SS - Neuroanesthesia 24.pptx

Neuroanesthesia Clay Freeman, DNP, CRNA Principles II – NRAN80526 1 Objectives Readings: Barash: Chap. 37 Barash: Chap. 51 Describe nervous s...

Neuroanesthesia Clay Freeman, DNP, CRNA Principles II – NRAN80526 1 Objectives Readings: Barash: Chap. 37 Barash: Chap. 51 Describe nervous system anatomy Discuss the physiology and anesthetic implications involved in neuroanesthesia Describe pharmacologic effects of anesthesia medications and its implication in neurosurgery Discuss anesthetic considerations and complications unique to neuroanesthesia Describe neural system pathophysiology and its anesthetic implications 2 Neuroanatomy CNS structurally consists of the brain & spinal cord Brain is divided into four structural components: Cerebrum Diencephalon Brainstem Cerebellum 3 Cerebrum Structures of the Cerebrum: Cerebral cortex – Cognition, movement, and sensation Hippocampus – Memory & learning Amygdala – Emotion, appetite, & response to pain/stressors Basal Ganglia – Fine movement o Caudate Nucleus o Globus Pallidus o Putamen o Substantia nigra o Red Nucleus 4  Cerebral Cortex Cerebral Cortex: outer 3mm layer of cerebral hemispheres Medial longitudinal fissure – Divides the cerebral hemispheres Hemispheres connect via the Corpus Callosum Lateral fissure of Sylvius – Divides temporal from frontal and parietal lobes Central sulcus of Rolando – Divides frontal and parietal Divided into four lobes: Frontal – Primary Motor cortex Parietal – Pain & touch sensory Occipital – Vision cortex Temporal – Auditory and speech centers Can be further divided into structurally distinct areas called 5 Brodmann areas  Diencephalon Diencephalon – Midline between the 2 hemispheres. Consists of the Thalamus, Hypothalamus, Epithalamus & Subthalamus. Thalamus “Relay Station” - integrates and transmits sensory to various cortical areas via separate pathways. Hypothalamus: is the primary neurohumoral organ 6 Cerebellum Cerebellum – integrates afferent information received from other areas of CNS & PNS to be transmitted to the cerebral cortex and to lower motor neurons for muscle tone, equilibrium (Vestibuloocular reflexes), and voluntary movement coordination Connected via cerebellar peduncles which have both efferent and afferent pathways Archicerebellum – Maintain Equilibrium Paleocerebellum – Muscle tone regulation Neocerebellum – Coordinates voluntary movement Contained within the posterior fossa 7  Brainstem Brainstem: midbrain, pons, medulla Responsible for… Consciousness via the Reticular Activating System, Autonomic functions including respiratory and cardiovascular control, and many reflexes (e.g., cough/gag, pupillary reflexes) - Contains ascending and descending fiber tracts - Extends to Foramen Magnum 8 Electrophysiol ogy 2 primary CNS cell types: Neuron Glial Cells Neurons conduct antegrade impulses from the dendrites  soma  axon  synaptic terminals Gray matter composed of cell bodies White matter composed of axons The majority of CNS neurons are either Multipolar motor neurons o innervate muscles & glands - or - Pseudounipolar sensory neurons 9  Neurons Nerve terminals contain neurotransmitters within vesicles Upon depolarization, voltage-gated Ca++ channels open which allow the vesicles to release the neurotransmitter into the synaptic cleft The postsynaptic neuron effect depends on the subsequent actions of the receptor activated Excitatory neurotransmitters hypopolarize the postsynaptic neuron Glutamate acts on AMPA & NMDA as the major excitatory neurotransmitter in the brain Inhibitory neurotransmitters hyperpolarize the postsynaptic neuron GABA is the major inhibitory transmitter in the brain 10 Glycine is the major inhibitory transmitter in  Cranial Nerves Cranial nerves are made up of sensory and/or motor neurons Cranial nerves exit the cranial cavity through foramina in the cranium. Except CN XI which arises from the superior part of the