This document discusses cardiac arrhythmias, specifically atrial fibrillation and atrial flutter. It defines arrhythmias as irregularities in heart rhythm and describes their classification as bradyarrhythmias or tachyarrhythmias based on heart rate. For atrial fibrillation and flutter, it covers causes, diagnosis involving ECG findings, treatment goals of rate control and preventing stroke, and management strategies including medication use, cardioversion, and anticoagulation. It provides guidelines on acute treatment and long-term management based on left ventricular function.
Atrial fibrillation is an irregular heartbeat caused by uncoordinated electrical activity in the atria. It can cause blood clots, heart failure, and stroke. Diagnosis involves an ECG and testing to check for underlying causes like thyroid problems. Treatment focuses on rate control with medications and preventing clots with anticoagulants. Rhythm control methods include cardioversion, medications, and ablation procedures to restore normal sinus rhythm or slow the heart rate. Long term anticoagulation is often needed due to the risk of stroke.
This document discusses various cardiac arrhythmias including their mechanisms and treatment. It begins by describing the three main mechanisms of cardiac arrhythmia: alterations in impulse initiation (automaticity), afterdepolarizations and triggered automaticity, and abnormal impulse conduction (reentry). It then discusses various specific arrhythmias in more detail, including types of heart block, tachycardias like atrial fibrillation, flutter and sinus tachycardia, as well as treatment options like antiarrhythmic drugs, catheter ablation, and pacemakers. In summary, the document provides an overview of the conduction system of the heart and covers the pathophysiology, classification, evaluation and management of different cardiac arrhythmias.
Cardiovascular system arrhythmia Disorders of heart Rate and rhythm and condu...Srh Alshemary
This document discusses cardiac arrhythmias, including their causes, mechanisms, classification, symptoms, diagnosis and treatment. Key points include:
- Arrhythmias can occur in structurally normal hearts or those with underlying heart disease.
- Mechanisms include increased automaticity, re-entry and triggered activity.
- Arrhythmias are classified as supraventricular (narrow QRS) or ventricular (wide QRS).
- Common symptoms include palpitations, chest pain and fainting. ECG is used for diagnosis.
- Treatment depends on type of arrhythmia but may include medications, cardioversion, ablation, or implantable devices. Anticoagulation is often needed to prevent stroke
Intraoperative arrhythmias are common, occurring in nearly 11% of patients under general anesthesia. They can be caused by preexisting cardiac conditions, medications, electrolyte abnormalities, procedures, or patient-specific factors. Bradyarrhythmias such as sinus bradycardia are usually treated pharmacologically with atropine or glycopyrrolate. Tachyarrhythmias like supraventricular tachycardia may require synchronized cardioversion. Ventricular arrhythmias should be promptly addressed and their underlying causes investigated and treated. Postoperative monitoring is important, especially for patients who required treatment for arrhythmias during surgery.
The document provides information on medications, cardiovascular physiology, the autonomic nervous system, and other topics relevant to ACLS (Advanced Cardiac Life Support). It lists medications commonly used in ACLS and their effects, including epinephrine, norepinephrine, isoproterenol, vasopressin, dopamine, and more. It also reviews concepts like the components of cardiac output, alpha and beta adrenergic receptors, and the effects of medications like atropine, calcium channel blockers, and antiarrhythmics. Useful links are provided for online ECG simulators and ACLS guidelines.
This document summarizes key information about atrial fibrillation (AF), including its causes, types, diagnosis, and treatment approaches. It describes AF as an irregularly irregular heart rhythm seen on ECG without P waves. Symptoms may include palpitations. Treatment focuses on rate control with medications or ablation, as well as rhythm control via cardioversion or ablation. Long-term anticoagulation is often needed to prevent thromboembolism like stroke. Catheter ablation of the pulmonary veins can cure AF in many patients.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
Cardiac arrhythmias refer to irregularities in the heart's electrical activity and rhythm. This document discusses the definition, physiology, types, diagnosis, and treatment of various cardiac arrhythmias including:
- Supraventricular tachycardias like atrial flutter and atrial fibrillation which originate above the ventricles.
- Ventricular arrhythmias including ventricular tachycardia and ventricular fibrillation. Causes include coronary artery disease and cardiomyopathy.
- Other arrhythmias like sinus tachycardia, junctional tachycardia, and multifocal atrial tachycardia. Diagnosis involves electrocardiograms and treatment depends on the type and severity
Atrial fibrillation is an irregular heartbeat caused by uncoordinated electrical activity in the atria. It can cause blood clots, heart failure, and stroke. Diagnosis involves an ECG and testing to check for underlying causes like thyroid problems. Treatment focuses on rate control with medications and preventing clots with anticoagulants. Rhythm control methods include cardioversion, medications, and ablation procedures to restore normal sinus rhythm or slow the heart rate. Long term anticoagulation is often needed due to the risk of stroke.
This document discusses various cardiac arrhythmias including their mechanisms and treatment. It begins by describing the three main mechanisms of cardiac arrhythmia: alterations in impulse initiation (automaticity), afterdepolarizations and triggered automaticity, and abnormal impulse conduction (reentry). It then discusses various specific arrhythmias in more detail, including types of heart block, tachycardias like atrial fibrillation, flutter and sinus tachycardia, as well as treatment options like antiarrhythmic drugs, catheter ablation, and pacemakers. In summary, the document provides an overview of the conduction system of the heart and covers the pathophysiology, classification, evaluation and management of different cardiac arrhythmias.
Cardiovascular system arrhythmia Disorders of heart Rate and rhythm and condu...Srh Alshemary
This document discusses cardiac arrhythmias, including their causes, mechanisms, classification, symptoms, diagnosis and treatment. Key points include:
- Arrhythmias can occur in structurally normal hearts or those with underlying heart disease.
- Mechanisms include increased automaticity, re-entry and triggered activity.
- Arrhythmias are classified as supraventricular (narrow QRS) or ventricular (wide QRS).
- Common symptoms include palpitations, chest pain and fainting. ECG is used for diagnosis.
- Treatment depends on type of arrhythmia but may include medications, cardioversion, ablation, or implantable devices. Anticoagulation is often needed to prevent stroke
Intraoperative arrhythmias are common, occurring in nearly 11% of patients under general anesthesia. They can be caused by preexisting cardiac conditions, medications, electrolyte abnormalities, procedures, or patient-specific factors. Bradyarrhythmias such as sinus bradycardia are usually treated pharmacologically with atropine or glycopyrrolate. Tachyarrhythmias like supraventricular tachycardia may require synchronized cardioversion. Ventricular arrhythmias should be promptly addressed and their underlying causes investigated and treated. Postoperative monitoring is important, especially for patients who required treatment for arrhythmias during surgery.
