VETM 5291 ECG I 2025 PDF

VETM 5291 ♥ Cardiovascular, Respiratory & Hemolymph Systems II Mandy Coleman, DVM, DACVIM (Cardiology) [email protected] By the end of this hour, you will be able to: § Label the x- and y-axes of the electrocardiogram (ECG) § Describe cell surface events when an upward deflection is recorded...

VETM 5291 ♥ Cardiovascular, Respiratory & Hemolymph Systems II Mandy Coleman, DVM, DACVIM (Cardiology) [email protected] By the end of this hour, you will be able to: § Label the x- and y-axes of the electrocardiogram (ECG) § Describe cell surface events when an upward deflection is recorded on the ECG § List the normal cardiac activation sequence from memory § For each component of the cardiac conduction system: § Describe relative velocity of conduction § Recall whether normal pacemaker activity is expected § Describe the method for recording a 6-lead ECG in a dog, and a base-apex ECG in a horse § When provided a normal ECG, label individual waves and explain the cellular events that each represents Voltage (mV) § Electrocardiogram (ECG or EKG) - records heart’s electrical activity from the body surface § Records extracellular signals produced by movement of depolarization/repolarization waves through time (sec) cardiac myocytes § Graph of voltage (mV, y-axis) over time (sec, x-axis) § Changes in voltage are recorded as waves/complexes, named by letters (P,QRS,T) Voltage (mV) § Evaluation of ECG gives clinician insight into: § Heart rate § Disturbances of heart rhythm and conduction time (sec) § Relative size of heart chambers (small animals only) § NOTE: ECG does NOT record mechanical activity and so can’t give insight into: § Whether the heart is contracting § Strength of cardiac contractions § Presence/absence of heart failure Remember: cardiac tissue is excitable! § At rest, myocytes are polarized – membrane is negatively charged (inside vs. outside) § When stimulated, resting myocyte depolarizes wave of depolarization (i.e., membrane polarity reverses) § Depolarized cell stimulates adjacent cell to depolarize § Depolarization “impulse” spreads as a wave § Extracellular currents associated with wave (depolarized cell) of depolarization are detected by the electrocardiogram § Cells must repolarize so this process can from: Mohrman DE, Heller JH. Cardiovascular Physiology, 8e happen again and again  wave of depolarization Negative portion Positive portion of electrical field of electrical field (depolarized cell) from: Mohrman DE, Heller JH. Cardiovascular Physiology, 8e  ECG screen/paper: 0 - + - + When ECG electrodes are placed on Electrocardiograph Negative electrode Positive electrode either side of a wave of depolarization, - + the electrical field can be measured wave of depolarization Negative portion Positive portion of electrical field of electrical field VERY IMPORTANT CONCEPT: By convention, if a wavefront of negative extracellular charges moves TOWARD the POSITIVE electrode, an upward deflection is recorded on the ECG! (depolarized cell) from: Mohrman DE, Heller JH. Cardiovascular Physiology, 8e At rest - outside of cell membrane is positively charged myocardial strip * Remember: a wavefront of negative charges moving toward the positive electrode = positive deflection  Effect of changing depolarization wavefront orientation relative to recording lead axis: = wavefront of depolarization A B C D E Recorded ECG deflection When a wavefront moves directly toward an electrode, in parallel with the lead axis, the largest possible deflection will be recorded (A and E)  Wavefront of depolarization (negative charges) - - Recording lead axis - + Lead A Negative Positive electrode electrode + + Lead C Lead B  Normal activation sequence RA LA LV RV Quiz yourself before moving on!  SA node Normal activation sequence Atrial muscle RA LA LV AV node RV His-Purkinje system (His bundle + bundle branches) Ventricular muscle  Quiz yourself before moving on! Conduction Pacemaker rate velocity (impulses/min) SA node Normal activation sequence Atrial muscle RA LA LV AV node RV His-Purkinje system (His bundle + bundle branches) Ventricular muscle  Conduction Pacemaker rate velocity (impulses/min) SA node 60-250 dominant pacemaker Normal activation sequence Atrial muscle fast None RA LA LV AV node slooow 40 – 60 RV Rescue pacemaker His-Purkinje system SUPER FAST 20 – 40 (His bundle + bundle Rescue pacemaker branches) Ventricular fast None muscle Atrial internodal tracts Rapidly-conducting tissue connecting SA and AV nodes Relatively resistant to effect of hyperkalemia (excess [K+]) Bundle of His/Bundle branches Divides into right and left bundle branches Rapidly conduct impulse to terminal Purkinje fibers Terminal Purkinje fibers Rapidly-conducting, subendocardial Penetrate inner ⅓ of myocardium in dogs and cats, so depolarization proceeds endocardium-to-epicardium Penetrate near-complete thickness in horses, cattle, birds § Patient in right lateral recumbency § Limbs parallel to one another, perpendicular to trunk § Calm environment, non-conducting surface to minimize artifacts § Electrode placement: § Forelimb electrodes (white/black) over elbows § Hindlimb electrodes (red/green) over stifles § Avoid contact with trunk and each other § “Black-and-white TV came before color; white on right and grass on the ground” § Some machines do not have a green (right hindlimb) electrode (grounding electrode) § Several standard leads used clinically § Lead = electrode pair (1 positive + 1 negative) § Lead axis = orientation of lead relative to heart § For this course, we will focus on lead II (used most frequently in the clinic) § Negative electrode on right forelimb (white) § Positive electrode on left hindlimb (red) § Lead axis oriented cranial-to-caudal, right-to-left Cranial Right Left Caudal LV RV  § No lead system is universally accepted in large animals - § Electrode placement for “base-to-apex” lead + + LA § Set machine to record in lead I (RA- to LA+) § Place white electrode (RA) over right jugular furrow or top of right scapular spine (base; “white on right”) - § Place black electrode (LA) over left apex beat + (“black on heart”) § Lead axis oriented cranial-to-caudal, right-to-left RA = Right Arm electrode LA = Left Arm electrode  Cranial Right Left Caudal blue = depolarized tissue pink arrow = direction of wave of depolarization  blue = depolarized tissue pink arrow = direction of wave of depolarization P wave = cell-by-cell atrial depolarization Positive in lead II + base-apex lead; frequently bifid (M-shaped) in horses  blue = depolarized tissue pink arrow = direction of wave of depolarization PR interval PR (PQ) interval: Includes depolarization of atria, AV node and His-Bundle PR interval approximates signal transmission through AV node Normal < 0.13 seconds (dog) or < 0.09 seconds (cat)  blue = depolarized tissue pink arrow = direction of wave of depolarization QRS complex = ventricular depolarization Should be tall, skinny and upright in lead II (in small animals) Normal < 0.06 seconds (dog), < 0.04 seconds (cat) In horses and ruminants, normal QRS complex is negatively deflected  blue = depolarized tissue pink arrow = direction of wave of depolarization ST segment ST segment Isoelectric (flat) line connecting the S and T waves All ventricular cells depolarized, no current flowing T wave = ventricular repolarization Ventricular repolarization is a complicated process T-wave may be negative, positive or biphasic – but must be there! Little emphasis placed on analysis in veterinary medicine  Ventricular depolarization Cranial Atrial Right Left depolarization Caudal Ventricular blue = depolarized tissue REpolarization pink arrow = direction of wave of depolarization  Bifid (notched) P waves are normal in horses − P QRS T P QRS T + negative electrode Negative QRS over right jugular furrow Normal sinus rhythm in a healthy horse complexes are normal in horses and cattle (base-apex lead) positive electrode over cardiac apex beat (left) T T P P QRS QRS Normal sinus rhythm in a healthy cow base-apex lead) From: Reddy BS, Sivajothi S. Electrocardiographic Parameters of Normal Dairy Cows during Different Ages. J Veter Sci Med. 2016;4(1): 5. By the end of this hour, you will be able to: § Label the x- and y-axes of the electrocardiogram (ECG) § Describe cell surface events when an upward deflection is recorded on the ECG § List the normal cardiac activation sequence from memory § For each component of the cardiac conduction system: § Describe relative velocity of conduction § Recall whether normal pacemaker activity is expected § Describe the method for recording a 6-lead ECG in a dog, and a base-apex ECG in a horse § When provided a normal ECG, label individual waves and explain the cellular events that each represents 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 Principles of Electrocardiography Part III: Approach to arrhythmia diagnosis (contd) VETM 5291︎ Cardio︎vascular, Respirato︎ry & Hemo︎lymph Systems II Mandy Co︎leman, DVM, DACVIM (Cardio︎lo︎gy) [email protected]  LEARNING OBJECTIVES ▪ By the end of this hour, 