Palpitation, Breathlessness, arrhythmia
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This document discusses breathlessness, palpitations, and arrhythmias. It begins by defining breathlessness and listing potential causes including lung problems, cardiac issues, and systemic illnesses. Evaluation for pulmonary and cardiac causes of breathlessness is described. Acute dyspnea management is outlined. Palpitations are defined and potential etiologies discussed. Arrhythmias are defined and mechanisms including automaticity and reentry are explained. The electrical conduction system of the heart is also briefly described.
![Evaluation for pulmonary causes
• PFTs: spirometry (screening/simple), lung
volumes, DLCO, O2 assessment; [assess for copd, asthma,
ILD]
• Exercise assessment (6MWT) [assess functional status of any
cardiopulm disease]
• Bronchoprovocation challenge [assess for asthma]
• Serial chest radiographs, CTA / HRCT chest [assess
for ILD, cancer, CHF, HP, other]
• Targeted Labs: cbc, chems, HPP, CVD, other [assess
for anemia, CVD, HP, sarcoid, vasculitis]
• Bronchoscopy [assess for any parenchymal lung disease that
produces infiltrates on CXR/CT]
• Surgical lung biopsy [assess for any parenchymal lung disease that
produces infiltrates on CXR/CT]](https://image.slidesharecdn.com/palpitation-140608072839-phpapp01/85/Palpitation-Breathlessness-arrhythmia-15-320.jpg?cb=1676626547)
![Mechanisms of cardiac arrhythmias
• Arrhythmic activity can be categorized as passive
(e.g., atrioventricular [AV] block) or active
• The mechanisms responsible for active cardiac
arrhythmias:
– Abnormal impulse formation:
• Automaticity (enhanced pacemaker, protected pacemaker
parasystole )
• triggered activity
– reentry (most common)](https://image.slidesharecdn.com/palpitation-140608072839-phpapp01/85/Palpitation-Breathlessness-arrhythmia-36-320.jpg?cb=1676626547)
![LBBB
ECG criteria for LBBB include a QRS duration O0.12 seconds, a broad
monomorphic R wave in leads I, V5, and V6, a wide S wave following an
initial small (or absent) R wave in the right precordial leads, and absence
septal Q waves in leads I, V5, and V6 (Fig. 6). The term incomplete
LBBB is used to describe these findings in patients who have a QRS complex
duration !0.12 seconds (usually 0.10–0.11 seconds) Left bundle branch
block ECG findings include (1) widened QRS complex (O0.12 seconds),
2) QS or rS complex in lead V1, (3) late intrinsicoid deflection and monophasic R
wave in lead V6, and (4) no Q wave in lead V6 [5].](https://image.slidesharecdn.com/palpitation-140608072839-phpapp01/85/Palpitation-Breathlessness-arrhythmia-126-320.jpg?cb=1676626547)
Palpitation, Breathlessness, arrhythmia
- 1. Breathlessness Palpitation Arrhythmia Dr. Doha Rasheedy Lecturer of Geriatric Medicine Department of Geriatric and Gerontology Ain Shams University
- 3. Breathlessness or shortness of breath • Difficulty in breathing / uncomfortable awareness of breathing. • It can be caused by various mechanisms related to different problems in the body. • In one’s lifetime, one may experience rare episodes of shortness of breath as part of high levels of activity like exhaustive exertion, or during environmental conditions such as high altitude or very warm or cold temperatures. Other than these extreme conditions, shortness of breath is commonly a sign of a medical problem.
- 4. When Is Shortness of Breath a Sign of a Medical Problem? If the shortness of breath is prolonged and persistent, it is likely to be related to a medical condition. If it is sudden and severe in intensity, even if it is of short duration, however, it may warrant medical evaluation. The following are other clues of existence of a medical problem: • Shortness of breath at rest • Shortness of breath with activity or exercise • Shortness of breath when lying down • Shortness of breath on exposure to allergens or provoking agents • Shortness of breath accompanied with: • Chest pain or chest discomfort • Discomfort or pain in 1 or both arms, pain radiating to jaw, or pain in the neck • Swelling in ankles and feet • Fluid weight gain or unintentional weight loss with loss of appetite • Unusual fatigue • Sweating • Yellow, green, or rusty colored sputum or phlegm or blood in the sputum • Fever • Wheezing or whistle-like sounds with breathing • Persistent, chronic cough • Blue discoloration of lips or fingertips • Fainting, dizzy spells, lightheadedness • Club-shaped deformation of fingertips
- 5. Causes
- 8. Lung Problems • Recent infections, such as bronchitis or pneumonia, or prolonged (chronic) infections, such as tuberculosis or chronic bronchitis. Shortness of breath may be accompanied by discolored phlegm and/or fever. • Asthma, chronic obstructive lung disease (COPD), and emphysema: The airways are narrowed with increased resistance to exhaling air from the lung, resulting in air entrapment in the lung. Shortness of breath may be accompanied by wheezing. With asthma, there is usually an allergy history, whereas with COPD or emphysema, there is usually a smoking history. • Lung cancer and other tumors: Shortness of breath is commonly accompanied by unintentional appetite and weight loss. There is usually a long history of heavy smoking. • Scarring and damage of lung tissue by toxins (such as asbestosis) or by systemic illnesses (such as rheumatoid arthritis). There is usually a known history of these systemic illnesses or occupational exposures.
