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Le#  Posterior  Hemiblock  

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Ischemic Heart Disease

�  Is most commonly due to atherosclerosis in coronary arteries

�  Ischemia occurs when blood supply to tissue is deficient �  Causes increased lactic acid from anaerobic metabolism

�  Often accompanied by angina pectoris (chest pain)

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CHEST  PAIN      

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259

ST Segment

•  Normal ST Segment is flat (isoelectric) – Same level with subsequent PR segment

•  Elevation or depression of ST segment by 1 mm or more, measured at J point IS ABNORMAL

•  “J” (Junction) point is the point between QRS and ST segment

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What’s a J point and where is it? •  J point – point to

mark end of QRS and beginning of ST segment – Evaluate ST elevation

0.04 seconds after J point

– Based on relationship to the baseline

– Used in assessing ST elevation

Ischemic Heart Disease

�  Detectable by changes in S-T segment of ECG

� Myocardial infarction (MI) is a heart attack �  Diagnosed by high levels of creatine phosphate (CPK) &

lactate dehydrogenase (LDH)

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Measuring for ST Elevation •  Find the J point •  Is the ST segment

>1mm above the isoelectric line in 2 or more contiguous leads?

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EARLY  REPOLARIZATION  

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Characteristic changes in AMI

�  ST segment elevation over area of damage

�  ST depression in leads opposite infarction

�  Pathological Q waves

�  Reduced R waves

�  Inverted T waves

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Myocardial Insult •  Ischemia

–  lack of oxygenation – ST depression or T wave inversion – permanent damage avoidable

•  Injury – prolonged ischemia – ST elevation – permanent damage avoidable

•  Infarct – death of myocardial tissue; damage

permanent; may have Q wave 4/18/12 badri@gmc 266

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ST elevation

R

P

Q

ST

•  Occurs in the early stages

•  Occurs in the leads facing the infarction

•  Slight ST elevation may be normal in V1 or V2

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Variable Shapes Of ST Segment Elevations in AMI

Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th ed: Mosby Elsevier; 2006. 4/18/12 badri@gmc 268

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Deep Q wave

R

P

Q

T

ST

•  Only diagnostic change of myocardial infarction

•  At least 0.04 seconds in duration

•  Depth of more than 25% of ensuing R wave

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T wave changes

R

P

Q

T

ST

•  Late change

•  Occurs as ST elevation is returning to normal

•  Apparent in many leads

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Bundle branch block

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Anterior wall MI Left bundle branch block

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Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q!

R!

P!

Q!T!

ST R!

P!

Q!

ST

P!

Q!T!

ST

R!

P!

S

T

P!

Q!T!

ST

R!

P!

Q!

T!

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Evolution of AMI A - pre-infarct (normal) B - Tall T wave (first few

minutes of infarct) C - Tall T wave and ST

elevation (injury) D - Elevated ST (injury),

inverted T wave (ischemia), Q wave (tissue death)

E - Inverted T wave (ischemia), Q wave (tissue death)

F - Q wave (permanent marking) 4/18/12 badri@gmc 274

EVOLUTION  OF  MI  

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Diagnostic criteria for AMI

•  Q wave duration of more than 0.04 seconds

•  Q wave depth of more than 25% of ensuing r wave

•  ST elevation in leads facing infarct (or depression in opposite leads)

•  Deep T wave inversion overlying and adjacent to infarct

•  Cardiac arrhythmias

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ACUTE  INFARCTION  

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Location of infarct combinations

aVR V1 V4 I

II

III

LATERAL

INFERIOR

ANT POST ANT

SEPTAL

ANT

LAT

aVL

aVF

V2

V3

V5

V6

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Lateral View – I, aVL, V5, V6

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Lateral infarction Lateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflex coronary artery 4/18/12 badri@gmc 280

Complications of Lateral Wall MI I, aVL, V5, V6

•  Monitor for lethal heart blocks

– Second degree type II – classical – Third degree heart block – complete

• Treat with TCP – Consider sedation for patient comfort – Monitor for capture – Monitor for improvement by measuring level

of consciousness and blood pressure 4/18/12 badri@gmc 281

Inferior View – II, III, aVF

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Inferior infarction Inferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery 4/18/12 badri@gmc 283

Complications of Inferior Wall MI II, III, aVF

•  May see Mobitz type I – Wenckebach –  Due to parasympathetic stimulation & not injury to conduction

system

•  Hypotension –  Right ventricle may lose some pumping ability

•  Venous return exceeds output, blood accumulates in right ventricle

–  Less blood being pumped to lungs to left ventricle and out to body

– Develop hypotension, JVD, with clear lung sounds •  Treated with additional fluid administered cautiously •  Ems to contact Medical Control prior to NTG administration

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Septal View – V1 & V2

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Complications of Septal Wall MI V1 & V2

