43 Fisiologia Cerebral Flashcards
Como é formado o poligono de Willis?
Quais as principais veias que drenam sangue do cerebro?
- Veias corticais superiores
- Veias corticais profundas
These veins drain into dural sinuses, of which the superior and inferior sagittal sinuses and the straight, transverse and sigmoid sinuses are the major dural sinuses. These ultimately drain into the right and left internal jugu- lar veins.A schematic representation of the cerebral venous circulation is shown
Qual a proporcao de drenagem de sangue cerebral pelas veias Jugulares Internas D+E?
- em 65%, D > E
- em 35% E > D
Onde deve ser colocado o cateter jugular de saturação venosa de oxigenio?
Na veia jugular dominante (geralmente a D)
Onde é produzido o liquido cerebro-raquidiano?
- Plexo coroide na lateral do terceiro e quarto ventriculos
- pouca contribuição de celulas endoteliais e de atividade metabolica
Onde é reabsorvido o LCR?
Granulacoes aracnoides nos seios durais.
O que é o sistema glinfático e qual o pp receptor?
- Sistema similar ao linfatico (inexistente no cerebro)
- O LCR entra o espace periarterial (entre vasos e astrocitos)
- Canais de aquaporina facilitam a troca de agua
- O LCR é transportado ao parênquima cerebral → espaco perivenoso → ventriculos
- Serve como um sistema de remoção de residuos.
Qual a imporatncia dos anestesicos no sistema glinfático? (2)
- ↑Transporte e ↑Clearance no sono e anestesia geral.
Among anesthetic agents, glymphatic transport is reduced by volatile agents but is less affected by dexmedetomidine.
Qual o valor de consumo de Oxigenio pelo cerebro?
3-3.5mlO₂/100g de tecido cerebral por minuto
Como é gasta a energia da taxa metabolica cerebarl?
- 60% eletrofisiologia (drogas interferem)
- 40% homeostase (drogas nao alteram, hipotermia altera)
Como calcular a Pressão de Perfusao Cerebral?
PPC = PAM - PIC
- PPC normal é 60-70
Problemas recorrentes na Neuroanestesia (5)
- Monitorizacao PAM, PIC, temp, etc
- DHEL: pCO2, glicemia, hidratacao
- Drogas: diureticos, corticoides, osmoticos, anticonv
- Complicacoes do posicionamento
- Complicacoes da anestesia
Quais as funções das celulas gliais? (4)
- Estrutura física de suporte ao cerebro
- Entrega e remocao de substratos metabólicos e resíduos
- Reabsorcao de neurotransmissores
- Funcao de Membrana Hemato-Encefalica
Fatores químicos, Metabólicos e Humorais que influenciam o FSC (7)
- TMC
- Anestesicos
- Temperatura
- Despertar, convulsoes
- PaCO₂, PaO₂
- Debito cardiaco
- Drogas vasoativas, vasodilatadores, vasopressores
Os mecanismos precisos em que a autorregulação cerebral é feita e seus acoplamentos neurovasculares sobrepostos nao sao conhecidos. O que diz a hipótese mitogênica?
- Mudancas na Pressao de Pulso Cerebral levam a mudanças diretas no tones vascular da musculatura lisa. (processo aparentemente passivo)
- Oxido nitrico e Canais de calcio participam na vasodilatacao associada com hipotensao
Como é a curva de autorregulacao cerebral Convencional que relaciona FSC e PAM?
Os mecanismos bioquimicos do acoplamento neurovasculares que regulam o FSC nao sao completamente definitos, mas os principais fatores parecem ser: (4)
- Metabólitos locais
- Acido Aracdonico
- Glutamato - (síntese e producao de NO)
- Glia
The net result therefore on vascular tone is determined by the relative contribution of multiple signaling pathways.
Figura: Cerebral neurovascular coupling. Synaptic activity leads to glutamate release, activation of glutamatergic receptors, and calcium entry in neurons. This results in a release of arachidonic acid (AA), prostaglandins (PGs), and nitric oxide (NO). Adenosine and lactate are generated from metabolic activity. These factors all lead to vascular dilation. Glutamate also activates metabotropic glutamate receptors (mGluR) in astrocytes, causing intracellular calcium entry, phospholipase A2 (PLA2) activation, release of AA and epoxyeicosatrienoic (EET) acid and prostaglandin E2 (PGE2). The latter two AA metabolites contribute to dilation. By contrast, AA can also be metabolized to 20-hydroxyl-eicosatetraenoic acid (20-HETE) in vascular smooth muscle. 20-HETE is a potent vascular constrictor. cGMP, Cyclic guanosine monophosphate; eNOS, endothelial nitric oxide synthase; NMDAR, N-methyl d-aspartate (NMDA) glutamate receptor; nNOS, neuronal nitric oxide synthase.
Quais drogas anestesicas nao suprimem a TMC? (2)
- Ketamina
- N₂O - oxido nitroso
Na dose de supressao no EEG, qual o padrao de Barbituricos e em relacao a Sevo/Isoflurano?
- Barbituricos: ↓FSC e ↓TMC uniforme em todo o cerebro
- Iso/Sevo: ↓TMC e ↓FSC mais intensos no neocortex
Qual o efeito da Hipotermia na TMC
- reduz TMC em 6-7% para cada °C de temperatura reduzida
- Ao contrario de anestesicos, reduções de temperatura alem da supressao do EEG provocam ainda mais decréscimo na TMC
Por que a hipotermia provoca reducao na TMC mesmo apos supressao do EEG?
