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Cardiovascular II Part 2 PVC Premature Ventricular Contraction 2.

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Presentation on theme: "Cardiovascular II Part 2 PVC Premature Ventricular Contraction 2."— Presentation transcript:


2 Cardiovascular II Part 2

3 PVC Premature Ventricular Contraction 2

4 Premature ventricular contracture With a PVC, diastolic volume is insufficient for ejection of blood into arterial system. – Therefore, no or weak pulse palpated. Few/day = OK, More/minute, the worse (>6). Common post MI, SNS activity,  K+, hypoxia. 3

5 V-Fib Ventricular Fibrillation 4

6 Ventricle quivers but does NOT contract!  – NO cardiac output and no pulses Cardiac Arrest!! Grossly disorganized pattern 5

7 V-Tach Ventricular Tachycardia 6

8 A bunch of PVC in a row – Rhythm originates below Bundle of His, in ventricular muscle. It is too fast, so ventricular filling is ineffective and CO is ineffective Wide, tall QRS complexes Stops spontaneously or continues Dangerous rhythm,  diastolic filling time   CO Can cause Cardiac Arrest 7

9 Class I Antidysrhythmics Diagram 8

10 Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node 9 Class I Antidysrhythmic

11 Class 1B: Lidocaine Ventricular Dysrhthmias 10

12 Class 1B: Lidocaine Ventricular Dysrhythmias 11

13 Class 1B: Lidocaine Effects on the Heart and the ECG 12

14 Class 1B: Lidocaine Effects on the Heart and the ECG 1.Blocks Na+ channels  slow conduction thru atria, ventricles, HIS-Purkinje 2.Reduces automaticity -Slows the heart rate down 3.Accelerates repolarization (shortens action potential) No anticholinergic effect No change in ECG – See a restoration of sinus normal 13

15 Lidocaine Precautions and Adverse Effects 14

16 Lidocaine Precautions and Adverse Effects Metabolized by Liver Therapeutic range 1.5 – 5.0 microgm/ml – Pretty narrow Adverse CNS Effects – Drowsiness, confusion, paresthesia Toxicity – Convulsions and respiratory arrest 15

17 Lidocaine Administration 16

18 Lidocaine Administration IV Push – 50-100mg (1mg/kg) – Comes in a preloaded syringe Infusion – 1-4mg/min – Diluted in D5W Special Considerations – Use for as short a time as possible – Reduce dosage in pts with liver disorders 17

19 Class III Antidysrhythmics Potassium Channel Blockers 18

20 Class III Antidysrhythmic Potassium Channel Blockers: Amiodarone Approved for V-tach and V-fib. Delay repolarization of the ventricles  Prolongs action potential and refractory period  Increases PR and QT intervals - as the QT interval lengthens, the person may develop additional dysrhythmias 19 Initial  catecholamine release  brief exacerbation of dysrhythmias - Catecholamines speed up the heart and lead to stronger heart beats  block catecholamine release  vasodilation / hypotension

21 Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node 20 Class III Antidysrhythmic

22 Non-Pharmacologic Treatment of Dysrhythmias 21

23 Non-Pharmacologic Treatment of Dysrhythmias Cardioversion –Synchronized, coordinated shocking of the heart –Atrial fib –V-tach Defibrillation –A shock that is delivered as soon as the buttons are pushed –V-fib 22

24 Automated External Defibrillator 23

25 Automated External Defibrillator Cardiac Arrest, AED “interrogates” rhythm. –Waits to see what the rhythm is and then delivers the shock as needed (timed for V- tach and not timed for V-fib.) Tells user what to do, eg. “Shock Now” Delivers shock for V-tach or V-fib. 24

26 Implantable Cardioverter/Defibrillator 25

27 Implantable Cardioverter/Defibrillator Like a pacemaker Monitors and analyzes rhythm Delivers shock to terminate V-tach, V-fib 26

28 Radiofrequency Catheter Ablation 27

29 Radiofrequency Catheter Ablation Cardiac cath and electrophysiologic (EP) test Identify cardiac tissue site which causes dysrhythmia while in the cath lab –Map the myocardium RF energy delivered to destroy the tissue so that that focus/area does not fire anymore –Remember, you can’t pace meatloaf Dead myocardium or heart tissue will not respond to pacing 28

30 Antidysrhythmic Drugs Summary 29

31 Antidysrhythmic Drugs Summary Class I – Depress phase 0 in depolarization – Block sodium channels Class II (Beta-blockers) – Depress phase 4 in depolarization – Block beta 1 & 2 adrenergic receptors HRContractility 30

32 Antidysrhythmic Drugs: Summary Class III (Potassium Channel Blockers) – Prolong phase 3 (repolarization) Class IV (Calcium Channel Blockers) – Depresses phase 4 depolarization – Prolongs phases 1 & 2 repolarization 31

