This document provides an outline and overview of anti-arrhythmic drugs. It begins with background information on arrhythmias and relevant studies. It then discusses the classification of arrhythmias and mechanisms of cardiac arrhythmia. The document outlines the Vaughan-Williams classification system for anti-arrhythmic drugs and provides examples of drugs from each class, including their formulations, dosages, mechanisms of action, uses and adverse effects. It emphasizes the sodium channel blocking properties of Class I drugs like quinidine, procainamide, and lignocaine.
This document provides an overview of antiarrhythmic agents. It begins by defining arrhythmia and discussing the normal cardiac rhythm and electrophysiology. It then examines the mechanisms of cardiac arrhythmias and various causes. Antiarrhythmic drugs are classified into four main classes based on their effects on the cardiac action potential. Examples from each class are discussed along with their mechanisms of action. The classes include sodium channel blockers, beta blockers, potassium channel blockers, and calcium channel blockers.
How should recently symptomatic patients be treated urgent cea or casuvcd
Recent symptomatic patients with carotid artery stenosis can be treated with either urgent carotid endarterectomy (CEA) or carotid artery stenting (CAS). While early studies found CEA to have better outcomes, more recent trials like CREST showed comparable rates of stroke and death between CEA and CAS. For recently symptomatic patients specifically, CEA may still be preferred to CAS due to concerns about stabilizing carotid plaque after stenting. Operator experience also impacts outcomes, so treatment should be individualized based on each patient's clinical situation.
Acute coronary syndrome (ACS) results from an imbalance between myocardial oxygen supply and demand due to diminished blood flow from an occlusive coronary artery thrombus. ACS is classified as ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation ACS (NSTE-ACS), which includes non-STEMI and unstable angina. Treatment involves antiplatelet and anticoagulant medications, revascularization procedures like percutaneous coronary intervention (PCI), and lifestyle modifications to prevent recurrent events.
Arrhythmias are caused by abnormal electrical activity in the heart and can be due to improper impulse generation or conduction. They are treated using antiarrhythmic drugs that work by sodium or calcium channel blockade, prolonging the refractory period, or blocking sympathetic effects. Common antiarrhythmic drug classes include Class I membrane stabilizers, Class II drugs that decrease catecholamine effects, Class III potassium channel blockers, and Class IV calcium channel blockers. Effective treatment depends on the underlying arrhythmia and may involve drugs, cardioversion, ablation, or pacing.
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.
The document discusses updates on stroke prevention and management. It summarizes recent findings related to primary stroke prevention involving homocysteine, folic acid, and B vitamins. It also discusses definitions and management of transient ischemic attacks, as well as treatments for acute ischemic stroke such as thrombolysis. Finally, it reviews options for secondary stroke prevention based on the underlying causes, emphasizing the use of antiplatelet agents for most etiologies according to American Stroke Association guidelines. The summary is provided in 3 sentences or less as requested.
This document defines cardiac dysrhythmias and discusses their incidence and causes in the perioperative period. It notes that dysrhythmias are common in patients undergoing surgery, occurring in over 70% of patients receiving general anesthesia. The causes include changes in cardiac ion channels from medications or clinical situations as well as pathological processes like injury or damage to the conduction system. Reentry and automaticity are two main mechanisms that can precipitate arrhythmias. Perioperative dysrhythmias are frequently benign but may become symptomatic in high-risk patients.
This document discusses perioperative dysrhythmias. It begins by defining dysrhythmias and noting they represent an important cause of complications during surgery. While most are benign, some can be lethal or symptomatic. The document then discusses the incidence, which is seen in 70.2% of patients undergoing general anesthesia and varies depending on surgery type and monitoring. It provides details on the mechanisms, causes, and types of perioperative dysrhythmias, as well as their presentation, treatment, and contributing risk factors.
This document provides an overview of antiarrhythmic agents. It begins by defining arrhythmia and discussing the normal cardiac rhythm and electrophysiology. It then examines the mechanisms of cardiac arrhythmias and various causes. Antiarrhythmic drugs are classified into four main classes based on their effects on the cardiac action potential. Examples from each class are discussed along with their mechanisms of action. The classes include sodium channel blockers, beta blockers, potassium channel blockers, and calcium channel blockers.
How should recently symptomatic patients be treated urgent cea or casuvcd
Recent symptomatic patients with carotid artery stenosis can be treated with either urgent carotid endarterectomy (CEA) or carotid artery stenting (CAS). While early studies found CEA to have better outcomes, more recent trials like CREST showed comparable rates of stroke and death between CEA and CAS. For recently symptomatic patients specifically, CEA may still be preferred to CAS due to concerns about stabilizing carotid plaque after stenting. Operator experience also impacts outcomes, so treatment should be individualized based on each patient's clinical situation.
Acute coronary syndrome (ACS) results from an imbalance between myocardial oxygen supply and demand due to diminished blood flow from an occlusive coronary artery thrombus. ACS is classified as ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation ACS (NSTE-ACS), which includes non-STEMI and unstable angina. Treatment involves antiplatelet and anticoagulant medications, revascularization procedures like percutaneous coronary intervention (PCI), and lifestyle modifications to prevent recurrent events.
Arrhythmias are caused by abnormal electrical activity in the heart and can be due to improper impulse generation or conduction. They are treated using antiarrhythmic drugs that work by sodium or calcium channel blockade, prolonging the refractory period, or blocking sympathetic effects. Common antiarrhythmic drug classes include Class I membrane stabilizers, Class II drugs that decrease catecholamine effects, Class III potassium channel blockers, and Class IV calcium channel blockers. Effective treatment depends on the underlying arrhythmia and may involve drugs, cardioversion, ablation, or pacing.
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.
The document discusses updates on stroke prevention and management. It summarizes recent findings related to primary stroke prevention involving homocysteine, folic acid, and B vitamins. It also discusses definitions and management of transient ischemic attacks, as well as treatments for acute ischemic stroke such as thrombolysis. Finally, it reviews options for secondary stroke prevention based on the underlying causes, emphasizing the use of antiplatelet agents for most etiologies according to American Stroke Association guidelines. The summary is provided in 3 sentences or less as requested.
This document defines cardiac dysrhythmias and discusses their incidence and causes in the perioperative period. It notes that dysrhythmias are common in patients undergoing surgery, occurring in over 70% of patients receiving general anesthesia. The causes include changes in cardiac ion channels from medications or clinical situations as well as pathological processes like injury or damage to the conduction system. Reentry and automaticity are two main mechanisms that can precipitate arrhythmias. Perioperative dysrhythmias are frequently benign but may become symptomatic in high-risk patients.