- Reduz atividade elétrica e homeostatica
This decrease occurs because anesthetic drugs reduce only the component of the CMR associated with neuronal function, whereas hypothermia decreases the rate of energy utilization associated with both electro- physiologic function and the basal component related to the maintenance of cellular integrity.
Qual o efeito da Hipertermia na funcao fisiológica cerebral?
- Entre 37-42°C, eleva FSC e TMC
- se > 42°C, reduz consumo cerebral de oxigenio (limiar toxico com desnaturação de proteinas)
Como é a variacao do FSC em relacao a PaCO₂?
Variacao direta:
- 1-2ml/100g/min de FSC para cada 1mmHg de variacao na PaCO₂, desde que valores normais
- Resposta atenuada com PaCO₂ < 25.
A magnitude da reducao da FSC causado por hipocapnia é mais intenso quando o FSC basal esta elevado (ex: durante anestesia com agentes voláteis)
- V ou F
Verdadeiro
Efeito da responsividade da PAM em relacao ao CO₂ em situacoes de hipotensao moderada e grave
- a elevacao no FSC na hipercarbia é reduzida
- Vasoconstriccao por hipocapnia é pouco afetada
Hipotensao grave:
- resposta vascular nao se altera
A, Relationship between cerebral blood flow (CBF) and partial pressure of carbon dioxide (Paco2). CBF increases linearly with increases in arterial Paco2. Below a Paco2 of 25 mm Hg, further reduction in CBF is limited. Similarly, the increase in CBF above a Paco2 of approximately 75 to 80 mm Hg is also attenuated. The cerebrovascular responsiveness to Paco2 is influenced significantly by blood pressure. With moderate hypotension (mean arterial pressure [MAP] reduction of <33%), the cerebrovascular responsiveness to changes in Paco2 is attenuated sig- nificantly. With severe hypotension (MAP reduction of approximately 66%), CO2 responsiveness is abolished.
Como é o efeito do nivel da PaCO₂ na curva de autoregulacao cerebral
- Na hipercarbia, a resposta cerebral autorregulatoria para hipertensao é atenuada
- Hipocapnia: o FSC é regulado em um limiar mais amplo de PAM
B, The effect of PaCO₂ variation on cerebral autoregulation. Hypercarbia induces cerebral vasodilation and, consequently, the autoregulatory response to hypertension is less effective. By contrast, hypocapnia results in greater CBF autoregulation over a wider MAP variation.
Quais os mediadores principais da vasodilatacao induzida por CO₂ (2)?
- NO
- Prostaglandinas
Por que a acidose metabolica tem pouco efeito imediato no FSC?
A BHE exclui H⁺ do espaco perivascular
- Em contrapartida, na acidose respiratória, o pH se altera rapidamente porque o CO₂ se difunde rapidamente atraves do endotélio cerebrovascular e BHE.
Por que as alteracoes da PaCO₂ no FSC ocorrem rapidamente, mas nao sao sustentadas?
- O pH retorna ao normal por causa da extrusão de bicarbonato.
Consequently, a patient who has had a sustained period of hyperventilation or hypoven- tilation deserves special consideration. Acute restoration of a normal Paco2 value will result in a significant CSF acido- sis (after hypocapnia) or alkalosis (after hypercapnia). former results in increased CBF with a concomitant increase in ICP that depends on the prevailing intracranial compliance. The latter conveys a theoretic risk for ischemia.
Como é a relacao de FSC e PaO₂?
PaO₂ entre 60-300 tem pouca influencia no FSC
- Se PaO₂ < 60, há aumento no FSC
Como é a relacao de FSC e SatO₂?
Linear e inversa
Below a Pao2 of 60 mm Hg, there is a rapid reduction in oxyhemoglo- bin saturation.
Both hemodilution and hypoxemic hypoxia lead to cerebral vasodilation and an increase in CBF.
- Das duas, qual a variável mais potente?
- hipoxia hipoxemica
The impact of a reduction in cerebral oxygen delivery (CDO2), either by hypoxemic hypoxia or by hemodilution, is depicted. CBF increases significantly either with hypoxia or hemodilution; however, the CBF response is much greater with hypoxia (upper panel). The total cerebral oxygen delivery is better maintained with hypoxia than hemodilution at a comparable level of arterial oxygen content (CaO2) because of the greater CBF increase that occurs with the former.
Quais mecanismos que alteram FSC conforme a PaO₂ (3)
- Liberacao de NO
- Canais-K-ATP-dependentes - na musculatura lisa, com hiperpolarizacao e vasodilatacao
- Medula rostral ventrolateral - sensor de oxigenio, ↑FSC sem elevar TMC
Quais as sistemas da inervacao da vasculatura cerebral?
- Colinergica (parassimp e nao-parassimp)
- Adrenergica (simpatica e nao-simpatica)
- Serotoninergica
- VIPergica
Qual o efeito do sistema simpatico na vasculatura cerebral durante hipotensao?
- Reduz a capacidade vasodilatadora dos vasos cerebrais
The contribution of the Sympathetic nervous system is of importance in the cerebrovascular response to hypertension.
