Winter pressure on hospital medical beds.
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Biomedical subjects
Publications and source records attributed to J M Rawles.
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To compare the seasonal variation in total mortality and deaths from cardiovascular, respiratory, and malignant disease, data were collected from North-East Scotland (Grampian region) and Kuwait. Seasonal differences were similar, in both timing and degree, for total mortality and deaths from circulatory disease, but were greater in Kuwait for respiratory disease. Peak mortality was during winter in both areas: in Grampian, when the climate is most uncomfortable, and in Kuwait, when the climate is at its most comfortable. Socioeconomic changes in Kuwait have been accompanied by a rapid fall in the degree of seasonality (deseasonality) for both total and infant mortality. These findings suggest that mortality peaks in winter, not because of a seasonally low temperature, but because of a seasonal fall in mean temperature irrespective of the annual mean temperature.
The composition of the seasonality of total death was ascertained. Vascular disease seasonality constitutes more than half. The remaining seasonality is influenced by respiratory disease. Surprisingly and of possible importance cancer mortality was not seasonal. Deaths from 'all other disease' and from 'injuries' is seasonal. Seasonality increases with age. In coronary and cerebrovascular disease death has a large seasonal fluctuation. On the other hand hospital admissions and survivors have a minor seasonal fluctuation--only cerebrovascular admissions reaching the chosen level of significance with a small seasonal amplitude. For vascular disease the ranking of seasonal fluctuation from greatest to least is--death outside hospital, total death, death inside hospital, admissions, survivors. It is death outside hospital presumably 'sudden' that imposes seasonality on coronary disease in general. For respiratory diseases not only death but hospital admissions and survivors have high amplitude seasonality with a much greater fluctuation than for death in vascular disease.
The delay between the onset of symptoms and the call for help is the longest single component of the time taken for patients with acute myocardial infarction to come under coronary care and receive thrombolytic therapy. In order to investigate factors influencing patient delay, visual analogue scores for pain, shortness of breath, and anxiety were obtained retrospectively from 250 patients with acute myocardial infarction, for the time of onset of symptoms, and for the time of the call for help. The predominant symptom was chest pain, followed by anxiety and breathlessness. Although all symptoms increased in severity after their onset, the initiation of a call was largely unexplained in terms of worsening symptoms. Patient delay had a skewed distribution with modal, median and mean values of up to 1 h, 1.5 h, and 11 h respectively. Patient delay was negatively correlated with the pain score at the time of calling, but most of the variance of patient delay could not be explained in terms of symptom scores. However, patient delay was independently and negatively related to maximum serum aspartate aminotransferase. During acute myocardial infarction, patients with higher cardiac enzyme levels experience more pain and delay less. This tendency for patients with more severe infarction and a greater risk of death to call for help sooner is an added reason for administering thrombolytic treatment at the first opportunity: those patients who call early have most to gain from prompt therapy.
Reduction of a rapid ventricular rate in atrial fibrillation results in a longer diastolic filling period and a higher left ventricular stroke volume but this is offset by reduced contractility and fewer beats per minute; the net effect on cardiac output is uncertain. Sequences of stroke distances were measured by Doppler ultrasound in 60 resting patients with atrial fibrillation to determine the relation between ventricular rate and linear cardiac output. The slope of the cardiac output/ventricular rate relation was positive in all 20 patients with a ventricular rate less than 90 beats per minute and negative in 16 (40%) of 40 patients with a ventricular rate greater than 90 beats per minute. In atrial fibrillation the ventricular rate can be regarded as "controlled" when the cardiac output/ventricular rate slope is positive and "uncontrolled" when the slope is negative--that is when reduction of ventricular rate would lead to increased cardiac output. As so defined, ventricular rate at rest was controlled in every patient when the ventricular rate was less than 90, controlled in 44 (73%) patients when the ventricular rate was 90-140 beats per minute, and uncontrolled in every case when it was greater than 140 beats per minute. Achieving a target ventricular rate of 90 beats per minute in patients with atrial fibrillation at rest would result in control with the least compromise of cardiac output.