This document discusses perioperative dysrhythmias. It begins by defining dysrhythmias and noting they represent an important cause of complications during surgery. While most are benign, some can be lethal or symptomatic. The document then discusses the incidence, which is seen in 70.2% of patients undergoing general anesthesia and varies depending on surgery type and monitoring. It provides details on the mechanisms, causes, and types of perioperative dysrhythmias, as well as their presentation, treatment, and contributing risk factors.
STEMI PPT for acute coronary syndome acute MIHima Bindu
A 67-year-old male presented with sudden onset of chest pain for 20 minutes. Clinical examination found tachycardia and signs of heart failure. ECG showed ST elevation myocardial infarction (STEMI) involving the anterior wall. The patient was diagnosed with STEMI and underwent primary percutaneous coronary intervention (PCI). During the procedure, the culprit lesion was identified in the left anterior descending artery and treated with stent placement. Post-procedure, the patient was started on dual antiplatelet therapy and anticoagulation medication. He was monitored in the intensive care unit and later transferred to the cardiology ward for further management of risk factors and secondary prevention.
This document discusses anti-arrhythmic drugs and updates. It begins by defining arrhythmias and explaining why they should be treated. It then discusses factors that can precipitate arrhythmias and classifications of arrhythmias based on origin. The document focuses on the Vaughn Williams classification of anti-arrhythmic drugs into classes I-IV based on their mechanisms of action and effects on ion channels. Several examples of drugs from each class are described in detail including their indications, mechanisms of action, dosages, and adverse effects.
Recent Advances In Thrombolysis In Stroke PatientAdamya Gupta
1) Recent advances in thrombolysis for stroke patients include extending the treatment window for intravenous rt-PA from 3 hours to 4.5 hours post-stroke onset based on the ECASS III trial results.
2) Intravenous rt-PA is still the standard of care for eligible patients within 4.5 hours, but endovascular thrombectomy is now recommended for eligible patients with a large vessel occlusion up to 24 hours from last known normal.
3) Treatment protocols now focus on a rapid door-to-needle time of 60 minutes or less for intravenous rt-PA and include advances in imaging such as CTA and perfusion imaging to identify patients that may benefit from endovascular thrombectomy.
"Clear!"
7
9.
Shout "Clear!" and press the shock button to deliver the shock.
10. Immediately resume CPR beginning with chest compressions for 2 minutes.
11. Check monitor for rhythm. If still in a shockable rhythm, repeat steps 7-10.
12. If rhythm converts to non-shockable, begin post-resuscitation care.
13. Document all interventions, time, rhythm, response to shocks.
To ensure safety of
caregivers and bystanders
To restore spontaneous
circulation
To determine if additional
shocks are needed
To provide appropriate
care based on patient's
rhythm
This document provides information on the management of stroke. It defines stroke and transient ischemic attack (TIA). It describes the different types of stroke and outlines the rationale for developing a stroke acute care pathway. The pathway includes components for TIA management, administration of thrombolysis for ischemic stroke patients within 3 hours of onset, organized inpatient care in a stroke unit, neurointervention, and stroke surgery. It provides details on each component, including evidence-based guidelines and levels of evidence. The goal is to establish an efficient system to rapidly diagnose and treat stroke patients according to best practices to improve outcomes.
The document discusses recent developments in stroke management. It summarizes that (1) endovascular therapy plus usual care is more effective than usual care alone for acute ischemic stroke patients with proximal arterial occlusion within 6 hours of onset, (2) early intensive blood pressure lowering is safe and may improve outcomes for intracerebral hemorrhage patients presenting within 6 hours with systolic BP 150-220 mmHg, and (3) stroke rehabilitation involving early mobilization, drug therapy to enhance motor recovery, and robotic training can improve functional recovery.
This document provides an overview of arrhythmia including its epidemiology, causes, clinical presentations, diagnosis, and management. It begins with an introduction to arrhythmia and defines different types. It then discusses that arrhythmia is more common in older patients and those with pre-existing heart conditions. The document outlines pharmacological treatments including different drug classes and non-pharmacological options like lifestyle changes, devices, and surgery. It emphasizes the pharmacist's role in counseling patients on antiarrhythmic medications and monitoring for side effects.
Evaluation of antiarrhythmic drugs (1)Nitin Shinde
This document discusses the evaluation of antiarrhythmic drugs. It begins with an introduction to arrhythmias and ECGs. It then describes various classification systems for antiarrhythmic drugs based on their mechanisms of action. The document focuses on experimental methods used to evaluate antiarrhythmic drugs, including in vitro techniques using isolated tissues and in vivo methods like inducing arrhythmias chemically, electrically, mechanically, or through exercise. Specific protocols are provided for evaluating drugs in models of aconitine-induced arrhythmias in rats, digoxin-induced arrhythmias in guinea pigs, and electrically-induced ventricular fibrillation thresholds in dogs. The goal is to determine if test compounds suppress or prevent
This document provides an overview of cardiac pacemakers, including:
- A brief history of the development of pacemakers from the first implant in 1958 to modern devices.
- The components, functions, and types of pacemakers including single vs dual chamber and permanent vs temporary pacing.
- Measurements taken during pacemaker implantation like impedance, sensing threshold, and pacing threshold to ensure proper function.
- Modes of pacing like VVI, DDD and indications for different modes. Potential complications of pacemaker therapy are also outlined.
The document serves as an introduction to pacemaker terminology, components, functions and the implantation process.
1) Cardiogenic shock is defined as hypotension, hypoperfusion, and elevated filling pressures caused by depressed left ventricular function following myocardial injury. Mortality from cardiogenic shock remains high at 50-70%.
2) Risk factors for cardiogenic shock include age over 65, female gender, large myocardial infarction, anterior infarction location, prior infarction history, diabetes, and hypertension. Post-mortem studies show extensive myocardial damage in patients who die from cardiogenic shock.
3) Early revascularization through percutaneous coronary intervention or coronary artery bypass grafting may improve survival outcomes for cardiogenic shock, especially in patients under age 75, according to the landmark SHOCK trial. Adjunctive therapies including intra
- The document provides guidelines for the management of acute coronary syndrome (ACS), including definitions, risk stratification, diagnostic criteria, treatment protocols for STEMI, NSTEMI/UA, and secondary prevention strategies.
