RU2469645C1 - Method of selection of pressure regulating preparation for adequate cerebral perfusion in acute cerebral injury - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: before and after the introduction of a pressure regulating preparation, acoustic stem-induced potentials are recorded, peak latencies and peak intervals P1-P3, P3-P5, PIPS are measured. If observing reduction of the peak intervals and the peak latencies, the preparation is considered as improving the functional state of cerebral stem structures; the prescribed preparation and doses are remained unchanged. Increase of the peak intervals and the peak latencies show the preparation to deteriorate the functional state of cerebral stem structures; the prescribed dose is to be lowered, or the preparation is to be changed. An unchanged value of the peak intervals and the peak latencies means deterioration of the functional state of cerebral stem structures; the preparations regulating haemodynamics are withdrawn; the acoustic stem-induced potentials are assessed after the preparation dose has been changed, or the preparation has been changed and in dynamics on the 3^rd, 5^th, 9^th days, as well as in case of patient's deterioration.

EFFECT: method extends the range of products for selection of the pressure regulating preparation in the acute cerebral injury.

7 tbl, 3 ex

Description

The method relates to medicine, namely to resuscitation and neurology, and can be used to treat patients with ischemic stroke.

In acute brain damage, whether it is the result of an injury, stroke or surgical intervention (for example, regarding a tumor), with the formation of a zone of necrosis, a delayed destructive process develops, the consequences of which are no less significant. Among the variety of pathophysiological mechanisms of secondary brain damage, an important role is given to vascular factors, which are understood as microcirculatory changes leading to cerebral ischemia, and general vascular effects - hypotension and decreased cardiac output, which significantly change the functioning of all organs and systems of the body. It should be borne in mind that a significant percentage of patients with ischemic stroke are people who have long suffered from hypertension, adapted to high numbers of blood pressure.

In ischemic stroke, intracranial pressure figures rarely reach critical values and remain at the level of 15-17 mm Hg. Therefore, given this from the generally accepted calculation formula: CPD = CAD-ICP, it becomes clear that to maintain the CPD = 70-80 mm Hg it is enough to keep GARDEN = 90 mm Hg, but for most patients suffering from hypertension, this is not enough.

As analogues, we considered the three methods described below for the prevention of cerebral ischemia.

Method of neurophysiological intraoperative monitoring of somatosensory evoked potentials (SSEP) during reconstructive and spinal surgery: Ryzhova O.E., Tikhodeev S.A., Vishnevsky A.A., Zhulev S.N., Belyakov N.A. Assessment of the possibilities of neurophysiological intraoperative monitoring during reconstructive surgery on the spine // Questions of Neurosurgery. N.N. Burdenko. -. 2003. - No. 1. - S. 27-32.

The tasks of conducting neurophysiological intraoperative monitoring of SSEP include early detection of functional changes in the nervous tissue of ischemic origin and their correction.

Monitoring of SSEP is carried out according to the standard technique bilaterally through alternating stimulation. Significant changes are considered to be a decrease in the amplitude of the response by more than 50% and / or an increase in latency by more than 10%.

There is a method of calculating and measuring indicators of the oxygen transport system: delivery, consumption, disposal: Intensive care: trans. from English add. ed. A.I. Martynov - M .: GEOTAR MEDICINE, 1998 .-- ISBN 5-88816-025-3. The ICU book // Paul L. Marino // Philadelphia, Williams & Wilkins. - ISBN 0-8121-1306-3. - S. 27-35. It lies in the fact that they determine the content of blood oxygen: bound to hemoglobin (Hb) and in a free or dissolved state. The total amount of gas in both fractions is called the oxygen content in the blood (CaO ₂ ). The oxygen content in arterial blood is determined by the formula taking into account the level of Hb equal to 14 g.%, Saturation of Hb with oxygen (SaO ₂ = 98%) and the partial pressure of O ₂ (pO ₂ ) in the blood (paO ₂ ), which is 100 mm Hg

Oxygen delivery (DO ₂ ) is the rate of oxygen transport by arterial blood, which depends on the amount of cardiac output (CB) and oxygen content in arterial blood. Normally, DO ₂ is determined with CaO ₂ equal to 18 vol.%, And a cardiac index of 3 l / (min · m ² ), according to the formula.

