Central haemodynamic changes during lower body positive pressure in patients with congestive cardiac failure.

Fifteen patients with moderately severe and severe chronic congestive heart failure were studied to determine the central haemodynamic results of short term increases in lower body positive pressure. Central haemodynamic variables were determined by Swan-Ganz thermodilution catheterisation and arterial cannulation. Graded increases in lower body positive pressure were applied to supine patients using Medical Anti-Shock Trousers (MAST). Increasing lower body positive pressure by 25 mm Hg and 55 mm Hg caused increases in mean right atrial pressure (6.0 to 13.2 to 17.9 mm Hg; p less than 0.001 and p less than 0.0001 respectively) and mean pulmonary artery pressure (26.8 to 35.5 to 41.3 mm Hg; p less than 0.05 and p less than 0.01 respectively). No significant changes were seen in left heart filling pressures or in pulmonary vascular resistance. Furthermore, there were no significant increases in indices of cardiac work (cardiac index, left ventricular stroke work index, right ventricular stroke work index or cardiac power output) despite the increased right heart filling pressures. These results show that in patients with longstanding severe congestive heart failure, short term increases in cardiac return may increase right heart pressures but do not appear to cause either beneficial or detrimental changes in left heart haemodynamic indices.

Repetitive monomorphic ventricular tachycardia aborted by sleep.

A 43-year-old woman with a 12-year history of palpitation was found to have recurrent monomorphic ventricular tachycardia resistant to beta-blockade but abolished by sleep.

The impact of a policy of collaborative management on mortality and morbidity from infective endocarditis.

The present study represents a comprehensive retrospective review of endocarditis in a large district general hospital since the inception of a formalized policy involving collaborative management a decade ago. The principle was to involve a recognised team of cardiologists, specialists in infectious disease and microbiologists in the treatment of the disease from the moment of its diagnosis. The pattern of infection has not altered in terms of prevalent organisms and valves infected since the change in management policy. There has, however, been a significant decline in the mortality, from 34 to 24% for all patients with endocarditis. Amongst those referred for collaborative management, the mortality has fallen to 6%. The single greatest improvement is a reduction in the number of patients dying of heart failure, the number of patients developing systemic emboli or requiring prosthetic valve replacement remaining unchanged. The results indicate that early referral to, and treatment by, a multidisciplinary team can significantly reduce the mortality from bacterial endocarditis.

The incidence and evolution of cardiomyopathy in Duchenne muscular dystrophy.

To assess the incidence, nature and evolution of cardiac disease in Duchenne muscular dystrophy, 328 patients were studied between 1976 and 1987 for periods varying from 3 to 11 years. Patients underwent regular clinical examination, electrocardiography, echocardiography and radiological assessment. Pre-clinical cardiac involvement was found in 25% of patients under 6 years old increasing to 59% between the ages of 6 and 10 years and then declining in incidence with age. Clinically apparent cardiomyopathy is first evident after 10 years of age and increases in incidence with age, being present in all patients over 18 years of age. Its clinical impact is discussed.

Cortisol level predicts myocardial infarction in patients with ischaemic chest pain.

Serum cortisol levels were studied in twenty patients with confirmed myocardial infarction and in twenty patients with severe chest pain admitted to the coronary care unit with suspected myocardial infarction but in whom a diagnosis of angina was subsequently made. Cortisol levels were significantly elevated in patients within five hours of the onset of symptoms in myocardial infarction (857 +/- 74 nmol/l; mean +/- SE) but remained within the normal range for those with angina (340 +/- 55 nmol/l). It is concluded that hypercortisolaemia accompanies myocardial infarction, but not angina, and that the psychological stresses of ischaemic chest pain and admission to the coronary care unit produce little, if any, elevation in serum cortisol levels unless there is significant myocardial necrosis. This observation may be of value to those conducting intervention studies in myocardial infarction since the early elevation of the cortisol levels to above the normal range in patients with ischaemic chest pain is both sensitive (70%) and specific (85%) for myocardial infarction.

