GEMC- Cardiovascular Board Review Session 1- Resident Training

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This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.

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GEMC- Cardiovascular Board Review Session 1- Resident Training

  1. 1. Project: Ghana Emergency Medicine Collaborative Document Title: Cardiovascular Board Review for www.EMedHome.com Author(s): Joe Lex, MD (Temple University School of Medicine) License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/ We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact open.michigan@umich.edu with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use. Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers. 1
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  3. 3. Cardiovascular Board Review for www.EMedHome.com Joe Lex, MD, FACEP, MAAEM Professor of Emergency Medicine Department of Emergency Medicine Temple University School of Medicine Philadelphia, PA USA 3
  4. 4. This Review Will Cover… 1. Cardiopulmonary Arrest / SIDS 2. Congenital Abnormalities 3. Disorders of Circulation Arterial Venous 4. Disturbances of Rhythm Ventricular Supraventricular 4
  5. 5. This Review Will Cover… 5. Diseases of the Myocardium Cardiac Failure Cardiomyopathy CHF Coronary Syndromes Myocardial Infarction Myocarditis Ventricular Aneurysm 5
  6. 6. This Review Will Cover… 6. Disease of the Pericardium Pericardial tamponade Pericarditis 7. Endocarditis 8. Hypertension 9. Tumors 10.Valvular disorders 6
  7. 7. Today – Part One 1. Cardiopulmonary Arrest / SIDS 2. Congenital Abnormalities 3. Disorders of Circulation Arterial Venous 4. Disturbances of Rhythm Ventricular Supraventricular 7
  8. 8. 3.1 Cardiopulmonary Arrest 8
  9. 9. Cardiopulmonary Arrest Abrupt cessation of pump function in heart No palpable pulse Unconscious and not breathing May be expected outcome to serious illness May be possible to reverse 9
  10. 10. Cardiopulmonary Arrest Shockable Ventricular tachycardia Ventricular fibrillation Non shockable Asystole Pulseless electrical activity (PEA) 10
  11. 11. Primary Causes Coronary heart disease Present in 60-70% Autopsy: 30% had recent MI Cardiomyopathy Cardiac rhythm disturbances Hypertensive heart disease Congestive heart failure 11
  12. 12. When Does It Occur? Most likely to occur in first few hours after awakening from sleep More likely to occur in winter rather than summer 12
  13. 13. Other Causes: Noncardiac Trauma Non-trauma bleeding Gastrointestinal Aortic rupture Intracranial hemorrhage Overdose Pulmonary embolism 13
  14. 14. Recognizing Arrest International Liaison Committee on Resuscitation (ILCOR) Diagnose cardiac arrest in all casualties who are unconscious and not breathing normally Carotid artery palpation no longer gold standard 14
  15. 15. Various Guidelines Resuscitation Guidelines BLS: Basic Life Support ALS: Advanced Cardiac Life Support PALS: Pediatric Advanced Life Support NRP: Neonatal Resuscitation Program 15
  16. 16. Cardiopulmonary Resuscitation Start as soon as possible, interrupt as little as possible  benefit  chest compressions Proper CPR  survival Tracheal intubation: no  survival Assisted ventilation may  outcome Prehospital intubation  survival 16
  17. 17. Automated External Defibrillator AED: they’re automated, not automatic Diagnoses shockable rhythm Tells operator to shock ILCOR recommends universal sign to identify location 17
  18. 18. ACLS Drugs Medications included in guidelines Not shown to  survival to hospital discharge from out of hospital cardiac arrest (OHCA) Includes epinephrine, atropine, amiodarone 18
  19. 19. ACLS Drugs Vasopressin: does not improve or worse outcomes Possible benefit in those with asystole especially if used early Epinephrine: appears to improve short term outcomes such as return of spontaneous circulation (ROSC) 19
  20. 20. ACLS Drugs in ET Tube Lidocaine: rarely used Epinephrine Atropine: no longer recommended for PEA Naloxone 20
  21. 21. Chain of Survival 21 1. Early recognition and call for help - To prevent cardiac arrest 2. Early CPR - To buy time 3. Early Defribilation - To restart the heart 4. Post resuscitation care - To restore quality of life
  22. 22. Chain of Survival Early recognition Each minute untreated arrest  survival ~10% Early CPR Blood and oxygen to vital organs Early defibrillation Only known effective therapy Early advanced care 22
  23. 23. Survival from Cardiac Arrest Initial emergency care by ambulance  ROSC ~15% Defibrillation in <5 min  ~30% 23
  24. 24. Therapeutic Hypothermia Cooling after cardiac arrest with return of spontaneous circulation (ROSC) but without return of consciousness improves outcomes Target temperature of 32–34 °C (90–93 °F) Death rates in hypothermia group  35% 24
  25. 25. 3.1.1 Sudden Infant Death Syndrome 25
  26. 26. SIDS Sudden Infant Death Syndrome aka SUDI: sudden unexpected death in infancy aka cot death or crib death Not predicted by medical history Unexplained after thorough forensic autopsy and detailed death scene investigation 26
  27. 27. SIDS Cause: unknown, many theories Prenatal associations: Maternal age: teenage mothers at greatest risk Delayed / poor prenatal care Maternal smoking 27
  28. 28. SIDS Postnatal associations: Low birth weight Exposure to tobacco smoke Prone sleeping position No breastfeeding Room temperature too high or low Excesses of bedding, clothing, soft sleep surfaces, stuffed animals 28
  29. 29. Differential Diagnosis Infant botulism Long QT syndrome (<2%) Helicobacter pylori infections Shaken baby syndrome / other nonaccidental trauma Overlying 29
  30. 30. Caring for Survivors Family-centered / team-oriented Provide personal, compassionate, individualized support to families Respect social, religious, cultural diversity Notify primary care physician Identify / report child maltreatment 30
  31. 31. 3.2 Congenital Abnormalities of the Cardiovascular System 31
  32. 32. Congenital Heart Disease (CHD) 32
  33. 33. Noncyanotic Defects Ventricular septal defect 20 – 25% Atrial septal defect 5 – 10% Patent ductus arteriosus 5 – 10% Coarctation of aorta 8% Pulmonic Stenosis 5 – 8% Aortic Stenosis 5% 33
  34. 34. Cyanotic: Terrible T’s Tetralogy of Fallot 10% Transposition of Great Arteries 5% Tricuspid Atresia 1 – 2% Total anomalous pulmonary venous return 1% Truncus Arteriosus <1% 34
  35. 35. Typical Presentations Cyanosis Shock Heart Failure 35
  36. 36. Present with Cyanosis Tetralogy of Fallot (to 12 weeks) Transposition of the great arteries Tricuspid atresia TAPVR Truncus arteriosus Pulmonary atresia Hypoplastic right or left heart All others birth to 2 weeks36
  37. 37. Present with Shock Coarctation of aorta Aortic stenosis from 1st week on 37
  38. 38. Present with Heart Failure Ventricular septal defects Patent ductus arteriosus from 4 weeks on 38
  39. 39. Some Clues Central cyanosis with minimal respiratory distress (“comfortably blue”): suggests CHD rather than pure pulmonary problem 39 Cornelia Csuk (Wikipedia)
  40. 40. Some Clues Worsening cyanosis with crying suggests cardiac rather than purely pulmonary etiology 40
  41. 41. Clue: Give 100% Oxygen Purely pulmonary: PaO2 should rise to 250 mm Hg Cyanotic CHD associated with  blood flow: PaO2 may occasionally reach as high as 150 mm Hg Cyanotic CHD associated with  blood flow: PaO2 will not rise >100 mm Hg 41