33 Management of Cardiac Dysrhythmias 32

34 Management of Cardiac Dysrhythmias REMEMBER: Many drugs used to treat dysrhythmias also may worsen them or cause new ones! 33


36 Coronary Circulation 35

37 Coronary Circulation Two main coronary arteries arise from coronary sinus (above aortic valve) – The orifices are above the aorta The heart perfuses during diastole because it is when the coronary arteries are open Primary factor responsible for perfusion of coronary arteries is BP in aorta  s aortic pressure ->  s coronary blood flow 36

38 Coronary Circulation Diagram 37

39 LV Coronary Circulation Diagram 38

40 Coronary Arteries 39

41 Coronary Arteries Right coronary artery – Nourishes right side, SA node, AV node – may lead to heart block Left coronary artery – A block in the left coronary artery leads to death because it sends blood to the left side of the heart and then to the body – Left anterior descending – Left circumflex 40

42 41


44 Coronary Heart Disease 43

45 Coronary Heart Disease Heart disease caused by impaired coronary blood flow (atherosclerosis) Cause angina, dysrhythmias, conduction defects, heart failure, sudden death, myocardial infarction (“heart attack”) If blood flow is temporarily inadequate (due to increased oxygen demand), ischemia produces pain (angina). Myocardial Infarction is myocardial cell/tissue death due to oxygen starvation 44

46 Assessment of Coronary Blood Flow 45

47 Assessment of Coronary Blood Flow ECG Exercise Stress Testing Pharmacologic Stress Testing – May give catecholamines, such as epinephrine, norepinephrine Nuclear Imaging Cardiac Catheterization /Coronary angiography 46

48 Collateral Circulation 47

49 Collateral Circulation With gradual occlusion of large coronary vessels, the smaller collateral vessels  in size and provide alternative channels for blood flow – Allow perfusion to the myocardium that is below and is distal to the blood flow One of the reasons CHD does not produce symptoms until it is far advanced is that the collateral channels develop at the same time the atherosclerotic changes are occurring. 48

50 Collateral Circulation Diagram 49

51 50 Collateral Circulation Diagram 50

52 Pathogenesis of CAD Atherosclerosis 51

53 Pathogenesis of CAD Atherosclerosis Most common cause of CAD Plaque disruption is most the frequent cause of MI, sudden death Can affect one or all three major coronary arteries/branches 52

54 Plaque 53

55 Plaque Plaques typically do not occlude the whole coronary artery but produce a narrowing that restricts blood flow. –In times of increased oxygen demand, such as with exercise, the restricted blood flow may produce ischemia in cells supplied by that artery. –This produces the pain of angina. 54

56 Plaque Rupture 55

57 Plaque Rupture A plaque may become unstable and rupture, causing a clot to form which may completely occlude the artery. –Results in no bloodflow –Occlusion of the artery causes death of the cardiac cells downstream that are supplied by that artery. –When the cells die, that is an infarction – hence the name myocardial infarction. –Have about 90 minutes to restore the blood flow to prevent permanent damage 56

58 Atherosclerosis in Coronary Artery 57

59 Atherosclerosis in Coronary Artery Plaque rupture and disruption of atheroma   lipid core/contents exposed to blood  platelet aggregation  coagulation cascade  fibrin clot  Give aspirin quickly to prevent or reduce the clotting  thrombosis, vasospasm  myocardial ischemia  Coronary arteries unable to supply blood to meet metabolic demands of the heart 58

60 Angina 59

61 Angina Angina: symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia 60

62 Stable Angina 61

63 Stable Angina Occurs with exertion or stress Predictable If plaque becomes unstable and ruptures, it leads to platelet aggregation and unstable angina 62

64 63

65 Variant or Vasospastic Angina 64

66 Variant or Vasospastic Angina Occurs during rest or with minimal activity (nocturnal, Prinzmetal’s) 65

67 Silent Myocardial Ischemia 66

68 Silent Myocardial Inschemia Occurs in the absence of anginal pain –Tend to be endocardial, in the inner layer of the myocardium 67

69 Unstable Angina 68

70 Unstable Angina Symptoms at rest lasting >20 minutes Marked limitations of ordinary activity (walking 1–2 blocks, climbing a flight of stairs) Recent acceleration in anginal signs, not responsive to nitroglycerine 69

71 70

72 Acute Myocardial Infarction 71

73 Acute Myocardial Infarction Acute myocardial infarction (STEMI or NSTEMI) –ST segment elevation myocardium infarction STEMI - complete occlusion of bloodflow – Significant change on the EKG NSTEMI – partial occlusion of a blood vessel by a thrombus 72

