Most people with supraventricular tachycardia don't need activity restrictions or treatment. For others, lifestyle changes, medication and heart procedures may be needed to control or eliminate the rapid heartbeats and related symptoms.
Types
Supraventricular tachycardia (SVT) falls into three main groups:
Atrioventricular nodal reentrant tachycardia (AVNRT). This is the most common type of supraventricular tachycardia.
Atrioventricular reciprocating tachycardia (AVRT). AVRT is the second most common type of supraventricular tachycardia. It's most commonly diagnosed in younger people.
Atrial tachycardia. This type of SVT is more commonly diagnosed in people who have heart disease. Atrial tachycardia doesn't involve the AV node.
Other types of supraventricular tachycardia include:
Sinus tachycardia
Sinus nodal reentrant tachycardia (SNRT)
Inappropriate sinus tachycardia (IST)
Multifocal atrial tachycardia (MAT)
Junctional ectopic tachycardia (JET)
Nonparoxysmal junctional tachycardia (NPJT)
Symptoms
The main symptom of supraventricular tachycardia (SVT) is a very fast heartbeat (100 beats a minute or more) that may last for a few minutes to a few days. The fast heartbeat may come and go suddenly, with stretches of typical heart rates in between.
Some people with SVT have no signs or symptoms.
Signs and symptoms of supraventricular tachycardia may include:
Very fast (rapid) heartbeat
A fluttering or pounding in the chest (palpitations)
A pounding sensation in the neck
Weakness or feeling very tired (fatigue)
Chest pain
Shortness of breath
Lightheadedness or dizziness
Sweating
Fainting (syncope) or near fainting
In infants and very young children, signs and symptoms of SVT may be difficult to identify. They include sweating, poor feeding, pale skin and a rapid pulse. If your infant or young child has any of these symptoms, ask your child's care provider about SVT screening.
When to see a doctor
Supraventricular tachycardia (SVT) is generally not life-threatening unless you have heart damage or other heart conditions. However, in extreme cases, an episode of SVT may cause unconsciousness or cardiac arrest.
Call your health care provider if you have an episode of a very fast heartbeat for the first time or if an irregular heartbeat lasts longer than a few seconds.
Some signs and symptoms of SVT may be related to a serious health condition. Call 911 or your local emergency number if you have an episode of SVT that lasts for more than a few minutes or if you have an episode with any of the following symptoms:
Chest pain
Shortness of breath
Weakness
Dizziness
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Causes
For some people, a supraventricular tachycardia (SVT
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
The document discusses cardiac arrest, which is defined as a sudden stop in blood circulation caused by the heart failing to contract. Potential causes of cardiac arrest are then listed in categories such as cardiac, respiratory, circulatory, and metabolic issues or toxic/environmental factors. Specific conditions are also outlined in lists of "6 H's" and "5 T's". The document concludes by describing shockable and non-shockable heart rhythms in cardiac arrest and the steps to take during a code blue situation, including initiating CPR, securing an airway, IV medications, and record keeping.
Ventricular fibrillation occurs when the ventricles of the heart quiver due to uncoordinated contractions of the heart muscle fibers. This prevents the heart from effectively pumping blood throughout the body. Ventricular fibrillation can be caused by stress, damage, or electrical changes to heart tissue. It requires immediate treatment through defibrillation or medications to prevent organ damage or death from lack of oxygen.
This document defines and describes sick sinus syndrome, which is a dysfunction of the sinoatrial node that can cause abnormal heart rhythms like bradycardia, tachycardia, and alternating slow and fast rhythms. It may be caused by certain drugs, aging, or underlying heart conditions. Symptoms can include fatigue, dizziness, and fainting. Diagnosis involves an electrocardiogram showing arrhythmias. Treatment options include medications or a pacemaker if symptoms are severe. The document also briefly discusses different types of heart block.
This document discusses supraventricular tachycardia (SVT), which are tachyarrhythmias originating from the atria or atrioventricular node that cause a rapid heart rate. SVTs are classified as either atrial or AV tachyarrhythmias based on their site of origin. Common causes include inherited conditions, structural heart abnormalities, coronary artery disease, and hyperthyroidism. Diagnosis involves an electrocardiogram (ECG), Holter or event monitor, exercise test, or electrophysiology study. Treatment depends on whether it is acute or long term, and may include vagal maneuvers, calcium channel blockers, cardioversion, or medications like digoxin, beta blockers,
This document discusses the classification, causes, symptoms, and treatment of bradycardia. It defines different types of bradycardia based on rhythm and heart block. Common causes include medications, cardiac disease, metabolic abnormalities, and neurological or infectious etiologies. Symptoms range from dizziness to hypotension and shock. Treatment follows ACLS algorithms and may include atropine, transcutaneous pacing, or addressing underlying causes. Case examples demonstrate ECG findings and management of hyperkalemia-induced complete heart block, athlete's heart, and inferior STEMI with complete heart block.
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
The document discusses cardiac arrest, which is defined as a sudden stop in blood circulation caused by the heart failing to contract. Potential causes of cardiac arrest are then listed in categories such as cardiac, respiratory, circulatory, and metabolic issues or toxic/environmental factors. Specific conditions are also outlined in lists of "6 H's" and "5 T's". The document concludes by describing shockable and non-shockable heart rhythms in cardiac arrest and the steps to take during a code blue situation, including initiating CPR, securing an airway, IV medications, and record keeping.
Ventricular fibrillation occurs when the ventricles of the heart quiver due to uncoordinated contractions of the heart muscle fibers. This prevents the heart from effectively pumping blood throughout the body. Ventricular fibrillation can be caused by stress, damage, or electrical changes to heart tissue. It requires immediate treatment through defibrillation or medications to prevent organ damage or death from lack of oxygen.
This document defines and describes sick sinus syndrome, which is a dysfunction of the sinoatrial node that can cause abnormal heart rhythms like bradycardia, tachycardia, and alternating slow and fast rhythms. It may be caused by certain drugs, aging, or underlying heart conditions. Symptoms can include fatigue, dizziness, and fainting. Diagnosis involves an electrocardiogram showing arrhythmias. Treatment options include medications or a pacemaker if symptoms are severe. The document also briefly discusses different types of heart block.