- 9. • Clot in the lung circulation (pulmonary embolus): Breathlessness is usually sudden and associated with rapid breathing and may be accompanied by chest pain. People with blood clots in the legs or pelvis (deep vein thrombosis, or DVT), debilitating medical conditions, immobility, or inherited tendency of forming clots may be prone to this condition. • Diseases of the lung sac (pleura): If the pleura thickens, becomes scarred, or gets filled with fluid or blood because of infection (pleurisy), cancer, or toxins (asbestosis), or if it becomes filled with air (called pneumothorax) because of trauma, it will hinder expansion of the lung, resulting in shortness of breath. • Diseases of the diaphragm : The diaphragm is the muscle that expands the lung. It may become paralyzed after chest surgery. • diseases of chest wall: Obesity and spine or chest wall deformities also can produce difficulty in breathing.
- 10. Cardiac causes
- 11. Systemic Illness Problems • Anemia, low red blood cell count: Because the red cells carry oxygen, when their number is extremely low, the oxygen demands of the body will not be met, resulting in shortness of breath. • Increased metabolic states such as high thyroid level, severe systemic infection (sepsis), or fever: The increased oxygen demands of the body will try to be met by breathing heavily and rapidly. • Kidney or chronic liver problems: Because of increased fluid in the lungs and body and impaired oxygen exchange in the lungs, patients may experience shortness of breath in the advanced stages of both conditions.
- 12. Nervous System Problems • Increased intracrainial tension: caused by trauma, tumors, stroke, or bleeding. When the portion of the brain that regulates respiration is affected, these rare conditions may result in difficulty in breathing. Other neurological symptoms usually precede shortness of breath. • Nerve and muscle disorders that affect the ability to coordinate and expand the chest and that affect movement of the diaphragm may produce difficulty in breathing. Muscular dystrophies, Guillain-Barre syndrome, ALS / Polio, myasthenia gravis.
- 13. other • Obesity • Physical deconditioning • Anxiety: Anxiety is sometimes accompanied by heavy and rapid breathing (hyperventilation). Shortness of breath usually resolves once the anxiety episode ends.
- 14. Urgently Life Threatening causes • Upper airway obstruction – Foreign body – Angioedema/anaphylaxis • Tension pneumothorax • Pulmonary embolism • Neuromuscular weakness – Myasthenia gravis – Guillain-Barre
- 15. Evaluation for pulmonary causes • PFTs: spirometry (screening/simple), lung volumes, DLCO, O2 assessment; [assess for copd, asthma, ILD] • Exercise assessment (6MWT) [assess functional status of any cardiopulm disease] • Bronchoprovocation challenge [assess for asthma] • Serial chest radiographs, CTA / HRCT chest [assess for ILD, cancer, CHF, HP, other] • Targeted Labs: cbc, chems, HPP, CVD, other [assess for anemia, CVD, HP, sarcoid, vasculitis] • Bronchoscopy [assess for any parenchymal lung disease that produces infiltrates on CXR/CT] • Surgical lung biopsy [assess for any parenchymal lung disease that produces infiltrates on CXR/CT]
- 16. Evaluation for Cardiac causes • ECG • Echocardiography • BNP • Exercise testing • Coronary angiography
- 18. Immediate Actions (in 10 minutes) • Supplemental oxygen • Pulse oximetry with complete vital signs • Decide need for endotracheal intubation • IV access, labs, and ABG • Portable chest x-ray • ECG if concerned for cardiac etiology • Brief history and focused physical exam • Form initial differential, begin treatment
- 19. Rapid Physical Exam • Vital signs – RR, HR, BP, temp, O2 Sat • Mental Status – Alert, confused, lethargic • Heart – JVP, muffled heart sounds, S3, S4 • Lungs – Rales, wheezing, diminished or absent BS, stridor – Respiratory accessory muscle use • Abdomen – Hepatomegaly, ascites • Skin – Diaphoresis, cyanosis • Extremities – Edema – Unilateral leg swelling • Neurologic – Focal neurologic deficits
- 20. Palpitation
- 21. Palpitation • The subjective awareness of the heart beating due to change in heart rate, rhythm, or force of cardiac contraction. • Palpitations can be symptomatic of life- threatening cardiac arrhythmias. However, most palpitations are benign
- 22. Etiology
- 23. Clinical manifestation • Fluttering, Skipping, or Pounding sensation in the chest. • Associated with light headiness, dizziness, dyspnea, presyncope or syncope. • Possible etiology:
- 25. Examination • Murmurs (valvular heart disease) • Midsystolic click (Mitral valve prolapse) • Elevated jugular venous pressure, rales (heart failure) • Thyroid enlargement or nodules
- 26. Work up • A 12-lead ECG evaluation is appropriate in all patients who complain of palpitations.(may not detect arrhythmia episode) Serious finding include: – previous myocardial infarction – left or right ventricular hypertrophy – atrial enlargement – atrial ventricular block – short PR interval and delta waves (Wolff-Parkinson-White syndrome), – prolonged QT interval. – finding of an isolated premature ventricular contraction or premature atrial contraction warrants further monitoring or exercise testing.
