular myocardial infarction.

This article sets out a summary of standards for departmental accreditation set by the British Society of Echocardiography (BSE) Departmental Accreditation Committee. Full accreditation standards are available at www.bsecho.org. The BSE were the first national organisation to establish a quality standards framework for departments that support the practice of individual echocardiographers. This is an updated version which recognises that, not only should all echocardiographers be individually accredited as competent to practice, but that departments also need to be well organised and have the facilities, equipment and processes to ensure the services they deliver are of an appropriate clinical standard. In combination with individual accreditation, departmental accreditation lays down standards to help ensure safe and effective patient care. These standards supersede the 2012 BSE Departmental Accreditation Standards. Standards are set to cover all potential areas of practice, including transthoracic (level 2) echocardiography, transoesophageal echocardiography, stress echocardiography, training, and emergency (level 1) echocardiography. The emergency echocardiography standard is a new addition to departmental accreditation and has been developed with input from the Intensive Care Society.

This report presents the case of a 42-year-old man with liver cirrhosis who presents with breathlessness. Initial investigations are unable to explain his persistent hypoxia and a diagnosis of hepatopulmonary syndrome is considered. Saline contrast echocardiography is utilised in confirming the diagnosis. Details of this case as well as practicalities in performing and interpreting saline contrast echocardiography are reviewed. Learning points Key features of hepatopulmonary syndrome are liver disease, hypoxia and pulmonary vascular dilatations. Saline contrast echocardiography is a simple inexpensive procedure to perform and key to confirming the diagnosis of hepatopulmonary syndrome. Detection can be improved by performing the scan in the stand-up position. Agitated saline contrast studies are more commonly performed to identify intra-cardiac shunts. Timing of contrast arrival in the left heart chambers is key to differentiating intra-cardiac shunting from extra-cardiac pulmonary transit.

Heart failure is a common and disabling condition with a dismal prognosis. Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme (ACE) inhibitors has proven to be a valuable therapeutic strategy in this condition, with well-proven morbidity and mortality benefits. Nonetheless, ACE inhibitors provide incomplete blockade of the RAAS and also inhibit the degradation of bradykinin. Although increased levels of bradykinin may have haemodynamic advantages by contributing to vasodilatation, they may also be largely responsible for some of the adverse effects of ACE inhibitors. Angiotensin II (Ang II) receptor antagonists offer more complete blockade of the RAAS without the potentiation of bradykinin, and it was therefore hoped that they would provide even greater benefits for patients with heart failure. So far, much of the initial promise of the Ang II receptor antagonists in heart failure has not been realised. There has been no conclusive demonstration of their superiority to ACE inhibitors in their effects on morbidity and mortality, and their equivalence to ACE inhibitors has not been proven. The Ang II receptor antagonists have, however, proven to be better tolerated than ACE inhibitors and they are therefore likely to be a reasonable alternative for those patients with heart failure who cannot tolerate ACE inhibition. Recent evidence has indicated that the Ang II type 1 receptor antagonist valsartan is of value when used in patients already receiving either an ACE inhibitor or a beta-blocker, but has also suggested that giving all three drugs together is deleterious. Further evidence about the value of Ang II receptor antagonists in heart failure may be provided by further studies, of which several are currently ongoing.