ELECTROCARDIOGRAPHY KEVIN REBECK PA-C. For more presentations

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1 ELECTROCARDIOGRAPHY KEVIN REBECK PA-C For more presentations

2 Objectives ECG History Pathophysiology Basics Case Historys

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8 Electrical activation of the heart In the heart muscle cell, or myocyte, electric activation takes place by means of the same mechanism as in the nerve cell, i.e., from the inflow of Na ions across the cell membrane. The amplitude of the action potential is also similar, being 100 mv for both nerve and muscle.

9 The duration of the cardiac impulse is, however, two orders of magnitude longer than in either nerve cell or sceletal muscle cell. As in the nerve cell, repolarization is a consequence of the outflow of K ions. The duration of the action impulse is about 300 ms.

10 Electrophysiology of the cardiac muscle cell

11 Mechanical contraction of Cardiac Muscle Associated with the electric activation of cardiac muscle cell is its mechanical contraction, which occurs a little later. An important distinction between cardiac muscle tissue and skeletal muscle is that in cardiac muscle, activation can propagate from one cell to another in any direction.

12 Normal Impulse Conduction Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

13 Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

14 The PQRST P wave - Atrial depolarization QRS - Ventricular depolarization T wave - Ventricular repolarization

15 The PR Interval Atrial depolarization + delay in AV junction (AV node/bundle of His) (delay allows time for the atria to contract before the ventricles contract)

16 Pacemakers of the Heart SA Node - Dominant pacemaker with an intrinsic rate of beats/minute. AV Node - Back-up pacemaker with an intrinsic rate of beats/minute. Ventricular cells - Back-up pacemaker with an intrinsic rate of bpm.

17 The ECG Paper Horizontally One small box s One large box s Vertically One large box mv

18 The ECG Paper (cont) 3 sec 3 sec Every 3 seconds (15 large boxes) is marked by a vertical line. This helps when calculating the heart rate. NOTE: the following strips are not marked but all are 6 seconds long.

19 Rhythm Analysis Step 1: Calculate rate. Step 2: Determine regularity. Step 3: Assess the P waves. Step 4: Determine PR interval. Step 5: Determine QRS duration.

20 Step 1: Calculate Rate 3 sec 3 sec Option 1 Count the # of R waves in a 6 second rhythm strip, then multiply by 10. Reminder: all rhythm strips in the Modules are 6 seconds in length. Interpretation? 9 x 10 = 90 bpm

21 Step 1: Calculate Rate R wave Option 2 Find a R wave that lands on a bold line. Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont)

22 Step 1: Calculate Rate Option 2 (cont) Memorize the sequence: Interpretation? Approx. 1 box less than 100 = 95 bpm

23 Step 2: Determine regularity R R Look at the R-R distances (using a caliper or markings on a pen or paper). Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular? Interpretation? Regular

24 Step 3: Assess the P waves Are there P waves? Do the P waves all look alike? Do the P waves occur at a regular rate? Is there one P wave before each QRS? Interpretation? Normal P waves with 1 P wave for every QRS

25 Step 4: Determine PR interval Normal: seconds. (3-5 boxes) Interpretation? 0.12 seconds

26 Step 5: QRS duration Normal: seconds. (1-3 boxes) Interpretation? 0.08 seconds

27 Rhythm Summary Rate Regularity P waves PR interval QRS duration Interpretation? bpm regular normal 0.12 s 0.08 s Normal Sinus Rhythm

28 Normal Sinus Rhythm (NSR) Etiology: the electrical impulse is formed in the SA node and conducted normally. This is the normal rhythm of the heart; other rhythms that do not conduct via the typical pathway are called arrhythmias.

29 NSR Parameters Rate Regularity P waves PR interval QRS duration bpm regular normal s s Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia

30 Arrhythmia Formation Arrhythmias can arise from problems in the: Sinus node Atrial cells AV junction Ventricular cells

31 SA Node Problems The SA Node can: fire too slow fire too fast Sinus Bradycardia Sinus Tachycardia Sinus Tachycardia may be an appropriate response to stress.

