ECG, EMG, NCS Flashcards

1
Q

Normal EMG insertional activity and causes of change

A

Normally is less than a few hundred milliseconds with no waxing and waning

First thing to increase with denervation and also seen increase in myositis due to membrane instability

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2
Q

What causes miniature end plate potentials

A

They are normal spontaneous relase of ACh at the NMJ

Small deflections on EMG

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3
Q

What can cause spontaneous bi/tri phasic waves of variable (usually downward or positive) readings on EMG

A

Consistent with fibrillation

Seen with denervation after 4-5 days
DDx: hypoTH, polyradiculoneuritis, DM, protozoal neuropathy, Botulism,

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4
Q

What are positive sharp waves

A

downward deflections on EMG that correlate to irritation of the myofibre or denervation.

They are shorter than normal voluntary unit APs and sharp return to negativity (upwards)

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5
Q

What can cause polyphasic, uniform shape, amplitude and frequency readings on EMG

A

Complex repetitive discharges

A symptom of chronic denervation, often occur spontaneously firing.

Also seen in some myopathies especially HAC associated

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6
Q

What is the term and cause for repetitive discharges of 20-80Hz that wax and wane .

Sometimes appearing as continuous positive sharp wave potentials

A

Myotonic potentials

Seen in muscular dystrophies and denervation

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7
Q

Key information garnered from EMG and what can it not do

A

Differentiates denervation from disuse atrophy (does take 4-5 days for changes to develop).

Can detect peripheral nerve axon loss

Cannot differentiate muscular from neuronal disease

Unable to determine the underlying derangement causing changes

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8
Q

What is CMAP on NCS and what features are evaluated

A

a simple biphasic waveform, initially upward (negative) then downward (positive)

Amplitude and area are a measure of the number of functioning axons
Differs with age and site.

Duration of the CMAP is also an indication of whether the signal from nerve is arriving all at once or if there is temporal dispersion

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9
Q

What causes reduced CMAP amplitude

A

Generalised axonopathies - less signal getting to muscle
(Botulism, MG, polyradiculoneuritis, tick envenomation)

Also can be affected by myopathies

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10
Q

What can cause slowed neuronal conduction with normal CMAP

A

Demyelination

eg: diabetic neuropathy; degenerative demyelination (eg peripheral myelinopathy of Golden Rets; chronic demyelinating polyneuropathy)

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11
Q

What can cause reduced CMAP and reduced conduction velocity

A

Loss of axons and demyelination

Hypothyroid polyneuropathy; feline relapsing polyneuropathy (JVIM 2022 case series); polyradiculoneuritis; PNST

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12
Q

What are F waves and F ratio

A

They are purely motor impulses measured after supramaximal stimulation of the ventral nerve root. They are a more sensitive means of detecting delayed conduction (latency) than M waves thus can more precisely identifiy polyneuropathy

F ratio is wheremultiple supramaximal stimuli are performed and the conduction is measured for the proximal and distal nerve segments
–> if F ratio is low there is more severe distal nerve lesion
–> if high then a proximal nerve lesion is more likely.
Normal values indicate a diffuse neuronal disorder

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13
Q

What can cause a decreased PROXIMAL CMAP with normal distal CMAP

A

A conduction block usually a result of segmental demyelination

Seen in diabetic neuropathies and sometimes hypoTH.

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14
Q

What can cause SNCV deficits

A

lesions distal to the dorsal root ganglion

So will be decreased in diabetic neuropathies, sensory polyradiculoneuritis, distal sensorimotor polyneuropathy (Dancing Dobermans)

May also see temporal dispersion of impulses

Sensory neuropathy affecting the dorsal horn may have normal recordings.