  42. 42. Clue: Chest X-Ray Boot-shaped heart: tetralogy of Fallot Egg-on-a-string silhouette: transposition of the great vessels Snowman-shaped or figure-of-eight heart: total anomalous pulmonary venous return (TAPVR) 42
  43. 43. Clue: Chest X-Ray Boot-shaped heart: tetralogy of Fallot 43 Source Undetermined
  44. 44. Tet Spell: Cyanosis When Crying 44
  45. 45. Tet Spell: Cyanosis When Crying 45Melimama (Wikimedia Commons)
  46. 46. Narrowing of pulmonary valve 46 Source Undetermined
  47. 47. Ventricular septal defect 47 Source Undetermined
  48. 48. Aorta displaced over VSD 48 Source Undetermined
  49. 49. Treatment for Tet Place in knee-to-chest position SVR   R to L shunt across VSD Supplemental O2 (limited value) Morphine: 0.1–0.2 mg/kg IV or IM Fentanyl as alternative Sodium bicarbonate: 1 mEq/kg IV  ketamine / propranolol / phenylephrine 49
  50. 50. Clue: Chest X-Ray Egg-on-a-string silhouette: transposition of the great vessels 50 Source Undetermined
  51. 51. Clue: Chest X-Ray Snowman or figure-of-8 heart: total anomalous pulmonary venous return (TAPVR) 51 Source Undetermined
  52. 52. Clue: Chest X-Ray Snowman or figure-of-8 heart: total anomalous pulmonary venous return (TAPVR) 52 Source Undetermined
  53. 53. Patent Ductus Ateriosus More severe / complex lesions may not be clinically apparent until ductus arteriosus begins to close First several weeks of life Defects with obstructive lesions of the pulmonary or systemic circulations will be unmasked Present with cyanosis, shock, both 53
  54. 54. Patent Ductus Ateriosus Preserves blood flow from aorta to the pulmonary circulation Or Preserves blood flow from main pulmonary artery to systemic circulation 54
  55. 55. Patent Ductus Arteriosus 55 National Institutes of Health (Wikipedia)
  56. 56. CHDs Requiring Patent Ductus To preserve blood flow from aorta to the pulmonary circulation: Tetralogy of Fallot Tricuspid atresia Pulmonary atresia Hypoplastic right heart syndrome Transposition of the great vessels 56
  57. 57. CHDs Requiring Patent Ductus To preserve blood flow from main pulmonary artery to systemic circulation: Severe coarctation of aorta Severe aortic stenosis Hypoplastic left heart syndrome 57
  58. 58. Patent Ductus Arteriosus Prostaglandin E2 is responsible for keeping ductus patent NSAIDs can help close a PDA If beneficial to prevent closure, administer prostaglandin analog: alprostadil, misoprostol History: prostglandins first isolated from seminal fluid of prostate 58
  59. 59. Prostaglandin E1 Therapy PGE1 infusion: start at 0.05 to 0.1 µg/kg/min Apnea common: intubate first Controlled ventilation will also help  work of breathing Other adverse reactions: fever, seizures, bradycardia, hypotension, flushing,  platelet aggregation 59
  60. 60. 3.3.1 Arterial 60Source Undetermined
  61. 61. 3.3.1.1 Arterial Aneurysm 61 Arcadian (Wikimedia Commons)
  62. 62. Aneurysms Dilation of arterial wall to >1.5 times its normal diameter Larger aneurysm  more likely to rupture Once stress on vessel wall exceeds tensile strength, it ruptures 62
  63. 63. Aneurysms True aneurysm: involves all three layers of arterial wall Atherosclerotic, syphilitic, congenital, ventricular False aneurysm / pseudo- aneurysm: collection of blood leaking out of artery, but confined next to vessel by surrounding tissue 63
  64. 64. Abdominal Aortic Aneurysm 64 Source Undetermined
  65. 65. Abdominal Aortic Aneurysm Disease of aging Occurrence expected to  as population of elderly grows Rare before age 50 years Average age at diagnosis: 65 to 70 Men >> women Most common and most important complication  rupture 65
  66. 66. Abdominal Aortic Aneurysm Normal diameter: 2 cm AAA: 3 cm <4 cm: rupture uncommon >5cm: high risk for rupture When unruptured, symptoms vague and nonspecific Symptomatic usually large and palpable 66
  67. 67. Signs & Symptoms Abdominal bruit: ~5 – 10% Most have normal femoral pulses Rupture often first manifestation CLASSIC TRIAD: pain, BP, pulsatile abdominal mass BP inconsistent, often late finding Contained retroperitoneal bleed 67
  68. 68. Signs & Symptoms Syncope (10%) Flank / back / abdominal pain Common misdiagnosis: kidney stone GI bleed from aortoduodenal fistula Extremity ischemia from thrombus embolization Shock Sudden death 68
  69. 69. Aorto-Enteric Fistula AAA erodes into GI tract Usually 3rd or 4th portion duodenum AKA Aorto-duodenal fistula Hematemesis, melenemesis, melena, or (if rapid transport) hematochezia History aortic graft placement greatly  clinical suspicion 69
  70. 70. Other Findings Periumbilical ecchymosis  Cullen Flank ecchymosis  Grey Turner 70 Source Undetermined Source Undetermined
  71. 71. Diagnosis: Radiograph May be picked up incidentally on plain x-ray  eggshell calcification Not sensitive or specific 71 Source Undetermined Source Undetermined
  72. 72. Diagnosis: Ultrasound Virtually 100% sensitive Measurement of aortic diameter accurate and reproducible Relatively inexpensive Requires no contrast agents or radiation exposure Performed at bedside CANNOT determine rupture 72
  73. 73. Diagnosis: Ultrasound 73 Source Undetermined
  74. 74. Diagnosis: Ultrasound 74 Source Undetermined
  75. 75. Diagnosis: CT Virtually 100% accurate Less subject to technical problems and interpretation errors IV contrast desirable, not essential Better than US at retroperitoneal bleeds 75
  76. 76. Diagnosis: CT 76 Source Undetermined
  77. 77. Ruptured = Unstable Large bore IV access x 2 Type & Cross 6 Units PRBC Volume controversial: permissive hypotension vs aggressive resuscitation Get to operating room as soon as possible 50% mortality 77
  78. 78. Post-Op Complications Graft infection: local vs general Most common: inguinal portion of aortofemoral graft Aortoenteric fistula: discussed above Pseudoaneurysm Endoleak: blood flow outside graft lumen but within aneurysm sac 78
  79. 79. 3.3.1.2 Aortic Dissection 79 Source Undetermined
  80. 80. Definition Tear of aorta intimal lining with expanding blood collection  forces layers apart  false lumen Death due to  blood supply to other organs, cardiac failure Rupture uncommon Aneurysm dissection RARE 80
  81. 81. Epidemiology Men > women Incidence  with age Hypertension in most patients History cardiac surgery in ~18% Bicuspid aortic valve in ~14% Atherosclerosis rarely involved at dissection site May have positive family history 81
  82. 82. Epidemiology 82 CardioNetworks (Wikimedia Commons)
  83. 83. Epidemiology Uncommon <40 years Other: stimulant use, exertion, trauma High-speed deceleration injury usually causes traumatic aortic rupture  different disease 83
  84. 84. Epidemiology Exception: congenital heart disease, giant-cell arteritis, Ehlers- Danlos or Marfan’s syndrome, >40% Marfan’s  aortic dissection Women with Marfan’s at risk during pregnancy 84
  85. 85. Marfan’s Syndrome Noted in 5–9% of people with aortic dissection 85 BQmUB2010144 (Wikimedia Commons)
  86. 86. Classification Anatomic classification important for diagnosis and therapy Stanford classification Type A  ascending: ~60% More lethal Type B  descending: ~40% Acute if <2 weeks duration About 2/3 are acute 86
  87. 87. Symptoms Pain in >90% of patients Painless  implies chronic Usually excruciating Occurs abruptly Most severe at onset Typically described as “sharp” more than “tearing” or “ripping” 87