- It outlines the pathophysiology of ACS as resulting from atherosclerotic plaque rupture and thrombus formation, and differentiates between STEMI, NSTEMI, and UA based on ECG changes and cardiac biomarker levels.
- Initial management involves optimal medical therapy, while risk stratification determines whether conservative treatment or an invasive strategy including angiography and revascularization is most appropriate for intermediate-to-high risk NSTEMI/
1. Coronary artery disease is caused by atherosclerosis developing in three stages, culminating in plaque rupture and thrombosis.
2. Risk factors for atherosclerosis and CAD include smoking, hyperlipidemia, hypertension, diabetes, male gender, increasing age, and family history.
3. Acute coronary syndromes include unstable angina, NSTEMI, and STEMI, differentiated by cardiac enzymes and ECG changes. High-risk patients with ongoing symptoms should receive urgent angiography and revascularization.
This document summarizes information on device therapy for congestive heart failure, including cardiac resynchronization therapy (CRT). It discusses:
1) The prevalence and mortality rates of heart failure in the US. Up to 30% of CHF patients have intraventricular conduction delays which increase mortality.
2) NYHA heart failure classifications and guidelines for CRT approval for classes III and IV.
3) Clinical trials that demonstrated the benefits of CRT including increased exercise capacity, quality of life, and decreased hospitalizations and mortality.
4) Anatomical challenges of CRT implantation via the coronary sinus and risks of the procedure. Proper lead placement is important to reduce asynchrony.
Antiarrhythmic therapy for supraventricular arrhythmiasKyaw Win
This document provides an overview of anti-arrhythmic drug therapy for supraventricular arrhythmias. It discusses the electrophysiology of the heart, definitions of arrhythmias, and classifications of anti-arrhythmic drugs. The four main classes of anti-arrhythmic drugs are described along with their mechanisms of action and uses for treating different types of supraventricular tachyarrhythmias. Guidelines for treating atrial fibrillation and some supraventricular tachycardias are also presented.
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
Modern devices such as implantable defibrillators (ICDs) and cardiac resynchronization therapy (CRT) are playing an expanding role in treating heart failure. CRT aims to improve synchronization of ventricular contractions in patients with left bundle branch block and a widened QRS complex. It has been shown to improve symptoms, exercise capacity, and reduce hospitalizations and mortality in moderate to severe heart failure patients. ICDs provide protection against sudden cardiac death from arrhythmias in patients with reduced left ventricular ejection fraction. Guidelines recommend considering CRT for appropriate candidates with LVEF <35% and QRS >120ms and considering ICDs for those with LVEF <35% who are not in NYHA
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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Similar to CLASSIFICATION OF ANTI-ARRHYTHMIC DRUGS - Copy.pptx
STEMI PPT for acute coronary syndome acute MIHima Bindu
A 67-year-old male presented with sudden onset of chest pain for 20 minutes. Clinical examination found tachycardia and signs of heart failure. ECG showed ST elevation myocardial infarction (STEMI) involving the anterior wall. The patient was diagnosed with STEMI and underwent primary percutaneous coronary intervention (PCI). During the procedure, the culprit lesion was identified in the left anterior descending artery and treated with stent placement. Post-procedure, the patient was started on dual antiplatelet therapy and anticoagulation medication. He was monitored in the intensive care unit and later transferred to the cardiology ward for further management of risk factors and secondary prevention.
This document discusses anti-arrhythmic drugs and updates. It begins by defining arrhythmias and explaining why they should be treated. It then discusses factors that can precipitate arrhythmias and classifications of arrhythmias based on origin. The document focuses on the Vaughn Williams classification of anti-arrhythmic drugs into classes I-IV based on their mechanisms of action and effects on ion channels. Several examples of drugs from each class are described in detail including their indications, mechanisms of action, dosages, and adverse effects.
Recent Advances In Thrombolysis In Stroke PatientAdamya Gupta
1) Recent advances in thrombolysis for stroke patients include extending the treatment window for intravenous rt-PA from 3 hours to 4.5 hours post-stroke onset based on the ECASS III trial results.
2) Intravenous rt-PA is still the standard of care for eligible patients within 4.5 hours, but endovascular thrombectomy is now recommended for eligible patients with a large vessel occlusion up to 24 hours from last known normal.
3) Treatment protocols now focus on a rapid door-to-needle time of 60 minutes or less for intravenous rt-PA and include advances in imaging such as CTA and perfusion imaging to identify patients that may benefit from endovascular thrombectomy.
"Clear!"
7
9.
Shout "Clear!" and press the shock button to deliver the shock.
10. Immediately resume CPR beginning with chest compressions for 2 minutes.
11. Check monitor for rhythm. If still in a shockable rhythm, repeat steps 7-10.
12. If rhythm converts to non-shockable, begin post-resuscitation care.
13. Document all interventions, time, rhythm, response to shocks.
To ensure safety of
caregivers and bystanders
To restore spontaneous
circulation
To determine if additional
shocks are needed
To provide appropriate
care based on patient's
rhythm
This document provides information on the management of stroke. It defines stroke and transient ischemic attack (TIA). It describes the different types of stroke and outlines the rationale for developing a stroke acute care pathway. The pathway includes components for TIA management, administration of thrombolysis for ischemic stroke patients within 3 hours of onset, organized inpatient care in a stroke unit, neurointervention, and stroke surgery. It provides details on each component, including evidence-based guidelines and levels of evidence. The goal is to establish an efficient system to rapidly diagnose and treat stroke patients according to best practices to improve outcomes.
The document discusses recent developments in stroke management. It summarizes that (1) endovascular therapy plus usual care is more effective than usual care alone for acute ischemic stroke patients with proximal arterial occlusion within 6 hours of onset, (2) early intensive blood pressure lowering is safe and may improve outcomes for intracerebral hemorrhage patients presenting within 6 hours with systolic BP 150-220 mmHg, and (3) stroke rehabilitation involving early mobilization, drug therapy to enhance motor recovery, and robotic training can improve functional recovery.
This document provides an overview of arrhythmia including its epidemiology, causes, clinical presentations, diagnosis, and management. It begins with an introduction to arrhythmia and defines different types. It then discusses that arrhythmia is more common in older patients and those with pre-existing heart conditions. The document outlines pharmacological treatments including different drug classes and non-pharmacological options like lifestyle changes, devices, and surgery. It emphasizes the pharmacist's role in counseling patients on antiarrhythmic medications and monitoring for side effects.
