Cardiovascular II Part 2 PVC Premature Ventricular Contraction 2 PVC Premature Ventricular Contraction • 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 V-Fib Ventricular Fibrillation 4 V-Fib Ventricular Fibrillation • Ventricle quivers but does NOT contract! – NO cardiac output and no pulses • Cardiac Arrest!! • Grossly disorganized pattern 5 V-Tach Ventricular Tachycardia 6 V-Tach Ventricular Tachycardia • 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 Class I Antidysrhythmics Diagram 8 Class I Antidysrhythmic Myocardium & His-Purkinje System SA Node & AV Node Lehne 5th ed Figure 47-2 9 Class 1B: Lidocaine Ventricular Dysrhthmias 10 Class 1B: Lidocaine Ventricular Dysrhythmias 11 Class 1B: Lidocaine Effects on the Heart and the ECG 12 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 Lidocaine Precautions and Adverse Effects 14 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 Lidocaine Administration 16 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 Class III Antidysrhythmics Potassium Channel Blockers 18 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 Initial catecholamine release brief exacerbation of dysrhythmias - Catecholamines speed up the heart and lead to stronger heart beats block catecholamine release vasodilation / hypotension 19 Class III Antidysrhythmic Myocardium & His-Purkinje System SA Node & AV Node Lehne 5th ed Figure 47-2 20 Non-Pharmacologic Treatment of Dysrhythmias 21 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 Automated External Defibrillator 23 Automated External Defibrillator • Cardiac Arrest, AED “interrogates” rhythm. – Waits to see what the rhythm is and then delivers the shock as needed (timed for Vtach and not timed for V-fib.) • Tells user what to do, eg. “Shock Now” • Delivers shock for V-tach or V-fib. 24 Implantable Cardioverter/Defibrillator 25 Implantable Cardioverter/Defibrillator • Like a pacemaker • Monitors and analyzes rhythm • Delivers shock to terminate V-tach, V-fib 26 Radiofrequency Catheter Ablation 27 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 Antidysrhythmic Drugs Summary 29 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 HR Contractility 30 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 Management of Cardiac Dysrhythmias 32 Management of Cardiac Dysrhythmias REMEMBER: Many drugs used to treat dysrhythmias also may worsen them or cause new ones! 33 CORONARY HEART DISEASE AND ACUTE MYOCARDIAL INFARCTION (MI OR AMI) 34 Coronary Circulation 35 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 Coronary Circulation Diagram 37 Coronary Circulation Diagram LV LV 38 Coronary Arteries 39 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 41 ISCHEMIC HEART DISEASE A.K.A CORONARY HEART DISEASE A.K.A CORONARY ARTERY DISEASE ANGINA 42 Coronary Heart Disease 43 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 Assessment of Coronary Blood Flow 45 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 Collateral Circulation 47 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 Collateral Circulation Diagram 49 Collateral Circulation Diagram 50 50 Pathogenesis of CAD Atherosclerosis 51 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 Plaque 53 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 Plaque Rupture 55 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 Atherosclerosis in Coronary Artery 57 Atherosclerosis in Coronary Artery Plaque rupture and disruption of atheroma lipid core/contents exposed to blood platelet aggregationcoagulation 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 Angina 59 Angina • Angina: symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia 60 Stable Angina 61 Stable Angina • Occurs with exertion or stress • Predictable • If plaque becomes unstable and ruptures, it leads to platelet aggregation and unstable angina 62 63 Variant or Vasospastic Angina 64 Variant or Vasospastic Angina • Occurs during rest or with minimal activity (nocturnal, Prinzmetal’s) 65 Silent Myocardial Ischemia 66 Silent Myocardial Inschemia • Occurs in the absence of anginal pain – Tend to be endocardial, in the inner layer of the myocardium 67 Unstable Angina 68 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 70 Acute Myocardial Infarction 71 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 73 74 Characteristics of Plaque Rupture 75 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 “Severe” Coronary Stenosis and Vulnerable Plaques Co-exist 77 “Severe” Coronary Stenosis and Vulnerable Plaques Co-exist Califf, Atlas of Heart Diseases 2001 78 Ischemia, Injury, and Infarction 79 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 Zones of Tissue Damage 81 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 82 An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis 83 An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis 84 Pathologic Changes in Zones of Injury 85 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 Extent of the Infarct 87 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 Types of Infarct 89 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 Porth, 2007, Essential of Pathophysiology, 2nd ed., Lippincott, p. 328. 90 Types of Coronary Heart Disease 91 92 Chest Pain Assessment 93 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 Categories (PQRST) 95 Categories (PQRST) risk for MI • 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 Chronic Ischemic Heart Disease 97 98 Stable Angina 99 Stable Angina • Fixed coronary obstruction • 02 Demand 02 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 Locations of Angina 101 Angina Usual distribution of pain Less common sites of pain distribution Typically precordial, substernal 102 Variant or Vasospastic Angina 103 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 104 – Person usually aware; High risk sudden death Variant or Vasospastic Angina Diagram 105 Variant or Vasospastic Angina Diagram A 38-year-old man was scheduled to undergo invasive coronary angiography after cardiac scintigraphy revealed silent ischemia of the anterior myocardial wall Hamon M and Hamon M. N Engl J Med 2006;355:2236 106 Acute Coronary Syndrome (ACS) 107 Acute Coronary Syndrome (ACS) Unstable or ruptured plaque NSTEMI STEMI 108 Acute Coronary Syndrome (ACS) Unstable Angina 109 Acute Coronary Syndrome (ACS) Unstable Angina 110 Unstable Angina • Severe • Clinical syndrome of myocardial ischemia ranging between stable angina and MI • Usually due to atherosclerotic plaque disruption, platelet aggregation 111 Presentations of Unstable Angina 112 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 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 114 Acute Coronary Syndrome (ACS) ST-segment Elevation 115 Acute Coronary Syndrome (ACS) ST-segment Elevation 116 ST Segment Elevation 117 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 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 394. 118 ECG STEMI vs. NSTEMI 119 ECG STEMI vs. NSTEMI 120 Non ST Segment Elevation Myocardial Infarction (NSTEMI) 121 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 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 123 ST Segment Elevation MI 124 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 Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 126 Diagnosis of CHD and MI 127 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 “Classic” Manifestations of MI 129 “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 ECG Changes 131 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 ST Segments 133 ST Segments • 1st to change during ischemia or MI because myocardial repolarization is altered. • Ischemia reduces membrane potential and shorten duration of AP in ischemic area. 134 Abnormal Q Waves 135 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 Serum Markers for Ischemia and MI 137 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 CK-MB 139 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 Troponin (TnC, TnI, TnT) 141 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 C-Reactive Protein (CRP) 143 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 Timeline of Cardiac Markers 145 Timeline of Cardiac Markers Troponin CK-MB Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5 146 Acute Coronary Syndrome Concept Map 147 ACS No ST Elevation Unstable Angina Pain is severe No ECG s No change in markers because they are not having an MI STEMI NSTEMI Unstable angina No ECG s Elevation of serum markers, including troponin and CKMB 148 Infarction Diagram 149 150