Tutorial in Basic ECG for Medical Students
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This is the lecture notes that I have been giving to the medical students (2nd, 3rd, final year) for the last two years (updated 2008).
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Approach to a patient with PR interval abnormality in ECG
TheĀ PR intervalĀ is the time from the onset of the P wave to the start of the QRS complex.
It reflects conduction through the AV node.
The normal PR interval is between 120 ā 200 ms (0.12-0.20s) in duration (three to five small squares).
If the PR interval is > 200 ms,Ā first degree heart blockĀ is said to be present.
PR interval < 120 ms suggestsĀ pre-excitationĀ (the presence of an accessory pathway between the atria and ventricles) orĀ AV nodal (junctional) rhythm.
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Arrhythmias general
The document discusses various types of arrhythmias and their mechanisms. It describes ectopic beats that originate from locations other than the sinoatrial node, and explains that they can cause single beats or take over the heart rhythm. The mechanisms of arrhythmias include altered automaticity, triggered activity, and reentry. Reentry involves unidirectional block and different conduction speeds that allow an impulse to circulate and repeat, creating a reentrant circuit. The document outlines several specific types of arrhythmias like atrial fibrillation, atrial flutter, atrioventricular nodal reentry, and Wolff-Parkinson-White syndrome.
Right bundle branch block
This document discusses right bundle branch block (RBBB) in the electrocardiogram (ECG). It begins by explaining normal ventricular conduction, then describes RBBB. Key points of RBBB include a QRS duration of over 110ms, an rSR' pattern or notched R wave in lead V1, and a wide and slurred S wave in leads I and V6. The document contrasts RBBB and left bundle branch block (LBBB) and provides illustrations of complete RBBB, incomplete RBBB, intermittent RBBB, and RBBB with left anterior fascicular block. It emphasizes using lead V1 and the direction of the terminal QRS force (upward for RBBB, downward for LBBB)
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ST Segment Elevations in ECG
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.
Systematic ECG Interpretation
This document provides an overview of electrocardiogram (ECG) interpretation. It discusses the components of a normal ECG tracing including rate, rhythm, axis, waveforms such as P, QRS, ST segments, and T waves. It describes how to systematically evaluate an ECG and identify abnormalities. Common abnormalities are outlined such as arrhythmias, conduction blocks, myocardial infarction, hypertrophy, and electrolyte disturbances. Causes of abnormalities in various ECG components are also reviewed. The goal is to provide clinicians a methodical approach to ECG interpretation.
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Approach to a patient with PR interval abnormality in ECG
TheĀ PR intervalĀ is the time from the onset of the P wave to the start of the QRS complex.
It reflects conduction through the AV node.
The normal PR interval is between 120 ā 200 ms (0.12-0.20s) in duration (three to five small squares).
If the PR interval is > 200 ms,Ā first degree heart blockĀ is said to be present.
PR interval < 120 ms suggestsĀ pre-excitationĀ (the presence of an accessory pathway between the atria and ventricles) orĀ AV nodal (junctional) rhythm.
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The document discusses electrocardiograms (ECGs) in the context of acute coronary syndrome. It begins by describing the normal conduction system and the 12 standard ECG leads. It then explains how ECGs are recorded and the positioning of limb and precordial leads. The document discusses ST segments, T waves, and how to evaluate for ST elevations. It defines acute coronary syndrome and describes the classifications of ST-elevation MI, non-ST-elevation MI, and unstable angina based on ECG and cardiac enzyme findings. Specific ECG patterns for lateral, inferior, septal, and posterior wall MIs are also shown.
Arrhythmias general
The document discusses various types of arrhythmias and their mechanisms. It describes ectopic beats that originate from locations other than the sinoatrial node, and explains that they can cause single beats or take over the heart rhythm. The mechanisms of arrhythmias include altered automaticity, triggered activity, and reentry. Reentry involves unidirectional block and different conduction speeds that allow an impulse to circulate and repeat, creating a reentrant circuit. The document outlines several specific types of arrhythmias like atrial fibrillation, atrial flutter, atrioventricular nodal reentry, and Wolff-Parkinson-White syndrome.
