This document provides a summary of a training chapter on 12-lead electrocardiogram (ECG) interpretation for paramedics. It outlines objectives of being able to recognize ST-elevation myocardial infarction (STEMI) on a 12-lead ECG. It discusses identifying important ECG features and relating them to lead locations on the heart. It emphasizes localization of STEMI rather than full interpretation. The document provides guidance on criteria for identifying STEMI and practicing recognition in various lead locations on sample ECGs.
The document discusses differentiating ST elevation myocardial infarction (STEMI) from other causes of ST elevation on an electrocardiogram (ECG). It provides examples of three sample ECGs, describing ECG 1 as showing typical inferior STEMI patterns, ECG 2 as most consistent with pericarditis given its global and concave ST elevation, and ECG 3 showing minimal changes consistent with benign early repolarization. Key factors for differentiation include the magnitude, morphology, distribution of ST elevation, and comparison to previous ECGs. The document emphasizes analyzing ST elevation in the full clinical context and pursuing safe care when in doubt.
ST segment elevations can be seen in acute myocardial infarction (AMI) but also have other causes. Non-AMI causes of ST elevation include left bundle branch block, left ventricular hypertrophy, pericarditis, Brugada syndrome, and early repolarization. The morphology, distribution, and magnitude of ST elevations, as well as other ECG features, can help differentiate AMI from other causes of ST elevation. It can be challenging to diagnose AMI using ECG criteria alone, as around half of AMI cases present without typical ST elevation patterns.
A 58-year-old man presented with shortness of breath and chest pain. An ECG showed ST segment elevation consistent with pericarditis. Pericarditis is inflammation of the pericardium and can be caused by uremia in patients with chronic kidney disease. The ECG changes in acute pericarditis include diffuse concave ST elevation and upright T waves, except in leads aVR and V1 which are usually depressed. This differs from a myocardial infarction which shows more convex ST elevation and the presence of Q waves.
Atrial tachycardias can originate from different sites in the atria and have various mechanisms. Common sites include the right atrial appendage, coronary sinus ostium, and crista terminalis. Mechanisms include focal automaticity, triggered activity, microreentry, and macroreentry. Macroreentry is the most common mechanism and can involve single or double loop circuits around anatomical barriers or scar tissue. Diagnosis involves electrocardiographic localization of the origin and electrophysiological testing including pacing maneuvers to evaluate for entrainment. Catheter ablation is often curative by targeting the arrhythmia origin site or critical portions of reentrant circuits.
This document provides an overview of electrocardiography (ECG or EKG):
- The ECG is essential for diagnosing cardiac rhythm abnormalities and chest pain, and guides treatment like thrombolysis for heart attacks.
- The history of ECG development is traced from early experiments in the 1800s to William Einthoven's invention of the first clinical ECG machine in the early 1900s.
- A normal ECG shows a regular rhythm between 60-100 beats per minute, visible P waves before each QRS complex, and normal durations for the P-R interval, QRS complex, and T wave.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
1. The document discusses different types of supraventricular tachycardia including AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia (AT).
2. It provides details on electrocardiogram patterns that can help differentiate the different types of SVT. Features like retrograde P waves, RP intervals, and the effect of ventricular pacing are discussed.
3. Ablation techniques for AVNRT and AVRT are covered, including approaches for mapping the circuits and terminating arrhythmias. The importance of making an accurate diagnosis is emphasized.
This document outlines techniques for differentiating supraventricular tachycardias (SVTs). It discusses features of SVT induction and baseline tachycardia characteristics, as well as diagnostic maneuvers that can be performed during tachycardia and after termination in sinus rhythm. These include the effects of atrial and ventricular extrastimulation or pacing on SVT cycle length, VA intervals, and atrial activation sequences to help identify the mechanism as atrial tachycardia, atrioventricular nodal reentrant tachycardia, or orthodromic reentrant tachycardia using an accessory atrioventricular connection. The document provides detailed descriptions and examples of applying these diagnostic tests.
The document discusses differentiating ST elevation myocardial infarction (STEMI) from other causes of ST elevation on an electrocardiogram (ECG). It provides examples of three sample ECGs, describing ECG 1 as showing typical inferior STEMI patterns, ECG 2 as most consistent with pericarditis given its global and concave ST elevation, and ECG 3 showing minimal changes consistent with benign early repolarization. Key factors for differentiation include the magnitude, morphology, distribution of ST elevation, and comparison to previous ECGs. The document emphasizes analyzing ST elevation in the full clinical context and pursuing safe care when in doubt.
ST segment elevations can be seen in acute myocardial infarction (AMI) but also have other causes. Non-AMI causes of ST elevation include left bundle branch block, left ventricular hypertrophy, pericarditis, Brugada syndrome, and early repolarization. The morphology, distribution, and magnitude of ST elevations, as well as other ECG features, can help differentiate AMI from other causes of ST elevation. It can be challenging to diagnose AMI using ECG criteria alone, as around half of AMI cases present without typical ST elevation patterns.
A 58-year-old man presented with shortness of breath and chest pain. An ECG showed ST segment elevation consistent with pericarditis. Pericarditis is inflammation of the pericardium and can be caused by uremia in patients with chronic kidney disease. The ECG changes in acute pericarditis include diffuse concave ST elevation and upright T waves, except in leads aVR and V1 which are usually depressed. This differs from a myocardial infarction which shows more convex ST elevation and the presence of Q waves.
Atrial tachycardias can originate from different sites in the atria and have various mechanisms. Common sites include the right atrial appendage, coronary sinus ostium, and crista terminalis. Mechanisms include focal automaticity, triggered activity, microreentry, and macroreentry. Macroreentry is the most common mechanism and can involve single or double loop circuits around anatomical barriers or scar tissue. Diagnosis involves electrocardiographic localization of the origin and electrophysiological testing including pacing maneuvers to evaluate for entrainment. Catheter ablation is often curative by targeting the arrhythmia origin site or critical portions of reentrant circuits.
This document provides an overview of electrocardiography (ECG or EKG):
- The ECG is essential for diagnosing cardiac rhythm abnormalities and chest pain, and guides treatment like thrombolysis for heart attacks.
- The history of ECG development is traced from early experiments in the 1800s to William Einthoven's invention of the first clinical ECG machine in the early 1900s.
- A normal ECG shows a regular rhythm between 60-100 beats per minute, visible P waves before each QRS complex, and normal durations for the P-R interval, QRS complex, and T wave.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
1. The document discusses different types of supraventricular tachycardia including AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia (AT).
2. It provides details on electrocardiogram patterns that can help differentiate the different types of SVT. Features like retrograde P waves, RP intervals, and the effect of ventricular pacing are discussed.
3. Ablation techniques for AVNRT and AVRT are covered, including approaches for mapping the circuits and terminating arrhythmias. The importance of making an accurate diagnosis is emphasized.
This document outlines techniques for differentiating supraventricular tachycardias (SVTs). It discusses features of SVT induction and baseline tachycardia characteristics, as well as diagnostic maneuvers that can be performed during tachycardia and after termination in sinus rhythm. These include the effects of atrial and ventricular extrastimulation or pacing on SVT cycle length, VA intervals, and atrial activation sequences to help identify the mechanism as atrial tachycardia, atrioventricular nodal reentrant tachycardia, or orthodromic reentrant tachycardia using an accessory atrioventricular connection. The document provides detailed descriptions and examples of applying these diagnostic tests.