At the same time, Sympathetic nerves reduce the vasodilatory capacity of the cerebral vessels during hypotension.
O que ocorre com o FSC no choque hemorrágico? (2)
- Diminui o FSC
- Desvia o ponto inferior para a direita da curva de autorregulacao
During shock, a sympathetically mediated vasoconstrictive effect shifts the lower end of the autoregulatory curve to the right. It is not clear what the relative contributions of humoral and neural mechanisms are to this phenomenon; however, a neurogenic component certainly exists because sym- pathetic denervation increases CBF during hemorrhagic shock.
Qual o efeito da Anemia no FSC?
- ↓Resistencia vascular cerebral
- ↑FSC
Em que pacientes a manipulação da viscosidade sanguinea é importante?
- AVEi com Ht > 55%
In healthy humans, variation of the hematocrit within the normal range (33%-45%) probably results in only modest alterations in CBF.
Qual a relacao entre Debito Cardiaco e FSC?
- Impacta a perfusao cerebral
- Relacao linear
A reduction in cardiac output of approximately 30% leads to a decrease in CBF by about 10%.
However, the CO-CBF relationship has not been demonstrated uniformly; in fact, augmentation of CO does not increase CBF in several disease states, including traumatic head injury, neurologic surgery, and cardiac surgery. Collectively, the available data suggest that CO does influence CBF and that this effect may be of particular rel- evance in situations in which circulating volume is reduced and in shock states.
The conventional view of cerebral autoregulation is that CBF is held constant as MAP increases between the lower limit and ULA. The currently available data, however, indicate that this view is now outmoded and is in need of revision.
- Quais sao as variáveis?
- TMC
- PAM e PPC
- DC
- PaCO₂, PaO₂
- Tonus simpatico
- Medicacoes - controle simpatico, vasomotores
- Anestesicos - supressao de metabolismo, acoplamento neurovascular, SNA
In these dynamic auto- regulatory curves, there is considerable heterogeneity in the LLA and ULA, as well as in the limits and slope of the plateau.
Como é o novo modelo de regulacao do FSC x PAM?
Given the multitude of factors that determine the capacity of the cerebral circulation to respond to changes in perfu- sion pressure, the premise that cerebral autoregulation is static is now untenable. Rather, cerebral autoregulation should be viewed as a dynamic process and that the mor- phologic form of the autoregulatory curve is the result of the integration of all the variables that affect cerebrovas- cular tone in an interdependent manner.8,23 Therefore, a continuum of vascular responsiveness in both the lower and upper limits and in the plateau probably exists as the ability of the cerebrovascular bed to dilate or constrict is exhausted. In a review of the available data from investi- gations in humans, the range of pressures that defined the LLA spanned from 33 mm Hg to as high as 108 mm Hg
- In these dynamic auto-regulatory curves, there is considerable heterogeneity in the LLA and ULA, as well as in the limits and slope of the plateau.
The capacity of the cere- bral circulation to adapt to increases in blood pressure is considerably greater than adaptation to hypotension.
- V ou F
Verdadeiro
Em relacao ao FSC, qual a diferenca na hipotensao causada por Vasodilatadodres Cerebrais ou por Choque hemorrágico?
Most drugs used to induce hypotension, including sodium nitroprusside, nitroglycerin, hydralazine, adenosine, and calcium channel blockers (CCBs), also cause cerebral vaso- dilation.
- As a result, CBF either increases or is maintained at pre-hypotensive levels.
In addition, when hypotension is induced with a cerebral vasodilator, CBF is maintained at lower MAP values than when induced by either hemorrhage or a noncerebral vasodilator.
Anestesicos que simultaneamente vasodilatam a circulação cerebral e causam ↑no volume sanguineo cerebral potencialmente elevam a pIC.
- Em que situacao esses efeitos sao atenuados?
- Quando a hipotensao for lentamente induzida, permitindo a atuação de mecanismos compensatórios
This probably reflects the more effective interplay of compensatory mechanisms (i.e., shifts in CSF and venous blood) when changes occur more slowly.
Qual o efeito dos agonistas 𝛂-adrenergicos no FSC e TMC?
- 𝛂1 : 0/↓FSC, sem efeito TMC
- 𝛂2: ↓FSC, ↓TMC
Administration of phenylephrine to patients undergoing cardiopulmonary bypass does not decrease CBF. In spinal cord–injured patients with relative hypotension, the admin- istration of the α1-agonist midodrine increased perfusion pressure and increased flow velocity in the middle cerebral artery (MCAfv) and the posterior cerebral artery. In healthy patients, and in those undergoing surgery in the beach chair position, the administration of phenylephrine main- tains or augments MCAfv.
Qual o efeito dos agonistas β-adrenergicos no FSC e TMC?
- se dose baixa, pouco efeito direto.
- ↑FSC, ↑TMC
The β1-receptor is probably the mediator of these effects.
Efeito aumentado se lesao da BHE
Qual o efeito dos agonistas dopaminergicos no FSC e TMC?
- Dopa: ↑FSC, sem efeito na TMC
- Dopa dose elevada: sem efeito no FSC e TMC
The likely predominant effect of dopamine in the normal cerebral vasculature, when administered in small doses, is probably slight vaso- dilation with a minimal change in the CMR. Increased CMR in discrete regions of the brain, such as the choroid plexus and basal ganglia, can occur. However, overall cortical blood flow is not influenced.
