This document discusses ECG monitoring and changes that can indicate intraoperative myocardial infarction. It provides details on normal ECG waves and intervals, abnormalities that can be seen in cases of ischemia or infarction, and management strategies for arrhythmias and signs of injury that present during surgery. Common risk factors for perioperative myocardial infarction are unstable coronary plaques, prolonged oxygen supply-demand mismatch in patients with stable coronary artery disease, and acute coronary syndromes. Intraoperative monitoring via ECG, echocardiogram, and cardiac biomarkers can help detect injury. Treatment focuses on optimizing hemodynamics, giving anti-ischemic medications, and consulting cardiology for possible intervention.
This document provides an overview of perioperative arrhythmias including:
- The anatomy and physiology of the cardiac conduction system.
- Types of arrhythmias like sinus bradycardia, heart blocks, bundle branch blocks, supraventricular tachycardias, atrial flutter/fibrillation, and Wolff-Parkinson-White syndrome.
- Causes, mechanisms, ECG features, and management strategies for different arrhythmias that can occur in the perioperative period. Antiarrhythmic drugs and electrical therapies like pacing and cardioversion are discussed as treatment options.
- The incidence of arrhythmias is high during anesthesia for surgery, ranging from 4-20% for non
Sinus node dysfunction refers to problems with the heart's natural pacemaker, the sinus node. This can cause abnormal heart rhythms. Types include sinus pause or arrest where there are missing P waves, and sinus arrhythmia where P wave intervals vary. Causes include aging, heart disease, medications, and autonomic dysfunction. Symptoms range from fatigue to fainting. Diagnosis involves electrocardiograms, heart monitoring, and testing sinus node function. Treatment is usually a pacemaker for chronic, symptomatic cases to control heart rate and relieve symptoms.
This document provides an overview of tachyarrhythmias, including their causes, clinical manifestations, and treatment approaches. It discusses various types of arrhythmias such as sinus tachycardia, atrial fibrillation, atrial flutter, premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. For each type, it outlines the etiology, characteristics, management strategies including medication and procedures. The document is an educational guide for healthcare providers on understanding and managing different cardiac arrhythmias.
This document provides an overview of normal cardiac impulse conduction and various cardiac arrhythmias based on electrocardiogram (ECG) findings. It describes the pacemaker tissues of the heart and normal P wave, PR interval, QRS complex, and ST-T wave patterns on ECG. Common arrhythmias are then summarized, including sinus bradycardia, sinus tachycardia, heart block, atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. For each arrhythmia, the document outlines key ECG features and potential underlying causes. The goal of the document is to provide guidance on systematically interpreting ECGs
This document discusses the anatomy, function, and assessment of the sinus node and sinus node dysfunction. It begins with an overview and description of the sinus node anatomy. It then discusses symptoms, diagnostic testing approaches including ECG, exercise testing, drug challenges, and long-term monitoring. Invasive assessment methods like sinus node recovery time and sinoatrial conduction time are also covered. The document provides details on performing, interpreting, and limitations of these invasive tests. Treatment options are also briefly mentioned.
Bradydysrhythmias are heart rhythms with a ventricular rate slower than 60 beats per minute in adults. They are commonly caused by problems with impulse formation or conduction in the heart's conduction system. Bradydysrhythmias can be classified as sinus bradycardia, AV blocks, junctional rhythms, or idioventricular rhythms. Treatment may include atropine or cardiac pacing depending on the specific rhythm abnormality and its symptoms.
IDENTIFICATION AND APPROACH TO BRADYARRHYTHMIAS .pptxDr Dravid m c
Explanation of SA Nodal and AV nodal block , ECG changes , identification clinical features and presentation of patients to emergency department, their approach and medical linea of treatment
This document provides an overview of perioperative arrhythmias including:
- The anatomy and physiology of the cardiac conduction system.
- Types of arrhythmias like sinus bradycardia, heart blocks, bundle branch blocks, supraventricular tachycardias, atrial flutter/fibrillation, and Wolff-Parkinson-White syndrome.
- Causes, mechanisms, ECG features, and management strategies for different arrhythmias that can occur in the perioperative period. Antiarrhythmic drugs and electrical therapies like pacing and cardioversion are discussed as treatment options.
- The incidence of arrhythmias is high during anesthesia for surgery, ranging from 4-20% for non
Sinus node dysfunction refers to problems with the heart's natural pacemaker, the sinus node. This can cause abnormal heart rhythms. Types include sinus pause or arrest where there are missing P waves, and sinus arrhythmia where P wave intervals vary. Causes include aging, heart disease, medications, and autonomic dysfunction. Symptoms range from fatigue to fainting. Diagnosis involves electrocardiograms, heart monitoring, and testing sinus node function. Treatment is usually a pacemaker for chronic, symptomatic cases to control heart rate and relieve symptoms.