The document provides information on medications, cardiovascular physiology, the autonomic nervous system, and other topics relevant to ACLS (Advanced Cardiac Life Support). It lists medications commonly used in ACLS and their effects, including epinephrine, norepinephrine, isoproterenol, vasopressin, dopamine, and more. It also reviews concepts like the components of cardiac output, alpha and beta adrenergic receptors, and the effects of medications like atropine, calcium channel blockers, and antiarrhythmics. Useful links are provided for online ECG simulators and ACLS guidelines.
This document summarizes key information about atrial fibrillation (AF), including its causes, types, diagnosis, and treatment approaches. It describes AF as an irregularly irregular heart rhythm seen on ECG without P waves. Symptoms may include palpitations. Treatment focuses on rate control with medications or ablation, as well as rhythm control via cardioversion or ablation. Long-term anticoagulation is often needed to prevent thromboembolism like stroke. Catheter ablation of the pulmonary veins can cure AF in many patients.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
Cardiac arrhythmias refer to irregularities in the heart's electrical activity and rhythm. This document discusses the definition, physiology, types, diagnosis, and treatment of various cardiac arrhythmias including:
- Supraventricular tachycardias like atrial flutter and atrial fibrillation which originate above the ventricles.
- Ventricular arrhythmias including ventricular tachycardia and ventricular fibrillation. Causes include coronary artery disease and cardiomyopathy.
- Other arrhythmias like sinus tachycardia, junctional tachycardia, and multifocal atrial tachycardia. Diagnosis involves electrocardiograms and treatment depends on the type and severity
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by irregular electrical activity in the atria. It increases in prevalence with age and can cause complications like heart failure, stroke, and systemic embolism.
2) Management of atrial fibrillation involves rate or rhythm control as well as long-term anticoagulation to prevent thromboembolism depending on stroke risk factors. The CHA2DS2-VASc score is used to assess this risk.
3) While antiarrhythmic drugs and cardioversion can restore normal sinus rhythm, rate control is preferred for many patients. Newer anticoagulants like dabigatran and rivar
Cardiac arrhythmias occur when the heart's electrical signals don't work properly, causing the heart to beat too fast, too slow, or irregularly. Arrhythmias can be harmless but some can cause life-threatening symptoms. Treatment may include medications, procedures, implanted devices, or surgery to control fast, slow, or irregular heartbeats. Types of arrhythmias include bradyarrhythmias and tachyarrhythmias. Tachyarrhythmias can be caused by enhanced automaticity, afterdepolarizations, or re-entry of electrical signals in the heart.
This document discusses antiarrhythmic agents and their mechanisms and classifications. It begins by describing the normal cardiac conduction pathway and different types of arrhythmias including their causes. Antiarrhythmic drugs are classified into four classes based on their effects on the cardiac action potential and ion channels. Class I drugs block fast sodium channels, class II are beta blockers, class III block potassium channels, and class IV block calcium channels. Examples from each class like quinidine, propranolol, amiodarone, and verapamil are described in more detail regarding their mechanisms and uses.
This document provides an overview of tachyarrhythmias and their mechanisms. It discusses the normal cardiac conduction system and describes how abnormalities can lead to arrhythmias via mechanisms like accelerated automaticity, triggered activity, and reentry. It then focuses on atrial fibrillation, describing its classification, causes, diagnosis, and treatment approaches like rate control and anticoagulation based on stroke risk scores. The document emphasizes the importance of evaluating hemodynamic stability and controlling heart rate for arrhythmia patients.
This document discusses antiarrhythmic drugs used to treat cardiac arrhythmias. It begins by defining arrhythmias and describing the causes. It then discusses the Vaughan Williams classification system for antiarrhythmic drugs. Class I drugs like quinidine, procainamide and flecainide work by blocking sodium channels. Class II drugs like propranolol are beta blockers. Class III drugs like amiodarone work by prolonging the action potential. The document provides details on specific drugs, their mechanisms of action, uses, doses and side effects. It emphasizes restoring normal rhythm and rate while preventing more dangerous arrhythmias.
This document discusses the management of peri-arrest arrhythmias. It defines arrhythmias and describes their assessment and general treatment options. It covers the management of specific arrhythmias like bradycardia and tachycardias. It also discusses the pharmacology of common antiarrhythmic drugs like amiodarone, atropine, digoxin. The document provides guidelines on stabilizing patients and restoring normal heart rhythm in peri-arrest settings.
A deep dive into management of cardiac arrhythmia from a Critical Care perspective. Covers brady- and tachyarrhythmias and management of both the stable and unstable patient.
The document discusses pharmacotherapy for arrhythmias, describing various types of arrhythmias caused by defects in impulse generation or propagation in the heart. It covers the mechanisms of different arrhythmias and classifications of antiarrhythmic drugs, focusing on classes I-IV and how they work by blocking sodium, potassium, or calcium channels to treat arrhythmias. Examples of commonly used antiarrhythmic drugs are provided for each class along with their mechanisms of action, effects, uses, and potential adverse effects.
1. Rate control is the initial approach for elderly patients with minor AF symptoms, while rhythm control may be considered for symptomatic patients despite rate control.
2. Catheter ablation is recommended for symptomatic patients where medical therapy fails, and can be considered as initial therapy in some selected patients.
3. Anticoagulation is recommended for AF patients based on their stroke risk profile according to CHA2DS2-VASc score. Warfarin requires careful management during pregnancy.
This document discusses various cardiac medications that are often mixed and matched to treat different heart conditions. It provides information on:
- How sodium-potassium pumps and calcium channels impact heart cell contraction and repolarization.
- Common classes of cardiac medications including antiarrhythmics, beta blockers, calcium channel blockers, ACE inhibitors, and ARBs.
- Specific medications within each class, their mechanisms and uses for treating arrhythmias, hypertension, heart failure, and other conditions.
This document discusses various cardiac medications that are often mixed and matched to treat different heart conditions. It provides information on:
- How sodium-potassium pumps and calcium channels impact heart cell contraction and repolarization.
- Common classes of cardiac medications including antiarrhythmics, beta blockers, calcium channel blockers, ACE inhibitors, and ARBs.
- Specific medications within each class, their mechanisms and uses for treating arrhythmias, hypertension, heart failure, and other conditions.
In patients with acute myocardial infarction (AMI), arrhythmias are common. 90% will develop some form of cardiac arrhythmia, with 25% occurring within the first 24 hours. Arrhythmias can be classified as tachyarrhythmias (ventricular, supraventricular) or bradyarrhythmias (bradycardias, heart blocks). Life-threatening ventricular arrhythmias like ventricular fibrillation and ventricular tachycardia are treated with defibrillation or antiarrhythmic drugs like amiodarone. Other arrhythmias seen in AMI include atrial fibrillation, sinus tachycardia, and various heart blocks. Temporary pacing may be needed for symptomatic bradyarrhythmias
This document presents information on various types of atrial arrhythmias. It discusses premature atrial complexes, atrial tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation, and wandering atrial pacemaker. For each type, it covers etiology, characteristics, and treatment approaches. The document is presented by Baby Haokip from the College of Nursing, NEIGRIHMS.