One hundred and thirty nine episodes of atrial fibrillation were identified from Holter recordings in 72 patients with paroxysmal atrial fibrillation. Paroxysms occurred more often by day than by night, suggesting that attacks are more closely associated with sympathetic than with vagal activity. In 41 patients who were not taking digoxin there were 79 episodes, and in 31 patients who were taking digoxin there were 60 episodes. Significantly more of the episodes that lasted for 30 minutes or more occurred in patients taking digoxin (13/17); the relative risk of a prolonged paroxysm associated with taking digoxin was 4.3 (95% confidence intervals 1.6-11.9). The mean (SD) ventricular rate at the onset of the paroxysms was not significantly different in those taking digoxin (140 (25) beats/min) and in those who were not (134 (22) beats/min). In paroxysmal atrial fibrillation, pretreatment with digoxin does not seem to reduce the frequency of paroxysms, or the ventricular rate when paroxysms occur, but it is associated with longer attacks.
In a retrospective 6 year follow up data were obtained for 536 of 566 (95%) consecutive patients admitted to a coronary care unit with acute chest pain. Their diagnoses were acute myocardial infarction in 290 (54%), myocardial ischaemia in 164 (31%), pericarditis in 16 (3%), and non-cardiac in 66 (12%). Six year mortality was 36%, 24%, 0%, and 16% respectively. In patients with acute myocardial infarction a higher mortality rate during follow up was associated with a higher than average age, a higher than average creatine kinase, previous myocardial infarction, Q wave infarction, and the presence of reciprocal changes. The presence of reciprocal changes was associated with higher than average concentration of serum creatine kinase, indicating more extensive infarction. Infarction complicated by ventricular fibrillation or left bundle branch block was associated with a higher death rate. The electrocardiogram recorded at the time of acute myocardial infarction contains much useful prognostic information.
Stroke distance was measured by means of doppler ultrasound in 100 consecutive patients with acute myocardial infarction. Mean stroke distance on days 1-5 after infarction was 72% of the predicted normal value for age and rose to 77% of normal by days 6-10. Stroke distance was lower after anterior (65%) than inferior infarction (75%), and was negatively correlated with peak serum aspartate aminotransferase (r = 0.47, p less than 0.001). Of 16 patients whose stroke distance on days 1-5 was below 50% of normal for age, 4 died, all within the first week. Of 84 patients whose stroke distance was 50% of normal or higher, only 1 died (at 13 days). The simple bedside measurement of stroke distance offers a practical method of monitoring left ventricular function in acute myocardial infarction: the measurement may have prognostic value.
1. The electrocardiogram was recorded for 3 min during spontaneous respiration in 70 subjects aged 15-86 years who were in sinus rhythm. Using a signal-averaging approach, the presence of respiratory variation of P-P intervals was analysed by multiple regression against a cosine function (cosinor analysis). 2. By cosinor analysis the phase of respiration when the intervals were longest was determined, together with the amplitude of the variation of the intervals around their mean value. 3. Respiratory variation of P-P intervals (respiratory sinus arrhythmia) was demonstrated in 84% of subjects; its amplitude decreased with age and respiratory rate. On average, the duration of P-P intervals varied by 2.8% around the mean, and the maximum duration occurred around the time of end-expiration. 4. By cosinor analysis, and allowing for variation of heart rate, P-R intervals showed an independent respiratory variation in 39% of cases, and its average amplitude was 1.2% around the mean. 5. The respiratory variation of P-R and P-P intervals showed similar phase relationships to respiration, suggesting that during respiration there is parallel alteration of sinoatrial and atrioventricular node function.