This document provides an overview of tachyarrhythmias, including their causes, clinical manifestations, and treatment approaches. It discusses various types of arrhythmias such as sinus tachycardia, atrial fibrillation, atrial flutter, premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. For each type, it outlines the etiology, characteristics, management strategies including medication and procedures. The document is an educational guide for healthcare providers on understanding and managing different cardiac arrhythmias.
This document provides an overview of normal cardiac impulse conduction and various cardiac arrhythmias based on electrocardiogram (ECG) findings. It describes the pacemaker tissues of the heart and normal P wave, PR interval, QRS complex, and ST-T wave patterns on ECG. Common arrhythmias are then summarized, including sinus bradycardia, sinus tachycardia, heart block, atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. For each arrhythmia, the document outlines key ECG features and potential underlying causes. The goal of the document is to provide guidance on systematically interpreting ECGs
This document discusses the anatomy, function, and assessment of the sinus node and sinus node dysfunction. It begins with an overview and description of the sinus node anatomy. It then discusses symptoms, diagnostic testing approaches including ECG, exercise testing, drug challenges, and long-term monitoring. Invasive assessment methods like sinus node recovery time and sinoatrial conduction time are also covered. The document provides details on performing, interpreting, and limitations of these invasive tests. Treatment options are also briefly mentioned.
Bradydysrhythmias are heart rhythms with a ventricular rate slower than 60 beats per minute in adults. They are commonly caused by problems with impulse formation or conduction in the heart's conduction system. Bradydysrhythmias can be classified as sinus bradycardia, AV blocks, junctional rhythms, or idioventricular rhythms. Treatment may include atropine or cardiac pacing depending on the specific rhythm abnormality and its symptoms.
IDENTIFICATION AND APPROACH TO BRADYARRHYTHMIAS .pptxDr Dravid m c
Explanation of SA Nodal and AV nodal block , ECG changes , identification clinical features and presentation of patients to emergency department, their approach and medical linea of treatment
1. The document discusses antiarrhythmic drugs and their classification and mechanisms of action.
2. Antiarrhythmic drugs are classified based on their effects on the cardiac action potential as Class I-IV. Class I drugs block sodium channels, Class II drugs are beta blockers, Class III drugs prolong the action potential duration, and Class IV drugs slow calcium channels.
3. Examples of different classes of drugs are provided along with their indications, mechanisms, effects, and side effects. The goal of antiarrhythmic therapy is to restore normal sinus rhythm and conduction while preventing more serious arrhythmias.
anti arrhythmic drugs anaesthesiology cardiacNeelkantRaju
1. The document discusses antiarrhythmic drugs and their classification and mechanisms of action. It focuses on Class I drugs that work by blocking sodium channels.
2. Class IA drugs like quinidine and procainamide have a moderate effect on sodium channels and are used for supraventricular and ventricular arrhythmias. They can cause side effects like QT prolongation.
3. Class IB drugs like lidocaine have a weak effect on sodium channels and are the drugs of choice for ventricular arrhythmias. They are used for ventricular arrhythmias due to ischemia or digoxin toxicity.
This document defines and describes various types of arrhythmias. It begins by defining arrhythmia as any change from the normal sequence of electrical impulses in the heart. Various cardiac and non-cardiac conditions can cause arrhythmias. The document then describes several specific types of arrhythmias in detail, including sinus bradycardia, sick sinus syndrome, sinus tachycardia, premature atrial contractions, atrial flutter, atrial fibrillation, junctional tachycardia, paroxysmal supraventricular tachycardia, premature ventricular contractions, ventricular fibrillation, pulseless electrical activity, asystole, and various types of heart block. Treatment options are provided for many of
This document defines and describes various types of arrhythmias. It begins by defining arrhythmia as any change from the normal sequence of electrical impulses in the heart. Various cardiac and non-cardiac conditions can cause arrhythmias. The document then describes several specific types of arrhythmias in detail, including sinus bradycardia, sick sinus syndrome, sinus tachycardia, premature atrial contractions, atrial flutter, atrial fibrillation, junctional tachycardia, paroxysmal supraventricular tachycardia, premature ventricular contractions, ventricular fibrillation, pulseless electrical activity, asystole, and various types of heart block. Treatment options are provided for each type
Arrhythmias 1DR NIKUNJ R SHEKHADA (MBBS,MS GEN SURG DNB CTS SR)DR NIKUNJ SHEKHADA
This document summarizes cardiac arrhythmias and the normal cardiac conduction system. It describes how arrhythmias occur due to problems in the sinus node, atrial cells, AV junction, or ventricular cells. Common arrhythmias discussed include sinus bradycardia, sinus tachycardia, atrial fibrillation, atrial flutter, supraventricular tachycardia, heart block, and bundle branch block. Causes, characteristics, and treatment approaches are provided for each type of arrhythmia. The normal cardiac conduction pathway and components of the ECG are also outlined.
