Clinical ECG: Atrial/Ventricular Arrhythmias Lecture PDF

Clinical ECG: Atrial / Ventricular Arrhythmias Scott Landman, OMS-III, Academic Medicine Scholar [email protected] Dr. Todd Cohen, Chief of Cardiology and Director of Medical Device Innovation [email protected]  Session Objectives 1. Distinguish an arrhythmia from artifact. 2. List the caus...

Clinical ECG: Atrial / Ventricular Arrhythmias Scott Landman, OMS-III, Academic Medicine Scholar [email protected] Dr. Todd Cohen, Chief of Cardiology and Director of Medical Device Innovation [email protected]  Session Objectives 1. Distinguish an arrhythmia from artifact. 2. List the causes of arrhythmias. 3. Distinguish a normal sinus rhythm from different bradyarrhythmias or tachyarrhythmias. 4. Sketch the algorithm to identify different tachyarrhythmias, identifying and creating a treatment plan along the way. First Aid (2021): 293, 294, 315, 316 Rate & Rhythm: What can go wrong? Arrhythmia= lack of normal rhythm Dysrhythmia= “doesn’t work properly” rhythm Tachyarrhythmia= fast arrhythmia Bradyarrhythmia= slow arrhythmia  Why do we care about arrhythmias? CO = SV x HR Brady Tachy Artifact Artifact occurs when something causes a disruption in monitoring. Some common causes are: ⮚AC interference - causes 60 Hz artifact ⮚Muscle contractions & tremors ⮚Respiratory artifact- patient movement - wandering baseline ⮚Loose electrode ⮚Broken lead wire Kaltura: Questions related to Objective #1  Steps in Analyzing a 12-lead ECG 1. Orient yourself Officer Ryan Reynolds Always Impresses Others 2. Calculate Rate 3. Determine Rhythm 4. Determine the Axis 5. Intervals and QRS Duration 6. “Others” ST segment & T wave Reading an ECG is a developed skill! Find the steps that work best for you and apply them in the same order for every ECG you read.  3 Mechanisms of Arrhythmias: 1.Re-entry 2.Automaticity 3.Triggered Activity Kaltura: Questions related to Objective #2 Bradyarrhythmias HR < 60 bpm Symptoms: Dizziness, Lightheadedness Palpitations, Pre-syncope Syncope Sinus Bradycardia (SB) Rate: 100 bpm Symptoms: Asymptomatic, Palpitations Shortness of breath, Fatigue Syncope, Lightheadedness Algorithm for Arrhythmias! Tachyarrhythmias Narrow QRS Regular Sinus Tachycardia Rate: > 100 bpm Rhythm: sinus tachycardia (normal p waves precede every QRS complex) Intervals: ○QRS: normal ○Conduction: P-R normal Causes: normal, physiologic response to pain, exercise, stress, infection, anemia, hyperthyroidism, dehydration or pulmonary embolism Treatment: includes identification of the underlying cause and correction. Supraventricular Tachycardia A tachycardia that originates in or depends on parts above the ventricles ○“supra” = above or earlier ○Any tachycardia that is not from the ventricles Broad description of a rhythm – there are many more precise ways to describe a rhythm (such as some of the rhythms to follow) Premature Atrial Contractions (PACs) Premature activation of the atria from an atrial site other than the sinus node Rate: normal or accelerated Rhythm: irregular ○ PAC P-waves usually have a different morphology than sinus P-waves because they originate from an ectopic pacemaker. Some can be embedded in T waves (or other places) Intervals: ○ P-R: ectopic beats may have a different P-R interval ○ QRS: usually normal Causes: occasional PACs are a normal occurrence; Occur more frequently in CHF, myocardial ischemia, COPD Normal p-waves Premature Atrial Contractions Focal Atrial Tachycardia (FAT) Regular atrial rhythm originating outside the SA node with rate >100 bpm ○ Specific atrial focus is firing – not SA node Most common location is the left atrium (63%) Rate: 150-250 bpm Rhythm: regular (p-waves almost hidden in T waves) Intervals: usually narrow QRS, normal PR Adenosine can reveal underlying atrial activity. AV Nodal Reentrant Tachycardia (AVNRT)* Most common type of paroxysmal SVT Results from a reentrant circuit at the site of the AV node → depolarizes the atrium & ventricle simultaneously Rate: 150-250 bpm Rhythm: Regular. P-waves may be retrograde or buried The mechanism involves the AV node, so it must be disabled in order to “break” the rhythm (bring back into sinus rhythm) ○ Vagal maneuvers (e.g. carotid sinus massage, coughing, Valsalva) ○ Adenosine Long-term treatment of choice is ablation.  