Right bundle branch block
This document discusses right bundle branch block (RBBB) in the electrocardiogram (ECG). It begins by explaining normal ventricular conduction, then describes RBBB. Key points of RBBB include a QRS duration of over 110ms, an rSR' pattern or notched R wave in lead V1, and a wide and slurred S wave in leads I and V6. The document contrasts RBBB and left bundle branch block (LBBB) and provides illustrations of complete RBBB, incomplete RBBB, intermittent RBBB, and RBBB with left anterior fascicular block. It emphasizes using lead V1 and the direction of the terminal QRS force (upward for RBBB, downward for LBBB)
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ST Segment Elevations in ECG
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Systematic ECG Interpretation
This document provides an overview of electrocardiogram (ECG) interpretation. It discusses the components of a normal ECG tracing including rate, rhythm, axis, waveforms such as P, QRS, ST segments, and T waves. It describes how to systematically evaluate an ECG and identify abnormalities. Common abnormalities are outlined such as arrhythmias, conduction blocks, myocardial infarction, hypertrophy, and electrolyte disturbances. Causes of abnormalities in various ECG components are also reviewed. The goal is to provide clinicians a methodical approach to ECG interpretation.
Ventricular tachycardia
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
ECG emergencies
1. The document discusses various ECG emergencies including narrow complex tachycardia, wide complex tachycardia, bradycardia, asystole, pulseless electrical activity, and myocardial infarction.
2. Treatment approaches for different arrhythmias are outlined, including electrical cardioversion for unstable ventricular tachycardia and defibrillation for pulseless ventricular fibrillation.
3. Management strategies for bradycardic rhythms like sinus bradycardia depend on severity and include atropine or pacing, while complete heart block may require withdrawal of aggravating medications.
LBBB
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ā„120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
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Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
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This document provides an overview of ECG interpretation including:
- The anatomy of the heart's conduction system and how ECG leads are attached
- How to read an ECG strip and calculate heart rate
- Normal P, QRS, and T waves along with intervals like PR and QT
- Abnormalities that can indicate conditions like blocks, arrhythmias, and hypertrophy
- Electrolyte imbalances that can affect the ECG tracing
It concludes with examples of ECG strips and questions to test the reader's understanding.
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ECG: Ventricular Premature Beats
1. The ECG shows a 45-year-old diabetic man with episodes of palpitations who presents with ventricular trigeminy.
2. Ventricular trigeminy is characterized by ventricular premature beats occurring after every two normal sinus beats with a compensatory pause.
3. Further investigation with Holter monitoring is recommended to better characterize the ventricular arrhythmia and assess for underlying cardiac disease.
Ventricular tachycardia
This document discusses ventricular tachycardia (VT), providing definitions and key characteristics. VT can be nonsustained (<30 seconds) or sustained (>30 seconds). ECG patterns include right bundle branch block (RBBB), left bundle branch block (LBBB), and various axis deviations. Idiopathic VT originates from the outflow tracts, mitral/tricuspid annuli, or fascicles. Specific VT types like bidirectional VT and torsades de pointes are also outlined. The document provides visual examples and differentiates VT from similar rhythms.
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Electrolyte and metabolic ECG abnormalities
This document discusses various electrolyte abnormalities and their ECG manifestations. Hyperkalemia causes widened and low amplitude P-waves, widened QRS complex with potential fusion of the QRS-T segment and loss of the ST segment, and tall tented T-waves. Hypokalemia results in ST depression and flattened T-waves and possible negative T-waves. Hypercalcemia speeds repolarization, causing tall peaked T-waves at mild levels and extremely wide QRS complex with low R-waves and disappearance of P-waves at severe levels. Hypocalcemia causes a narrowed QRS complex, reduced PR interval, flattened and inverted T-waves, and prolonged QT and ST intervals. Hypomag
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Bundle branch blocks
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This document provides a tutorial on electrocardiography (ECG) including:
- The basics of ECG calibration and electrical impulse propagation.
- Descriptions of the P wave, QRS complex, ST segment, T wave, and other ECG components.
- Identification of abnormalities including hypertrophy, infarction, arrhythmias, and axis deviations.
- Guidance on interpreting ECG findings related to conditions like myocardial infarction, hypertrophy, and conduction blocks.
- Algorithms for managing cardiac arrest and arrhythmia rhythms.
- Recommended resources for further ECG education.
ECG Basics
This document provides a summary of basics of electrocardiography (ECG/EKG). It discusses the history and development of ECG technology. It describes the components of a normal ECG waveform including the P, QRS, and T waves. It explains how to determine heart rate from an ECG and identify different arrhythmias based on the waveform. Key anatomical structures involved in heart's electrical conduction system are also outlined.