The consumption of oxygen (VO ₂ ) is the final stage of oxygen transport to tissues and represents the oxygen supply of tissue metabolism. The Fick equation defines oxygen consumption as a derivative of cardiac output (CB) and arteriovenous difference in oxygen content (CaO ₂ -CvO ₂ ).

The absorption of oxygen from capillaries is carried out depending on its metabolic needs (except in cases of impaired ability to extract oxygen from capillary blood). When oxygen uptake worsens, VO ₂ will determine the rate of metabolic processes. This situation usually occurs in patients in critical conditions, and is described in detail in sepsis, multiple trauma, burns. Therefore, VO ₂ as an indicator of the metabolic rate in these cases should be determined in each patient.

The oxygen utilization coefficient (KUO ₂ ) is the part of oxygen absorbed by the tissues from the capillary bed; KUO _{2 is} defined as the ratio of oxygen consumption to its delivery.

The rate of oxygen delivery under normal conditions significantly exceeds consumption - this allows tissues to adapt to a decrease in oxygen delivery by increasing its utilization. KUO ₂ during heavy muscular work is able to increase up to 60-80% (at rest KUO ₂ is usually equal to 22-32%).

Also, this technique is used to assess cerebral blood flow, based on the data of arteriovenous difference in arterial oxygen and jugular vein (Tsarenko S.V. Intensive care for craniocerebral injury. M.: Publishing House "Medicine", 2004).

A well-known technique for non-invasive determination of cerebral oximetry in the para-infrared range, which allows to assess the correspondence of oxygen delivery and consumption by the brain and vascular regulation: S.V. Tsarenko, V.V. Krylov, D.N. Tyurin, V.V. Lazarev, D.L. Tsymlyakov, A.V. Karzin. Cerebral oximetry in the para-infrared range. Possibilities of use in the neuroresuscitation department. // Anesthesiology and resuscitation. - 1998 - No. 4 - P.43-47.

The cerebral oximetry method consists in the fact that a special sensor is placed on previously treated skin of the patient, which is free of hairline. The preferred location of the sensor over one of the frontal areas. Through the cable, the sensor is connected to the oximeter itself. The screen displays the current values of cerebral blood saturation in the studied region of the brain, as well as the trend of the indicator. It reflects the oxygen saturation of the blood of the brain itself, and not the scalp: Cerebral oximetry in dead subjects / Schwarz G., Litscher G., Kleinert R., et al. // J Neurosurg - Anest. - 1996 .-- 8 (3). - P.189-93, and venous, since it is known that the vascular bed of the brain is 80% composed of venous vessels.

The disadvantage of this method is that it is designed to diagnose cerebral ischemia, that is, in fact, to assess the effectiveness of cerebral microcirculation, and one can only judge the state of the functional activity of brain structures indirectly.

But the use of these methods in patients with ischemic stroke does not allow us to choose the optimal level of average blood pressure to maintain and improve the function of the brain stem structures and to judge the adequacy of cerebral perfusion.

The known method, selected as a prototype, the correction of arterial hypertension in the practice of intensive care of patients with traumatic brain injury and vascular diseases of the brain: S.V. Tsarenko, V.V. Krylov, D.N. Tyurin, V.V. Lazarev , D.L. Tsimlyakov. Correction of arterial hypertension in the practice of intensive care of patients with traumatic brain injury and vascular diseases of the brain. // Bulletin of intensive care. - 1999 - No. 2.

