Csilla Molnár

Acetazolamide as a vasodilatory stimulus in cerebrovascular diseases and in conditions affecting the cerebral vasculature

Pathologic processes affecting the brain vessels may damage cerebral vasodilatory capacity. Early detection of cerebral dysfunction plays an important role in the prevention of cerebrovascular diseases. In recent decades acetazolamide (AZ) has frequently been used for this purpose. In the present work the mechanism of action and the previous studies are reviewed. The authors conclude that AZ tests are useful in cerebrovascular research. Further investigations are recommended to prove how impaired reserve capacity and reactivity influence the stroke risk in patients and whether these tests may indicate therapeutic interventions.

Cerebrovascular Reactivity and Reserve Capacity in Type II Diabetes Mellitus

The aim of the study was to test the hypothesis that cerebrovascular reserve capacity and cerebrovascular reactivity are impaired in patients suffering from non insulin-dependent diabetes mellitus. We also intended to investigate factors which may influence resting cerebral blood flow velocity and cerebrovascular reserve capacity. A total of 28 patients suffering from type II diabetes mellitus and 20 healthy control subjects were studied. Based on diabetes duration patients were divided into two groups: subjects with > 10 years and those with < or = 10 years disease duration. Middle cerebral artery mean blood flow velocities were measured at rest and after intravenous administration of 1g acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated. Blood glucose, insulin, glycosylated hemoglobin, hemostatic factors (fibrinogen, alpha-2 macroglobulin and von Willebrand factor antigen) were determined. Cerebrovascular reactivity and reserve capacity values were compared between the two diabetic subgroups and controls. Correlations between laboratory parameters and cerebrovascular reserve were investigated by linear regression analysis. Resting cerebral blood flow velocity was similar in controls and in the two diabetic subgroups. Cerebrovascular reactivity was elevated for a shorter time in patients with > 10 years disease duration than in controls and short-term diabetic patients. Cerebrovascular reserve capacity was lower in the long-term diabetes group (means +/- SD: 39.6 +/- 20.7%) than in patients with < or = 10 years disease duration (63.3 +/- 17.4%, p < 0.02 after Bonferroni correction). Cerebrovascular reserve capacity was inversely related to the duration of the disease (R = 0.53, p < 0.003). None of the determined laboratory factors had any relation with resting cerebral blood flow and cerebrovascular reserve capacity. The vasodilatory ability of cerebral arterioles is diminished in long-standing type II diabetes mellitus.

Transcranial Doppler Study of the Cerebral Hemodynamic Changes During Breath-Holding and Hyperventilation Tests

Background and purpose. The aim of the present study was to assess the time course of hyperventilation (HV) and breath‐holding (BH) tests in healthy volunteers. Subjects and Methods. Young healthy volunteers (n= 29) underwent continuous registration of the middle cerebral artery mean blood flow velocity (MCAV) during and after 30 seconds of BH and 60 seconds of HV. Absolute values as well as percentage changes of the MCAV are reported. In 13 subjects, determination of capillary blood gas parameters (pH, pCO2, pO2, and O2 saturation) was performed before tests, after BH and after HV. Results. MCAV during 30 seconds of breath‐holding starts to increase after 10 seconds and reaches its highest level at 30 seconds. After breathing normally, MCAV normalizes within 30 seconds. Hyper‐ ventilation results in a decrease in MCAV, which reaches a plateau at 20 to 30 seconds after starting to hyperventilate, and blood flow velocity did not change significantly any further until the end of the procedure. The normalization of the MCAV is incomplete at 30 seconds after finishing hyperventilation. None of the capillary blood gases changed significantly after breathholding, whereas capillary pH, pO2, and oxygen saturation increased and pCO2 decreased after hyperventilation. No relationship was found between capillary blood gas parameters and MCAV values. Conclusions. The authors concluded that breathholding and hyperventilation tests seem to be a practical alternative to acetazolamide and the CO2 inhalation method in the assessment of cerebral hemodynamics.

Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test

IntroductionThe pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE.MethodsPatients fulfilling the criteria of clinical sepsis and showing disturbance of consciousness of any severity were included (n = 14). Non-septic persons whithout previous diseases affecting cerebral vasoreactivity served as controls (n = 20). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15 and 20 minutes after intravenous administration of 15 mg/kgBW acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity, CVR) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity, CRC) were compared among the groups.ResultsAbsolute blood flow velocities after adminsitration of the vasodilator drug were higher among control subjects than in SAE. Assessment of the time-course of the vasomotor reaction showed that patients with SAE reacted slower to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that patients with SAE reacted to a lesser extent to the drug than did control subjects (CRC controls:46.2 ± 15.9%, CRC SAE: 31,5 ± 15.8%, P < 0.01).ConclusionsWe conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological finding has to be assessed in further studies.