spinal cord. Useful mnemonics for cranial nerves Names: Oh, Oh, Oh To Touch And Feel Very Good Velvet, Absolute Heaven Function: 11 Some Say Marry Money, But My Brother Says Big Brains 12 Picasso 13  Cranial Nerve Function Cranial nerve highlights: Trigeminal Cardiac Reflex Eye movement controlled by 3, 4, and 6 Parasympathetic output from 3, 7, 9, and 10… *& 5* Vagus Nerve (X) performs 75% of all parasympathetic activity 14  Glial Cells Besides Neurons, the other primary CNS cell type is the Glial Cell Glial cells are more abundant (5x) and supportive in nature Maintain ionic environment Modulate action potential conduction Control reuptake of neurotransmitters Repair neurons Glial cell subtypes: Astrocytes Ependymal cells Oligodendrocytes Microglia 15  Blood-Brain Barrier The environment of the brain is kept in homeostasis via the Blood-Brain Barrier. The Blood-Brain Barrier consists of: In the CNS, capillary endothelial cells are connected to one another via intercellular clefts called Tight Junctions Endothelial cell membranes are made up of a lipid bilayer to prevent the passage of polar molecules Astrocytes interpose between capillaries and neurons to aid in maintenance 16  Blockade Water moves freely across the blood-brain barrier via bulk flow Lipid soluble substances pass easily which drug manufactures consider when designing drugs CO2 but not H+ The blood-brain barrier can be compromised by: O2 Acute hypertension Volatile anesthetics Shock Stroke/Ischemia Infection Local tumor Polar molecules require active transport Trauma ions Radiation glucose Seizures 17 Circumventricular Organs Areas of the Blood-brain barrier are compromised by the presence of fenestrated capillaries Increased permeability in these highly vascular areas serve as points of neuroendocrine control Subfornical Organ (SFO) Subcommissural Organ (SCO) Area Postrema (AP) Neurohypophysis (NH) Organum Vasculosum of the Lamina Terminalis (OVLT) 18  Cerebrospinal Fluid CSF provides CNS cushioning, buoyancy and also serves as an excretory pathway CSF found in Ventricles, Cisterns, and Subarachnoid space of brain & SC Volume split evenly between cranial vault & SC ~150ml total volume CSF is formed primarily by active transport of Na+ by the ependymal cells in the choroid plexus Produces ~20mL/hr or 500mL/day Composition & Osmotic pressure is similar to plasma Production decreased by carbonic anhydrase inhibitors, spironolactone, furosemide, corticosteroids, isoflurane, and vasoconstrictors 19  CSF Circulation CSF ultimately absorbed by the Arachnoid Villi of the superior sagittal sinus and drains into venous circulation Complete turnover of CSF volume occurs ~3x/day More Mnemonics Leave Lateral Ventricles Pathology Me Monro (foramen) Hydrocephalus due to accumulation of CSF in 3 Third Ventricle excess Silvers Aqueduct of Sylvius 4 Fourth Ventricle Obstructive: blockage in CSF flow (most Luscious Foramen of Luschka common) Margaritas Foramen of Magendie vs 20  Blood-CSF Barrier Blood-CSF barrier similar to the blood-brain barrier Although endothelial cells are fenestrated in the choroid plexus, tight junctions are used in the epithelium as a barrier Free movement of water and lipid-soluble substances Requires carrier-mediated active transport for glucose, amino acids, and ions A compromised blood-CSF barrier is particularly concerning for infections of the CNS 21  Venous Drainage Veins traverse through the arachnoid and meningeal layers of the dura mater to flow into the nearest sinuses From the Subarachnoid space to between the periosteal & meningeal layers of the Dura Mater Cerebral venous circulation is divided into 2 functional components: Superior sagittal sinus o Collects from the cerebral cortex and cerebellum Inferior sagittal sinus/Vein of Galen: o Collects from basal ganglia structures These connect at the Sinus Confluence All venous blood ultimately drains via the internal 22 jugular veins  