The essence of the method lies in the fact that cerebral blood flow is estimated using an indicator such as cerebral perfusion pressure (CPP), which is the difference between mean blood pressure and intracranial pressure. The mean arterial pressure (SBP) is calculated by the formula: SBP = ADdiast. + Pulse Hell / 3, where Pulse Hell = ADsyst.- ADdiast. Thus, the SBP is located between systolic and diastolic pressures, closer to diastolic. This indicator is widely used in neurosurgery to calculate cerebral perfusion pressure: CPD = ICP-ICP. Normal CPD is 80 mmHg; when it is reduced to 50 mm Hg metabolic signs of ischemia and a decrease in brain electrical activity occur. Several studies on patients with severe traumatic brain injury have shown an increase in mortality and poor outcomes with a drop in CPD <70 mm Hg. for a long time. Continuous monitoring of blood saturation in the jugular vein is another important method for monitoring the adequacy of cerebral blood flow. Saturation in the jugular vein (SjO ₂ ) reflects a saturation of venous blood flowing from the cranial cavity, which is normally 65-75%. If blood flow drops to a critical level, venous saturation (rSO ₂ ) begins to decrease, that is, the brain begins to consume more oxygen from the blood to maintain oxygen flow.

To maintain optimal blood pressure and CPP, it is highly informative to compare these indicators with the data of the arteriovenous difference in oxygen (AVDO ₂ - arterio-venous difference). An increase in AVDO2 can reflect both the potential danger of ischemic changes due to a decrease in blood flow, and be a manifestation of real neuron ischemia with an increase in oxygen consumption. Calculation of AVDO2 can be carried out both by invasively determining the saturation of hemoglobin with oxygen in the blood of the carotid artery and jugular vein, and using non-invasive indicators. For non-invasive assessment of hemoglobin oxygen saturation in arterial blood, pulse oximetry is used, and parainfrared spectroscopy (cerebral oximetry - rSO ₂ ) is used in venous blood of the brain. The possibility of this approach is explained as follows. With sufficient accuracy, hemoglobin saturation in different arteries can be considered the same. Therefore, non-invasive determination of this indicator using pulse oximetry (SpO ₂ ) is close to the saturation value of hemoglobin in the arteries (SaO ₂ ) supplying the brain, while cerebral oxygenation (rSO ₂ ) reflects the saturation of hemoglobin with oxygen in the brain tissue.

The disadvantage of this method is that the use of the method in patients with ischemic stroke does not allow you to choose the optimal level of average blood pressure to maintain and improve the function of the stem structures of the brain, and therefore, objectively judge the adequacy of cerebral perfusion.

The objective of this method is to test the drug that regulates the pressure, to determine the optimal level of blood pressure individually for each patient.

The task is achieved by a method of selecting a drug that regulates pressure for adequate cerebral perfusion in acute brain damage, including determining the average blood pressure. Before and after the administration of the pressure-regulating drug, acoustic stem evoked potentials (ASWP) are recorded, peak latencies and peak-to-peak intervals P1-P3, P3-P5, P1-P5 are measured. With a reduction in peak-to-peak intervals and a decrease in peak latency, the drug is evaluated as improving the functional state of the brain stem structures, the selected drug and dosage are left unchanged. With an increase in inter-peak intervals and an increase in latency of the peaks, the drug is evaluated as impairing the functional state of the brain stem structures, the dose is reduced or the drug is replaced. The constant peak-to-peak intervals and peak latency are estimated as deterioration of the functional state of the brain stem structures; hemodynamic-regulating drugs are canceled. ASVP indicators are evaluated after changing the dosage of the drug, its replacement and in the dynamics of the study on days 3, 5, 9, as well as when the patient worsens.