32 Atrial Cell Problems Atrial cells can: fire occasionally from a focus Premature Atrial Contractions (PACs) fire continuously due to a looping re-entrant circuit Atrial Flutter

33 Teaching Moment A re-entrant pathway occurs when an impulse loops and results in selfperpetuating impulse formation.

34 Atrial Cell Problems Atrial cells can also: fire continuously from multiple foci or fire continuously due to multiple micro re-entrant wavelets Atrial Fibrillation Atrial Fibrillation

35 Teaching Moment Multiple micro reentrant wavelets refers to wandering small areas of activation which generate fine chaotic impulses. Colliding wavelets can, in turn, generate new foci of activation. Atrial tissue

36 AV Junctional Problems The AV junction can: fire continuously due to a looping re-entrant circuit block impulses coming from the SA Node Paroxysmal Supraventricular Tachycardia AV Junctional Blocks

37 Ventricular Cell Problems Ventricular cells can: fire occasionally from 1 or more foci fire continuously from multiple foci fire continuously due to a looping re-entrant circuit Premature Ventricular Contractions (PVCs) Ventricular Fibrillation Ventricular Tachycardia

38 Sinus Rhythms Sinus Bradycardia Sinus Tachycardia

39 Rhythm #1 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 30 bpm regular normal 0.12 s 0.10 s Sinus Bradycardia

40 Sinus Bradycardia Deviation from NSR - Rate < 60 bpm

41 Sinus Bradycardia Etiology: SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval).

42 Rhythm #2 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 130 bpm regular normal 0.16 s 0.08 s Sinus Tachycardia

43 Sinus Tachycardia Deviation from NSR - Rate > 100 bpm

44 Sinus Tachycardia Etiology: SA node is depolarizing faster than normal, impulse is conducted normally. Remember: sinus tachycardia is a response to physical or psychological stress, not a primary arrhythmia.

45 Premature Beats Premature Atrial Contractions (PACs) Premature Ventricular Contractions (PVCs)

46 Rhythm #3 Rate? Regularity? P waves? 70 bpm occasionally irreg. 2/7 different contour PR interval? 0.14 s (except 2/7) QRS duration? Interpretation? 0.08 s

47 Premature Atrial Contractions Deviation from NSR These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.

48 Premature Atrial Contractions Etiology: Excitation of an atrial cell forms an impulse that is then conducted normally through the AV node and ventricles.

49 Teaching Moment When an impulse originates anywhere in the atria (SA node, atrial cells, AV node, Bundle of His) and then is conducted normally through the ventricles, the QRS will be narrow ( s).

50 Rhythm #4 Rate? Regularity? P waves? PR interval? QRS duration? 60 bpm occasionally irreg. none for 7th QRS 0.14 s 0.08 s (7th wide) Interpretation? Sinus Rhythm with 1 PVC

51 PVCs Deviation from NSR Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes. When there are more than 1 premature beats and look alike, they are called uniform. When they look different, they are called multiform.

52 PVCs Etiology: One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles.

53 Teaching Moment When an impulse originates in a ventricle, conduction through the ventricles will be inefficient and the QRS will be wide and bizarre.

54 Ventricular Conduction Normal Signal moves rapidly through the ventricles Abnormal Signal moves slowly through the ventricles

55 Supraventricular Arrhythmias Atrial Fibrillation Atrial Flutter Paroxysmal Supraventricular Tachycardia

56 Rhythm #5 Rate? Regularity? P waves? PR interval? QRS duration? 100 bpm irregularly irregular none none 0.06 s Interpretation? Atrial Fibrillation

57 Atrial Fibrillation Deviation from NSR No organized atrial depolarization, so no normal P waves (impulses are not originating from the sinus node). Atrial activity is chaotic (resulting in an irregularly irregular rate). Common, affects 2-4%, up to 5-10% if > 80 years old

58 Atrial Fibrillation Etiology: Recent theories suggest that it is due to multiple re-entrant wavelets conducted between the R & L atria. Either way, impulses are formed in a totally unpredictable fashion. The AV node allows some of the impulses to pass through at variable intervals (so rhythm is irregularly irregular).