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Ventricular tachycardia
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
ECG emergencies
1. The document discusses various ECG emergencies including narrow complex tachycardia, wide complex tachycardia, bradycardia, asystole, pulseless electrical activity, and myocardial infarction.
2. Treatment approaches for different arrhythmias are outlined, including electrical cardioversion for unstable ventricular tachycardia and defibrillation for pulseless ventricular fibrillation.
3. Management strategies for bradycardic rhythms like sinus bradycardia depend on severity and include atropine or pacing, while complete heart block may require withdrawal of aggravating medications.
LBBB
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ā„120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
Ventricular tachycardia
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
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This document provides an overview of ECG interpretation including:
- The anatomy of the heart's conduction system and how ECG leads are attached
- How to read an ECG strip and calculate heart rate
- Normal P, QRS, and T waves along with intervals like PR and QT
- Abnormalities that can indicate conditions like blocks, arrhythmias, and hypertrophy
- Electrolyte imbalances that can affect the ECG tracing
It concludes with examples of ECG strips and questions to test the reader's understanding.
Ecg changes in mi
This document summarizes electrocardiogram (ECG) findings related to myocardial infarction (MI). It describes the ECG changes that occur in the hyperacute, evolved, and chronic phases of MI. These include ST segment elevation, T wave changes, Q wave development, and other abnormalities. It also discusses ECG patterns related to injury of specific coronary artery territories and criteria for diagnosing MI when a left bundle branch block is present.
ECG: Ventricular Premature Beats
1. The ECG shows a 45-year-old diabetic man with episodes of palpitations who presents with ventricular trigeminy.
2. Ventricular trigeminy is characterized by ventricular premature beats occurring after every two normal sinus beats with a compensatory pause.
3. Further investigation with Holter monitoring is recommended to better characterize the ventricular arrhythmia and assess for underlying cardiac disease.
Ventricular tachycardia
This document discusses ventricular tachycardia (VT), providing definitions and key characteristics. VT can be nonsustained (<30 seconds) or sustained (>30 seconds). ECG patterns include right bundle branch block (RBBB), left bundle branch block (LBBB), and various axis deviations. Idiopathic VT originates from the outflow tracts, mitral/tricuspid annuli, or fascicles. Specific VT types like bidirectional VT and torsades de pointes are also outlined. The document provides visual examples and differentiates VT from similar rhythms.
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This document describes various types of cardiac murmurs and added heart sounds. It defines different types of murmurs such as systolic, diastolic, and continuous murmurs. It also describes how to characterize murmurs based on timing, location, intensity, and other factors. Specific heart conditions are discussed in relation to the murmurs and sounds they may cause, such as mid-systolic murmurs indicating aortic stenosis or holosystolic murmurs indicating mitral regurgitation. Grading scales for murmur intensity and examples of maneuvers that may modify murmurs are also provided.
Electrolyte and metabolic ECG abnormalities
This document discusses various electrolyte abnormalities and their ECG manifestations. Hyperkalemia causes widened and low amplitude P-waves, widened QRS complex with potential fusion of the QRS-T segment and loss of the ST segment, and tall tented T-waves. Hypokalemia results in ST depression and flattened T-waves and possible negative T-waves. Hypercalcemia speeds repolarization, causing tall peaked T-waves at mild levels and extremely wide QRS complex with low R-waves and disappearance of P-waves at severe levels. Hypocalcemia causes a narrowed QRS complex, reduced PR interval, flattened and inverted T-waves, and prolonged QT and ST intervals. Hypomag
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In a myocardial infarction transmural ischemia develops. In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.
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Myocardial infarction (MI) ecg localisation
This document discusses various non-coronary causes of ST-elevation on electrocardiograms (ECGs) including ventricular aneurysms, pericarditis, early repolarization patterns, left ventricular hypertrophy, left bundle branch block, hypothermia, cardioversion, intraventricular hemorrhage, hyperkalemia, Brugada pattern, type 1C antiarrhythmic drugs, hypercalcemia, pulmonary embolism, hypothermia, myocarditis, and tumor invasion of the left ventricle. It then discusses left ventricular aneurysms, early repolarization, acute pericarditis, hyperkalemia, hypothermia, increased intracranial pressure, Brugada syndrome, Tak
Brady arryhthmias
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
ECG- ST segment
This document contains a lecture on ST segment abnormalities from Professor Dr. Md Toufiqur Rahman. It discusses the normal ST segment and various causes of ST elevation and depression. ST segment abnormalities most commonly indicate myocardial ischemia or infarction. Other causes of ST elevation discussed include pericarditis, early repolarization, left bundle branch block, left ventricular hypertrophy, ventricular aneurysm, Brugada syndrome, ventricular pacing, and raised intracranial pressure. The lecture includes examples and descriptions of ST segment changes in each condition.