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 “no︎rmal 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 General approach to ECG interpretation ▪ 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  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 T T T T P P T T T T T QRS QRS QRS QRS QRS QRS QRS 6-month-old F German shepherd dog, presented for routine examination  Ventricular Premature Depolarizations/Complexes 25 mm/sec; HR 90 bpm 6-month-old F German shepherd dog, presented for routine examination ▪ Abno︎rmal impulses arising fro︎m ventricular tissue ▪ How do you know these abnormal beats (arrows) have a ventricular origin? + II  Ventricular Premature Depolarizations/Complexes 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 co︎mplexes (“PVC”; used widely in human medicine) ▪ VPCs are building blocks for more complex ventricular arrhythmias (e.g., ventricular tachycardia) + II  Ventricular Premature Depolarizations/Complexes 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 ▪ Depo︎larizatio︎n starts in ventricle + do︎esn’t use specialized electrical co︎nductio︎n system, so︎ it is sloooow (cell-by-cell) ▪ WIDE QRS > 0.06 sec (dog) or > 0.04 sec (cat)  Ventricular Premature Depolarizations/Complexes Ventricular Ventricular couplet with R-on-T couplet with R-on-T 25 mm/sec; HR 90 bpm VPC VPC VPC VPC 6-mo︎nth-o︎ld F German shepherd do︎g, presented fo︎r ro︎utine examinatio︎n ▪ ECG characteristics ▪ Can be single, o︎r o︎ccur in pairs (“co︎uplet”) o︎r in threes (“triplet”) Ventricular Single Ventricular Single triplet VPC co︎uplet VPC  Ventricular Premature Depolarizations/Complexes Ventricular Ventricular co︎uplet with R-o︎n-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, o︎r o︎ccur in pairs (“co︎uplet”) o︎r in threes (“triplet”) ▪ Can be uniform (all complexes identical) or multiform (different morphologies) Uniform VPCs  Ventricular Premature Depolarizations/Complexes 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, o︎r o︎ccur in pairs (“co︎uplet”) o︎r in threes (“triplet”) ▪ Can be uniform (all complexes identical) or multiform (different morphologies) ▪ “R-on-T” pheno︎meno︎n: QRS o︎f VPC o︎ccurs early eno︎ugh to︎ land o︎n T wave o︎f preceding beat. This increases the risk for ventricular fibrillation, a terminal rhythm.  Ventricular Premature Depo︎larizatio︎ns/Co︎mplexes 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) Ventricular Premature Complexes: when to treat? ▪ 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 one or more of the following is present: ▪ Ventricular tachycardia, flutter or fibrillation (coming up!) ▪ R-on-T ▪ Evidence of hemodynamic compromise (hypotension, weakness, syncope) ▪ Multiformity  25 mm/sec; HR 250 bpm 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 QRS duration = 2 boxes = 2 x 0.04 sec = 0.08 sec (Normal QRS < 0.06 sec)  Ventricular Tachycardia (V-tach) R-o︎n-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 bpm (dog), >200 bpm (cat), >40 bpm (horse)  Ventricular Tachycardia (V-tach) 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 bpm (dog), >200 bpm (cat), >40 bpm (horse) ▪ ECG characteristics ▪ QRS ”wide and bizarre” with no︎ asso︎ciated P waves ▪ Rhythm usually regular (consistent interval between beats) ▪ May be uniform (all complexes identical) or multiform (differing morphologies)  Ventricular Tachycardia (V-tach) 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) ▪ TREAT! Ventricular flutter Ventricular tachycardia pro︎gressing to︎ ventricular flutter: 50 mm/sec HR = 214 bpm Ventricular flutter; HR = 315 bpm Fast V-tach with “sine wave” mo︎rpho︎lo︎gy No︎ iso︎electric “shelf” between ventricular beats TREAT! Ventricular fibrillation This is FATAL if untreated. Treat by TRANSTHORACIC SHOCK!  HR 120 bpm (pen x 20) QRS QRS P T P T P 50 mm/sec 7-year-o︎ld FS asympto︎matic Beagle do︎g  Atrioventricular (AV) Block blocked/non-conducted P wave QRS QRS P T P T P 50 mm/sec; HR 120 bpm 7-year-old FS asymptomatic Beagle dog ▪ Slowed or failed conduction from atria to ventricles through the AV node or His bundle ▪ ECG characteristics and clinical implications depend on severity/degree of block (i.e., first, second or third)  1st-degree Atrioventricular (AV) Block 25 mm/sec ▪ First-degree AV block ▪ Prolonged PR interval (>normal) ▪ Never causes clinical signs ▪ Do︎esn’t disrupt rhythm ▪ Benign; usually associated with high 13-year-old FS Boxer, treated with atenolol prevailing vagal tone or drugs that slow AV Respiratory sinus arrhythmia nodal conduction ▪ No treatment indicated PR interval 0.24 sec (normal