Evaluation of antiarrhythmic drugs (1)Nitin Shinde
This document discusses the evaluation of antiarrhythmic drugs. It begins with an introduction to arrhythmias and ECGs. It then describes various classification systems for antiarrhythmic drugs based on their mechanisms of action. The document focuses on experimental methods used to evaluate antiarrhythmic drugs, including in vitro techniques using isolated tissues and in vivo methods like inducing arrhythmias chemically, electrically, mechanically, or through exercise. Specific protocols are provided for evaluating drugs in models of aconitine-induced arrhythmias in rats, digoxin-induced arrhythmias in guinea pigs, and electrically-induced ventricular fibrillation thresholds in dogs. The goal is to determine if test compounds suppress or prevent
This document provides an overview of cardiac pacemakers, including:
- A brief history of the development of pacemakers from the first implant in 1958 to modern devices.
- The components, functions, and types of pacemakers including single vs dual chamber and permanent vs temporary pacing.
- Measurements taken during pacemaker implantation like impedance, sensing threshold, and pacing threshold to ensure proper function.
- Modes of pacing like VVI, DDD and indications for different modes. Potential complications of pacemaker therapy are also outlined.
The document serves as an introduction to pacemaker terminology, components, functions and the implantation process.
1) Cardiogenic shock is defined as hypotension, hypoperfusion, and elevated filling pressures caused by depressed left ventricular function following myocardial injury. Mortality from cardiogenic shock remains high at 50-70%.
2) Risk factors for cardiogenic shock include age over 65, female gender, large myocardial infarction, anterior infarction location, prior infarction history, diabetes, and hypertension. Post-mortem studies show extensive myocardial damage in patients who die from cardiogenic shock.
3) Early revascularization through percutaneous coronary intervention or coronary artery bypass grafting may improve survival outcomes for cardiogenic shock, especially in patients under age 75, according to the landmark SHOCK trial. Adjunctive therapies including intra
- The document provides guidelines for the management of acute coronary syndrome (ACS), including definitions, risk stratification, diagnostic criteria, treatment protocols for STEMI, NSTEMI/UA, and secondary prevention strategies.
- It outlines the pathophysiology of ACS as resulting from atherosclerotic plaque rupture and thrombus formation, and differentiates between STEMI, NSTEMI, and UA based on ECG changes and cardiac biomarker levels.
- Initial management involves optimal medical therapy, while risk stratification determines whether conservative treatment or an invasive strategy including angiography and revascularization is most appropriate for intermediate-to-high risk NSTEMI/
1. Coronary artery disease is caused by atherosclerosis developing in three stages, culminating in plaque rupture and thrombosis.
2. Risk factors for atherosclerosis and CAD include smoking, hyperlipidemia, hypertension, diabetes, male gender, increasing age, and family history.
3. Acute coronary syndromes include unstable angina, NSTEMI, and STEMI, differentiated by cardiac enzymes and ECG changes. High-risk patients with ongoing symptoms should receive urgent angiography and revascularization.
This document summarizes information on device therapy for congestive heart failure, including cardiac resynchronization therapy (CRT). It discusses:
1) The prevalence and mortality rates of heart failure in the US. Up to 30% of CHF patients have intraventricular conduction delays which increase mortality.
2) NYHA heart failure classifications and guidelines for CRT approval for classes III and IV.
3) Clinical trials that demonstrated the benefits of CRT including increased exercise capacity, quality of life, and decreased hospitalizations and mortality.
4) Anatomical challenges of CRT implantation via the coronary sinus and risks of the procedure. Proper lead placement is important to reduce asynchrony.
Antiarrhythmic therapy for supraventricular arrhythmiasKyaw Win
This document provides an overview of anti-arrhythmic drug therapy for supraventricular arrhythmias. It discusses the electrophysiology of the heart, definitions of arrhythmias, and classifications of anti-arrhythmic drugs. The four main classes of anti-arrhythmic drugs are described along with their mechanisms of action and uses for treating different types of supraventricular tachyarrhythmias. Guidelines for treating atrial fibrillation and some supraventricular tachycardias are also presented.
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
Modern devices such as implantable defibrillators (ICDs) and cardiac resynchronization therapy (CRT) are playing an expanding role in treating heart failure. CRT aims to improve synchronization of ventricular contractions in patients with left bundle branch block and a widened QRS complex. It has been shown to improve symptoms, exercise capacity, and reduce hospitalizations and mortality in moderate to severe heart failure patients. ICDs provide protection against sudden cardiac death from arrhythmias in patients with reduced left ventricular ejection fraction. Guidelines recommend considering CRT for appropriate candidates with LVEF <35% and QRS >120ms and considering ICDs for those with LVEF <35% who are not in NYHA
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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3. INTRODUCTION
• Cardiac arrhythmias are a frequent problem in
clinical practice, occurring in up to 25% of patients
treated with digitalis, 50% of anesthetized patients,
and over 80% of patients with acute myocardial
infarction
Arrhythmia is defined as an abnormality of the cardiac
rate, rhythm or both
6/2/2023 3
7. Relevant Studies
• The Cardiac Arrhythmia Suppression Trial I -
CAST-I
"Mortality and morbidity in patients receiving
encainide, flecainide, or placebo". The New England
Journal of Medicine. 1991. 324(12):781-788
“Among patients with recent MI and increased
ventricular ectopy, use of antiarrhythmics
suppresses ventricular ectopy, but increases
mortality.”
6/2/2023 7
8. …
• The Cardiac Arrhythmia Suppression Trial II - CAST-II
"As with the antiarrhythmic agents used in CAST
(flecainide and encainide), the use of moricizine in
CAST-II to suppress asymptomatic or mildly
symptomatic ventricular premature depolarizations to
try to reduce mortality after myocardial infarction is not
only ineffective but also harmful."
6/2/2023 8
9. …
• Canadian Amiodarone Myocardial Infarction
Arrhythmia Trial (Pilot) - CAMIAT
“Amiodarone reduces the incidence of ventricular
fibrillation or arrhythmic death among survivors of
acute myocardial infarction with frequent or repetitive
VPDs. Amiodarone, in moderate loading and
maintenance dosages with adjustments in response to
plasma levels, VPD suppressions, and side effects,
results in effective VPD suppression and acceptable
levels of toxicity.”
