1. In six healthy subjects the amplitude and phase of respiratory sinus arrhythmia were determined at five different respiratory cycle lengths ranging from 3 to 9.5 s. 2. At each respiratory cycle length the carotid baroreceptor-heart rate reflex response was determined by cyclical neck suction at −40 mmHg at five different cycle lengths covering the same range of 3–9.5 s. 3. The application of cyclical neck suction increased the amplitude of respiratory sinus arrhythmia in all but the longest respiratory cycle lengths. 4. With increasing respiratory cycle length the amplitude of sinus arrhythmia increased, and R-R intervals were at their longest at an earlier phase of the respiratory cycle. Similarly, with increasing suction cycle length the amplitude of the cardiac interval response increased and the phase angle decreased. 5. The cardiac interval responses to respiration and to neck suction at different frequencies were independent of each other, the heart rate at any moment resulting from the algebraic summation of the two responses.

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 < 0.001 and r = 0.44, P < 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 < 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.

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. The major components of the blood fibrinolytic enzyme system were measured in patients with congestive cardiac failure, in control patients with heart disease but not in failure, and in control subjects without heart disease. 2. Heart disease in the absence of failure was associated with an increase in fibrinogen, fibrin degradation products and α 1 -antitrypsin, but not with any alteration of plasminogen activator, plasminogen, the serum inhibitor of plasminogen activation or α 2 -macroglobulin. 3. Compared with patients with heart disease, there were decreased amounts of plasminogen activator and plasminogen and increased amounts of the serum inhibitor of plasminogen activation and the antiplasmin α 1 -antitrypsin in patients with cardiac failure. Fibrinogen, fibrin degradation products and α 2 -macroglobulin were not significantly altered. 4. Plasminogen activator as measured by the euglobulin lysis time correlated inversely with the height of the jugular venous pressure, but not with liver size, the extent of oedema, chest X-ray appearances, amounts of blood urea or bilirubin. 5. The release of plasminogen activator in response to venous stasis was decreased in patients with cardiac failure.