Structure of the Anesthesia Intensive Care Units: Recommendations of the Intensive Care Section of the Spanish Society of Anaesthesiology. / Estructura de las unidades de cuidados intensivos de anestesia: recomendaciones de la Sección de Cuidados Intensivos de la Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor (SEDAR).

BACKGROUND AND OBJECTIVE: In this article, the Intensive Care Section of the Spanish Society of Anesthesiology (SCI-SEDAR) establishes new recommendations based on the standards published by the Ministry of Health, Consumer Affairs and Social Welfare and aligned with the principle international guidelines, and develops a tool to improve quality and efficiency. MATERIALS AND METHOD: Over a 12-month period (2018), 3 members of the SCI-SEDAR defined the methodology, developed the recommendations and selected the panel of experts. Due to the limited evidence available for many of the recommendations and the significant structural differences between existing anesthesia intensive care units, we chose a modified Delphi approach to determine the degree of consensus. RESULTS: The panel consisted of 24 experts from 21 institutions. The group put forward 175 recommendations on 8 sections, including 129 with strong consensus and 46 with weak consensus. CONCLUSIONS: The SCI-SEDAR has established a series of structural recommendations that should be used when renovating or creating new anesthesia intensive care units.

Alpha 2-adrenoceptors in the brain of suicide victims: increased receptor density associated with major depression.

To examine directly in the brain the status of the alpha 2-adrenoceptor in major depression, the specific binding of the agonists [3H]clonidine and [3H]UK 14304 was quantitated in various brain regions of suicide victims with a retrospective diagnosis of depression or other psychiatric disorders. In depressed suicides, the binding capacity of [3H]clonidine was found to be increased in the hypothalamus (Bmax 35%-55% greater), and to a lesser extent in the frontal cortex, as compared with that in matched controls, schizophrenic suicides, or suicides with various diagnosis. The binding capacity of [3H]UK 14304 also was found increased in the frontal cortex (Bmax 30% greater), and to a lesser extent in the hypothalamus, of depressed suicides. In other brain regions such as the amygdala, hippocampus, and cerebellum there also was a tendency for an increased receptor density associated with suicide. Moreover, in the frontal cortex of suicides, the potency of norepinephrine in displacing the binding of the antagonist [3H]idazoxan also was found increased (Ki decreased eight-fold). The results indicate that the density and affinity of alpha 2A-adrenoceptors in the high-affinity state are increased in the brain of depressed suicides.

Modulation by central postsynaptic alpha 2-adrenoceptors of the jaw-opening reflex induced by orofacial stimulation in rats.