  88. 88. Symptoms: pain Anterior chest: think ascending aorta Neck and jaw: think aortic arch Interscapular: think descending thoracic aorta Lumbar / abdomen: think below diaphragm 88
  89. 89. Symptoms Pain migration consistent with propagation Occurs in <20% Onset often accompanied by visceral pain symptoms: nausea, vomiting, diaphoresis, severe apprehension, lightheadedness 89
  90. 90. Blood Pressure Variable at presentation Proximal: ~35% BP, ~25% BP Distal: ~70% BP, ~5% BP Severe BP  grave prognosis Associated with severe aortic insufficiency, pericardial tamponade, rupture 90
  91. 91. Blood Pressure Pseudohypotension: false BP Involvement of brachiocephalic artery supplying right arm Involvement of left subclavian artery supplying left arm 91
  92. 92. 92 Rob Swatski (Flickr)
  93. 93. 93 brachiocephalic artery supplies right arm Rob Swatski (Flickr)
  94. 94. left subclavian artery supplies left arm 94Rob Swatski (Flickr)
  95. 95. Aortic Insufficiency Occurs in half to two-thirds of ascending aortic dissections Aortic insufficiency murmur audible in one-third of proximal dissections May be inaudible if BP 95
  96. 96. Aortic Insufficiency 96
  97. 97. Myocardial Infarction 1–2% of dissections Involves coronary arteries RCA > LCA Inadvertently treat with lysis  >70% mortality 97
  98. 98. Diagnosis Difficult, often missed D-dimer <500 mcg/mL MAY be able to rule out (not definitive) Wide mediastinum on chest x-ray: moderate sensitivity, low specificity Up to 20%  normal chest x-ray Calcium sign suggestive 98
  99. 99. Wide Mediastinum 99 Source Undetermined
  100. 100. Calcium Sign 100Source Undetermined
  101. 101. Computerized Tomography Noninvasive Requires peripheral vein injection of iodinated contrast Sensitivity 96 – 100% Specificity 96 – 100% Poorly identifies site of intimal tear 101
  102. 102. Computerized Tomography 102 Source Undetermined
  103. 103. Computerized Tomography 103 Source Undetermined
  104. 104. MRI Current gold standard Sensitivity = 98%, specificity = 98% Locates intimal tear, secondary tears, involved branch vessels Non-invasive test, no iodinated contrast material Disadvantage: not always available, time consuming 104
  105. 105. MRI 105 Source Undetermined
  106. 106. Transesophageal Echo (TEE) Sensitivity ~98%, specificity ~97% Relatively non-invasive: patient swallows echocardiography probe Especially good to evaluate aortic insufficiency, coronary artery involvement 106
  107. 107. Transesophageal Echo (TEE) 107 Source Undetermined
  108. 108. Aortogram No longer “gold standard” 108 Source Undetermined
  109. 109. Management Stanford type A (ascending aortic): surgical management Stanford type B (uncomplicated distal aortic): medical management 109J. Heuser (Wikipedia)
  110. 110. Management Presenting as hypertensive emergency  strict blood pressure control Target mean arterial pressure (MAP) of 60 to 75 mmHg Also:  shear-force dP/dt (force of blood ejection from left ventricle) 110
  111. 111. Management 1st line treatment: beta-blocker Rapidly acting, titratable parenteral agent preferred Esmolol, propranolol, labetalol Do NOT use vasodilators alone  cause reflex tachycardia May be used as supplement to control BP 111
  112. 112. Risk of Death 25% in first 24 hours 50% in first 48 hours 75% in first week 90% in first month 112
  113. 113. 3.3.1.3 Arterial Thromboembolism 113 Source Undetermined
  114. 114. Peripheral Arterial Disease Defined as ankle-brachial index (ABI) of <0.9 Prevalent in ~15% over age 70 Risk factors: diabetes, tobacco use Acute occlusion  irreversible changes in peripheral nerves and skeletal muscle tissue in 4 – 6 hrs 114
  115. 115. Peripheral Arterial Disease ABI = SBP arm / SBP leg Normal >0.9; <0.4  critical Cuff inflated proximal to artery in question 90% sensitive, 98% specific for hemodynamically significant leg artery stenosis (i.e. >50% occlusion in major leg arteries) 115
  116. 116. Peripheral Arterial Disease “Six Ps": pain, pallor, poikilothermia (coldness), pulselessness, paresthesias, and paralysis Pain earliest symptom, may  with limb elevation Mottling, splotchiness, cool temperature also common  distal pulse unreliable finding 116
  117. 117. Peripheral Arterial Disease Claudication  cramplike pain, ache, tiredness brought on by exercise and relieved by rest Reproducible, resolves within 2 to 5 minutes of rest Acute limb ischemia pain not well localized, not relieved by rest or gravity 117
  118. 118. Peripheral Arterial Disease Claudication  cramplike pain, ache, tiredness brought on by exercise and relieved by rest 118 NHLBI (Wikipedia)
  119. 119. Peripheral Arterial Disease Most common cause acute arterial occlusion: thromboembolic disease Differential diagnosis: vasculitis, Raynaud disease, thromboangiitis obliterans, blunt or penetrating trauma, or low-flow shock states (sepsis) 119
  120. 120. Acute Arterial Occlusion Stabilize Fluid resuscitation, pain control Dependent positioning can  perfusion pressure ECG,  echocardiography to assess for conditions associated with embolism 120
  121. 121. Acute Arterial Occlusion Give aspirin Unfractionated heparin: 80 U/kg bolus, 18 U/kg//hr Definitive treatment in consultation with vascular surgeon and interventional radiologist Preferred: catheter-directed embolectomy 121
  122. 122. Acute Arterial Occlusion Reperfusion injury after revascularization can cause myoglobinemia, renal failure, hyperkalemia, and metabolic acidosis 122 Source Undetermined
  123. 123. Chronic Arterial Occlusion If no immediate limb threat and no co-morbidities: discharge on aspirin (75 milligrams daily) Close vascular surgical follow-up 123 Source Undetermined
  124. 124. 3.3.2.1 Venous Thromboembolism Covered in another section, but… 124
  125. 125. Phlegmasia cerulea dolens Literally: painful blue edema Uncommon severe form of DVT Extensive thrombotic occlusion of major and collateral extremity veins Sudden severe pain, swelling, cyanosis, edema High risk of massive pulmonary embolism, even when treated 125
  126. 126. Phlegmasia cerulea dolens 126Source Undetermined
  127. 127. 3.4 Disturbances of Cardiac Rhythm 127
  128. 128. Sinus Rhythm Rate: 60 – 100 beats / minute Rhythm: regular with 1:1 relationship of P to QRS PR interval: 0.12 – 0.20 seconds QRS complex: 0.06 – 0.10 seconds P waves upright in Leads I, II, AVF 128
  129. 129. 3.4.1 Cardiac Dysrhythmias 129
  130. 130. Premature Atrial Contraction Extra beat Originates outside sinus node from ectopic atrial pacemaker Usually interspersed throughout underlying rhythm Underlying rhythm is usually sinus 130
  131. 131. Premature Atrial Contraction Ectopic P wave Upright in Lead II Appears earlier than next expected sinus beat Has different configuration than normal P wave May or may not be conducted through AV node 131
  132. 132. Premature Atrial Contraction QRS complex usually normal May be widened due to aberrant conduction QRS generally followed by noncompensatory pause SA node reset  returning sinus beat occurs ahead of schedule 132
  133. 133. Premature Atrial Contraction 133 Source Undetermined
  134. 134. Premature Atrial Contraction Most frequent cause of EKG pause Can be normal variant Can be caused by drugs or underlying disease Can precipitate supraventricular tachycardia, atrial fibrillation, atrial flutter 134
  135. 135. Premature Atrial Contraction 135 Source Undetermined
  136. 136. Premature Atrial Contraction Asymptomatic: no treatment indicated Frequent or symptomatic: correct underlying cause 136