Bundle branch blocks
Bundle branch blocks occur when the left or right bundle branch is blocked, preventing normal conduction of electrical impulses through the ventricles. Right bundle branch block is usually benign but can worsen prognosis in acute myocardial infarction by indicating occlusion of the proximal left anterior descending artery. Left bundle branch block is more serious as it can mask signs of myocardial infarction and worsen prognosis in acute infarction. The Sgarbossa criteria can help diagnose myocardial infarction in the presence of left bundle branch block. Left anterior and posterior hemiblocks involve conduction abnormalities localized to one side of the ventricles.
SVT
This document discusses supraventricular tachycardia (SVT), which are tachyarrhythmias originating from the atria or atrioventricular node that cause a rapid heart rate. SVTs are classified as either atrial or AV tachyarrhythmias based on their site of origin. Common causes include inherited conditions, structural heart abnormalities, coronary artery disease, and hyperthyroidism. Diagnosis involves an electrocardiogram (ECG), Holter or event monitor, exercise test, or electrophysiology study. Treatment depends on whether it is acute or long term, and may include vagal maneuvers, calcium channel blockers, cardioversion, or medications like digoxin, beta blockers,
Supraventricular tachyarrythmias
This document describes different types of supraventricular tachycardias (SVTs), which are rapid heart rhythms originating above the ventricles. It defines SVTs and paroxysmal supraventricular tachycardia (PSVT), and lists common symptoms. The types of SVTs are categorized based on their origin in the sinoatrial node, atria, or atrioventricular node/junction. Each type has a distinct electrocardiogram appearance and cause, such as reentry circuits, ectopic foci, or increased node automaticity. Common examples include AV nodal reentrant tachycardia, atrial fibrillation, atrial flutter, and Wolff-Parkinson-
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The ECG represents the electrical activity of the heart. It can provide insight into cardiac pathophysiology by analyzing the distinctive waveforms of each cardiac event. The ECG can identify arrhythmias, ischemia, infarction, pericarditis, chamber hypertrophy, and electrolyte disturbances. The standard 12-lead ECG consists of 3 limb leads, 3 augmented limb leads, and 6 precordial leads, which provide different views of the heart. Analysis of the P wave, PR interval, QRS complex, ST segment, T wave, and QT interval can reveal normal sinus rhythm or abnormalities that require further investigation.
Ekg Tutorial
This document provides an overview of how to systematically interpret an electrocardiogram (EKG or ECG). It describes evaluating the rhythm, rate, axis, intervals, waves, and arriving at a final diagnosis by considering abnormalities in relationship to clinical data. Key aspects include assessing the P wave, QRS complex, ST segment, T wave, and U wave in each lead in a specified order. Factors that can affect the ST segment, T wave, and U wave are also discussed.
ECG BY Dr.MOHAMED RAMADAN
this is a simple work to understand how to read an ECG for medical students
by
M.RAMADAN
E C G M O H A M E D R A M A D A N
This document provides a summary of the basics of electrocardiography (ECG). It discusses the history and development of ECG technology. It describes the normal cardiac conduction system and the waves that make up a normal ECG, including the P, QRS, and T waves. It outlines the 12 standard ECG leads and how they are positioned on the body. It reviews criteria for interpreting common cardiac abnormalities based on ECG findings such as hypertrophy, infarction, and arrhythmias.
ECG BASICS.pptx
Electrocardiogram Basics, Recognition of common pathologies and treatment of common ECG abnormalities
ECG easy way
The ECG represents the electrical activity of the heart during the cardiac cycle. Each waveform provides insight into cardiac physiology and pathology. The ECG can be used to identify arrhythmias, ischemia, infarction, conduction abnormalities, chamber enlargement, and electrolyte disturbances. It consists of 12 leads that view the heart from different angles. The waveform intervals like P wave, PR interval, QRS complex, and ST segment must be carefully analyzed to interpret the ECG tracing.