1. The modulation by alpha 2-adrenoceptors of the jaw-opening reflex (digastric electromyographic responses) elicited by orofacial electrical stimulation (OF-JOR) in pentobarbitone anaesthetized rats was investigated. 2. Increasing doses of clonidine (0.1-1000 micrograms kg-1, i.v.) reduced, in a dose-dependent manner until abolition, the amplitude and duration of the OF-JOR and increased the latency to onset. The sum of amplitudes of the reflex was the most sensitive parameter to the inhibitory effects of clonidine (ED50 = 13.9 micrograms kg-1). 3. Pretreatment with the alpha 2-adrenoceptor antagonist, idazoxan (0.03-1 mg kg-1, i.v.), caused a dose-dependent shift (1.5 to 37 fold) to the right of the dose-response curve for clonidine without significant change of maximum inhibitory effect, in a manner compatible with competitive antagonism (ED50B = 29.0 micrograms kg-1). Pretreatment with yohimbine (0.3 mg kg-1, i.v.) also antagonized the inhibitory effect of clonidine on the OF-JOR. In contrast, the alpha 2-adrenoceptor antagonist ARC-239 (0.3 mg kg-1, i.v.) did not antagonize the effect of clonidine on the reflex. 4. In rats pretreated with reserpine (5 mg kg-1, s.c., 18 h) the OF-JOR was not modified, but the potency of clonidine in inhibiting the reflex was potentiated (ED50 value decreased to 6.8 micrograms kg-1) without a significant change of maximum inhibitory effect. 5. Increasing doses of amphetamine (0.1-3000 micrograms kg-1, i.v.) caused a dose-related, but partial, inhibition of the OF-JOR (ED50 = 135 micrograms kg-1; Emax = 67%). Pretreatment with idazoxan (0.1 mg kg-1, i.v.)induced a nine fold shift to the right of the dose-response curve for amphetamine, while treatment with the depleting drug alpha-methyl-p-tyrosine (150mg kg-1 daily, i.p., for 14 days) abolished the inhibitory effect of this indirect adrenoceptor agonist on the OF-JOR.6. Morphine (0.1-3000 microgkg-1, i.v.) also reduced the OF-JOR in a dose-dependent manner (ED50 value about 325 microg kg-1) but, in contrast to clonidine, it failed to inhibit the reflex fully (Emax = 48%).As expected, pretreatment with the opioid antagonist naloxone (1 mg kg-1, i.v.) abolished the inhibitory effect of morphine on the OF-JOR, while it did not alter that of clonidine.7. Chronic, but not acute, pretreatment with idazoxan (3 mg kg-1 daily, i.p. for 14 days) led to a marked potentiation of the inhibitory effect of clonidine on the OF-JOR (ED50 value decreased to 4.2 microg kg-1), without a significant change of maximum inhibitory effect.8. Together the results indicate that clonidine evokes a potent inhibition of the OF-JOR in rats through the activation of postsynaptic alpha2-adrenoceptors. It is suggested that this functional response represents a simple and useful in vivo model for studying various regulatory mechanisms of central alpha2-adrenoceptors.

Acute ethanol intoxication may not alter alpha 2-adrenoceptors in the human brain.

The specific binding of the alpha 2-adrenoceptor agonists [3H]clonidine and [3H]bromoxidine (UK 14304) was measured in the postmortem brain of ethanol intoxicated nonalcoholic subjects (blood ethanol concentration: 1.37 +/- 0.30 g/l) and matched controls. In the frontal cortex, the density of binding sites for [3H]clonidine (Bmax = 58 +/- 7 fmol/mg protein) and [3H]bromoxidine (UK 14304) (Bmax = 49 +/- 7 fmol/mg protein) in ethanol intoxicated subjects did not differ from those in the control groups (Bmax = 68 +/- 4 and 56 +/- 8 fmol/mg protein for the respective radioligand). The dissociation constants (KD) were also similar in both groups. The binding capacities (Bmax) and KD values for both radioligands also were found unchanged in the hypothalamus, amygdala, head of caudate, hippocampus and cerebellum. The results demonstrate that, contrary to the beta-adrenoceptor, the presence of ethanol in the human brain does not alter the high-affinity state of the alpha 2-adrenoceptor in the frontal cortex and possibly also in other brain regions.

mu-Opioid receptor and alpha 2-adrenoceptor agonist binding sites in the postmortem brain of heroin addicts.

The biochemical status of human brain mu-opioid receptors and alpha 2-adrenoceptors during opiate dependence was studied by means of the binding of [3H] [D-Ala2, MePhe4, Gly-ol5] enkephalin (DAGO) and [3H]clonidine, respectively, in postmortem brains of heroin addicts who had died by opiate overdose or other causes. In the frontal cortex, thalamus and caudate of heroin addicts the density (Bmax) and affinity (KD) of mu-opioid receptors were similar to those in controls. In contrast, the density of alpha 2-adrenoceptors in heroin addicts was found to be significantly decreased in frontal cortex (Bmax 31% lower), hypothalamus (Bmax 40% lower) and caudate (Bmax 32% lower) without changes in KD values. When heroin addicts were divided into two subgroups according to the presence or absence of morphine in body fluids, only the group with positive screening for morphine showed relevant decreases in brain alpha 2-adrenoceptor density (Bmax 36-48% lower), whereas the decreases in receptor density observed in the subgroup with negative screening for morphine did not reach statistical significance. The results suggest that desensitization of brain alpha 2A-adrenceptors is a relevant adaptative receptor mechanism during opiate addiction in humans.