  137. 137. Sinus Tachycardia Rate: >100 beats / minute (usually <160 beats / minute) Rhythm: regular with 1:1 relationship of P to QRS PR interval: 0.12 – 0.20 seconds QRS complex: 0.06 – 0.10 seconds P waves upright in Leads I, II, AVF 137
  138. 138. Sinus Tachycardia Newborn: 110 – 150 bpm 2 years: 85 – 125 bpm 4 years: 75 – 115 bpm 6 years+: 60 – 100 bpm 138
  139. 139. Sinus Tachycardia P-wave hidden in T-wave 139 Source Undetermined
  140. 140. Sinus Tachycardia P-wave hidden in T-wave “Camel hump” appearance 140 Source Undetermined
  141. 141. Sinus Tachycardia P-wave hidden in T-wave “Camel hump” appearance 141 Source Undetermined Arpingstone (Wikimedia Commons)
  142. 142. Sinus Tachycardia Common causes Drugs Fever Hyperthyroid Pulmonary embolism Hypovolemia Anemia Hypoxia Pain Anxiety: diagnosis of exclusion 142
  143. 143. Sinus Tachycardia Treatment: fix underlying cause Acute myocardial infarction: may be useful to treat “inappropriate” tachycardia with beta-blocker to slow heart rate Cocaine toxicity: may be helpful to treat with benzodiazepine 143
  144. 144. Sinus Bradycardia Rate: <60 beats / minute Rhythm: regular with 1:1 relationship of P to QRS PR interval: 0.12 – 0.20 seconds QRS complex: 0.06 – 0.10 seconds P waves upright in Leads I, II, AVF 144
  145. 145. Sinus Bradycardia 145 Source Undetermined
  146. 146. Sinus Bradycardia Common causes Acute inferior wall MI Vasovagal event (e.g. vomiting)  vagal tone (e.g. athlete) Vagal stimulation (e.g. pain) Hypothermia Hypothyroidism Brainstem herniation Myocarditis Sick sinus syndrome 146
  147. 147. Sinus Bradycardia Common causes, pharmacologic Beta-blocker Calcium-channel blocker Digoxin Amiodarone Opiate Central alpha-2 agonist (clonidine, dexmedetomidine) GABA-ergic agent (barbiturate, benzodiazepine, baclofen, GHB) Organophosphate poisoning 147
  148. 148. Sinus Bradycardia Treat if symptomatic Shock Hypotension Short of breath Chest pain  mentation Congestive heart failure PVCs in acute myocardial infarction148
  149. 149. Sinus Bradycardia Atropine 0.5-1mg q5 minutes prn Total: 0.03 – 0.04 mg/kg Acute myocardial infarction: may worsen ischemia, precipitate dysrhythmia Mobitz II and 3°AV Block with wide complex: atrial rate AV block ventricular rate, BP 149
  150. 150. Sinus Bradycardia Atropine ineffective in patient with heart transplant Atropine dose <0.5mg can be parasympathomimetic Produce further  in heart rate 150
  151. 151. Sinus Bradycardia Transcutaneous pacing (TCP) Treatment of choice if no response to atropine or severe symptoms May need analgesic / sedative Transvenous pacing Persistent symptomatic bradycardia More about pacing in Part 3 151
  152. 152. Sinus Bradycardia Dopamine 5-20 mcg/kg/min No response to atropine and / or TCP not readily available Epinephrine 2-10 mcg/min Particularly useful if significant hypotension 152
  153. 153. Sinus Bradycardia Isoproterenol 2-10 mcg/min Only in low doses as last resort Significant negative effects  myocardial oxygen consumption Peripheral vasodilatation Serious dysrhythmias 153
  154. 154. 3.4.1.1 Ventricular Dysrhythmias 154
  155. 155. Premature Ventricular Contractions Abnormal QRS complexes and T waves occurring in another underlying rhythm 155 Source Undetermined
  156. 156. Premature Ventricular Contractions Six characteristics: 1. Occur earlier than expected normal QRS (premature) 2. Wider than normal QRS, usually ≥0.12 sec 3. Bizarre QRS morphology 156
  157. 157. Premature Ventricular Contractions 4. No preceding P wave: retrograde conduction occasionally causes inverted P wave after QRS 5. ST and T deflection opposite that of QRS: generally followed by compensatory pause 6. SA node not reset, so next P wave occurs at usual time 157
  158. 158. Premature Ventricular Contractions Bigeminy: every other beat PVC Trigeminy: every 3rd beat PVC Quadrigeminy: every 4th beat Couplet: 2 consecutive PVCs Triplet: 3 consecutive PVCs 158
  159. 159. Premature Ventricular Contractions Common Causes Hypokalemia Hypomagnesemia Cardiomyopathy Hyperthyroidism Myocardial Infarction Hypoxia CHF Mechanical: catheter in RV Myocardial contusion 159
  160. 160. Premature Ventricular Contractions Common causes: Drugs Alcohol / tobacco / caffeine Cocaine Digitalis or quinidine toxicity Most common dysrhythmia seen with digitalis toxicity Methylxanthines: theophyline 160
  161. 161. Premature Ventricular Contractions Treatment No symptoms  no treatment May be normal variant Correct underlying cause Pull back central line Deflate Swann balloon to avoid floating in to outflow track 161
  162. 162. Premature Ventricular Contractions Escape PVCs associated with bradycardia Treat with atropine: lidocaine may suppress existing functioning rhythm 162
  163. 163. Premature Ventricular Contractions Associated with acute MI or ischemia  treatment controversial CONSIDER: frequent (> 30/hr), multiform / multifocal or associated with runs of ventricular tachycardia Occur in couplets R-on-T phenomenon during ventricular depolarization 163
  164. 164. Premature Ventricular Contractions Associated with acute MI or ischemia Treat underlying ischemia / infarction: oxygen, nitroglycerine, morphine, ASA, fibrinolytic therapy If these measures fail, most experts say watchful waiting, but a few advocate treatment 164
  165. 165. Premature Ventricular Contractions Pharmacologic agent: lidocaine 1 – 1.5mg/kg bolus, then 2 – 4 mg/min drip. May repeat boluses 0.5 – 0.75mg/kg every 5 – 10 minutes as needed to maximum total 3mg/kg 165
  166. 166. Premature Ventricular Contractions Pharmacologic agent if lidocaine ineffective: procainamide 15 – 18 mg / kg IV until… …favorable response noted …QRS widens 50% >original width …hypotension develops …total 17mg / kg administered 166
  167. 167. Premature Ventricular Contractions Pharmacologic agent: magnesium sulfate Decreases frequency of PVCs 1 – 2 grams slow IV push over 1 – 2 minutes followed by infusion of 1 – 2 gms/hr 167
  168. 168. Ventricular Tachycardia 168 Source Undetermined
  169. 169. Ventricular Tachycardia Three or more consecutive PVCs occurring at a rate >100 / minute Non-sustained: 3 ventricular beats for maximum 30 seconds Sustained: lasts >30 seconds (less if treated by electrocardioversion within 30 seconds) 169
  170. 170. Ventricular Tachycardia Monomorphic VT: all ventricular beats have same configuration Polymorphic VT: ventricular beats have a changing configuration and heart rate is 100-333 bpm Biphasic VT: ventricular tachycardia with a QRS complex that alternates from beat to beat 170
  171. 171. Monomorphic VTach 171 Source Undetermined
  172. 172. Polymorphic VTach 172 Source Undetermined
  173. 173. Bidirectional VTach 173 Source Undetermined
  174. 174. Ventricular Tachycardia P waves: usually absent If present: retrograde or not related to QRS (AV- dissociation) QRS complexes: wide (≥ 0.12 sec) and may be bizarre 174
  175. 175. Ventricular Tachycardia ± Fusion beat: cross between bizarre QRS and normal QRS Pathognomonic for ventricular tachycardia 175 Source Undetermined
  176. 176. Ventricular Tachycardia ± Capture beat: atrial impulse penetrates AV node from above to stimulate (“capture”) ventricles QRS looks normal: ventricular conduction via normal pathway Rare Pathognomonic for ventricular tachycardia 176
