VETM 5291 ECG II 2025 Slides PDF

VETM 5291♥ Cardiovascular, Respiratory & Hemolymph Systems II Mandy Coleman, DVM, DACVIM (Cardiology) [email protected] § By the end of the next 2 hours, you will be able to: § List and discuss the steps comprising a systematic approach to ECG interpretation § When provided an ECG, determ...

VETM 5291♥ Cardiovascular, Respiratory & Hemolymph Systems II Mandy Coleman, DVM, DACVIM (Cardiology) [email protected] § By the end of the next 2 hours, you will be able to: § List and discuss the steps comprising a systematic approach to ECG interpretation § When provided an ECG, determine heart rate (with and without a Bic pen) and whether the rhythm is sinus § Define “cardiac arrhythmia” and “normal sinus rhythm” § List the ECG criteria of a normal sinus rhythm § When given a lead II electrocardiogram, determine whether the rhythm is controlled by the sinus node § Contrast the expected appearance of the QRS complex in patients affected by supraventricular, versus ventricular, arrhythmias § For each specific arrhythmia discussed in class, describe: § The electrocardiographic criteria for diagnosis § Associated conditions or diseases § Be systematic: 1. Note lead and paper speed settings Most common paper speeds: 25 mm/sec and 50 mm/sec 2. What is the heart rate? 3. Is there an underlying sinus rhythm? 4. If not sinus rhythm: describe and name rhythm abnormality What is the paper speed (mm/s) setting? § 25 mm/sec paper speed § Each small (mm) box = 0.04 sec § Each big box = 5 mm = 0.2 sec § 25 small boxes = 1 sec § 50 mm/sec paper speed § Each small (mm) box = 0.02 sec § Each big box = 5 mm = 0.1 sec § 50 small boxes = 1 sec  § To determine heart rate: § Count the number of QRS complexes in a 3-second period § Multiply by 20 to get beats/60 seconds (beats/minute) 3 sec (75 mm) 25 mm/sec 7 QRS complexes in 3 seconds x 20 = 140 beats/minute § Standard Bic pen with cap on: 150 mm long = 3 seconds at 50 mm/sec = 6 seconds at 25 mm/sec § To determine average heart rate: § Count # of QRS complexes inside the pen length § Multiply by 10 if at 25 mm/sec (”Pen times 10”) or by 20 if at 50 mm/sec 25 mm/sec paper speed Heart rate = “pen x 10” = 11 x 10 = 110 beats/minute 50 mm/sec paper speed Heart rate = “pen x 20” = 6 x 20 = 120 beats/minute  25 mm/sec; Heart rate = 140 bpm Rhythm occurring when depolarization of the cardiac muscle begins at the sinus node If the sinus node is firing and “calling the shots”, the following should be present in lead II most of the time (i.e. there is an “underlying sinus rhythm”): § Positive P waves in lead II (small animals) or base-apex lead (large animals) occurring at a ”reasonable rate” (i.e., 0-300 bpm) for SA node? § A P wave for every QRS complex and a QRS complex for every P wave § Consistent PR intervals (i.e., P is linked to and “causing” QRS) Recall: P waves should be positive in lead II if atrial depolarization wave originates from the sinus node! § Any alteration in the rate, regularity or normal sequence of electrical activation of the heart § Essentially, any heart rhythm that: § Originates outside the sinoatrial (SA) node, or § Occurs at an abnormally high or low rate, or § Creates beats at irregular intervals …is termed an arrhythmia § Can cause clinical signs, cardiac injury § ↓ cardiac output can cause hypotension, myocardial ischemia § Most likely with sustained, very fast or very slow rhythms § super fast HR = inadequate filling time = ↓stroke volume + coronary perfusion § super slow HR = inadequate cardiac output (most important during physical exertion) § Some arrhythmias (e.g., ATRIAL FIBRILLATION) cause loss of atrio-ventricular synchrony § Loss of atrial “booster” = further ↓ in diastolic filling (especially detrimental at high HR) § Tachycardia-induced cardiomyopathy § Can cause sudden death  A clinically relevant scheme for classifying arrhythmias… Sinus bradycardia Atrioventricular (AV) block Bradyarrhythmias Atrial standstill Sinus tachycardia Sick sinus syndrome Atrial premature complexes