L&J Chp 28: Physiology, Pathophysiology, Anesthetic Management of Patients with Neurologic Disease Flashcards
Electromyelography
-Measurement of electrical activity within the muscle
EMG recordings
Made with needle inserted into a muscle –> analysis of waveforms, firing rates of single or multiple motor units can give diagnostic information
Clinical applications of EMG
- Diagnostic disorders of the spinal cord (acute disc herniation)
- Disorders of peripheral nerves (traumatic neuropathies(
- Disorders of the NMJ (myasthenia gravis)
- Muscle disorders (myotonia, polymyositis)
Contents of the intracranial space
- Brain tissue 80-85%
- Cerebral blood volume (CBV) 5-8%
- CSF (7-10%)
Intracranial pressure
Represents the pressure caused by brain tissue, cerebral blood volume, and CSF within the non-distensible cranial space
Monroe-Kelly Hypothesis
For ICP to remain normal, volume increase in any one of the three components must be matched by a decrease in another
Consequences of space-occupying brain tumors, TBI, subarachnoid hemorrhage
May all cause vasomotor paralysis, increase in ICP with subsequent decrease in CBF and impaired oxygen delivery
Rapidly increasing ICP
Arterial hypertension
Bradycardia
Respiratory irregularity
What is the response called for increased ICP?
Vasomotor response Cushing's response Cushing's reflex Cushing reaction Cushing's law Cushing's phenomenon Cushing's triad
Consequences of rapidly increasing ICP
-Cerebral herniation with brainstem compression, unconsciousness, subsequent death
Normal ICP
10-15mm Hg
Cerebral Perfusion Pressure Equation
MAP - ICP
why important to maintain normotension in these patients (>80 mm Hg)
Abnormal ICP
20-30mm Hg
What happens after TBI metabolically?
- Brain may increase metabolic activity –> ramification of glutamate release, excitotoxicity
- Euglycemic or hypoglycemic patients’ blood glucose concentrations may not allow for adequate substrate delivery to compensate for hypermetabolic brain –> metabolic crisis
Definition of a metabolic crisis
- Simultaneous decrease in glucose below 0.7mmol/L
- Increase in lactate-to-pyruvate ratio >40 in microdialyzate fluid
- Why important to frequently measure serum glucose concentrations during neuroanesthesia as both severe hypo/hyperglycemia impact a patient outcome after brain injury
Cerebral blood flow autoregulation
-Multifactorial process that maintains constant CBF despite changes in systemic BP, CPP over wide range
CBF Autoregulation
Enables the brain to match blood supply with its metabolic demand both regionally and globally
- -Usually intact during light planes of anesthesia
- -Impaired/abolished during deep anesthesia
Effect of volatile anesthetic agents on CBF autoregulation
-Attenuate autoregulation up to a point when CBF becomes passively dependent upon CPP
Upper limit of flow autoregulation in a normotensive patient
MAP 130-150 mmHg
Lower limit of flow autoregulation in a normotensive patient
MAP 60 mm Hg
Decrease in MAP below lower limit results in CBF decrease and increase in arteriovenous oxygen difference
What happens above/below the limits of autoregulation?
CBF becomes flow-dependent
CBF autoregulation: at a MAP of 40 mm Hg
Symptoms of cerebral ischemia including dizziness, hyperventilation, mental impairment occur
T/F: CPP can decrease by approximately 30% before lower limit of autoregulation is reached
True
Rule of them useful clinically when planning management of a hypertensive/normotensive patient
Brain function
Intimately related to cerebral perfusion, metabolism
Characteristic features of cerebral metabolism
- High cellular energy demands utilizing ATP energy obtained from aerobic glucose oxidation
- No oxygen, minimal glucose and glycogen substrate reserves relative to consumption rates
- Low concentrations of high-energy phosphate compounds
What is the brain dependent on?
-Adequate blood for minute-to-minute delivery of oxygen and glucose
Normal cerebral metabolic rate for glucose
4.5mg/100g/min
Metabolic rate will be decreased during anesthesia, hypothermia, and/or hypercapnia
How do volatile anesthetic agents affect the relationship btw CBF and CMRO2?