Cardiac arrhythmias are abnormal heart rhythms that can be caused by issues with impulse formation, conduction, or both. The document defines different types of arrhythmias and their causes. It discusses evaluation and management approaches including pharmacological therapy with antiarrhythmic drugs, electrical cardioversion, pacemaker implantation, catheter ablation procedures, and surgery. Common arrhythmias like atrial fibrillation, atrial flutter, premature beats, and ventricular tachycardia are explained in terms of their presentation and treatment.
The document defines and classifies different types of arrhythmias. It discusses the etiology, symptoms, electrocardiogram characteristics and treatment options for various arrhythmias including sinus arrhythmia, atrial fibrillation, ventricular tachycardia, premature contractions, and more. Anti-arrhythmia medications are also categorized based on their mechanisms of action.
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.
Varner Medical Antiarrhythmics 2009.pptMaggieAlex1
This document summarizes drugs used to treat cardiac arrhythmias. It defines arrhythmias as variations in cardiac impulse formation or propagation. It describes how different classes of drugs target specific ion channels like sodium, potassium, and calcium channels to modify the cardiac action potential in ways that suppress arrhythmias, such as by slowing conduction, prolonging refractory periods, or decreasing automaticity. Side effects and uses are provided for each major drug class, including local anesthetics, beta blockers, antiarrhythmics that block potassium channels, calcium channel blockers, and other miscellaneous agents like adenosine, digoxin, atropine, and magnesium. Non-pharmacological treatments like cardioversion, ablation, and
This document discusses dysrhythmias, which are disorders of the heart's electrical conduction or rhythm. Dysrhythmias can be diagnosed by electrocardiogram and may cause changes in blood pressure or pumping of the heart. Common types of dysrhythmias discussed include normal sinus rhythm, sinus bradycardia, sinus tachycardia, premature atrial complexes, atrial flutter, and atrial fibrillation. Nursing management focuses on treating the underlying cause, controlling heart rate, and preventing complications like stroke.
This document discusses antiarrhythmic drugs, which are used to treat abnormal heart rhythms known as cardiac arrhythmias. It defines arrhythmias and describes their causes and mechanisms. It then classifies antiarrhythmic drugs into four main classes based on their effects on ion channels in the heart muscle. For each class, it provides examples of drugs, their mechanisms of action, uses, and common side effects. The classes are sodium channel blockers, beta blockers, potassium channel blockers, and calcium channel blockers.
This document discusses gout and hyperuricemia. It defines gout as a type of inflammatory arthritis caused by uric acid crystals depositing in joints. Gout is associated with hyperuricemia, an elevated uric acid level. The document reviews risk factors, pathophysiology, clinical presentation, diagnosis, and treatment approaches including lifestyle changes, medications to treat acute attacks, and long-term urate-lowering therapy. It provides details on medications commonly used to treat gout such as allopurinol, febuxostat, colchicine, NSAIDs, and corticosteroids.
The document defines shock and describes its various types, including hypovolemic, cardiogenic, obstructive, and distributive shock. It discusses the pathophysiology, clinical presentation, diagnosis, and general treatment approach for shock. Regarding treatment, it emphasizes early correction of pulse, ventilation, oxygenation, and fluid administration. It then provides specific protocols for resuscitation in cases of hypovolemia and septic shock.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by irregular electrical activity in the atria. It increases in prevalence with age and can cause complications like heart failure, stroke, and systemic embolism.
2) Management of atrial fibrillation involves rate or rhythm control as well as long-term anticoagulation to prevent thromboembolism depending on stroke risk factors. The CHA2DS2-VASc score is used to assess this risk.
3) While antiarrhythmic drugs and cardioversion can restore normal sinus rhythm, rate control is preferred for many patients. Newer anticoagulants like dabigatran and rivar
Cardiac arrhythmias occur when the heart's electrical signals don't work properly, causing the heart to beat too fast, too slow, or irregularly. Arrhythmias can be harmless but some can cause life-threatening symptoms. Treatment may include medications, procedures, implanted devices, or surgery to control fast, slow, or irregular heartbeats. Types of arrhythmias include bradyarrhythmias and tachyarrhythmias. Tachyarrhythmias can be caused by enhanced automaticity, afterdepolarizations, or re-entry of electrical signals in the heart.
This document discusses antiarrhythmic agents and their mechanisms and classifications. It begins by describing the normal cardiac conduction pathway and different types of arrhythmias including their causes. Antiarrhythmic drugs are classified into four classes based on their effects on the cardiac action potential and ion channels. Class I drugs block fast sodium channels, class II are beta blockers, class III block potassium channels, and class IV block calcium channels. Examples from each class like quinidine, propranolol, amiodarone, and verapamil are described in more detail regarding their mechanisms and uses.
This document provides an overview of tachyarrhythmias and their mechanisms. It discusses the normal cardiac conduction system and describes how abnormalities can lead to arrhythmias via mechanisms like accelerated automaticity, triggered activity, and reentry. It then focuses on atrial fibrillation, describing its classification, causes, diagnosis, and treatment approaches like rate control and anticoagulation based on stroke risk scores. The document emphasizes the importance of evaluating hemodynamic stability and controlling heart rate for arrhythmia patients.
This document discusses antiarrhythmic drugs used to treat cardiac arrhythmias. It begins by defining arrhythmias and describing the causes. It then discusses the Vaughan Williams classification system for antiarrhythmic drugs. Class I drugs like quinidine, procainamide and flecainide work by blocking sodium channels. Class II drugs like propranolol are beta blockers. Class III drugs like amiodarone work by prolonging the action potential. The document provides details on specific drugs, their mechanisms of action, uses, doses and side effects. It emphasizes restoring normal rhythm and rate while preventing more dangerous arrhythmias.
This document discusses the management of peri-arrest arrhythmias. It defines arrhythmias and describes their assessment and general treatment options. It covers the management of specific arrhythmias like bradycardia and tachycardias. It also discusses the pharmacology of common antiarrhythmic drugs like amiodarone, atropine, digoxin. The document provides guidelines on stabilizing patients and restoring normal heart rhythm in peri-arrest settings.
A deep dive into management of cardiac arrhythmia from a Critical Care perspective. Covers brady- and tachyarrhythmias and management of both the stable and unstable patient.
The document discusses pharmacotherapy for arrhythmias, describing various types of arrhythmias caused by defects in impulse generation or propagation in the heart. It covers the mechanisms of different arrhythmias and classifications of antiarrhythmic drugs, focusing on classes I-IV and how they work by blocking sodium, potassium, or calcium channels to treat arrhythmias. Examples of commonly used antiarrhythmic drugs are provided for each class along with their mechanisms of action, effects, uses, and potential adverse effects.