Cardiac Supraventricular tachycardia Arrhythmias Atrial fibrillation Supraventricular Atrial flutter Tachyarrhythmias Ventricular premature complexes Accelerated idioventricular rhythm Ventricular Ventricular tachycardia Ventricular fibrillation Ventricular flutter  Supraventricular origin (comes from above the ventricles [i.e., atria or AV junction]) Normal abnormal impulse (comes from the sinus node) QRS complex identical to sinus beat (skinny and upright in lead II) P-wave buried in preceding T Ventricular origin (comes from the ventricles) abnormal impulse QRS complex “wide and bizarre” Not preceded by P-wave WIDE = QRS > 0.06 sec (dog); > 0.04 sec (cat)  Supraventricular origin (comes from above the ventricles [i.e., atria or AV junction]) Normal abnormal impulse (comes from the sinus node) Why should you know how to identify a rhythm’s origin? QRS complex identical to sinus beat (skinny and upright in lead II) In general: ventricular arrhythmias are more P-wavedangerous! buried in preceding T Ventricular origin (comes from the ventricles) abnormal impulse QRS complex “wide and bizarre” Not preceded by P-wave WIDE = QRS > 0.06 sec (dog); > 0.04 sec (cat)  25 mm/sec 8-year-old MC Boston terrier; routine evaluation  Heart rate 70 bpm (pen x 10) 25 mm/sec QRS P T 8-year-old MC Boston terrier; routine evaluation  25 mm/sec; HR, 70 bpm QRS P T 8-year-old MC Boston terrier; routine evaluation § ECG characteristics § Sinus rhythm with cyclic slowing and speeding of rate (“regularly irregular” rhythm) § Cycle often associated with respiration (speeds on inhale, slows on exhale) § Associated with high prevailing vagal (parasympathetic) tone § Normal finding in dogs and fit horses § Rare in cats in-clinic § May be exaggerated in diseases associated with high vagal tone (e.g., respiratory, intraocular, GI) § No treatment necessary  25 mm/sec 10-year-old MC Whippet, presented with seizures after ingesting cocaine  22 QRS complexes HR 220 bpm 25 mm/sec QRS P T 10-year-old MC Whippet, presented with seizures after ingesting cocaine  25 mm/sec; HR 220 bpm QRS P T 10-year-old MC Whippet, presented with § ECG characteristics seizures after ingesting cocaine § Sinus rhythm with fast heart rate § Rate cutoffs used for diagnosis of tachycardia are species-specific: Dogs > 160 bpm Cats > 200 bpm Horses > 44 bpm Cattle > 80 bpm Small ruminants, foals, calves > 120 bpm  25 mm/sec; HR 220 bpm QRS P T 10-year-old MC Whippet, presented with § ECG characteristics seizures after ingesting cocaine § Sinus rhythm with fast heart rate § 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 tachycardia: catecholamines, atropine, terbutaline, aminophylline, theophylline, caffeine, chocolate toxicity, amphetamines, cocaine § Treatment: address the underlying cause  25 mm/sec Lead II Lead III 11-year-old FS English setter, previously diagnosed with severe mitral valve disease; acute onset lethargy  HR 170 bpm QRS 25 mm/sec Lead II T Lead III 11-year-old FS English setter, previously diagnosed with severe mitral valve disease; acute onset lethargy  QRS 25 mm/sec; HR 180 bpm Lead II T Lead III 11-year-old FS English setter, previously diagnosed with severe mitral valve disease; acute onset lethargy § Most common ectopic supraventricular tachyarrhythmia seen clinically § How do you know this is supraventricular in origin? § Dogs and cats: almost always associated with advanced heart disease (atrial enlargement) § Giant-breed dogs + horses: may occur in absence of underlying heart disease (“lone A-fib”); decreased performance/exercise intolerance as 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”] QRS) § 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)  25 mm/sec; HR 180 bpm 11-year-old FS English setter, previously diagnosed with severe mitral valve disease; acute onset lethargy § ECG characteristics § Absence of P waves § Irregular, “sawtooth” baseline caused by fibrillation (f) waves § Supraventricular QRS complexes (narrow and upright in lead II) § Irregularly irregular rhythm (no pattern to R-R intervals) § Rapid heart (“ventricular response”) rate (usually) § A rapid, irregularly irregular, supraventricular arrhythmia without P waves is A-fib until proven otherwise!  