The document provides information about interpreting electrocardiograms (ECGs) from patients with pacemakers. It discusses various pacemaker modes, assessing capture and sensing functions, underlying cardiac rhythms, and what follow up actions may be needed based on the ECG patterns. Examples are presented to illustrate dual chamber pacing, assessing atrial and ventricular sensing, pacemaker-mediated tachycardia, undersensing, failure of capture, and magnet mode behavior.
This document discusses peripheral pulmonary artery stenosis, including its description, associated conditions, classification, clinical features, diagnosis using imaging modalities like echocardiography and angiography, and treatment options like balloon angioplasty. Peripheral pulmonary artery stenosis can involve the main pulmonary artery or its branches and is present in 2-3% of congenital heart disease cases. Diagnosis relies on cardiac catheterization and angiography to determine severity and anatomy. Balloon angioplasty is an option for treating moderate or severe stenosis when surgery is difficult.
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
This document discusses various types of tachyarrhythmias categorized by their anatomical location and electrophysiological mechanisms. It describes atrial arrhythmias including sinus tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. It also discusses atrioventricular node reentrant tachycardia, atrioventricular reentrant tachycardia, junctional tachycardia, and ventricular arrhythmias including monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation. Key features and mechanisms of each type are outlined to aid in diagnosis and classification.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
This document discusses ECG patterns in congenital heart disease. It begins by outlining the significance of ECG in diagnosing congenital heart defects. It then provides an overview of normal ECG changes in children and how they evolve over time as hemodynamics change. Next, it describes how ECG can help identify situs and ventricular position. It then discusses the characteristic ECG patterns seen in common acyanotic defects like atrial septal defects and ventricular septal defects. It also covers cyanotic defects like transposition of the great arteries. The document provides detailed information on ECG features, associated conditions, complications and evolution over time for many different congenital heart defects.
1. This document provides an overview of a training course on complex supraventricular tachycardia (SVT) differentiation. It discusses various SVT etiologies and electrocardiogram patterns.
2. Mechanisms of SVT discussed include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia (AT). The document also reviews electrophysiology study findings that help differentiate the mechanisms.
3. Case examples are presented to demonstrate electrophysiology study techniques for SVT diagnosis and ablation, including ventricular overdrive pacing, ventricular extrastimuli, and induction protocols.
This document discusses wide complex tachycardia (WCT), which is ventricular in origin 80% of the time. In patients with structural heart disease, 95% of WCT is ventricular tachycardia (VT). VT can be life-threatening and cause sudden death or tachycardia-induced cardiomyopathy. The document describes types of VT based on morphology and duration, symptoms of VT, features that appear on ECGs during VT like abnormal wide QRS complexes and AV dissociation, and examples of patients presenting with potential VT.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
This document discusses sudden cardiac arrest and death (SCD). It defines SCD and provides data on its prevalence. It outlines various risk factors for SCD including personal or family history of heart disease, smoking, hypertension, obesity, and more. The document discusses ECG predictors of SCD and various cardiac conditions that can cause SCD like coronary artery disease, cardiomyopathies, channelopathies and more. It also outlines the management of sudden cardiac arrest including assessing rhythm and providing defibrillation and CPR if needed. Prevention strategies discussed include antiarrhythmic drugs, ICD implantation, catheter ablation and surgery.
ECG-T wave inversion , Dr. Malala Rajapaksha ,Cardiology unit,General Hospit...malala720
This is a presentation on “What are the deferential Diagnosis a clinician think of when the clinician encounter T inversions in an ECG of a patient”. This will be help full in day today clinical practice and also in academic purposes.
This document discusses electrophysiological diagnosis and management of atrioventricular reentrant tachycardia (AVRT). It describes the historical discovery of Wolff-Parkinson-White syndrome and mechanisms of tachyarrhythmias including reentry. Characteristics of orthodromic and antidromic AVRT are provided along with techniques for evaluating accessory pathways including baseline observations, programmed stimulation, and catheter ablation. Precise localization of accessory pathways is important for successful ablation.
Myocardial Protection in Pediatric Cardiac SurgerySlide Sharer
1. The document discusses various methods of myocardial protection that have been used in pediatric cardiac surgery over time, including potassium-induced cardiac arrest, hypothermia, and cardioplegic arrest.
2. Cardioplegic arrest techniques have evolved from early pharmacological agents to modern approaches using blood or crystalloid cardioplegia solutions along with hypothermia. Debate continues around the optimal cardioplegia type and delivery method.
3. The immature pediatric myocardium has physiological differences from the adult heart, including a primary reliance on glucose metabolism rather than fatty acids, that require consideration in myocardial protection strategies.
This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. Evaluation involves analyzing the ECG for P wave presence and morphology, QRS duration and morphology, and the relationship between P waves and QRS complexes. Treatment involves vagal maneuvers, adenosine, calcium channel blockers, beta blockers
This document discusses the current management of cardiogenic shock. It defines cardiogenic shock and describes its causes, predictors of mortality, and pathophysiology. Treatment involves hemodynamic support, volume management, inotropic drugs, and early revascularization, which significantly reduces mortality. Mechanical circulatory support devices like IABP, Tandem Heart, Impella, and ECMO can further improve hemodynamics and outcomes when used as adjuncts to optimal medical therapy. Timing of revascularization is critical, with survival benefits seen for up to 48 hours after myocardial infarction onset. Special considerations are discussed for managing shock in the elderly, from mechanical causes, and with specific device therapies.
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mpdrranjithmp
This document discusses the mechanisms of ventricular tachycardia (VT), including disorders of impulse formation (enhanced automaticity and triggered activity) and disorders of impulse conduction (re-entry). Re-entry is the most common mechanism underlying VT associated with healed myocardial infarction. The surface ECG can provide clues about the location of the re-entry circuit. Treatment depends on whether the VT is tolerated or not, with cardioversion used for hemodynamically unstable VT and medications or an ICD for recurrent VT.
[Int. med] jugular venous pressure from SIMS LahoreMuhammad Ahmad
The jugular venous pressure (JVP) provides an indirect measure of central venous pressure. Normally the JVP is 6-8 cm H2O above the right atrium. Deviations from this range indicate hypovolemia or impaired cardiac filling. The JVP is examined by observing pulsations in the right internal jugular vein and measuring the vertical distance between the pulsation and sternal angle. An elevated JVP indicates venous hypertension from conditions like heart failure. The JVP waveform has an a wave from atrial contraction and a v wave from venous filling. Abnormalities in the waves can indicate conditions like heart block or tricuspid regurgitation. An elevated JVP is a sign of right-sided heart
The 12-lead ECG is a diagnostic test that helps identify conditions like acute coronary syndrome and myocardial infarction. Obtaining a 12-lead ECG in the field is important to identify ST elevations that could indicate a heart attack and speed up treatment times. The placement of the ECG leads and the patterns in the complexes can provide clues to determine the type and location of any heart issues. It is important for paramedics to become proficient in performing and interpreting 12-lead ECGs to help ensure the best outcomes for patients experiencing potential cardiac events.