1. Rate control is the initial approach for elderly patients with minor AF symptoms, while rhythm control may be considered for symptomatic patients despite rate control.
2. Catheter ablation is recommended for symptomatic patients where medical therapy fails, and can be considered as initial therapy in some selected patients.
3. Anticoagulation is recommended for AF patients based on their stroke risk profile according to CHA2DS2-VASc score. Warfarin requires careful management during pregnancy.
This document discusses various cardiac medications that are often mixed and matched to treat different heart conditions. It provides information on:
- How sodium-potassium pumps and calcium channels impact heart cell contraction and repolarization.
- Common classes of cardiac medications including antiarrhythmics, beta blockers, calcium channel blockers, ACE inhibitors, and ARBs.
- Specific medications within each class, their mechanisms and uses for treating arrhythmias, hypertension, heart failure, and other conditions.
This document discusses various cardiac medications that are often mixed and matched to treat different heart conditions. It provides information on:
- How sodium-potassium pumps and calcium channels impact heart cell contraction and repolarization.
- Common classes of cardiac medications including antiarrhythmics, beta blockers, calcium channel blockers, ACE inhibitors, and ARBs.
- Specific medications within each class, their mechanisms and uses for treating arrhythmias, hypertension, heart failure, and other conditions.
In patients with acute myocardial infarction (AMI), arrhythmias are common. 90% will develop some form of cardiac arrhythmia, with 25% occurring within the first 24 hours. Arrhythmias can be classified as tachyarrhythmias (ventricular, supraventricular) or bradyarrhythmias (bradycardias, heart blocks). Life-threatening ventricular arrhythmias like ventricular fibrillation and ventricular tachycardia are treated with defibrillation or antiarrhythmic drugs like amiodarone. Other arrhythmias seen in AMI include atrial fibrillation, sinus tachycardia, and various heart blocks. Temporary pacing may be needed for symptomatic bradyarrhythmias
This document presents information on various types of atrial arrhythmias. It discusses premature atrial complexes, atrial tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation, and wandering atrial pacemaker. For each type, it covers etiology, characteristics, and treatment approaches. The document is presented by Baby Haokip from the College of Nursing, NEIGRIHMS.
Cardiac arrhythmias are abnormal heart rhythms that can be caused by issues with impulse formation, conduction, or both. The document defines different types of arrhythmias and their causes. It discusses evaluation and management approaches including pharmacological therapy with antiarrhythmic drugs, electrical cardioversion, pacemaker implantation, catheter ablation procedures, and surgery. Common arrhythmias like atrial fibrillation, atrial flutter, premature beats, and ventricular tachycardia are explained in terms of their presentation and treatment.
The document defines and classifies different types of arrhythmias. It discusses the etiology, symptoms, electrocardiogram characteristics and treatment options for various arrhythmias including sinus arrhythmia, atrial fibrillation, ventricular tachycardia, premature contractions, and more. Anti-arrhythmia medications are also categorized based on their mechanisms of action.
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.
Varner Medical Antiarrhythmics 2009.pptMaggieAlex1
This document summarizes drugs used to treat cardiac arrhythmias. It defines arrhythmias as variations in cardiac impulse formation or propagation. It describes how different classes of drugs target specific ion channels like sodium, potassium, and calcium channels to modify the cardiac action potential in ways that suppress arrhythmias, such as by slowing conduction, prolonging refractory periods, or decreasing automaticity. Side effects and uses are provided for each major drug class, including local anesthetics, beta blockers, antiarrhythmics that block potassium channels, calcium channel blockers, and other miscellaneous agents like adenosine, digoxin, atropine, and magnesium. Non-pharmacological treatments like cardioversion, ablation, and
This document discusses dysrhythmias, which are disorders of the heart's electrical conduction or rhythm. Dysrhythmias can be diagnosed by electrocardiogram and may cause changes in blood pressure or pumping of the heart. Common types of dysrhythmias discussed include normal sinus rhythm, sinus bradycardia, sinus tachycardia, premature atrial complexes, atrial flutter, and atrial fibrillation. Nursing management focuses on treating the underlying cause, controlling heart rate, and preventing complications like stroke.
This document discusses antiarrhythmic drugs, which are used to treat abnormal heart rhythms known as cardiac arrhythmias. It defines arrhythmias and describes their causes and mechanisms. It then classifies antiarrhythmic drugs into four main classes based on their effects on ion channels in the heart muscle. For each class, it provides examples of drugs, their mechanisms of action, uses, and common side effects. The classes are sodium channel blockers, beta blockers, potassium channel blockers, and calcium channel blockers.
This document discusses gout and hyperuricemia. It defines gout as a type of inflammatory arthritis caused by uric acid crystals depositing in joints. Gout is associated with hyperuricemia, an elevated uric acid level. The document reviews risk factors, pathophysiology, clinical presentation, diagnosis, and treatment approaches including lifestyle changes, medications to treat acute attacks, and long-term urate-lowering therapy. It provides details on medications commonly used to treat gout such as allopurinol, febuxostat, colchicine, NSAIDs, and corticosteroids.
The document defines shock and describes its various types, including hypovolemic, cardiogenic, obstructive, and distributive shock. It discusses the pathophysiology, clinical presentation, diagnosis, and general treatment approach for shock. Regarding treatment, it emphasizes early correction of pulse, ventilation, oxygenation, and fluid administration. It then provides specific protocols for resuscitation in cases of hypovolemia and septic shock.
1) Venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE), results from blood clots forming in the veins. VTE is potentially fatal and is more likely to occur in immobilized patients, those with hypercoagulable disorders, or after trauma or surgery.
2) PE occurs when a clot breaks off and lodges in the lung arteries, partially or fully blocking blood flow. Patients with PE have a higher risk of recurrent VTE than those with DVT alone.
3) Treatment of VTE involves both prevention and acute phase treatment, with the goals of preventing PE/complications and reducing mortality and treatment side
This document discusses hyperlipidemia and dyslipidemia. It begins by defining hyperlipidemia and dyslipidemia as elevated blood levels of lipoproteins including cholesterol, triglycerides, and phospholipids. Abnormal lipoprotein levels increase the risk of coronary heart disease. The document then covers the pathophysiology of lipoprotein transport and metabolism. It describes the clinical presentation of hyperlipidemia, which is often asymptomatic initially. Diagnosis involves lipid profiling and classification of cholesterol and triglyceride levels. The focus of treatment is lowering LDL cholesterol through lifestyle changes and lipid-lowering drugs like statins when necessary.
