急性脑卒中急性期血压调控与早期预后的相关性研究

目的 探讨急性脑卒中急性期血压调控与早期预后的相关性。方法 本研究对20005年9月至2006年12月发病72h内入院的急性脑卒中符合人选标准的患者，据单、双日随机分为A、B两组。于入院24h内、7d、14d进行神经功能缺损评分，调控血压并记录其他影响预后的危险因素。结果共纳入急性脑卒中患者692例，血压与预后呈U型关系。入院时血压升高的发生率为71．24％，合并高血压组较不合并高血压组预后差。血压调控在140—180/180—90mmHg时预后最好，为U型关系的分界值。脑卒中急性期高血压是近期预后不良的独立危险因素，高血糖、白细胞升高与预后不良呈正相关。结论 急性脑卒中患者急性期血压调控是早期预后的独立影响因素。     

Intracranial pressure and cerebral perfusion pressure in patients developing brain death

PurposeWe investigated whether a critical rise of intracranial pressure (ICP) leading to a loss of cerebral perfusion pressure (CPP) could serve as a surrogate marker of brain death (BD).Materials and methodsWe retrospectively analyzed ICP and CPP of patients in whom BD was diagnosed (n = 32, 16-79 years). Intracranial pressure and CPP were recorded using parenchymal (n = 27) and ventricular probes (n = 5). Data were analyzed from admission until BD was diagnosed.ResultsIntracranial pressure was severely elevated (mean ± SD, 95.5 ± 9.8 mm Hg) in all patients when BD was diagnosed. In 28 patients, CPP was negative at the time of diagnosis (− 8.2 ± 6.5 mm Hg). In 4 patients (12.5%), CPP was reduced but not negative. In these patients, minimal CPP was 4 to 18 mm Hg. In 1 patient, loss of CPP occurred 4 hours before apnea completed the BD syndrome.ConclusionsBrain death was universally preceded by a severe reduction of CPP, supporting loss of cerebral perfusion as a critical step in BD development. Our data show that a negative CPP is neither sufficient nor a prerequisite to diagnose BD. In BD cases with positive CPP, we speculate that arterial blood pressure dropped below a critical closing pressure, thereby causing cessation of cerebral blood flow.     

Systemic arterial pressure wave reflections during acute hemorrhage

OBJECTIVE: To determine the effects of hemorrhage on wave-reflection-induced systolic pressure augmentation in the aorta. DESIGN: Randomized, controlled laboratory experiment. SETTING: University research laboratory. SUBJECTS: Twenty-five anesthetized pigs randomized to surgical controls (n = 7), hemorrhage (n = 9, H), and hemorrhage with reinfusion (n = 9, HR). INTERVENTIONS: Hemorrhage of 1 mL/kg/min over 20 mins followed by observation (H) or reinfusion (HR) of shed blood. MEASUREMENTS AND MAIN RESULTS: High-fidelity systemic arterial pressure waveforms, from ascending aorta to femoral artery, were transduced and archived digitally using intravascular semiconductor catheter-tipped pressure transducers. Wave-reflection-induced systolic pressure augmentation was determined using the augmentation index in the ascending aorta (AIaa) and distal descending aorta (AIda). Pulse wave velocity, wave travel times, and lumped pressure wave reflection sites were also calculated. AI values were positive at baseline with greater decreases in AIda compared with AIaa observed following hemorrhage, with negative values achieved for AIda alone. AI returned to control values following reinfusion. Lumped reflection site positions and pressure contour maps suggested that a single lumped reflection site (lower abdomen/pelvis) at baseline was replaced by two discrete sites (upper abdomen and pelvis) following hemorrhage, which only recovered following reinfusion. Hemorrhage was associated with hemodynamic conditions that favored late return of wave reflection from the trunk and with the absence of significant changes in systemic vascular resistance. CONCLUSIONS: Hemorrhage-induced early return of pressure wave reflection from the abdominal vasculature is associated with systolic pressure augmentation in the ascending aorta and has the potential to worsen afterload conditions and decrease coronary artery perfusion and cardiac performance. Hemorrhage-induced splanchnic vasoconstriction causing pressure wave reflection may explain these loading conditions in the ascending aorta, and systolic pressure augmentation may be a more useful guide to left ventricular afterload than systemic vascular resistance.     