Ecg easy way
The ECG measures the electrical activity of the heart. Each component of the ECG waveform provides important information about the heart's structure and function. Abnormalities seen on the ECG can help identify arrhythmias, conduction defects, chamber enlargement, ischemia, infarction and other cardiac pathologies. A thorough understanding of normal ECG patterns is required to accurately interpret ECG tracings and diagnose cardiac conditions.
Ecgrevised2 090808155046 Phpapp01
The document provides an overview of electrocardiography (ECG) basics including lead positions, ECG paper and timing, standardization, the normal ECG waves including P, PR, QRS, ST segments, T waves, and QT interval, and abnormalities. Key findings of right and left ventricular hypertrophy, atrial enlargement, bundle branch blocks, myocardial infarction, and various degrees of atrioventricular block are also summarized.
Understanding ecg
ecg basics made easy, with description of most common ecg types especially in emergency situation.
easy to memorize points and mnemonics included.
approach to ecg diagnosis.
sample ecgs.
Basic ECG &rhythm interpretation
The document provides an overview of electrocardiography (ECG), including its history, importance, physiology, leads, waves, intervals, and abnormalities. Key points covered include the names and functions of the P, QRS, and T waves, as well as common abnormalities like ST segment elevation/depression, T wave inversion, and arrhythmias. The summary analyzes ECGs to recognize conditions like myocardial infarction and ventricular hypertrophy.
Similar to Tutorial in Basic ECG for Medical Students (20)
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Tutorial in Basic ECG for Medical Students
- 1. Tutorial in ECG Dr. Chew Keng Sheng Emergency Medicine Universiti Sains Malaysia http://emergencymedic.blogspot.com
- 3. Vertical and horizontal perspective of the ECG Leads Leads Anatomical II, III, aVF Inferior surface of heart V1 to V4 Anterior surface of heart I, aVL, V5, and V6 Lateral surface of heart V1 and aVR Right atrium
- 4. Location of MI and Affected Coronary Arteries Location of MI Affected Artery Lateral Left circumflex Anterior LAD Septum LAD Inferior RCA Posterior RCA Right Ventricle RCA
- 5. Right Sided & Posterior Chest Leads
- 8. Instant Recognition of Axis Deviation
- 9. Cardiac Axis Normal Axis Right Axis deviation Left Axis Deviation Lead I Positive ļ Negative ļÆ Positive ļ Lead II Positive ļ Positive ļ Negative ļÆ Lead III Positive Positive Negative
- 15. P Pulmonale and P Mitrale
- 16. Ā
- 17. RAH and LAH Right Atrial Hypertrophy Left Atrial Hypertrophy
- 22. Conditions with Tall R in V1
- 23. Right Atrial and Ventricular Hypertrophy
- 24. COPD
- 26. Ā
- 27. Hypertrophy Strain Pattern vs ACS
- 29. Variable Shapes Of ST Segment Elevations in AMI Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th ed: Mosby Elsevier; 2006.
- 33. QT Interval
- 34. Long QT Syndrome
- 38. Calculation of Heart Rate
- 43. Note that by this time, if 3 rd shock is required, it is the DRUG ->SHOCK-> CPR sequence. It is the same sequence thereafter The drugs to be given at this stage are vasopressors Cardiac Arrest
- 44. After the 3 rd sequence and giving adrenaline/vasopressin, consider giving antiarrhythmics like amiodarone for VF or magnesium for torsades de pointes. The sequence is still the same DRUG->SHOCK-> CPR. At any time, if rhythm becomes non-shockable, follow the non-shockable algorithm Cardiac Arrest
- 45. For cardiac arrest, the first thing to know is whether the rhythm is shockable or not shockable. In periarrest rhythms (bradyarrhythmias and tachyarrhythmias, the first thing to know is whether it STABLE or NOT STABLE
- 47. Atropine 0.5 mg each bolus up to 3 mg. Atropine as temporizing measure only. Needs transcutaneous/transvenous pacing
- 50. * For polymorphic VT ā if patients become unstable, perform defibrillation rather than cardioversion. If ever in doubt whether to perform cardioversion or defibrillation, then perform DEFIBRILLATION Rule of thumb ā if your eye cannot synchronize to each QRS complex, neither can the machine!
- 53. Narrow complexes and regular ā attempt vagal maneuver and adenosine; Narrow complexes but not regular- likely AF. Donāt give adenosine. May attempt rate control using beta blocker or diltiazem
- 54. Amiodarone can be given for both regular and irregular broad complexes
- 56. Thank You Contact me: Dr. K.S. Chew [email_address] http://emergencymedic.blogspot.com