This document discusses supraventricular tachycardia (SVT), which are tachyarrhythmias originating from the atria or atrioventricular node that cause a rapid heart rate. SVTs are classified as either atrial or AV tachyarrhythmias based on their site of origin. Common causes include inherited conditions, structural heart abnormalities, coronary artery disease, and hyperthyroidism. Diagnosis involves an electrocardiogram (ECG), Holter or event monitor, exercise test, or electrophysiology study. Treatment depends on whether it is acute or long term, and may include vagal maneuvers, calcium channel blockers, cardioversion, or medications like digoxin, beta blockers,
This document discusses the classification, causes, symptoms, and treatment of bradycardia. It defines different types of bradycardia based on rhythm and heart block. Common causes include medications, cardiac disease, metabolic abnormalities, and neurological or infectious etiologies. Symptoms range from dizziness to hypotension and shock. Treatment follows ACLS algorithms and may include atropine, transcutaneous pacing, or addressing underlying causes. Case examples demonstrate ECG findings and management of hyperkalemia-induced complete heart block, athlete's heart, and inferior STEMI with complete heart block.
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
This document provides an outline for a module on ventricular tachyarrhythmias. It begins with module objectives of differentiating types of ventricular tachycardias using ECGs. The outline then describes ventricular tachyarrhythmias, discusses characteristics like mechanisms and sustained vs nonsustained types. It classifies ventricular tachyarrhythmias as monomorphic or polymorphic, and provides subcategories within each with descriptions and ECG recognition details. Specific arrhythmias discussed include idiopathic VT, bundle branch reentry, ventricular flutter, fibrillation, and Torsades de Pointes.
1) When encountering a patient with tachycardia, first check if they have a pulse and if they are stable or unstable. Then treat according to the ACLS tachycardia algorithm.
2) For stable tachycardia, further assess if the QRS is narrow or wide, regular or irregular to determine the likely rhythm and appropriate treatment.
3) Unstable tachycardia requires immediate synchronized cardioversion without delay.
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
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
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
The document discusses cardiogenic shock, outlining its definition, causes, pathophysiology, diagnosis and management, with a focus on shock complicating myocardial infarction. Cardiogenic shock occurs in 5-8% of patients hospitalized with ST-elevation myocardial infarction and has a high mortality rate of 70-80% despite emerging treatments. The document provides details on the hemodynamic parameters defining cardiogenic shock and reviews the various mechanisms that can lead to left or right ventricular failure and shock.
An aortic dissection occurs when blood tears the inner layer of the aorta, separating it from the middle layer. It is classified by location and timing of symptoms. Risk factors include hypertension, connective tissue disorders, and family history. Treatment depends on location but may include surgery, endovascular stent grafting, or medical management of blood pressure. Prognosis depends on type and treatment, with mortality rates declining with advances in surgical and endovascular techniques.
This document discusses aortic stenosis and aortic regurgitation. It defines aortic stenosis as a narrowing of the aortic valve opening, with common causes being a bicuspid aortic valve, calcification, or rheumatic heart disease. Symptoms include angina, syncope, and dyspnea. Diagnosis involves echocardiography. Treatment options are balloon valvuloplasty or valve replacement. Aortic regurgitation is defined as retrograde blood flow through the aortic valve during diastole. Common causes are rheumatic fever, hypertension, or a bicuspid valve. Symptoms progress from palpitations to dyspnea. Physical exam may reveal a wide pulse pressure.
The document provides information on inferior wall myocardial infarction (MI), including:
1. Definitions, epidemiology, etiology, clinical features, diagnosis, treatment and complications of inferior wall MI are discussed. Worldwide over 7 million people experience STEMIs or NSTEMIs annually.
2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen.
3. The history of pioneers in cardiology and development of techniques like echocardi
The document discusses aortic regurgitation, including its anatomy, etiology, pathophysiology, epidemiology, clinical manifestations, diagnosis, and management. Key points include:
- Aortic regurgitation occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole.
- Causes include conditions like infective endocarditis, bicuspid aortic valve, hypertension, and Marfan syndrome.
- In acute severe cases, a rapid increase in left ventricular preload can cause pulmonary edema and cardiogenic shock. Chronic cases involve left ventricular dilation and hypertrophy to compensate for the increased preload over time.
- Physical exam may
1. The ECG shows a 45-year-old diabetic man with episodes of palpitations who presents with ventricular trigeminy.
2. Ventricular trigeminy is characterized by ventricular premature beats occurring after every two normal sinus beats with a compensatory pause.
3. Further investigation with Holter monitoring is recommended to better characterize the ventricular arrhythmia and assess for underlying cardiac disease.
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
Mitral stenosis is characterized by obstruction of blood flow from the left atrium to the left ventricle due to thickening and immobility of the mitral valve leaflets. The most common cause is rheumatic heart disease. As the stenosis progresses, the left atrial pressure rises, leading to pulmonary congestion and right-sided heart failure over time. On examination, findings may include an accentuated S1, opening snap, and mid-diastolic murmur with presystolic accentuation. Chest x-ray may show an enlarged left atrium and signs of pulmonary congestion. Treatment involves rate control for atrial fibrillation, diuretics, and potentially balloon valvuloplasty or
This document provides a template for systematically interpreting electrocardiograms (ECGs). It outlines 13 sections to analyze, including ECG type and recording, rate, rhythm and axis, P wave, PR interval, QRS complex, ST segment, T wave, and U wave. Additional features like delta waves are also addressed. Various abnormalities are defined and associated diagnoses are provided. The template aims to help clinicians make accurate ECG interpretations through a standardized approach.
Aortic valve stenosis is a narrowing of the aortic valve opening between the left ventricle and aorta. It is most commonly caused by age-related calcification of the normal three-leafed valve. As the opening narrows, the left ventricle must work harder to pump blood through, causing thickening of its walls. In later stages, the ventricle dilates and pumping function deteriorates. Symptoms range from shortness of breath to chest pain and syncope. While medical therapy has limited effect, severe symptomatic stenosis requires surgery to replace the valve.
A 38-year-old female presented to the emergency room with severe headache, shortness of breath, dizziness, confusion, nausea and palpitations. She has a history of hypertension and was diagnosed with a myocardial infarction one week ago. Evaluation showed signs of cardiogenic shock. The plan is to perform ECG, CT scan, echocardiogram, cardiac enzymes, blood gas analysis and V/Q scan. The learning goals are to discuss cardiogenic shock, its causes, clinical presentation, diagnosis and treatment.