This document provides information on osteoarthritis (OA), including its pathophysiology, risk factors, clinical presentation, diagnosis, and treatment approaches. It discusses how OA most commonly affects weight-bearing joints in older adults. The goals of treatment are outlined as relieving pain, maintaining mobility, and preserving joint integrity. First-line treatment involves non-pharmacological approaches like education, exercise, and weight loss, along with acetaminophen and topical or oral NSAIDs. For patients who do not respond to initial treatment, options include tramadol, duloxetine, intra-articular corticosteroids, and opioids. Treatment is tailored based on the specific joints affected, with topical therapies emphasized for hand
This document discusses stable and acute ischemic heart disease. It begins by defining coronary heart disease and coronary artery disease. It then discusses the etiology, pathophysiology, risk factors, classification, clinical presentation, and desired outcomes of stable ischemic heart disease. It covers the general treatment approach including risk factor modification, drug therapy using antiplatelet agents, ACE inhibitors, statins, beta-blockers, calcium channel blockers, and nitrates. It then discusses acute coronary syndromes including unstable angina, non-ST-elevation myocardial infarction, and ST-elevation myocardial infarction. It covers risk stratification, general treatment approach, and early pharmacotherapy for ST-elevation myocardial infarction.
Acute coronary syndromes (ACS) include unstable angina and myocardial infarction, which are forms of coronary heart disease caused by reduced blood flow due to plaque rupture and clot formation in the coronary arteries. The document discusses the epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and treatment of ACS. It provides details on evaluating patients using biomarkers, ECG, risk scores, restoring blood flow through procedures like PCI or fibrinolysis, and employing antiplatelet and anticoagulant medications in the early treatment of ACS.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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2. Definition
Arrhythmias = loss of heart rhythm
Occurs when the electrical impulses in the heart that
coordinate heartbeats don't function properly
Causes the heart to beat too fast, too slow or
irregularly
Can be broadly grouped into bradyarrhythmias and
tachyarrhythmias.
2
3. Normal conduction of the heart
Sinoatrial node
Atrioventricular node
Bundle of His
Purkinje fibers 3
5. Pathogenesis
3 basic mechanisms:
enhanced or suppressed automaticity
• Due to
• Ischemia, scarring, electrolyte disturbances, medications, advancing
age, excess catecholamine activity
triggered activity
• Attempt to depolarize before or after the cell is fully repolarized
• torsades de pointes- initiated by early after-depolarization
• ventricular arrhythmias caused by digitalis toxicity- delayed after-
depolarization
re-entry
• Most common
• Supraventricular and monomorphic ventricular tachycardia
5
6. Risk Factors
Coronary artery disease
High blood pressure
Diabetes
Smoking
High cholesterol
Obesity
Excessive alcohol use
Drug abuse
Stress
Family history of heart disease
Advancing age
Certain medications, dietary
supplements and herbal remedies
6
7. Signs and symptoms
Most common signs &
symptoms:
Palpitation
A slow heartbeat
An irregular heartbeat
Feeling pauses between
heartbeats
More serious signs &
symptoms:
Anxiety
Weakness, dizziness, and
lightheadedness
Fainting or nearly fainting
Sweating
Shortness of breath
Chest pain (angina)
7
9. CLASS I: SODIUM CHANNEL BLOCKING DRUGS
IA - lengthen APD (Action Potential Duration)- (longer QT
interval)
Moderate slowing of phase 0 (medium Na blockade)
used for supraventricular & ventricular arrhythmias
Disopyramide, Quinidine, Procainamide
IB - Shorten APD
Minimal slowing of phase 0 (least Na blockade)
therefore shorter QT interval
Used primarily in ventricular arrhythmias
Lidocaine, Mexiletene, Tocainide, Phenytoin
IC - no effect APD
Maximal slowing of phase 0 (greatest Na blockade)
Effective for both ventricular & supraventricular
9
10. CLASS II: BETA-BLOCKING AGENTS
↓ AV nodal conduction
↑ PR interval & prolong AV nodal refractoriness
In the SA node, they reduce automaticity
Reduce adrenergic activity
In the atria and ventricles, they reduce contractility
reduce calcium entry (during fast and slow potentials) and
depress phase 4 depolarization (in slow potentials only)
Propranolol, Esmolol, Metoprolol, Sotalol
10
11. CLASS III: POTASSIUM CHANNEL BLOCKERS
Prolong effective refractory period by prolonging
Action Potential
↑↑ Refractory Period with little or no effect on
conduction velocity & automaticity
Amiodarone & Dronedarone (dAlso has sodium, calcium,
and B-blocking actions)
Ibutilide & Dofetilide (pure Kr blockers)
Sotalol (also B blocker)
Bretylium
11
12. CLASS IV: CALCIUM CHANNEL BLOCKERS
Blocks cardiac calcium currents
velocity of AV nodal conduction decreases,
•↑ PR interval
increase refractory period
• esp. in Ca2+ dependent tissues (i.e. AV node)
• Antidysrhythmic benefits derive from suppressing AV
nodal conduction
Verapamil, Diltiazem
12
13. Supraventricular arrhythmias
Originate from above the bifurcation (branching) of the
bundle of His
Include
Atrial fibrilation
Atrial flutter
Paroxysmal sinus tachycardia
Etopic atrial tachycardia
Paroxysmal supraventricular tachycardias (PSVT)
14. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Atrial fibrillation and atrial flutter are common
supraventricular tachycardias.
Atrial fibrillation is characterized by extremely rapid (atrial
rate of 400–600 beats/min) and disorganized atrial
activation
Atrial flutter occurs less frequently than AF, This
arrhythmia is characterized by rapid (270 to 330 atrial
beats/min) but regular atrial activation.
14
15. ATRIAL FIBRILLATION/FLUTTER
Causes/Etiology:
Cardiac: atrial septal defect, Previous cardiac surgery,
HTN, Coronary arterial disease, cardiomyopathy, mitral
valve disease, Pericarditis
Systemic: alcohol, CVA, chronic pulmonary disease,
electrolyte abnormalities, fever, hypothermia,
Hyperthyroidism, Sleep apnea, Alcohol abuse, Smoking,
Excessive caffeine consumption.
Patients with AF are at risk for thrombotic stroke
risk increases following restoration of normal sinus rhythm,
• or in patients with other comorbidities (HF, cardiomyopathy,
congenital heart disease, thyrotoxicosis)
Pathophysiology: Predominant mechanism is reentry, usually
16. Diagnosis
ECG shows irregularly irregular supraventricular rhythm
with no discernible, consistent atrial activity (P waves);
ventricular response usually 120–180 beats/min.
Desired Outcomes
Prevent thromboembolic complications.
16
17. ATRIAL FIBRILLATION/FLUTTER
Management
Treatment (Desired Outcomes)
Relieve symptoms
Slowing ventricular rate: (Digoxin, BBs, CCBs)
Restoring normal sinus rhythm
Chemical cardioconversion: (ibutilide, propafenone,
flecainide)
Electrical: (DCC) Hemodynamically unstable patients
Preventing AF recurrences
Class IA, IC, III antiarrhythmic agents for maintenance of sinus
rhythm
Reduce risk of stroke
18. Atrial Fibrillation and Atrial Flutter
Acute Treatment
with signs and/or symptoms of hemodynamic instability
(e.g., severe hypotension, angina, or pulmonary edema,
qualifies as a medical emergency
DCC is indicated as first-line therapy in an attempt to
immediately restore sinus rhythm (without regard to the risk
of thromboembolism).