6/2/2023 9
10. …
• Sudden Cardiac Death in Heart Failure Trial - SCD-
HeFT
“Among patients with NYHA class II or III CHF and
reduced LVEF, treatment with an ICD was associated
with a reduction in all-cause mortality compared with
placebo, but there was no difference between
amiodarone and placebo. The ICD was programmed for
VF treatment only
6/2/2023 10
11. …
• On long-term follow-up, there was potentially some
attenuation in benefit beyond 6 years, although the
crossover rate to the ICD arm was >50%. Benefit was
highest among patients with ischemic
cardiomyopathy and NYHA class II symptoms.”
6/2/2023 11
12. …
• Multicenter Automatic Defibrillator Implantation
Trial II - MADIT-II
Moss AJ, et al. "Prophylactic Implantation of a
Defibrillator in Patients with Myocardial Infarction and
Reduced Ejection Fraction". The New England Journal
of Medicine. 2002. 346(12):877-883.
“In post-MI patients with systolic dysfunction (EF
≤30%), prophylactic ICD reduced all-cause mortality
compared to standard medical therapy.”
6/2/2023 12
15. 100
60
Normal range
150 Simple tachyarrhythmia
200 Paroxysmal TA
350 Atrial flutter
. 500 Atrial fibrillation
40 Mild bradyarrhythmias
20 moderate BA
Severe BA
6/2/2023 15
18. Pacemaker AP
Phase 4: pacemaker
potential
Na influx, K efflux and Ca
influx until the cell
reaches threshold and
then turns into phase 0
Phase 0: upstroke:
Due to Ca++ influx
Phase 3:
repolarization:
Due to K+ efflux
Pacemaker cells (automatic cells) have
unstable membrane potential so they can
generate AP spontaneously
6/2/2023 18
19. +30 mV
0 mV
-80 mV
-90 mV
OUTSIDE
MEMBRANE
INSIDE
Na+
0
4
3
2
1
K+
Ca++ K+
Atp
K+
Na+
K+
Ca++
Na+
K+
Na+
Resting
open
Inactivated
Phase zero
depolarization
Early
repolarization
Plateau phase
Rapid
Repolarization
phase
Phase 4
depolarization
Myocardiac AP
6/2/2023 19
21. ECG…
• P wave: atrial depolarization
• PR-Interval reflects AV nodal conduction time
• QRS DURATION reflects conduction time in ventricles
• T-wave: ventricular repolarization
• QT interval is a measure of ventricular APD
6/2/2023 21
29. MODERNIZED OXFORD
CLASSIFICATION
• It now introduces new classes incorporating
additional targets, including:
• Class 0: ion channels involved in automaticity
• Class V: mechanically sensitive ion channels
• Class VI: connexins controlling electrotonic cell
coupling
• Class VII: molecules underlying longer term signalling
processes affecting structural remodeling
6/2/2023 29
30. CLASSIFICATION BASED ON CLINICAL
USE
• Drugs used for supraventricular arrhythmias
– Adenosine, Verapamil, Diltiazem
• Drugs used for ventricular arrhythmias
– Lignocaine, Mexelitine, Bretylium
• Drugs used for supraventricular as well as ventricular
arrhythmias
– Amiodarone, - blockers, Disopyramide, Procainamide
6/2/2023 30
31. VAUGHAN-WILLIAMS-SINGH
Phase 4
Phase 0
Phase 1
Phase 2
Phase 3
0 mV
-
80m
V
II
I
III
IV
Class I: block Na+ channels
Ia (Quinidine, Procainamide,
Disopyramide) (1-10s)
Ib (Lignocaine) (<1s)
Ic (Flecainide) (>10s)
Class II: ß-adrenoceptor antagonists
(Atenolol, Sotalol)
Class III: prolong action potential and
prolong refractory period
(Amiodarone, Dofetilide, Sotalol)
Class IV: Ca2+ channel antagonists
(Verapamil, Diltiazem)
6/2/2023 31
32. NA+ CHANNEL BLOCKER
• Bind to and block Na+ channels (and K+ also)
• Act on initial rapid depolarization (slowing effect)
• Local Anaesthetic (higher concentration): block nerve
conduction
• Do not alter resting membrane potential (Membrane
Stabilisers)
6/2/2023 32
33. …
• At times, post repolarization refractoriness
• Bind preferentially to the open channel state
• Use dependence: The more the channel is in use, the
more drug is bound
6/2/2023 33
34. IA IB IC
Moderate Na channel
blockade
Mild Na channel
blockade
Marked Na channel
blockade
Slow rate of rise of
Phase 0
Limited effect on
Phase 0
Markedly reduces rate
of rise of phase 0
Prolong refractoriness
by blocking several
types of K channels
Little effect on
refractoriness as there
is minimal effect on K
channels
Prolong refractoriness
by blocking delayed
rectifier K channels
Lengthen APD &
repolarization
Shorten APD &
repolarization
No effect on APD &
repolarization
Prolong PR, QRS QT unaltered or
slightly shortened
Markedly prolong PR
& QRS
6/2/2023 34
35. …
• IA: Ʈrecovery moderate (1-10sec)
Prolong APD
• IB: Ʈrecovery fast (<1sec)
Shorten APD in some heart
tissues
• IC: Ʈrecovery slow(>10sec)
Minimal effect on APD
6/2/2023 35
37. Quinidine
• Historically first antiarrhythmic drug used
• In 18th century, the bark of the cinchona plant was used
to treat “rebellious palpitations”
Pharmacological effects
threshold for excitability
automaticity
prolongs AP
6/2/2023 37
38. …
Formulation: It is a stereoisomer of quinine, originally
derived from the bark of the cinchona tree
Dosage: Orals and injectables
Tablet (sulfate):100 to 600 mg/dose orally every 4 to 6
hours; begin at 200 mg/dose and titrate to desired effect
(maximum daily dose: 3 to 4 g)
Extended Release: 324 to 648 mg (gluconate) orally every
8 to 12 hours or 300 to 600 mg (sulfate) orally every 8 to
12 hours
6/2/2023 38
39. …
IV: 800 mg of quinidine gluconate diluted to 50 mL and
given at a rate not to exceed 1 mL/min
Clinical Pharmacokinetics
• well absorbed
• 80% bound to plasma proteins (albumin)
• extensive hepatic oxidative metabolism
6/2/2023 39
40. …
Uses
• To maintain sinus rhythm in patients with atrial
flutter or atrial fibrillation
• To prevent recurrence of ventricular tachycardia or
VF
6/2/2023 40
41. …
Adverse Effects:
Non cardiac
• Diarrhea, thrombocytopenia
• Cinchonism and skin rashes
Cardiac
• Marked QT-interval prolongation and Torsades de
pointes (2-8% )
• Hypotension and tachycardia
6/2/2023 41
42. …
Drug interactions
• Metabolized by CYP450
• Increases Digoxin levels
• Cardiac depression with beta blockers
• Inhibits CYP2D6
6/2/2023 42
43. Disopyramide
• Exerts electrophysiologic effects very similar to those of
Quinidine
• Better tolerated than Quinidine
• Exert prominent anticholinergic actions
• Negative ionotropic action
6/2/2023 43
44. …
• Formulation: made up of Disopyramide phosphate
• Dose: Mainly orals
400-800 mg/day. The recommended dose for most
adults is 600 mg/day
Patients < 50 kg may be given 400 mg/day
Immediate-release form: The dose is divided and
administered every 6 hours
Extended-release form: The dose is divided and
administered every 12 hours
6/2/2023 44
46. Procainamide
• Lesser vagolytic action, depression of contractility
and fall in BP
• Metabolized by acetylation to N-acetyl Procainamide
which can block K+ channels
• Does not alter plasma Digoxin levels
6/2/2023 46
47. …
• Formulation: 4-amino-N-2-(diethylamino)ethyl-benzamide
• Dosage: Orals and injectables
• IV:
Loading dose: 15 to 18 mg/kg administered as slow infusion
over 25 to 30 minutes or 100 mg/dose at a rate not to exceed
50 mg/minute repeated every 5 minutes as needed to a total
dose of 1 gram.