Increased density of I2-imidazoline receptors in human glioblastomas.

A glial location has been proposed for the non-adrenoceptor [3H]idazoxan binding site termed the I2-imidazoline receptor. The specific binding of [3H]idazoxan in the presence of (-)adrenaline was measured in membranes from excised human glioblastomas (n = 6), meningiomas (n = 6) and normal brains (n = 6). The pharmacological profile of the [3H]idazoxan binding in astrocytic tumours was similar to that in normal brain, compatible with the presence of I2-imidazoline receptors. There was a higher density of I2-imidazoline receptors in astrocytic tumours (Bmax = 266 +/- 18 fmol mg-1 protein; p < 0.001) than in normal brain (Bmax = 54 +/- 4 fmol mg-1 protein), with no differences in affinity values. Almost no [3H]idazoxan-specific binding was shown in meningiomas. The results suggest that I2-imidazoline receptors may be a selective marker for glial tumours in the evaluation of intracranial neoplasms.

Alpha 2-adrenoceptors in human forebrain: autoradiographic visualization and biochemical parameters using the agonist [3H]UK-14304.

The regional distribution and biochemical parameters of alpha 2-adrenoceptors in post-mortem human brain tissue were analyzed in autoradiographic and membrane binding studies, using the full agonist, [3H]UK-14304. Autoradiographic visualization of these receptors in the forebrain revealed a heterogeneous anatomical distribution with high levels in the neocortex, ventral hypothalamus, hippocampus and some thalamic nuclei, among others. In membrane binding studies, analyses of saturation curves indicated the presence of a single population of sites for [3H]UK-14304 both in the human and rat brain. There was a good correlation between the density of alpha 2-adrenoceptors obtained by both procedures. [3H]UK-14304 is a feasible ligand to localise and quantify alpha 2-adrenoceptors in human post-mortem material by autoradiographic and membrane binding techniques.

Decreased density and sensitivity of alpha 2-adrenoceptors in the brain of spontaneously hypertensive rats.

The specific binding of the agonist [corrected], [3H]clonidine, to neural membranes and clonidine-induced mydriasis were used to evaluate the density and sensitivity [corrected] of alpha 2-adrenoceptors in the brain of spontaneously hypertensive rats (SHR) and sex- and age-matched normotensive Wistar-Kyoto (WKY) rats. In hypertensive rats (SHR) the density of alpha 2-adrenoceptors was reduced in the cerebral cortex, hypothalamus and medulla oblongata (20-27%), as was the dose-pupillary response curve for clonidine (1.8-fold). The results demonstrated that this model of genetic hypertension is associated with desensitization of alpha 2-adrenoceptors in the brain.

Non-adrenoceptor [3H]idazoxan binding sites (I2-imidazoline sites) are increased in postmortem brain from patients with Alzheimer's disease.

The I2-imidazoline site (a non-adrenergic mitochondrial site for which a glial location has been proposed and that is associated with the B-form of the enzyme monoamine oxidase) was evaluated in postmortem cortical membranes from 9 subjects with Alzheimer's disease (AD) and 9 matched-controls by using [3H]idazoxan (0.6-30 nM) in the presence of 10(-6) M (-)-adrenaline to prevent binding to alpha 2-adrenoceptors. In AD the density (Bmax) of I2-imidazoline sites was significantly higher (+63%) than in controls whereas no differences were apparent in affinity values (Kd). The results support the hypothesis that the I2 imidazoline site has a major location on glial (astrocyte) cells.