Arterial Circulation Blood supply to the brain is fed by an Anterior & Posterior circulation Anterior (majority of blood supply) Arises from the Aorta Fed by Internal carotid arteries (x2) - each artery serves ipsilateral hemisphere only Enters skull through the foramen lacerum Posterior Arises from the Subclavian Artery Fed by the Vertebral arteries (x2) Enters skull through foramen magnum Converges into the Basilar artery Feeds the posterior fossa/Cerebellum 23  Circle of Willis The circulations converge at the Circle of Willis The Circle of Willis is crucial for its ability to provide redundancy for cerebral blood flow Cerebral cortex supplied by: Anterior cerebral artery - most of the medial and superior surfaces and the frontal pole Middle cerebral artery - lateral surface and the temporal pole Posterior cerebral artery - inferior surface and the occipital pole 24 1 more time ACA, Anterior Cerebral Artery MCA, Middle Cerebral Artery PCA, Posterior Cerebral Artery 25 NeuroPhysiology 26 Neurophysiol ogy The brain relies on a steady supply of oxygen and glucose via a disproportionately high degree of blood flow Brain is ~2% of body weight but 15% of total cardiac output 20% of the total oxygen uptake Average: 50ml / 100g tissue/min Gray matter has a greater requirement of blood flow Gray: 80ml/100g tissue/min White: 20ml/100g tissue/min Cerebral blood flow is adaptive to avoid fluctuations and pauses in supply 27 < 20ml/100g tissue/min  signs of ischemia Cerebral Blood Flow Regulation of Cerebral Blood Flow is managed by several determinants of Flow-Metabolism Coupling: Cerebral perfusion pressure Autoregulation Myogenic Neurogenic Metabolic Venous Pressure Extrinsic mechanisms Gas tensions (PaO2 & PaCO2) Temperature blood viscosity 28 Cerebral Perfusion Pressure CPP is a major determinant of CBF CPP = MAP – ICP Normal CPP 60-80mmHg Outside the range of regulation, CBF becomes completely pressure dependent 29  Contemporary Model With chronic hypertension: Autoregulation shifts so that CBF becomes more dependent on CPP Autoregulation is… modulated by iatrogenic interventions such as administration of volatile anesthetics - or - debilitated by various disease processes including tumors, head trauma, AV Malformations, aneurysms, stroke. 30  Autoregulati on CBF is kept constant even with changes in CPP due to Autoregulation Myogenic – local effect Intrinsic vascular smooth muscle response to changes in vascular transmural pressures. Ex) Increased pressure  Constriction Metabolic – moderate effect Local responses to CO2, O2, H+, Metabolic by-products (adenosine, lactate, prostaglandins, thromboxane, etc) Neurogenic – larger vessels Cerebral vasculature is innervated by adrenergic, cholinergic, serotonergic, and gabaminergic nerve fibers. 31 Cerebral Metabolism Aerobic vs Anaerobic metabolism Aerobic: Sufficient O2, Oxidative phosphorylation occurs 1 glucose = 36 ATP Anaerobic: Glycolysis produces only 2 ATP Pyruvate  lactic acid Brain has low levels of glycogen stores ~60% of metabolism supports ionic gradients Na-K pumps utilize largest portion ~40% homeostasis of neurons & glial cells 32  Cerebral Metabolism Neurovascular Coupling – CMR changes affect proportional change in CBF CBF can parallel metabolic needs from 20-300ml/100g tissue/min Ex) Increased neuronal activity  Glutamate release  synthesis and release of NO (vasodilator) CMR increased by: Hyperthermia, seizures, ketamine, N2O CMR decreased by: Hypothermia (~6%/°C), anesthetics 33  CO2 PaCO2 rapidly affects CBF in a directly proportional manner Every 1mmHg of PaCO2 affects CBF by 1mL/100g/min CO2 readily crosses the blood-brain barrier but NOT H+ However, H+ is the cause of vasodilation CO2 undergoes carbonic anhydrase reaction with water in the CSF & cerebral tissues to form H+ ions  PaCO2 range of adaptation of CBF is 25-75mmHg  PaCO2 effects on CBF are also time-limited: CSF 34 adapts to pH changes