•  Monitor for lethal heart blocks – Second degree type II – classical – Third degree heart block – complete

•  Treat with TCP

•  Rare to have a septal wall MI alone – Often associated with anterior and/or lateral

wall involvement

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Anterior View – V3 & V4

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Anterior infarction Anterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary artery

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Complications of Anterior Wall MI V3 & V4

•  Occlusion of left main coronary artery – the “widow maker” –  Cardiogenic shock and death without prompt reperfusion

•  Second degree AV block type II –  Often symptomatic –  Often progress to 3rd degree heart block –  Prepare to initiate TCP

•  Third degree heart block – complete –  Rhythm usually unstable –  Rate usually less than 40 beats per minute –  Prepare to initiate TCP

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ST T changes- MI anteroseptal/// axis???

�  ST T in V1-V5/ aVL

�  Axis

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ST    DEPRESSION  

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�  ST in V1-V4

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ISCHEMIC    T    WAVES  LAHB    RBBB  

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INFEROLATERAL  ISCHEMIA  

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Hypertrophy Strain Pattern vs. ACS

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DIGOXIN  EFFECT  

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PERICARDITIS  

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Patient Presenting with Coronary Chest Pain – AMI Until Proven Otherwise

•  Oxygen –  May limit ischemic injury –  New trends/guidelines coming out in 2011 SOP’s

•  Aspirin - 324 mg chewed (PO) –  Blocks platelet aggregation (clumping) to keep

clot from getting bigger –  Chewing breaks medication down faster & allows

for quicker absorption –  Hold if patient allergic

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•  Nitroglycerin - 0.4 mg SL every 5 minutes –  Dilates coronary vessels to relieve vasospams –  Increases collateral blood flow –  Dilates veins to reduce preload to reduce

workload of heart •  Watch for hypotension •  If inferior wall MI (II, III, aVF), contact Medical

Control prior to administration –  If pain persists, move to Morphine –  Check for recent male enhancement drug use

(ie: viagra, cialis, levitra) •  Side effect could be lethal hypotension

Acute Coronary Syndrome Medications cont.

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Acute Coronary Syndrome Region X EMS Medications cont.

•  Morphine - 2 mg slow IVP – Decreases pain & apprehension – Mild venodilator & arterial dilator

• Reduces preload and afterload – Given if pain level not changed after

nitroglycerin – Give 2mg slow IVP repeated every 2 minutes

as needed – Max total dose 10 mg

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T wave •  The normal T wave is asymmetrical, the

first half having a more gradual slope than the second half

•  The T wave should generally be at least 1/8 but less than 2/3 of the amplitude of the corresponding R wave

•  T wave amplitude rarely exceeds 10 mm •  Abnormal T waves are symmetrical, tall,

peaked, biphasic or inverted.

T wave

•  As a rule, the T wave follows the direction of the main QRS deflection. Thus when the main QRS deflection is positive (upright), the T wave is normally positive.

•  Other rules – The normal T wave is always negative in lead

aVR but positive in lead II. – Left-sided chest leads such as V4 to V6

normally always show a positive T wave. 306

HYPERKALEMIA: PEAKED T WAVES

See a normal EKG…

HYPOKALEMIA: PROMINENT U WAVES

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QT interval •  QT interval decreases when heart rate increases •  A general guide to the upper limit of QT interval.

For HR = 70 bpm, QT<0.40 sec. –  For every 10 bpm increase above 70 subtract 0.02

sec. –  For every 10 bpm decrease below 70 add 0.02 sec

•  As a general guide the QT interval should be 0.35- 0.45 s, and should not be more than half of the interval between adjacent R waves (R-R interval).

QT Interval

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Long QT Syndrome

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Prolonged QTc

•  During sleep •  Hypocalcemia •  Ac myocarditis •  AMI •  Drugs like

quinidine,procainamide,tricyclic antidepressants

•  Hypothermia •  HOCM

•  Advanced AV block or high degree AV block

•  Jervell-Lange –Neilson syndrome •  Romano-ward syndrome

Shortened QT

•  Digitalis effect •  Hypercalcemia •  Hyperthermia •  Vagal stimulation

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QT Interval

•  The QT interval increases slightly with age and tends to be longer in women than in men.

•  Bazett's correction is used to calculate the QT interval corrected for heart rate (QTc): QTc = QT/ Sq root [R-R in seconds]

U wave •  Normal U waves are small, round, symmetrical

and positive in lead II, with amplitude < 2 mm (amplitude is usually < 1/3 T wave amplitude in same lead)

•  U wave direction is the same as T wave direction in that lead

•  More prominent at slow heart rates and usually best seen in the right precordial leads.

•  Origin of the U wave is thought to be related to afterdepolarizations which interrupt or follow repolarization

Final Impression “ Does the ECG correlate with the clinical scenario ?”