  177. 177. Ventricular Tachycardia ± Capture beat: atrial impulse penetrates AV node from above to stimulate (“capture”) ventricles 177 Source Undetermined
  178. 178. Ventricular Tachycardia Deflection of ST segment and T wave is generally opposite that of QRS complex Rate: >100 bpm, usually 150 – 200 Rhythm: generally regular, but beat-to-beat variation may occur 178
  179. 179. Ventricular Tachycardia QRS axis: generally constant Monomorphic: QRS complexes look the same Polymorphic: QRS complexes have varying morphology Current therapeutic modalities based on this classifications 179
  180. 180. Wide Complex Tachycardia 180 Source Undetermined
  181. 181. V-Tach vs. Aberrant SVT 1. Ventricular tachycardia vs. 2. SVT with aberrant conduction due to bundle branch block vs. 3. SVT with aberrant conduction due to WPW Assume ventricular tachycardia Unstable  synchronized cardioversion 181
  182. 182. V-Tach vs. Aberrant SVT PROBABLY V-TACH Age >35  PPV 85% Structural heart disease Ischemic heart disease Previous MI Congestive heart failure Cardiomyopathy FHx sudden cardiac death 182
  183. 183. V-Tach vs. Aberrant SVT MAYBE ABERRANCY Prior ECG  bundle branch block with identical morphology Prior ECG  evidence of WPW Patient has history of similar successfully terminated with adenosine or vagal maneuvers 183
  184. 184. V-Tach vs. Aberrant SVT Stable  procainamide or amiodarone Both convert SVT or V-Tach Procainamide contraindicated with cyclic anti-depressant overdose Adenosine may initially slow either rhythm, but it may recur 184
  185. 185. V-Tach vs. Aberrant SVT Stable  procainamide or amiodarone Drug therapy fails synchronized cardioversion 185
  186. 186. V-Tach vs. Aberrant SVT EKG suggests V-Tach Absence typical RBBB / LBBB morphology Extreme axis deviation: QRS positive in aVR, negative in I + aVF Very broad complexes: >160ms AV dissociation: P and QRS complexes at different rates 186
  187. 187. V-Tach vs. Aberrant SVT EKG suggests V-Tach Fusion beats: sinus and ventricular beat coincide to produce hybrid complex Capture beats: sinoatrial node transiently ‘captures’ ventricles in midst of AV dissociation to produce a QRS complex of normal duration 187
  188. 188. V-Tach vs. Aberrant SVT ± Fusion beat: cross between bizarre QRS and normal QRS Pathognomonic for VT 188 Source Undetermined
  189. 189. V-Tach vs. Aberrant SVT ± Capture beat: atrial impulse penetrates AV node from above to stimulate (“capture”) ventricles Pathognomonic for VT 189 Source Undetermined
  190. 190. V-Tach vs. Aberrant SVT EKG suggests V-Tach Positive or negative concordance throughout chest leads Leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen 190
  191. 191. 191 Source Undetermined
  192. 192. 192 Source Undetermined
  193. 193. V-Tach vs. Aberrant SVT EKG suggests V-Tach RSR’ complexes with taller left rabbit ear Most specific finding in favor of VT In RBBB, right rabbit ear is taller 193 Source Undetermined Source Undetermined
  194. 194. V-Tach vs. Aberrant SVT Verapamil accelerates heart rate, drops blood pressure and does not convert rhythm Adenosine can convert catecholamine-induced VT to sinus (very rare) CANNOT use adenosine to distinguish VT from SVT aberrancy 194
  195. 195. Torsades de Pointes AKA Polymorphic ventricular tachycardia (PVT) 195 Source Undetermined
  196. 196. Torsades de Pointes “Twisting of the points” QRS complexes “twist” around the isoelectric line Must be evidence of both PVT and QT prolongation Rate: usually 200-240 196
  197. 197. Torsades de Pointes Causes: drugs Class IV antidysrhythmics: quinidine, procainamide Class I-C: propafenone, flecainide Tricyclic antidepresssants Droperidol / haloperidol Phenothiazines 197
  198. 198. Torsades de Pointes Drug combinations: e.g. terfenadine + ketoconazole or erythromycin Other causes: hypomagnesemia, hypokalemia 198 Source Undetermined
  199. 199. Torsades de Pointes During short runs, “twisting” may not be apparent Bigeminy in patient with known prolonged QT may herald imminent TdP TdP with heart rate >220 beats / minute more likely to degenerate into ventricular fibrillation 199
  200. 200. Ventricular Flutter 200 Source Undetermined
  201. 201. Ventricular Flutter Extreme ventricular tachycardia Loss of organized electrical activity Rapid, profound hemodynamic compromise Usually short lived due to progression to ventricular fibrillation Treat as ventricular fibrillation 201
  202. 202. Ventricular Flutter Continuous sine wave No identifiable P waves, QRS complexes, or T waves Rate usually > 200 beats / min ECG looks identical when viewed upside down! 202
  203. 203. 203 Source Undetermined
  204. 204. Ventricular Fibrillation 204 Source Undetermined
  205. 205. Ventricular Fibrillation Most common: fine or coarse zigzag pattern without discernible P waves, QRS complexes or T waves Sometimes looks like ventricular tachycardia Patient without pulse, unresponsive: treatment same 205
  206. 206. Ventricular Fibrillation Most important shockable cardiac arrest rhythm Ventricles attempt to contract at rates of up to 500 / minute Ventricles unable to contract in synchronised manner  immediate loss of cardiac output 206
  207. 207. Ventricular Fibrillation Heart no longer effective pump Invariably fatal without ACLS Prolonged ventricular fibrillation: coarse VF  fine VF  asystole Due to progressive depletion of myocardial energy stores 207
  208. 208. Ventricular Fibrillation Treatment: DEFIBRILLATE IMMEDIATELY 3 successive “stacked” shocks, checking only the monitor between shocks Start with 200J If persistent, defibrillate again with 200-300J and then 360J 208
  209. 209. Ventricular Fibrillation If defibrillation unsuccessful, start ACLS Look for reversible causes (H’s & T’s) 209
  210. 210. Reversible Causes 5 H’s Hypovolemia (most common) Hypoxemia Hydrogen ions (acidosis) Hyperkalemia / Hypokalemia Hypothermia 5 T’s Tablets (drugs) Tamponade (cardiac) Tension pneumothorax Thrombosis, coronary Thrombosis, pulmonary 210
  211. 211. Ventricular Fibrillation Persists despite treatment of reversible cause  give anti- fibrillatory drug Amiodarone or procainamide Lidocaine as last resort Continue shocks every 30 – 60 seconds while meds being drawn Defibrillate with 360J after each drug dose 211
  212. 212. Pulseless Electrical Activity 212 Source Undetermined
  213. 213. Pulseless Electrical Activity Electrical activity other than V-Tach or V-Fib without pulse Electromechanical dissociation (EMD) Idioventricular rhythms Ventricular escape rhythms Bradyasystolic rhythms THIS IS CARDIAC ARREST 213
  214. 214. Pulseless Electrical Activity Often occur in association with 5 H’s and 5 T’s 214
  215. 215. Pulseless Electrical Activity Causes: same as ventricular fibrillation and pulseless ventricular tachycardia Treatment: ACLS CPR, intubation, start an IV Search for and treat underlying cause 215
  216. 216. Pulseless Electrical Activity Hypoxia: ventilate 100% oxygen Hypovolemia: administer fluid bolus Hypothermia: check core body temperature, warm prn Hydrogen ions: bicarbonate for suspected severe acidosis Hyperkalemia: seek EKG changes 216
  217. 217. Pulseless Electrical Activity Epinephrine 1 mg every 3–5 min Atropine NO LONGER RECOMMENDED (2010 ACLS) Sodium bicarbonate not recommended EXCEPT preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose 217
