Basic Approach to ECG Interpretation and Arrhythmia Diagnosis Flashcards
describe the general approach to ECG interpretation
- note lead and paper speed settings
-most common paper speeds: 25mm/sec and 50mm/sec - what is the heart rate?
- is there an underlying sinus rhythm?
- if not sinus rhythm: describe and name rhythm abnormality
describe paper speed settings
25mm/sec paper speed (1/25th of a second = each box):
-each small (mm) box = 0.04 sec!!!!!
-each big box = 5mm = 0.2 sec
-default for most machines but ALWAYS check
50 mm/sec
-each small (mm) box = 0.02 sec!!!!
-each big box = 5mm = 0.1 sec
-50 small boxes = 1 sec
describe how to determine heart rate on ECG
- count number of QRS complexes in a 3-second period
- multiple by 20 to get beats/60sec (beats/min)
- for rapid HR determination:
-standard BIC pen with cap on is 150mm long
=3 seconds at 50mm/sec
=6 seconds at 25mm/sec
-to determine average HR: count number of QRS complexes inside pen length, multiply by 10 if at 25mm/sec (pen times ten), or by 20 if at 50mm/sec
describe how to determine if there is an underlying sinus rhythm
- rhythm occurring when depolarization of the cardiac muscle begins at the sinus node
- if the sinus node is firing and calling the sots, the following should be present in lead II MOST of the time
-positive P waves in lead II (small animals) or base-apex lead (large animals) occurring at a reasonable rate (0-300bpm) for SA node
-a P wave for every QRS complex and a QRS complex for every P wave
-consistent PR intervals (P is linked to and “causing” QRS)
define arrhythmia/dysrhythmia
- any alteration in the rate, regularity, or normal sequence of electrical activation of the heart
- essentially, any heart rhythm that:
-originates outside the SA node
-occurs at an abnormally high or low rate
-creates beats at irregular intervals
- can cause clinical signs and cardiac injury
-decreased cardiac output can cause hypotension or myocardial ischemia
-most likely with sustained, very fast, or very slow rhythms:
–super fast HR: inadequate filling time = decreased stroke volume and decreased coronary perfusion
–super slow HR: inadequate cardiac output (most important during physical exertion)
-some arrhythmias (like A FIB!!) cause loss of atrio-ventricular synchrony
–loss of atrial booster = further decrease in diastolic filling (esp detrimental at high HR)
-tachycardia-induced cardiomyopathy
-can cause sudden death!
describe supraventricular versus ventricular arrhythmias
- supraventricular: comes from above the ventricles (atria or AV junction)
-abnormal impulse: QRS complex identical to sinus beat (skinny and upright in lead II)
-P wave buried in preceding T - ventricular: comes from the ventricles
-QRS complex wide and bizarre, not preceded by P-wave
-WIDE = QRS > 0.06 sec (dog); >0.04 sec (cat)
-ventricular are MOER DANGEROUS
describe sinus arrhythmia
ECG characteristics:
1. sinus rhythm with cyclic slowing and speeding of rate (regularly irregular) rhythm
- cycle often associated with respiration (speeds on inhale, slows on exhale)
- mechanism: associated with high prevailing vagal (parasympathetic tone)
-normal finding in dogs and FIT horses
-rare in cats in clinic (too stressed usually)
-may be exaggerated in diseases associated with high vagal tone (resp, intraocular, GI)
- treatment: no treatment necessary
describe sinus tachycardia
ECG characteristics:
1. sinus rhythm with fact heart rate
- rate cutoffs used for diagnosis of tachycardia are species specific
-dogs: >160 bpm
-cats: >200bpm
-horses: >44bpm
-cows: >80bpm
-small ruminants, foals, calves: >120bpm - mechanism: physiologic response to
-conditions associated with high sympathetic tone: fear, excitement, exercise, pain, fever, hyperthyroidism, hypovolemia, cardiac tamponade, heart failure, hypoxia, anemia
-DRUGS causing sinus tachycardiaL catecholamines, atropine, terbutaline, aminophylline, theophylline, caffeine, chocolate toxicity, amphetamines, cocaine
- treatment: address underlying cause!