The novelty of the method:

- before and after administration of the pressure-regulating drug, acoustic stem evoked potentials (ASWP) are recorded, peak latencies and peak-to-peak intervals (ms) are measured: P1-P3, P3-P5, P1-P5;

- with a reduction in peak-to-peak intervals and a decrease in peak latency, the drug is evaluated as improving the functional state of the brain stem structures, the selected drug and dosage are left unchanged;

- with an increase in inter-peak intervals and an increase in latency of the peaks, the drug is assessed as impairing the functional state of the brain stem structures, reduce the dose or replace the drug;

- the constant magnitude of the inter-peak intervals and peak latency is estimated as a deterioration in the functional state of the brain stem structures, hemodynamic-regulating drugs are canceled;

- ASWP indicators are evaluated after changing the dosage of the drug, its replacement and in the dynamics of the study on 3, 5, 9 days, as well as with a worsening of the patient's condition.

The set of essential features of the invention allows to obtain a new technical result, which consists in creating a method that allows you to test and select a drug that supports the optimal level of blood pressure, individually for each patient, which allows you to save and improve the functions of the brain stem structures. The advantage of this approach is a quick indirect assessment of the effectiveness and feasibility of the use and dosage of vasoactive drugs to optimize cerebral blood flow, based on the high sensitivity of ASWP.

In the very first hours, after an acute violation of cerebral circulation, it is necessary to create the most favorable conditions for the course of reparative and restoration processes through conservative measures. At the moment, the most accessible form of exposure in the conditions of resuscitation department on the ischemic component of brain damage is drug therapy: a change in the rheological properties of blood, an effect on the coagulation system and vascular tone. However, the approach to choosing the optimal level of mean arterial pressure (SBP) as a complex indicator of the adequacy of cardiac output to the volume of the vascular bed (vascular tone) for a particular patient remains empirical, despite its prognostic value. Correction of hypotension and hypertension, the development of which is associated with a violation of the regulation of vascular tone, should take into account the risk of secondary hemorrhagic complications. It is necessary to restore adequate perfusion in the ischemic zone as soon as possible while observing the hemodynamic interests of the organism as a whole.

ASWPs reflect the conduction of an afferent excitation wave along the pathways of general sensitivity passing through the stem sections of the brain and through the spinal thalamic tracts to the cortex. With brain damage, the severity of ASWP at various levels of leads varies significantly: Gnezditsky V.V. Evoked brain potentials in clinical practice. - M .: "MEDpress-inform", 2003. - S.93-111.

The method is as follows. An individual selection of medications that regulate hemodynamics is carried out on the basis of the sequential test use of vasoactive drugs under the control of ASWP.

The ASVP study was carried out on the Neuro MVP apparatus of the Neurosoft company (Russia), acoustic stem evoked potentials (ASVP), which are caused by monoauricular irritation with sound signals of a certain frequency and volume, were recorded; evoked responses of various neural groups are recorded on the scalp using a highly sensitive amplifier with high resolution capabilities of small time intervals of neuron activity. Stimulation was carried out by an R-click, which means the sound click was generated by retracting the membrane (rarefaction - from English retraction). A masking white noise of 60 dB intensity was applied to the contralateral ear. The stimulation intensity was set at 70 dB above the threshold of audibility. To record responses, an active electrode is used, mounted on the Cz vertex, connected to the second input of the amplifier (+). A mastoid electrode connected to the first input (-) is used as a referent. In this case, an upward deviation corresponds to positivity above the Cz electrode. A ground electrode is placed on the forehead at the point Fpz. Peak latency is determined by the highest point of the positive component. For a better identification of the components of ASAW, records are compared for ipsilateral and contralateral registration. Peak latencies are measured (ms): P1 is the distal part of the auditory nerve, P3 is the bilateral superior olivary complex, P5 is the lower tuberculosis of the quadrupole, peak-to-peak intervals (ms) are measured: P1-P3, P3-P5, P1-P5, mean blood pressure is calculated (SBP) and prescribe drugs that regulate pressure, after which they carry out the control registration of ASAW. With a reduction in peak-to-peak intervals and a decrease in peak latency, the drug is evaluated as improving the functional state of the brain stem structures, the selected drug and dosage are left unchanged. With an increase in inter-peak intervals and an increase in latency of the peaks, the drug is evaluated as impairing the functional state of the brain stem structures, the dose is reduced or the drug is replaced. The constant magnitude of the inter-peak intervals and peak latency is estimated as a deterioration in the functional state of the brain stem structures and hemodynamic drugs are canceled. ASVP indicators are evaluated after changing the dosage of the drug, its replacement and in the dynamics of the study on days 3, 5, 9, as well as when the patient worsens.