O que acontece com a curva de autorregulação em situacoes de trauma, doenca ou disfuncao cerebral?
Dependente de uma pressao adequada (Ex: HIC)
Efeito dos BCCa no FSC e TMC
Ao considerar a ↓PAM e ΔPaCO₂, ↑FSC e nao altera TMC.
A reatividade a ΔPaCO esta preservada
Principal canal de Ca nos vasos cerebrais
Tipo-L
Qual o efeito dos iECA e BRA2 no FSC e TMC?
- Sem efeito no FSC
- ↑TMC
They do not affect resting CBF, and autoregulation is maintained.
Efeito da idade avançada no FSC e TMC
↓15-20% aos 80 anos
Cerebral circulatory responsiveness to changes in Paco2 and to hypoxia are slightly reduced in the healthy aged brain
Relacao entre FSC e Volume Sanguineo Cerebral
Although CBV and CBF usually vary in parallel, the magnitude of change in CBV is less than the magnitude of change in CBF
Por que a maneira como as drogas anestesicas e tecnicas influenciam o FSC é importante na neuroanestesia? (2)
- A entrega de substratos energéticos depende do FSC
- Manejo da PIC
Em que situacoes uma mudanca no Volume Sanguineo Cerebral e FSC variam independentemente? (3)
1) isquemia cerebral
- VSC eleva, FSC reduz
2) PA elevada
- Autorregulacao faz vasoconstricao para manter FSC e com isso cai VSC
- quando a autorregulacao nao esta adequada ou quando o limite superior ~150mmHg é excedido, VSC e FSC elevam em paralelo junto com ↑PAM.
3) PA baixa
- vasodilatacao eleva VSC e pode prejudicar o FSC
Qual o efeito de Barbituricos no FSC, TMC, autorregulacao e resposta a ΔCO₂?
- ↓FSC, ↓TMC
- Preserva autorregulacao e resposta a ΔCO₂
In patients with severe head injury in whom barbiturate coma was maintained for 72 hours, the blood concentration of thiamylal required to maintain EEG burst suppression was observed to be increased by the end of the first 24 hours and continued to increase over the next 48 hours.
Qual o efeito do Propofol no FSC, TMC, autorregulacao e resposta a ΔCO₂?
- ↓FSC, ↓TMC
- Preserva autorregulacao e resposta a ΔCO₂, mesmo em surto-supressão no EEG
Diferencas de Barbituricos e Propofol na TMC e FSC
- Ambos diminuem FSC de maneira similar
- Propofol reduz menos a TMC
- Ambos suprimem EEG
Azul: TMC, Laranja: FSC
Qual o efeito do Etomidato no FSC, TMC, PIC, autorregulacao e resposta a ΔCO₂?
- ↓FSC, ↓TMC
- Reduz a PIC apenas quando atividade no EEG preservada
- Autorregulacao nao foi avaliada
- Preserva resposta a ΔCO₂
The CMR suppression caused by etomidate is regionally variable and occurs predominantly in forebrain structures.
Forebrain: Prosencéfalo (diencéfalo + telencéfalo)
Problemas do uso de Etomidato em neurocirurgias (4)
- Pode ter grau de atividade epileptogenica
- Pode piorar hipoxia cerebral e acidose
- Supressao adrenocortical - inibicao 11β-hidroxilase
- Lesao renal - veiculo de propileno glycol
Efeito dos Narcóticos na TMC e FSC
- Pouco efeito, com ↓FSC, ↓TMC
Se dose muito elevada, pode provocar rigidez muscular e ↑PIC, provavelmente por congestao cerebral venosa
Qual o efeito da Morfina 1-2mg/kg no FSC, TMC e autorregulacao?
- Sem alteracoes em FSC e TMC
- Se liberacao de histamina: vasodilatacao cerebral com ↑Volume Sang Cerebral e ↑FSC, conforme a resposta da PA
- Autorregulacao preservada em PAM 60-120mmHg
Qual o efeito do Fentanyl no FSC, TMC e autorregulacao e resposta a ΔCO₂?
- ↓FSC, ↓TMC
- Preserva autorregulacao cerebral e resposta a ΔCO₂
In sedative doses of 1.5 μg/kg, fentanyl increased CBF in the frontal, temporal, and cerebellar areas simultaneous with decreases in discrete areas associated with pain-related processing.
In conclusion, fentanyl will cause a moderate global reduction in CBF and CMR in the normal quiescent brain and will, similar to morphine, cause larger reductions when administered during arousal.
Qual o efeito do Alfentanyl no FSC, TMC e autorregulacao e resposta a ΔCO₂?
- Nenhum efeito
In general, alfentanil does not significantly impact the cerebral circulation, provided that alfentanil induced reduc- tion in MAP is prevented.
Qual o efeito do Sufentanyl no FSC, TMC, resposta autorreguladora e PIC?
- Nenhuma ou pouca reducao em FSC e TCM, conforme a dose.
- Pode elevar a PIC
In some investigations in humans, sufentanil was associated with modest increases in ICP. The increases in ICP associated with sufentanil are likely the consequence, in part, of a normal autoregulatory response to the sudden reduction in MAP that can occur as a consequence of sufentanil administration. Therefore sufentanil and fentanyl should be administered in a manner that does not produce a sudden reduction of MAP.