The document provides information about interpreting electrocardiograms (ECGs) from patients with pacemakers. It discusses various pacemaker modes, assessing capture and sensing functions, underlying cardiac rhythms, and what follow up actions may be needed based on the ECG patterns. Examples are presented to illustrate dual chamber pacing, assessing atrial and ventricular sensing, pacemaker-mediated tachycardia, undersensing, failure of capture, and magnet mode behavior.
This document discusses peripheral pulmonary artery stenosis, including its description, associated conditions, classification, clinical features, diagnosis using imaging modalities like echocardiography and angiography, and treatment options like balloon angioplasty. Peripheral pulmonary artery stenosis can involve the main pulmonary artery or its branches and is present in 2-3% of congenital heart disease cases. Diagnosis relies on cardiac catheterization and angiography to determine severity and anatomy. Balloon angioplasty is an option for treating moderate or severe stenosis when surgery is difficult.
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
This document discusses various types of tachyarrhythmias categorized by their anatomical location and electrophysiological mechanisms. It describes atrial arrhythmias including sinus tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. It also discusses atrioventricular node reentrant tachycardia, atrioventricular reentrant tachycardia, junctional tachycardia, and ventricular arrhythmias including monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation. Key features and mechanisms of each type are outlined to aid in diagnosis and classification.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
This document discusses ECG patterns in congenital heart disease. It begins by outlining the significance of ECG in diagnosing congenital heart defects. It then provides an overview of normal ECG changes in children and how they evolve over time as hemodynamics change. Next, it describes how ECG can help identify situs and ventricular position. It then discusses the characteristic ECG patterns seen in common acyanotic defects like atrial septal defects and ventricular septal defects. It also covers cyanotic defects like transposition of the great arteries. The document provides detailed information on ECG features, associated conditions, complications and evolution over time for many different congenital heart defects.
1. This document provides an overview of a training course on complex supraventricular tachycardia (SVT) differentiation. It discusses various SVT etiologies and electrocardiogram patterns.
2. Mechanisms of SVT discussed include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia (AT). The document also reviews electrophysiology study findings that help differentiate the mechanisms.
3. Case examples are presented to demonstrate electrophysiology study techniques for SVT diagnosis and ablation, including ventricular overdrive pacing, ventricular extrastimuli, and induction protocols.
This document discusses wide complex tachycardia (WCT), which is ventricular in origin 80% of the time. In patients with structural heart disease, 95% of WCT is ventricular tachycardia (VT). VT can be life-threatening and cause sudden death or tachycardia-induced cardiomyopathy. The document describes types of VT based on morphology and duration, symptoms of VT, features that appear on ECGs during VT like abnormal wide QRS complexes and AV dissociation, and examples of patients presenting with potential VT.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
This document discusses sudden cardiac arrest and death (SCD). It defines SCD and provides data on its prevalence. It outlines various risk factors for SCD including personal or family history of heart disease, smoking, hypertension, obesity, and more. The document discusses ECG predictors of SCD and various cardiac conditions that can cause SCD like coronary artery disease, cardiomyopathies, channelopathies and more. It also outlines the management of sudden cardiac arrest including assessing rhythm and providing defibrillation and CPR if needed. Prevention strategies discussed include antiarrhythmic drugs, ICD implantation, catheter ablation and surgery.
ECG-T wave inversion , Dr. Malala Rajapaksha ,Cardiology unit,General Hospit...malala720
This is a presentation on “What are the deferential Diagnosis a clinician think of when the clinician encounter T inversions in an ECG of a patient”. This will be help full in day today clinical practice and also in academic purposes.
This document discusses electrophysiological diagnosis and management of atrioventricular reentrant tachycardia (AVRT). It describes the historical discovery of Wolff-Parkinson-White syndrome and mechanisms of tachyarrhythmias including reentry. Characteristics of orthodromic and antidromic AVRT are provided along with techniques for evaluating accessory pathways including baseline observations, programmed stimulation, and catheter ablation. Precise localization of accessory pathways is important for successful ablation.
Myocardial Protection in Pediatric Cardiac SurgerySlide Sharer
1. The document discusses various methods of myocardial protection that have been used in pediatric cardiac surgery over time, including potassium-induced cardiac arrest, hypothermia, and cardioplegic arrest.
2. Cardioplegic arrest techniques have evolved from early pharmacological agents to modern approaches using blood or crystalloid cardioplegia solutions along with hypothermia. Debate continues around the optimal cardioplegia type and delivery method.
3. The immature pediatric myocardium has physiological differences from the adult heart, including a primary reliance on glucose metabolism rather than fatty acids, that require consideration in myocardial protection strategies.
This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. Evaluation involves analyzing the ECG for P wave presence and morphology, QRS duration and morphology, and the relationship between P waves and QRS complexes. Treatment involves vagal maneuvers, adenosine, calcium channel blockers, beta blockers
This document discusses the current management of cardiogenic shock. It defines cardiogenic shock and describes its causes, predictors of mortality, and pathophysiology. Treatment involves hemodynamic support, volume management, inotropic drugs, and early revascularization, which significantly reduces mortality. Mechanical circulatory support devices like IABP, Tandem Heart, Impella, and ECMO can further improve hemodynamics and outcomes when used as adjuncts to optimal medical therapy. Timing of revascularization is critical, with survival benefits seen for up to 48 hours after myocardial infarction onset. Special considerations are discussed for managing shock in the elderly, from mechanical causes, and with specific device therapies.
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mpdrranjithmp
This document discusses the mechanisms of ventricular tachycardia (VT), including disorders of impulse formation (enhanced automaticity and triggered activity) and disorders of impulse conduction (re-entry). Re-entry is the most common mechanism underlying VT associated with healed myocardial infarction. The surface ECG can provide clues about the location of the re-entry circuit. Treatment depends on whether the VT is tolerated or not, with cardioversion used for hemodynamically unstable VT and medications or an ICD for recurrent VT.
[Int. med] jugular venous pressure from SIMS LahoreMuhammad Ahmad
The jugular venous pressure (JVP) provides an indirect measure of central venous pressure. Normally the JVP is 6-8 cm H2O above the right atrium. Deviations from this range indicate hypovolemia or impaired cardiac filling. The JVP is examined by observing pulsations in the right internal jugular vein and measuring the vertical distance between the pulsation and sternal angle. An elevated JVP indicates venous hypertension from conditions like heart failure. The JVP waveform has an a wave from atrial contraction and a v wave from venous filling. Abnormalities in the waves can indicate conditions like heart block or tricuspid regurgitation. An elevated JVP is a sign of right-sided heart
The 12-lead ECG is a diagnostic test that helps identify conditions like acute coronary syndrome and myocardial infarction. Obtaining a 12-lead ECG in the field is important to identify ST elevations that could indicate a heart attack and speed up treatment times. The placement of the ECG leads and the patterns in the complexes can provide clues to determine the type and location of any heart issues. It is important for paramedics to become proficient in performing and interpreting 12-lead ECGs to help ensure the best outcomes for patients experiencing potential cardiac events.
