Evening-to-morning blood pressure variations in snoring patients with and without obstructive sleep apnea.

This study was designed to test a hypothesis that patients with sleep apnea have higher blood pressure in the morning, following a night spent in apnea and hypoxemia, than in the evening. To accomplish this, we prospectively studied a set of 611 patients referred to our clinic because of suspicion of sleep apnea. All patients had full nocturnal polysomnography, including measurement of snoring. Blood pressure was measured in the evening, prior to onset of sleep, and in the morning, immediately on awakening. We found that patients without apnea and hypoxemia had lower blood pressure in the morning compared with the evening value, while patients with severe sleep apnea and hypoxemia had higher blood pressure in the morning; these evening-to-morning blood pressure differences, although statistically significant, were small, typically 1 to 4 mm Hg. Morning blood pressures were higher in patients with sleep apnea and hypoxemia than in nonapneic normoxic patients. However, this difference disappeared after the groups were matched for age and body mass index. We conclude that (1) patients with sleep apnea and nocturnal hypoxemia lose the expected morning dip in arterial blood pressure, and (2) age and body mass index are more important correlates of blood pressure than apnea and nocturnal oxygen desaturation. We speculate that the loss of evening-to-morning drop in blood pressure, if present over a long period of time, may lead to sustained elevations in arterial blood pressure frequently observed in patients with sleep apnea.     

The effect of sleep on normal and high blood pressure

Twenty-five normal young men at basal conditions showed a drop of blood pressure from 110 to 101 by falling asleep.In normals the greatest drop, due solely to sleep, comes at about the fourth hour of sleep, but this lower level continues throughout the sleeping state. There is a slowing of pulse in sleep parallel to the drop in blood pressure.Of thirty-six patients with elevated blood pressure, but one showed a normal fall of blood pressure in sleep. Sixteen showed a fall due to sleep, which reached a level regarded as normal by ordinary criteria. Twenty showed less fall, varying from no change at all to more or less greater change, but remaining abnormal throughout.Patients whose blood pressure fell to normal in sleep had less evidence of disease, less disability and less elevation of blood pressure. Patients who maintained an elevated blood pressure in sleep showed more signs of disease, had more disability and more elevation of blood pressure.     

阻塞性睡眠呼吸暂停对动态血压影响的研究

目的　探讨阻塞性睡眠呼吸暂停 (OSA)夜间低氧血症对动态血压变化的影响。方法　选择阻塞性睡眠呼吸暂停综合征 (OSAS)患者 60例和正常对照组 2 0例进行多导睡眠图检查和 2 4h血压监测。结果　轻度OSAS患者的动态血压及其昼夜节律的改变与正常对照组相比无显著性差异 ;中度OSAS患者的nMDP及血压昼夜节律与正常对照组相比已有显著性差异 ;而重度OSAS组的动态血压改变则更加明显 ,2 4hMDP、2 4hMAP、dMSP、dMDP、dMAP、nMSP、nMDP、nMAP均明显高于对照组 ,其中 2 4hMDP、dMDP、dMAP、nMSP、nMDP与轻、中度组比较有显著性差异 ,同时夜间血压下降节律紊乱 ,昼夜血压差值减小。OSAS患者 2 4hMDP、dMDP、nMSP、nMDP、nMAP与睡眠呼吸暂停低通气指数 (AHI)呈显著正相关 ,而 2 4hMSP、2 4hMAP、nMSP、nMAP、ΔSBP、ΔDBP与睡眠中经皮血氧饱和度(SpO2 )降低大于 0 0 4的总次数、SpO2 低于 0 90的时间均呈正相关 ,而与睡眠中SpO2 最低值、SpO2 平均值呈负相关。结论　OSAS患者各期血压的平均水平与AHI、呼吸暂停持续时间及SpO2 降低的程度显著相关 ,OSAS的病情越重 ,这种血压变化及昼夜节律改变越显著     

Calculated mean arterial blood pressure in critically ill neonates

Summary Mean arterial pressure (MAP) is the area under the pressure wave form averaged over the cardiac cycle. A widely used rule of thumb to estimate MAP of peripheral arterial pressure waves in adults is adding one-third of the pulse pressure (PP) to diastolic arterial pressure (DAP). However, radial artery pressure waves in newborns differ from those in adults and resemble proximal aortic pressure waves, so that the above-mentioned calculation of MAP may not be correct. The present study was set up to obtain an arithmetical approximation to derive MAP from blood pressure waves measured in the radial artery of the neonate. We accurately recorded about 300 invasively obtained blood pressure curves in the radial artery of 10 neonates admitted for intensive care. We found that MAP in the radial artery in these neonates can be well approximated by adding 46.6% PP to DAP (range 43.0–50.1%). We suggest that the rule of thumb to derive MAP from radial artery waves in the neonate to be approximately the average of systolic and diastolic pressure, as opposed to adding one-third of the pulse pressure to the diastolic value in the adult.Abbreviations ABP Arterial blood pressure - SAP Systolic arterial pressure - DAP Diastolic arterial pressure - MAP Mean arterial pressure - PP Pulse pressure - MAP% (MAP-DAP)/(SAP-DAP)×100% (i.e., level of the MAP in the wave, expressed in % PP) - PDA Patent ductus arteriosus - IRDS Idiopathic respiratory distress syndrome     