25 mm/sec; HR 180 bpm 11-year-old FS English setter, previously diagnosed with severe mitral valve disease; acute onset lethargy § Treatment § Rhythm control (i.e., convert to sinus rhythm) § Used in horses and giant-breed dogs with lone A-fib § Medical antiarrhythmic therapy (quinidine in horses) vs. electrical cardioversion (horses, dogs) § Rate control (i.e., reduce AV node conduction to slow ventricular response rate) § Most common approach in dogs and cats § Oral antiarrhythmics (e.g., calcium channel blockers, beta-adrenergic blockers, digoxin)  25 mm/sec; HR 120 bpm 6-month-old F German shepherd dog, presented for routine examination  25 mm/sec; HR 120 bpm QRS T QRS P P T T T T QRS QRS QRS 6-month-old F German shepherd dog, presented for routine examination  25 mm/sec; HR 90 bpm 6-month-old F German shepherd dog, presented for routine examination § Abnormal impulses arising from ventricular tissue § How do you know these abnormal beats (arrows) have a ventricular origin? § Ventricular premature depolarizations (VPD) = complexes (VPC) = premature ventricular complexes (“PVC”; used widely in human medicine) § VPCs are building blocks for more complex ventricular arrhythmias (e.g., ventricular tachycardia) + II  25 mm/sec; HR 90 bpm 6-month-old F German shepherd dog, presented for routine examination § ECG characteristics § Premature (earlier than next expected sinus beat) § No related P wave § ”Wide and bizarre” QRS § Depolarization starts in ventricle + doesn’t use specialized electrical conduction system, so it is sloooow (cell-by-cell) § WIDE QRS > 0.06 sec (dog) or > 0.04 sec (cat)  Ventricular Ventricular couplet with R-on-T couplet with R-on-T 25 mm/sec; HR 90 bpm VPC VPC VPC VPC 6-month-old F German shepherd dog, presented for routine examination § ECG characteristics § Can be single, or occur in pairs (“couplet”) or in threes (“triplet”) § Can be uniform (all complexes identical) or multiform (different morphologies) § “R-on-T” phenomenon: QRS of VPC occurs early enough to land on T wave of preceding beat. This increases the risk for ventricular fibrillation, a terminal rhythm.  25 mm/sec; HR 90 bpm 6-month-old F German shepherd dog, presented for routine examination § Potential causes (VPCs and other ventricular tachyarrhythmias): § H – heart disease/injury (especially primary myocardial diseases in dogs, myocarditis, myocardial hypoxia) § E – electrolyte derangements (hyper/hypo-kalemia, hypocalcemia, hypomagnesemia) § A – algesia (pain), adrenergic stimulation § D – drugs (anesthetics, stimulants) § S – splenic disease, sepsis, SIRS, systemic inflammation (e.g., IMHA, pancreatitis)  R-on-T 25 mm/sec; HR 250 bpm T T QRS QRS 7-year-old MC Doberman with dilated cardiomyopathy  R-on-T 25 mm/sec; HR 250 bpm T T QRS QRS 7-year-old MC Doberman with dilated cardiomyopathy § Rapid rhythm originating from the ventricles § 4 or more VPCs in a row at a rate >160 beats per minute § ECG characteristics § QRS morphology ”wide and bizarre” § Rapid rhythm (rate > 160 in a dog, >200 in a cat, >40 in a horse) § Rhythm usually regular § May be uniform (all complexes identical) or multiform (differing morphologies)  25 mm/sec; HR 250 bpm 7-year-old MC Doberman with dilated cardiomyopathy § This is a very dangerous rhythm! § If there is severe underlying heart disease or if rate very rapid (i.e., >250/min in dog), animal can experience weakness or syncope (fainting) § If sustained, can precipitate CHF § Can degenerate to ventricular fibrillation (FATAL) § Single VPCs are unlikely to cause clinical signs or increase risk for sudden death § Treat underlying disease § Consider longer-term ECG monitoring (Holter) to evaluate for occult complexity § Treat if there is: § Ventricular tachycardia § R-on-T § Evidence of hemodynamic compromise § Multiformity § Underlying heart disease