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15
Q

How is Repetitive nerve stimulation performed and what are expected findings in MG

A

2-3Hz stimulation of the nerve and monitoring evoked CMAPs - with each subsequent CMAP expressed as a % of the first

This rate is fast enough to deplete ACh stores in nerve terminals

MG results in >10% decement in subsequent CMAPs compared to first.
Same for congenital MG

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16
Q

What can cause reduced CMAP amplitude on NCS and fibrillation potentials with sharp P waves

A

Indicates denervation changes on EMG and reduced impulse reaching muscle on NCS

DDx: HypoTH, polyradiculoneuritis, myopathies, degenerative motor neuropathies (seen in Britt Spaniel and Maine Coon cat), relapsing polyneuropathy of cats

17
Q

What can cause normal EMG findings with reduced conduction velocity, temporal dispersion and normal CMAP

A

Consistent with demyelination
CMAP may be affected later in disease

DDx: Chronic demyelinating polyneuropathy, diabetic polyneuropathy)

18
Q

What is the cord dorsum potential useful for

A

it is a measure of sensory activity assessing the dorsal horn and interneurons (so the other part compared to SNCV)

Assesses the severity and distribution of abnormalities in the proximal sensory nerve, dorsal nerve root and spinal cord. So can help in diagnosis of nerve root injury or sensory polyganglioradiculoneuropathy

19
Q

ECG:
increased HR can be severe with signs of haemodynamic compromise
Irregularly irregular rhythm
no organized P-waves
normal QRS complexes

A

A fib

ORCA study - rate control important

Digoxin - slows atrial conduction

Diltiazem - slows nodal Ca influx thus inhibiting stage 4

add B block if still too high rate

20
Q

Increased HR
P waves normal (may not be visible) , but dissociated from QRS
QRS is wide and bizarre with negative deflection
R-R interval is irregular
abnormal QRS complexes are occurring in paroxysmal runs, with R on T occurring.

A

Ventricular tachycardia

R on T can be an indication of severe disease and impending VFib

21
Q

DDx for bradyarrhythmia

A

Physiologic - sleep, fitness
Increased vagal tone - resp, GI or CNS disease
SA node disease - fibrosis, atrial stretch, neoplasia, myocarditis
Metabolic ddz - hyperK, hypoTH, hypothermia, hypoglycemia, uraemia
Autonomic NS disease
Drugs - beta blockers, digoxin, diltiazem, sedation (alpha2 agonists, phenothiazines)

22
Q

Different AV block ECG findings

A

1 = PR interval is prolonged

2 (Mobitz I) = variable PR interval, gradually increases until blocked beat (P wave with no conduction)

2 (Mobitz II) = regular PR interval with intermittent blocked conduction

3 = no correlation b/w P and QRS waves. P waves fire with normal rhythm, unrelated QRS complexes may arise from AV node (40-60bpm) or from purkinjie fibres (20-40bpm)
No ability to increase HR with exertion

vagolytic drugs or sympathomimetics but tends not to help

23
Q

Holter monitor findings in SSS

A

slow irregular atrial rate (severe sinus bradycardia); long asystole with no escape beats; impaired AV conduction (2nd or 3rd degree); slow and irregular ventricular escape beats; paroxysms of SVT alternating with severe sinus bradycardia

Definitive electrophysiologic diagnosis of SSS requires demonstration of abnormal sinus node recovery time or sinoatrial conduction time after overdrive pacing, in practice, a clinical diagnosis of SSS is often made based on abnormal sinoatrial node (SAN) activity on the surface electrocardiogram (ECG), with corresponding clinical signs of low cardiac output (i.e. syncope, staggering, weakness).

Haemodynamic compromise due to bradycardia

Breeds: Min Schnauzer, WHWT; Cocker Spaniel, Doberman, Boxer

24
Q

TX options for SSS

A

If response to atropine test - ie HR increases then can try:

Theophylline - weak chronotropic and ionotropic effects through PDE3i effects altering myocardial Ca translocation

Isoproterenol = B1 and 2 agonist, no alpha effects

25
Q

Digoxin MOA, uses, adverse effects

A

antiarrhythmic effect due to neuroendocrine and baroreceptor effects and parasympathomimetic action on SA and AV node and atrial muscle.
Reduces conduction velocity through nodes and prolongs refractory period

Ionotropic effects increase contractility and CO
Increase diuresis reducing preload

Mainly used in SVT and AFib to slow ventricular rate
Commonly used in combination with a beta blocker or a calcium channel blocker

AEs:
Usually correlated with blood toxic levels
Cardiac - arrhythmia, worsening CHF,
Extracardiac - mild GI, anorexia, weight loss, diarrhea.
Avoid in renal failure (renally excreted)
Contraindicated in presence of ventricular tachyarrhythmia