Maintenance dose: 1 to 4 mg/minute by continuous infusion
• IM:
50 mg/kg divided into fractional amounts of 1/8 to 1/4 and
injected every 3 to 6 hours or 0.5 to 1 gram every 4 to 8 hours
6/2/2023 47
48. …
• Orals:
Immediate-release: 250 mg orally every 3 hours
Sustained-release: 500 mg every 6 hours
Twice daily formulation: 1000 mg every 12 hours
6/2/2023 48
49. …
• Cardiac adverse effects like Quinidine
• Can cause SLE not recommended >6 months
• Use: Monomorphic VT, WPW Syndrome
6/2/2023 49
50. Class IB drugs
Lignocaine, Phenytoin,
Mexiletine
Block sodium channels
and shorten
repolarization
6/2/2023 50
52. Lignocaine
• Blocks inactivated sodium channels more than open
state
• Relatively selective for partially depolarized cells
• Selectively acts on diseased myocardium
• Rapid onset and shorter duration of action
• Useful in ventricular arrhythmias and Digitalis
induced ventricular arrhythmias
6/2/2023 52
53. • Formulation: Lidocaine hydrochloride
• Dosage: Mainly injectable
• Initial dose: 50 to 100 mg IV bolus once over 2 to 3
minutes; may repeat after 5 minutes if necessary not
to exceed up to 300 mg in a 1-hour period
Following bolus administration: 1 to 4 mg/min
continuous IV infusion
6/2/2023 53
54. …
Pharmacokinetics:
• High first pass metabolism
• Metabolism dependent on hepatic blood flow
• T ½ = 8min – distributive, 2hrs – elimination
• Propranolol decreases half life of Lignocaine
• Dose= 50-100mg bolus followed by 20-40mg every
10-20min IV
6/2/2023 54
56. • Local anaesthetic
• Inactive orally
• Given IV for antiarrhythmic action
• Na+ channel blockade which occurs
• Only in inactive state of Na+ channels
• CNS side effects in high doses
• Action lasts only for 15 min
• Inhibits Purkinje fibres and ventricles but
• No action on AVN and SAN so
• Effective in Ventricular arrhythmias only
6/2/2023 56
57. Mexiletine
• Oral analogue of Lignocaine
• No first pass metabolism in liver
• Uses:
– Chronic treatment of ventricular arrhythmias
associated with previous MI
– Unlabelled use in diabetic neuropathy
6/2/2023 57
58. …
• Formulation: Mexiletine hydrochloride
• Dosage: mainly orals
• Initial dose: 200 mg orally every 8 hours
A minimum of 2-3 days between dose adjustments is
recommended
Dose may be adjusted in 50 or 100 mg increments up
or down
• The dose should not exceed 1200 mg/day
6/2/2023 58
59. …
• Tremor is early sign of Mexiletine toxicity
• Hypotension
• Bradycardia,
• Widened QRS,
• Dizziness and
• Nystagmus
6/2/2023 59
60. Class IC drugs
Encainide, Flecainide, Propafenone
Have minimal effect on
repolarization
Are most potent sodium
channel blockers
• Risk of cardiac arrest and
sudden death-so not used
commonly
• May be used in severe
ventricular arrhythmias
6/2/2023 60
62. Propafenone
• Structural similarity with Propranolol and has -
blocking action
• Undergoes variable first pass metabolism
• Reserve drug for ventricular arrhythmias, re-entrant
tachycardia involving accessory pathway
6/2/2023 62
63. …
• Formulation: Propafenone hydrochloride
• Dosage: Mainly orals
Initial dose: 150 mg orally every 8 hours; may increase
dose after at least 3 to 4 days to 225 mg orally every 8
hours; if additional therapeutic effect is needed, may
increase dose to 300 mg orally every 8 hours
Maximum dose: 900 mg/day
6/2/2023 63
65. Class II: Beta blockers
• -receptor stimulation:
• ↑ Automaticity
• ↑ AV conduction velocity
• ↓ Refractory period
• -adrenergic blockers competitively block
catecholamine induced stimulation of cardiac -
receptors
6/2/2023 65
66. …
• Depress phase 4 depolarization of pacemaker cells
• Slow sinus as well as AV nodal conduction:
↓HR, ↑PR
• ↑ERP, prolong AP Duration by ↓AV conduction
• Reduce myocardial oxygen demand
• Well tolerated and Safer
6/2/2023 66
67. β Adrenergic
Stimulation
β Blockers
↑ magnitude of Ca2+ current &
slows its inactivation
↓ Intracellular Ca2+ overload
↑ Pacemaker current→↑
heart rate
↓Pacemaker current→↓
heart rate
↑ DAD & EAD mediated
arrhythmias
Inhibits after-depolarization
mediated automaticity
Epinephrine induces
hypokalemia (β2 action)
Propranolol blocks this action
6/2/2023 67
68. Use in arrhythmia
• Control supraventricular arrhythmias, Atrial flutter,
fibrillation and PSVT
• Treat tachyarrhythmias caused by:
-Hyperthyroidism, Pheochromocytoma and during
anaesthesia with halothane
6/2/2023 68
69. …
• Digitalis induced tachyarrythmias
• Prophylactic in post-MI
• Ventricular arrhythmias in prolonged QT syndrome
6/2/2023 69
70. Esmolol