Qual o efeito do Remifentanyl no FSC?
- DOSES SEDATIVAS: pouco ↑FSC
- Doses elevadas: FSC mantido ou pouco reduzido.
sedative doses of remifentanil alone can cause minor increases in CBF. With larger doses or with the concomitant administration of anesthetic adjuvants, CBF is either unaltered or modestly reduced.
Qual o efeito dos Benzodiazepinicos no FSC, TMC e autorregulacao?
- ↓FSC, ↓TMC
- Preserva autorregulacao cerebral e resposta a ΔCO₂
The extent of the maximal reductions of CBF and CMR produced by benzodiazepines is probably interme- diate between the decreases caused by narcotics (modest) and barbiturates (substantial). It appears that benzodiaz- epines should be safe to administer to patients with intra- cranial hypertension, provided that respiratory depression (and an associated increase in Paco2) or hypotension do not occur.
Qual o efeito do Flumazenil no FSC, TMC e autorregulacao?
- reverte benzos e efeitos na TMC, FSC e PIC.
- Em pacientes com descontrole da PIC, pode causar overshoot.
In contrast, severe increases in ICP occurred when flumazenil was given to patients with severe head injury in whom ICP was not well controlled. The CBF overshoot effect is unexplained, but it may be a neurogenically medi- ated arousal phenomenon. Flumazenil should be used cau- tiously to reverse benzodiazepine sedation in patients with impaired intracranial compliance.
Qual o efeito do Droperidol no FSC, TMC e autorregulacao?
- Pouco efeito
Qual o efeito da Ketamina no FSC, TMC e PIC?
- ↑FSC e ↑TMC
- sem efeito na PIC quando administrada com outros agentes sedativos.
Substantial increases occur in limbic system structures with modest changes or small decreases in cortical structures.
The (S)-ketamine enantiomer substantially increases CMR, whereas the (R) enantiomer tends to decrease the CMR, particularly in the temporomedial cortex and in the cerebellum.These changes in the CMR are accompanied by corresponding changes in CBF.
The anticipated increase in ICP with an increase in CBF has not been confirmed to occur in humans. When examined in their entirety, the available data indicate that ketamine does not increase ICP in patients with nontraumatic neurologic illness nor in patients with traumatic brain injury. Accord- ingly, although ketamine is probably best avoided as the sole anesthetic drug in patients with impaired intracranial compliance, it may be cautiously given to patients who are simultaneously receiving adjunctive sedative drugs.
Qual o efeito da Lidocaina no FSC, TMC e PIC?
- ↓FSC, ↓TMC, ↓PIC
- se doses mais elevadas, reducao ma CMRO₂ maior do que em barbituricos.
Pode prevenir elevacao da PIC em caso de succao endotraqueal ou colocação de pinos na cabeça ou incisões de pele.
Although large doses of lidocaine can produce seizures in humans, lidocaine-induced seizures have not been reported in anesthetized humans. Nonetheless, lidocaine doses should be adjusted to achieve serum levels less than the seizure threshold (>5-10 μg/mL) in awake humans. After a 2-mg/kg bolus, peak serum concentrations of 6.6 to 8.5 μg/ mL are below the seizure threshold. Bolus doses of 1.5 to 2.0 mg/kg therefore seem appropriate.
Qual o efeito dos anestesicos voláteis no FSC e TMC?
- Equilibrio entre a reducao no FSC causado pela supressao na TMC e a elevacao do FSC causado por vasodilatacao cerebral direta
- Apos 1MAC ➡️↑FSC, ↑VSC, ↑PIC
When administered at a dose of 0.5 MAC, CMR suppres- sion–induced reduction in CBF predominates, and net CBF decreases in comparison with the awake state. At 1 MAC, concentrations of isoflurane, sevoflurane, or desflurane, CBF remains unchanged; at this concentration, CMR sup- pression and vasodilatory effects are in balance. Beyond 1 MAC, the vasodilatory activity predominates, and CBF sig- nificantly increases, even though the CMR is substantially reduced (Fig. 11.11). Vasodilation with increasing doses of volatile agents lead to an attenuation of cerebral autoregulation. With large doses, autoregulation is abolished and cerebral perfusion becomes pressure passive.
Qual o comportamento da curva de autoregulacao do FSC x PAM, conforme a dose do anestesico volatil? (2)
- Desvio para a Esquerda
- Atenuação da resposta autorregulatório.
O que é a perda do acoplamento neurovascular causada pelos anestesicos voláteis?
- Doses > 1MAC provocam ↑FSC
Does anestesicos volateis mais utilizados, qual a ordem de potencia vasodilatadora?
- halothane ≫ enflurane > desflurane ≈ isoflurane > sevoflurane.
Sobre a anestesia com Xenonio, qual o efeito de 1MAC no FSC, TMC, autorregulacao cerebral e reatividade a CO₂?
- ↓FSC, ↓TMC, ↓PIC
- Preserva autorregulacao cerebral e reatividade a CO₂
De maneira inversa, ↑FSC na substancia branca.
Qual o mecanismo de acao do Xenonio? (2)
- Antagonismo nao competitivo de NMDAr
- Activation of the TREK two-pore K+ channel may also play a role.
Qual o efeito do aumento da dose de Sevoflurano no FSC em diferentes locais do cerebro?