This document outlines a STEMI recognition class consisting of 6 modules: 1) Introduction to 12-lead EKGs, 2) Identifying the J point, 3) Identifying ST elevation and depression, 4) Lead views and what areas of the heart each lead represents, 5) Practice exercises, and 6) Putting it all together to recognize STEMIs by identifying ST elevation in two or more contiguous leads. The class teaches students to systematically analyze each lead one by one to check for ST elevation compared to the TP segment baseline in order to diagnose STEMIs.
The document provides information about electrocardiography (ECG) including its history, how an ECG machine works, how to perform an ECG, ECG waveform interpretation, and common cardiac rhythms and abnormalities. It discusses key aspects of an ECG such as rate, rhythm, cardiac axis, P waves, PR interval, and common rhythms including normal sinus rhythm, atrial fibrillation, ventricular tachycardia, and more.
This document provides an overview of ECG interpretation, including conduction pathways, a systematic method of interpretation, and common abnormalities seen in critical care. It discusses supraventricular and ventricular arrhythmias, bundle branch blocks, heart block, and life-threatening arrhythmias such as ventricular tachycardia, ventricular fibrillation, and asystole. It also covers the basics of 12-lead ECG interpretation including lead placement and axis.
The document discusses the electrocardiogram (ECG), which shows the electrical pattern generated by the heart as it activates from the atria to the ventricles. The ECG uses leads to provide a 3D view of the direction of depolarization. The conduction system of the heart includes the sinoatrial node, AV node, bundle of His, bundle branches, and Purkinje fibers. The normal ECG shows the P wave, QRS complex, and T wave representing atrial depolarization, ventricular depolarization, and ventricular repolarization, respectively. The positions of the leads determine which part of the heart is visualized on the ECG.
Chapter 5 - Making Sense of the 12 Leadryanhall911
This document is a chapter from the Ontario Base Hospital Group about interpreting 12-lead electrocardiograms (ECGs). It discusses the standard ECG printout format and how it relates to time. It also describes the benefits and limitations of machine analysis, how to locate the isoelectric line for voltage measurements, and how to validate a 12-lead ECG by checking for normal wave progression and looking for signs of lead reversals. The overall aim is to help acute care providers accurately interpret ECGs.
Stress tests use physical or pharmacological stress to detect coronary artery disease. Exercise treadmill testing is commonly used but has limitations. Myocardial perfusion imaging and stress echocardiography can detect ischemia through abnormal perfusion or wall motion changes during stress. The choice of stress test depends on the patient's clinical characteristics and contraindications to certain stress modalities.
Abstract Interpretation meets model checking near the 1000000 LOC mark: Findi...Peter Breuer
Slides for presentation on "Abstract Interpretation meets model checking near the 1000000 LOC mark" at 5th International Workshop on Automated Verification of Infinite-State Systems (AVIS'06), Apr 1, 2006. A preprint of the full paper is available at http://www.academia.edu/2494187/Abstract_Interpretation_meets_Model_Checking_near_the_10_6_LOC_mark .
A Question Of Interpretation: the role of archivists in an online ageAmanda Hill
This document summarizes the changing role of archivists in the digital age. Technology and user expectations have changed the way archivists provide access to archival materials. Archivists are no longer gatekeepers as users can now find archival materials online through search engines and platforms like Archives Hub. Archivists must adapt by improving online finding aids, using less jargon, and better understanding different types of online users to ensure valued archival materials remain accessible and interpreted for new audiences.
This document summarizes a port container supply chain project aimed at improving forecast accuracy, identifying commodity routes, and constructing an integrated planning model. The project involves 7 key stages: 1) mapping stakeholders and interactions, 2) illustrating import/export hotspots, 3) generating rolling commodity forecasts, 4) developing an integrated constraint model, 5) integrating the model with financial forecasts, 6) participating in benchmarking, and 7) publishing a monthly dashboard report. The goal is to provide management visibility into potential supply chain issues and identify constraint points to improve the overall port supply chain.
Läkaren Martin Fahlén tar upp några exempel på sjukdomar och besvär som kan komma från geologiska ursprung och berättar på ett intressant sätt om ämnet i allmänhet.
This document provides information on public speaking, specifically introductions, conclusions, and outlining a speech.
The introduction should capture attention, give reason to listen, and indicate the main idea. Methods to get attention include humor, startling statements, questions, and brief stories.
The conclusion is important to achieve the speech's purpose and signal the end. It should restate the central idea, summarize main points, or end with a rhetorical question or vision of the future.
An outline organizes the introduction, body, and conclusion into a clear, sentence-form structure. It details the main points, subpoints, and supporting materials to check flow and prepare note cards. Outlining provides a framework for an effective
1. The document discusses ECG intervals and waveforms that can aid in medical diagnoses. It describes the normal ranges and clinical significance of intervals like the PR and QT intervals.
2. Key ECG patterns are summarized that indicate normal sinus rhythm as well as various arrhythmias like atrial fibrillation, supraventricular tachycardia, and heart blocks.
3. Abnormal QRS complexes, ST segments, T waves, and other waveform changes associated with conditions like pericarditis, ischemia, and hypertrophy are outlined.
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This document provides information about introductions and conclusions in public speaking. It discusses 10 ways to begin an introduction, including using humor, startling statements, rhetorical questions, or brief stories. It also lists 6 ways to conclude a speech, such as restating the central idea, summarizing main ideas, or issuing a call to action. The document then provides an outline for a sample speech on the benefits of walking, with the introduction citing a quote on walking being the best medicine and stating the central idea that walking strengthens both the heart and mind.
Health service impact from mass-gatherings: A systematic literature reviewJamie Ranse
Ranse J, Hutton A, Keene T, Lenson S, Luther M, Bost N, Johnston A, Crilly J, Cannon M, Jones N, Hayes C, Burke B. (2016) Health service impact from mass-gatherings: A systematic literature review; paper presented at the 14th International Conference for Emergency Nurses. Alice Springs, Australia. 20th October.
An electrocardiogram (ECG or EKG) records the electrical activity of the heart. It is a painless test that provides important information about heart function and any problems with heart rhythm or electrical conduction. The ECG traces the heart's electrical signals as waves on paper or a computer screen. Abnormal wave patterns or intervals can indicate conditions like arrhythmias, heart attacks, or damage to the heart muscle. The ECG is a very commonly used test that provides valuable data to diagnose cardiac issues.
This document provides an overview of electrocardiography (ECG) and ECG interpretation. It discusses the conduction system of the heart and how ECG works to record and display the heart's electrical activity. A systematic 8-step approach to ECG interpretation is outlined, examining rate, rhythm, intervals, waves, segments, and arriving at an overall interpretation. Common ECG patterns for myocardial ischemia, injury, and infarction are reviewed.
This document provides an introduction to prehospital 12-lead ECGs. It discusses how acquiring a 12-lead ECG in the field can help expedite reperfusion treatment for ST-elevation myocardial infarction patients by allowing for earlier diagnosis. Faster reperfusion therapy is important for reducing mortality, as death of heart muscle tissue occurs beyond the site of coronary artery blockage. The document reviews lead placement and how to interpret the 12-lead ECG to identify the location of any heart attack.