This document discusses aortic regurgitation (AR), which occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion of the aorta. Common causes include rheumatic heart disease, bicuspid aortic valves, hypertension, and Marfan syndrome. Over time, the left ventricle must work harder to compensate for the backflow of blood, which can lead to enlarged and weakened heart muscles. Symptoms may include palpitations, chest pain, and shortness of breath. Diagnosis involves listening for an early diastolic murmur and confirming the diagnosis with echocardiogram
The electrocardiogram (ECG) records the electrical activity of the heart during each cardiac cycle. It detects the P wave, QRS complex, and T wave which represent atrial depolarization, ventricular depolarization, and ventricular repolarization, respectively. The ECG is used to analyze the heart rate, rhythm, and intervals between waves to diagnose cardiac conditions. Common arrhythmias include premature beats, supraventricular tachycardias like atrial flutter, and atrial fibrillation which is characterized by disorganized atrial activity and an irregular ventricular response.
Cardiac arrhythmias are abnormalities in the heart's rhythm. There are two main types: bradycardia, a slow heart rate, and tachycardia, a fast heart rate. Various arrhythmias are described including sinus bradycardia, heart block, atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, ventricular fibrillation, and ventricular tachycardia. Treatment depends on the type of arrhythmia and may include medication, cardioversion, ablation, or pacemaker implantation. Diagnosis involves ECG, echocardiogram, blood tests, and other cardiac tests. Lifestyle changes and avoiding arrhythmia triggers can help management.
This document provides an outline for a module on ventricular tachyarrhythmias. It begins with module objectives of differentiating types of ventricular tachycardias using ECGs. The outline then describes ventricular tachyarrhythmias, discusses characteristics like mechanisms and sustained vs nonsustained types. It classifies ventricular tachyarrhythmias as monomorphic or polymorphic, and provides subcategories within each with descriptions and ECG recognition details. Specific arrhythmias discussed include idiopathic VT, bundle branch reentry, ventricular flutter, fibrillation, and Torsades de Pointes.
1) When encountering a patient with tachycardia, first check if they have a pulse and if they are stable or unstable. Then treat according to the ACLS tachycardia algorithm.
2) For stable tachycardia, further assess if the QRS is narrow or wide, regular or irregular to determine the likely rhythm and appropriate treatment.
3) Unstable tachycardia requires immediate synchronized cardioversion without delay.
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
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
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
The document discusses cardiogenic shock, outlining its definition, causes, pathophysiology, diagnosis and management, with a focus on shock complicating myocardial infarction. Cardiogenic shock occurs in 5-8% of patients hospitalized with ST-elevation myocardial infarction and has a high mortality rate of 70-80% despite emerging treatments. The document provides details on the hemodynamic parameters defining cardiogenic shock and reviews the various mechanisms that can lead to left or right ventricular failure and shock.
An aortic dissection occurs when blood tears the inner layer of the aorta, separating it from the middle layer. It is classified by location and timing of symptoms. Risk factors include hypertension, connective tissue disorders, and family history. Treatment depends on location but may include surgery, endovascular stent grafting, or medical management of blood pressure. Prognosis depends on type and treatment, with mortality rates declining with advances in surgical and endovascular techniques.
This document discusses aortic stenosis and aortic regurgitation. It defines aortic stenosis as a narrowing of the aortic valve opening, with common causes being a bicuspid aortic valve, calcification, or rheumatic heart disease. Symptoms include angina, syncope, and dyspnea. Diagnosis involves echocardiography. Treatment options are balloon valvuloplasty or valve replacement. Aortic regurgitation is defined as retrograde blood flow through the aortic valve during diastole. Common causes are rheumatic fever, hypertension, or a bicuspid valve. Symptoms progress from palpitations to dyspnea. Physical exam may reveal a wide pulse pressure.
The document provides information on inferior wall myocardial infarction (MI), including:
1. Definitions, epidemiology, etiology, clinical features, diagnosis, treatment and complications of inferior wall MI are discussed. Worldwide over 7 million people experience STEMIs or NSTEMIs annually.
2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen.
3. The history of pioneers in cardiology and development of techniques like echocardi
The document discusses aortic regurgitation, including its anatomy, etiology, pathophysiology, epidemiology, clinical manifestations, diagnosis, and management. Key points include:
- Aortic regurgitation occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole.
- Causes include conditions like infective endocarditis, bicuspid aortic valve, hypertension, and Marfan syndrome.
- In acute severe cases, a rapid increase in left ventricular preload can cause pulmonary edema and cardiogenic shock. Chronic cases involve left ventricular dilation and hypertrophy to compensate for the increased preload over time.
- Physical exam may
1. The ECG shows a 45-year-old diabetic man with episodes of palpitations who presents with ventricular trigeminy.
2. Ventricular trigeminy is characterized by ventricular premature beats occurring after every two normal sinus beats with a compensatory pause.
3. Further investigation with Holter monitoring is recommended to better characterize the ventricular arrhythmia and assess for underlying cardiac disease.
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
Mitral stenosis is characterized by obstruction of blood flow from the left atrium to the left ventricle due to thickening and immobility of the mitral valve leaflets. The most common cause is rheumatic heart disease. As the stenosis progresses, the left atrial pressure rises, leading to pulmonary congestion and right-sided heart failure over time. On examination, findings may include an accentuated S1, opening snap, and mid-diastolic murmur with presystolic accentuation. Chest x-ray may show an enlarged left atrium and signs of pulmonary congestion. Treatment involves rate control for atrial fibrillation, diuretics, and potentially balloon valvuloplasty or
This document provides a template for systematically interpreting electrocardiograms (ECGs). It outlines 13 sections to analyze, including ECG type and recording, rate, rhythm and axis, P wave, PR interval, QRS complex, ST segment, T wave, and U wave. Additional features like delta waves are also addressed. Various abnormalities are defined and associated diagnoses are provided. The template aims to help clinicians make accurate ECG interpretations through a standardized approach.
Aortic valve stenosis is a narrowing of the aortic valve opening between the left ventricle and aorta. It is most commonly caused by age-related calcification of the normal three-leafed valve. As the opening narrows, the left ventricle must work harder to pump blood through, causing thickening of its walls. In later stages, the ventricle dilates and pumping function deteriorates. Symptoms range from shortness of breath to chest pain and syncope. While medical therapy has limited effect, severe symptomatic stenosis requires surgery to replace the valve.
A 38-year-old female presented to the emergency room with severe headache, shortness of breath, dizziness, confusion, nausea and palpitations. She has a history of hypertension and was diagnosed with a myocardial infarction one week ago. Evaluation showed signs of cardiogenic shock. The plan is to perform ECG, CT scan, echocardiogram, cardiac enzymes, blood gas analysis and V/Q scan. The learning goals are to discuss cardiogenic shock, its causes, clinical presentation, diagnosis and treatment.