• β1 selective agent
• Very short elimination t1/2: 9 mins
• Metabolized by RBC esterases
• Rate control of rapidly conducted AF
Uses:
• Arrythmia associated with anaesthesia
• Supraventricular tachycardia
6/2/2023 70
71. …
• Formulation: Esmolol hydrochloride
• Dosage: Mainly injectibles
Optional loading dose (500 mcg/kg IV over 1 minute),
then 50 mcg/kg/min IV for 4 minutes; if the response is
adequate, the infusion may be maintained at 50
mcg/kg/min
Maintenance dose: 25 to 200 mcg/kg/min IV
-Maximum dose: 200 mcg/kg/min IV
-Duration: Maintenance infusions may be continued for
up to 48 hours
6/2/2023 71
75. …
• Formulation: (2-{4-[(2-butyl-1-benzofuran-3-yl)carbonyl]-
2,6-diiodophenoxy}ethyl)diethylamine
• Dosage: Both Injectibles and orals
• IV:
Initial dose: 1000 mg over the first 24 hours of therapy,
delivered by the following infusion regimen:
-Loading infusions: 150 mg over the first 10 minutes (15
mg/min), followed by 360 mg over the next 6 hours (1
mg/min)
-Maintenance infusion: 540 mg over the remaining 18
hours (0.5 mg/min)
Maximum dose: Initial infusion rate: 30 mg/min
6/2/2023 75
76. …
• Oral
Loading dose: 800 to 1600 mg orally per day for 1 to 3
weeks
Adjustment dose: 600 to 800 mg orally per day for 1
month, then switch to maintenance dose
Maintenance dose: 400 mg orally per day
Maximum dose: 600mg/day
6/2/2023 76
77. • Pharmacokinetics:
– Variable absorption 35-65%
– Slow onset 2days to several weeks
– Duration of action: weeks to months
• Dose:
– Loading dose: 150mg over 10min
– Then 1mg/min for 6 hrs
– Then maintenance infusion of 0.5mg/min for 24
hr
…
6/2/2023 77
78. …
• Uses:
– Can be used for both supraventricular and
ventricular tachycardia
• Adverse effects:
– Cardiac: heart block, QT prolongation, bradycardia,
cardiac failure, hypotension
– Pulmonary: pneumonitis leading to pulmonary
fibrosis
6/2/2023 78
79. …
– Bluish discoloration of skin
– Corneal microdeposits
– GIT disturbances, hepatotoxicity
– Blocks peripheral conversion of T4 to T3 can cause
hypothyroidism or hyperthyroidism
6/2/2023 79
80. • Antiarrhythmic
• Multiple actions
• Iodine containing
• Orally used mainly
• Duration of action is very long (t ½ = 3-8 weeks)
• APD & ERP increases
• Resistant AF, VT, Recurrent VF are indications
• On prolonged use- pulmonary fibrosis
• Neuropathy may occur
• Eye: corneal microdeposits may occur
6/2/2023 80
81. • Bretylium:
– Adrenergic neuron blocker used in resistant
ventricular arrhythmias
• Sotalol:
– Beta blocker
• Dofetilide, Ibutilide:
– Selective K+ channel blocker, less adverse events
– use in AF to convert or maintain sinus rhythm
– May cause QT prolongation
6/2/2023 81
82. Newer class III drugs
• Dronedarone
• Vernakalant
• Azimilide
• Tedisamil
6/2/2023 82
83. Calcium channel blockers (Class IV)
• Inhibit the inward
movement of calcium ↓
contractility, automaticity,
and AV conduction.
• Verapamil and Diltiazem
6/2/2023 83
84. Verapamil
• Formulation: Verapamil hydrochloride
• Dosage: Mainly Orals
-Chronic atrial fibrillation in digitalized patients: 240
to 320 mg/day orally in 3 or 4 divided doses
-Prophylaxis of paroxysmal supraventricular
tachycardia (PSVT) in non-digitalized patients: 240 to
480 mg/day orally in 3 or 4 divided doses
• Maximum dose: 480mg/day
6/2/2023 84
85. …
• Uses:
– Terminate PSVT
– Control ventricular rate in atrial flutter or
fibrillation
• Drug interactions:
– Displaces Digoxin from binding sites
– ↓Renal clearance of Digoxin
6/2/2023 85
87. Adenosine
Purine nucleoside having short and rapid action
IV suppresses automaticity, AV conduction and
dilates coronaries
Drug of choice for PSVT
Has very short half life
Adverse effects:
Nausea, dyspnea, flushing and headache
6/2/2023 87
95. CONCLUSION
• Since arrhythmia is associated with high morbidity
and mortality, it is expedient to know what drug to
use in what situation so as to reduce these
unfavourable outcomes
6/2/2023 95
96. REFERENCES
• Kumar and Clark, Textbook of Clinical Medicine
• Katzung, Textbook of Pharmacology
• Medical school lecture notes
• Sideshare notes
• https://en.wikipedia.org/wiki/Cardiac_Arrhythmia_Suppression_Trial
• https://www.nigeriamedj.com/article.asp?issn=0300-
1652;year=2015;volume=56;issue=6;spage=429;epage=432;aulast=Okeahialam
• [Agents Used in Cardiac Arrhythmias -(Robert D. Harvey; Augustus O. Grant)]
• https://www.mayoclinic.org/tests-procedures/maze-procedure/pyc-
20384973#:~:text=Maze%20is%20a%20surgical%20procedure,to%20make%20several%20precise
%20incisions.