describe atrial fibrillation
- most common ectopic supraventricular tachyarrhythmia seen clinically
- dogs and cats: almost always associated with advanced heart disease (atrial enlargement)
- giant breed dogs ad horses: may occur in absence of underlying heart disease (lone A-fib): decreased performance/exercise tolerance as a first sign is common
- disorganized atrial activity; simultaneous atrial depolarization waves bombard AV node at 500-600/min
-AV node can’t conduct all impulses, acts as a filter
-because His-purkinje system is still used to depolarize ventricles, QRS is normal (narrow, supraventricular) - hemodynamic consequences:
-loss of atrial kick (important at high heart rates): decreased exercise tolerance/performance
-precipitation of heart failure in patients with heart disease
-if sustained, tachycardia may lead to worsening myocardial function (tachycardia-induced cardiomyopathy)
describe A fib ECG characteristics
- absence of P waves
- irregular, sawtooth baseline cause by fibrillation (f) waves
- supraventricular QRS complexes: narrow and upright in lead II
- irregularly irregular rhythm: no pattern to P-R intervals
- rapid heart (ventricular response) rate (usually)
- a rapid, irregularly irregular, supraventricular arrhythmia without p waves is A fib until proven otherwise!!!!!!!!!!!!
describe treatment of A-fib
- rhythm control: convert to sinus rhythm
-used in horses and giant breed dogs with lone a-fibn
-medical antiarrhythmic therapy (quinidine in horses) vs. electrical cardioversion (horses, dogs) - rate control: reduce AV node conduction to slow ventricular response rate
-most common approach in dogs and cats, oral anti-arrhythmics
describe ventricular premature depolarizations/complexes
- abnormal impulses arising from ventricular tissue
-ventricular origin? very wide and bizarre (>0.06 sec!) - building blocks for more complex arrhythmias (V-tach)
- ECG characteristics:
-premature: earlier than next expected sinus beat
-no related P wave
-wide and bizarre QRS
–depolarization starts in ventricle and doesn’t use specialized electrical conduction system so is slowwww (cell-by-cell)
–WIDE QRS >0.06sec (dog), >0.04sec (cat)
describe ECG characteristics of ventricular premature depolarizations/complexes
- premature: earlier than next expected sinus beat
- no related P wave
- wide and bizarre QRS
-depolarization starts in ventricle and doesn’t use specialized electrical conduction system so is slowwww (cell-by-cell)
-WIDE QRS >0.06sec (dog), >0.04sec (cat)
- can be single, or occur in pairs or in threes (couplet, triplet)
- can be uniform (all complexes identical) or multiform (different morphologies)
-multiformity tends to be more dangerous (firing from multiple locations) - R on T phenomenon:
-QRS of VPC occurs early enough to land on T wave of preceding beat
-increases the risk for ventricular fibrillation, a terminal rhythm
-repolarization and depolarization occurring at same time in different parts of the ventricle
describe the causes of VPCs (HEADS)
H: heart disease/injury: esp primary myocardial dz in dogs, myocarditis, myocardial hypoxia
E: electrolyte derangements (hypo/hyperkalemia, hypocalcemia, hypomagnesemia)
A: algesia: pain, adrenergic stimulation
D: drugs: anesthetics, stimulants
S: splenic dz, sepsis, SIRS, systemic inflammation (IMHA, pancreatitis)
happens for multiple reasons, many of them are EXTRA cardiac
describe when to treat VPCs
- single VPCs are unlikely to cause clinical signs or increase risk for sudden death
-treat underlying disease
-consider longterm ECG monitoring (Holter) to eval for occult complexity - treat if one or more of the following is present (4):
-ventricular tachycardia, flutter, or fibrillation
-R on T
-evidence of hemodynamic compromise (hypotension, weakness, syncope)
-multiformity