1. Irregular narrow complex tachycardia with no discernible P waves. Diagnosis is atrial fibrillation.
2. Regular narrow complex tachycardia with short RP intervals and variable relationship between P waves and QRS complexes. Diagnosis is AV nodal reentrant tachycardia (AVNRT).
3. Regular narrow complex tachycardia with sawtooth flutter waves and 2:1 conduction. Diagnosis is atrial flutter.
This document provides guidelines for managing supraventricular tachycardia (SVT) in adult patients. SVT is defined as a tachycardia with atrial and/or ventricular rates over 100 bpm involving tissue above the His bundle. Common types of SVT include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), multifocal atrial tachycardia (MAT), sinus node reentry tachycardia, and junctional tachycardia. The document reviews the clinical presentation, differential diagnosis, evaluation and treatment of these arrhythmias. It
Arrhythmias refer to abnormalities in the cardiac rhythm. There are two main types: bradycardia where the heart rate is slow, and tachycardia where the heart rate is fast. Specific arrhythmias include sinus bradycardia, various types of heart block, atrial fibrillation, atrial flutter, AV nodal re-entry tachycardia, ventricular tachycardia, and ventricular fibrillation. Diagnosis involves electrocardiography and other tests. Treatment depends on the type of arrhythmia but may include medications, catheter ablation, pacemaker implantation, or cardioversion. Lifestyle modifications and avoiding arrhythmia triggers can also help management.
This document discusses various ventricular dysrhythmias, including premature ventricular contractions, ventricular tachycardia, torsades de pointes, ventricular fibrillation, asystole, ventricular escape rhythms, and artificial pacemaker rhythms. It provides details on the origin, characteristics, clinical significance, and treatment approaches for each dysrhythmia. Artificial pacemakers are discussed in terms of basic types, chambers paced/sensed, and classification codes. Assessment of pacemaker function and potential issues like failure to capture are also reviewed.
This document provides an overview of heart conduction and various types of arrhythmias or disturbances in heart rhythm. It begins with a description of normal heart conduction and then defines arrhythmia. Various mechanisms of arrhythmia are described including increased automaticity, triggered automaticity, and reentry. Arrhythmias are classified based on heart rate as tachyarrhythmias or bradyarrhythmias, and based on site of impulse generation as supraventricular or ventricular arrhythmias. Specific types of arrhythmias are defined including sinus arrhythmias, atrial arrhythmias like atrial fibrillation and flutter, junctional arrhythmias, and ventricular arrhythmias. Treatment options for arrhythmias include medications
This document discusses the diagnosis and management of cardiac arrhythmias. It begins with an introduction stating that cardiac arrhythmias lead to sudden cardiac death for 250,000 people annually in the United States. The document then covers the history of understanding arrhythmias, the major types of arrhythmias and heart blocks, how to analyze arrhythmias, evaluate patients presenting with arrhythmias, investigate arrhythmias, and manage common arrhythmias like atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia. Treatment options discussed include medical management, surgical correction, ablation, pacemakers, and defibrillators.
This document discusses different types of cardiac arrhythmias including bradyarrhythmias which are slow heart rhythms and tachyarrhythmias which are fast heart rhythms. It describes specific arrhythmias like sinus bradycardia, atrial fibrillation, atrial flutter, atrioventricular reciprocating tachycardia, ventricular fibrillation, and ventricular tachycardia. It also discusses diagnostic studies, management through lifestyle changes and medications, and treatment options like cardioversion, pacemakers, surgery, and ablation for various arrhythmias.
This document provides an overview of pericardial diseases. It begins with the anatomy and functions of the pericardium. It then discusses various pericardial diseases like acute pericarditis, pericardial effusion, and cardiac tamponade. For acute pericarditis, it describes the key symptoms of chest pain, pericardial friction rub, and ECG changes. It also outlines the diagnostic criteria and treatment approaches for pericardial effusion and cardiac tamponade, including the use of echocardiography, medications, and pericardiocentesis.
Cardiac arrhythmia refers to any abnormal heart rhythm and can cause the heart rate to be too fast, too slow, or irregular. Common types include sinus tachycardia, ventricular tachycardia, sinus bradycardia, paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, premature atrial contractions, premature ventricular contractions, and nodal rhythm. Treatment depends on the specific arrhythmia but may include medications, cardioversion, pacemakers, ablation, or defibrillation.
- An ECG records the electrical activity of the heart over time using electrodes placed on the skin. It detects tiny electrical changes arising from the heart muscle contracting during each heartbeat.
- The cardiac impulse originates in the sinoatrial node and travels through the atria and ventricles via specialized conduction pathways before the ventricles contract.
- A standard 12-lead ECG provides multiple views of the heart to analyze the rate and rhythm of the heart as well as measure key intervals like the PR interval, QRS duration, and QT interval to identify any abnormalities.
