L&J Chp 28: Physiology, Pathophysiology, Anesthetic Management of Patients with Neurologic Disease

Question 1

Electromyelography

Answer 1

-Measurement of electrical activity within the muscle

Question 2

EMG recordings

Answer 2

Made with needle inserted into a muscle –> analysis of waveforms, firing rates of single or multiple motor units can give diagnostic information

Question 3

Clinical applications of EMG

Answer 3

• 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)

Question 4

Contents of the intracranial space

Answer 4

• Brain tissue 80-85%
• Cerebral blood volume (CBV) 5-8%
• CSF (7-10%)

Question 5

Intracranial pressure

Answer 5

Represents the pressure caused by brain tissue, cerebral blood volume, and CSF within the non-distensible cranial space

Question 6

Monroe-Kelly Hypothesis

Answer 6

For ICP to remain normal, volume increase in any one of the three components must be matched by a decrease in another

Question 7

Consequences of space-occupying brain tumors, TBI, subarachnoid hemorrhage

Answer 7

May all cause vasomotor paralysis, increase in ICP with subsequent decrease in CBF and impaired oxygen delivery

Question 8

Rapidly increasing ICP

Answer 8

Arterial hypertension
Bradycardia
Respiratory irregularity

Question 9

What is the response called for increased ICP?

Answer 9

Vasomotor response
Cushing's response
Cushing's reflex 
Cushing reaction
Cushing's law 
Cushing's phenomenon 
Cushing's triad

Question 10

Consequences of rapidly increasing ICP

Answer 10

-Cerebral herniation with brainstem compression, unconsciousness, subsequent death

Question 11

Normal ICP

Answer 11

10-15mm Hg

Question 12

Cerebral Perfusion Pressure Equation

Answer 12

MAP - ICP

why important to maintain normotension in these patients (>80 mm Hg)

Question 13

Abnormal ICP

Answer 13

20-30mm Hg

Question 14

What happens after TBI metabolically?

Answer 14

• 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

Question 15

Definition of a metabolic crisis

Answer 15

• 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

Question 16

Cerebral blood flow autoregulation

Answer 16

-Multifactorial process that maintains constant CBF despite changes in systemic BP, CPP over wide range

Question 17

CBF Autoregulation

Answer 17

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

Question 18

Effect of volatile anesthetic agents on CBF autoregulation

Answer 18

-Attenuate autoregulation up to a point when CBF becomes passively dependent upon CPP

Question 19

Upper limit of flow autoregulation in a normotensive patient

Answer 19

MAP 130-150 mmHg

Question 20

Lower limit of flow autoregulation in a normotensive patient

Answer 20

MAP 60 mm Hg

Decrease in MAP below lower limit results in CBF decrease and increase in arteriovenous oxygen difference

Question 21

What happens above/below the limits of autoregulation?

Answer 21

CBF becomes flow-dependent

Question 22

CBF autoregulation: at a MAP of 40 mm Hg

Answer 22

Symptoms of cerebral ischemia including dizziness, hyperventilation, mental impairment occur

Question 23

T/F: CPP can decrease by approximately 30% before lower limit of autoregulation is reached

Answer 23

True

Rule of them useful clinically when planning management of a hypertensive/normotensive patient

Question 24

Brain function

Answer 24

Intimately related to cerebral perfusion, metabolism

Question 25

Characteristic features of cerebral metabolism

Answer 25

1. High cellular energy demands utilizing ATP energy obtained from aerobic glucose oxidation 2. No oxygen, minimal glucose and glycogen substrate reserves relative to consumption rates 3. Low concentrations of high-energy phosphate compounds

Question 26

What is the brain dependent on?

Answer 26

-Adequate blood for minute-to-minute delivery of oxygen and glucose

Question 27

Normal cerebral metabolic rate for glucose

Answer 27

4.5mg/100g/min | Metabolic rate will be decreased during anesthesia, hypothermia, and/or hypercapnia

Question 28

How do volatile anesthetic agents affect the relationship btw CBF and CMRO2?

Answer 28

- -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

Question 29

What are the consequences of losing auto regulation of CBF with CMRO2?

Answer 29

CBF is passively dependent on CPP

Question 30

Normal mean global CBF in humans

Answer 30

45-65mL/100g/min

Question 31

What are the two types of arteries that supply the cerebral hemispheres?

Answer 31

1. conducting vessels | 2. penetrating vessels

Question 32

Cerebral arteries: conducting arteries

Answer 32

Non-resistance vessels --> carotid, vertebral, occipital, spinal artery together with their major and minor branches

Question 33

Cerebral arteries: penetrating arteries

Answer 33

AKA nutrient arterioles --> enter brain parenchyma at right angles to surface vessels Site of primary CBF regulation

Question 34

Even though the vessels receive automatic innervation...

Answer 34

neurogenic tone not essential to normal CBF regulation

Question 35

Why do cats with spring-held mouth gags have increased risk of post anesthetic neurological deficits, cortical blindness, or hearing deficits?

Answer 35

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

Question 36

Consequences of MAP increasing above the upper limit of auto regulation?

Answer 36

- - 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

Question 37

Constancy of CBF

Answer 37

Achieved by active vascular response thus rendering CBF directly proportional to CPP, inversely proportional to cerebrovascular resistance (CVR)

Question 38

What happens when have an increase in perfusion pressure?

Answer 38

-Elicit arteriolar constriction

Question 39

What happens when have a decrease in perfusion pressure?

Answer 39

Arteriolar dilation

Question 40

CBF auto regulation results from...

Answer 40

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

Question 41

Drainage of blood flow from the brain

Answer 41

- 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

Question 42

Chronic cerebral arterial hypertension

Answer 42

--Cerebral vessels adapt to higher perfusion pressure by hypertrophy of the vessel wall --> displaces autoregulatory curve to the right

Question 43

Differences with chronically hypertensive patients

Answer 43

- 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

Question 44

Effect of hypovolemic hypotension on CBF autoregulation

Answer 44

- 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

Question 45

Effect of moderate changes in PaO2 (arterial hypoxemia, arterial hyperoxemia)

Answer 45

-Do not exert measurable influence on CBF

Question 46

At what PaO2 do we see increase in CBF?

Answer 46

50mm Hg or below Same PO2 at which progressive brain tissue lactic acidosis appears so suggests hypoxia in CBF regulated by the periarteriolar pH

Question 47

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

Answer 47

True

Question 48

Intracerebral Steal Syndrome

Answer 48

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

Question 49

Robin Hood Syndrome (inverse steal syndrome)

Answer 49

Increase in CVR in normal cerebral regions will shunt blood into areas of vasomotor paralysis

Question 50

What conditions cause inadequate cerebral perfusion and hypoxia? What are the consequences?

Answer 50

Pathologic conditions including transient cardiac arrest, traumatic brain injury, brain tumor, or meningitis Will lead to severe tissue lactic acidosis, vasomotor paralysis, increased ICP