Cerebrovascular Reactivity in Hypertensive and Healthy Adolescents: TCD With Vasodilatory Challenge

Background. Adolescent hypertension predicts hypertension and increased cardiovascular morbidity in adulthood. The aim of the present work was to test whether cerebrovascular reactivity to CO2 is altered among hypertensive adolescents. Methods. From the population‐based cohort of the Debrecen Hypertension Study, 113 hypertensive and 58 normotensive adolescents underwent transcranial Doppler measurements at rest and after 30 seconds of breath holding. Results. Systolic, mean, and diastolic blood flow velocities were higher among hypertensive individuals at rest. Taking the absolute blood flow velocity parameters into account, after breath holding, only the pulsatility index was significantly higher in the hypertensive group. The percentage change of the different blood flow parameters showed less intensive change in hypertensive teenagers. Conclusion. Cerebral vasoreactivity is decreased among hypertensive individuals as compared to healthy controls.

Assessment of target-organ damage in adolescent white-coat and sustained hypertensives

Aims and scope The aim of the present study was to assess whether a difference exists between intima–media thickness and the left ventricular mass index in healthy nonhypertensive, white-coat hypertensive and sustained hypertensive adolescents. Patients and methods Fifty-nine normotensive and 120 hypertensive adolescents were enrolled in our study. Hypertensive patients were classified into white-coat hypertension (WCH) and sustained hypertension groups based on 24-h ambulatory blood pressure measurements. Both normotensive and hypertensive individuals underwent routine laboratory tests, intima–media thickness measurements on the common carotid arteries and transthoracic echocardiography to measure the left ventricular mass index (LVMI). Results Intima–media thickness was higher both in WCH and sustained hypertension compared with healthy normotensive individuals (controls: 0.048 ± 0.01 cm, WCH: 0.056 ± 0.01 cm, sustained hypertension: 0.054 ± 0.012 cm, both P < 0.001 compared with controls, nonsignificant difference between the two hypertensive groups). There was no difference between the LVMI of control individuals and WCH (LVMI: 35.5 ± 10.3 g/m2.7 and 37.7 ± 11.2 g/m2.7 respectively, P = 0.87). LVMI in sustained hypertension group (LVMI: 44.1 ± 14.1 g/m2.7) was significantly higher both compared with WCH (P < 0.05), and healthy adolescents (P < 0.001). Conclusion Target-organ damage develops in a stepwise fashion in adolescent hypertension. An increased intima–media thickness can be demonstrated not only in the sustained but also in the white-coat form of adolescent hypertension.

Impaired cerebral vasoreactivity in white coat hypertensive adolescents

Background and purpose:  Although its incidence is not high, adolescent hypertension may predict hypertension and increased cardiovascular risk in adulthood. Therefore, the aim of the present study was to assess whether cerebrovascular reactivity is altered in adolescent white coat and sustained hypertensive patients compared to healthy teenagers.

Active warming of critically ill trauma patients during intrahospital transfer: A prospective, randomized trial

ZusammenfassungHintergrundHypothermia ist ein oft beobachtbares Phänomen bei Traumapatienten während der Akutversorgung. Bekannte Komplikationen einer akzidentellen Hypothermie sind Wundheilungsstörungen, kardiale Komplikationen, hämodynamische Instabilität, Defizite im Immunsystem und vermehrter Blutverlust. In der folgenden Studie verglichen wir passiv gewärmte vs. aktiv gewärmte Patienten auf dem Transport von einer Intensivstation zum CT.MethodenDreißig Intensivpatienten wurden randomisiert zur einer aktiv gewärmten Gruppe, abgedeckt mit einer Carbonfiberwärmedecke (42°C) während des gesamtem Transport und zur einer passiv gewärmten Gruppe, die mit einer ausgeschalteten Carbonfiberdecke versorgt waren. In beiden Gruppen waren die Carbonfiberdecke mit konventionellen Wolldecken abgedeckt. Es wurden die Vitalparameter und die Körpertemperaturen gemessen.ErgebnisseDie Ausgangsdaten der Patienten waren in beiden Gruppen vergleichbar. Die Ausgangstemperatur in Gruppe A war 36,4°C±0,2°C und blieb stabil bei 36,4°C±01°C, die Temperatur in Gruppe B startete bei 36,4°C±0,2°C und sank statistisch signifikant auf 34,7°C±0,6°C.SchlussfolgerungenDie Hypothermie ist ein gängiges Problem, wenn Patienten wegen der diagnostischen Maßnahme einen innerklinischen Transport benötigen. Das aktive Wärmen dieser Patienten während des Transports kann die Körpertemperatur stabil normotherm halten. We können daher zur Erhaltung der Normothermia das aktive Wärmen von Patienten während eines Transports empfehlen.SummaryObjectiveHypothermia in trauma victims is a frequently observed phenomenon in acute care. Known complications of hypothermia are impaired wound healing, cardiac complications, hemodynamic instability, impaired immune function and increased blood loss. We compared active warming versus passive warming in hypothermia in critical-care patients undergoing intrahospital transfer from ICU to computer tomography (CT).MethodsThirty critically ill patients were randomized either to an actively warmed group, covered with a carbon-fiber heating blanket (set to 42°C) during the entire transport including the time spent in the CT, or to a passively warmed group, covered with a carbon-fiber heating blanket (switched off) during the entire transport and in the CT. The carbon-fiber blanket was covered with a conventional wool blanket in both groups. Vital parameters and core temperatures were recorded.ResultsPatients’ characteristics and vital parameters were similar in each treatment group. Initial average core temperature in group A was 36.4°C±0.2°C and remained stable at 36.4°C±0.1°C; core temperature in group B started at 36.4°C±0.2°C but decreased to 34.7°C±0.6°C.ConclusionsHypothermia is common when critically ill trauma patients require intrahospital transport for diagnostic procedures. Resistive heating during intrahospital transport kept the core temperature stable and assured normothermia in all actively warmed patients. We therefore recommend active warming for critically ill trauma patients during intrahospital transport.