- 1MAC: ↓FSC no cortex e cerebelo
- > 1.5MAC: ↓FSC no cortex, ↑FSC no cerebelo
Qual a relacao entre os anestesicos voláteis e PIC?
- Apesar de grande ↑FSC, ha pouca ↑VSC, o que nao implica em elevada PIC
Although a reasonable correlation exists between vasodilation-induced increases in CBF and CBV, the magni- tude of changes in CBF is considerably greater than that in CBV (see Fig. 11.9). Hence, changes in CBF do not reliably predict changes in CBV and, by extension, in ICP.
Como esta a autorregulacao cerebral e a responsividade ao CO₂ com os anestesicos voláteis?
- preserva responsividade ao CO₂
- autorregulacao prejudicada com ↑PA
The autoregulatory response to increasing blood pressure may be pertinent during acute episodes of hyperten- sion, such as during laryngoscopy or mismatch of surgical stimulation to anesthetic depth.
in patients with abnormal intracranial compliance, the potential for volatile anesthetic–induced increases in CBV and ICP exist.
- Quais as condicoes em maior risco? (3)
- Lesao em massa (volumosa ou rapidamente expansiva)
- PIC instavel
- Disturbio fisiologico cerebral que prejudique a responsividade ao CO₂ ou acoplamento neurovascular
Em uma anestesia venosa com propofol profduzindo supressao maxima de TMC, o que acontece com o FSC se for iniciado um agente anestesico volatil e qual a implicacao pratica?
- ↑FSC significativo
In essence, antecedent CMR suppres- sion unmasks the vasodilatory action of volatile anesthetics. These data also suggest that caution must be exercised in the administration of volatile anesthetics in pathologic conditions, such as traumatic brain injury, in which metabolism is already reduced.
Sobre a anestesia com N₂O, qual o efeito de 1MAC no FSC, TMC, PIC e reatividade a CO₂?
- ↑FSC, ↑TMC, ↑PIC
- Efeito estimulador simpato-adrenal
- Preserva reatividade a CO₂
In sharp contrast, when N₂O is administered in combination with intravenous drugs, including barbiturates, benzodiazepines, narcotics, and propofol, its cerebral-vasodilating effect is attenuated or even completely inhibited.
The most dramatic increases in ICP or CBF in humans and experimental animals have occurred when N₂O was administered alone or with minimal background anesthesia
Em que situacoes evitar N₂O na neurocirurgia? (2)
- ↑PIC persistente
- risco de embolia aerea
Como os BNM Nao-Despolarizantes podem afetar a PIC e PPC (3)
- Prevencao de tosse e straining pelo relaxamento - acao indireta na ↓ PIC
- Laudanosina: Metabolito do atracurio, pode ser epileptogenica. Sem efeito no FSC, PIC e TMC.
- liberacao de histamina: ↓PAM, ↓PPC, ↑PIC,
It is not entirely clear whether histamine directly causes cerebral vasodilation or whether it is a secondary (autoregulatory) response to a reduction in the MAP.
Although succinylcholine can produce increases in ICP, it can still be used for a rapid sequence induction of anesthesia. No change in ICP was observed after the administration of succinylcholine, 1 mg/kg, to 10 nonparalyzed, ventilated neurosurgical patients in the intensive care unit, 6 of whom had sustained a head injury.
- V ou F?
Verdadeiro
Por que nao usar Enflurano em neurocirurgias? (3)
- Potencial Epileptogenico
- Producao ↑LCR
- Reabsorcao ↓LCR
The most deleterious potential combination of effects in a patient with poor intracranial compliance is increased CSF production and decreased reabsorption. This pattern occurs with enflurane in the dog, which is perhaps another reason (in addition to the poten- tial for epileptogenesis in the presence of cerebral injury and hypocapnia) for omission of enflurane in this circumstance.
Em que situacao o potencial epileptogenico do Enflurano é exacerbado?
Hipocapnia
Quais agentes anestesicos aumentam a secreção de LCR?
- Enflurano
- Desflurano
Quais agentes anestesicos diminuem a secreção de LCR?
- Halotano
- Etomidato
Quais agentes anestesicos aumentam a absorcao de LCR? (3)
- Isoflurano
- Fentanyl
- Etomidato
Quais agentes anestesicos diminuem a absorcao de LCR?
- Halotano
- Enflurano
Quais os efeitos dos seguintes anestesicos inalatorios na secreção e absorcao do Liquor?
- Qual o mais adequado, na teoria, para HIC?
- Halotano - diminui ambos, se anulam
- Enflurane - ↑sec ↓absorcao = ↑PIC
- Isoflurano - apenas ↑absorcao
- Desflurano - apenas ↑sec = ↑PIC
Qual anestesico inalatorio em altas doses de inducao esta associado a convulsões em criancas, mesmo sem historia previa?
Sevoflurano
In two healthy humans, EEG burst suppression with 2 MAC sevoflurane was accompanied by epileptiform discharges that were observed during EEG monitoring. These discharges were associated with a significant increase in CBF, thus demonstrating that neurovascular coupling was preserved.
Qual droga pode ser usada em doses baixas para ativar focos epileptogenicos com o propósito de localiza-los no EEG no intraop?
Etomidato
In the experience of the authors (unpublished), selective activation of a quiescent focus can be achieved with 0.1 mg/kg etomidate. Larger doses are more likely to lead to generalized activation
In the face of a declining CBF and therefore oxygen supply, neuronal function deteriorates in what manner?