This document provides guidance on acquiring a 12-lead electrocardiogram (ECG). It describes the goals of acquisition as being clear, accurate and fast ECGs without increasing scene time. Placement of the 10 chest and limb leads is outlined in detail. Sources of artifact are discussed and remedies provided, such as preparing the skin, limiting patient movement and cable movement, and avoiding electromagnetic interference. Maintaining patient dignity during chest lead placement is also addressed.
Chapter 10 - 12 lead Interpretation - Part 2ryanhall911
This document provides a 3-sentence summary of a chapter on 12-lead ECG interpretation from an Ontario Base Hospital Group training manual:
The chapter reviews key concepts for interpreting 12-lead ECGs in acute coronary syndrome patients, including ST segment depression, T-wave inversion, Q-waves, reciprocal changes, and the evolution of ECG patterns over time during a myocardial infarction. It emphasizes that while ST elevation has high specificity for STEMI, a normal ECG does not rule out AMI since not all AMIs exhibit STE and early AMIs may not show changes yet. The document aims to help emergency responders properly recognize and interpret 12-lead ECG findings for acute myocardial infarction.
The document discusses 12-lead EKG interpretation for emergency providers, noting that while technology is advancing in EMS, many providers lack proficiency in 12-lead interpretation because courses often teach unnecessary information. It emphasizes the importance of recognizing serious rhythms like VF and VT and interpreting the rhythm strip first before assessing the 12-lead, and of understanding the concept of grouped leads which relate directly to cardiac anatomy.
This document provides an overview of performing and interpreting electrocardiograms (ECGs). It outlines the objectives of understanding ECGs, including defining an ECG, performing one, and interpreting various cardiac pathologies. The document explains that an ECG is a tracing of the heart's electrical activity and describes the process for recording one, including electrode placement and the cardiac conduction system. It also provides a high-level overview of the typical waves, segments and intervals seen on an ECG tracing.
This document provides an overview of performing and interpreting electrocardiograms (ECGs). It outlines the objectives of understanding ECGs, including defining an ECG, performing one, and interpreting various cardiac pathologies. The document explains that an ECG is a tracing of the heart's electrical activity and describes the process for recording one, including electrode placement and the cardiac conduction system. It also provides a high-level overview of the typical waves, segments and intervals seen on an ECG tracing and how the different leads view the heart.
This document provides an overview of acute coronary syndromes (ACS) for paramedics. It begins by defining ACS and outlining the pathophysiology, including plaque rupture, thrombus formation, and vasoconstriction as the three initiating events. It then describes the timeline from ischemia to injury to infarction. The document details the three types of ACS (unstable angina, non-ST-elevation MI, and ST-elevation MI) and reviews anatomy of the coronary arteries. Finally, it outlines treatment for ACS, including oxygen, aspirin, nitroglycerin, IV access if indicated, and 12-lead ECG acquisition. The goal is rapid recognition and treatment of patients experiencing sudden myocardial ischemia
This document provides an overview of acute coronary syndromes (ACS) for paramedics. It begins by defining ACS and outlining the pathophysiology, including plaque rupture, thrombus formation, and vasoconstriction as the three initiating events. It then describes the timeline from ischemia to injury to infarction. The document details the three types of ACS presentations: classic chest pain, atypical chest pain, and ischemic equivalents. It concludes by outlining the general therapy paramedics should provide for ACS patients, including oxygen, vital signs, aspirin, nitroglycerin, IV access if indicated, and 12-lead ECG acquisition.
This document discusses how to diagnose an acute myocardial infarction (MI) using a 12-lead electrocardiogram (ECG). It explains that an MI is diagnosed by looking for ST segment elevation in certain leads that view different areas of the heart. Specifically, it states that ST elevation in leads V1-V4 indicates an anterior wall MI, leads II, III, and aVF indicate an inferior wall MI, and leads I, aVL, and V5-V6 indicate a lateral wall MI. The document uses examples of 12-lead ECGs to illustrate how to determine if a patient is experiencing an anterior, inferior, or anterolateral MI.
This document discusses the challenges in differentiating between ST elevation myocardial infarction (STEMI) and pericarditis based on electrocardiogram (ECG) findings. While pericarditis is classically taught to present with diffuse ST elevation and PR segment depression, in reality the findings can be more localized. STEMI can also occasionally present with concave ST elevation. The document provides factors that favor STEMI over pericarditis, including ST depression beyond leads aVR and V1, convex or horizontal ST elevation, and greater ST elevation in lead III than II. It emphasizes getting serial ECGs when the diagnosis is unclear and discusses an example where PR depression occurred due to atrial injury in the setting of acute
This document introduces a standardized method for electrocardiogram (ECG) interpretation. It begins by dedicating the document to Dr. Alan E. Lindsay, a master teacher of electrocardiography. It then outlines a 6 step method for ECG interpretation: 1) Measurements, 2) Rhythm analysis, 3) Conduction analysis, 4) Wave analysis, 5) Hypertrophy analysis, and 6) Miscellaneous abnormalities analysis. The document provides background information on the components of a 12-lead ECG and emphasizes following a systematic approach to avoid missing important abnormalities.
This document provides an introduction to electrocardiogram (ECG) interpretation. It outlines a standardized 6-step method for analyzing ECGs, including measurements, rhythm analysis, conduction analysis, waveform description, interpretation, and comparison to previous ECGs. The method emphasizes a systematic approach to avoid missing abnormalities. The document also reviews ECG waves, intervals, lead placements, and how to measure the frontal plane QRS axis.
This document provides an overview of 12-lead ECG interpretation for EMS professionals. It reviews cardiac anatomy and the relationship between anatomical structures and the 12 leads. It describes the components of the 12-lead ECG device and format. Key waveform components like the QRS complex, ST segment, and T wave are defined. The document explains how the 12 leads are grouped and relate to different views and walls of the heart, such as the inferior, lateral, anterior, and septal walls. Interpretation of ST segment elevation is discussed as it relates to recognizing acute myocardial infarction.
This document provides an overview of essential 12-lead ECG interpretation for recognizing acute myocardial infarction (AMI). It reviews the goals of recognizing and localizing AMI on ECGs and becoming comfortable with 12-lead interpretation. Key points covered include identifying ST segment elevation and reciprocal changes, understanding lead views of different cardiac walls, and recognizing that while ST elevation suggests AMI, other conditions can also cause ST elevation and a normal ECG does not rule out AMI. The overall goal is to understand what and where to look for on 12-lead ECGs to recognize AMI.
12 lead introduction review of the basicsHarvey Conner
The 12-lead ECG provides 12 pictures of the heart that can be interpreted in under 60 seconds. There are 3 limb leads, 3 augmented limb leads, and 6 precordial leads that each represent a different view of the heart. Understanding the vector, or direction of electrical flow, of each lead helps identify abnormalities in cardiac depolarization. The mean QRS axis can be determined from leads I, II, and III and indicates the quadrant of cardiac electrical activity. Interpreting 12-lead ECGs involves recognizing common patterns that indicate conditions like myocardial infarction.