Clinical example 1

Patient K.E., 50 years old, medical history No. 615, was admitted to the clinic 02/06/11, at 11 hours 35 minutes. The patient's condition is extremely serious. Coma I (SCH - 8 points). After the examination, which included a clinical and neurological examination, X-ray, clinical and biochemical, ECG, brain CT, transcranial dopplerometry of the cerebral vessels (TCD), the diagnosis was made: Acute ischemic stroke in the cerebellar artery pool. Occlusive hydrocephalus. Right-sided hemiparesis. Coma I.

The patient was admitted to the intensive care unit on 02/06/11 in a serious condition and was in the intensive care unit for 11 days, after which she was transferred to the neurology department for further treatment.

On admission: HELL 130/80 mm Hg, SBP = 97 mm Hg, CVP = 60 mm water. Art., ICP = 25 mm Hg, CPD = 78 mm Hg, according to the TCD, a ventricular drainage was applied and an intraparenchymal ICP control sensor was installed, artificial lung ventilation was performed to synchronize the patient with the ventilator, medication relaxation, catheterization of the right subclavian vein was performed for dynamic control of CVP, noninvasive monitoring of the state of central hemodynamics was carried out by the method of integrated tetropolar rheovasography on the Diamant hardware complex (Russia), invasive control of the ICP level was carried out It was equipped with a Codman apparatus (USA).

Intensive therapy was carried out, aimed at maintaining normal blood gas, water-electrolyte and acid-base conditions.

Upon admission to the department on the first day, an ASWP study was conducted using the Neuro MVP apparatus of Neurosoft (Russia): decompensation of stem structures with impaired functions of the brain stem nuclei with subcompensated violations of the functions of conducting along the trunk of Table 1:

Table 1 ASWP baseline Latency Incentives Left On right Normative values P1, ms 2,58 2.23 1.7 P3, ms 4.68 4.4 3.9 P5, ms 6.3 6.43 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 2.1 2.18 2.1 P3-P5, ms 1,62 2.03 1.9 P1-P5, ms 3.73 4.21 four

The patient was prescribed intravenous dopamine at a dose of 15 mcg / kg / min. Against the background of drug administration, an increase in blood pressure of 160/90 mm Hg was achieved, i.e. GARDEN = 113 mmHg, ICP = 20 mmHg, CPD = 93 mmHg A study of ASWP after correction of hemodynamics of the drug.

table 2 ASVP indicators after a sample of a drug that increases SBP Latency Incentives Left On right Normative values P1, ms 2.48 2.18 1.7 P3, ms 4.28 4.2 3.9 P5, ms 6.1 6.28 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 2.0 2.03 2.1 P3-P5, ms 1,6 2.01 1.9 P1-P5, ms 3.6 4.04 four

From table 2 it is seen that against the background of an increase in SBP by 17%, latencies and intervals tend to decrease, and in some parts of the brain stem they normalize, which indicates an improvement in the functional state of the brain stem structures and allows us to conclude that the level of SBP chosen by us is favorable . The prescribed drug and its dosage are left unchanged.

On the 3rd day (02/09/11), the patient's condition was serious, but some improvement was noted: hemodynamic reactions were less pronounced during treatment and diagnostic procedures. Blood pressure during therapy 150/90 mm Hg, SBP = 110 mm Hg, ICP = 16 mm Hg, CPD = 94 mm Hg, dopamine dose 15 μg / kg / min.

A study of ASWP was performed (Table 3), which showed a deterioration in the functional state of stem structures due to dysfunction and a slowdown in conduct on the rostral sections of the brain stem on both sides. The latencies of the peaks P3, P5, intervals P1-P3, P3-P5, P1-P5 decreased.