  218. 218. Pulseless Electrical Activity Tablets: history, toxidrome Tamponade: distended neck veins, EMBU Tension pneumothorax: breath sounds, ease of manual ventilation Thrombosis, heart: assess EKG Thrombosis, lungs: EMBU for right heart strain 218
  219. 219. Asystole / Flatline CPR Epinephrine 5 H’s and 5 T’s Atropine and defibrillation NO LONG RECOMMENDED 219 Source Undetermined
  220. 220. 3.4.1.2 Supraventricular 220
  221. 221. Supraventricular Tachycardia Any tachydysrhythmia arising from above the level of Bundle of His Often used synonymously with AV nodal re-entry tachycardia (AVNRT) Paroxysmal SVT (pSVT): abrupt onset / offset, characteristically seen with re-entrant tachycardias involving AV node such as AVNRT 221
  222. 222. Supraventricular Tachycardia Atrial rate: 120-200 beats / minute Rhythm: regular P waves: abnormal, may be hidden in preceding T wave If P waves visible: 1:1 P to QRS ratio QRS: usually narrow, may be wide due to aberrant conduction Extra beats: none 222
  223. 223. Supraventricular Tachycardia Can be classified based on site of origin (SA or AV node) or regularity (regular or irregular) Classification based on QRS width not helpful Influenced by pre-existing bundle branch block, rate-related aberrant conduction, accessory pathways 223
  224. 224. Supraventricular Tachycardia 224 Source Undetermined
  225. 225. Supraventricular Tachycardia 225 Source Undetermined
  226. 226. Supraventricular Tachycardia 226Source Undetermined
  227. 227. Supraventricular Tachycardia Treatment Vagal maneuvers: may respond Adenosine: mainstay of treatment Calcium-channel blocker, beta- blocker, amiodarone: 2nd line MAY be effective: procainamide, amiodarone, sotalol 227
  228. 228. Supraventricular Tachycardia Treatment Vagal maneuvers: may respond 228
  229. 229. Supraventricular Tachycardia NO LONGER RECOMMENDED Vasopressors: norepinephrine, methoxamine, phenylephrine Cholinergic drugs: edrophonium DC synchronized cardioversion: rarely required Catheter ablation: for recurrent episodes not amenable to medicine 229
  230. 230. Multifocal Atrial Tachycardia Form of supraventricular tachycardia Irregular rhythm sometimes mistaken for atrial fibrillation Originates from many different atrial sites Characterized by P waves of varying shape 230
  231. 231. Multifocal Atrial Tachycardia P waves: 3 morphologies in 1 lead Atrial rate: 100 – 180 beats/minute Rhythm: irregularly irregular PP, PR, and RR intervals vary QRS complex: normal configuration Nonconducted (blocked) P waves frequently present, particularly when the atrial rate is rapid 231
  232. 232. Multifocal Atrial Tachycardia 232 Source Undetermined
  233. 233. Multifocal Atrial Tachycardia 233Source Undetermined
  234. 234. Multifocal Atrial Tachycardia Causes Most common: decompensated COPD Congestive heart failure Sepsis Theophylline toxicity Right atrial dilatation (cor pulmonale) Hypoxia / hypercarbia 234
  235. 235. Multifocal Atrial Tachycardia Treatment Correct underlying disease process Unsuccessful, patient symptomatic: Calcium channel blocker: slows ventricular rate,  atrial ectopy Magnesium:  atrial ectopy Metoprolol: slows ventricular rate Digoxin / cardioversion usually ineffective 235
  236. 236. AV Node + His Bundle = AV Junction 236 Madhero88 (Wikipedia)
  237. 237. Junctional Premature Contractions Far less common than PACs/PVCs From ectopic focus in AV node or bundle of His ABOVE bifurcation P wave: different shape / deflection Usually inverted in II, III, and AVF Can occur before, during or after QRS complex 237
  238. 238. Junctional Premature Contractions When P wave precedes QRS: PR interval is shorter than normal QRS complex premature QRS complex normal shape Unless aberrant conduction Usually compensatory pause: SA node NOT reset so next P wave occurs at its usual time 238
  239. 239. Junctional Premature Contractions 239 Source Undetermined Source Undetermined
  240. 240. Junctional Premature Contractions Causes: digitalis toxicity, coronary artery disease, congestive heart failure, acute myocardial infarction (especially inferior wall) Treat underlying cause If precipitate lethal dysrhythmias: intravenous procainamide 240
  241. 241. Junctional Escape Sinus intrinsic rate: ~75 beats / minute Junctional intrinsic rate: 40 – 60 beats/minute If sinus too slow, junctional may take over as “back-up” rhythm Hence “junctional escape” 241
  242. 242. Junctional Escape 242 Source Undetermined
  243. 243. Junctional Tachycardia Ectopic pacemaker in AV junction overtakes sinus node Rate >100 beats / minute  junctional tachycardia 243 Source Undetermined
  244. 244. Accelerated Junctional Rhythm Ectopic AV junction pacemaker too fast for junctional escape, but too slow for junctional tachycardia 244 Source Undetermined
  245. 245. Atrial Fibrillation Uncoordinated atrial activation and random ventricular depolarization Rhythm: irregularly irregular Most common sustained dysrhythmia; 2% of the general population 5% of people > 60 years old P waves absent  no PR interval 245
  246. 246. Atrial Fibrillation Atria discharge electrical impulses to ventricles No single impulse depolarizes atria completely Atria don’t pump Occasional impulse gets through to AV node 246
  247. 247. Atrial Fibrillation May see small irregular deflections in the baseline (“f waves”) Atrial rate: 400 – 700 beats/minute QRS complexes: normal, unless aberrant conduction Ventricular response rate: variable, generally 160 – 180 beats/minute 247
  248. 248. Atrial Fibrillation 248 Source Undetermined
  249. 249. Atrial Fibrillation 249Source Undetermined
  250. 250. Atrial Fibrillation If rate >200 beats/minute + wide QRS complex: think Wolf- Parkinson-White syndrome with antegrade conduction through accessory pathway If regular, slow ventricular rate: think digitalis toxicity No extra beats 250
  251. 251. Atrial Fibrillation: Causes Ischemic heart disease Hypertension Valvular heart disease (esp. mitral) Acute infection Electrolyte disturbance (hypokalemia, hypomagnesemia) Thyrotoxicosis Drugs (e.g. sympathomimetics) Pulmonary embolus Pericardial disease Acid-base disturbance Pre-excitation syndromes Cardiomyopathies: dilated, hypertrophic Pheochromocytoma251
  252. 252. Atrial Fibrillation: Type 1st detected episode vs. recurrent Paroxysmal (<7 days): terminated spontaneously Persistent (>7 days): sustained or terminated therapeutically Permanent (>1 year): cardioversion failed or not attempted 252
  253. 253. Atrial Fibrillation: Treatment Treatment depends on: Cardiovascular stability Duration of dysrhythmia Underlying cause / condition Presence / absence of accessory pathway 253
  254. 254. Atrial Fibrillation: Treatment 1. Treat underlying condition 2. Determine risk for stroke High risk for cardiogenic thromboembolism: cardiac surgery, AMI, hyperthyroidism, myocarditis, acute pulmonary disease 254
  255. 255. Atrial Fibrillation: Treatment Other risks for stroke: Cardiac: congestive heart failure, coronary artery disease, elevated systolic blood pressure Non-Cardiac: prior stroke or TIA, hypertension, advanced age, diabetes 255
  256. 256. Atrial Fibrillation: Treatment Control rhythm: restore and maintain sinus rhythm Control rate: allow atrial fibrillation to continue, control ventricular rate 256
  257. 257. Atrial Fibrillation: Treatment Unstable: immediate synchronized cardioversion Sedate if possible Start with 100J Last resort if digitalis toxic: start with 10J Heparinize if >48 hrs or hypertrophic cardiomyopathy 257
