Derek J. Rowlands

Atrial function after cardioversion

Abstract The immediate hemodynamic changes occurring after D.C. cardioversion have been measured in 18 patients with rheumatic, ischemic, or thyrotoxic heart disease. Sinus rhythm was successfully restored in 13 patients. Twelve out of 13 successfully cardioverted patients developed clearly visible right atrial “a” waves. Five out of 8 successfully cardioverted patients developed left atrial “a” waves. The lower incidence of return of effective atrial systole on the left side, despite the return of normal atrial excitation, is explained by the more severe left-sided disease. Seven out of 12 successfully cardioverted patients had increased cardiac indices after cardioversion. The other 5 patients showed either no change or minor falls. When discernible left atrial “a” waves returned after cardioversion, appreciable increases in cardiac output occurred (range 11 to 55 per cent). When no discernible left atrial “a” wave returned, changes in cardiac output were slight. Significant reduction in cardiac output occurred in 2 out of 4 cases in which cardioversion failed. In 3 out of 4 cases in which cardioversion failed, a temporary increase in mean left atrial pressure occurred. A similar temporary increase in left ventricular end-diastolic pressure occurred in the single case in which this was measured.

The effect of the dextro isomer of propranolol on sinus rate and cardiac arrhythmias

Abstract Previous workers have shown experimentally that dl -propranolol, in addition to its β-blocking action, has a direct depressant effect on cardiac muscle and terminates arrhythmias due to digitalis overdosage. The dextro isomer of propranolol has very little β-blocking activity compared with dl -propranolol, but has an equivalent direct myocardial action. In this investigation d -propranolol, and in most cases dl -propranolol also, was given to 25 patients in sinus rhythm and 59 with cardiac arrhythmias. d -Propranolol had much less effect than dl -propranolol on sinus rate and on ventricular rate in atrial flutter and fibrillation. In supraventricular and ventricular ectopic beats and tachycardias, however, either both drugs were ineffective or they had approximately equivalent effects. d -Propranolol terminated digitalis arrhythmias. It is suggested from these observations that the actions of dl -propranolol on the sinus node and on the atrioventricular node in atrial flutter and fibrillation are through β blockade. In other ectopic arrhythmias and in digitalis intoxication, its action is by a mechanism or mechanisms other than β blockade.

Postural hypotension in amyloid disease

Abstract A patient with primary amyloidosis who developed severe postural hypotension during the course of the nephrotic syndrome is described; hemodynamic studies demonstrated that this was due to autonomic dysfunction and revealed evidence of central and peripheral cardiovascular denervation. Pathological examination showed extensive infiltration of sympathetic ganglia and nerves with amyloid material. Postural hypotension was the only clinical evidence of neurological involvement in the absence of other manifestations of autonomic disturbance or signs of peripheral neuropathy.

Graphical representation of QT rate correction formulae: an aid facilitating the use of a given formula and providing a visual comparison of the impact of different formulae

The QT interval on the electrocardiogram is an increasingly important measurement, especially in relation to drug action and interaction. The QT interval varies inversely as the heart rate and numerous rate correction formulae have been proposed. It is difficult to compare the effect of applying different formulae at different heart rates and for different measured QT intervals. A simple graphical display of the results from different formulae is proposed. This display is dependent on the concept of the absolute correction factor. This graphical presentation is useful (a) in comparing the effect of the application of different formulae and (b) in directly reading the correction produced by any individual formula.

Study of right ventricular function in ischaemic heart disease using radionuclide angiocardiography

A technique for the estimation of LVEF from first passage radionuclide angiocardiography was adapted to provide estimates of RVEF. In 17 subjects with no history of cardiovascular disease mean LVEF was 0.71±0.08 and mean RVEF 0.65±0.08. Mean values for 15 subjects with coronary artery disease but no previous history of myocardial infarction were 0.66±0.10 for LVEF and 0.65±0.08 for RVEF. Depressed ejection fractions were found after acute myocardial infarction. LVEF was lower after anterior (0.43±0.06) than inferior (0.51±0.10) infarction. RVEF was normal in the majority of subjects with anterior infarction (0.58±0.10) but was depressed after inferior infarction (0.50±0.05). Similar, although less marked, results were found in a group of subjects with old myocardial infarction.

The management of arrhythmias following an acute myocardial infarction.

Arrhythmias are extremely common early after AMI. An arrhythmiasis defined by exclusion, either because the sequence of myocardial depolarisation is other than normal or because certain arbitrary limits are exceeded. It follows that the term “arrhythmia” encompasses a complex heterogeneous group. Although arrhythmias are defined in electrical terms they are only important because of their immediate, delayed or potential haemodynamic consequences. These occur because of changes in heart rate, loss of atrial transport function, increased myocardial oxygen consumption, decreased myocardial blood flow or loos of synchronicity of ventricular contraction. The sensible and effective management of arrhythmias following acute myocardial infarction requires an appraisal of the haemodynamic consequences, if any, which follow the initiation of the arrhythmia. The indications for treating an arrhythmia must be the immediate, delayed or potential haemodynamic loss rather than the mere preseence of a rhythm which falls outside the limits of normal. This distinction is perhaps most clearly seen in the case of atrio-ventricular conduction disturbances.

“An example of apparently normal electrocardiogram originating from incorrect electrocardiographic acquisition in a patient with ST-segment elevation myocardial infarction”: Aslanger et al

I read with interest the article by Aslanger et al entitled “An example of apparently normal electrocardiogram originating from incorrect electrocardiographic acquisition in a patient with ST-segment elevation myocardial infarction.” The report provides a valuable reminder of the need to be able to recognize any limb lead connection error. Such errors are, of course, very common. In the case described, appropriate treatment would not have been given had another record not been taken within a short time interval. The authors have done a valuable service in reporting this case, but there are one or two items in the discussion that might benefit from clarification. The authors state that “lead II was evidently disconnected.” This is not a correct interpretation of the electrocardiographic (ECG) findings. The appearances are those of inadvertent interchange between the right arm and right leg connections. Furthermore, the stated relations between the “unipolar” leads (aVR, aVL, aVF) and the “bipolar” leads (I, II, III), in a standard ECG recording, are incorrect.