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60 Rhythm #6 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? Atrial Flutter 70 bpm regular flutter waves none 0.06 s

61 Atrial Flutter Deviation from NSR No P waves. Instead flutter waves (note sawtooth pattern) are formed at a rate of bpm. Only some impulses conduct through the AV node (usually every other impulse).

62 Atrial Flutter Etiology: Reentrant pathway in the right atrium with every 2nd, 3rd or 4th impulse generating a QRS (others are blocked in the AV node as the node repolarizes).

63 Rhythm #7 Rate? Regularity? P waves? PR interval? QRS duration? bpm Regular regular Normal none 0.16 s none 0.08 s Interpretation? Paroxysmal Supraventricular For more presentations Tachycardia (PSVT)

64 PSVT Deviation from NSR The heart rate suddenly speeds up, often triggered by a PAC (not seen here) and the P waves are lost.

65 PSVT Etiology: There are several types of PSVT but all originate above the ventricles (therefore the QRS is narrow). Most common: abnormal conduction in the AV node (reentrant circuit looping in the AV node).

66 Ventricular Arrhythmias Ventricular Tachycardia Ventricular Fibrillation

67 Rhythm #8 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 160 bpm regular none none wide (> 0.12 sec) Ventricular Tachycardia

68 Ventricular Tachycardia Deviation from NSR Impulse is originating in the ventricles (no P waves, wide QRS).

69 Ventricular Tachycardia Etiology: There is a re-entrant pathway looping in a ventricle (most common cause). Ventricular tachycardia can sometimes generate enough cardiac output to produce a pulse; at other times no pulse can be felt.

70 Rhythm #9 Rate? Regularity? P waves? PR interval? QRS duration? none irregularly irreg. none none wide, if recognizable Interpretation? Ventricular Fibrillation

71 Ventricular Fibrillation Deviation from NSR Completely abnormal.

72 Ventricular Fibrillation Etiology: The ventricular cells are excitable and depolarizing randomly. Rapid drop in cardiac output and death occurs if not quickly reversed

73 AV Nodal Blocks 1st Degree AV Block 2nd Degree AV Block, Type I 2nd Degree AV Block, Type II 3rd Degree AV Block

74 Rhythm #10 Rate? Regularity? P waves? PR interval? QRS duration? 60 bpm regular normal 0.36 s 0.08 s Interpretation? 1st Degree AV Block

75 1st Degree AV Block Deviation from NSR PR Interval > 0.20 s

76 1st Degree AV Block Etiology: Prolonged conduction delay in the AV node or Bundle of His.

77 Rhythm #11 Rate? Regularity? P waves? PR interval? QRS duration? 50 bpm regularly irregular nl, but 4th no QRS lengthens 0.08 s Interpretation? 2nd Degree AV Block, Type I

78 2nd Degree AV Block, Type I Deviation from NSR PR interval progressively lengthens, then the impulse is completely blocked (P wave not followed by QRS).

79 2nd Degree AV Block, Type I Etiology: Each successive atrial impulse encounters a longer and longer delay in the AV node until one impulse (usually the 3rd or 4th) fails to make it through the AV node.

80 Rhythm #12 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 40 bpm regular nl, 2 of 3 no QRS 0.14 s 0.08 s 2nd Degree AV Block, Type II

81 2nd Degree AV Block, Type II Deviation from NSR Occasional P waves are completely blocked (P wave not followed by QRS).

82 2nd Degree AV Block, Type II Etiology: Conduction is all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His.

83 Rhythm #13 Rate? Regularity? P waves? PR interval? QRS duration? 40 bpm regular no relation to QRS none wide (> 0.12 s) Interpretation? 3rd Degree AV Block

84 3rd Degree AV Block Deviation from NSR The P waves are completely blocked in the AV junction; QRS complexes originate independently from below the junction.

85 3rd Degree AV Block Etiology: There is complete block of conduction in the AV junction, so the atria and ventricles form impulses independently of each other. Without impulses from the atria, the ventricles own intrinsic pacemaker kicks in at around beats/minute.