- 27. • 24-hour ECG monitoring, ambulatory event monitor, implantable loop recorder: For assessment of infrequent palpitation
- 28. • ECG exercise testing is appropriate in patients who have palpitations with physical exertion and patients with suspected coronary artery disease or myocardial ischemia. •
- 29. • Echocardiography to evaluate structural abnormalities and ventricular function.
- 30. Electrophysiological testing • Failed documentation of arrhythmia by 24- hour ECG monitoring, ambulatory event monitor, implantable loop recorder
- 31. Blood tests • may be appropriate in the following conditions: – complete blood cell count for suspected anemia or infection – electrolytes for arrhythmia from suspected electrolyte imbalance – thyroid-stimulating hormone for suspected hyperthyroidism or hypothyroidism. – ABG: hypoxia:
- 33. Arrhythmia
- 34. Definition of Arrhythmia • Any abnormality in the Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation.
- 35. The electrical system of the heart
- 36. Mechanisms of cardiac arrhythmias • Arrhythmic activity can be categorized as passive (e.g., atrioventricular [AV] block) or active • The mechanisms responsible for active cardiac arrhythmias: – Abnormal impulse formation: • Automaticity (enhanced pacemaker, protected pacemaker parasystole ) • triggered activity – reentry (most common)
- 37. Automaticity • Cells in the sinus node possess the fastest intrinsic rates. Thus the SA node is the primary pacemaker in the normal heart. When impulse generation or conduction within or out of the SA node is impaired, latent or subsidiary pacemakers within the atria or ventricle are capable of taking control of pacing the heart. The intrinsically slower rates of these latent pacemakers result in bradycardia.
- 38. Enhanced automaticity • Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker. • Factors that enhance automaticity include: acute cardiac ischemia, hypoxemia, hypokalemia, hypomagnesemia, acid–base disturbances, high sympathetic tone, or the use of sympathomimetic agents. • Examples: Ectopic atrial tachycardia or multifocal tachycardia in patients with chronic lung disease OR ventricular ectopy after MI
- 39. Protected automaticity (Parasystole) • Latent pacemakers throughout the heart are generally reset by the propagating wavefront initiated by the dominant pacemaker and are therefore unable to activate the heart. • An exception to this rule occurs when the pacemaking tissue is protected from the impulse of sinus origin. A region of entrance block arises when cells exhibiting automaticity are surrounded by ischemic, infarcted, or otherwise compromised cardiac tissues that prevent the propagating wave from invading the focus, but which permit the spontaneous beat generated within the automatic focus to exit and activate the rest of the myocardium. • A pacemaker region exhibiting entrance block and exit conduction defines a parasystolic focus. • The ectopic activity generated by a parasystolic focus is characterized by premature ventricular complexes. • This rhythm is fairly rare. Although it is usually considered benign, any premature ventricular activation can induce malignant ventricular rhythms in the ischemic myocardium or in the presence of a suitable myocardial substrate.
- 40. REENTRY
- 41. Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Reentry Requires… Electrical Impulse Cardiac Conduction Tissue 1. 2 distinct pathways that come together at beginning and end to form a loop. 2. A unidirectional block in one of those pathways. 3. Slow conduction in the unblocked pathway.
- 42. Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Premature Beat Impulse Cardiac Conduction Tissue 1. An arrhythmia is triggered by a premature beat 2. The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway Repolarizing Tissue (long refractory period) Reentry Mechanism
- 43. 3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue Reentry Mechanism
- 44. 4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue Reentry Mechanism
- 45. Atrial Reentry • atrial tachycardia • atrial fibrillation • atrial flutter Atrio-Ventricular Reentry • WPW • SVT Ventricular Re-entry • ventricular tachycardia AV Nodal Reentry •SVT Reentry Circuits SA Node
- 46. Triggered activity • abnormal fluxes of positive ions (usually calcium) into cardiac cells. • Two subclasses traditionally recognized: (1) early, and (2) delayed. EADs interrupt or retard repolarization during phase 2 and/or phase 3 of the cardiac action potential, whereas DADs occur after full repolarization. • If the after- depolarizations are of sufficient amplitude, they can trigger the rapid sodium channels and thus cause another action potential to be generated.
- 47. • Delayed after-depolarizations arise during the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias. • Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced
- 48. Sinus Arrhythmia
- 49. Sinus tachycardia • Sinus rate > 100 beats/min (100-180) • Causes: 1. Some physical condition: exercise, anxiety, exciting, alcohol, coffee 2. Some disease: fever, hyperthyroidism, anemia, myocarditis 3. Some drugs: Atropine, Isoprenaline • Needn’t therapy
- 50. Sinus Bradycardia • Sinus rate < 60 beats/min • Normal variant in many normal and older people • Causes: Trained athletes, during sleep, drugs (ß- blocker) , Hypothyriodism, CAD or SSS • Symptoms: 1. Most patients have no symptoms. 2. Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope. • Needn’t specific therapy, If the patient has severe symptoms, planted an pacemaker may be needed.
- 51. Sinus Arrest or Sinus Standstill • Sinus arrest or standstill is recognized by a pause in the sinus rhythm. • Causes: myocardial ischemia, hypoxia, hyperkalemia, higher intracranial pressure, sinus node degeneration and some drugs (digitalis, ß-blocks). • Symptoms: dizziness, amaurosis, syncope • Therapy is same to SSS
- 52. • Sinus pause or arrest means failure of sinus node discharge with lack of atrial activation of sinus origin. This results in absence of P waves and periods of ventricular asystole if lower pacemakers (junctional or ventricular) do not initiate escape beats. • The resulting pause in sinus activity should not be in multiples of preceding sinus cycle length (P-P interval). • Pauses longer than 3 sec need careful clinical correlation with symptoms and warrant further evaluation.