Serum cortisol levels predict infarct size and patient mortality.

We have investigated prospectively the serum cortisol response to acute myocardial infarction in 70 consecutive patients admitted to a coronary care unit and we have shown that the levels are significantly raised early in the course of the illness and prior to elevation of the cardiac specific enzyme fraction, creatine kinase MB. The magnitude of the cortisol response is related to the size of the ensuing infarction (rs = 0.54) as calculated from the total creatine kinase MB release (P < 0.001) and very high levels (> 2000 mumol/l) are predictive of mortality (P < 0.05). Serum cortisol levels may have a role in the early identification of myocardial infarction and in predicting those patients with a poor prognosis.

Nurse initiated thrombolysis in the accident and emergency department: safe, accurate, and faster than fast track.

OBJECTIVE: To reduce the time between arrival at hospital of a patient with acute myocardial infarction and administration of thrombolytic therapy (door to needle time) by the introduction of nurse initiated thrombolysis in the accident and emergency department. METHODS: Two acute chest pain nurse specialists (ACPNS) based in A&E for 62.5 hours of the week were responsible for initiating thrombolysis in the A&E department. The service reverts to a "fast track" system outside of these hours, with the on call medical team prescribing thrombolysis on the coronary care unit. Prospectively gathered data were analysed for a nine month period and a head to head comparison made between the mean and median door to needle times for both systems of thrombolysis delivery. RESULTS: Data from 91 patients were analysed; 43 (47%) were thrombolysed in A&E by the ACPNS and 48 (53%) were thrombolysed in the coronary care unit by the on call medical team. The ACPNS achieved a median door to needle time of 23 minutes (IQR=17 to 32) compared with 56 minutes (IQR=34 to 79.5) for the fast track. The proportion of patients thrombolysed in 30 minutes by the ACPNS and fast track system was 72% (31 of 43) and 21% (10 of 48) respectively (difference=51%, 95% confidence intervals 34% to 69%, p<0.05). CONCLUSION: Diagnosis of acute myocardial infarction and administration of thrombolysis by experienced cardiology nurses in A&E is a safe and effective strategy for reducing door to needle times, even when compared with a conventional fast track system.

Assessing cardiac pumping capability by exercise testing and inotropic stimulation.

In heart failure both functional capacity and prognosis are primarily determined by the degree of pump dysfunction. Although data on haemodynamic function at rest may indicate impaired cardiac function, they do not assess the capacity of the heart to respond to stress. Maximal bicycle ergometry and incremental intravenous inotropic stimulation in 31 patients with moderately severe heart failure were evaluated as methods of stressing the heart to determine cardiac pumping capability, which is defined as the cardiac power obtained during maximal stimulation. There was good agreement between the cardiac pumping capabilities assessed by these two methods. Maximal cardiac power output was better than maximal cardiac output and left ventricular stroke work index in representing cardiac pumping capability, because it was less dependent on the type of stimulation used during evaluation. Inotropic challenge is at least as effective as exercise testing in assessing cardiac pumping capability in heart failure, and may be a better method in patients who find physical exercise difficult.

The clinical and echocardiographic diagnosis of infective endocarditis.

We report the results of a series of 75 patients admitted to the East Birmingham Hospital between 1976 and 1984. Rheumatic heart disease is now an uncommon predisposing factor. The viridans streptococci are a decreasing cause of infection while staphylococcal infections are increasing and often occur on previously normal heart valves. The presenting symptoms of the disease are usually non-specific and the classical physical signs of endocarditis are uncommon. Blood culture and echocardiography are the most useful investigations in establishing the diagnosis. The diagnosis of endocarditis should be considered in all febrile patients, especially if they are ill, who have a cardiac murmur or persistent bacteraemia.

Tuberculous retropharyngeal abscess producing respiratory obstruction.

Oropharyngeal tuberculosis is a rare presentation of the disease even in the presence of extensive pulmonary tuberculosis. A case is described in which a retropharyngeal abscess, causing stridor and threatening respiratory obstruction, was the only manifestation of Mycobacterium tuberculosis infection.