AVNRT PAC SLOW FAST SLOW FAST pathway pathway pathway pathway Short RP Long RP Short RP Long RP HIS HIS AVNRT (cont.) AV Reentrant Tachycardia (AVRT)* This involves a reentrant circuit as well: ○ Accessory pathway: abnormal connection between the atria and ventricles. ○ Two conduction pathways: the AV node (normal) and accessory pathway Retrograde P wave seen after the QRS ○ The accessory pathway can repolarize the p- wave ○ QRS can be either normal (orthodromic) or prolonged (antidromic) – depending on the pathways Treatment is similar to AVNRT AVRT AVRT  Wolff-Parkinson-White Syndrome** Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway. In WPW the accessory pathway is often referred to as the Bundle of Kent, or AV bypass tract. WPW Syndrome: ECG features & Treatment ECG Findings ○ Shortened PR interval ○ Delta wave – slurring slow rise of initial portion of the QRS ○ QRS > 120ms (when pre-excited) ○ ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex Treatment: ○ Catheter ablation ○ Vagal Maneuvers ○ Meds: Adenosine, Verapamil, Procainamide WPW – Delta Waves Tachyarrhythmias Narrow QRS Irregular Atrial Fibrillation (A fib) Firing of multiple impulses from numerous ectopic pacemakers in the atria→ chaotic asynchronous activity in atrial tissue ○ Common location of focal origin is in LA near site of pulmonary veins Rate: ○ Atria is firing ~300-650 bpm – heart is quivering Rhythm: irregularly irregular (NO p-waves) Intervals: PR unmeasurable; usually narrow QRS Causes: a/w HTN (most common), COPD, CHF, underlying heart disease, aging, stress, infection, alcohol, thyrotoxicosis, caffeine Management Options of A-Fib Rate control = Rhythm control Rate control= Beta-blockers (Metoprolol), Calcium Channel Blockers (Diltiazem), Digoxin Rhythm control= Amiodarone, Sotalol, Flecainide Anticoagulation prevent cerebrovascular accident= Warfarin, Enoxaparin, Rivaroxaban, Apixab, or Dabigatran Emergency= Electrical Cardioversion (DCCV) “Should do the trick”: Ablation → Pulmonary vein isolation Catheter Ablation for A Fib CHA2DS2-VASc Risk Stratification CHADS2-VASc Score: 0 → “low risk” 1 → “low-mod risk”→ antiplatelet or anticoagulant ≥ 2 → “mod-high risk”→ anticoagulant Atrial Flutter Atrial flutter is a type of SVT caused by a re-entry circuit within the right atrium that transverses the cavo-tricuspid isthmus ○ The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a predictable atrial rate around 300 bpm (range 200-350) Ventricular rate is determined by the AV conduction ratio (degree of AV block) The most common AV ratio is 2:1, resulting in a ventricular rate of ~150 bpm Atrial Flutter – ECG Narrow complex tachycardia Rate: regular atrial activity at ~300 bpm, variable AV block Rhythm: Flutter waves (“saw-tooth” pattern) - II, III, aVF ○ Loss of the isoelectric baseline ○ Fixed or variable AV Block – regular or irregular Intervals: PR unmeasurable; usually a narrow QRS Atrial Flutter Management Difficult to control rate with pharmacology Anticoagulation Cardioversion if unstable Ablation of the Cavo-tricuspid isthmus ○ Lower right atrium between IVC and tricuspid valve ○ *most common site  Multifocal Atrial Tachycardia (MAT) Numerous atrial foci fire intermittently Can resemble A Fib/Flutter Rate: 100-250 bpm Rhythm: irregular (>3 different p-wave shapes) Intervals: QRS narrow, PR interval variable Cause: most common in COPD/hypoxemia, hypomagnesemia and hypokalemia Treatment: Verapamil. Treat underlying cause Multifocal Atrial Tachycardia (cont.) Tachyarrhythmias Wide QRS Premature Ventricular Contractions (PVCs) Ectopic beats that originate below the branching point of the Bundle of His Impulse is generated below AV node → wide QRS usually without preceding