  258. 258. Atrial Fibrillation: Treatment Stable, onset <48hrs: pharmacologic Control ventricular rate first Goal <100 beats/minute Calcium channel blocker: diltiazem Beta blocker: esmolol, metoprolol If EF < 40% Digoxin, diltiazem, amiodarone: will not further depress cardiac function 258
  259. 259. Atrial Fibrillation: Treatment Stable, onset <48hrs: pharmacologic Patient takes digoxin: add MgSO4 (2.5gm IV x 20mins, then 2.5gm infused over 2 hrs) May slow heart rate even more and / or convert to sinus rhythm WPW: amiodarone Avoid beta blocker, calcium channel blocker 259
  260. 260. Atrial Fibrillation: Treatment Stable: onset / duration > 48hrs (higher risk systemic embolization) No immediate cardioversion if possible Cardioversion anticipated in 24 hrs Consider heparin Consider cardiology consult for TEE to exclude atrial clot 260
  261. 261. Atrial Flutter Rapid atrial rhythm: 250-300/min Slower ventricular response 2o to nodal delay Always occurs with AV block Not all impulses conducted Variable conduction 2:1, 3:1, 4:1, etc. P waves: sawtooth pattern Called “F” or flutter waves 261
  262. 262. Atrial Flutter Best seen: inferior leads, V1, V2 PR interval (when present) always normal Not every P wave followed by QRS complex QRS complexes  normal configuration 262
  263. 263. Atrial Flutter Ventricular rate: most common ~150 beats / minute Depends on degree of block May be variable Suspect atrial flutter with 2:1 block in patients with regular ventricular rate of 130 – 150 beats / minute 263
  264. 264. Atrial Flutter Causes: similar to atrial fibrillation Often associated with post-cardiac surgery and peri-infarction periods Usually transitional rhythm between sinus rhythm and atrial fibrillation Treatment determined by stability, duration, accessory pathway 264
  265. 265. Atrial Flutter – 3:1 block 265 Source Undetermined
  266. 266. Atrial Flutter Treatment: unstable Sedate (if possible) Synchronized cardioversion: start with 50J Treatment: stable Vagal maneuvers and adenosine may be useful to slow rate for diagnostic confirmation 266
  267. 267. Atrial Flutter Rate control first Diltiazem (first choice), verapamil, esmolol, metoprolol Digoxin no longer first line Magnesium may be useful adjuvant 267
  268. 268. Atrial Flutter Rhythm control second Procainamide Synchronized cardioversion Accessory pathway present Avoid calcium channel blocker, beta blocker, digoxin, adenosine Synchronized cardioversion Procainamide if stable 268
  269. 269. 269 Source Undetermined
  270. 270. Pre-Excitation Syndromes 270
  271. 271. Pre-Excitation Syndromes Pre-excitation: early activation of ventricles due to impulses bypassing AV node via accessory pathway AV node would normally slow this down 271
  272. 272. Pre-Excitation Syndromes WPW: accessory pathway referred to as Bundle of Kent, or atrioventricular bypass tract Accessory pathway can conduct impulses anterograde (towards ventricle) retrograde (away from ventricle) in both directions 272
  273. 273. Pre-Excitation Syndromes Majority of pathways allow conduction in both directions Retrograde-only: ~15% of cases Anterograde-only: very rare 273
  274. 274. Orthodromic (left) Conduction 274 Orthodromic Circular Tachycardia in a patient with an accessory pathway Tom Lück (Wikipedia)
  275. 275. Orthodromic (left) Conduction 275 Tom Lück (Wikipedia) Source Undetermined
  276. 276. Antedromic (right) Conduction 276 Drj (Ecgpedia)
  277. 277. Antedromic (right) Conduction 277 Drj (Ecgpedia)
  278. 278. WPW in Sinus Rhythm PR: <120ms Delta wave: slurring slow rise of initial portion of QRS QRS: prolonged >110ms ST segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex 278
  279. 279. Pre-Excitation Syndromes Pseudo-infarction pattern in up to 70% of patients Due to negatively deflected delta waves in inferior / anterior leads (“pseudo-Q waves”), or as a prominent R wave in V1-3 (mimicking posterior infarction). 279
  280. 280. Pre-Excitation Syndromes Suspect accessory pathway if ventricular rate > 200/min Synchronized cardioversion may be 1st line, regardless of stability Procainamide prolongs refractory period of accessory pathway May be therapy of choice in hemodynamically stable patient 280
  281. 281. Pre-Excitation Syndromes CONTRAINDICATED: calcium channel blockers, beta blockers, digoxin, adenosine All block AV nodal conduction All can  conduction down accessory pathway, producing  in ventricular response  ventricular fibrillation 281
  282. 282. Pre-Excitation Syndromes Lown-Ganong-Levine Syndrome Accessory pathway (James fibers) connects atria directly to proximal His bundle, completely bypassing AV node Very short PR interval Narrow QRS complexes No evidence of delta waves 282
  283. 283. Pre-Excitation Syndromes 283 Source Undetermined
  284. 284. 3.4.2 Conduction Disorders 284
  285. 285. Bundle Branch Blocks Conduction abnormality, not rhythm disturbance Ventricles depolarize in sequence rather than simultaneously Produces wide QRS complex 285
  286. 286. Bundle Branch Blocks Incomplete BBB  QRS ranges from 0.09 – 0.11 seconds Complete BBB  QRS ≥0.012 sec ST segment has slope opposite that of terminal half of QRS complex 286
  287. 287. 287
  288. 288. Right BBB 288 Source Undetermined Source Undetermined
  289. 289. Right BBB Unifasciular Right ventricle activation delayed Left ventricle activated normally  early part of QRS complex unchanged Depolarization spreads across septum from left ventricle 289
  290. 290. Right BBB Delayed right ventricular activation produces secondary R wave (R’) in right precordial leads (V1-3) and wide, slurred S wave in lateral leads V-6V-1 290 Source Undetermined Source Undetermined
  291. 291. Right BBB Also causes 2o repolarization abnormalities: right precordial leads show ST depression and T wave inversion Isolated RBBB: cardiac axis unchanged Left ventricular activation proceeds normally via left bundle branch 291
  292. 292. Right BBB Criteria Long QRS >120 ms RSR’ pattern in V1-3 Wide, slurred S wave in lateral leads (I, aVL, V5-6) ST depression, T wave inversion in right precordial leads (V1-3) 292
  293. 293. Right BBB Criteria ST depression, T wave inversion in right precordial leads (V1-3) 293 Source Undetermined
  294. 294. 294
  295. 295. Left BBB Septum is usually activated left  right, producing small Q waves in lateral leads LBBB: septal depolarization reversed (right  left) Impulse spreads first to RV through right bundle branch and then to LV through septum 295
  296. 296. Left BBB This sequence extends QRS duration to >120 ms Eliminates normal septal Q waves in lateral leads Depolarization direction produces tall R waves in lateral leads (I, V5- 6) and deep S waves in right precordial leads (V1-3) 296
  297. 297. Left BBB Depolarization from right to left produces tall R waves in lateral leads (I, V5-6) and deep S waves in right precordial leads (V1-3) usually leads to left axis deviation V6 V1 297 Source Undetermined Source Undetermined
  298. 298. Left BBB Criteria QRS 120 ms Dominant S wave in V1 Broad monophasic R wave in lateral leads (I, aVL, V5-V6) No Q waves in lateral leads (I, V5- V6; small Q waves allowed in aVL) Prolonged R wave peak time >60 ms in left precordial leads (V5-6) 298
  299. 299. Left BBB R waves in lateral leads may be: ‘M’ shaped or notched 299 Source Undetermined
  300. 300. Left BBB R waves in lateral leads may be: Monophasic rather than biphasic 300 Source Undetermined