This document provides an overview of diagnosing myocardial infarction (MI) using electrocardiograms (ECGs). It discusses that an MI is best diagnosed using a 12-lead ECG rather than just a rhythm strip. The 12-lead ECG views the heart from 12 angles and can identify ST elevation in different regions to locate the MI. Anterior MIs involve leads V1-V4, lateral MIs involve leads I, aVL, V5-V6, and inferior MIs involve leads II, III, and aVF. The document walks through examples of anterior, lateral, inferior, and anterolateral MIs.
This document provides an overview of using electrocardiograms (ECGs) to diagnose acute myocardial infarction (AMI). It discusses how the 12-lead ECG can identify ST elevation in different regions of the heart to determine if the AMI is anterior, lateral, or inferior. Specifically, anterior AMIs show ST elevation in leads V1-V4, lateral AMIs in leads I, aVL, and V5-V6, and inferior AMIs in leads II, III, and aVF. The document aims to teach learners to recognize ST elevation patterns associated with different AMI locations.
The document discusses principles of electrocardiography (ECG). It explains that an ECG complex consists of a PQRST waveform. The P wave indicates atrial depolarization while the QRS wave is produced by ventricular depolarization. It provides a brief history of ECG, noting that Willem Einthoven developed the bipolar triaxial lead system still used today. The document also lists common indications for ECG, such as arrhythmias, shock, or murmurs. It discusses the normal cardiac conduction system and rules for interpreting the polarity of deflections in ECG complexes.
This document provides an overview of electrocardiography (ECG) and how to perform and interpret an ECG. It defines an ECG as a tracing of the heart's electrical activity. It describes how to properly perform an ECG, including electrode placement and recording the trace. Basic cardiac electrophysiology and the components of the ECG waveform are explained. The document outlines how to systematically interpret an ECG, including checking patient details, calibration, rate, rhythm, axis, and waveform components in each lead. Pathologies that can be identified on ECG such as MI, AF, and various conduction abnormalities are also listed.
Similar to Chapter 6 - Introduction to 12 Lead Interpretation (20)
The facial nerve, also known as cranial nerve VII, is one of the 12 cranial nerves originating from the brain. It's a mixed nerve, meaning it contains both sensory and motor fibres, and it plays a crucial role in controlling various facial muscles, as well as conveying sensory information from the taste buds on the anterior two-thirds of the tongue.
Fit to Fly PCR Covid Testing at our Clinic Near YouNX Healthcare
A Fit-to-Fly PCR Test is a crucial service for travelers needing to meet the entry requirements of various countries or airlines. This test involves a polymerase chain reaction (PCR) test for COVID-19, which is considered the gold standard for detecting active infections. At our travel clinic in Leeds, we offer fast and reliable Fit to Fly PCR testing, providing you with an official certificate verifying your negative COVID-19 status. Our process is designed for convenience and accuracy, with quick turnaround times to ensure you receive your results and certificate in time for your departure. Trust our professional and experienced medical team to help you travel safely and compliantly, giving you peace of mind for your journey.www.nxhealthcare.co.uk
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This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is a summary of Pneumothorax:
Pneumothorax, also known as a collapsed lung, is a condition that occurs when air leaks into the space between the lung and chest wall. This air buildup puts pressure on the lung, preventing it from expanding fully when you breathe. A pneumothorax can cause a complete or partial collapse of the lung.
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Chapter 6 - Introduction to 12 Lead Interpretation
1. ONTARIO
BASE HOSPITAL GROUP
Chapter 6
for 12 Lead Training
-Introduction to 12 Lead Interpretation-
Ontario Base Hospital Group
Education Subcommittee
2008
TIME IS
MUSCLE
2. Introduction to 12 Lead
OBHG Education Subcommittee
Interpretation
REVIEWERS/CONTRIBUTORS
Neil Freckleton, AEMCA, ACP
Hamilton Base Hospital
Jim Scott, AEMCA, PCP
Sault Area Hospital
Ed Ouston, AEMCA, ACP
Ottawa Base Hospital
Laura McCleary, AEMCA, ACP
SOCPC
Tim Dodd, AEMCA, ACP
Hamilton Base Hospital
Dr. Rick Verbeek, Medical Director
AUTHOR
Greg Soto, BEd, BA, ACP
Niagara Base Hospital
2008 Ontario Base Hospital Group SOCPC
3. Chapter 6 - Objectives
Recognize the usefulness of ECG data provided
by computerized 12 Lead ECG
Identify important features of ECG such as Q, R,
S, T waves and relate to 12 Lead interpretation
Find J-points and compare to TP segments
Recognize ST-elevation and relate to clinical
significance
Become comfortable with recognizing and
locating AMI on 12 Lead ECG
Practice a bit of 12 Lead interpretation
OBHG Education Subcommittee
4. 12 Lead Interpretation
Interpretation vs. STEMI Recognition
It is important to note that upon
completion of this training, it is not
expected that paramedics will be
“interpreting” a 12 Lead but rather
recognizing STEMI patients
OBHG Education Subcommittee
5. Learning 12 Lead ECG
OBHG Education Subcommittee
Interpretation
Common Paramedic responses prior to
learning 12 Lead ECG Interpretation:
I can’t interpret a 12 Lead ECG like a
Cardiologist!
Are you kidding me?
Common Paramedic responses after learning
12 Lead ECG Interpretation:
Hey – that wasn’t as hard as I thought it
would be!
6. Essential Interpretation
OBHG Education Subcommittee
Goals
Recognize and localize
AMI on the ECG
Feel comfortable with 12
Lead interpretation
18. OBHG Education Subcommittee
12-Lead ECG
AMI recognition
Two things to know
What to look for
Where to look
Local medical oversight will determine the criteria used
to identify a STEMI patient. All stakeholders must be
consulted to determine what criteria should be utilized
in a given centre.
19. OBHG Education Subcommittee
What to look for
Example - ST segment elevation
One millimetre or more (one small
box) in limb leads
Two millimetres or more (two small
boxes) in chest leads
Present in two anatomically
contiguous leads
20. OBHG Education Subcommittee
Contiguous Leads
Limb leads that “look” at the same area
of the heart
OR
Numerically consecutive chest leads
21. OBHG Education Subcommittee
Contiguous Leads
Inferior wall: II, III, avF
Lateral wall: I, aVL, V5, V6
Septum: V1 and V2
Anterior wall: V3 and V4
Posterior wall: V7, V8, V9
(leads placed on the patient’s back 5th
intercostal space creating a 15 lead EKG)
40. OBHG Education Subcommittee
AMI Localization
AAnntteerriioorr:: VV33,, VV44
SSeeppttaall:: VV11,, VV22
IInnffeerriioorr:: IIII,, IIIIII,, AAVVFF
LLaatteerraall:: II,, AAVVLL,, VV55,, VV66
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
41. OBHG Education Subcommittee
AMI Recognition
I Lateral
II Inferior
III Inferior
aVR
aVL Lateral
V1 Septal
aVF Inferior
V2 Septal
V3 Anterior
V4 Anterior
V5 Lateral
V6 Lateral
42. OBHG Education Subcommittee
AMI Recognition
Know what to look for
ST elevation
> 1mm in limb leads
> 2mm chest leads
Two contiguous leads
Know where you are looking
You will soon have this memorized
43. Mnemonic for Location
Rhyme, phrase or device for remembering
something
“LII – LI – ASS (backwards) – ALL”
L = I (Lateral)
I = II (Inferior)
I = III (Inferior)
L = aVL (Lateral)
I = aVF (Inferior)
S = V1 (Septal)
S = V2 (Septal)
A = V3 (Anterior)
A = V4 (Anterior)
L = V5 (Lateral)
L = V6 (Lateral)
OBHG Education Subcommittee
44. Using mnemonic on ECG
You may want to write the Letters in the
corner of each Lead when interpreting
OBHG Education Subcommittee
L
L L
L
I
I I
S
S
A
A
Teaching Point:
Paramedics are often intimidated by 12 Lead ECG before learning STEMI interpretation and surprised that it was not more difficult to learn after training.
