cardiovascular ii part 2
DESCRIPTION
Cardiovascular II Part 2. PVC Premature Ventricular Contraction. 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. - PowerPoint PPT PresentationTRANSCRIPT
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Cardiovascular II Part 2
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PVCPremature Ventricular Contraction
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PVCPremature 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.
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V-FibVentricular Fibrillation
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V-FibVentricular Fibrillation
• Ventricle quivers but does NOT contract! – NO cardiac output and no pulses
• Cardiac Arrest!!
• Grossly disorganized pattern
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V-TachVentricular Tachycardia
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V-TachVentricular 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
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Class I AntidysrhythmicsDiagram
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Lehne 5th ed Figure 47-2
Myocardium& His-Purkinje
System
SA Node &AV Node
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Class I Antidysrhythmic
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Class 1B: Lidocaine Ventricular Dysrhthmias
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Class 1B: Lidocaine Ventricular Dysrhythmias
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Class 1B: LidocaineEffects on the Heart and the ECG
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Class 1B: LidocaineEffects 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
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LidocainePrecautions and Adverse Effects
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LidocainePrecautions 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
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LidocaineAdministration
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LidocaineAdministration
• 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
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Class III AntidysrhythmicsPotassium Channel Blockers
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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
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Initial catecholamine release brief exacerbation of dysrhythmias
- Catecholamines speed up the heart and lead to stronger heart beatsblock catecholamine release vasodilation /
hypotension
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Lehne 5th ed Figure 47-2
Myocardium& His-Purkinje
System
SA Node &AV Node
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Class III Antidysrhythmic
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Non-Pharmacologic Treatment of Dysrhythmias
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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
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Automated External Defibrillator
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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.
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Implantable Cardioverter/Defibrillator
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Implantable Cardioverter/Defibrillator
• Like a pacemaker
• Monitors and analyzes rhythm
• Delivers shock to terminate V-tach, V-fib
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Radiofrequency Catheter Ablation
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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
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Antidysrhythmic DrugsSummary
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Antidysrhythmic DrugsSummary
• 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
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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
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Management of Cardiac Dysrhythmias
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Management of Cardiac Dysrhythmias
REMEMBER:Many drugs used to treat dysrhythmias
also may worsen them or cause new ones!
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CORONARY HEART DISEASE ANDACUTE MYOCARDIAL INFARCTION(MI OR AMI) 34
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Coronary Circulation
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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
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Coronary CirculationDiagram
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LV LV
Coronary CirculationDiagram
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Coronary Arteries
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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
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ISCHEMIC HEART DISEASEA.K.A CORONARY HEART DISEASE A.K.A CORONARY ARTERY DISEASEANGINAMYOCARDIAL INFARCTION
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Coronary Heart Disease
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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
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Assessment of Coronary Blood Flow
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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
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Collateral Circulation
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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.
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Collateral CirculationDiagram
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Collateral CirculationDiagram
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Pathogenesis of CAD Atherosclerosis
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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
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Plaque
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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.
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Plaque Rupture
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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
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Atherosclerosis in Coronary Artery
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Atherosclerosis in Coronary ArteryPlaque 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
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Angina
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Angina
• Angina: symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia
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Stable Angina
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Stable Angina
• Occurs with exertion or stress
• Predictable
• If plaque becomes unstable and ruptures, it leads to platelet aggregation and unstable angina
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Variant or Vasospastic Angina
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Variant or Vasospastic Angina
• Occurs during rest or with minimal activity (nocturnal, Prinzmetal’s)
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Silent Myocardial Ischemia
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Silent Myocardial Inschemia
• Occurs in the absence of anginal pain– Tend to be endocardial, in the inner layer of the
myocardium
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Unstable Angina
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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
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Acute Myocardial Infarction
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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
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Characteristics of Plaque Rupture
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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
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“Severe” Coronary Stenosis and Vulnerable Plaques Co-exist
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“Severe” Coronary Stenosis and Vulnerable Plaques Co-exist
78Califf, Atlas of Heart Diseases 2001
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Ischemia, Injury, and Infarction
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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
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Zones of Tissue Damage
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Zones of Tissue DamageGoal 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
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An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis
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An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis
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Pathologic Changes in Zones of Injury
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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
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Extent of the Infarct
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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
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Types of Infarct
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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
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Types of Coronary Heart Disease
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Chest Pain Assessment
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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
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Categories (PQRST)
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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
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Chronic Ischemic Heart Disease
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Stable Angina
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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
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Locations of Angina
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Usual distribution of pain
Less common sites of pain distribution
Typically precordial, substernal
Angina
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Variant or Vasospastic Angina
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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 death104
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Variant or Vasospastic AnginaDiagram
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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 AnginaDiagram
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Acute Coronary Syndrome (ACS)
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Acute Coronary Syndrome (ACS)
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NSTEMI STEMI
Unstable or ruptured plaque
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Acute Coronary Syndrome (ACS)
Unstable Angina
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Acute Coronary Syndrome (ACS)Unstable Angina
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Unstable Angina• Severe
• Clinical syndrome of myocardial ischemia ranging between stable angina and MI
• Usually due to atherosclerotic plaque disruption, platelet aggregation
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Presentations of Unstable Angina
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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
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Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 114
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Acute Coronary Syndrome (ACS)ST-segment Elevation
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Acute Coronary Syndrome (ACS)ST-segment Elevation
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ST Segment Elevation
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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
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ECGSTEMI vs. NSTEMI
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ECGSTEMI vs. NSTEMI
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Non ST Segment Elevation Myocardial Infarction (NSTEMI)
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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
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Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 123
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ST Segment Elevation MI
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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
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Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392. 126
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Diagnosis of CHD and MI
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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
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“Classic” Manifestations of MI
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“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 skin130
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ECG Changes
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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
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ST Segments
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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.
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Abnormal Q Waves
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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
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Serum Markers for Ischemia and MI
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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
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CK-MB
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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
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Troponin (TnC, TnI, TnT)
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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
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C-Reactive Protein (CRP)
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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
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Timeline of Cardiac Markers
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Timeline of Cardiac Markers
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Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5
Troponin
CK-MB
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Acute Coronary SyndromeConcept Map
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NSTEMIUnstable angina
No ECG sElevation of serum markers, including troponin and CK-MB
Unstable AnginaPain is severeNo ECG sNo change in markers because they are not having an MI
ACS
No ST Elevation STEMI
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InfarctionDiagram
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