within 6-8hrs  O2 Changes in PaO2 has minimal effect on CBF at 60- 300 mmHg However, rapid changes in CBF are seen at a PaO2 < 60mmHg Remember: at PaO2 of 60 mmHg, there is a rapid reduction in SpO2 Hypoxia  ATP-dependent K+ channel activation  vasodilation The rostral ventrolateral medulla monitors oxygen levels in the brain and responds via neurogenic and local humoral mechanisms to affect CBF 35 Integrated Contemporary Model 36 Venous Pressure Increases in venous pressure results in decreased venous drainage This increases Intracranial Volume  increases Intracranial Pressure(ICP) 2 clinically important related concepts: Highlights importance of proper positioning Intrathoracic pressure (Cough/PEEP) = ↑ venous pressure 37  Intracranial Pressure Intracranial contents contained within the cranial vault (~1500ml) Brain tissue (85%) CSF (10%) Cerebral Blood Volume - CBV (5%) Normal ICP: 5-15mmHg Intracranial hypertension: >20mmHg Crucial in calculating Cerebral Perfusion Pressure (CPP) CPP = [MAP-CVR] - ICP Gold standard measurement is with intraventricular 38 catheter  External Ventricular Drain Indications: Acute Symptomatic Hydrocephalus ICP monitoring Bridge for malfunctioning/infected VP shunts Cerebral “Relaxation” Targeted therapies (Abx) Sterile management techniques Flushless transducer systems Primed with preservative-free saline Gravity drain Leveled to external auditory meatus 39 External Ventricular Drain *Recommendations* Clamp for transport Coordinate with surgeon for intraoperative management Label ports & lines Report & note changes in CSF color, drainage >20mL or 0/hr, line disconnections, or loss of waveform 40  Intracranial Pressure Monro-Kellie Doctrine: Increases in volume of any one component is compensated by a decrease in another component. Brain parenchyma: Included in the content of brain tissue is intracellular fluid. CSF: plays the greatest role in volume compensation to maintain normal ICP. As the volume of an intracranial component expands, CSF can: 1. Translocate to the more distensible spinal subarachnoid space 2. Increase absorption (Sensitive) 3. Decrease production (relatively insensitive) 41 CBV: Smallest Intracranial component of most  Intracranial Hypertension Intracranial Hypertension results in reduced CPP and oxygen delivery due to elevated ICP Cushing’s Triad: ↓CPP  ↑MAP  Baroreceptor reflex (↓ HR). Compression of medulla  irregular respirations Result: Hypertension + Bradycardia + Irregular Respirations Other S/S of Intracranial Hypertension: Headache, N/V, papilledema, Pupil dilation (mydriasis), Focal deficits, Seizure, Coma, & EKG (ST elevation, Long QT, Inverted T) Intracranial hypertension is a compounding issue: Cerebral ischemia  local swelling  decreased CPP  42 More ischemia  Rinse & Repeat Cerebral Ischemia High energy needs coupled with very limited storage capacity of essential substrates, makes the brain highly sensitive to ischemia. Central concept of ischemic damage is the reduced energy necessary to produce adequate amounts of ATP Ischemia results in inefficient Glycolysis rather than oxidative phosphorylation ATPase ion pumps begin to fail increasing intracellular Na+, a decrease in K+, & especially Ca++ increases Cause neurons to depolarize and release excitatory neurotransmitters (Glutamate) causing further depolarization and allowing more Ca ++ to enter via NMDA (N-methyl-D- aspartate) receptor channels Calcium is the dominant factor to the ischemic damage process. Ca++ normally functions in the activation of various enzymes used in cellular metabolism. However, Sustained elevation of Ca++ increases action of enzymes causing structural damage to the neuronal membranes 43  Ew…more Neuronal membranes release fatty acids when destabilized Primarily arachidonic acid (precursor via the cyclo-oxygenase pathway) Prostaglandins and leukotrienes increased = altered membrane permeability  further neuron damage Also