ECG, EMG, NCS Flashcards
Normal EMG insertional activity and causes of change
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
What causes miniature end plate potentials
They are normal spontaneous relase of ACh at the NMJ
Small deflections on EMG
What can cause spontaneous bi/tri phasic waves of variable (usually downward or positive) readings on EMG
Consistent with fibrillation
Seen with denervation after 4-5 days
DDx: hypoTH, polyradiculoneuritis, DM, protozoal neuropathy, Botulism,
What are positive sharp waves
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)
What can cause polyphasic, uniform shape, amplitude and frequency readings on EMG
Complex repetitive discharges
A symptom of chronic denervation, often occur spontaneously firing.
Also seen in some myopathies especially HAC associated
What is the term and cause for repetitive discharges of 20-80Hz that wax and wane .
Sometimes appearing as continuous positive sharp wave potentials
Myotonic potentials
Seen in muscular dystrophies and denervation
Key information garnered from EMG and what can it not do
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
What is CMAP on NCS and what features are evaluated
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
What causes reduced CMAP amplitude
Generalised axonopathies - less signal getting to muscle
(Botulism, MG, polyradiculoneuritis, tick envenomation)
Also can be affected by myopathies
What can cause slowed neuronal conduction with normal CMAP
Demyelination
eg: diabetic neuropathy; degenerative demyelination (eg peripheral myelinopathy of Golden Rets; chronic demyelinating polyneuropathy)
What can cause reduced CMAP and reduced conduction velocity
Loss of axons and demyelination
Hypothyroid polyneuropathy; feline relapsing polyneuropathy (JVIM 2022 case series); polyradiculoneuritis; PNST
What are F waves and F ratio
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
What can cause a decreased PROXIMAL CMAP with normal distal CMAP
A conduction block usually a result of segmental demyelination
Seen in diabetic neuropathies and sometimes hypoTH.
What can cause SNCV deficits
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.
How is Repetitive nerve stimulation performed and what are expected findings in MG
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
What can cause reduced CMAP amplitude on NCS and fibrillation potentials with sharp P waves
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
What can cause normal EMG findings with reduced conduction velocity, temporal dispersion and normal CMAP
Consistent with demyelination
CMAP may be affected later in disease
DDx: Chronic demyelinating polyneuropathy, diabetic polyneuropathy)
What is the cord dorsum potential useful for
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
ECG:
increased HR can be severe with signs of haemodynamic compromise
Irregularly irregular rhythm
no organized P-waves
normal QRS complexes
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
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.
Ventricular tachycardia
R on T can be an indication of severe disease and impending VFib
DDx for bradyarrhythmia
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)
Different AV block ECG findings
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
Holter monitor findings in SSS
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
TX options for SSS
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