- 53. Sinoatrial exit block (SAB) • SAB: Sinus pulse was blocked so it couldn’t active the atrium. • In SA exit block, the impulse is formed in the sinus node but fails to conduct to the atria, unlike sinus arrest. This particular arrhythmia is recognized on ECG by pauses resulting from the absence of normal P waves and the duration of the pause measuring an exact multiple of the preceding P-P interval • Causes: CAD, Myopathy, Myocarditis, digitalis toxicity • Symptoms: dizziness, fatigue, syncope • Therapy is same to SSS
- 54. Sinoatrial exit block (SAB) • SA block can also be described in the same way as AV block. In first- degree SA block, there is significant prolongation of the time for the sinus impulse to exit into the atria (SA conduction time). This cannot be identified clinically or electrocardiographically. • Similar to AV block, second-degree SA block can be type I (Wenckebach) or type II. In type I there is progressive prolongation of SA conduction, manifested on surface ECG as progressive shortening of P-P interval, prior to the pause created by loss of a P wave. In type II SA exit block, the P-P intervals remain constant before the pause. • Third-degree or complete SA block will manifest as absence of P waves, with long pauses resulting in lower pacemaker escape rhythm; it is impossible to diagnose with certainty without invasive sinus node recordings..
- 55. Sick Sinus Syndrome (SSS) • SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node automaticity and SA conduction. • Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor, trauma and congenital disease. • With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms • Bradycardia-tachycardia syndrome: These patients are at increased risk for thromboembolism, and the issue of long-term anticoagulation should be addressed to prevent strokes.
- 56. Sick Sinus Syndrome (SSS) ECG Recognition: 1. Sinus bradycardia, ≤40 bpm; 2. Sinus arrest > 3s 3. Type II SAB 4. Nonsinus tachyarrhythmia ( SVT, AF or Af).
- 58. Sick Sinus Syndrome (SSS) • Therapy: 1. Treat the etiology 2. Treat with drugs: anti-bradycardia agents, the effect of drug therapy is not good. 3. Artificial cardiac pacing.
- 59. Tachyarrhythmias • Supraventricular tachycardia • Atrial fibrillation • Atrial flutter • Ventricular tachycardia » Monomorphic » Polymorphic (Torsades de pointe) • Ventricular fibrillation
- 60. Premature contractions • The term “premature contractions” are used to describe non sinus beats. • Common arrhythmia • The morbidity rate is 3-5%
- 61. Atrial premature contractions (APCs) • APCs arising from somewhere in either the left or the right atrium. • Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemia • Symptoms: many patients have no symptom, some have palpitation, chest incomfortable. • Therapy: Needn’t therapy in the patients without heart disease. Can be treated with ß-blocker, propafenone, verapamil.
- 62. Atrial tachycardia • Classify by automatic atrial tachycardia (AAT); intra-atrial reentrant atrial tachycardia (IART); chaotic atrial tachycardia (CAT). • Etiology: atrial enlargement, MI; chronic obstructive pulmonary disease; drinking; metabolic disturbance; digitalis toxicity; electrolytic disturbance.
- 63. Atrial tachycardia • May occur transient; intermittent; or persistent. • Symptoms: palpitation; chest uncomfortable, tachycardia may induce myopathy.
- 64. Intra-atrial reentry tachycardia (IART) • ECG characters: 1. Atrial rate is around 130-150bpm; 2. P’ wave is different from sinus P wave; 3. P’-R interval ≥ 0.12” 4. Often appear type I or type II, 2:1 AV block; 5. EP study: atrial program pacing can induce and terminate tachycardia
- 65. Automatic atrial tachycardia (AAT) • ECG characters: 1. Atrial rate is around 100-200bpm; 2. P’ wave is different from sinus P wave; 3. P’-R interval≥ 0.12” 4. Often appear type I or type II, 2:1 AV block; 5. EP study: Atrial program pacing can’t induce or terminate the tachycardia
- 67. Chaotic atrial tachycardia (CAT) • Also termed “Multifocal atrial tachycardia”. • Always occurs in COPD or CHF, • Have a high in-hospital mortality ( 25-56%). Death is caused by the severity of the underlying disease. • ECG characters: 1. Atrial rate is around 100-130bpm; 2. The morphologies P’ wave are more than 3 types. 3. P’-P’, P’-R and R-R interval are different. 4. Will progress to af in half the cases 5. EP study: Atrial program pacing can’t induce or terminate the tachycardia
- 69. MAT • Automatic atrial rhythm from various different foci • Seen in hypoxia, COPD, atrial stretch and local metabolic imbalance. • Three or more types of p waves and a rate > 100 • Digoxin worsens it, so treat with oxygen and slow calcium channel blocker like verapamil or diltiazem.
- 70. Therapy • IRAT: RFCA, Ic and IV class anti-tachycardia agents • AAT: Digoxin, IV, II, Ia and III class anti- tachycardia agents; RFCA • CAT: treat the underlying disease, verapamil or amiodarone. • Associated with SSS: Implant pace-maker.