Table 3 ASVP indicators for 3 days Latency Incentives Left On right Normative values P1, ms 2,33 2.23 1.7 P3, ms 4.6 4.4 3.9 P5, ms 6.5 6.8 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 2.21 2.18 2.1 P3-P5, ms 2,4 2,8 1.9 P1-P5, ms 4.61 4.98 four

It was decided to reduce the dose of dopamine to 7-8 μg / kg / min, given the decrease in ICP while maintaining the level of CPD. BP = 120/80 mmHg, SBP = 93 mmHg, ICP = 14 mmHg, CPD = 79 mmHg. A study of ASWP was carried out. The latency of the peaks and the intervals decreased (Table 4). Positive dynamics is noted due to the improvement of the excitation along the trunk and the improvement of the functions of the nuclei of the brain stem.

Table 4 ASVP indices on the 3rd day after a dose reduction Latency Incentives Left On right Normative values P1, ms 2,3 1.9 1.7 P3, ms 4,5 4.3 3.9 P5, ms 6.4 6.6 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 1.8 2.0 2.1 P3-P5, ms 2,4 2.6 1.9 P1-P5, ms 4.2 4.6 four

On the 5th day (02/11/11), the patient changed the regime of forced mechanical ventilation with pressure control to support pressure. A study of ASWP. The functional state of stem structures is unchanged. The dose of dopamine was left unchanged.

On day 9 (02.15.11), the patient's condition is stable, stabilization of central hemodynamics, normalization of intracranial pressure are noted, according to transcranial dopplerometry, the reactivity of cerebral vessels is restored, support by vasopressors is canceled: HELL = 100-110 / 82 mm Hg, GARDEN = 90 mm Hg, ICP = 12 mm Hg, CPD = 78 mm Hg, according to ASVP, subcompensation is preserved (Table 5.).

Table 5 ASVP indicators for 9 days Latency Incentives Left On right Normative values P1, ms 2,3 1.8 1.7 P3, ms 4.1 4.0 3.9 P5, ms 6.4 6.7 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 1.8 2.1 2.1 P3-P5, ms 2.5 2,3 1.9 P1-P5, ms 4.3 4.4 four

Thus, the patient’s body is able to independently maintain adequate indicators of systemic hemodynamics to ensure the necessary microcirculation in the affected area of the brain.

On the 15th day (02.21.11), the patient was transferred to the neurological department.

Clinical example 2

Patient S.V., 59 years old, medical history No. 235, was admitted to the hospital on 01/19/11, at 14 hours 10 minutes. The patient's condition is extremely serious. A standard examination was carried out: clinical and neurological examination, X-ray, CT of the brain, transcranial dopplerometry of the cerebral vessels (TCD), clinical and biochemical blood tests, ECG.

Diagnosis: Acute ischemic stroke in the pool of the right midbrain artery. Left-side hemiparesis. Deep coma.

The patient was admitted to the department on 01.19.11. The condition is extremely serious: respiratory decompensation, (BP = 170/90 mm Hg), SBP = 116 mm Hg, CVP = 90 mm water. Art., ICP = 21 mm Hg, CPD = 96 mm Hg, an intraparenchymal ICP control sensor was installed, artificial ventilation of the lungs was performed to synchronize the patient with the ventilator, medication relaxation, for the purpose of dynamic control of CVP and infusion The catheterization of the right subclavian vein was performed, for non-invasive monitoring of the central hemodynamic state, the method of integral tetropolar rheovasography was used on the hardware complex “Diamond” (Russia), invasive control of the ICP level was carried out I «Codman» device (USA).