complicating the ischemia, is the build up of lactic acid and H + Causing further deterioration in the intracellular environment A preexisting high serum glucose accelerates this process The dynamic zones of ischemia are similar to the zones described in myocardial infarction. Core: Inner most region is completely ischemic resulting in membrane destruction CBF and neuronal death. Functional impairment < 20ml/100g/min Penumbra: outer region of intermediate perfusion Duration > 2 hours is likely Receives collateral blood flow but demonstrates signs of ischemia irreversible Can survive if flow is restored, but if ischemia is prolonged: neuronal death. 44 Cerebral Protection Cerebral protection aims at attempting to limit or reduce the various mechanisms of ischemic injury via physiologic and pharmacologic techniques. Hypothermia is the Gold Standard among the protective physiologic techniques. What it does: Reduces electrophysical activity Decreases Ca++ entry Decreases glutamate release Stabilizes proteins Slows the normal and harmful enzymatic activity Decreased free radical formation Decreased protein kinase ~5% change in CMR for every 1°C change in temperature CBF also changes ~6% / 1°C 45 Moderate hypothermia with core temperatures of 32 – 34°C may be worth CP2 Glucose during cerebral ischemia paradox: Although the normal brain is dependent on a continuous supply of glucose, the ischemic brain finds extensive glucose availability to be detrimental Hyperglycemia allows some ATP production, BUT at the cost of accumulation of lactate (the end product of glycolysis). The lactate accumulation sets up an intracellular acidosis, which causes further adverse neurologic outcomes. Studies have supported that hyperglycemia both pre-ischemic and during ischemia results in worse outcomes Human studies do not support giving insulin to create hypoglycemia with cerebral ischemia. 46 Most guidelines recommend normalization of plasma glucose  Neuroanaesthe sia Neuroanaesthesia is the practice of applied cerebrovascular physiology and pharmacology Use of techniques and agents to control CMR & CBF which subsequently manipulates CBV CP Induction P Goal: to prevent increases in ICP, and decreases in CPP. Maintenance Goal: provide adequate substrate delivery and control brain tension by controlling the CBF/CBV. Emergence Goal: prevent increases in ICP and to rapidly assess patient outcomes 47 Neuroanaesthe sia Anesthetics modulate autoregulation by suppression of metabolism, switching neurovascular coupling to a higher flow–metabolism ratio, decreasing autonomic neural activity, and direct effect on cerebral vasomotor tone Indirectly by alteration of cardiac function and systemic circulatory tone 48 Pharmacolo gy Focus attention towards effects of anesthetic drugs on CBF and CMR. Other clinical considerations: autoregulation effects, CO 2 responsiveness, CBV, Effects on CSF dynamics, interactions with the BBB, and epileptogenesis. 49 Pharmacolo gy Barbiturates decrease the CMR (up to 60%) and CBF in a dose-dependent fashion until isoelectric EEG Barbiturates decrease CMR: Reducing Ca++ influx Na+ channel blockade Inhibits free radical formation Potentiates GABA activity Inhibits glucose transfer across the blood-brain barrier Robin Hood, or reverse steal phenomenon Barbiturates produce vasoconstriction only in normal brain tissue, thus redistributing blood flow to ischemic areas. Barbiturates facilitate CSF absorption, thus reducing ICP. Barbiturates have anticonvulsant properties, reducing the potential of seizure activity. 