- 71. Atrial fibrillation • Prevalence increases with increasing age of the population: 0.5% in ages 50–59 years and 8.8% in ages 80–89 years. A classification by Camm has divided AF into the following: • Paroxysmal: characterized by self-terminating episodes that generally last <7 days (most <24 hours), • persistent AF generally lasts >7 days and often requires electrical or pharmacologic cardioversion. • Permanent: established AF. Cannot be terminated by drugs or DC cardioversion. Patients need rate control therapy plus consideration of anticoagulation. Ablation can be successful
- 73. Common Causes • Ischaemic heart disease • Alcohol: chronic alcohol consumption • Thyrotoxicosis • Mitral valve disease: LA dilatation caused by mitral stenosis and/or regurgitation • Hypertension: accounts for about 50% cases • Cardiac surgery: right atrial cannulation; thoracotomy. • Pyrexial illness, chest infection, etc.
- 74. Less Common Causes • General anaesthesia • Hypoxia: chronic pulmonary disease • Pulmonary embolism • After ASD closure • Chest trauma • Pregnancy • Heart muscle disease: dilated cardiomyopathy , hypertrophic • Obstructive sleep apnoea • Provocation by pacing wire, catheter in either atrium • Part of the rhythm spectrum of sinoatrial disease • Malignant infiltration.
- 75. • If no cause is apparent and the heart is otherwise normal clinically and on echocardiography, the term ‘lone AF’ is used.
- 76. Treatment 1- Anticoagulation Stroke Risk and Stratification for long term anticoagulation CHADS2 Scoring System: • A total score of 0–1 should be managed with soluble aspirin. A score of 2 or more should be anticoagulated with warfarin, but the hypertension must be well controlled.
- 77. Rhythm control • Cardioversion can be accomplished using either antiarrhythmic drugs or the direct-current approach. In situations where urgent cardioversion is needed, such as marked hypotension, the direct- current approach is preferred. The need for anticoagulation prior to cardioversion must be considered: • There is general consensus that AF that has been present for <48 hours can be cardioverted without prior anticoagulation, but there are no randomized trial data to support this, and probable systemic emboli can occur in this situation. • Because often it is impossible to time accurately the onset of AF, anticoagulation therapy is recommended for AF of uncertain duration. • There are two basic strategies to deal with cardioversion: (1) oral warfarin with a therapeutic INR (2–3) for 3 to 4 weeks before cardioversion followed by continued warfarin thereafter or (2) transesophageal echocardiography (TEE) and heparin immediately before cardioversion followed by oral warfarin thereafter. • Anticoagulation should be continued for 1 month after successful cardioversion
- 78. DC Cardioversion • Start with 200J shock (100 J if in atrial fl utter). If failure to cardiovert: second shock, 300 J. If failure: give disopyramide 100 mg i.v or flecainide 50–100 mg slowly over 5–10 min. Third shock 360 J with paddles in anteroposterior position. • If still fails: consider treatment with amiodarone for 1 month and a further attempt, or just accept AF as definitive rhythm and treat with rate control and long-term warfarin. • Successful cardioversion: Disopyramide, ß blockade or amiodarone helps maintain sinus rhythm.
- 79. Pharmacological cardioversion • This is most likely to succeed with recent-onset AF. • Flecainide 2 mg/kg i.v. over 10 min is the drug of choice but should be avoided in patients with poor LV function because it has a negative inotropic effect. • Disopyramide 50– 150 mg i.v. slowly over 5 min is an alternative. • Fibrillatory waves may coarsen and the ventricular response increase before sinus rhythm is achieved. • Amiodarone given orally (200 mg three times daily up to 400 mg three times daily for 1 week) may also result in version to sinus rhythm. The dose is reduced after 1 week. Amiodarone is also very useful given intravenously: 5 mg/kg over 4 h in 5% dextrose. The maximum intravenous dose over 24 h in an adultis 1200 mg. An immediate result should not be expected: it may take 24–48 h to convert the patient back to sinus rhythm. The patient can be converted to oral amiodarone when practical.
- 81. Rate control • In permanent AF, drug therapy is used to control the rate of ventricular response by increasing AV node refractoriness. • Control of the ventricular rate involves both acute and chronic phases. In the acute phase, intravenous diltiazem, metoprolol, esmolol, or verapamil have all been demonstrated to provide slowing of AV nodal conduction within 5 minutes; these drugs are indicated for patients with severe symptoms related to a rapid ventricular rate.
- 82. • Target rate: is 60 to 80 beats/min at rest and between 90 and 115 beats/min during moderate exercise. • Digoxin may provide effective control of the resting heart rate but is often ineffective during exertion. • β Adrenergic blockers or calcium channel antagonists provide much better control of the ventricular rate during exercise and should be considered for most patients. • Digoxin is most useful in the setting of impaired systolic function, and can be used in combination withβ blockers or calcium antagonists if these agents do not provide adequate rate control.