Upon admission to the department according to the ASVP study, signs of dysfunction of the brain stem nuclei at the level of the lower third of the bridge, coarser to the right, increase in latencies P1, P3, P5 and intervals P1-P3 and P1-P5 are recorded (Table 6)

Table 6 ASWP baseline Latency Incentives Left On right Normative values P1, ms 2,53 2.83 1.7 P3, ms 3.9 5.18 3.9 P5, ms 5.7 7.03 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 2.1 2,35 2.1 P3-P5, ms 1.85 1.9 1.9 P1-P5, ms 3.95 4.25 four

In order to reduce blood pressure, 20.0 ml, 25% of magnesium sulfate was intravenously administered bolus. Blood pressure 140/80 mm Hg, GARDEN = 100 mm Hg (decreased by 16%), ICP = 18 mmHg, CPD = 82 mmHg A control study of ASWP showed a deterioration in the functional state, an increase in the dysfunction of the nuclei and the pathways (Table 7).

Table 7 Latency Incentives Left On right Normative values P1, ms 2.6 3.0 1.7 P3, ms 4.47 5.5 3.9 P5, ms 6.93 7.13 5.7 Intervals Incentives Left On right Normative values P1-P3, ms 2.6 2,4 2.1 P3-P5, ms 2.45 3,5 1.9 P1-P5, ms 5.05 5.9 four Note: for brevity, the table below is not given, but describes the main changes in indicators

This level of SBP caused a negative dynamics of indicators. It was decided not to reduce the GARDEN.

On the 3rd day of January 22, 2011, the patient's condition remains extremely severe. Positive dynamics of neurophysiological indicators is not traced. An attempt was made to increase the SBP: with the SBP = 125 mm Hg, which is 18% higher than the initial one, the functional state of the stem structures worsened. Therefore, it was decided not to use drugs that increase blood pressure.

On the 5th day of January 24, 2011, the patient's condition without significant dynamics. BP = 130/80 mmHg, SBP = 97 mmHg, ICP = 14 mmHg, CPD = 83 mmHg In the study of ASWP, a pronounced dysfunction of excitation at the caudal-rostral levels with a gross damage to the nuclei of the bridge and midbrain remains. After intravenous administration of 1.0 ml of a 1% solution of mesatone HELL = 160/90 mm Hg, SBP = 113 mm Hg. (an increase of 16.5% from the original), ICP = 12 mm Hg, CPD = 101 mm Hg, a decrease in the latencies of the peaks P1 and P5 on both sides, as well as a shortening of the intervals P1-3, P3-5 and P1-5 on the right. Considering the revealed changes, a 4% dopamine solution at a dose of 15 μg / kg / min was added to the treatment in order to maintain blood pressure and average blood pressure at optimal levels.

On the 9th day, the general condition of the patient improved slightly: the patient was transferred to an intermittent mode of ventilation. The functional state of the brain stem structures remains unchanged. Adjustments were made to therapy: the dopamine dose was reduced to 5 μg / kg / min., Blood pressure = 150/90 mm Hg, SBP = 110 mm Hg, ICP = 8 mm Hg, CPD = 102 mm Hg, the functional state of stem structures does not change. On the 10th day, dopamine is canceled, there are no dynamics in neurophysiological indicators.

The patient was treated in the intensive care unit for 17 days and was transferred to the neurological department without significant improvement and without dynamics in neurological status.

Clinical example 3

Patient K.N., 71 years old, medical history No. 1531, was admitted to the clinic on 06.10.09 at 6 hours 10 minutes. The patient's condition is serious. A standard examination was performed: clinical neurological, radiological, general blood test, general urine analysis, ECG. Diagnosis: Acute ischemic stroke in the left cerebral artery basin. Right-sided hemiparesis.

