cardiovascular ii part 2

Cardiovascular II Part 2

PVCPremature Ventricular Contraction

2

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.

3

V-FibVentricular Fibrillation

4

V-FibVentricular Fibrillation

• Ventricle quivers but does NOT contract! – NO cardiac output and no pulses

• Cardiac Arrest!!

• Grossly disorganized pattern

5

V-TachVentricular Tachycardia

6

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

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

13

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

Lehne 5th ed Figure 47-2

Myocardium& His-Purkinje

System

SA Node &AV Node

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Class III Antidysrhythmic

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

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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41

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

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.

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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.

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

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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

meet metabolic demands of the heart58

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

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

81

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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

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

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

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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

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Porth, 2007, Essential of Pathophysiology, 2nd ed., Lippincott, p. 328.

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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risk forMI

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

101

Usual distribution of pain

Less common sites of pain distribution

Typically precordial, substernal

Angina

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– Person usually aware; High risk sudden death104

Variant or Vasospastic AnginaDiagram

105

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

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

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

118

Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 394.

ECGSTEMI vs. NSTEMI

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ECGSTEMI vs. NSTEMI

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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

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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

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 skin130

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

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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

146

Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5

Troponin

CK-MB

Acute Coronary SyndromeConcept Map

147

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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