- 83. Catheter ablation • Recent approaches to catheter ablation of AF, especially paroxysmal AF, have been to eliminate triggering foci, primarily within the pulmonary veins
- 84. Atrial Flutter • There are several types of atrial flutter, all having rapid, regular atrial rates, generally 240 to 340 beats/min, because of a reentrant mechanism in the atria. • Types: – Typical, also called counterclockwise atrial flutter is characterized by negative sawtooth flutter waves in ECG leads II, III, and aVF – reverse typical, also called atypical or clockwise atrial flutter by positive flutter waves in ECG leads II, III, and aVF • Both types use the sub-Eustachian or cavotricuspid isthmus (i.e., the isthmus between the tricuspid annulus on one side and the inferior vena cava–Eustachian ridge- coronary sinus on the other) as a part of the reentrant circuit • Usually a 2:1 conduction pattern.
- 85. Atrial Flutter
- 86. Management Acute Treatment of Atrial Flutter atrial flutter should be treated acutely to restore sinus rhythm, or at the very least, to control the ventricular response rate as needed. • Cardioversion: Transthoracic direct current (DC) cardioversion of atrial flutter to sinus rhythm has a very high likelihood of success. • Pharmacological cardioversion: Antiarrhythmic drug therapy to restore sinus rhythm is primarily intravenous ibutilide, procainamide. • Drug therapy may also be used to slow the ventricular response rate as needed: • Useful agents include β blockers, verapamil, diltiazem, and digitalis, alone or in combination. It is often difficult to achieve sufficient AV nodal block to slow adequately the ventricular response during atrial flutter, and 2:1 AV conduction frequently recurs. • Rapid atrial pacing can also be used to restore sinus rhythm.
- 87. Long-Term Treatment of Atrial Flutter Catheter Ablation Therapy: is highly successful, typically 90 percent or greater, to cure atrial flutter.3 This coupled with the recognized difficulty in achieving adequate long-term suppression with antiarrhythmic drug therapy make catheter ablation a first-line treatment option for many patients. • Because classical atrial flutter is usually preceded by a variable period of AF, successful ablation of the atrial flutter reentrant circuit per se may not prevent either the new appearance or the recurrence of AF. Antiarrhythmic Drug Therapy • Selection of an antiarrhythmic drug to treat atrial flutter mirrors that to treat AF. However, this form of therapy is no longer the treatment of choice for long-term therapy in most patients with atrial flutter, because catheter ablation to cure atrial flutter has superseded it. Anticoagulant Therapy • In patients with atrial flutter, daily warfarin therapy to achieve an INR between 2 and 3 (target 2.5) is recommended using the same criteria as for AF. In addition, several studies indicate that the incidence of stroke associated with atrial flutter approaches that of AF Antitachycardia Pacemaker Therapy • Although available and effective, little use has been made of implantation of an antitachycardia pacemaker to treat (interrupt) atrial flutter. Antitachycardia pacing can be used acutely in patients with atrial flutter who have an implanted pacemaker or defibrillator with the capability of temporary rapid atrial pacing therapies.
- 90. Ventricular Premature Contractions (VPCs) • Etiology: 1. Occur in normal person 2. Myocarditis, CAD, valve heart disease, hyperthyroidism, Drug toxicity (digoxin, quinidine and anti-anxiety drug) 3. electrolyte disturbance, anxiety, drinking, coffee
- 91. VPCs • Manifestation: 1. palpitation 2. dizziness 3. syncope 4. loss of the second heart sound
- 92. PVCs • Therapy: treat underlying disease, antiarrhythmia • No structure heart disease: 1. Asymptom: no therapy 2. Symptom caused by PVCs: antianxiety agents, ß- blocker and mexiletine to relief the symptom. • With structure heart disease (CAD, HBP): 1. Treat the underlying diseas 2. ß-blocker, amiodarone 3. Class I especially should be avoided because of proarrhytmia and lack of benefit of prophylaxis
- 93. Ventricular tachycardia Non-sustained VT • three or more ventricular premature beats at a rate of >100 beats/min terminating in <30 s. Sustained VT • VT lasting >30 s, or requiring termination resulting form haemodynamic compromise in <30 s. VT may be monomorphic with a stable single QRS morphology, or polymorphic with a changing multiform QRS morphology
- 95. Ventricular Flutter • This is a term occasionally used to describe monomorphic VT at a rate of approximately 300/min. No isoelectric interval between QRS complexes. Ventricular Fibrillation • This is a rapid ventricular rate >300/min with marked variability in QRS cycle length and QRS amplitude.
- 97. Management of VT in a Haemodynamically Stable Patient • Establish intravenous access. Check blood for K , acid– base balance and arterial blood gases and correct if necessary. • Start amiodarone 300 mg in 5% dextrose over 10 min then aim to deliver a total of 1200 mg over 24 h. • Assume hypomagnesaemia. Give 10 mmol magnesium sulphate over 30 min. • If VT persists, or haemodynamics deteriorates: for DC shock. It is much safer to shock a patient early for VT than to try several different antiarrhythmic drugs.
- 98. Management of VT in a Haemodynamically Unstable Patient • Establish intravenous access. Check blood for K, acid–base balance and blood gases in all patients and correct if necessary (including artifi cial ventilation • Cardiac massage may help correct the arrhythmia. • High-flow oxygen. • DC synchronized shock 200 J. If fails: DC shock 360 J. • Give amiodarone 300 mg i.v. in 20 ml 5% dextrose over 5–10 min. If unavailable, give lidocaine 100–200 mg bolus followed by infusion. • Assume hypomagnesaemia. Give 10 mmol magnesium sulphate over 30 min • If still in VT: further 360 J shock. • Consider overdrive pacing. • Consider alternative antiarrhythmic drug, e.g. intravenous mexiletine.
