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Slide 2 Cardiovascular II Part 2 Slide 3 PVC Premature Ventricular Contraction 2 Slide 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 Slide 5 V-Fib Ventricular Fibrillation 4 Slide 6 Ventricle quivers but does NOT contract! NO cardiac output and no pulses Cardiac Arrest!! Grossly disorganized pattern 5 Slide 7 V-Tach Ventricular Tachycardia 6 Slide 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 Slide 9 Class I Antidysrhythmics Diagram 8 Slide 10 Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node 9 Class I Antidysrhythmic Slide 11 Class 1B: Lidocaine Ventricular Dysrhthmias 10 Slide 12 Class 1B: Lidocaine Ventricular Dysrhythmias 11 Slide 13 Class 1B: Lidocaine Effects on the Heart and the ECG 12 Slide 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 Slide 15 Lidocaine Precautions and Adverse Effects 14 Slide 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 Slide 17 Lidocaine Administration 16 Slide 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 Slide 19 Class III Antidysrhythmics Potassium Channel Blockers 18 Slide 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 Slide 21 Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node 20 Class III Antidysrhythmic Slide 22 Non-Pharmacologic Treatment of Dysrhythmias 21 Slide 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 Slide 24 Automated External Defibrillator 23 Slide 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 Slide 26 Implantable Cardioverter/Defibrillator 25 Slide 27 Implantable Cardioverter/Defibrillator Like a pacemaker Monitors and analyzes rhythm Delivers shock to terminate V-tach, V-fib 26 Slide 28 Radiofrequency Catheter Ablation 27 Slide 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 cant pace meatloaf Dead myocardium or heart tissue will not respond to pacing 28 Slide 30 Antidysrhythmic Drugs Summary 29 Slide 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 Slide 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 Slide 33 Management of Cardiac Dysrhythmias 32 Slide 34 Management of Cardiac Dysrhythmias REMEMBER: Many drugs used to treat dysrhythmias also may worsen them or cause new ones! 33 Slide 35 CORONARY HEART DISEASE AND ACUTE MYOCARDIAL INFARCTION (MI OR AMI) 34 Slide 36 Coronary Circulation 35 Slide 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 Slide 38 Coronary Circulation Diagram 37 Slide 39 LV Coronary Circulation Diagram 38 Slide 40 Coronary Arteries 39 Slide 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 Slide 42 41 Slide 43 ISCHEMIC HEART DISEASE A.K.A CORONARY HEART DISEASE A.K.A CORONARY ARTERY DISEASE ANGINA MYOCARDIAL INFARCTION 42 Slide 44 Coronary Heart Disease 43 Slide 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 Slide 46 Assessment of Coronary Blood Flow 45 Slide 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 Slide 48 Collateral Circulation 47 Slide 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 Slide 50 Collateral Circulation Diagram 49 Slide 51 50 Collateral Circulation Diagram 50 Slide 52 Pathogenesis of CAD Atherosclerosis 51 Slide 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 Slide 54 Plaque 53 Slide 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 Slide 56 Plaque Rupture 55 Slide 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 Slide 58 Atherosclerosis in Coronary Artery 57 Slide 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 Slide 60 Angina 59 Slide 61 Angina Angina: symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia 60 Slide 62 Stable Angina 61 Slide 63 Stable Angina Occurs with exertion or stress Predictable If plaque becomes unstable and ruptures, it leads to platelet aggregation and unstable angina 62 Slide 64 63 Slide 65 Variant or Vasospastic Angina 64 Slide 66 Variant or Vasospastic Angina Occurs during rest or with minimal activity (nocturnal, Prinzmetals) 65 Slide 67 Silent Myocardial Ischemia 66 Slide 68 Silent Myocardial Inschemia Occurs in the absence of anginal pain Tend to be endocardial, in the inner layer of the myocardium 67 Slide 69 Unstable Angina 68 Slide 70 Unstable Angina Symptoms at rest lasting >20 minutes Marked limitations of ordinary activity (walking 12 blocks, climbing a flight of stairs) Recent acceleration in anginal signs, not responsive to nitroglycerine 69 Slide 71 70 Slide 72 Acute Myocardial Infarction 71 Slide 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 Slide 74 73 Slide 75 74 Slide 76 Characteristics of Plaque Rupture 75 Slide 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 Slide 78 Severe Coronary Stenosis and Vulnerable Plaques Co-exist 77 Slide 79 Severe Coronary Stenosis and Vulnerable Plaques Co-exist 78 Califf, Atlas of Heart Diseases 2001 Slide 80 Ischemia, Injury, and Infarction 79 Slide 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 Slide 82 Zones of Tissue Damage 81 Slide 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 Slide 84 An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis 83 Slide 85 An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis 84 Slide 86 Pathologic Changes in Zones of Injury 85 Slide 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 Slide 88 Extent of the Infarct 87 Slide 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 Slide 90 Types of Infarct 89 Slide 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. Slide 92 Types of Coronary Heart Disease 91 Slide 93 92 Slide 94 Chest Pain Assessment 93 Slide 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 Slide 96 Categories (PQRST) 95 Slide 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 Slide 98 Chronic Ischemic Heart Disease 97 Slide 99 98 Slide 100 Stable Angina 99 Slide 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 Slide 102 Locations of Angina 101 Slide 103 Usual distribution of pain Less common sites of pain distribution Typically precordial, substernal Angina 102 Slide 104 Variant or Vasospastic Angina 103 Slide 105 Variant or Vasospastic Angina Prinzmetals 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 Slide 106 Variant or Vasospastic Angina Diagram 105 Slide 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 Slide 108 Acute Coronary Syndrome (ACS) 107 Slide 109 Acute Coronary Syndrome (ACS) 108 NSTEMISTEMI Unstable or ruptured plaque Slide 110 Acute Coronary Syndrome (ACS) Unstable Angina 109 Slide 111 Acute Coronary Syndrome (ACS) Unstable Angina 110 Slide 112 Unstable Angina Severe Clinical syndrome of myocardial ischemia ranging between stable angina and MI Usually due to atherosclerotic plaque disruption, platelet aggregation 111 Slide 113 Presentations of Unstable Angina 112 Slide 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 Slide 115 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 114 Slide 116 Acute Coronary Syndrome (ACS) ST-segment Elevation 115 Slide 117 Acute Coronary Syndrome (ACS) ST-segment Elevation 116 Slide 118 ST Segment Elevation 117 Slide 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. Slide 120 ECG STEMI vs. NSTEMI 119 Slide 121 ECG STEMI vs. NSTEMI 120 Slide 122 Non ST Segment Elevation Myocardial Infarction (NSTEMI) 121 Slide 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 Slide 124 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 123 Slide 125 ST Segment Elevation MI 124 Slide 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 Slide 127 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 126 Slide 128 Diagnosis of CHD and MI 127 Slide 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 Slide 130 Classic Manifestations of MI 129 Slide 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 Slide 132 ECG Changes 131 Slide 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 Slide 134 ST Segments 133 Slide 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 Slide 136 Abnormal Q Waves 135 Slide 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 Slide 138 Serum Markers for Ischemia and MI 137 Slide 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 Slide 140 CK-MB 139 Slide 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 Slide 142 Troponin (TnC, TnI, TnT) 141 Slide 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 Slide 144 C-Reactive Protein (CRP) 143 Slide 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 Slide 146 Timeline of Cardiac Markers 145 Slide 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 Slide 148 Acute Coronary Syndrome Concept Map 147 Slide 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 Slide 150 Infarction Diagram 149 Slide 151 150