74 73

75 74

76 Characteristics of Plaque Rupture 75

77 Characteristics of Plaque Rupture Spontaneous – SNS activation  BP,  HR,  contraction – Triggering event (stress: emotional, physical) Diurnal – Plaque rupture is more common in the first hour of arising – SNS “surge” on arising SNS major player – Beta-adrenergic blockers Block the adrenergic response so the patients will not have the same response to a SNS surge 76

78 “Severe” Coronary Stenosis and Vulnerable Plaques Co-exist 77

79 “Severe” Coronary Stenosis and Vulnerable Plaques Co-exist 78 Califf, Atlas of Heart Diseases 2001

80 Ischemia, Injury, and Infarction 79

81 Ischemia, Injury, and Infarction Three Zones of Damage Infarction = Necrosis – MI, dead cells – Beyond hope of recovery but can stop in from increasing Injury – Some recovery possible Can still perfuse it and restore it to become viable – Not dead yet Ischemia – Full recovery possible Do not want the patient to extend the size of the infarct – Increase oxygen – Decrease the demand on the heart 80

82 Zones of Tissue Damage 81

83 82 Zones of Tissue Damage Goal is to limit the area of necrosis (infarction) ! Necrotic myocardial cells are gradually replaced with scar tissue Scar tissue cannot contract or conduct action potentials, cannot respond to drugs or pacing

84 An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis 83

85 An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis 84

86 Pathologic Changes in Zones of Injury 85

87 Pathologic Changes in Zones of Injury Ischemic areas cease to function within minutes Irreversible damage/death to myocardial cells occurs within 20-40 minutes Early reperfusion (20min) after onset of ischemia can prevent necrosis, prevent further ischemia and necrosis 86

88 Extent of the Infarct 87

89 Extent of the Infarct Extent of infarct depends on : Location Extent of occlusion Amount of heart tissue supplied by vessel, duration of occlusion Metabolic needs of the affected tissue Extent of collateral circulation – A couch potato will probably have a lot more collateral circulation 88

90 Types of Infarct 89

91 Types of Infarct Transmural infarct – Full thickness of ventricular wall, – Occurs with obstruction of a single artery; – May involve RV, LV and/or IV septum Subendocardial infarct – Involve inner 1/3 to 1/2 ventricular wall, – May occur with severely narrowed arteries or with occlusion of a very small artery 90 Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 328.

92 Types of Coronary Heart Disease 91

93 92

94 Chest Pain Assessment 93

95 Chest Pain Assessment P – Provocation Q – Quality – Tell me about it... – Describe the pain R – Region/Radiation S – Severity T – Timing – Does it occur at night or during the day – Predictability 94

96 Categories (PQRST) 95

97 Categories (PQRST) Angina that occurs with stress (physical/emotional) – Relieved within minutes by rest or NTG (nitroglycerine) Angina that occurs with rest Is of new onset Increasing intensity 96  risk for MI

98 Chronic Ischemic Heart Disease 97

99 98

100 Stable Angina 99

101 Stable Angina Fixed coronary obstruction  0 2 Demand   0 2 supply  pain – Physical/emotional stress, cold Provoked by stressor – Relieved with rest/NTG (nitroglycerine) Not everyone with CHD has angina – Sedentary lifestyle (couch potatoes), development of collateral circulation, altered perception pain 100

102 Locations of Angina 101

103 Usual distribution of pain Less common sites of pain distribution Typically precordial, substernal Angina 102

104 Variant or Vasospastic Angina 103

105 Variant or Vasospastic Angina “Prinzmetal’s angina” –Comes and goes without any predictability Due to coronary artery spasms Occurs during rest or with minimal exertion, frequently nocturnal Mechanism is uncertain –Possibilities may include SNS activation, VSM Ca ++ channel dysfunction, imbalance of endothelial cell vasodilating/constricting substances Dysrhythmias can occur –Person usually aware; High risk sudden death 104

106 Variant or Vasospastic Angina Diagram 105

107 Hamon M and Hamon M. N Engl J Med 2006;355:2236 A 38-year-old man was scheduled to undergo invasive coronary angiography after cardiac scintigraphy revealed silent ischemia of the anterior myocardial wall Variant or Vasospastic Angina Diagram 106

108 Acute Coronary Syndrome (ACS) 107

109 Acute Coronary Syndrome (ACS) 108 NSTEMISTEMI Unstable or ruptured plaque

110 Acute Coronary Syndrome (ACS) Unstable Angina 109

111 Acute Coronary Syndrome (ACS) Unstable Angina 110

112 Unstable Angina Severe Clinical syndrome of myocardial ischemia ranging between stable angina and MI Usually due to atherosclerotic plaque disruption, platelet aggregation 111

113 Presentations of Unstable Angina 112

114 Presentations of Unstable Angina 1.Symptoms at rest (> 20 minutes) 2.Severe, frank pain, new onset (< 1month) - Pain crescendos 3.More severe, prolonged, or frequent 113

115 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 114

116 Acute Coronary Syndrome (ACS) ST-segment Elevation 115

117 Acute Coronary Syndrome (ACS) ST-segment Elevation 116

118 ST Segment Elevation 117

119 ST Segment Elevation ST segment elevations are indicative of myocardial damage or ischemia. It may take some time (minutes to hours) for the changes to show up, and they may not be present in all EKG leads. –The placement of the leads and the occurrence of ST elevation indicates where the MI is occurring 118 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 394.