- -May uncouple tight relationship of CBF and CRMO2 –> resulting in an increased blood flow despite dose-dependent decrease in CRMO2
- -Attenuate autoregulation –> may be lost at higher doses
What are the consequences of losing auto regulation of CBF with CMRO2?
CBF is passively dependent on CPP
Normal mean global CBF in humans
45-65mL/100g/min
What are the two types of arteries that supply the cerebral hemispheres?
- conducting vessels
2. penetrating vessels
Cerebral arteries: conducting arteries
Non-resistance vessels –> carotid, vertebral, occipital, spinal artery together with their major and minor branches
Cerebral arteries: penetrating arteries
AKA nutrient arterioles –> enter brain parenchyma at right angles to surface vessels
Site of primary CBF regulation
Even though the vessels receive automatic innervation…
neurogenic tone not essential to normal CBF regulation
Why do cats with spring-held mouth gags have increased risk of post anesthetic neurological deficits, cortical blindness, or hearing deficits?
Maximally opened mouths in cats may be associated with disrupted CBF, reduced direct blood flow to the Reina or inner ear –> most likely caused by stretching of vasculature of maxillary artery and adjacent muscles including temporalis, masseter, pterygoid m
Consequences of MAP increasing above the upper limit of auto regulation?
- Blood flow exceeds ability of cerebral vasculature to constrict
- Pronounced increases in CBF cause forced dilation of arterioles –> may be associated with disruption of the BBB, subsequent edema +/- hemorrhage
Constancy of CBF
Achieved by active vascular response thus rendering CBF directly proportional to CPP, inversely proportional to cerebrovascular resistance (CVR)
What happens when have an increase in perfusion pressure?
-Elicit arteriolar constriction
What happens when have a decrease in perfusion pressure?
Arteriolar dilation
CBF auto regulation results from…
Myogenic responses of smooth muscle cells of the arteriolar wall to stretch cause caused by distending transmural pressure rather than by activation of the autonomic nerve fibers of perivascular nerves
Drainage of blood flow from the brain
- Thin-walled, valveless cerebral veins drain blood into relatively thick-walled dural sinuses
- Site of entry of cerebral vein into dural sinus anatomically presents relatively fixed orifice, physiologically presents significant resistance to flow
Chronic cerebral arterial hypertension
–Cerebral vessels adapt to higher perfusion pressure by hypertrophy of the vessel wall –> displaces autoregulatory curve to the right
Differences with chronically hypertensive patients
- tolerate higher arterial pressure much better than normotensive patients
- displacement of autoregulatory curve to the right means lower limit also shifted right –> increased risk of ischemia during systemic hypotension
- Do not tolerate same acceptable lower limits (eg MAP 60-70) for arterial BP as normotensive patients
Effect of hypovolemic hypotension on CBF autoregulation
- CVR increases –> increased vessel tone displaces curve to the right
- Increases lower limit of CBF auto regulation and lowest tolerated pressure
- Brain ischemia develops at a higher perfusion pressure than during pharmacologically induced hypotension where CVR is decreased
Effect of moderate changes in PaO2 (arterial hypoxemia, arterial hyperoxemia)
-Do not exert measurable influence on CBF
At what PaO2 do we see increase in CBF?
50mm Hg or below
Same PO2 at which progressive brain tissue lactic acidosis appears so suggests hypoxia in CBF regulated by the periarteriolar pH
T/F: anoxia or anoxia + hypercapnia can constitute a pronounced cerebral vasodilation may cause a fatal increase in ICP and mass displacement (brain herniation) in patients with space-occupying intracranial lesions
True
Intracerebral Steal Syndrome
If CVR decreases in non-ischemic, normal regions of the brain (eg via isoflurane anesthesia), blood may be shunted away from the area of vasomotor paralysis
Robin Hood Syndrome (inverse steal syndrome)
Increase in CVR in normal cerebral regions will shunt blood into areas of vasomotor paralysis
What conditions cause inadequate cerebral perfusion and hypoxia? What are the consequences?
Pathologic conditions including transient cardiac arrest, traumatic brain injury, brain tumor, or meningitis
Will lead to severe tissue lactic acidosis, vasomotor paralysis, increased ICP