Time required for equilibration of arterial oxygen pressure after setting optimal positive end-expiratory pressure in acute respiratory distress syndrome

OBJECTIVE: To evaluate the time course of Pao2 change following the setting of optimal positive end-expiratory pressure (PEEP) in patients with acute respiratory distress syndrome (ARDS). DESIGN: Prospective clinical study. SETTING: Multidisciplinary intensive care unit of a university hospital. PATIENTS: Twenty-five consecutive patients with ARDS. INTERVENTIONS: ARDS was diagnosed during pressure-regulated volume control ventilation with tidal volume of 7 mL/kg actual body weight, respiratory rate of 12 breaths/min, inspiratory/expiratory ratio of 1:2, Fio2 of 1, and PEEP of 5 cm H2O. A critical care attending physician obtained pressure volume curves and determined the lower inflection point. Following a rest period of 30 mins with initial ventilation variables, PEEP was set at 2 cm H2O above the lower inflection point, and serial blood samples were collected during 1-hr ventilation with optimal PEEP. Arterial blood gas analyses were performed at 1, 3, 5, 7, 9, 11, 15, 20, 30, 45, and 60 mins. MEASUREMENTS AND MAIN RESULTS: Twenty-five patients were found eligible for the study. Three patients were excluded due to deterioration of oxygen saturation and hemodynamic instability following the initiation of optimal PEEP. Eight cases (36%) were considered to be of pulmonary origin and 14 cases (64%) of extrapulmonary origin. Optimal PEEP levels were 14 +/- 3 cm H2O and 14 +/- 4 cm H2O in pulmonary and extrapulmonary ARDS, respectively. Pao2 demonstrated a 130 +/- 101% increase at the end of 1-hr period in total study population. This improvement did not differ significantly between pulmonary and extrapulmonary forms of ARDS (135 +/- 118% vs. 127 +/- 95%, p = .8). Mean 90% oxygenation time was found to be 20 +/- 19 mins. In the subset of patients with ARDS of pulmonary origin, 90% oxygenation time was 25 +/- 26 mins, whereas it was 17 +/- 15 mins in patients with ARDS of extrapulmonary origin (p = .8). CONCLUSIONS: Our data showed that 20 mins would be adequate for obtaining a blood gas sample in ARDS patients with pulmonary and extrapulmonary origin after application of optimal PEEP 2 cm H2O above the lower inflection point.     

Impaired cerebrovascular reactivity after acute traumatic brain injury can be detected by wavelet phase coherence analysis of the intracranial and arterial blood pressure signals

The objective of the study was to evaluate the wavelet spectral energy of oscillations in the intracranial pressure (ICP) signal in patients with acute traumatic brain injury (TBI). The wavelet phase coherence and phase shift in the 0.006–2 Hz interval between the ICP and the arterial blood pressure (ABP) signals were also investigated. Patients were separated into normal or impaired cerebrovascular reactivity, based on the pressure reactivity index (PRx). Spectral energy, phase coherence and phase shift in the low frequency and cardiorespiratory intervals were compared for the two groups. Data were prospectively collected and analyzed retrospectively in 22 patients, within the first week after acute TBI. The ICP and ABP signals were continuously recorded for $ \cong $ ? 40 min and the wavelet transform was used to calculate the spectral energy and phase of the signals. The average ICP wavelet energy spectrum showed distinct peaks around 1.0 (cardiac), 0.25 (respiratory) and 0.03 Hz. Patients with normal cerebrovascular reactivity (negative PRx) had 38.6 % (±SD 16.7 %) of the mean wavelet energy below the lower limit of the respiratory frequency band (0.14 Hz) compared to only 18.1 % (±SD 17.8 %) in patients with altered cerebrovascular reactivity (positive PRx) (difference: p = 0.0057). Wavelet phase coherence between the ABP and ICP signals was statistically significant (p < 0.05) in the 0.006–2 Hz interval. The phase shift between the ABP and ICP signals was around zero in the 0.14–1.0 Hz interval. Seven patients with PRx between ?0.4943 and ?0.1653 had a phase shift in the interval 0.07–0.14 Hz, whereas 15 patients with PRx between ?0.1019 and 0.3881 had a phase shift in the interval 0.006–0.07 Hz. We conclude that the wavelet transform of the ICP signal shows spectral peaks at the cardiac, respiratory and 0.03 Hz frequencies. Normal cerebrovascular reactivity seems to be manifested as increased spectral energy in the frequency interval <0.14 Hz. A phase shift between the ICP and ABP signals in the interval 0.07–0.14 Hz indicates normal cerebrovascular reactivity, while a phase shift in the interval 0.006–0.07 Hz indicates altered cerebrovascular reactivity.     