Hyperventilation-induced cerebrovascular reactivity among hypertensive and healthy adolescents

Background: It is known that cerebral vasoreactivity is altered in adult arterial hypertension but no information is available about cerebral arteriolar function in hypertensive adolescents. Therefore, the aim of the present work was to assess cerebral vasoreactivity responses in adolescent hypertension. Methods: 113 hypertensive and 58 normotensive adolescents were assessed with transcranial Doppler sonography by using voluntary hyperventilation (HV) as vasoconstrictory stimulus. Absolute blood flow velocities (systolic, mean and diastolic) and pulsatility indices (PIs) at rest and after HV, as well as percentage change of the blood flow velocities after HV were compared among the groups. Results: Blood flow velocities at rest were significantly higher in hypertensive individuals, while PIs were similar in the two groups. After HV, all blood flow velocity parameters were higher among hypertensive teenagers than in healthy controls, while PIs did not differ between the two groups. Taking the relative changes after HV into account, it was found that HV induced a more pronounced change of the systolic and mean blood flow velocities of the control subjects than in hypertensive adolescents. Conclusions: Cerebrovascular reactivity to hypocapnia is decreased in hypertensive adolescents as compared to healthy teenagers. Further studies are needed to clarify the clinical significance of altered cerebral microvascular function in adolescent hypertension.

The relative exposure of the operating room staff to sevoflurane during intracerebral surgery.

BACKGROUND: Our primary aim in this study was to investigate whether escape of the volatile anesthetic sevoflurane from the surgical site during craniotomy for tumor resection increases the exposure of the neurosurgeon to the anesthetic when compared with the anesthesiologist. METHODS: Initially, the release of sevoflurane from the surgical site was measured during 35 tumorectomies starting from opening to closure of the dura. Volatile anesthetic absorbers were placed at three detection sites: 1) the surgeon’s breathing zone, 2) the anesthesiologist’s breathing zone, and 3) the farthest corner of the operation room. In the second sampling series that included 16 patients, the detector that had been in the corner of the operating room in the first series was now placed in the vicinity of the patient’s mouth (within 5 cm). Sevoflurane captured by the absorbers was quantified by an independent chemist using chromatography. RESULTS: Absorbers in the surgeon’s breathing zone (0.24 ± 0.04 ppm) captured a significantly lower amount of sevoflurane compared with absorbers in the anesthesiologist’s breathing zone (1.40 ± 0.37 ppm) and comparable with that in the farthest corner of the operation room (0.25 ± 0.07 ppm). There was no correlation between the amount of absorbed sevoflurane and the size of craniotomy window, even when adjusting for the variation in duration of surgery. In the second series of sampling, absorbers in the proximity of the patient’s mouth captured the highest amount of sevoflurane (1.54 ± 0.55 ppm), followed by the anesthesiologist’s (1.14 ± 0.43 ppm) and the surgeon’s (0.15 ± 0.05 ppm) breathing zones. CONCLUSIONS: The close proximity of the surgeon’s breathing zone to the craniotomy window does not appear to be a source of increased exposure to sevoflurane. The observed higher exposure of the anesthesiologist to sevoflurane in the operating room environment warrants further exploration.