Right lateral transthoracic approach mimicking standard transesophageal echocardiographic views in a patient with giant left atrium.

We describe the case of a patient with long-standing severe mitral periprosthetic regurgitation and a giant left atrium. The patient was referred for surgery. On the third postoperative day, after resuture of the dehiscence of the valve sewing ring, the patient complained of dyspnea. Transthoracic ultrasound examination was performed to eliminate pleural effusion. The severe right lateral displacement of an aneurysmatic left atrial cavity contacting with the thoracic wall allowed us to obtain excellent images of the posterior cardiac anatomy by a right lateral thoracic view. The new transthoracic approach made it possible to safely assess the atrial side of the mitral prosthesis, eliminating mitral regurgitation after surgery without transesophageal echocardiographic examination.

Intermittent electromechanical dissociation as an unusual sign of prosthetic valve thrombosis in a patient with prosthetic fibrous ingrowth.

We describe the echocardiographic features of an unusual hemodynamic phenomenon of intermittent electromechanical dissociation during regular sinus tachycardia in a patient with prosthetic mitral valve thrombosis. Thrombolysis with a solution of recombinant tissue-type plasminogen activator resulted in the disappearance of electromechanical dissociation and was effective in stabilizing the patient's condition. The later discovery of panus covering the valve ring after the lysis of clots confirmed surgery as the definitive treatment.

Left ventricular pseudoaneurysm with left atrium tamponade: a rare postinfarction complication.

A 65-year-old man was readmitted to the hospital with deep-vein thrombophlebitis 3 weeks after suffering a small infarction. Two days after the patient was readmitted severe symptoms of cardiac failure developed. Transthoracic echocardiographic examination showed an unusual echo-free space adjacent to the lateral wall of the left atrium. No further diagnostic information could be obtained from precordial examinations. Single-plane transesophageal echocardiography demonstrated the presence of a ruptured aneurysm in the posterolateral wall of the left ventricle and a pseudoaneurysm, which was severely compressing the left atrial cavity. On color-flow Doppler examination a tear was detected in the wall of the left ventricular aneurysm close to the posterior atrioventricular sulcus. Pericardial adhesions because of coronary artery bypass grafting performed 10 years before may have contributed to the unusual location of this left ventricular pseudoaneurysm, complicated with left atrium tamponade after myocardial infarction.

Atrial tamponade causing acute ischemic hepatic injury after cardiac surgery.

A patient developed late cardiac tamponade after aortic valve replacement and coronary artery bypass grafting. Nausea and dramatic elevations of serum aminotransferases were the initial clinical manifestations of cardiac tamponade. Severe acute ischemic hepatic injury secondary to isolated compression of both atrial cavities by two loculated thrombi was diagnosed.

[Pseudoaneurysm of the mitral-aortic fibrosa secondary to the partial detachment of a mechanical aortic prosthesis]. / Seudoaneurisma de la fibrosa mitroaórtica secundario a la desinserción parcial de una prótesis mecánica aórtica.

We report a patient with an iatrogenic pseudoaneurysm of the mitral-aortic intervalvular fibrosa under the level of a prosthetic aortic valve. Partial detachment of the proximal suture line of the sewing ring is the most probable etiology. This unusual pathology was well demonstrated by transesophageal echocardiography incidentally in an asymptomatic patient who died of a brain haematoma. Aspects related to the diagnosis, treatment and prognosis of this infrequent finding are discussed.

[Myocardial stunning in the context of a subarachnoid hemorrhage]. / Aturdimiento miocárdico en el contexto de hemorragia subaracnoidea.

Myocardial stunning has been poorly described in patients with cerebrovascular accidents. We present a patient in whom severe anteroapical wall motion abnormalities and extensive anterior ST-segment elevation developed after subarachnoid hemorrhage. Total recovery ensued within 2 days. Coronary vasospasm induced by stroke-related sympathetic surge might be the determinant factor of this cardiac event.