This document discusses aortic regurgitation (AR), which occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion of the aorta. Common causes include rheumatic heart disease, bicuspid aortic valves, hypertension, and Marfan syndrome. Over time, the left ventricle must work harder to compensate for the backflow of blood, which can lead to enlarged and weakened heart muscles. Symptoms may include palpitations, chest pain, and shortness of breath. Diagnosis involves listening for an early diastolic murmur and confirming the diagnosis with echocardiogram
The electrocardiogram (ECG) records the electrical activity of the heart during each cardiac cycle. It detects the P wave, QRS complex, and T wave which represent atrial depolarization, ventricular depolarization, and ventricular repolarization, respectively. The ECG is used to analyze the heart rate, rhythm, and intervals between waves to diagnose cardiac conditions. Common arrhythmias include premature beats, supraventricular tachycardias like atrial flutter, and atrial fibrillation which is characterized by disorganized atrial activity and an irregular ventricular response.
Cardiac arrhythmias are abnormalities in the heart's rhythm. There are two main types: bradycardia, a slow heart rate, and tachycardia, a fast heart rate. Various arrhythmias are described including sinus bradycardia, heart block, atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, ventricular fibrillation, and ventricular tachycardia. Treatment depends on the type of arrhythmia and may include medication, cardioversion, ablation, or pacemaker implantation. Diagnosis involves ECG, echocardiogram, blood tests, and other cardiac tests. Lifestyle changes and avoiding arrhythmia triggers can help management.
The document provides information on electrocardiogram (ECG) findings and their significance in patients presenting with syncope. It discusses diagnostic criteria and risk stratification tools for evaluating causes of syncope, including the CHESS criteria and San Francisco Syncope Rule. Important ECG findings that warrant further investigation or indicate an underlying cardiac condition are highlighted, such as arrhythmias, conduction abnormalities, signs of ischemia, and structural heart disease. Specific arrhythmias and cardiac conditions like long QT syndrome and Brugada syndrome are also reviewed in the context of evaluating syncope.
This document discusses drug therapy for heart failure. It begins by defining heart failure and describing the stages and phenotypes. The main causes of heart failure are then outlined, including ischemic heart disease, hypertension, cardiomyopathy, infections, toxins, and valvular disease. The document discusses the pathophysiology of heart failure in terms of ventricular dysfunction, compensatory mechanisms like the Frank-Starling mechanism and neurohormonal activation, and the determinants of ventricular function. General treatment measures and pharmacological management are described for different stages of heart failure.
Arrhythmias refer to abnormalities in the cardiac rhythm. There are two main types: bradycardia where the heart rate is slow, and tachycardia where the heart rate is fast. Specific arrhythmias include sinus bradycardia, various types of heart block, atrial fibrillation, atrial flutter, AV nodal re-entry tachycardia, ventricular tachycardia, and ventricular fibrillation. Diagnosis involves electrocardiography and other tests. Treatment depends on the type of arrhythmia but may include medications, catheter ablation, pacemaker implantation, or cardioversion. Lifestyle modifications and avoiding arrhythmia triggers can also help management.
This document provides an overview of cardiology and cardiovascular disease. It discusses the leading causes of death worldwide, including coronary heart disease and diseases of the heart muscles and valves. It then covers topics like case history taking in cardiology, common symptoms like chest pain and shortness of breath, methods for examining the cardiovascular system, and risk factors for conditions like coronary heart disease.
The document discusses various types of cardiac arrhythmias including their definitions, causes, clinical manifestations and management. It describes normal sinus rhythm and defines arrhythmias as any change from the normal heart rhythm. Common arrhythmias discussed include sinus tachycardia, sinus bradycardia, premature atrial complexes, premature ventricular complexes, atrial flutter, atrial fibrillation and ventricular tachycardia. It provides EKG images to demonstrate the different arrhythmias and compares characteristics of supraventricular and ventricular arrhythmias. Causes, clinical significance and treatment approaches for different arrhythmias are also summarized.
This document provides an overview of cardiovascular disorders and congenital heart disease in children. It presents two case studies, the first involving a 10-day-old infant with signs of impending cardiopulmonary failure, and the second a 10-year-old boy with chest pain and shortness of breath diagnosed with myocarditis. Key topics covered include ductal-dependent lesions, cyanotic and acyanotic congenital heart disease, myocarditis, pericarditis, and their clinical features, diagnostic evaluation and management.
Acute Coronary Syndrome (ACS) can present as ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), or unstable angina. STEMI is diagnosed based on ST elevation on ECG along with elevated troponin levels. NSTEMI and unstable angina involve non-ST elevation changes on ECG and elevated troponins. Immediate treatment focuses on antiplatelet therapy, analgesia, and reperfusion through percutaneous coronary intervention or thrombolysis depending on timing of symptoms. Long term management aims to prevent complications and recurrence through medications, lifestyle changes, and cardiac rehabilitation.
Here are the responses:
A. The diagnosis is hypovolemic shock likely due to gastrointestinal bleeding given the sudden onset of symptoms.
B. The treatment of choice at current time is aggressive fluid resuscitation with crystalloids like normal saline to restore intravascular volume and blood pressure. Other supportive treatments like oxygen supplementation and cardiac monitoring should also be started. Blood samples should be sent for complete blood count and coagulation profile to check for anemia and bleeding diathesis which may require blood transfusion. Endoscopy may be needed later to identify the source of bleeding once the patient is stabilized hemodynamically. The primary goal currently is to resuscitate the patient from shock through fluid administration.
This document provides an overview of cardiac arrhythmias including their classification, mechanisms, clinical manifestations, diagnostic approaches and management strategies. It discusses various specific arrhythmias in detail such as atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular arrhythmias, sick sinus syndrome and heart block. Treatment options covered include pharmacological therapies using different classes of antiarrhythmic drugs, procedures like cardiac ablation and use of devices like pacemakers.
1. A 65-year-old woman presented with a fall and hip fracture. Her ECG showed complete heart block with a ventricular rate of 45 beats per minute, requiring a permanent pacemaker.
2. A 50-year-old woman with rheumatic heart disease was in atrial fibrillation with a controlled ventricular rate of 60-65 beats per minute on her ECG. The ECG showed signs of digoxin use and possible hypokalemia, requiring questions about appetite and potassium levels.