  301. 301. Incomplete Left BBB Typical LBBB morphology with QRS duration <120ms 301 Source Undetermined
  302. 302. Heart Blocks 302
  303. 303. Atrioventricular Block Impaired conduction between atria and ventricles Normal: SA node sets pace  impulses travel to ventricles AV block: message does not reach ventricles or impaired along way 303
  304. 304. 1st Degree AV Block PR interval >200ms (five small squares) “Marked” 1o block: PR > 300ms 304Source Undetermined
  305. 305. 1st Degree AV Block May be normal variant  vagal tone Athletic training Inferior MI Mitral valve surgery Myocarditis (e.g. Lyme disease) Hypokalaemia 305
  306. 306. 1st Degree AV Block AV nodal-blocking drugs: beta- blockers, calcium channel blockers, digoxin, amiodarone 306 Source Undetermined
  307. 307. 1st Degree AV Block Does not cause hemodynamic disturbance No specific treatment required 307
  308. 308. 2nd Degree, Mobitz I AKA Wenckebach Progressive prolongation of PR interval culminating in non- conducted P wave PR interval is longest immediately before dropped beat PR interval is shortest immediately after dropped beat 308
  309. 309. 2nd Degree, Mobitz I P-P interval relatively constant Greatest increase in P-R interval typically between 1st and 2nd beats of cycle 309 Source Undetermined
  310. 310. 2nd Degree, Mobitz I R-R interval progressively shortens with each beat of cycle Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4 310 Source Undetermined
  311. 311. 2nd Degree, Mobitz I Usually reversible conduction block at level of AV node Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct impulse His-Purkinje cells tend to fail suddenly and unexpectedly (i.e. producing Mobitz II block) 311
  312. 312. 2nd Degree, Mobitz I Drugs: beta & calcium channel blockers, digoxin, amiodarone  vagal tone (e.g. athletes) Inferior wall MI Myocarditis After cardiac surgery: mitral valve repair, Tetralogy of Fallot repair 312
  313. 313. 2nd Degree, Mobitz I Usually benign rhythm Minimal hemodynamic disturbance Low risk of progression to 3o block Asymptomatic: no treatment Symptomatic: atropine usually works Permanent pacing: rarely required 313
  314. 314. 2nd Degree, Mobitz II 314 Source Undetermined Source Undetermined
  315. 315. Mobitz II: Description Intermittent non-conducted P waves without progressive prolongation of PR interval PR interval in conducted beats remains constant P waves at constant rate 315
  316. 316. Mobitz II: Description RR interval surrounding dropped beat(s): exact multiple of preceding RR interval 2x preceding RR interval for single dropped beat 3x preceding RR interval for two dropped beats 316
  317. 317. Mobitz II: Mechanism Usually due to conduction failure at His-Purkinje system (i.e. below AV node) 317 Madhero88 (Wikipedia)
  318. 318. Mobitz II: Mechanism More likely then Mobitz I to be due to structural damage to conducting system Typically have pre-existing LBBB or bifascicular block Produced by intermittent failure of remaining fascicle “bilateral bundle-branch block” 318
  319. 319. Mobitz II: Mechanism In ~75%: conduction block distal to Bundle of His  broad QRS complexes 319 Source Undetermined
  320. 320. Mobitz II: Mechanism In ~25%: conduction block within His Bundle itself  narrow QRS complexes 320 Source Undetermined
  321. 321. Mobitz II: Mechanism Recall Mobitz I  AV node fatigue Mobitz II is “all or nothing” His-Purkinje cells suddenly fail to conduct supraventricular impulse May be fixed relationship between P waves and QRS complexes… …but may be no pattern to conduction blockade 321
  322. 322. Mobitz II: Causes 1 Anterior MI: septal infarct with necrosis of bundle branches Idiopathic fibrosis of conducting system Cardiac surgery close to septum, like mitral valve repair Inflammatory conditions: rheumatic fever, myocarditis, Lyme disease 322
  323. 323. Mobitz II: Causes 2 Autoimmune: lupus, systemic sclerosis Infiltrative myocardial disease: amyloidosis, hemochromatosis, sarcoidosis Hyperkalemia Drugs: beta- & calcium channel blockers, digoxin, amiodarone 323
  324. 324. Mobitz II: Significance Much more likely than Mobitz I to be associated with hemodynamic compromise, severe bradycardia, progression to 3rd degree block Hemodynamic instability can be sudden and unexpected  syncope (Stokes-Adams attacks) or sudden cardiac death 324
  325. 325. Mobitz II: Significance Risk of asystole: ~35% per year Mandates admission for cardiac monitoring, backup temporary pacing, ultimately insertion of permanent pacemaker 325 Source Undetermined
  326. 326. 3rd Degree / Complete Block 326 Source Undetermined Source Undetermined
  327. 327. 3rd Degree / Complete Block No atrial impulses conducted Atria and ventricles beat independently of one another 327 Source Undetermined
  328. 328. 3rd Degree / Complete Block No atrial impulses conducted Atria and ventricles beat independently of one another 328 Source Undetermined
  329. 329. 3rd Degree / Complete Block No atrial impulses conducted Atria and ventricles beat independently of one another 329 Source Undetermined
  330. 330. 3rd Degree / Complete Block P waves: normal PR interval: variable  P waves not related to QRS complexes PP interval: regular RR interval: regular Perfusing rhythm maintained by junctional or ventricular escape rhythm 330
  331. 331. 3rd Degree / Complete Block Block can occur at level of AV node, bundle of His or bundle branches QRS complexes: narrow or wide depending on location of block Above His bundle  narrow At or below His bundle  wide 331
  332. 332. 3rd Degree / Complete Block End point of either Mobitz I or II Progressive fatigue of AV nodal cells 2o to increased vagal tone in acute phase of inferior MI Sudden complete conduction failure throughout His-Purkinje system 2o to septal infarction in acute anterior MI 332
  333. 333. 3rd Degree / Complete Block High risk of ventricular standstill and sudden cardiac death Urgent admission for cardiac monitoring, backup temporary pacing, and (usually) insertion of permanent pacemaker 333
  334. 334. AND FINALLY… 334
  335. 335. Sinus Node Dysfunction 335
  336. 336. Sinus Node Dysfunction AKA “sick sinus syndrome” Abnormality of cardiac impulse formation AND intra-atrial and AV nodal conduction Wide variety / combinations of bradyarrhythmias and tachyarrhythmias Most common in elderly 336
  337. 337. Sinus Node Dysfunction Presenting symptoms may include: Dizziness Palpitations Dyspnea Fatigue Lethargy Syncope 337
  338. 338. Sinus Node Dysfunction Causes: intrinsic Idiopathic degenerative fibrosis Ischemia Cardiomyopathies Infiltrative diseases: sarcoidosis, haemochromatosis Congenital abnormalities 338
  339. 339. Sinus Node Dysfunction Causes: extrinsic Drugs: digoxin, beta- & calcium channel blockers Autonomic dysfunction Hypothyroidism Electrolyte abnormalities: hyperkalemia 339
  340. 340. Sinus Node Dysfunction Diagnosis: documentation of bradyarrhythmia or tachyarrhythmia in associated with these symptoms 340 Source Undetermined Source Undetermined
  341. 341. Sinus Node Dysfunction Treatment: stable Refer to cardiologist for demand pacemaker and antidysrhythmic therapy Treatment: unstable Bradydysrhythmia  rate stimulation Atropine, isoproternol, pacemaker Tachydysrhythma  rate control Digoxin, beta- or calcium channel blocker 341
  342. 342. 342

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