2025 ECG Quiz 5 Flashcards

Myocardial Ischemia and Infarction

1
Q

WHAT IS MYOCARDIAL
INFARCTION

A

Occlusion of coronary arteries = acute
coronary syndrome
* Causes myocardial hypoperfusion resulting in
cellular death

AKA: “Heart attack”

May lead to:
* Arrhythmias
* Heart failure
* Cardiogenic shock
* Heart rupture
* Cardiac arrest
* Death

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2
Q

WHAT CAUSES
MYOCARDIAL INFARCTION

A

Coronary Artery Disease
* Narrowing caused by build up of plaque (atherosclerosis)

Coronary Thrombosis
* Blood clot blockage.
* Commonly associated with
coronary narrowing due to
atherosclerosis.

Coronary Artery Spasm
* Cocaine, stress, cold, etc.

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3
Q

ACUTE CORONARY
SYNDROME

A

Any condition brought on by a sudden reduction or
blockage of blood flow to the heart

Stable angina vs Unstable
angina

NSTEMI vs STEMI

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4
Q

STABLE VS UNSTABLE
ANGINA

A

Stable angina: vessel unable
to dilate enough to allow
adequate blood flow

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5
Q

STABLE VS UNSTABLE
ANGINA

A

Unstable angina: Thrombus
forms on ruptured plaque
causing partial occlusion

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6
Q

NSTEMI VS STEMI

A

Non-STEMI
* Partial occlusion
* Cellular death occurs in
subendocardial tissue

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7
Q

NSTEMI VS STEMI

A

STEMI
* Total occlusion
* True emergency
* Cellular death occurs
throughout entire wall of
heart, or transmural

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8
Q

3 COMPONENTS OF MI
DIAGNOSIS

A

History and physical exam

Cardiac enzymes

ECG changes

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9
Q

HISTORY AND PHYSICAL
EXAM

A

Prolonged, severe chest pain
* Classic symptom of cardiac ischemia
* Diffuse chest pain
* May radiate to jaw, neck, left arm, back
* Angina: ischemic chest pain
* Generalized weakness
* Lightheadedness and syncope
* Shortness of breath
* Diaphoresis and pallor
* Nausea and vomiting
* Anxiety/”feeling of impending doom”

Woman and Diabetics can show Atypical signs… dont see the crushing chest pain

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10
Q

CARDIAC ENZYMES

A

Troponin (TnI, TnT)
* Most important cardiac marker
* High sensitivity and specificity
* Rises early and stays elevated
longer than other enzymes
* Valuable for early/late detection
* Provides information pertaining to
acute MI severity and reperfusion

Myoglobin
* Limited specificity, but
high sensitivity makes it
useful for early
detection.

Creatine kinase MB isoenzyme (CKMB)
* High sensitivity & specificity = valuable in assessment of AMI severity & reperfusion
* Limited value early/late

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11
Q

ELECTROCARDIOGRAM

A

During an AMI, the ECG evolves
through 3 stages:
* T wave peaking followed by T wave inversion
* ST segment elevation
* Appearance of new Q waves
* Changes begin immediately after
infarct.
* 12-lead EKG can help aid in localization of infarct.

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12
Q

TREATMENT OF MI

A

THROMBINS2
* Thienopyridines
* P2Y12 receptor blockers
* Heparin/enoxaparin, Reninangiotensin
system blockers
* Oxygen
* Morphine
* Beta blocker
* Intervention
* Nitroglycerin
* Statin
* Salicylate (Aspirin)

Management:
* IV Access, ECG, Cardiac
Monitoring, SpO2, CXR
* Send Cardiac Enzyme Labs
* Begin THROMBINS2 if suspected MI from ECG
* Consider revascularization
interventions:
Percutaneous coronary
Intervention (PCI)
Intra-coronary stent (ICS)
Coronary artery bypass graft (CABG)

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13
Q

ST SEGMENT
ELEVATION
MI (STEMI)

A
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14
Q

T WAVE ALTERATIONS

A

1st sign: T waves peak
* Changes due to local hyperkalemia in ischemic myocardium.
* At this point ischemia can be reversible if blood flow is restored promptly
* Must be in two sequential anatomical leads i.e. V1,V2; V5,V6

Hours later: T waves invert
* May persist for months to years.
* Note: T-wave inversion can occur due to causes other than MI. However, in MI, T waves invert symmetrically.