Progressive manner rather than in an all-or-none fashion
Brain tissue in which neuronal dysfunction is temporarily reversible but within which neuronal death will occur if flow is not restored; such regions are referred to as the:
Ischemic Penumbra
How different is complete cerebral ischemia, as occurs during cardiac arrest, and incomplete cerebral ischemia, as may occur during occlusion of a major cerebral vessel or severe hypotension?
- Presenca de circulacao colateral
The important difference is that the residual (i.e., collateral) blood flow during incomplete ischemia may result in enough delivery of oxygen to allow some generation of ATP and thereby stave off the catastrophic irreversible membrane failure that occurs within minutes during normothermic complete cerebral ischemia.
This difference in the rate of failure of the energy supply (Fig. 11.19)234,235 can result in signifi- cantly greater apparent tolerance for focal or incomplete ischemia than for complete global ischemia (e.g., cardiac arrest).
Qual o evento central que ocorre durante uma isquemia cerebral?
Falencia energetica
- ATP é necessario para manutencao do gradiente iônico da membrana
Energy failure is rapidly attended by membrane depolarization and influx of sodium (Na+) and calcium (Ca2+) into the neuron. Volt- age-dependent Ca2+ channels are then activated, and Ca2+ gains entry into the cytosol. Depolarization of presynaptic terminals also results in the release of massive quantities of excitatory neurotransmitters, particularly glutamate, into the synaptic cleft. Activation of glutamatergic recep- tors, the NMDAR, and the α-amino-3-hydroxy-5-methyl- 4-isoxazopropionic acid receptors (AMPARs), adds to the influx of Na+ and Ca2+ (Fig. 11.20). Initiation of cellular signaling by the activation of the mGluR leads to the release of stored Ca2+ from the endoplasmic reticulum (ER) via inositol 1,4,5-triphosphate (IP3) receptors. Ionic influx is accompanied by an influx of water, and neuronal swell- ing rapidly occurs after membrane depolarization. The injury that is initiated by excessive glutamatergic activity is referred to as excitotoxicity.
Quais os principais eventos que levam a lesao celular durante isquemia cerebral? (5)
- deplecao ATP
- ↑Glutamato
- Entrada de Ca²⁺ do extracelular, Ret Endop, Mitocondria
- Ativacao AMPAR e NMDAr, com entrada de Na⁺
- lesao de membrana celular e liberado de AA com radicais livres
Qual o nome do dano iniciado pelo excesso de atividade glutamatergica?
Excitotoxicidade
Qual substancia inicia a apoptose neuronal a partir de lesao mitocondrial?
- Citocromo C
The nature of neuronal death probably encompasses a spectrum in which some neurons undergo either necrosis or apoptosis, whereas oth- ers undergo cell death that has features of both necrosis and apoptosis.
- V ou F
Verdadeiro
Despite intense investigative efforts, pharmacologic agents that can protect the brain against ischemic injury have not been identified.
- V ou F
Verdadeiro
Qual anestesico volatil é um potente supressor da TMC?
Isoflurano
The neuroprotective effect of isoflurane is not substantially different from that of other volatile anesthet- ics. Sevoflurane reduces ischemic injury in animal models of focal280 and hemispheric ischemia;281 its efficacy is not different from that of halothane. Desflurane also reduces neuronal injury to the same extent that isoflurane does.282 The available data therefore suggest that adequate anes- thesia, per se, may have a protective effect261,262 versus the awake state, but there does not appear to be any difference in neuroprotective efficacy among the volatile anesthetics.
Quais as terapias utilizadas no manejo do paciente com isquemia cerebral que apresentam beneficios neuroprotetores? (3)
- tPA para trombolise
- Trombectomia mecanica
- Nimodipino e nicardipino para HSA
With the exception of tissue plasminogen activator (tPA) for thrombolysis, mechanical thrombectomy, and the CCBs nimodipine and nicardipine for the management of SAH, pharmacologic neuroprotective agents are not available for the treatment of patients with cerebral ischemia.
Alvo de PAM no paciente pos-AVEi e quando necessita tratamento?
- PAM 70-80mmHg
- tratar se PA > 180/105 pos-trombolise
Although the target MAP should obviously be based on knowledge of a patient’s preexisting blood pres- sure, data to provide specific guidelines are insufficient in humans. In the majority of patients, maintenance of the MAP in the 70 to 80 mm Hg range should be adequate.
Alvo de PA em pacientes com vasoespasmo induzido por HSA
PAs ~180mmHg
Alvo de PPC em pacientes com TCE
60-70mmHg
Alvo PaCO₂ na isquemia cerebral
Normocapnia
Recomendacoes da Hipotermia pos-AVE para neuroprotecao
- Nao recomendada
At the current time, however, hypothermia for purposes of neuroprotection in the setting of acute ischemic stroke is not recommended.