1. In 50 subjects with atrial fibrillation we have attempted to demonstrate variation of ventricular rate with respiration, as evidence of cardioregulatory reflex activity. 2. The electrocardiogram was recorded for 3 min during spontaneous respiration. The presence of respiratory variation of R-R intervals was analysed by multiple regression against a cosine function (cosinor analysis), making it possible to determine the phase of respiration when the intervals were longest. 3. Variation in ventricular rate with respect to respiration was demonstrated (P less than 0.05) in seven (14%) cases. On average, R-R intervals were longest at the end of inspiration; this contrasts with sinus rhythm where P-P, P-R and R-R intervals are longest around the time of end-expiration. 4. These results suggest that in atrial fibrillation the beat-to-beat ventricular rate may be under the influence of cardioregulatory reflexes, but the effect of respiration is weak and paradoxical.
1. Carotid baroreceptor-heart rate sensitivity has been measured non-invasively by a modified neck-chamber method that utilizes all cardiac intervals recorded in 6 min during 84 respiratory cycles. 2. In a replication study in 10 subjects the mean baroreflex sensitivity was 5.52 ms/mmHg and the mean (SD) difference between determinations was 0.70 (0.74) ms/mmHg. 3. Baroreflex sensitivity was measured in 48 untreated subjects of mean age 43 (range 20-71) years with blood pressures ranging from 104 to 202 mmHg (13.9 to 26.9 kPa) systolic and 52 to 120 mmHg (6.9 to 16.0 kPa) diastolic [average 142/87 mmHg (18.9/11.6 kPa)]. Both systolic and diastolic pressures correlated with age (r = 0.53, P less than 0.001 and r = 0.44, P less than 0.01). 4. Baroreflex sensitivity determined throughout respiration was log-normally distributed with a median value of 2.24 ms/mmHg, which declined with age (r = -0.63, P less than 0.001). 5. After allowing for the effects of age, baroreflex sensitivity throughout respiration was not independently related to either systolic or diastolic blood pressure.
We assessed the relative contributions of raised cardiac output and increased peripheral resistance to elevation and lability of blood pressure in patients with borderline and sustained hypertension. Ninety-five untreated patients were admitted to hospital for assessment. Using Doppler ultrasound, linear cardiac output was measured as minute distance on the day of admission and 24 h later; blood pressure was measured at the same times, enabling calculation of linear resistance (analogous to peripheral vascular resistance). In sustained, but not borderline, hypertension linear resistance was increased at the first measurement (+ 36%, P less than 0.001), but mean minute distance did not differ significantly from normal in either group. Between the first and second measurements in borderline and sustained hypertension there were significant falls of mean blood pressure (-9%, P less than 0.001 and -4%, P less than 0.01). In borderline, but not sustained, hypertension there was an associated fall of linear resistance (-11%, P less than 0.05); in neither group was there a significant change of minute distance. Both elevation and lability of blood pressure in borderline and sustained hypertension are due more to changes of peripheral resistance than to changes of cardiac output.
The electrocardiogram was recorded for 100 seconds in 50 patients with atrial fibrillation to determine the relations between QT intervals and both the mean and instantaneous ventricular rates. The mean ventricular rate was 94 beats per minute with a mean QT interval of 357 ms. The mean QTc, corrected beat by beat with Bazett's formula, was 444 ms--longer than reported for sinus rhythm. Between subjects, the mean QT interval was linearly related to the mean RR interval, with a slope of +21%. Within all 50 recordings there was a statistically significant correlation between QT intervals and immediately preceding RR intervals, with an average slope of +7%. This within subject QT/RR interval slope was greater at faster mean ventricular rates. In atrial fibrillation, as in sinus rhythm, the QT interval is a function of both the mean ventricular rate and the instantaneous ventricular rate, with the mean ventricular rate predominating; a simple correction of QT intervals for heart rate is therefore inadequate. Comparison of uncorrected QT intervals with those of earlier published series of people in sinus rhythm, however, suggested that atrial fibrillation is associated with prolongation of the mean QT interval.