The patient was admitted to the neuroresuscitation department on 10/06/09. The condition is extremely serious: deep stunning, respiratory decompensation - performed mechanical ventilation, blood pressure = 160/110 mm Hg; GARDEN 120 mm Hg; ICP - 20 mmHg

The department conducted an ASWP study - decompensation (peaks on the left do not differentiate, latencies and intervals are increased on the right (P1 3 ms, P3 6 ms; P5 8 ms; peak-to-peak interval P1-5 increased more than 10 ms). It was decided to reduce the SBP by 15%, for this patient, sulphate magnesia was administered intravenously at a dose of 1.5 g / hour, blood pressure decreased to 130/90 mm Hg - SBP = 103 mm Hg Against this background, peak latencies increased and peak-to-peak intervals increased. reduced to 1.0 g / h. GARDEN reached the level of 113 mm Hg, which is 6% less than the initial one (BP = 140/100 mm Hg) - when recording and ASWP, the dynamics are positive, despite the decompensation of the function of stem structures and previous ICP figures: the peaks on the left do not differentiate, on the right the latency of the peaks P1 2.7 ms, P3 5.6 ms; P5 6.5 ms; the peak-to-peak interval P1-5 decreased to 7 ms.The dose of the drug was considered optimal.

The next day (10/07/09) the patient's condition is extremely serious, but stable. In the study of ASWP there are no changes, but the SBP at a dose of magnesia of 1.0 g / hour was 103 mm Hg. (HELL = 130/90 mmHg). They tried to reduce the dose of the drug to 0.75 g / hour, followed by an increase in the SBP to 115 mm Hg. and deterioration (the peaks on the left do not differentiate, on the right, the latency of the P1 peaks increased from 2.7 to 3.5 ms, P3 from 5.6 to 7 ms; P5 6.5 ms did not change; the peak-to-peak interval P1-5 increased to 8 ms. Therefore, they returned to the previous dose.

10/09/09 - 3 days: the patient is conscious, general condition without significant dynamics, neurologically there is no dynamics either. In the study of ASWP: on the left, an increase in the latency of the peaks P1 3.5 ms, P3 5.6 ms, P5 7 ms; peak-to-peak interval P1-5 8 ms, right latency of peaks P1 2.7 ms, P3 7 ms; P5 6.5 ms; the peak-to-peak interval P1-5 is 6 ms., the dynamics have improved (peaks on the affected side are differentiated). There is no need to change the therapy.

On the 5th day (11.10.09), the patient's condition improved slightly: they transferred to spontaneous breathing with insufflated moistened oxygen. Neurologically - weak positive dynamics. In a control study of ASWP, subcompensation of stem structures. After the abolition of magnesia with SBP = 90 mm Hg (HELL = 130/70 mm Hg) - subcompensation is maintained.

On day 16, the patient was transferred to the neurology department.

The proposed method, in contrast to the prototype, allows to control and objectively evaluate the feasibility of prescribing drugs that increase or decrease the SBP, and the effect of its level on the functional state of the brain stem structures for the timely prevention of secondary ischemia in the damage zone.

The method allows:

- substantiate approaches to the correction of hemodynamic parameters in patients in the acute period of ischemic stroke;

- prevent secondary cerebral ischemia;

- controlling the dynamics of the functional state of the brain stem structures, select an individual treatment regimen, drug and its dosage.

The method can be applied in practical resuscitation.

Claims (1)

A method for selecting a pressure-regulating drug for adequate cerebral perfusion in acute brain damage, including determining average blood pressure, characterized in that before and after administration of the pressure-regulating drug, acoustic stem evoked potentials (ASVP) are recorded, peak latencies and inter-peak latencies are measured intervals P1-P3, P3-P5, P1-P5; and with a reduction in peak intervals and a decrease in peak latency, the drug is assessed as improving the functional state of the brain stem structures, the selected drug and dosage are left unchanged; with an increase in inter-peak intervals and an increase in latency of peaks, the drug is assessed as impairing the functional state of the brain stem structures, reduce the dose or replace the drug; the constant magnitude of the peak-to-peak intervals and peak latency is estimated as a deterioration in the functional state of the brain stem structures, drugs that regulate hemodynamics are canceled; ASVP indicators are evaluated after changing the dosage of the drug, its replacement and in the dynamics of the study on the 3rd, 5th, 9th day, and also when the patient's condition worsens.