P-wave Causes: a/w electrolyte abnormalities, hypoxia, hyperthyroidism, catecholamines, drug toxicities; can occur in both structurally normal or abnormal heart Treat if: ○ A/w acute MI ○ Occur as couplets, bigeminy, trigeminy ○ Are multifocal, or ○ Are frequent (>6/min) or symptomatic  Monomorphic Ventricular Tachycardia Usually occurs in diseased hearts Without treatment - deteriorates into ventricular fibrillation Rhythm: p-waves are usually obscured/not present, are unrelated to the QRS complex Causes: CAD, acute MI, digitalis toxicity, CHF, ventricular aneurysms, cardiomyopathy, electrolyte abnormalities Treatment: ○ Symptomatic/Unstable: electrical cardioversion ○ Pharm: Amiodarone, Lidocaine Ventricular Fibrillation (V fib) Chaotic electrical activity from the ventricles that causes the absence of cardiac output Treatment: ○Immediate defibrillation and ACLS protocols ○Identification and treatment of the underlying cause (often ischemic e.g. acute MI) Torsades de Pointes Upward & downward deflection of QRS complexes around the baseline P-wave usually obscured if present, QRS complexes are wide, bizarre morphology Causes: drugs that prolong QT interval, MI, electrolyte imbalances (esp. hypo-Mg, hypo-K, hypo-Ca) Can progress to V Fib Treatment: ○ Synchronized cardioversion if patient unstable ○ IV Magnesium, IV Potassium ○ Overdrive pacing Kaltura: Questions related to Objective #3+4  Summary Slide Premature Atrial Contractions (PAC’s)- activation of the atria from an atrial site other than the SA node Focal Atrial Tachycardia- Single atrial myocyte (not the SA node) firing at a rate > 100 bpm AV nodal reentrant tachycardia (AVNRT)- reentrant circuit at the AV node AV reentrant tachycardia w/ accessory pathway (AVRT)- accessory pathway leads to two conduction pathways WPW- activation of the ventricles due to bypassing of the AV node via an accessory pathway (ECG delta wave) Atrial flutter- re-entry circuit within the right atrium transversing the cavo-tricuspid isthmus (ECG “saw- tooth” pattern) Atrial Fibrillation- atria are firing at 300-650 bpm originating from the pulmonary veins (no p-waves) Multifocal Atrial Tachycardia- multiple atrial myocytes firing creating three distinct p-waves Premature ventricular contraction (PVC’s)- impulse generated below the bifurcation of the His bundle Monomorphic Ventricular Tachycardia- uniform wide QRS complex Ventricular Fibrillation- minimal cardiac output, requires immediate defibrillation Torsades de Pointes- associated w/ prolonged QT interval, MI, and electrolyte imbalances (first line txt- IV Magnesium) How I would approach the lecture: 1. Distinguish an arrhythmia from artifact. a. What is an arrhythmia? b. What is artifact and what causes artifact? c. Why do we care about tachy and bradyarrhythmias? i. Can alter CO2 or oxygen demand! How I would approach the lecture: 2. List the causes of arrhythmias. a. Review an approach to a rhythm strip i. Need to know how to identify abnormalities b. 3 Mechanisms of Arrhythmias i. Re-entry= AVNRT or AVRT ii. Automaticity= meds alter rate iii. Triggered Activity= Torsades de Pointes, V- fib, V-tach etc. (emergencies) How I would approach the lecture: 3. Distinguish a normal sinus rhythm from different bradyarrhythmias or tachyarrhythmias. a. Discuss Sx, Causes & Tx of: i. Sinus Bradycardia, Sinus Tachycardia, “SVT”, PAC, FAT, AVNRT, WPW, A Fib, A Flutter, MAT, PVC, V tach, V fib, Torsade How I would approach the lecture: 4. Sketch the algorithm to identify different tachyarrhythmias, identifying and creating a treatment plan along the way. a. While we did the pathologies, we grouped them: walking through ID-ing: i. Narrow vs Wide QRS ii. Regular vs Irregular Final Slide: Questions: Scott Landman: [email protected] More exposure→ better EKG skills -ECG Lectures Mon 12-1 PM EST with Dr. Cohen via Zoom -Will be sent out to the class each week by Dr. Cohen’s Research Team Feedback on the lecture: https://comresearchdata.nyit.edu/redcap/surveys/?s=HRCY448FWYXREL4R