ECG: Ischemia Flashcards
Explain the cellular changes that occur in ischemic myocytes in phase 4
o Decreased O2 supply → anaerobic metabolism
o pH drops
o [H+] activated K+ channels open → K+ efflux
• AKA “K[ATP]” channel but ATP often still present
• Open channel = Cl- follows K+ (charge balance)
• K+ gradient lost (locally)
• Em becomes less negative (depolarizes)
o Na+/K+ ATPase pumps slow, further decrease K+ gradient
o Overall: a temporary, transient state!
• Protective: functionally disable cell’s contractility but allows longer survival during ischemia
Explain the cellular changes that occur in ischemic myocytes in phase 0 or 1
o Membrane potential effect on Na+ channels
• -100 mV = max Na+ channel availability
• -90 mV = high Na+ channel availability
• -60 mV = fast Na+ channels inactivated (nodal)
• -40 mV = myocyte unexcitable
o Decreased Em → decreased Na+ channel availability = decreased rate of depolarization → slower upstroke
o Decreased rate of depolarization → smaller overshoot (phase 1)
Explain the cellular changes that occur in ischemic myocytes in phase 2 or 3
o Plateau phase is lower and shorter
• L-type Ca2+ channels are less active
• K+ current dominates the balance
o Repolarization is quicker and occurs earlier
Explain how ischemia affects the ST segment at the macro level of the ECG
• Normally: ST is flat because cells all at same potential
• With ischemia: now a voltage potential between normal and ischemic tissues
o Surface ECG electrodes nearest ischemic regions register the largest ST segment shift
• During systole: ischemic cells less depolarized in phase 2 than normal cells
o If ischemic tissue appears “closer” to electrode → voltage gradient recorded as upward ST segment
o If ischemic tissue farther → downward shift
Contrast how different ischemic distributions (subendocardial vs. transmural) change the ST segment.
Can elevate ST segment in two ways:
1) Ischemia in epicardium
• Results in gradient towards the electrode
• Results in ST elevation
• Uncommon: ex. Pericarditis or penetrating injury to heart
2) Transmural ischemia
• Caused by acute MI with trans myocardial ischemia
• Results in ST elevation
• More common
Can depress ST segment:
1) Subendocardial ischemia
• Voltage gradient oriented away from electrode
• Results in ST depression
• Subendocardium more vulnerable than epicardium
2) Reciprocal Changes
• When electrode overlies normal myocardium “across” from ischemic injury in large transmural segment on opposite side of heart
• Mirror images of ST segment elevation over true injury site
Utilize the vector orientation of the leads to localize Anterior myocardial infarction to a region of the left ventricle
o Usually due to left anterior coronary artery occlusion
o Seen in leads V1-V4
o May get reciprocal ST depression in inferior leads (injury currents flowing along posterior/superior axis
Utilize the vector orientation of the leads to localize Lateral myocardial infarction to a region of the left ventricle
o Usually due to circumflex coronary artery occlusion
o Seen in leads V3-V6, I, aVL (especially V5 and V6)
Utilize the vector orientation of the leads to localize Inferior myocardial infarction to a region of the left ventricle
o Usually due to posterior descending artery (from the right coronary) occlusion
• In 15% population, could be from dominant circumflex artery
o Seen in leads II, III, and aVF
o May get reciprocal ST depression in V1-V3
Explain the mechanism of T wave inversion during myocardial infarction.
o Often in leads showing ST elevation or near border zone of injury
o Also due to altered duration of AP repolarization
o Caused by potential gradients between ischemic and normal regions during repolarization phase
• Ischemic cells: shorter AP, repolarizes early
o Negative T wave if net repolarization vector directed from endo- to epicarium → T wave inversion in leads over injured region
o Usually begins >24 hours, maximized >72 hours
o Not specific to ischemia
• Also in hypertrophy, metabolic changes, drugs, drinking ice water, normal variant in some leads (III, V1-V2)
• Only supports diagnosis of ischemia
o Gradually resolve over few weeks
Explain the mechanism of Q wave development during myocardial infarction.
• Q wave development
o As myocardium dies → area becomes electrically silent
• Depolarization occurs away from infarct → negative deflection (Q wave) on surface ECG leads
o Develop 6-12 hours after infarction
o Diagnostic criteria: • Depth >1 mm • Duration >40 ms • Seen in 2 or more adjacent leads • Associated with characteristic acute ischemic ST and T changes
Discuss the typical time progression of ECG changes in a classic “Q-wave” MI.
Acute phase (minutes-few hours)
o Tall peaked T waves (may be early and missed)
o ST elevation in leads overlaying injury segments
• Possible reciprocal changes
o Gradual T wave inversion over injury site and border regions
Evolving phase (>6 hours- several days)
o ST elevation gradually decreases
o Q waves develop
o Continued T wave inversion over injury site and border regions
Resolving phase (2 weeks –months)
o ST elevation resolves
o T waves revert to upright or may remain variable inverted
o Q waves persist but may partially resolve in small infarcts
LV aneurysm (weeks- months)
o Persistent ST elevation over infarct site
• May increase with tachycardia
o Do imaging study to identify