Persistence of cerebral blood flow after brain death

Persistent cerebral blood flow occasionally confounds confirmatory tests for brain death and results in the anguish of delayed diagnosis, unnecessary use of expensive resources, and loss of transplant opportunities. We reviewed the literature to examine the reasons, frequency, and meaning of this problem. We found that this phenomenon occurs: (1) before increasing intracranial pressure completely shuts down flow; (2) in infants with pliable skulls; and with (3) decompressing fractures, (4) ventricular shunts, (5) ineffective deep brain flow, (6) reperfusion, (7) brain herniation, (8) jugular reflux, (9) emissary veins, and (10) pressure injection artifacts. Isolated venous sinus visualization is common (occurring in up to 57%) but represents trivial blood flow and confirms brain death. Arterial flow is much less common (2.6% incidence in our series). Normal flow occurs but is rare. Arterial flow does not exclude brain death, but the diagnosis should be confirmed by repeated studies or other means.     

Central arterial pressure and arterial pressure pulse: new views entering the second century after Korotkov

The ubiquitous brachial cuff method gained widespread clinical acceptance for blood pressure recording after confirmation of its prognostic value in 1917. This method displaced radial pulse waveform analysis by sphygmography, which also gave prognostic Information but was difficult to use. Since that time, brachial cuff sphygmomanometry has migrated from the physician's office to 24-hour monitoring and home use, with electronic methods replacing the Korotkov sound technique for determining systolic and diastolic pressure. Detailed instrumental studies, required by regulatory bodies, revealed inaccuracies of all cuff methods for recording true intra-arterial pressure. A major source of inaccuracy in assessing left ventricular load is the amplification of the pressure wave in its transit from the central aorta to upper limb arteries, as extensively studied by Earl H. Wood at the Mayo Clinic in Rochester, Minn, in the 1950s. This limitation can be overcome by combining newer methods using radial artery waveform analysis in conjunction with conventional cuff sphygmomanometry to noninvasively measure the central aortic pressure waveforms. Recent studies using radial tonometry have proved that this is more effective than conventional manometry in predicting cardiovascular events and gauging response to therapy. Measurement of central as well as peripheral arterial pressure and physiology is becoming increasingly used as an office practice and a laboratory procedure.     

Long-term causes of death after traumatic brain injury.

OBJECTIVE: To determine which causes of death are more frequent in persons with traumatic brain injury (TBI), and by how much, compared with the general population. Our focus was the period beginning 1 yr after injury. DESIGN: Subjects were 2320 Californians with long-term mental disability after a TBI at age 10 yr or more, followed up between 1988 and 1997. The units of study were person-years, each linked to the subject's age, gender, level of ambulation, time since injury, and cause of death (if any) for the specific year. Observed numbers of cause-specific deaths were compared with numbers expected according to general population mortality rates. RESULTS: Mortality was higher between 1.0 and 5.0 yr postinjury than after 5.0 yr and was strongly related to reduced mobility. Death rates were elevated for circulatory diseases, respiratory diseases, choking/suffocation, and seizures, with seizure deaths being relatively frequent, even among the most ambulatory. CONCLUSIONS: Death rates for several causes are elevated in persons with long-term sequelae of TBI. The increased risk of choking/suffocation should be of interest to caregivers. Life expectancy seems to be reduced, even for patients who are fully ambulatory.     

Vegetative regulation of arterial pressure in patients with arterial hypertension and non-insulin-dependent diabetes mellitus (NIDDM)

72 patients with NIDDM (duration 5.3 +/- 3.1 years) aged 41-60 years were examined. They had also mild or moderate hypertension (duration 12.1 +/- 4.5). Control groups consisted of 15 NIDDM patients free of hypertension, 15 hypertensive patients without diabetes, 15 healthy subjects. All the patients have undergone 24-h monitoring of arterial pressure (APM) and computed cardiointervalography (CIG). As shown by CIG, hypertensive patients with NIDDM had sympathotonia which resulted from hypofunction of parasympathetic and hyperfunction of the sympathetic nervous systems. APM demonstrated enhanced variability of arterial pressure and its inadequate fall at night in patients of this group and normotensive patients with diabetes.     

A 24-hour profile of arterial pressure: vegetative regulation in persons with isolated systolic arterial hypertension

A total of 117 persons were studied: 60 patients with isolated systolic arterial hypertension (ISAH) (22 males, 38 females; mean age 68.7 +/- 4.2 years), 22 males with ISAH (mean age 20.1 +/- 2.7 years), 15 healthy elderly subjects and 20 healthy young males. The analysis of heart rhythm variability and the results of 24-h arterial pressure monitoring specified an individual 24-h profile of arterial pressure and effects of vegetative regulation on this profile.