Lymphocyte beta adrenoceptor upregulation and improved cardiac response to adrenergic stimulation following converting enzyme inhibition in congestive heart failure.

To determine the effect of ACE inhibitor therapy on lymphocyte beta-adrenoceptor function and density, as well as the in vivo myocardial response to beta-agonist stimulation, we studied 12 patients with chronic severe heart failure before and after 16 weeks' treatment with quinapril. Lymphocyte beta-adrenoceptor function (intracellular cAMP production in response to isoprenaline) was studied as a surrogate tissue for myocardium, and increased significantly after quinapril at concentrations of isoprenaline between 10(-3) and 50 mmol.l-1. Lymphocyte beta-adrenoceptor density (six patients) measured by [125I] iodocyanopindolol binding, increased from 242 +/- 72 (mean +/- SEM) to 884 +/- 17 receptors/cell (P < 0.05). Changes in functional myocardial beta-adrenoceptor status were determined by measuring changes in haemodynamic responses to exercise and to incremental dobutamine infusion. Following quinapril there were significant improvements in cardiac index, stroke volume and cardiac power output during sub-maximal exercise testing and dobutamine infusion; stroke work index in response to dobutamine (but not exercise) improved significantly. ACE inhibitors cause lymphocyte beta-adrenoceptor upregulation in heart failure, which is associated with an improved cardiac pumping capacity in response to beta-agonist stimulation.

The correlation of cardiac power output to exercise capacity in chronic heart failure.

Cardiac haemodynamics are deranged in chronic heart failure but fail to predict the exercise capacity of the patient. Cardiac power output is a descriptor of cardiac function derived from preload, blood pressure and cardiac output. Forty-one patients with moderately severe and severe chronic heart failure were exercised on a cycle ergometer to determine the relationship between traditional haemodynamics and cardiac power output and exercise capacity. Resting cardiac power output was no more predictive of exercise capacity than resting stroke-work index or resting cardiac index (r = 0.53, 0.61 and 0.51 respectively). Maximum cardiac power output and the ability to increase cardiac power output, however, were correlated with exercise capacity (r = 0.79 and 0.80). It is concluded that resting cardiac power output does not predict subsequent exercise capacity but that maximum cardiac power output and the ability to increase cardiac power output on stimulation are good descriptors of functional cardiac reserve.

Domiciliary investigation of sleep-related hypoxaemia in Duchenne muscular dystrophy.

In Duchenne muscular dystrophy (DMD) nocturnal oxygen desaturation occurs during rapid eye movement (REM) sleep. Polysomnography, which requires hospital admission, will detect sleep-related breathing abnormalities. In order to avoid the inconvenience of hospital admission for the disabled patient, we investigated overnight oxygenation in ten boys with DMD by domiciliary oximetry. In four boys the results of oximetry were compared with those of a polysomnographic recording. The "repeatability" of domiciliary oximetry was assessed in six boys by performing oximetry on two non-consecutive nights. Older boys with DMD may develop a cardiomyopathy. In order to assess cardiac rhythm and ST segment changes we performed simultaneous Holter monitoring and oximetry in seven boys with overnight hypoxaemia. Six of the initial ten boys studied demonstrated episodic nocturnal hypoxaemia and there was a strong correlation between minimum oxygen saturation overnight and daytime arterial oxygen and carbon dioxide tensions (PaO2 r = 0.89; PaCO2 r = -0.87). Despite adequate REM time during polysomnography, greater oxygen desaturation was found during domiciliary oximetry. No difference was found in the severity of desaturation recorded in the boys who were studied on two separate occasions. Five boys demonstrated marked heart rate variation during hypoxaemic episodes and more serious arrhythmias occurred overnight in the three most hypoxaemic boys. Domiciliary oximetry is a simple, repeatable method of assessing overnight oxygenation and compares well with polysomnography. In boys with advanced DMD and severe nocturnal hypoxaemia, 24 h electrocardiographic monitoring may detect potentially life-threatening arrhythmias.