6/2/2023 96
Editor's Notes
RMP IS -90 MV
Cardiac bounded by a lipoprotein membrane which has receptor channels crossing it
WHEN AN ATRIAL OR VENTRICULAR CELL RECIEVES An action potential it starts depolarising in response to it..and sodium starts entering it
Intracellular negativity starts diminishing
When such depolarisation reaches a threshold potential, the sodium channels open abruptly
Na enters cell in large quantities
CELL MEMBRANE ACTION POTENTIAL CHANGES FROM -90 TO ALMOST +30MV
Phase 0: rapid depolarisation…fast selective inflow of na ions
During latter part, ca ions also enter the cell via na channels
Frther in phase 1 and 2 ca ions enter thru slow ca channels
THE CONFORMATION OF THE SODIUM CHANNELS HENCE CHANGES TO INACTIVE STATE
The ca which enters the cell in dis manner causes release of ca from sarcoplasmic reticulumraising the conc of ca within the cells
This intracellular free ca interacts with actin myocin system and causes contraction of heart
Afetr this, phase 1: short rapid repolarisation due to beginning of outflow of potassium and entry of cloride ions into the cells, MEMBRANE CHARGE CHANGES FROM +30 TO ALMOST 0 MV IN VERY SHORT TIME
Phase 2 : prolonged plateau phase.. Balance bw ca enterin the cell and k leavin the cell..VOLTAGE SENSITIVE SLOW l type CA CHANNELS OPEN …SLOW INWARD CA CURRENT BALANCED BY SLOW OUTWARD K CURRENT..DEPOLARISATION = REPOLARISATION
Phase 3 : rapid repolarisation.. CA CHANNELS CLOSE…K CHANNELS OPEN..Contimued extrusion of k…RESUMES INITIAL NEGATIVITY
FROM PHASE 0 TO 3 THERE HAS BEEN A GAIN OF NA AND A LOSS OF K ..THIS IS NOW REVERTED AND BALANCED BY NA K ATPASE
Phase 4: resting phase..ELECTRICALLY STABLE… Ionic reconstitution of cell is reachieved by na k exchange pump
RMP MAINTAINED BY OUTWARD K LEAK CURRENTS AND NA CA EXCHANGERS
The cycle is then repeated
Inactivation gates of sodium channels in resting membranes close over the potential range of -75 to -55mv
Cardiac sodium channel protein shows 3 different conformations
Depolarisation to threshold voltage results in opening of the activation gates of sodium channel thus causing markerdly increased sodium permeability
Brief intense sodium current , conductance of fast sodium channel suddenly increases in response to depolarising stimulUs
Very large influx of na accounts for phase 0 depolarisation
Clusure of inactivation gates result
Remain inactivated till mid phase 3 to permit a new propagated response to external stimulus…refractory period..
Cardiac calcium channels are L type
Phase 1 and 2 : turning off nodium current, waxing and waning of calcium curent, slow development of repolarising potassium current, calcium enters ..potassium leaves..
Phase 3: complete inactivation of sodium and calcium currents and full opening of potassium
2 types of main potassium currents involved in phase 3 : ikr and iks
Certain potassium channels are open at rest also…”inward rectifier” channels
In addition there are 2 energy requiring exchange pumps in cardiac myocyte cell membrane…na k exchange pump…and and na-ca exchange pump
Normally na ions concentrated extracellularly and vice versa for k cions
Thus have a tendency odf diffusion along concentration gradient
This diffusion is opposed by na k pump
This pump operates contimuously and does not switch on and off during action potential of cardiac cells
↓ Automaticity
↓ Excitability
↓ Conduction velocity
Refractory period
Direct action : prolonged in all cardiac tissues
Vagolytic action :
Atria: ↑
AV node : ↓
Ventricles : unaltered
Over all : ↑ atrial , ↑ ventricular, ↓ AV node
Contractility
BP
ECG
Extracardiac
Depresses skeletal muscle
Quinine like antimalarial , antipyretic and oxytocic action
Prominent cardiac depressant and antivagal action
Use: second line drug for preventing recurrences of ventricular arrhythmia
No affect on sinus rate due to opposing actions
Can also cause mental depression, erectile dysfunction, and hypotension
50 % EXCRETED UNCHANGED IN URINE
Also discuss about procaine
Class Ib drug blocks sodium channels more in inactivated state than open state but do not delay the channel recovery, they do not depress AV conduction or prolong APD Even shorten
Than with long APD ( Na + channels remain inactivated for long period of time
Normal ventricular fibres are minmally affected , depolarized damaged fibres are significantly depressed
Brevity of AP and lack of lidocaine effect on channel recovery may explain its inefficacy in atrial arrhythmias
No significant hemodynamic effect
No significant autonomic actions
IV preparation must not contain preservative, symapthomimetic or vasoconstrictor
1-3 mg/min infusion
Clinical Pharmacokinetics
High first pass metabolism
half-life 1–2 hours
a loading dose of 150–200 mg administered over about 15 minutes
should be followed by a maintenance infusion of 2–4 mg/min
400 mg loading dose then 200 mg 8 hrly
Contraindicated in patients with AV block as it may accelerate AV block
450- 750 mg of Mexiletine orally per day provides significant relief in diabetic neuropathy
Can precipitate CHF by depressing AV CONDUCTION and ALSO CAN CAUSE bronchospasm.
Dose = 200 mg tds
Morcizine has properties of all 3 classes but as it prolongs QRS it has been placed along with class Ic drugs
Beta receptor stimulation causes increased automaticity, steeper phase 4, Increased AV conduction velocity and decreased refractory period
Beta adrenergic blockers competitively block catecholamine induced stimulation of cardiac beta receptors
Slow sinus as well as AV nodal conduction which results in decrease in HR and increase PR atrial depolarization, QT and QRS are not significantly altered.
Propranolol, Acebutolol and Esmolol have been approved for antiarrhythmic use
Class III drugs block outward K+ channels during phase III of action potential
These drugs prolong the duration of action potential without affecting phase 0 of action potential or resting membrane potential they instead prolong ERP
HENCE IT DECREASES HEART RATE AS WELL AS AV conduction, better efficacy with lower risk of development of Torsades de pointes
Many drug interactions
Bretylium became obsolete because of poor bioavailability and development of tolerance, reintroduced as anti-arrhythmic for parenteral use. Main adverse effect is postural hypotension, nausea and vomiting. Long term use may result in swelling of parotid gland particularly at meal time. It is contraindicated in digitalis induced arrhythmias and cardiogenic shock
Dronaderone: Amiodarone like drug without iodine atoms so no pulmonary or thyroid toxicity. Has shorter half life 1-2 days compared to months
Vernakalant mixed sodium and potassium channel blocker
Azimilide: blocks rapid and slow components of potassium channels low incidence of torsades de pointes
Tedisamil:
Timeline of findings from landmark trials in atrial fibrillation management, including treatment of concomitant conditions and prevention (green), anticoagulation (blue), rate control therapy (orange), rhythm control therapy (red), and atrial fibrillation surgery (purple).