1685644652805_1685644176287_1685644169732_CARDIAC ARRYTHMIAS AND MANAGEMENT...PratimaSingh928775
Cardiac arrhythmias refer to irregularities in heart rhythm. They can be characterized by rate, rhythm, origin, conduction pathways, and other factors. Causes include coronary artery disease, electrolyte imbalances, structural heart changes, and various medical conditions. Symptoms depend on the type of arrhythmia but may include palpitations, dizziness, chest pain, and fainting. Diagnosis involves EKGs, holter monitors, echocardiograms, and other tests. Treatment includes medications to restore normal rhythm or prevent dangerous arrhythmias, cardioversion, pacemakers, ablation, and defibrillators. Management depends on the specific arrhythmia and may involve drugs, ablation, cardioversion,
This document discusses ischemic heart disease and acute coronary syndrome. It covers the anatomy of the heart, pathophysiology of coronary artery disease, management of stable angina, and prognosis. Key topics include diagnosis of ischemic heart disease, treatment of risk factors, drug therapy for angina, stress testing, revascularization options, and the differences between NSTEMI and STEMI.
- Anaesthesia impairs pulmonary function by reducing lung volume and compliance while increasing airway resistance. This leads to atelectasis formation and V/Q mismatch, resulting in hypoxemia.
- General anaesthesia decreases functional residual capacity (FRC) by 20% from reduced respiratory muscle tone. Atelectasis occurs in 90% of patients and impacts oxygenation.
- Factors like age, obesity, and pre-existing lung disease worsen oxygenation and gas exchange under anaesthesia due to increased shunting and V/Q mismatch. Patient positioning, use of muscle relaxants, and type of anaesthesia also influence respiratory function.
Spinal anaesthesia involves injecting local anaesthetic into the subarachnoid space to block spinal nerves. It was first introduced in the late 1800s. The spinal cord and nerves are surrounded by meninges including the dura, arachnoid and pia mater. Cerebrospinal fluid flows in the subarachnoid space. Spinal anaesthesia is performed using a small needle inserted between vertebrae to access this space and inject anaesthetic. The level and extent of nerve blockade depends on factors like drug used, dose, patient positioning and anatomy. It provides anaesthesia for surgeries below the level of injection while sparing consciousness above.
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1. The document discusses antiarrhythmic drugs and their classification and mechanisms of action.
2. Antiarrhythmic drugs are classified based on their effects on the cardiac action potential as Class I-IV. Class I drugs block sodium channels, Class II drugs are beta blockers, Class III drugs prolong the action potential duration, and Class IV drugs slow calcium channels.
3. Examples of different classes of drugs are provided along with their indications, mechanisms, effects, and side effects. The goal of antiarrhythmic therapy is to restore normal sinus rhythm and conduction while preventing more serious arrhythmias.
anti arrhythmic drugs anaesthesiology cardiacNeelkantRaju
1. The document discusses antiarrhythmic drugs and their classification and mechanisms of action. It focuses on Class I drugs that work by blocking sodium channels.
2. Class IA drugs like quinidine and procainamide have a moderate effect on sodium channels and are used for supraventricular and ventricular arrhythmias. They can cause side effects like QT prolongation.
3. Class IB drugs like lidocaine have a weak effect on sodium channels and are the drugs of choice for ventricular arrhythmias. They are used for ventricular arrhythmias due to ischemia or digoxin toxicity.
This document defines and describes various types of arrhythmias. It begins by defining arrhythmia as any change from the normal sequence of electrical impulses in the heart. Various cardiac and non-cardiac conditions can cause arrhythmias. The document then describes several specific types of arrhythmias in detail, including sinus bradycardia, sick sinus syndrome, sinus tachycardia, premature atrial contractions, atrial flutter, atrial fibrillation, junctional tachycardia, paroxysmal supraventricular tachycardia, premature ventricular contractions, ventricular fibrillation, pulseless electrical activity, asystole, and various types of heart block. Treatment options are provided for many of
This document defines and describes various types of arrhythmias. It begins by defining arrhythmia as any change from the normal sequence of electrical impulses in the heart. Various cardiac and non-cardiac conditions can cause arrhythmias. The document then describes several specific types of arrhythmias in detail, including sinus bradycardia, sick sinus syndrome, sinus tachycardia, premature atrial contractions, atrial flutter, atrial fibrillation, junctional tachycardia, paroxysmal supraventricular tachycardia, premature ventricular contractions, ventricular fibrillation, pulseless electrical activity, asystole, and various types of heart block. Treatment options are provided for each type
Arrhythmias 1DR NIKUNJ R SHEKHADA (MBBS,MS GEN SURG DNB CTS SR)DR NIKUNJ SHEKHADA
This document summarizes cardiac arrhythmias and the normal cardiac conduction system. It describes how arrhythmias occur due to problems in the sinus node, atrial cells, AV junction, or ventricular cells. Common arrhythmias discussed include sinus bradycardia, sinus tachycardia, atrial fibrillation, atrial flutter, supraventricular tachycardia, heart block, and bundle branch block. Causes, characteristics, and treatment approaches are provided for each type of arrhythmia. The normal cardiac conduction pathway and components of the ECG are also outlined.