The important point to emphasize is that paramedics are examining 12 Lead ECGs for very specific findings – ST-elevation. Physicians of all specialities read 12 Lead ECGs for ST-elevation and many other more complex interpretations. Paramedics are looking at the ECG, for the most part, to identify if the patient is a candidate for triage for early AMI reperfusion. Many other features of prehospital 12 Lead ECG may be interesting to learn but ST-elevation is MUST KNOW.
Further, for paramedics with experience in ECG Rhythm Interpretation, explain that ST-elevation on a 12 Lead ECG is easier to learn and much quicker to master than Rhythm Interpretation.
You may wish to retell the following amusing story to highlight the above point:
Tim Phelan, a paramedic from Florida with extensive experience in teaching prehospital 12 Lead ECG, was trying to demonstrate the ease of learning 12 Lead interpretation. One day he and his medic partner spent 30 minutes teaching interpretation to the Janitor in the hospital for which they worked. At the end of this session he seemed to be reasonably comfortable with what STEMI looked like and could locate the AMI. Later Tim and his partner got in trouble for this seemingly innocuous activity. One day, while cleaning floors in the ICU, the Janitor happened upon a conversation between an ICU nurse and physician about the location of an AMI in a newly admitted patient. The Janitor had a look at the ECG himself and noted, “Looks like an Anterior MI to me”. Turns out he was spot on in his interpretation causing some ruffled feathers in the Unit.
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After a brief review of essential terminology, participants move directly into AMI recognition and localization. In fact, participants will be able to recognize and localize myocardial infarction approximately 30 minutes into this module! A fact that is mentioned in previous slide and re-emphasized here.
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The 12-lead can provide a computer generated interpretation. The computer’s interpretive algorithm is designed to favor “specificity”. In other words, when the machine says “ACUTE MI SUSPECTED” it needs to always be right. The program is almost perfect in that regard, and when you see “ACUTE MI SUSPECTED” the machine is right about 98% of the time.
However, in order to attain that specificity, if the computer isn’t absolutely sure that an AMI is present, it will not say anything about it. Depending on the version of the software in your 12-lead machine, the computer may miss as many as one half of the cases where AMI could be suspected on the ECG.
In other words YOU are the primary interpreter, the computer is your backup.
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The computer is very good at measuring intervals and durations. For example, it is actually much better than we are at measuring the PR-interval and the QRS width.
This information is always provided and can be very useful to review in interpreting the 12 Lead ECG.
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Some of you may be wondering how anyone can make a sound interpretation with only 2.5 seconds shown in each lead.
Ask the group to look at the highlighted beat in the lead two rhythm strip, ask them to determine the rate, rhythm and interpretation. Of course it cannot be done.
As you well know, when you use an ECG to determine the cardiac rate, rhythm & interpretation, certain sampling time is required. Usually, at least a six second tracing is necessary, and complex rhythms may require even more sampling time.
However, do not be intimidated by the short sampling time in each of the 12-leads. What is different about 12-lead interpretation is this: Only one beat from each lead is needed to make an interpretation. The 2.5 seconds in each lead is usually long enough to capture one good, representative beat. Having said that one ST-segment may be enough to examine, looking at more than one complex may be helpful especially if there is wandering baseline or artifact at any point.
Recognition of AMI involves analyzing the shape of one beat in each lead. With that in mind let’s look at the shape of the waveforms in each lead.
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R wave: The first positive deflection.
No matter where it occurs in the complex, the first positive deflection is called the R wave.
The R wave includes not only the upstroke of the positive deflection, but the downstroke returning to the baseline as well.
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Q Wave: A negative deflection preceding the R wave.
If there is any negative deflection in front of the R wave, it is labelled the Q wave.
The Q wave includes the negative down stroke and the return to baseline.
&lt;number&gt;
S wave: A negative deflection following the R wave.
Like the Q wave and the R wave, the S wave includes both the departure from and return to the baseline.
&lt;number&gt;
J-Point: The junction between the end of the QRS and the beginning of the ST segment.
The J-point is found by looking for the point where the QRS stops and makes a sudden sharp change of direction.
You may opt to point out to the students that they have already found hundreds of J-points. Every time they have ever measured the width of a QRS, they have found the J-point. While they may not have labeled it as such, the end of the QRS complex is the J-point.
&lt;number&gt;
ST segment: The ECG segment between the J-point and the beginning of the T wave.
The ST segment is probably the single most important element to identify on the ECG when looking for evidence of AMI.
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They are not yet concerned with ST elevation or depression, simply identifying the J-point and ST segment.
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Review J-points and ST segment.
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The first level of 12-lead interpretation is simply a matter of knowing two facts:
1. What changes an AMI can place on the 12-lead, and
2. Knowing which part of the heart that each lead “sees.”
Lets look at each in more detail.
&lt;number&gt;
ST segment elevation, measured at the J-point, of 1mm or more is considered an abnormal finding in limb leads (I, II, III, aVF, aVL). Two mm or more is considered an abnormal finding in chest leads (V1 – V6).
Why different definitions of STEMI in limb and chest leads?
The limb leads are a long way away from each other and are not as sensitive as chest (or precordial) leads. It has been found that requiring at least 2mm or more of elevation in chest leads more accurately depicts patterns associated with acute infarct.
When that elevation is found in at least two anatomically contiguous leads, it is considered presumptive evidence of AMI.
NOTE: The concept of anatomically contiguous leads is simple, but may be difficult to explain. Essentially it means two leads looking at adjoining area of tissue. The difficulty comes when trying to determine which leads are contiguous with other leads. Here is one explanation:
If two leads have the same name (i.e., lateral or inferior) they are contiguous. Also, in the chest leads, if they are numerically consecutive, they are also contiguous. For example V2 is called a septal lead, and V3 an anterior lead, but they are anatomically contiguous. Reason:
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With an appropriate clinical presentation, ST segment elevation is presumptive evidence of acute myocardial infarction.
These patients benefit from immediate reperfusion, usually in the form of a thrombolytic drug or PCI (Percutaneous Coronary Intervention).