120 ECG STEMI vs. NSTEMI 119

121 ECG STEMI vs. NSTEMI 120

122 Non ST Segment Elevation Myocardial Infarction (NSTEMI) 121

123 Non ST Segment Elevation Myocardial Infarction (NSTEMI) How is this different from unstable angina or STEMI? Unstable angina, plaque disruption but no thrombus or occlusion of the coronary artery, therefore no myocardial cell death (no MI). NSTEMI, a thrombus partially occludes a coronary artery. Depending on the degree of occlusion and oxygen demand of downstream heart cells, there may be myocardial cell death (an MI) but insufficient to produce ST segment elevations. The patient may not have unstable angina The amount of the infarction depends on how much blood flow is getting through 122

124 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 123

125 ST Segment Elevation MI 124

126 ST Segment Elevation MI Characterized by ischemia of cardiac tissue Area of infarction is determined by the coronary artery that is affected and by its distribution of blood flow – 40-50% of time – LAD Influences CO, BP, and likelihood of survival or death – 30-40% of time – RCA Will see blocks on the EKG due to SA node or AV node dysfunction – 15-20% of time - LCA 125

127 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 126

128 Diagnosis of CHD and MI 127

129 Diagnosis of CHD and MI Good history and identification of risk factors R/O Other causes of CP, such as GERD ECG Serum myocardial markers Stress testing – May be exercise or pharmacological Cardiac catheterization 128

130 “Classic” Manifestations of MI 129

131 “Classic” Manifestations of MI Abrupt onset or progression of unstable, non-ST elevation, which then moves to become ST elevation Pain is severe, crushing, “someone sitting on my chest” Radiates to left arm, jaw, neck MI pain is prolonged, not relieved by rest and/or NTG (unlike angina) N/V, SNS activation   HR,  RR, diaphoresis, cool/clammy skin 130

132 ECG Changes 131

133 ECG Changes T wave inversion ST segment elevation Abnormal Q wave (may not appear immediately) –Wider and bigger where the MI is present Once a QI develops, it does not ever go away Changes can occur over time, depending on duration of ischemia (extent and location) Changes may not be present in all leads – take 12-lead EKG –Will only be present over the area that is infarcted 132

134 ST Segments 133

135 ST Segments 1 st to change during ischemia or MI because myocardial repolarization is altered. Ischemia reduces membrane potential and shorten duration of AP in ischemic area. 134

136 Abnormal Q Waves 135

137 Abnormal Q Waves Develop because there is no depolarizing current conduction from necrotic tissue May not appear immediately Diagnostic of MI Q waves are permanent after MI 136

138 Serum Markers for Ischemia and MI 137

139 Serum Markers for Ischemia and MI Necrotic cells release intracellular enzymes into blood stream Measure these in blood – The larger the number, the larger the amount of necrotic tissue – CK-MB (Creatine-kinase-myocardial bands) – Troponin – C-reactive Protein An inflammatory marker 138

140 CK-MB 139

141 CK-MB CK is normal in all muscle cells – Has three isoenzymes BB, MM, MB CK-MB Creatine kinase -myocardial bands is cardiac specific Elevated within 8 hours after MI Returns to normal in 2-3 days Nl ~ 24-195 IU/L 140

142 Troponin (TnC, TnI, TnT) 141

143 Troponin (TnC, TnI, TnT) Very cardiac specific – Most sensitive marker Part of the actin-myosin filament Elevate more quickly than the CK-MB – Rises within 3 hours after MI – Remains elevated 3-4 days and up to 10 days Diagnostic of MI; No change with ischemia Nl ~ 0.4 ng/ml 142

144 C-Reactive Protein (CRP) 143

145 C-Reactive Protein (CRP) Marker of chronic inflammation May be a marker of risk Identifies people before they are symptomatic May guide preventative therapy in the future Non-specific because it increases with any inflammatory response 144

146 Timeline of Cardiac Markers 145

147 Timeline of Cardiac Markers 146 Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5 Troponin CK-MB

148 Acute Coronary Syndrome Concept Map 147

149 NSTEMI Unstable angina No ECG  s Elevation of serum markers, including troponin and CK- MB Unstable Angina Pain is severe No ECG  s No change in markers because they are not having an MI ACS No ST Elevation STEMI 148

150 Infarction Diagram 149

151 150

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