1. Irregular narrow complex tachycardia with no discernible P waves. Diagnosis is atrial fibrillation.
2. Regular narrow complex tachycardia with short RP intervals and variable relationship between P waves and QRS complexes. Diagnosis is AV nodal reentrant tachycardia (AVNRT).
3. Regular narrow complex tachycardia with sawtooth flutter waves and 2:1 conduction. Diagnosis is atrial flutter.
This document provides guidelines for managing supraventricular tachycardia (SVT) in adult patients. SVT is defined as a tachycardia with atrial and/or ventricular rates over 100 bpm involving tissue above the His bundle. Common types of SVT include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), multifocal atrial tachycardia (MAT), sinus node reentry tachycardia, and junctional tachycardia. The document reviews the clinical presentation, differential diagnosis, evaluation and treatment of these arrhythmias. It
Arrhythmias refer to abnormalities in the cardiac rhythm. There are two main types: bradycardia where the heart rate is slow, and tachycardia where the heart rate is fast. Specific arrhythmias include sinus bradycardia, various types of heart block, atrial fibrillation, atrial flutter, AV nodal re-entry tachycardia, ventricular tachycardia, and ventricular fibrillation. Diagnosis involves electrocardiography and other tests. Treatment depends on the type of arrhythmia but may include medications, catheter ablation, pacemaker implantation, or cardioversion. Lifestyle modifications and avoiding arrhythmia triggers can also help management.
This document discusses various ventricular dysrhythmias, including premature ventricular contractions, ventricular tachycardia, torsades de pointes, ventricular fibrillation, asystole, ventricular escape rhythms, and artificial pacemaker rhythms. It provides details on the origin, characteristics, clinical significance, and treatment approaches for each dysrhythmia. Artificial pacemakers are discussed in terms of basic types, chambers paced/sensed, and classification codes. Assessment of pacemaker function and potential issues like failure to capture are also reviewed.
This document provides an overview of heart conduction and various types of arrhythmias or disturbances in heart rhythm. It begins with a description of normal heart conduction and then defines arrhythmia. Various mechanisms of arrhythmia are described including increased automaticity, triggered automaticity, and reentry. Arrhythmias are classified based on heart rate as tachyarrhythmias or bradyarrhythmias, and based on site of impulse generation as supraventricular or ventricular arrhythmias. Specific types of arrhythmias are defined including sinus arrhythmias, atrial arrhythmias like atrial fibrillation and flutter, junctional arrhythmias, and ventricular arrhythmias. Treatment options for arrhythmias include medications
This document discusses the diagnosis and management of cardiac arrhythmias. It begins with an introduction stating that cardiac arrhythmias lead to sudden cardiac death for 250,000 people annually in the United States. The document then covers the history of understanding arrhythmias, the major types of arrhythmias and heart blocks, how to analyze arrhythmias, evaluate patients presenting with arrhythmias, investigate arrhythmias, and manage common arrhythmias like atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia. Treatment options discussed include medical management, surgical correction, ablation, pacemakers, and defibrillators.
This document discusses different types of cardiac arrhythmias including bradyarrhythmias which are slow heart rhythms and tachyarrhythmias which are fast heart rhythms. It describes specific arrhythmias like sinus bradycardia, atrial fibrillation, atrial flutter, atrioventricular reciprocating tachycardia, ventricular fibrillation, and ventricular tachycardia. It also discusses diagnostic studies, management through lifestyle changes and medications, and treatment options like cardioversion, pacemakers, surgery, and ablation for various arrhythmias.
This document provides an overview of pericardial diseases. It begins with the anatomy and functions of the pericardium. It then discusses various pericardial diseases like acute pericarditis, pericardial effusion, and cardiac tamponade. For acute pericarditis, it describes the key symptoms of chest pain, pericardial friction rub, and ECG changes. It also outlines the diagnostic criteria and treatment approaches for pericardial effusion and cardiac tamponade, including the use of echocardiography, medications, and pericardiocentesis.
Cardiac arrhythmia refers to any abnormal heart rhythm and can cause the heart rate to be too fast, too slow, or irregular. Common types include sinus tachycardia, ventricular tachycardia, sinus bradycardia, paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, premature atrial contractions, premature ventricular contractions, and nodal rhythm. Treatment depends on the specific arrhythmia but may include medications, cardioversion, pacemakers, ablation, or defibrillation.
- An ECG records the electrical activity of the heart over time using electrodes placed on the skin. It detects tiny electrical changes arising from the heart muscle contracting during each heartbeat.