3. A 20-year-old woman presented with chest pain and her ECG showed a pattern consistent with Wolff-Parkinson-White syndrome type B with right posterior accessory pathway location
Samir rafla ecg arrhythmia for medical students- added amr kamalSamirRafla1
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An arrhythmia is an irregular heartbeat that occurs when the heart's electrical signals don't work properly, causing the heart to beat too fast, too slow, or irregularly. Some key types discussed include sinus tachycardia, sinus bradycardia, premature atrial contractions, atrial flutter, atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, and heart block. Causes can include direct damage to the conduction system, inflammation, electrolyte imbalances, and drugs. Treatment depends on the specific type but may include medications, catheter ablation, cardioversion, or pacemaker implantation.
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The document discusses several types of arrhythmias and heart block conditions. It describes sinus tachycardia as a condition where the sinoatrial node discharges impulses faster than normal, over 100 beats per minute. Paroxysmal supraventricular tachycardia is described as a condition with an abnormal focus discharging regular impulses over 150 beats per minute. The third type discussed is atrial flutter, where there is an abnormal focus discharging rapid regular impulses between 250-350 beats per minute, with only some impulses conducted to the ventricles.
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2. Patient with Supraventricular Tachycardia
Elisa Vasquez, 53 years old, is admitted to the
car diac unit with complaints of palpitations,
lightheadedness, and shortness of breath. Her
history reveals rheumatic fever at age 12 with
subsequent rheumatic heart disease and mitral
stenosis. An intravenous line is in place and she
is receiving oxygen. Marcia Lewin, RN, is
assigned to Ms. Vasquez.
SCENARIO
SCENARIO
3. Demographic data
Name:Mrs
Age:
Sex:Female
Diagnosis: Supraventricular Tachycardia
Elisa Vasquez
53 years
Complaints on admission:complaints of palpitations,
lightheadedness, and shortness of breath
𝙃𝙞𝙨𝙩𝙤𝙧𝙮 𝙊𝙁 𝙄𝙇𝙇𝙉𝙀𝙎𝙎
Ms. Vasquez is still complaining of palpitations
and tells Ms. Lewin, “I feel so nervous and weak
and dizzy.
Presenting complaints
4. . Vital signs: T 98.8° F (37.1°C), R 26, BP 95/60. Peripheral
pulses weak but equal, mucous membranes pale pink, skin
cool and dry. Fine crackles noted in both lung bases. A loud
S3 gallop and a diastolic murmur are noted. Ms. Vasquez is
still complaining of palpitations and tells Ms. Lewin, “I feel
so nervous and weak and dizzy.” Ms. Vasquez’s cardiologist
orders 2.5 mg of verapamil to be given slowly via
intravenous push and tells Ms. Lewin to prepare to assist
with synchronized cardioversion if drug therapy does not
control the ventricular rate."
Present medical history
complaints of palpitations, lightheadedness, and
shortness of breath at time of admission. An
intravenous line is in place and she is receiving
oxygen.
5. 𝙋𝙖𝙨𝙩 𝙢𝙚𝙙𝙞𝙘𝙖𝙡 𝙝𝙞𝙨𝙩𝙤𝙧𝙮
Her history reveals rheumatic fever at age 12 with
subsequent rheumatic heart disease and mitral stenosis.
𝙉𝙤 𝙤𝙩𝙝𝙚𝙧 𝙙𝙖𝙩𝙖 𝙖𝙗𝙤𝙪𝙩 𝙥𝙖𝙩𝙞𝙚𝙣𝙩 𝙤𝙧 𝙛𝙖𝙢𝙞𝙡𝙮 𝙞𝙨 𝙖𝙫𝙖𝙞𝙡𝙖𝙗𝙡𝙚
𝙞𝙣 𝙨𝙘𝙚𝙣𝙖𝙧𝙞𝙤
𝙋𝙝𝙮𝙨𝙞𝙘𝙖𝙡 𝙚𝙭𝙖𝙢𝙞𝙣𝙖𝙩𝙞𝙤𝙣
. Vital signs: T 98.8° F (37.1°C), R 26, BP 95/60.
Peripheral pulses weak but equal, mucous membranes
pale pink, skin cool and dry. Fine crackles noted in both
lung bases. A loud S3 gallop and a diastolic murmur
An intravenous line is in place and she is receiving
oxygen.
palpitations 𝙥𝙧𝙚𝙨𝙚𝙣𝙩
6. Mid-diastolic murmurs start after S2 and end before S1.
They are due to turbulent flow across the atrioventricular
(mitral & tricuspid) valves during the rapid filling phase
from mitral or tricuspid stenosis. Late diastolic
(presystolic) murmurs start after S2 and extend up to S1
and have a crescendo configuration.
third heart sound (S3), also known as the “ventricular
gallop,” occurs just after S2 when the mitral valve
opens, allowing passive filling of the left ventricle. ... A
S3 can be a normal finding in children, pregnant
females and well-trained athletes; however, a S4 heart
sound is almost always abnormal.
13. 𝙍𝙚𝙫𝙞𝙚𝙬 𝙤𝙛 𝙖𝙣𝙖𝙩𝙤𝙢𝙮 𝙖𝙣𝙙 𝙥𝙝𝙮𝙨𝙞𝙤𝙡𝙤𝙜𝙮
The heart itself is made up of 4 chambers, 2 atria and
2 ventricles. De-oxygenated blood returns to the right
side of the heart via the venous circulation. It is
pumped into the right ventricle and then to the lungs
where carbon dioxide is released and oxygen is
absorbed.
• main functions of the heart are:
Pumping oxygenated blood to the other body parts.
Pumping hormones and other vital substances to
different parts of the body.
Receiving deoxygenated blood and carrying
metabolic waste products from the body and
pumping it to the lungs for oxygenation.
Maintaining blood pressure
14. The sequence of electrical events during one full
contraction of the heart muscle:
An excitation signal (an action potential) is created by
the sinoatrial (SA) node.
The wave of excitation spreads across the atria,
causing them to contract.
Upon reaching the atrioventricular (AV) node, the
signal is delayed.
It is then conducted into the bundle of His, down the
interventricular septum.
The bundle of His and the Purkinje fibres spread the
wave impulses along the ventricles, causing them to
contract.
𝘾𝙤𝙣𝙙𝙪𝙘𝙩𝙞𝙣𝙜 𝙨𝙮𝙨𝙩𝙚𝙢 𝙤𝙛 𝙝𝙚𝙖𝙧𝙩
15.
16.
17. QRS duration represents the time for ventricular
depolarization. The duration is normally 0.06 to 0.10
seconds.
18.
19.