50 Exception: methohexital which can produce excitatory phenomena, and has been used  IV Hypnotics Propofol, is similar to barbiturates in producing a dose- dependent reduction in CBF and CMR. Currently the most commonly used induction agent Propofol decreases CBF and CMR up to ~50%. Preserves cerebral autoregulation Decreases ICP > volatile anesthetics Significant anticonvulsant activity Monitor for decreases in CPP which can exacerbate cerebral ischemia. Etomidate near parallel CBF and CMR changes. ~40% reductions with CBF CMR suppression is preferentially focused to the cerebral cortex Myoclonic movements are not epileptic activity BUT etomidate does precipitate seizure activity at lower 51  Inhalation Anesthetics CMR is decreased in a concentration-dependent manner with the volatile anesthetics (up to 50%). Isoflurane produces the greatest decrease in CMR Volatile anesthetic agents are potent cerebrovascular dilators, and increase CBF in a dose-related manner. Increases in CBF are greatest with halothane, and least with isoflurane and sevoflurane. Appears to be time-limited: 3-6 hours All volatile agents affect ICP by: decreasing cerebrovascular resistance (cerebrovascular dilation) Luxury Perfusion Attenuation of autoregulation Volatile anesthetics alter CBF to CMR ratio The cerebral response to CO2 is maintained with all the agents, CBF ↑ therefore, hyperventilation can attenuate the effects on CBF. CMR ↓ The effect of a decrease in CO2 is greatest with isoflurane. 52 Volatile anesthetics affect CSF formation and absorption.  Inhale At high concentrations, autoregulation is abolished and cerebral perfusion becomes passive Volatile agents increase CBF in normal tissue, but not ischemic areas (where vasculature is already maximally dilated) thus redistributing blood away from ischemic areas (circulatory steal phenomena). Isoflurane is classically considered to be the volatile anesthetic agent of choice in neuroanesthesia. Causes the greatest decrease in CMR (40% - 50%) Least potent cerebral vasodilator. Nitrous oxide increases CBF, CMR, & ICP. Increase in CBF also noted when used in combination with volatile agents. - Additive vasodilating effect of N2O in the presence of a volatile agent 53  Goodies Benzodiazepines are useful anesthetic adjuncts due to their anxiolytic, anticonvulsant, and amnestic effects. Reductions in CBF and CMR Some concern with post-op delirium Opioid-based anesthetic techniques are popular in neuroanesthesia because it provides hemodynamic stability and a predictable emergence. Opioids have minimal effects on CBF and CMR …but… Autoregulation and cerebral CO2 responsiveness is maintained with opioids. Exception: Meperidine(Demerol) is not used in because the active metabolite (normeperidine) is a known convulsant. 54  Ketamine Ketamine causes a dramatic increase in CBF (up to 60%) lesser increase in CMR: thalamic/limbic increased activity with suppression of somatosensory areas Impedes CSF absorption ↑CBF + ↑CSF = Increases ICP* Historically, ketamine was not used in neuroanesthesia  However, it provides protection against neuronal cell death 55 Neuromuscular Blocking Agents The only direct effect of nondepolarizing muscle relaxants on cerebral physiology occurs due to the release of histamine. Histamine directly dilates the cerebral vasculature Atracurium has significant histamine release. Pancuronium demonstrates sympathetic effects on induction Succinylcholine can produce increases in ICP Attenuated with a defasciculating dose of nondepolarizers ~ May want to avoid in patients with CVA, coma, encephalitis, and head injury. 56  Uppers & Downers Vasopressors Vasodilators Goal of maintaining CBF by maintaining MAP 50-150mmHg All antihypertensive agents that cause smooth muscle relaxation can produce In the absence of autoregulation cerebral vasodilation and increase ICP. nitroglycerine and nitroprusside can be CBF is directly affected by alterations in used when the dose is increased CPP gradually over several minutes, without increasing ICP. Phenylephrine (pure α-1 agonist) produces no Hydralazine has a longer onset, thus a effect on CBF or CMR. subsequent less increase in ICP. Antihypertensive agents may be useful in Dopamine produces a decrease in CBF at low deliberate hypotensive techniques since (