86 Remember When an impulse originates in a ventricle, conduction through the ventricles will be inefficient and the QRS will be wide and bizarre.

87 Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. 12-Lead ECG Rhythm Strip

88 The 12-Lead ECG The 12-Lead ECG sees the heart from 12 different views. Therefore, the 12-Lead ECG helps you see what is happening in different portions of the heart. The rhythm strip is only 1 of these 12 views.

89 The 12-Leads The 12-leads include: 3 Limb leads (I, II, III) 3 Augmented leads (avr, avl, avf) 6 Precordial leads (V 1 - V 6 )

90 Views of the Heart Some leads get a good view of the: Lateral portion of the heart Anterior portion of the heart Inferior portion of the heart

91 One way to diagnose an acute MI is to look for elevation of the ST segment. ST Elevation

92 Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction. ST Elevation (cont)

93 Anterior View of the Heart The anterior portion of the heart is best viewed using leads V 1 - V 4.

94 Anterior Myocardial Infarction If you see changes in leads V 1 - V 4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

95 Putting it all Together Do you think this person is having a myocardial infarction. If so, where?

96 Interpretation Yes!, this person is having an acute anterior wall myocardial infarction.

97 Other MI Locations Now that you know where to look for an anterior wall myocardial infarction let s look at how you would determine if the MI involves the lateral wall or the inferior wall of the heart.

98 Other MI Locations First, take a look again at this picture of the heart. Lateral portion of the heart Anterior portion of the heart Inferior portion of the heart

99 Other MI Locations Second, remember that the 12-leads of the ECG look at different portions of the heart. The limb and augmented leads see electrical activity moving inferiorly (II, III and avf), to the left (I, avl) and to the right (avr). Whereas, the precordial leads see electrical activity in the posterior to anterior direction. Limb Leads Augmented Leads Precordial Leads

100 Other MI Locations Now that you know where to look for an anterior wall myocardial infarction let s look at how you would determine if the MI involves the lateral wall or the inferior wall of the heart.

101 Other MI Locations First, take a look again at this picture of the heart. Lateral portion of the heart Anterior portion of the heart Inferior portion of the heart

102 Other MI Locations Now, using these 3 diagrams let s figure where to look for a lateral wall and inferior wall MI. Limb Leads Augmented Leads Precordial Leads

103 Anterior MI Remember the anterior portion of the heart is best viewed using leads V 1 - V 4. Limb Leads Augmented Leads Precordial Leads

104 Lateral MI So what leads do you think the lateral portion of the heart is best viewed? Leads I, avl, and V 5 - V 6 Limb Leads Augmented Leads Precordial Leads

105 Inferior MI Now how about the inferior portion of the heart? Leads II, III and avf Limb Leads Augmented Leads Precordial Leads

106 Putting it all Together Now, where do you think this person is having a myocardial infarction?

107 Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and avf.

108 Putting it all Together How about now?

109 Anterolateral MI This person s MI involves both the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6, I, and avl)!

110 ST Elevation and non-st Elevation MIs

111 ST Elevation and non-st Elevation MIs When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time. The ECG changes over time with each of these events

112 ECG Changes Ways the ECG can change include: ST elevation & depression T-waves Appearance of pathologic Q-waves peaked flattened inverted

113 ECG Changes & the Evolving MI There are two distinct patterns of ECG change depending if the infarction is: Non-ST Elevation ST Elevation ST Elevation (Transmural or Q-wave), or Non-ST Elevation (Subendocardial or non-q-wave)

114 ST Elevation Infarction The ECG changes seen with a ST elevation infarction are: Before injury Normal ECG Ischemia Infarction Fibrosis ST depression, peaked T-waves, then T-wave inversion ST elevation & appearance of Q-waves ST segments and T-waves return to normal, but Q-waves persist

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116 ST Elevation Infarction Here s a diagram depicting an evolving infarction: A. Normal ECG prior to MI B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves C. Infarction from ongoing ischemia results in marked ST elevation D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves

117 ST Elevation Infarction Here s an ECG of an inferior MI: Look at the inferior leads (II, III, avf). Question: What ECG changes do you see? ST elevation and Q-waves Extra credit: What is the rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!