20. normal PR interval is 0.12 to 0.20 seconds, or 120 to
200 milliseconds.
normal
duration
(interval) of
the QRS
complex is
between
0.08 and
0.10
seconds —
that is, 80
and 100
milliseconds
21. SUPRAVENTRICULAR’ TACHYCARDIAS
SUPRAVENTRICULAR’ TACHYCARDIAS AV NODAL
RE-ENTRY TACHYCARDIA (AVNRT) This is due to re-entry in
the right atrium and AV node, and tends to occur in hearts
that are otherwise normal. It produces episodes of regular
tachy-cardia with a rate of 140–220/min that last from a few
seconds to many hours.
patient is usually aware of a fast heart beat and
may feel faint or breathless.
Polyuria may occur, and also angina if there is
underlying coronary disease
Attacks may be terminated by carotid sinus
pressure or Valsalva manoeuvre, but if not, i.v.
adenosine or verapamil will restore sinus rhythm in
most cases
𝘿𝙚𝙛𝙞𝙣𝙞𝙩𝙞𝙤𝙣
22. ECG (Fig. 8.3) usually shows a regular tachycardia
with normal QRS complexes but occasionally
there may be rate-dependent bundle branch block
When there is severe haemodynamic com-promise,
the tachycardia should be terminated by DC
cardioversion
• If attacks are frequent or disabling, prophylactic
oral therapy (e.g. β-blocker, verapamil) may be
indicated but catheter ablation (p. 228) offers a
very high chance of complete cure and is usually
preferable to long-term drug treatment.
23. ATRIOVENTRICULAR RE-ENTRANT
TACHYCARDIA (AVRT) AND WOLFF–
PARKINSON–WHITE SYNDROME
An abnormal band of rapidly conducting tissue
(‘accessory pathway’) con-nects the atria and
ventricles. In around half of cases, premature
activation of ventricular tissue via the pathway
produces a short PR interval and a ‘slur-ring’ of
the QRS complex, called a delta wave
As the AV node and bypass tract have different
conduction speeds and refractory periods, a re-
entry circuit can develop, causing tachycardia;
when associated with symp-toms, the condition is
known as Wolff–Parkinson–White syndrome.
𝙋𝙖𝙩𝙝𝙤𝙥𝙝𝙮𝙨𝙞𝙤𝙡𝙤𝙜𝙮 𝙤𝙛 𝙨𝙫𝙩
25. The incidence of SVT is approximately 35
cases per 100,000 patients with a
prevalence of 2.25 cases per 1,000 in the
general population. Atrial fibrillation and
atrial flutter are the most common
subtypes of SVT, affecting approximately 2
million patients in the United States.
𝙄𝙣𝙘𝙞𝙙𝙚𝙣𝙘𝙚
26. 𝘽𝙤𝙤𝙠 𝙥𝙞𝙘𝙩𝙪𝙧𝙚
𝙋𝙖𝙩𝙞𝙚𝙣𝙩 𝙥𝙞𝙘𝙩𝙪𝙧𝙚
𝙎𝙩𝙧𝙪𝙘𝙩𝙪𝙧𝙖𝙡 𝙖𝙣𝙤𝙢𝙖𝙡𝙞𝙩𝙮
(𝙈𝙄𝙏𝙍𝘼𝙇 𝙎𝙏𝙀𝙉𝙊𝙎𝙄𝙎
• 𝙂𝙚𝙣𝙙𝙚𝙧
• 𝙁𝙚𝙢𝙖𝙡𝙚 𝙥𝙖𝙩𝙞𝙚𝙣𝙩
𝙢𝙤𝙧𝙚 𝙥𝙧𝙤𝙣𝙚
Estrogen and progesterone
levels rise and fall in
women with a normal
menstrual cycle during the
days of the month. The
rise of progesterone and
the fall of estrogen
correspond with: More
frequent episodes of
supraventricular
tachycardia (SVT)
• 𝘼𝙜𝙚
Coronary artery
disease, other heart
problems and
previous heart surgery.
Congenital heart
diseas
Thyroid 𝙥𝙧𝙤𝙗𝙡𝙚𝙢𝙨
Drugs and
𝙨𝙪𝙥𝙥𝙡𝙚𝙢𝙚𝙣𝙩𝙨
Anxiety or emotional
stress.
Physical fatigue.
Diabetes.
• Anxiety
𝙍𝙞𝙨𝙠 𝙛𝙖𝙘𝙩𝙤𝙧𝙨
27. SYMPTOMS
Book picture
•
•
•
rapid tachycardia of
abrupt onset and
termination
Dizziness can occur
initially because of
hypotension
continuous pulsing
cannon A waves in
the jugular venous
waveform (described
as the “frog” sign)
?𝙋𝙖𝙩𝙞𝙚𝙣𝙩 𝙥𝙞𝙘𝙩𝙪𝙧𝙚
• ECG shows
supraventricular
tachycardia (SVT) with
a rate of 154. Vital
signs: T 98.8° F (37.1°C)
, R 26, BP 95/60
• nervous and weak and
dizzy.
28. • palpitations and
heart racing,
frequently
associated with
complaints of
dyspnea, weakness,
chest pain, dizziness,
or even frank
syncope.
• patients with
underlying
structural heart
disease,
symptoms can be
more severe
𝘽𝙤𝙤𝙠 𝙥𝙞𝙘𝙩𝙪𝙧𝙚
• Peripheral pulses weak but
equal, mucous
membranes pale pink, skin
cool and dry. Fine crackles
noted in both lung bases.
A loud S3 gallop and a
diastolic murmur.
• complaining of palpitations
𝙋𝙖𝙩𝙞𝙚𝙣𝙩 𝙥𝙞𝙘𝙩𝙪𝙧𝙚
• lightheadedness, and
shortness of breath
• history reveals rheumatic
fever at age 12 with
subsequent rheumatic heart
disease and mitral stenosis.
29. 𝘿𝙞𝙖𝙜𝙣𝙤𝙨𝙩𝙞𝙘 𝙀𝙫𝙖𝙡𝙪𝙖𝙩𝙞𝙤𝙣
𝘽𝙊𝙊𝙆 𝙋𝙄𝘾𝙏𝙐𝙍𝙀
𝙋𝙖𝙩𝙞𝙚𝙣𝙩 𝙥𝙞𝙘𝙩𝙪𝙧𝙚
• History, physical
examination, and an
electrocardiogram (ECG)
con-stitute an appropriate
initial evaluation of
patients presenting with
symptoms suggestive of
paroxysmal SVT.
History, physical
examination, and an
electrocardiogram (ECG)
• Ambulatory 24- or 48-
hour Holter recording
• A cardiac event
monitor,Implantable
loop recorders can be
helpful in selected
cases with rare
episodes associated
with severe symptoms
of hemodynamic
instability (e.g.,
syncope).