The effect of continuous positive airway pressure therapy on blood pressure and arterial stiffness in hypertensive patients with obstructive sleep apnea

Aim

We aimed to evaluate the effect of continuous positive airway pressure (CPAP) therapy on blood pressure (BP) and arterial stiffness in hypertensive patients with obstructive sleep apnea (OSA).

Patients and methods

We studied 38 hypertensive patients who suffered from severe OSA. Ambulatory BP measurement was performed at baseline and after at least 3 months of uninterrupted CPAP therapy. In 19 of these patients, we also measured pulse wave velocity (PWV) at baseline, after the first night of CPAP therapy and at 3 months. Fifteen normotensive subjects without OSA comprised the control group.

Results

CPAP therapy reduced systolic BP from 141.5?±?12.1 to 133.5?±?9.7 mmHg (p?=?0.007) and diastolic BP from 87.8?±?6.8 to 83?±?5.4 mmHg (p?=?0.004). CPAP also reduced the PWV from 8.81?±?1.4 to 8.18?±?1 m/s after the first night of CPAP therapy (p?=?0.003) and to 7.37?±?1 m/s at 3 months (p?=?0.007).

Conclusions

To the best of our knowledge, this is the first study demonstrating that CPAP therapy in hypertensive patients with OSA improves arterial stiffness from the first night and that this favorable effect is maintained for at least 3 months of CPAP use. A reduction in BP was also observed, even though BP control was not always achieved.     

Sodium thiopental and mean arterial pressure during cardiopulmonary bypass

Sodium thiopental is known to have a number of cardiovascular effects, but injection into the cardiopulmonary bypass reservoir has not been studied. The effect of sodium thiopental on mean arterial blood pressure during cardiopulmonary bypass was assessed in 150 patients undergoing elective coronary artery bypass grafting. Sodium thiopental 3 mg · kg(-1) was administered via the cardiopulmonary bypass reservoir. Mean arterial pressure was recorded just before drug administration and at 15-sec intervals up to 120 sec afterwards. Compared to the baseline value, mean arterial pressure was significantly higher at 30, 45, 60, and 75 sec after drug administration, and it was significantly lower at 90, 105, and 120 sec. Sodium thiopental, in addition to its effects on myocardial tissue, acts initially as a potent vasopressor, and shortly after, as a potent vasodilator.     

Short-term effect of dynamic exercise on arterial blood pressure

BACKGROUND. To quantify the duration of postexercise hypotension at different exercise intensities, we studied six unmedicated, mildly hypertensive men matched with six normotensive controls. METHODS AND RESULTS. Each subject wore a 24-hour ambulatory blood pressure monitor at the same time of day for 13 consecutive hours on 3 different days. On each of the 3 days, subjects either cycled for 30 minutes at 40% or 70% maximum VO2 or performed activities of daily living. There was no intensity effect on the postexercise reduction in blood pressure, so blood pressure data were combined for the different exercise intensities. Postexercise diastolic blood pressure and mean arterial pressure were lower by 8 +/- 1 (p less than 0.001) and 7 +/- 1 mm Hg (p less than 0.05), respectively, than the preexercise values for 12.7 hours in the hypertensive group. These variables were not different before and after exercise in the normotensive group. Systolic blood pressure was reduced by 5 +/- 1 mm Hg (p less than 0.05) for 8.7 hours after exercise in the hypertensive group. In contrast, systolic blood pressure was 5 +/- 1 mm Hg (p less than 0.001) higher for 12.7 hours after exercise in the normotensive group. When the blood pressure response on the exercise days was compared with that on the nonexercise day, systolic blood pressure (135 +/- 1 versus 145 +/- 1 mm Hg) and mean arterial pressure (100 +/- 1 versus 106 +/- 1 mm Hg) were lower (p less than 0.05) on the exercise days in the hypertensive but not in the normotensive group. We found a postexercise reduction in mean arterial pressure for 12.7 hours independent of the exercise intensity in the hypertensive group. Furthermore, mean arterial pressure was lower on exercise than on nonexercise days in the hypertensive but not in the normotensive group. CONCLUSION. These findings indicate that dynamic exercise may be an important adjunct in the treatment of mild hypertension.     

The effect of pressure pulsations on time mean flow rate.