Possiveis beneficios da hipotermia pos-AVE
Melhora PIC e PPC
Possiveis complicacoes da hipotermia pos-AVE
- Trombocitopenia
- Bradicardia
- Ectopia ventricular
- Hipotensao
- Infeccao
- ↑PIC intratavel durante reaquecimento, mesmo se gradual
Recomendacoes da Hipotermia pos-PCR para neuroprotecao
- Recomendada
Recomendacoes de controle glicemico no paciente pos Isquemia Cerebral
Normoglicemia 140-180mg/dl
Hiper e hipo sao deleterias
Recomendacoes de manipulação do volume vascular e Ht no paciente pos Isquemia Cerebral
Flebotomia apenas se Ht > 55%
Recomendacoes da PaO₂ no paciente pos isquemia cerebral
- PaO₂ < 300
Hyperoxia is associated with vasoconstriction and reduc- tion in microvascular tissue flow, generation of reactive oxygen species, and augmentation of inflammation.
Quanto tempo devem ser postergadas as cirurgias eletivas apos AVE
- 4-6 semanas
CEA: Carotid Endarterectomy
Alvo de PA em pacientes cronicamente hipertensos
- reducao 20-25% do basal
Firm guidelines have not been established. However, from the vantage of cerebral well-being, limiting elective MAP reduction 20% to 25% of resting mean levels seems appropriate for both hypertensive and normo- tensive patients. The same guidelines might apply in both populations, because in chronic hypertension, both the LLA and ULA are shifted to the right with apparently little distortion.
No Tu de Cerebro, como é formado o edema na regiao peritumoral? (3)
Vasogenico, Hidrocefalico e/ou Estatico
- Vasogenico, com extravasamento de proteinas plasmáticas do espaco vascular
- Hidrocefalico: obstrucao do fluxo LCR
- Estatico: obstrucao venosa do tumor
Como esta o FSC nos tumores cerebrais?
- geralmente ↓FSC
- Gliomas de alto-grau: ↑FSC
Measurement of regional CBF in the area of the tumor might also be a useful predictor of the grade of intracranial gliomas; both regional CBF and regional CBV are greater with high-grade gliomas.
Como estao o FSC e TMC em convulsão generalizada?
- Ambos elevados
During relatively brief episodes of continuous seizures, the brain seems able to meet the high metabolic demands.204 However, even with effective ventilation and maintenance of perfusion pressure, when seizures continue for a prolonged period, they can lead to the development of irreversible neuronal damage.
Que paciente precisa de prevencao par convulsões?
Incisao cortical importante
Principal definidor do equilibrio da PIC
Taxa Metabolica Cerebral
Qual opioide esta associado a elevacao da PIC?
Sufentanyl
Entretanto, nao ha nada na literatura que justifique nao utilizar Sufentanyl em Neurocirurgia
Qual o efeito do Isoflurano na TMC, FSC e PAM conforme a CAM?
Qual o nome deste comportamento?
- 0-0.5 CAM: ↓TMC, FSC, PAM
- 0.5-1 CAM: FSC volta a linha de base. ↓TMC, ↓PAM
- 1-1.5 CAM: FSC↑, caem TMC e PAM
Resumo: apos 0.5 CAM, aumenta FSC para linha de base e depois dispara - Desacoplamento Fluxo/Metabolismo. Restante cai.
Por que anestesicos inalatorios provocam aumento na TMC em doses elevadas?
Vasodilatacao Cerebral Direta (dose dependente)
Anestesico inalatorio que mais provoca aumento no FSC
Halotano (~200%)
Anestesicos inalatorios que mais provocam reducao da TMC e qual a diferenca deles no FSC?
Sevoflurano e Enflurano
- O Sevo flurano provoca menos aumento do FSC em relacao ao Enflurano e outros anestesicos inalatorios.
Qual o efeito do aumento da CAM na curva de autorregulação da FSC x PAM?
- O aumento da dose provoca vasodilatacao cerebral: a mesma PA provoca um FSC maior
- Ao chegar em mais de 2 CAM, a curva é quase perdida e se assemelha a uma retae: a PAM basicamente define o FSC
Isto retrata a perda da autorregulacao cerebral
Como o CO₂ interfere no FSC?
- Passa livremente na BHE e deixa o pH mais acido
- libera NO e Prostaglandinas - causa vasodilatacao cerebral e ↑FSC
- Para cada 1mmHg alterado, ha alteracao de 1 ml de Fluxo Sanguineo no cérebro
Qual a relacao entre PaCO₂, pH LCR, FSC ao longo do tempo em caso de Hiperventilação?
- ↓PaCO₂, ↑pH-LCR, ↓FSC
Caso mantida:
- Efeito nao sustentado
- Devido a Anidrase Carbonica, o pH do LCH e o FSC tendem a retornar a normalidade
- Aumenta a quebra de HCO₃⁻ para ↑H⁺ e ↑CO₂
A figura abaixo representa a relação existente entre o fluxo sanguíneo cerebral e a pressão parcial arterial de gás carbônico.
Assinale a afirmação correta:
A) A CURVA A nos neonatos está deslocada para a esquerda.
B) Fármacos vasodilatadores cerebrais deslocam a CURVA A para a direita.
C) A CURVA B representa a resposta ao CO₂ na hipotensão arterial profunda.
D) Fármacos vasoconstrictores cerebrais deslocam a CURVA A para a POSIÇÃO B.
Resposta: C
A. Nos neonatos, essa reatividade nao esta completamente definida. Desvia para Direita
B. Vasodilatador potencializa a resposta, joga para Esquerda, fluxo maior
C. Nao adianta vasodilatar o cerebro se nao tem sangue para chegar la.
D. Nunca vai abolir completamente, mas vai atenuar.