• An echocardiographic
examination
33. Stable client with sustained VT (with pulse and no
signs or symptoms of decreasedcardiac output)
• a. Administer oxygen as prescribed.
b. Administer antidysrhythmics as prescribed.
3. Unstable client with VT (with pulse and signs and
symptoms of decreasedcardiac output) a. Administer
oxygen and antidysrhythmic ther-apy as prescribed.
b. Prepare for synchronized cardioversion if the client
is unstable.
c. Attempt cough cardiopulmonary resuscita-tion
(CPR) by asking the client to cough hard every 1 to 3
seconds.
4. Pulseless client with ventricular tachycardia:
defibrillation and CPR
𝙉𝙐𝙍𝙎𝙄𝙉𝙂 𝙈𝘼𝙉𝘼𝙂𝙀𝙈𝙀𝙉𝙏
34. ASSESSMENT
Ms. Lewin’s assessment reveals that Ms. Vasquez is
moderately anxious. Her ECG shows supraventricular
tachycardia (SVT) with a rate of 154. Vital signs: T 98.8° F
(37.1°C), R 26, BP 95/60. Peripheral pulses weak but
equal, mucous membranes pale pink, skin cool and dry.
Fine crackles noted in both lung bases. A loud S3 gallop
and a diastolic murmur are noted. Ms. Vasquez is still
complaining of palpitations and tells Ms. Lewin, “I feel so
nervous and weak and dizzy.” Ms. Vasquez’s cardiologist
orders 2.5 mg of verapamil to be given slowly via
intravenous push and tells Ms. Lewin to prepare to assist
with synchronized cardioversion if drug therapy does not
control the ventricular rate."
Nursing care plan
35. DIAGNOSIS
Ms. Lewin formulates the following nursing diagnoses for Ms.
Vasquez.
• Decreased cardiac output related to inadequate ventricular
fill-ing associated with rapid tachycardia
• Ineffective tissue perfusion:cerebral/cardiopulmonary/
peripheral related to decreased cardiac 𝙤𝙪𝙩𝙥𝙪𝙩
• Anxiety related to unknown outcome of altered health 𝙨𝙩𝙖𝙩𝙚
EXPECTED OUTCOMES The expected outcomes for the
plan of care specify that Ms.
Vasquez will:
• Maintain adequate cardiac output and tissue perfusion.
• Demonstrate a ventricular rate within normal limits and
stable vital signs.
• Verbalize reduced anxiety.
• Verbalize an understanding of the rationale for the
treatment measures to control the heart rate
𝙉𝙪𝙧𝙨𝙞𝙣𝙜 𝙘𝙖𝙧𝙚 𝙥𝙡𝙖𝙣
36. •
•
Nursing Interventions
Monitoring and Managing the Dysrhythmia
• Minimizing Anxiety When the patient experiences
episodes of dysrhyth-mia, the nurse stays with the
patient and provides assurance of safety and
security while maintaining a calm and reassuring
attitude.
•
•
Promoting Home and Community-Based Care
TEACHING PATIENTS SELF-CARE.
When teaching patients about dysrhythmias, the
nurse fi rst assesses the patient’s understanding,
clarif i es misinformation, and then shares
needed information in terms that are
understandable and in a manner that is not
frighten-ing or threatening.
37. Valsalva maneuver
a. The physician instructs the client to bear down or
induces a gag reflex in the client to stimulate a
vagal response b. Monitor the heart rate, rhythm,
andBP.
c. Observe the cardiac monitor for a change in
rhythm.
d. Record an electrocardiographic rhythm strip
before, during, and after the procedure.
e. Provide an emesis basin if the gag reflex is
stimulated, and initiate precautions to prevent
aspiration.
f. Have a defibrillator and resuscitative equip-ment
available.
38. MANAGEMENT OF DYSRHYTHMIAS
. . Vagal maneuver:induce vagal stimulation of the
cardiac conduction system and are used to terminate
supraventricular tachydysrhythmias.
a. The physician instructs the client to turn the head
away from the side to be massaged
. Carotid sinus massage
b. The physician massages over one carotid artery for a few
seconds to determine whether a change in cardiac rhythm
occurs.
c. The client should be on a cardiac monitor;
an electrocardiographic rhythm strip before, during, and after
the procedure should be documented on the chart.
d. Have a defibrillator and resuscitative equip-ment available.
e. Monitor vital signs, cardiac rhythm, and level of
consciousness following the procedure.
45. B. . Cardioversion is synchronized countershock to convert
an undesirable rhythm to a stable rhythm.
b. Cardioversion can be an elective procedure performed by
the physician for stable tachy-dysrhythmias resistant to
medical therapies or an emergent procedure for
hemodynami-cally unstable ventricular or supraventricular
tachydysrhythmias.
c. A lower amount of energy is used than with defibrillation.
d. The defibrillator is synchronized to the cli-ent’s R wave to
avoid discharging the shock during the vulnerable period (T
wave).
e. If the defibrillator were not synchronized, it could
discharge on the T wave and cause VF.
46. 2. Preprocedure interventions
a. Obtain an informed consent if an elective procedure.
b. Administer sedation as prescribed.
c. Ifanelectiveprocedure,holddigoxin(Lanoxin) 48 hours
preprocedure as prescribed to prevent postcardioversion
ventricular irritability.
d. If an elective procedure for atrial fibrillation or atrial
flutter, the client should receive anticoagulant therapy for
4 to 6 weeks preprocedure.
3. During the procedure
a. Ensure that the skin is clean and dry in the area where
the electrode paddles will be placed.
b. Stop the oxygen during the procedure to avoid the
hazard of fire.
c. Be sure that no one is touching the bed or the client
when delivering the countershock.
47. 4. Postprocedure interventions
a. Priority assessment includes ability of the cli-ent
to maintain the airway and breathing.
b. Resume oxygen administration as prescribed.
c. Assess vital signs.
d. Assess level of consciousness.
e. Monitor cardiac rhythm.
f. Monitor for indications of successful response,
such as conversion to sinus rhythm, strong
peripheral pulses, an ade-quateBP, and adequate
urine output.
g. Assess the skin on the chest for evidence of
burns from the edges of the paddles.
48. Defibrillation
1. Defibrillation is an asynchronous countershock
used to terminate pulseless ventricular tachycar-
dia (VT) or VF.
2. Three rapid consecutive shocks are delivered,
with the first at an energy of 200 J.