NOTE: In later chapters of this program the participant will be introduced to the full spectrum of Acute Coronary Syndromes (ACS). You may opt to acknowledge that other criteria for reperfusion will be added in later in the program. However, it is appropriate to begin with ST segment elevation.
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In order to determine if the ST segment is elevated it is necessary to have a reference point.
The TP segment is the best reference to the isoelectric line.
Do not compare the ST segment to the PR segment because the PR can be depressed, giving the illusion of ST segment elevation.
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This time find not only the J-point, but determine if the ST segment is elevated one millimeter or more above the TP segment.
#1 No
#2 Yes
#3 Yes
#4 No (likely BBB)
#5 Yes
#6 No
&lt;number&gt;
EXERCISE: approximately 2 minutes
Instructions:
Review the 12-lead ECG.
Go lead by lead, and pick one good complex in each lead.
Find the J-point and ST segment.
Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now).
Place a checkmark next to any lead with 1mm of ST segment elevation.
Review findings with group, pointing out every J-point and ST segment. Note leads II, III and aVF display elevation.
Remember ST segment elevation is presumptive evidence for AMI. Knowing which part of the heart leads II, III and aVF “sees” would tell you where the infarct is located.
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Each lead has one, and only one, positive electrode. We can think of the positive electrode as a camera or an eye. The view is from the positive electrode toward the negative electrode. The portion of the left ventricle that each leads “sees” is determined by the location of that positive electrode on the patient’s body.
Different placements of the electrodes will yield different viewpoints.
There are six positive electrodes on the chest, yielding six leads.
There are four electrodes on the limbs from which the ECG machine makes another six leads.
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Here’s what they look like on a patient. You may want to make a humorous remark that this gentleman looks like a younger Saddam Hussein experiencing chest pain.
The ECG machine simultaneously derives the 12-leads from the various positive electrodes.
Let’s discuss which part of the heart each lead “looks” at.
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The positive electrode for leads II, III, and aVF is attached to the left leg. The ECG monitor uses this one electrode as the positive electrode for all three leads.
From that perspective, these leads “look up” and “see” the inferior wall of the left ventricle.
NOTE: A heart model is helpful at this juncture, particularly to remind students that the heart does not sit “straight up” in the chest.
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NOTE: This is a posterior view of the heart.
The portion of the heart that rests on the diaphragm is called the “inferior wall”.
Leads II, III, and aVF, “look” up and see the inferior wall.
When ST segment elevation is noted in II, III and aVF, suspect an inferior infarction.
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Leads I and aVL share the positive electrode on the left arm.
From the perspective of the left arm, these leads “see” the lateral wall of the left ventricle.
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V5 and V6 are positioned on the lateral wall of the left chest which is why these two leads also “see” the lateral wall of the left ventricle.
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Portions of the lateral wall are shown here from both the anterior and posterior perspective.
Leads I, aVL, V5 and V6 “see” the lateral wall. When ST segment elevation is seen in these leads, consider a lateral wall infarction.
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The positive electrode for these two leads is placed on the anterior wall of the left chest. This correlates to their designation as anterior leads.
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Of course, ST segment elevation in V3 and V4 implies an anterior wall infarction.
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These leads are positioned one on each side of the sternum. From that placement they “look through” the right ventricle and “see” the septal wall.
NOTE: The septum is left ventricular tissue.
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V1 and V2 “look through” the right ventricle to “see” the septum.
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This represents the 3x4 format of the 12-lead ECG.
Each box represents one lead, and the viewpoint of that lead is indicated.
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Each box represents one lead, and the viewpoint of that lead is indicated.
NOTE: Refer participants to their pocket card where this information is summarized as well.
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This mnemonic device may work for some learners to remember the locations of the walls of the heart in relation to the 12 Lead ECG. However, emphasize to the learners that commitment to memorizing the locations of leads is essential for fast and consistent recognition.
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Greg Soto Note:
I have found the best way to teach interpretation is to begin, at this point, to have each participant interpret the 12 Leads while going around the room. If they miss anything or are incorrect be sure to point out proper interpretation while supporting participants. Encourage each participant to use the same following consistent approach:
Review the 12-lead ECG.
Go lead by lead, and pick one good complex in each lead.
Find the J-point and ST segment.
Compare the ST to the TP segment, looking for (ignore ST depression for now).
Place a check mark next to any lead with ST segment elevation.
Localize the area of infarction.
Acute antero-septal wall infarction
After reviewing this ECG, check in with the group. Press to see if everyone feels comfortable with the information presented to this point. If so, proceed to the next topic. The broader pattern of ECG changes are produced by infarction.
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Instructions:
Review the 12-lead ECG.
Go lead by lead, and pick one good complex in each lead.
Find the J-point and ST segment.
Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now).
Place a check mark next to any lead with 1mm of ST segment elevation.
Localize the area of infarction.
ST↑: Leads I, aVL, V1-V6 = Extensive Anterior STEMI
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Instructions:
Review the 12-lead ECG.
Go lead by lead, and pick one good complex in each lead.
Find the J-point and ST segment.
Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now).
Place a check mark next to any lead with 1mm of ST segment elevation.
Localize the area of infarction.
Inferior wall infarction
Note ST depression in I, AVL and V1-V3. The ask the participants to compare the elevation in aVF to the depression in aVL. Ask them if aVF elevation pattern looks similar to aVL if it were flipped upside down? Tell them there is a reason for this – it is called reciprocal changes.
Lets talk about one cause of ST depression, known as reciprocal ST depression.
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Instructions:
Review the 12-lead ECG.
Go lead by lead, and pick one good complex in each lead.
Find the J-point and ST segment.
Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now).
Place a check mark next to any lead with 1mm of ST segment elevation.
Localize the area of infarction.
Extensive anterior (septal + anterior + lateral)
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Instructions:
Determine which leads show ST elevation.
Which leads show ST depression.
Localize the area of infarction.
Determine if a reciprocal pattern exists.
ST elevation exists in II, III and aVF. ST depression in I and aVL
Does it fit the reciprocal pattern? Yes.
NOTE: Not every lead on each side of the seesaw must be elevated or depressed in order to assume reciprocal changes. Rather it is more a matter of at least some leads on one end of the seesaw being elevated and some being depressed.
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Instructions:
Determine which leads show ST elevation.
Which show ST depression.
Localize the area of infarction.
Determine if a reciprocal pattern exists.
Here the elevation is in leads I, aVL, V1-V5
And the depression is in leads II, III and aVF
Extensive anterior infarction, with reciprocal depression
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ST segments are iso-electric.
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Ask group to look for ST elevation.
The ST elevation implied epicardia ischemia (injury pattern).
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Inferolateral STEMI with RCs and Q-waves in II, III, aVF & V5.
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Instructions for presenter:
Review the 12-lead ECG slowly with the participants .
Go lead by lead, and pick one good complex in each lead.
Find the J-point and ST segment.
Compare the ST to the TP segment, looking for 1mm (one small box) of elevation in limb leads and 2 mm in chest leads (ignore ST depression for now).
Place a check mark next to any lead with ST segment elevation.
Localize the area of infarction.
Acute inferior wall infarction
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Inverted T-waves in aVL, V1 – V3
Leads us into next discussion.