- The cardiac impulse originates in the sinoatrial node and travels through the atria and ventricles via specialized conduction pathways before the ventricles contract.
- A standard 12-lead ECG provides multiple views of the heart to analyze the rate and rhythm of the heart as well as measure key intervals like the PR interval, QRS duration, and QT interval to identify any abnormalities.
1685644652805_1685644176287_1685644169732_CARDIAC ARRYTHMIAS AND MANAGEMENT...PratimaSingh928775
Cardiac arrhythmias refer to irregularities in heart rhythm. They can be characterized by rate, rhythm, origin, conduction pathways, and other factors. Causes include coronary artery disease, electrolyte imbalances, structural heart changes, and various medical conditions. Symptoms depend on the type of arrhythmia but may include palpitations, dizziness, chest pain, and fainting. Diagnosis involves EKGs, holter monitors, echocardiograms, and other tests. Treatment includes medications to restore normal rhythm or prevent dangerous arrhythmias, cardioversion, pacemakers, ablation, and defibrillators. Management depends on the specific arrhythmia and may involve drugs, ablation, cardioversion,
This document discusses ischemic heart disease and acute coronary syndrome. It covers the anatomy of the heart, pathophysiology of coronary artery disease, management of stable angina, and prognosis. Key topics include diagnosis of ischemic heart disease, treatment of risk factors, drug therapy for angina, stress testing, revascularization options, and the differences between NSTEMI and STEMI.
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- Anaesthesia impairs pulmonary function by reducing lung volume and compliance while increasing airway resistance. This leads to atelectasis formation and V/Q mismatch, resulting in hypoxemia.
- General anaesthesia decreases functional residual capacity (FRC) by 20% from reduced respiratory muscle tone. Atelectasis occurs in 90% of patients and impacts oxygenation.
- Factors like age, obesity, and pre-existing lung disease worsen oxygenation and gas exchange under anaesthesia due to increased shunting and V/Q mismatch. Patient positioning, use of muscle relaxants, and type of anaesthesia also influence respiratory function.
Spinal anaesthesia involves injecting local anaesthetic into the subarachnoid space to block spinal nerves. It was first introduced in the late 1800s. The spinal cord and nerves are surrounded by meninges including the dura, arachnoid and pia mater. Cerebrospinal fluid flows in the subarachnoid space. Spinal anaesthesia is performed using a small needle inserted between vertebrae to access this space and inject anaesthetic. The level and extent of nerve blockade depends on factors like drug used, dose, patient positioning and anatomy. It provides anaesthesia for surgeries below the level of injection while sparing consciousness above.
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The visual pathway allows us to see and process visual information. It begins when light enters the eye and is focused onto the retina where it is converted into neural signals. These signals then travel through the optic nerve and optic chiasm into the lateral geniculate nucleus and ultimately to the primary visual cortex in the occipital lobe of the brain where visual information is assembled into the images we perceive.
The visual pathway allows us to see and process visual information. It begins when light enters the eye and is focused onto the retina where it is converted into neural signals. These signals then travel through the optic nerve and optic chiasm into the lateral geniculate nucleus and ultimately to the primary visual cortex in the occipital lobe of the brain where visual information is assembled into the images we perceive.
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ECG MONITORING AND ECG CHANGES OF INTRAOPERATIVE MYOCARDIAL.pptx
1. ECG MONITORING AND ECG CHANGES
OF INTRAOPERATIVE MYOCARDIAL
INFARCTION
Dr.PRIYANGA RAVI,
SECOND YEAR ANAESTHESIA RESIDENT,
GOVERNMENT MEDICAL COLLEGE,
BHAVNAGAR.
2. STANDARD -12 LEAD
ELECTROCARDIOGRAM
• A graphical recording of the electrical activity of the
heart over time.
• It is a bedside investigation.
• Gold standard for diagnosis of cardiac arrythmias.
• Allows for detection of conduction abnormalities.
• Screening tool for ischemic heart disease during stress
tests.
• Helpful with non-cardiac diseases (e.g.pulmonary
embolism or hypothermia)
• Its a simple ,cheap and easily available investigation.
8. • Speed of the paper-25mm/sec
• 1 horizontal small box-0.04second
• 1 horizontal large box -0.2 second
• 1 vertical small box is 1mm-0.1 MV
9.
10. ELECTROCARDIOGRAM WAVES
• P WAVE-depolarization of atria (atria begin
contracting about 25msec after the start of the
p-wave.
• QRS –COMPLEX-ventricular
depolarization(ventricles begin contracting
shortly after the peak of the R wave)
• T WAVE-ventricular repolarization.
11. EINTHOVEN’S LAW
• In the ecg at any given instant ,the potential of
any wave in lead II is equal to sum of the
potentials in lead I and lead III.