3. Ifunsuccessful,theshockisrepeatedat200to300J.
4. The third and subsequent shocks will be 360 J.
Before defibrillating a client be sure that the
oxygen is shut off to avoid the hazard of fire and
be sure that no one is touching the bed or the
client.
D. Use of paddle electrodes
E. Automatic external defibrillator
F. Implantable cardioverter-defibrillator (ICD)
53. Evaluation Expected Patient Outcomes Expected
patient outcomes may include:
1. Maintains cardiac output
a. Demonstrates heart rate, blood pressure, respi-
ratory rate, and level of consciousness within normal
ranges
b. Demonstrates no or decreased episodes of
𝙙𝙮𝙨𝙧𝙝𝙮𝙩𝙝𝙢𝙞𝙖
2. Experiences reduced anxiety
3. Expresses understanding of the dysrhythmia and its
treatment
54. 1. What is the scientific basis for using carotid
massage to treat supraventricular tachycardias?
Was this an appropriate ma-neuver in the case of
Ms.Vasquez?
2. What other treatment options might the
physician have used to treat Ms.Vasquez’s
supraventricular tachycardia if she had been
asymptomatic with stable vital signs?
3. Develop a teaching plan for Ms.Vasquez
related to her pre-scription for furosemide.
Evaluation questions?
?
55. ℍ𝕖𝕒𝕝𝕥𝕙 𝕖𝕕𝕦𝕔𝕒𝕥𝕚𝕠𝕟 𝕗𝕠𝕣 𝕡𝕒𝕥𝕚𝕖𝕟𝕥 𝕙𝕒𝕧𝕚𝕟𝕘 𝕤𝕧𝕥
• Have less alcohol and caffeine
Don't smoke
Lower your stress
Eat foods that are healthy for your heart
Don't take recreational drugs, especially stimulants that can over-excite the heart
muscle. Some herbs and supplements can have this same effect. Always check with
your healthcare team before you take any non-prescribed medicines.
Stay well hydrated and get enough sleep
• 𝘼𝙜𝙚
Coronary artery disease, other heart problems
and previous heart surgery.
Congenital heart diseas
Thyroid 𝙥𝙧𝙤𝙗𝙡𝙚𝙢𝙨
Drugs and 𝙨𝙪𝙥𝙥𝙡𝙚𝙢𝙚𝙣𝙩𝙨
Anxiety or emotional stress.
Physical fatigue.
𝕄𝕒𝕜𝕖 𝕡𝕒𝕥𝕚𝕖𝕟𝕥 𝕒𝕨𝕒𝕣𝕖
𝕒𝕓𝕠𝕦𝕥 𝕥𝕙𝕚𝕤 𝕣𝕚𝕤𝕜 𝕗𝕒𝕔𝕥𝕠𝕣𝕤 𝕗𝕠𝕣
𝕊𝕦𝕡𝕣𝕒𝕧𝕖𝕟𝕥𝕣𝕚𝕔𝕦𝕝𝕒𝕣
𝕥𝕒𝕔𝕙𝕪𝕔𝕒𝕣𝕕𝕚𝕒
57. 𝘿𝙄𝙎𝘾𝙃𝘼𝙍𝙂𝙀 𝙋𝙇𝘼𝙉𝙉𝙄𝙉𝙂
Perform vagal maneuvers as directed when you have
symptoms of SVT. Lie down flat and bear down like you
are having a bowel movement. Do this for 10 to 30
seconds.
Do not drink caffeine or alcohol. These can increase your
risk for SVT.
Keep a record of your symptoms. Write down what you
ate or what you were doing before an episode of SVT.
Also write down anything you did to make the SVT stop.
Bring your record to follow up visits with your healthcare
provider.
Eat heart-healthy foods. These include fruits, vegetables,
whole-grain breads, low-fat dairy products, beans, lean
meats, and fish. Replace butter and margarine with
heart-healthy oils such as olive oil and canola oil.
58. • Exercise regularly and maintain a healthy weight.
Ask about the best exercise plan for you. Ask your
healthcare provider what a healthy weight is for
you. Ask him or her to help you create a safe
weight loss plan if you are overweight.
59. • Do not smoke. Nicotine and other chemicals in
cigarettes and cigars can cause heart and lung
damage. Ask your healthcare provider for
information if you currently smoke and need help
to quit. E-cigarettes or smokeless tobacco still
contain nicotine. Talk to your healthcare provider
before you use these products.
Manage other health conditions. Take medicine
as directed and follow your treatment plan. Your
healthcare provider may need to change a
medicine you are taking if it is causing your SVT.
Do not stop taking any medicine unless directed
by your provider.
60. 𝙎𝙪𝙢𝙢𝙖𝙧𝙮???
Supraventricular tachycardias (SVTs) are a group
of tachyarrhythmias arising from abnormalities
in pacemaker activity and/or conduction
involving myocytes of the atria and/or AV node.
Types of SVT include atrioventricular nodal
reentrant tachycardia (AVNRT; approx. two-thirds
of cases), atrioventricular reciprocating (or
reentrant) tachycardia (AVRT), focal atrial
tachycardia (FAT), multifocal atrial tachycardia
(MAT), and junctional tachycardia. AVNRT and
AVRT are caused by abnormal conduction
circuits that form an unending loop of conduction
referred to as reentry.
61. 𝘾𝙤𝙣𝙘𝙡𝙪𝙨𝙞𝙤𝙣
supraventricular tachycardias produce serious
symp-toms and can dramatically impair quality of
life. Apart from the obvious haemodynamic and
thromboembolic risks already discussed, the
psychological impact of SVT should not be
underestimated. Patients feel insecure and
vulnerable when their hearts inexplicably accelerate
and they become aware of an abnormal cardiac
rhythm.
Whilst many will respond to reassurance, many
others do not. Many fear for their lives each time the
arrhythmia occurs.
Supraventricular tachycardias frequently threaten
the quality of life but only rarely threaten life
62. 𝘽𝙞𝙗𝙡𝙞𝙤𝙜𝙧𝙖𝙥𝙝𝙮
1. Holter NJ: New method for heart studies. Science,
1961; 134: 1214–1229.
2. Bleifer SB, Bleifer DJ, Hansmann DR, Sheppard JJ,
and Karpmann HL: Diagnosis of occult arrhythmias by
Holter electrocardiography. Prog Cardiovasc Dis 1974;
16: 569–599.
3. Lipski J, Cohen L, Espinoso J, Motro M, Dack S, and
Donoso E: Value of Holter monitoring in assessing
cardiac arrhythmias in symptomatic patients. Am J
Cardiol 1976; 37: 102–109.