18
19. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
If patients are hemodynamically stable, there is no
emergent need to restore sinus rhythm.
Instead, the focus should be directed toward controlling
the patient’s ventricular rate.
Achieving adequate ventricular rate control is a treatment
goal for all patients with AF.
19
20. ATRIAL FIBRILLATION AND ATRIAL FLUTTER
Acute Treatment
Initial therapy, drugs that slow conduction and ↑
refractoriness in the AV node (e.g., βBs,
nondihydropyridine CCBs, or digoxin).
use of digoxin for achieving ventricular rate control,
especially in patients with normal LV systolic function
(left ventricular ejection fraction [LVEF] >40%) not
recommended.
its relatively slow onset & its inability to control heart rate during
exercise.
digoxin , ineffective for controlling ventricular rate under
conditions of ↑ed sympathetic tone (i.e., surgery,
thyrotoxicosis)
20
21. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
IV βBs (propranolol, metoprolol, esmolol),
diltiazem, or verapamil is preferred
a relatively quick onset and can effectively control the
ventricular rate at rest and during exercise.
β- blockers are also effective for controlling ventricular rate
under conditions of increased sympathetic tone.
21
22. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
Drug selection to control ventricular rate in the acute
setting should be primarily based on the patient’s LV
function.
In patients with normal LV function (LVEF >40%), IV
βBs, diltiazem, or verapamil is recommended as first-
line therapy
If LVEF ≤40%, IV diltiazem or verapamil should be
avoided because of their potent negative inotropic
effects. 22
23. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
If Exacerbation of HF symptoms, IV administration of
either digoxin or amiodarone should be used as first-
line therapy to achieve ventricular rate control.
IV amiodarone can also be used in patients who are
refractory to or have C/Is to βBs, nondihydropyridine CCBs,
and digoxin
But use of amiodarone for controlling ventricular rate may
also stimulate the conversion of AF to sinus rhythm, and
place the patient at risk for a thromboembolic event.
23
24. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
Because a rhythm control strategy does not confer any
advantage over a rate-control strategy in the management
of AF
Now it remains acceptable to allow patients to remain in
AF, while being chronically treated with AV nodal-blocking
agents to achieve adequate ventricular rate control (e.g.,
HR <80 beats/min at rest and <100 beats/min during
exercise).
24
25. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
The selection of an AV nodal-blocking agent to control ventricular
rate in the chronic setting primarily based on the patient’s LV
function.
normal LV function
In patients with normal LV function (LVEF >40%), oral βBs,
diltiazem, or verapamil are preferred over digoxin because of
their relatively quick onset and maintained efficacy during
exercise.
When adequate ventricular rate control cannot be achieved with
one of these agents, the addition of digoxin may provide an
additive lowering of the heart rate.
25
26. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
LV dysfunction
Verapamil and diltiazem should not be used (LVEF ≤40%).
βBs (i.e., metoprolol, carvedilol, or bisoprolol) and digoxin are
preferred, as these agents are also concomitantly used to treat
chronic HF;
if possible, βBs should be considered over digoxin in this situation
because of their survival benefits in patients with LV systolic
dysfunction.
If patients are having an episode of decompensated
HF, digoxin is preferred first-line therapy
26
27. AF……ANTICOAGULATION
In those patients in whom it is decided to restore sinus
rhythm, one must consider that this very act (regardless of
whether an electrical or pharmacologic method is chosen)
places the patient at risk for a thromboembolic event.
the return of sinus rhythm restores effective contraction in
the atria, which may dislodge poorly adherent thrombi.
Administering antithrombotic therapy prior to cardioversion
not only prevents clot growth & formation of new thrombi
but also allows existing thrombi to become organized &
well-adherent to the atrial wall. 27
28. AF…..ANTICOAGULATION THERAPY
Indicated for
CVA Prevention in Atrial fibrillation
Preparation for atrial fibrillation cardioversion
Atrial fibrillation < 48 hours
Consider Heparin (UFH, lMWH) while considering cardioversion
Consider early atrial fibrillation cardioversion
Atrial fibrillation >48 hours
Warfarin – 3 weeks before cardioversion
Consider atrial fibrillation cardioversion
Continue warfarin for 4 weeks after cardioversion
Dosing
Target INR 2-3
Tight INR control is important
INR 1.5-1.9 with 2 fold risk of severe CVA
INR 1.5-1.9 with 3 fold risk of mortality
29. AF……ANTICOAGULATION
patients become at ↑ed risk of thrombus formation and a
subsequent embolic event particularly if duration of AF
exceeds 48 hours.
patients with AF for longer than 48 hours or an unknown
duration should receive warfarin (target INR 2.5; range: 2.0
to 3.0) for at least 3 weeks prior to cardioversion.
After restoration of sinus rhythm, full atrial contraction
returns gradually to a maximum contractile force over a 3-
to 4-week period.
warfarin continued for at least 4 weeks after effective
cardioversion and return of sinus rhythm 29
30. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
methods of restoring sinus rhythm in patients with AF or
atrial flutter:
pharmacologic cardioversion and
DCC.
The disadvantages of pharmacologic cardioversion are the
risk of significant side effects
the inconvenience of drug–drug interactions (e.g.,
digoxin–amiodarone), and
drugs are generally less effective when compared to
DCC.
The advantages of DCC are that it is quick and more often
30
31. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
Pharmacologic cardioversion appears to be most effective
when initiated within 7 days after the onset of AF
Single, oral loading doses of propafenone (600 mg) or
flecainide (300 mg) are effective for conversion of
recent onset AF and provide a simple regimen.
A method called the “pill-in- the-pocket” approach was
recently endorsed by the treatment guidelines.
In patients with AF that is longer than 7 days in duration,
only dofetilide, amiodarone, and ibutilide have proven
efficacy for cardioversion.
31
32. ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
Selection of an antiarrhythmic drug should be based on whether the
patient has structural heart disease (SHD) (e.g., LV dysfunction,
coronary artery disease, valvular heart disease, LV hypertrophy)
In the absence of any structural heart disease, the use of a single,
oral loading dose of flecainide or propafenone is a reasonable
approach for cardioversion
In patients with underlying SHD, these antiarrhythmics should be
avoided , and amiodarone or dofetilide should be used instead.
amiodarone can be administered safely on an outpatient basis
because of its low proarrhythmic potential, dofetilide can only be
initiated in the hospital.