Saccadic eye movement recording was performed in 53 patients with non-compressive myelopathy. Twenty one patients (40%) had subclinical abnormalities of saccadic movement, supporting a diagnosis of probable multiple sclerosis. When used in addition to the measurement of visual evoked potentials and brainstem auditory evoked responses, the detection of subclinical abnormalities increased from 40% to 57%. The detection rate of abnormalities by saccadic eye movement recording was equal to that of visual evoked responses, but more than of brainstem auditory evoked responses. Prolonged latency of gaze was the most common saccadic latency abnormality detected. The majority of saccadic velocity abnormalities could be explained by disease in the medial longitudinal bundle. An unusual finding was that abduction velocity was increased in six patients. It is concluded that the simple measurement of saccadic eye movement is a valuable addition to other ancillary investigations for the diagnosis of multiple sclerosis. It also allows analysis of oculomotor function, commonly disordered in multiple sclerosis, but rarely investigated.
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The longest component of the total delay in coming under coronary care is patient delay, and it has been suggested that public education might be used to make it shorter. The patterns of patient delay were studied in 450 patients with acute myocardial infarction uncomplicated by cardiac arrest out of hospital, of whom 243 had a previous history of ischaemic heart disease. Patient delays had a skewed distribution with a modal delay of up to one hour, a median delay of two hours, and a mean delay of 10 hours. Two thirds of patients had sought help from their general practitioners within four hours of the onset of symptoms. During the first four hours the longer that patients delayed the lower was the subsequent mortality (27%, 18%, and 9% for delays of one hour or less, up to two hours, and up to four hours, respectively), but patients who delayed four to eight hours had the highest mortality of all (38%). Neither the median value nor the pattern of patient delays was altered by a previous history of ischaemic heart disease. There were pronounced differences in doctor delays, depending on the patient's age, delay time, and ultimate place of treatment, showing that the doctors' behaviour was influenced before they had seen their patients. Nevertheless, the median total delay for patients aged up to 70 was one hour 35 minutes, and a higher proportion of patients were seen early after infarction than in recent hospital trials of thrombolytic treatment. These findings suggest that the patients' call for help and the doctors' response may be at an instinctive level according to the patients' distress; these patterns of behaviour may be difficult to modify by public education.
Cytotoxic chemotherapeutic agents, particularly the anthracyclines, are known to be cardiotoxic, but toxic effects on the aorta have not previously been documented. In this study, diameters of ascending and descending thoracic aortae were measured by computerized tomography in 69 patients with lymphoma, before and after first-line treatment with one of 7 different regimes. Minor increases in aortic diameter over the study period due to the aging process were expected. These increases were greater than anticipated in both the ascending and the descending aortae after chemotherapy with CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisolone) and CVP (cyclophosphamide, vincristine, and prednisolone) regimes. Smaller changes, or changes which were not statistically significant, were noted after MVPP (mustine, vinblastine, procarbazine, and prednisolone), ChlVPP (chlorambucil, vinblastine, procarbazine, and prednisolone), ChlVP (chlorambucil, vincristine and prednisolone), mediastinal radiotherapy, and radiotherapy plus MVPP (MVPP/XRT). Cardiovascular damage associated with certain forms of cytotoxic therapy is not confined to the heart, but also affects the aorta.
Sixty patients with atrial fibrillation (AF) have been studied with Doppler ultrasound to establish the relationship between the duration of R-R intervals and subsequent left ventricular stroke outputs, assessed as stroke distance. Using multiple regression analysis, most of the beat-to-beat variation of stroke distance could be explained in terms of the two preceding R-R intervals (Mean R = 0.82). The relative contribution of these two intervals to the variation of stroke distance was assessed in each patient. In all patients there was a positive correlation between stroke distance and the preceding R-R interval, largely due to the influence of this interval on diastolic filling or preload. In all but one patient the correlation with the second previous R-R interval was negative, the mechanism being changing contractility due to operation of the force-frequency effect. On average, 58% of the variance in stroke distance could be explained by alteration of the previous R-R interval and 10% by alteration of the second previous R-R interval. The relative contribution of the previous R-R interval (preload) falls as left ventricular function declines, and also as mean ventricular rate rises. However, there is a wide individual variation in the pattern of left ventricular function, which may be represented graphically as the haemodynamic profile.