- 99. Long-term Prophylaxis • Once successfully cardioverted, prophylactic therapy is started orally and ICD implantation is considered . • The effect of the chosen drug is monitored with 24- hour Holter). It is important to keep the serum K between 4.5 and 5.5 mmol/l. • If VT was secondary to MI or acute myocarditis, it is probably wise to continue drug therapy for 3 months in the first instance, and then repeat 24-hour monitoring both on the drug and after its withdrawal. In some cases more than one drug will be necessary and indefinite oral therapy may be required.
- 100. Regimens of choice are one or more of these drugs: • Disopyramide 100 mg three or four times daily • Mexiletine 200 mg three times daily • Amiodarone 200 mg three times daily for 1 week then reducing • Propafenone 150–300 mg three times daily • ß-Blocking agent flecainide 100–200 mg twice daily. Drugs of second choice may be added or tried separately: • Procainamide 375 mg 4-hourly • Quinidine durules, two twice daily • Phenytoin 100 mg three times daily to 200 mg twice daily. The best combinations (e.g. disopyramide or mexiletine and amiodarone).
- 101. Ventricular flutter and fibrillation 1. Cardio-Pulmonary Resuscitate (CPR) 2. ICD
- 102. Long QT Syndromes • A long QT interval may be congenital (inherited gene defects) or acquired (drug or electrolyte effects), resulting from abnormalities of the ion channels controlling the duration of repolarization. • long QT interval may predispose to VT often of the polymorphic torsades de pointes type. Acquired Long QT Interval • This is most commonly drug-induced or secondary to hypocalcaemia or hypomagnesaemia. It may occur in anorexia nervosa. Prolongation of the QT interval is part of the therapeutic benefit of drugs such as amiodarone and sotalol, and the finding of a long QT interval is not necessarily an indication to stop the drug unless the QT interval is >500 ms.
- 103. Management of Torsades de Pointes • Torsades respond poorly to conventional drugs and may be made worse by class Ia agents, e.g. lidocaine, or class III agents. The probable culprit drug is stopped. Consider the following: • Pacing: temporary or permanent. Atrial pacing at 90–110/min shortens the QT interval, helping to prevent torsades. • Magnesium sulphate infusion (even if magnesium level is normal): 1–2 g i.v. over 2–3 min (equivalent to 2–4 ml 50% magnesium sulphate). Then infuse at 2–8 mg/min. • Isoprenaline infusion 2–10 µg/min, intravenous magnesium (even if magnesium level is normal) or overdrive atrial pacing to rates of 90–110/min. • Potassium replacement to get K to 4.5–5.0 mmol/l.
- 106. • paroxysmal supraventricular tachycardia (PSVT) refers to a clinical syndrome characterized by a rapid, regular tachycardia with abrupt onset and termination. • Approximately two-thirds of cases of PSVT result from AV nodal reentrant tachycardia (AVNRT). Orthodromic AV reentrant tachycardia (AVRT), which involves an accessory pathway, is the second most common cause of PSVT, accounting for approximately one-third of cases. • The heart rate may be 140–240 beats/min (usually 160– 220 beats/min) and is regular (despite exercise or change in position) The P wave usually differs in contour from sinus beats and is often buried in the QRS complex.
- 107. Treatment Mechanical Measures: • increase in vagal tone and include the Valsalva maneuver • Carotid sinus massage is often performed by physicians but should be avoided if the patient has carotid bruits or a history of transient cerebral ischemic attacks
- 108. Drug Therapy • Adenosine: a 6 mg bolus is administered. If no response is observed after 1–2 minutes, a second 12 mg bolus should be given, followed by a third if necessary. • Intravenous verapamil may be given as a 2.5 mg bolus, followed by additional doses of 2.5–5 mg every 1–3 minutes up to a total of 20 mg if BP and rhythm are stable. If the rhythm recurs, further doses can be given. Oral verapamil, 80–120 mg every 4–6 hours, can be used as well in stable patients who are tolerating the rhythm without difficulty, but avoid it if there is any concern that the arrhythmia may be ventricular in origin. • Intravenous diltiazem (0.25 mg/kg over 2 minutes, followed by a second bolus of 0.35 mg/kg if necessary and then an infusion of 5–15 mg/h) may cause less hypotension and myocardial depression. • Esmolol, a short-acting -blocker, may also be effective; the initial dose is 500 mcg/kg intravenously over 1 minute followed by an infusion of 25–200 mcg/min. Metoprolol is also effective and can be given in 5 mg boluses every 5 minutes and repeated up to two times
- 109. Cardioversion • If the patient is hemodynamically unstable or if adenosine and verapamil are contraindicated or ineffective, synchronized electrical cardioversion (beginning at 100 J) is almost universally successful. If digitalis toxicity is present or strongly suspected, as in the case of paroxysmal tachycardia with block, electrical cardioversion should be avoided
- 110. Catheter Ablation • Because of concerns about the safety and the intolerability of antiarrhythmic medications, radiofrequency ablation is the preferred approach to patients with recurrent symptomatic reentrant supraventricular tachycardia, whether it is due to dual pathways within the AV node or to accessory pathways.