118 Non-ST Elevation Infarction Here s an ECG of an inferior MI later in time: Now what do you see in the inferior leads? ST elevation, Q-waves and T-wave inversion

119 Non-ST Elevation Infarction The ECG changes seen with a non-st elevation infarction are: Before injury Normal ECG Ischemia ST depression & T-wave inversion Infarction Fibrosis ST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists

120 Non-ST Elevation Infarction Here s an ECG of an evolving non-st elevation MI: Note the ST depression and T-wave inversion in leads V 2 -V 6. Question: What area of the heart is infarcting? Anterolateral

121 Left Ventricular Hypertrophy

122 LVH

123 Left Ventricular Hypertrophy Compare these two 12-lead ECGs. What stands out as different with the second one? Normal Left Ventricular Hypertrophy Answer: The QRS complexes are very tall (increased voltage)

124 Left Ventricular Hypertrophy Why is left ventricular hypertrophy characterized by tall QRS complexes? As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage. LVH Increased QRS voltage ECHOcardiogram

125 Left Ventricular Hypertrophy Criteria exists to diagnose LVH using a 12-lead ECG. For example: The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm. However, for now, all you need to know is that the QRS voltage increases with LVH.

126 Bundle Branch Blocks

127 Bundle Branch Blocks Turning our attention to bundle branch blocks Remember normal impulse conduction is SA node AV node Bundle of His Bundle Branches Purkinje fibers

128 Normal Impulse Conduction Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

129 Bundle Branch Blocks So, depolarization of the Bundle Branches and Purkinje fibers are seen as the QRS complex on the ECG. Therefore, a conduction block of the Bundle Branches would be reflected as a change in the QRS complex. Right BBB

130 Bundle Branch Blocks With Bundle Branch Blocks you will see two changes on the ECG. 1. QRS complex widens (> 0.12 sec). 2. QRS morphology changes (va ries depending on ECG lead, and if it is a right vs. left bundle branch block).

131 Bundle Branch Blocks Why does the QRS complex widen? When the conduction pathway is blocked it will take longer for the electrical signal to pass throughout the ventricles.

132 Right Bundle Branch Blocks What QRS morphology is characteristic? For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V 1 and V 2 ). V 1 Rabbit Ears

133 Left Bundle Branch Blocks What QRS morphology is characteristic? For LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V 1 and V 2 ). Normal Broad, deep S waves

134 ARTIFACT ON THE ECG 135

135 FIND THE ARTIFACT 136

136 WANDERING BASELINE 137

137 SOMATIC TREMOR 138

138 ELECTRICAL INTERFERANCE 139

139 Reciprocal changes Lateral MI

140 Inferolateral MI ST elevation II, III, avf ST depression in avl, V1-V3 are reciprocal changes

141 Anterolateral / Inferior Ischemia LVH, AV junctional rhythm, bradycardia

142 Left Bundle Branch Block Monophasic R wave in I and V6, QRS > 0.12 sec Loss of R wave in precordial leads QRS T wave discordance I, V1, V6 Consider cardiac ischemia if a new finding

143 Left Bundle Branch Block Monophasic R wave in I and V6, QRS > 0.12 sec Loss of R wave in precordial leads QRS T wave discordance I, V1, V6 Consider cardiac ischemia if a new finding

144 First Degree Heart Block, Mobitz Type I (Wenckebach) PR progressively lengthens until QRS drops

145 Right Ventricular Myocardial Infarction Found in 1/3 of patients with inferior MI Increased morbidity and mortality ST elevation in V4-V6 of Right-sided EKG

146 Right Sided Leads

147 Ventricular Tachycardia

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149 Case #1 70 year old male with history of diabetes mellitus and hypertension occasionally feels lightheaded. He recently fainted while standing.