32
33. TABLE Guidelines for Selecting AADs for Maintenance of Sinus Rhythm
in Patients with Recurrent Paroxysmal (Persistent) AF
No structural heart disease
1st line: flecainide, propafenone, or sotalol
2nd line: amiodarone, dofetilide, or dronedarone (catheter ablation be
considered as alternative to AAD)
Heart failure
1st line: amiodarone or dofetilide
2nd line: catheter ablation
Coronary artery diseasea
1st line: sotalol (to be used only if patients have normal LV systolic
function)
2nd line: amiodarone, dofetilide, or dronedaroneb (catheter ablation
alternative to AAD)
Hypertension
Presence of significant LVH: 1st line: amiodarone; 2nd line: catheter
ablation
Absence of significant LVH:
The normal electrical conduction of the heart allows electrical propagation to be transmitted from the Sinoatrial Node through both atria and forward to the Atrioventricular Node.
3The impulses then enter the base of the ventricle at the Bundle of His and then follow the left and right bundle branches along the interventricular septum. These specialized fibers conduct the impulses at a very rapid velocity (about 2 m/sec). The bundle branches then divide into an extensive system of Purkinje fibers that conduct the impulses at high velocity (about 4 m/sec)
Prolong action potential duration by increasing repolarization and refractoriness (amiodarone, sotalol, bretylium, dofetilide, azimilide, ibutilide)
Supraventricular arrhythmias
PSVT:
Is reentry to Av node and HR 180-200bpm
Mgt: Valsalva maneuver, DCC if hemodynamic instability
Pharmacologic: that slow conduction & ↑refractoriness: Adenosine=DOC, CCBs, BBs or digoxin occasionally IA & IC
WPWS:
excitation of ventricle before regular impulse arrival via AV node
Non cologic Mgt: Radiofrequency catheter ablation
Pharmacologic mgt: drugs that slow AV conduction and ↑ refractory period: Class I agent s but IB is least effective
ATRIAL FIBRILLATION AND ATRIAL FLUTTER At. Flatter 270 to 330 atrial beats/min but regular atrial activation.
At. Fibr 400 to 600 atrial beats/min with disorganized atrial activation.
ATRIAL FIBRILLATION AND ATRIAL FLUTTER Acute Treatment
Hemodynamically unstable-medical emergency: restore sinus rhythm is the goal …. DCC
Hemodynamically stable: controlling ventricular rate is the goal…. drugs that slow conduction and ↑ refractoriness in AV node (BBs, NDP CCBs, Digoxine, Amiodareone)
Normal EF: βBs, NDP CCBs first line
LVD: BBs preferred
Exacerbation of HF symptoms: Digoxin, Amiodareone (Thromboembolic risk) preferred
ATRIAL FIBRILLATION AND ATRIAL FLUTTER chronic management
Rate-control strategy: AV nodal-blocking agents (BBs, CCBs, Digoxin)
normal LV function: βBs, diltiazem, or verapamil or βBs, diltiazem, or verapamil + digoxin
LV dysfunction: βBs >digoxin (Avoid CCBs)
If episode of decompensated HF: Digoxin preferred
Rhythm control strategy
methods of restoring sinus rhythm in patients with AF or atrial flutter: is cardioversion
pharmacologic cardioversion ()
within 7 days and/or no SHD: Single, oral loading doses of propafenone (600 mg) or flecainide (300 mg)
After 7 days and/or has SHD: dofetilide and amiodarone,
DCC
Sinus rhythm restoration (both of electrical or pharmacologic) places the patient at risk for a thromboembolic event……antithrombotic therapy prior to cardioversion mandatory
Atrial fibrillation < 48 hours, Consider Heparin for 24 hrs then …. considering early AF cardioversion
Atrial fibrillation >48 hours (↑ risk & prolonged risk of clot): Warfarin – 3 weeks before cardioversion…Consider AF cardioversion….Continue warfarin for 4 weeks after cardioversion
CVA prevention with anticoagulant in AF is also indicated
ATRIAL FIBRILLATION AND ATRIAL FLUTTER Acute Treatment
Hemodynamically unstable-medical emergency: restore sinus rhythm is the goal …. DCC
Hemodynamically stable: controlling ventricular rate is the goal…. drugs that slow conduction and ↑ refractoriness in AV node (BBs, NDP CCBs, Digoxine, Amiodareone)
Normal EF: βBs, NDP CCBs first line
LVD: BBs preferred
Exacerbation of HF symptoms: Digoxin, Amiodareone (Thromboembolic risk) preferred
ATRIAL FIBRILLATION AND ATRIAL FLUTTER chronic management
Rate-control strategy: AV nodal-blocking agents (BBs, CCBs, Digoxin)
normal LV function: βBs, diltiazem, or verapamil or βBs, diltiazem, or verapamil + digoxin
LV dysfunction: βBs >digoxin (Avoid CCBs)
If episode of decompensated HF: Digoxin preferred
Rhythm control strategy
methods of restoring sinus rhythm in patients with AF or atrial flutter: is cardioversion
pharmacologic cardioversion ()
within 7 days and/or no SHD: Single, oral loading doses of propafenone (600 mg) or flecainide (300 mg)
After 7 days and/or has SHD: dofetilide and amiodarone,
DCC
AF for >48 hours…. warfarin for at least 3 weeks prior ……. Cardioversion ……warfarin continued for at least 4 weeks after
CREBROVASCULAR ACCIDENT = CVA.
PATHOPHYSIOLOGY
Predominant mechanism is reentry, usually associated with organic heart disease causing atrial distention (eg, ischemia or infarction, hypertensive heart disease, valvular disorders).