Young kids might have inverted T-Wave normal???

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15
Q

T WAVE ALTERATIONS

A

Young kids might have inverted T-Wave normal???

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16
Q

ST SEGMENT ELEVATION

A
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17
Q

Q WAVE APPEARANCE

18
Q

WHY Q WAVES FORM

A

Myocardium dies and cannot conduct
electrical current.

Electrical forces move away from area of infarction.

Causes deep negative deflection, a Q wave.

19
Q

RECIPROCAL CHANGES

A

Electrical forces move toward sites distant from infarction.

Affect ST segment (depression), Q waves,
and T waves.

20
Q

STEMI SUMMARY

A

T wave “peaks”

Signifies myocardial ischemia

ST segment elevation; merges with T wave

Signifies myocardial injury

Signifies to baseline within a few hours

T Wave inverts
* Inverts symmetrically
* May resolve or persist for months/years

New Q waves appear

Signifies permanent myocardial
infarction
* Persist for lifetime of patient

21
Q

PEAKED T
WAVES

22
Q

ST SEGMENT
ELEVATION

23
Q

Q WAVE
APPEARANCE

A

Q-Waves can persist for life

24
Q

STEMI-LOCALIZING THE
INFARCT

A

Location of infarct affects prognosis and
treatment.

Two major systems of blood supply to
myocardium:
* Right coronary artery

  • Left coronary artery (left main coronary artery):
  • Left anterior descending artery
  • Left circumflex artery
25
Q

ANATOMICAL
CATEGORIES OF
INFARCTION

A

Inferior

Lateral

Anterior

Posterior

26
Q

ANATOMICAL
CATEGORIES OF
INFARCTION

A

Inferior

Lateral

Anterior

Posterior

27
Q

LOCALIZING
ACS AND
INFARCTION

28
Q

INFERIOR
INFARCTION

29
Q

LATERAL
INFARCTION

30
Q

ANTERIOR
INFARCTION

31
Q

POSTERIOR
INFARCTION

A

Since no ECG lead reflects posterior electrical activity, changes are reciprocal of those in anterior leads

Can attach V8 and V9??? Look at more

32
Q

RIGHT VENTRICULAR
INFARCTIONS

33
Q

PRACTICE

A

V6 - large ST elevation
Also in aVF and aVL

Lateral infarction

34
Q

PRACTICE

A

V2 and V3 - ST elevation

Peaked T-Waves

Anterior infarction

35
Q

PRACTICE

A

Lead II - ST Elevation
Lead I and aVF - small ST Elevation

Inferior and Lateral Infarction

36
Q

PRACTICE

A

Inferior and Lateral Infarction

37
Q

NON-STEMI

A

More common than STEMIs.

NO ST-segment elevation or deep Q waves.

Only changes are T-wave inversion and ST depression

Usually caused by either:
* Nonocclusive thrombosis of major
coronary artery
* Complete occlusion of small offshoot

Involve less than entire thickness of heart muscle

Lower initial mortality; higher later re-infarction mortality

38
Q

DISTINGUISHING ANGINA
FROM NON-STEMI

A

EKG findings resemble those of a non- STEMI
* ST-segment depression
* T-wave inversion

Distinction is made by measuring cardiac
enzymes:
* Significantly elevated with a non-
STEMI
* Normal with uncomplicated angina

Angina associated with ST elevation and normal enzymes, the T is different though? = Crinsmetal Ingina? From the book… look at more

39
Q

SORTING OUT THE DIFFERENT ISCHEMIC
SYNDROMES

40
Q

LIMITATIONS OF THE ECG
IN DIAGNOSING INFARCTION

A

Diagnosis of myocardial infarction with
EKG relies on:
* T-wave changes
* ST-segment changes
* Q-wave formation

Some underlying cardiac conditions
mask these effects:
* Wolff–Parkinson–White
* Left ventricular hypertrophy
* Left bundle branch block… if see on ECG, need to rule out infarction before can do anything (will never show the ST changes)