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151 Case #1 ECG

152 Sinus Bradycardia Sinus Bradycardia with First degree block Ask Patient about HTN Meds that may slow HR down, if none pt needs 24 hour holtor monitor, if further bradycardia Pt may need Pacemaker

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154 Case #2 58 year old Female with no significant past medical history presents with Fatigue, lightheadedness and shortness of breath.

155 Case #2 ECG

156 Atrial Fibrilation A-Fib with Rapid Ventricular Response, LVH; Rate control First with: Ca+ Blocker, Beta-Blocker or Amioderone.

157 Case #3 78 year old Female with History of HTN, DM, HL, CAD admitted for Syncope complains of palpitations and lightheadedness.

158 Case #3 ECG

159 Monomorphic VT Activate: ACLS protocol Wide complex : ventricular pacing Prepare for cardioversion

160 Case #4 67 year old male with history of diabetes, hypertension,pacemaker, COPD presents with chest pain.

161 Case #4 ECG

162 Case #5 38 year old female with history of DM, HTN, CKD presents with 2 days of nausea and abdominal pain.

163 Case #5 ECG

164 Hyperkalemia Peaked T waves with a K of: 7.7. As Hyperkalemia progresses: PR interval increases QRS then widens, P Waves dissapear A Sine wave pattern developes

165 Next step: Calcium Gluconate ( Stablilizes Cell Membrane) Insulin & D50 - (Drives Potasium into the cells) Kavexalate ( Removes Potasium & Albuterol inhaler & Lasix)

166 Case #6 60 year-old man with history of HTN, HL, CAD presents with nausea, shortness of breath and chest pain.

167 Case #6 ECG

168 STEMI + STTW elevation in Inferior Lateral leads. Inferior MI + for Right Coronary Artery Etiology

169 Case # 7 53 year old hypertensive black male smoker presents with two hours of : diaphoresis, nausea, vomiting, and the worst tooth ache of his life

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171 Torsades de Pointes Notice twisting pattern Treatment: Magnesium 2 grams IV

172 56 year old white female Racing heart after dialysis Mg K-3.5

173 Torsades de Pointes

174 Prolonged QT Normal Men 450ms Women 460ms Corrected QT (QTc) QTm/ (R-R) Causes Drugs (Na channel blockers) Hypocalcemia, hypomagnesemia, hypokalemia Hypothermia AMI Congenital Increased ICP

175 Prolonged QT QT > 450 ms Inferior and anterolateral ischemia

176 34 year old white female + sharp CP, worse with inspiration, 3 hours duration, + smoking, +anxiety, + Family History CAD

177 Nuclear Stress Test

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179 Your Grandmother 76 year old 3 weeks post-op left hip replacement, ex-smoker, +HTN, + Hemoptysis.

180 Acute Pulmonary Embolism S I Q III T III in 10-15% T-wave inversions, especially occurring in inferior and anteroseptal simultaneously RAD

181 62 Year Old Male Dialysis Patient +Lupus etilogy for Renal failure. Felt so good didn t have dialysis for two weeks, started having: Nausea & Vomiting

182 Hyperkalemia Tall, narrow and symmetric T waves

183 46 Year Old Female Hypertensive First line treatment for HTN: Thiazide diuretic and ACE Inhibator for one month, One month follow up labs with K of: 2.7

184 Hypokalemia U waves Can also see PVCs, ST depression, small T waves

185 Wellen s Sign ST elevation and biphasic T wave in V2 and V3 Sign of large proximal LAD lesion

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187 44 Year Old white female + Palpatations, dizzyness, diaphoresis, SOB, near syncope, racing heart beat

188 Wolff-Parkinson-White Syndrome Short PR interval <0.12 sec Prolonged QRS >0.10 sec Delta wave Can simulate ventricular hypertrophy, BBB and previous MI

189 74 Year Old male with CHF CHF 20% EF, HTN, CAD/CABG, A-fib,Dementia, DM, Hyperlipidemia, Renal Insufficinecy, Gout, Meds: Betablocker, ACE, Digoxin, ASA, Lasix & K

190 Digitalis Effect