• II=I+III
17. ECG INTERPRETATION
• Patient name and date
• Standardization
• Rate
• Rythm
• P wave
• PR segment
• QRS complex
• ST segment
• T wave
• QT interval
• U wave
19. OVERDAMPING AND
UNDERDAMPING
• Overdamping-When the pressure of the stylus
is too firm on the paper so that it’s movements
are retarded-deflection fractionally wider and
dimisnished amplitude.
• Underdamping-when the writing stylus is not
pressed firmly enough against the paper-sharp
spikes at the corners
20. RATE
• Formula 1: 300/number of big squares
between R-R
• Formula 2: 1500/small squares between R-R
• For irregular heart rates ,get the number of
QRS complexes in a 6-second strip;then
multiply by 10
47. HR->100BPM- ADULT PATIENT may be as high as 150bpm.
Rhythm-regular
DANGEROUS-IHD,MS,AS,OBSTRUCTIVE CARDIOMYOPATHY
48. CAUSES
• PHYSIOLOGICAL;excitement,exertion,pregnancy,pain,fever
• Lighter planes of anaesthesia
• DRUGS
• Cardiac vagal tone blockers(atropine,and other
anticholinergic agents)
• Sympathetic tone stimulants-(eg-
epinephrine,norepinephrine,dopamine,cocaine,amphetami
nes,ketamine,ether,pancuranium.
• Hypotension.
• Hyperthyroidism
• Pheochromocytoma
49. MANAGEMENT
• The underlying cause should be treated.
• Hypovolemia and lighter planes of anaesthesia
are the most common causes.
• In patient with ischemic and stenotic valvular
disease
• B adrenergic blockers.
57. • Origin is from a site in the atria other than the
SA node.
• Rate <100/min
• Rhythm-irregular
• P wavw –abnormal
• Printreval-variable
• QRS –normal configuration
• Incomplete compensatory pause
62. MANAGEMENT
• Hemodynaically stable,then
amiodarone,administered in one or more
doses of 150mg given iv in 100ml saline or
D5W over 10 minutes ,followed by an iv
infusion of 1 mg/min for 6 hours and
0.5mg/min thereafter.
• Hemodynamically unstable-synchronised
cardioversion (200J)
64. • A form of polymorphic VT
• RATE 150-200
• Rhythm may be irregular
• P waves absent
• Qrs complexes-wide appears twisting around a
central axis
• Can occur in patients with prolonged qt intrevel
• Responds to iv magnesium
• If unstable-electrical defibrillation
72. PERIOPERATIVE MYOCARDIAL
INFARCTION
• Defining PMI,however is often difficult because most
PMIs occur without clinical symptoms in
anaesthetiszed and sedated patients.
• ECG changes are subtle and or transient,the creatine
kinase –MB iso enzyme has limited sensitivity and
specificity because of co existing skeletal muscle
injury.
• The majority of patients with an acute MI will have
elevation in troponins within 2-3 hours of MI
• CTnl has been shown to be exclusive to cardiac muscle.
73. PATHOPHYSIOLOGY
– Two distinct mechanisms may lead to PMI
• Acute coronary syndrome.
• Prolonges myocardial oxygen supply demand
imbalance in the presence of stable coronary
artery disease,designated type 1 and type 2 by
the universal definition of MI.
74. ACUTE CORONARY SYNDROME
(TYPE 1 PMI)
• Acute coronary syndrome occurs when an
unstable or vulnarable plaque undergoes
spontaneous rupture,fissuring or erosion,leading
to acute coronary thrombosis,ischemia,and
infarction.
• Serial cTn concentration are necessary to
distinguish acute from chronic myocardial
injury,and preoperative cTn concentrations from
the interpretation of postoperative measurments.
76. • Leads to Increased coagulability and
decreased fibrinolysis .
ACUTE CORONARY THROMBOSIS
ACS-TYPE-1 MI
77. SEVERE ,YET STABLE CAD
• Increased sympathetic hyperactivity ,post
operative pain ,withdrawl of b-blockers leads
to increased myocardial 02 demand and
decreased 02 supply thereby leads to increase
in heart rate/arrythmia.
PROLONGED ST DEPRESSION ISCHEMIA>> TYPE II MI
78. NON –CARDIAC SURGERY
BASELINE RISK +INTRAOPERATIVE FACTORS
SURGICAL TRAUMA
INFLAMMATION/CYTO
KINE RELEASE
PLATELET ACTIVATION
CATECHOLAMINE/COR
TISOL
SURGE/BLEEDING
HYPERTENSION
HYPOTENSION
TACHYCARDIA
BRADYCARDIA
HYPOXEMIA
ANEMIA
HEART
FAILURE
SEPSIS
RENAL
FAILURE
VOLUME
OVERLOAD
PULMONARY
EMBOLISM
VALVULAR
HEART
DISEASES
NON ISCHEMIC
MYOCARDIAL
INJURY
ATHEROSCLEROTIC
CORONARY PLAQUE
DISRUPTION
MYOCARDIAL
OXYGEN
DEMAND
MISMATCH WITH
STABLE CAD
MYOCARDIAL INJURY AFTER NON-CARDIAC SURGERY
79. ECG CRITERIA TO DIAGNOSE
ACUTE MYOCARDIAL ISCHEMIA
• Atleast 2 anatomical contiguous lead with
the following
1. ST elevation at the J point of atleast1mm (depending on location)
2. ST DEPRESSION of atleast 0.5 mm and or T wave inversion of atleast
1mm
80.