There are two methods of restoring SR in patients with AF or atrial flutter: pharmacologic cardioversion and DCC. The decision to use either of these methods is generally a matter of clinical preference. The disadvantages of pharmacologic cardioversion are the risk of significant side effects (e.g., drug-induced TdP),32 the potential for drug–drug interactions (e.g., digoxin–amiodarone), and the lower efficacy of AADs when compared with DCC. The advantages of DCC are that it is quick and more often successful (80% to 90% success rate). The disadvantages of DCC are the need for prior sedation/anesthesia and a risk (albeit small) of serious complications such as sinus arrest or ventricular arrhythmias. Contrary to past beliefs, DCC carries very little risk in patients who are receiving digoxin and have no evidence of digoxin toxicity
ATRIAL FIBRILLATION AND ATRIAL FLUTTER Acute Treatment
Hemodynamically unstable-medical emergency: restore sinus rhythm is the goal …. DCC
Hemodynamically stable: controlling ventricular rate is the goal…. drugs that slow conduction and ↑ refractoriness in AV node (BBs, NDP CCBs, Digoxine, Amiodareone)
Normal EF: βBs, NDP CCBs first line
LVD: BBs preferred
Exacerbation of HF symptoms: Digoxin, Amiodareone (Thromboembolic risk) preferred
ATRIAL FIBRILLATION AND ATRIAL FLUTTER chronic management
Rate-control strategy: AV nodal-blocking agents (BBs, CCBs, Digoxin)
normal LV function: βBs, diltiazem, or verapamil or βBs, diltiazem, or verapamil + digoxin
LV dysfunction: βBs >digoxin (Avoid CCBs)
If episode of decompensated HF: Digoxin preferred
Rhythm control strategy
methods of restoring sinus rhythm in patients with AF or atrial flutter: is cardioversion
pharmacologic cardioversion ()
within 7 days and/or no SHD: Single, oral loading doses of propafenone (600 mg) or flecainide (300 mg)
After 7 days and/or has SHD: dofetilide and amiodarone,
DCC
AF for >48 hours…. warfarin for at least 3 weeks prior ……. Cardioversion ……warfarin continued for at least 4 weeks after
ATRIAL FIBRILLATION AND ATRIAL FLUTTER chronic management
Rate-control strategy: AV nodal-blocking agents (BBs, CCBs, Digoxin)
normal LV function: βBs, diltiazem, or verapamil or βBs, diltiazem, or verapamil + digoxin
LV dysfunction: βBs >digoxin (Avoid CCBs)
If episode of decompensated HF: Digoxin preferred
Rhythm control strategy
methods of restoring sinus rhythm in patients with AF or atrial flutter: is cardioversion
pharmacologic cardioversion ()
within 7 days and/or no SHD: Single, oral loading doses of propafenone (600 mg) or flecainide (300 mg)
After 7 days and/or has SHD: dofetilide and amiodarone,
DCC
AF for >48 hours…. warfarin for at least 3 weeks prior ……. Cardioversion ……warfarin continued for at least 4 weeks after
aIf AF is less than 48 hours in duration, anticoagulation prior to cardioversion is unnecessary; initiate anticoagulation with unfractionated heparin, a low-molecular-weight heparin, apixaban, dabigatran, or rivaroxaban as soon as possible either before or after cardioversion for patients at high risk for stroke (this anticoagulant regimen or no antithrombotic therapy may be considered in low-risk patients). bAblation may be considered for patients who fail or do not tolerate at least 1 AAD or as first-line therapy (before AAD therapy) for select patients with recurrent symptomatic paroxysmal AF. cChronic antithrombotic therapy should be considered in all patients with AF and risk factors for stroke regardless of whether or not they remain in sinus rhythm. (AAD, antiarrhythmic drug; AF, atrial fibrillation; AFl, atrial utter; BB, β-blocker; CCB, calcium channel blocker [ie, verapamil or diltiazem]; DCC, direct current cardioversion; TEE, transesophageal echocardiogram.)
CVA Prevention in Atrial Fibrillation
Preparation for Atrial Fibrillation Cardioversion
Atrial Fibrillation longer than 48 hours
Cardioversion without Anticoagulation risks embolus
Protocol: Anticoagulation for Cardioversion Protocol
Assumes Atrial Fibrillation >48 hours or unknown
See Atrial Fibrillation Acute Management for <48 hour
Delayed cardioversion
Anticoagulation on Coumadin for 3 weeks
Atrial Fibrillation Cardioversion
Anticoagulation on Coumadin for 4 more weeks
Early cardioversion
Intravenous Heparin for 24 hours
Transesophageal Echocardiogram excludes atrial clot
Atrial Fibrillation Cardioversion
Anticoagulation on Coumadin for 4 more weeks
Atrial Fibrillation Cardioversion to sinus rhythm Atrial Fibrillation less than 48 hours
Consider Heparin while considering cardioversion
Consider early Atrial Fibrillation Cardioversion
Atrial Fibrillation more than 48 hours
Coumadin for 3 weeks before cardioversion
Consider Atrial Fibrillation Cardioversion
Continue Coumadin for 4 weeks after cardioversion
See Atrial Fibrillation Anticoagulation
Early cardioversion ok if cleared with TEE first
See Atrial Fibrillation Anticoagulation
direct-current cardioversion [DCC]
bDronedarone should only be used in this situation if the patient has normal LV systolic function.
Emerging Anti-Xa Inhibitors
The introduction of LMWH and fondaparinux transformed the initial treatment of VTE from a purely inpatient endeavor to one where the majority of patients can be treated as outpatients. However, the need for daily subcutaneous injections is a significant barrier for some patients.39 Warfarin therapy poses even greater challenges as discussed previously and the required monitoring is labor intensive and stressful for patients and anticoagulation providers.40 These shortcomings in available anticoagulants have driven the search for replacements with rapid onset of effect that can be administered orally without the need for anticoagulant monitoring. Two such agents that target factor Xa, rivaroxaban and apixaban are in advanced stages of clinical development. Rivaroxaban has been approved in Europe and Canada for prevention of VTE following orthopedic surgery.40
Pharmacology and Pharmacokinetics
Rivaroxaban and apixaban are potent and selective inhibitors of factor Xa that do not require antithrombin to exert their anticoagulant effect.39 Both drugs have good oral bioavailability (80% and 50% for rivaroxaban and abixaban, respectively) and reach peak plasma concentrations in about 3 hours.39 The terminal half-life of rivaroxaban is 5 to 9 hours and 9 to 14 hours for abixaban.39 Both drugs are excreted in the urine and feces and are metabolized by CYP 3A4 (among others) and CYP-independent mechanisms.39 Inhibitors of CYP3A4 and P-glycoprotein may increase plasma concentrations of either drug.40
Monitoring
Rivaroxaban and abixaban prolong the PT and the aPTT. For rivaroxaban, the effect on PT and aPTT is short-lived and only appreciable at peak concentrations. Apixiban's effect on PT and aPTT is minimal at therapeutic concentrations. Both drugs can be monitored using factor Xa inhibition assay; however, clinical trials have demonstrated that routine coagulation monitoring is unnecessary for either.
Oral Direct Thrombin Inhibitors
Recent progress has also been made in the development of oral DTIs. These agents appear promising and offer various advantages such as oral administration, predictable pharmacokinetics and pharmacodynamics, a broader therapeutic window, no need for routine laboratory monitoring, no significant drug interactions, and fixed dose administration without the need of dosing adjustments.42 Several of these compounds are being investigated with dabigatran etexilate being in most advanced phases of clinical development. A previous oral DTI (ximelagatran) was denied FDA approval because of concerns of drug-induced liver toxicity. Dabigatran is being investigated in the prevention and treatment of venous thrombosis and for stroke prevention in atrial fibrillation. Available data suggest that dabigatran is at least as effective and safe as LMWH in the prevention of VTE after major orthopedic surgery and at least as effective and safe as warfarin in patients with atrial fibrillation.51,52 Dabigatran has been approved in Canada and Europe for VTE prevention after hip and knee replacement surgery, but it is not yet approved by the FDA. Dabigatran shows promise as an effective and convenient oral anticoagulant. The first safe, oral DTI to make it to the U.S. market has the potential to revolutionize the provision of antithrombotic therapy.