- 111. Atrioventricular Block • AV block is a delay or failure in transmission of the cardiac impulse from atrium to ventricle. • Etiology: Atherosclerotic heart disease; myocarditis; rheumatic fever; cardiomyopathy; drug toxicity; electrolyte disturbance, collagen disease, lev’s disease.
- 112. AV Block AV block is divided into three categories: 1. First-degree AV block 2. Second-degree AV block: further subdivided into type I and type II 3. Third-degree AV block: complete block
- 113. First Degree AV Block • Delay at the AV node results in prolonged PR interval • PR interval>0.2 sec. • Leave it alone
- 114. Second Degree AV Block Type 1 (Wenckebach) • Increasing delay at AV node until a p wave is not conducted. • Often comes post inferior MI with AV node ischemia • Gradual prolongation of the PR interval before a skipped QRS. QRS are normal! • No pacing as long as no bradycardia.
- 115. Second Degree AV Block Type 2 • Diseased bundle of HIS with BBB. • Sudden loss of a QRS wave because p wave was not transmitted beyond AV node. QRS are abnormal! • May be precursor to complete heart block and needs pacing.
- 116. Third Degree AV Block • Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles. • Must treat with pacemaker.
- 117. AV Block • Treatment: 1. I or II degree AV block needn’t antibradycardia agent therapy 2. II degree II type and III degree AV block need antibradycardia agent therapy 3. Implant Pace Maker
- 118. Intraventricular Conduction Abnormalities • There are multiple types of IVCA: Block of one fascicle • right bundle branch block (RBBB), • left anterior fascicular block (LAFB), • left posterior fascicular block (LPFB) Bifascicular blocks, • left bundle branch block (LBBB), • The combination of RBBB and LAFB, or RBBB and LPFB, trifascicular block denotes a block in all three fascicles.
- 119. Right bundle branch block ECG findings include: • (1) widened QRS complex (O0.12 seconds), • (2) deep, wide S wave in left-sided leads (I, V5, and V6), and • (3) secondary R wave in right precordial leads (rsr-, rSR-, or rsR- ).
- 121. Left anterior fascicular block • The ECG findings of LAFB include a QRS complex generally<0.12 seconds, a leftward axis shift (usually -45 to - 90 ), rS pattern in the inferior leads (II, III, and aVF), and qR pattern in leads I and aVL.
- 122. Left posterior fascicular block Electrocardiographic findings in LPFB include: 1. a rightward axis shift, 2. an rS pattern in leads I and aVL, 3. and a qR pattern in lead III and often in lead aVF. 4. The QRS complex duration is usually normal
- 123. Bifascicular block • is the combination of an RBBB and an LAFB, or an RBBB plus an LPFB. • In addition, because the left bundle branch is composed of an anterior and a posterior fascicle, LBBB can be thought of as bifascicular block. • Bifascicular blocks are of particular importance in the setting of an acute MI, because their presence may suggest impending complete heart block. • The most common type of bifascicular block is the combination of an RBBB and an LAFB
- 124. RBBB and an LAFB • The ECG is characterized by features of an RBBB (QRS duration • O0.12 seconds, rsR# or qR in leads V1 and V2, wide or deep S waves in leads I and V6), in addition to a leftward QRS axis and the findings of LAFB (see earlier discussion) in the limb leads.
- 125. RBBB and an LPFB • will demonstrate findings of an RBBB, plus a right axis deviation and the other findings of LPFB
- 126. LBBB ECG criteria for LBBB include a QRS duration O0.12 seconds, a broad monomorphic R wave in leads I, V5, and V6, a wide S wave following an initial small (or absent) R wave in the right precordial leads, and absence septal Q waves in leads I, V5, and V6 (Fig. 6). The term incomplete LBBB is used to describe these findings in patients who have a QRS complex duration !0.12 seconds (usually 0.10–0.11 seconds) Left bundle branch block ECG findings include (1) widened QRS complex (O0.12 seconds), 2) QS or rS complex in lead V1, (3) late intrinsicoid deflection and monophasic R wave in lead V6, and (4) no Q wave in lead V6 [5].
- 127. Classification of Anti-arrhythmics Cla ss Action Exa mples Side Ef fects 1A Fa st sodium chan nel blocker va ries depola riza tion a nd a ction potential dura tion Q uinidine, proca ina mide, disop yra mide Cla ss: na usea , vomiting Q uinidine: h emolytic a nemia, thrombo cytope nia , tinnitus Procaina mide: lupus 1B Lido ca ine, Mex iletine Lido ca ine: dizziness, confusion, seizures, coma Mex iletine: tremor, a taxia, ras h 1C Fleca inide, Prop afen one Fleca inide: pro-a rrhythmia , na usea , dizzy ness 2 beta-b lockers SA nod e & AV node conduction Prop ra nolol, metop rolol Cla ss: CHF, b ronchospa sm, bra dyca rdia , hypo tension 3 Prolong a ction poten tia l by blocking K+ c ha nnels Amioda rone, sota lol Amioda rone: hepa titis, pulmona ry fibro sis, thyroid disorde rs, periphe ra l neu ro pa thy So talol: bronchospa sm 4 calcium cha nnel blockers AV node conduction Vera pa mil, dilitia zem Cla ss:A V block, hypotension, bra dycar dia, constipa tion
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