81. ACUTE MI
• MI is defined as myocardial cell death due to prolonged
myocardial ischemia.It is diagnosed by a rise of cardiac
biomarker value above the 99th percentile limit with at least 1
of the following
1. Symptoms of ischemia
2. New ST segment T wave changes or new left bundle branch
block
3. New pathological Q waves
4. Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality
5. Identification of an intracoronary thrombus by angiography or
autopsy OR;cardiac death with symptoms suggestive
myocardial ischemia.
82. NON SURGICAL MI
1. Typical presentation
,hence early
diagnosis
1. Commonly occurs
outside the hospital
2. ST segment elevation
3. Q wave MI
4. Atherosclerotic
thrombus
obstructing coronary
artery
PERIOPERATIVE MI
1. Mostly silent,Atypical
presentation and
difficult to diagnose
2. Usually in the
hospitalised patients
within few days of
surgical procedure
3. ST segment
depression
4. None Q wave MI
5. Mismatch between
oxygen supply and
demand
83.
84. INTRAOPERATIVE MONITORS
FOR ISCHEMIA
ELECTROCARDIOGRAPHY
MYOCARDIAL ISCHEMIA
DRUG EFFECTS(DIGITALIS)
MYOCARDIAL ISCHEMIA
CONDUCTION CHANGES
LEFT VENTRICULAR HYPERTROPHY
PULMONARY CAPILLARY WEDGE PRESSURE
•MYOCARDIAL ISCHEMIA
•MITRAL REGURGITATION
•INCREASE IN AFTERLOAD
•DECREASE IN PULMONARY COMPLIANCE
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
• Myocardial ischemia
• Acute hypovolemia
• Pre existing myocardial disease
85.
86. MANAGEMENT OF MYOCARDIAL
ISCHAEMIA IN NON CARDIAC
SURGICAL PATIENTA
1. CONFIRM DIAGNOSIS
• Obtain 12 lead ECG
• Consider transoesophageal or transthoracic
echocardiogram if hemodynamic instability is
detected.
• Obtain baseline and 4 hour troponin levels.
87. OPTIMISE MYOCARDIAL
OXYGEN SUPPLY AND DEMAND
BALANCE
• Pause the surgery if appropriate while the situation is stabilized
• Achieve physiologic goals as mentioned earlier;low/normal heart
rate,normal blood pressure,normal oxygen saturations with the least
FIO2 possible,avoid hypothermia,avoid excessive fluid.
• Administer medications ;beta blockers to achieve low or normal
heart rate provided no hypotension,consider giving aspirin (via
nasogastric tube if under general anaesthesia)and a glyceryl
trinitrate infusion
• Consider use of intra-aortic balloon pump,as guided by
cardiologisits.
89. PROVEN INDICATIONS FOR
REVASCULARISATION
• Significant left main disease
• 3 vessel CAD and LV dysfunction
• 2 vessel CAD with proximal LAD
involvement
• Intractable ischemia
90.
91. • CONSIDER ABANDONING SURGERY
This will be situation-specific and involve a multidisciplinary
discussion.consider include the following
1. How unstable is the patient?
2. How urgent is the surgery?
3 .Can the surgery stio rapidly if the patient deteriorates?
If the surgery is continued ,having an experienced surgeon to
ensure shortest surgical time might be benefit to the patient.
92. CONSULT CARDIOLOGIST
• If the evidence of ST elevation MI is present
on ECG,or there is haemodynamic instability
,emergent cardiologist opinion is
recommended to consider need for PCI
• Thrombolysis is usually contraindicated if
surgical incision has been made except in
minimally invasive surgeries.
93. POST OPERATIVE
CONSIDERATONS
1. Postoperative management will be patient specific but
considerations include-
• Postoperative placement ;consider more intensive monitoring as
appropriate ,including need for telemetry.
• Consider need for seriel ECG monitoring or troponin depending on
index of suspicion of MI
• Ensure cardiology follow up or in-patient review if infarct is
suspected.
• Ensure good analgesia,euvolaemia.and the ddition of beta
blockers(blood pressure allowing )to minimise tachycardia.
• Maintain normal oxygen saturations with judicious oxygen
therapy.
• Commence aspirin and consider PGY12 inhibitor as guided by
cardiology opinion.