The flow rate of Newtonian fluids (water and a 1:1 water/glycerol mixture) was studied in small rigid tubes (415, 441, 706, and 1403 μm diameter). The time mean flow rates produced by steady pressure gradients were compared with the flow rates produced by superimposing cyclically varying pulses on the same mean pressure gradients. Pulse frequencies between zero and 4 Hz and pulse amplitudes of 20 and 40% of the upstream mean pressure were applied. Two cases were considered. In the first, long tubes ($\text{L}\text{D}\text{= 96}\text{and}\text{216}$) in which entrance effects are insignificant were used. The second case employed short tubes ($\text{L}\text{D}\text{= 30, 24,}\text{and}\text{21}$), where the entrance effects are important. The latter situation more closely corresponds with the conditions that exist in the small arterial distributing system than does the long tube model. Earlier theoretical studies of flow in long tubes predict that superimposed pressure oscillations do not modify the time mean flow rates when compared with static perfusion. Our results confirm these predictions. No theoretical studies have yet been made to predict the effects of superposition of pressure pulses on steady flow in short rigid tubes. Our experimental results demonstrate that in this case superposition of pulses produce only minor changes in the mean flow. The largest observed deviations were about 4%. However, statistically significant changes most frequently observed were only of the order of 1–2%. We interprete this to mean that pulsation adds no new nonlinearities of importance to those produced by the entrance effects in steady flow. Extrapolating these results to the circulation, one may conclude that any effects of the arterial pulse on the time mean flow rate through vascular regions composed of frequently branching vessels must be due to effects such as wall distensibility, non-Newtonian behavior of blood, and vascular smooth muscle reactivity.     

Variability of direct arterial blood pressure in essential hypertension--relationships between the fall of blood pressure during sleep and awake resting hemodynamic parameters

The relationship of continuous ambulatory intra-arterial blood pressure over a 24-hour period and awake resting hemodynamic parameters measured by echocardiography was studied in 21 patients with essential hypertension (WHO stage I & II): Left ventricular wall thickness at end-diastole correlated strongly with average SBP and weakly with average DBP during both waking and sleeping periods. Variability of blood pressure taken during waking and sleeping periods was not significantly correlated with any hemodynamic parameters measured by echocardiography. Variability of SBP during sleep had a significant correlation with age; however the fall of blood pressure during sleep had no significant correlation with age. Fall of blood pressure during sleep was significantly correlated to resting awake TPR. In patients with essential hypertension, the above results demonstrate that subjects with thicker left ventricular wall have higher average continuous blood pressure over 24-hours and suggest that there is a tendency for greater falls in blood pressure during sleep to occur in subjects with higher TPR and that older subjects have greater variabilities of SBP during sleep.     

The acute effects of continuous positive airway pressure and oxygen administration on blood pressure during obstructive sleep apnea.

We have measured blood pressure continuously with a digital artery blood pressure monitor in eight patients with severe obstructive sleep apnea (OSA) during 30 min each of wakefulness, OSA, OSA with added oxygen to keep saturation above 96 percent at all times (OSA+O2), and nasal continuous positive airway pressure (CPAP) therapy. Mean blood pressures were not different between wakefulness, OSA, OSA+O2, and CPAP, although the variability in blood pressure was significantly greater during OSA and OSA+O2 than during wakefulness and CPAP. The addition of oxygen did not attenuate the variability in blood pressure. Using multiple linear regression modeling to further dissect out the principal variables determining the postapneic blood pressure rise, we found that only apnea length (r2 = 0.28, p less than 0.0001) and pulse rate changes (r2 = 0.15, p less than 0.0001) remained significantly related to SBPmax, while hypoxemia did not. We found the same trends in the other variables SBPten, DBPmax, and DBPten. Hypoxemia made a small contribution to the size of DBPmax, although this was small by comparison with apnea length. We conclude that CPAP treatment of OSA does not lower mean blood pressure acutely, although it significantly reduces the large oscillations in blood pressure seen in patients with untreated OSA. The rise in blood pressure following each apnea is not primarily due to arterial desaturation but is related to apnea length and may be caused by increased sympathetic activity secondary to arousal.     

Observations on arterial blood pressure during attacks of angina pectoris

Blood pressure readings were obtained during spontaneous attacks of angina pectoris in twenty-three patients. In seven, the previous blood pressure readings were known. In three, the attacks were allowed to end spontaneously, and in twenty relief was obtained by administering nitroglycerin.In every instance the level of the systolic pressure was distinctly higher during pain than when the patient was free from pain. Although this may not be an invariable relationship, this study and a survey of the cases recently reported leads one to the conclusion that a failure of the blood pressure to rise in anginal attacks is rare.Evidence is presented to show that in patients with angina pectoris, pain alone, e. g., that of renal colic, neither produces an elevation in blood pressure nor brings on an attack of angina.Although we suspect that a temporary elevation in blood pressure is an important factor in the production of anginal attacks and may even be a necessary immediate cause of the attack, a final decision as to this relationship will require further investigation.