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30 Cards in this Set
- Front
- Back
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A systematic approach to looking at EKG
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Rate
Rhythm Intervals (PR/QRS/QT) Axis (we won't do) Hypetrophy (we won't do) Infarct (=QRST changes) |
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Sweep speed
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The “sweep speed” of this EKG (how fast the electronic pen moves across the paper) is 25 mm/s.
-Each little box is 1 mm -So 25 mm/s = 25 little boxes per second Each big box contains 5 little boxes -So there are 5 big boxes per second |
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Rate: the 300 rule, 10 second EKG strip
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300 bpm = 1 beat for every big box
Divide 300 by number of big boxes for each interval to get rate Irregular rhythm? -Each EKG is 10 second strip -Count total QRS complexes and multiply by 6 |
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Key questions of rhythm analysis
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Is the rhythm regular?
Are there P waves? -If so, is the P wave upright in lead II (r arm to l leg)? The route from SA to AV node. Is the P related to the QRS? |
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Atrial fibrillation EKG
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Atrial (and usually ventricular) rhythm are irregular
Look for P wave, irregular |
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Atrial flutter EKG
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The atrial rhythm is regular
Ventricular rhythm can be regular or irregular depending on AV node conduction Typical appearance is "sawtooth pattern" of atrial flutter waves in inferior leads (leads II, III, aVF) |
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Junctional escape rhythm EKG
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No P waves
This is a junctional escape rhythm with no atrial activity at all The sinus node is not working Yes, it’s a little slower than 40 bpm, but it’s still a junctional rhythm (narrow QRS) |
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Sinus rhythm EKG
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Regular rhythm, one P wave for every QRS
And the P wave is upright in lead II |
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Ectopic atrial rhythm EKG
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Inverted P wave in lead II
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Complete AV Block and ventricular escape rhythm EKG
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P wave not related to QRS
QRS wide Slow rate |
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PR interval
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Verify sinus rhythm (upright P-wave in II)
-If not sinus rhythm, PR interval is less useful --Whether it’s useful depends on the specific arrhythmia Precise measurement is not usually necessary (unless you have my job) All that really matters is whether the PR is short, prolonged, or normal. Normal=less than 1 big box and more than three little boxes |
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Short PR interval
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Main context of this is WPW syndrome
Accessory pathway conducts more quickly than normal AV node, so conduction time from atrium to ventricle is shorter than normal The “delta wave” is the beginning of the QRS - and it’s early |
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Prolonged PR interval
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Unfortunately, this is also called “first-degree AV block”
-A misnomer, because there is no block – all the P waves get through -The term is very entrenched, so learn it Beginning of P wave to beginning of QRS is greater than one large block |
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Types of heart block
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First-degree AV block
-Not really block, just very slow conduction through the AV node -Beginning of P wave to begining of QRS is greater than one large block -No P waves are dropped (if even one is dropped, it becomes second degree) Second-degree AV block -Some P waves are blocked and never make it to the ventricles -But only one P wave blocked at a time Third-degree AV block (Complete AV block) -No P waves are conducted -Hopefully some kind of escape rhythm takes over |
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Second degree AV block
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Mobitz 1 (Wenckebach)
-Almost always within the AV node -Can be caused by drugs that affect the AV node -Usually responds to atropine, isoproterenol, dopamine while waiting for pacemaker implant or for offending drugs to “wash out” -PR interval prolongs before block, then shortens up a bit with the next beat, then starts prolonging again… -QRS is usually normal width (normal QRS interval) Mobitz 2 Usually below the AV node (His bundle or LBBB+RBBB) -Not caused by drugs Very rare exceptions exist Rarely responds to meds – need urgent pacemaker PR interval constant and then suddenly blocks QRS is usually wide -Usually due to a bundle branch block (as seen intermittently here) |
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Third degree AV block (AKA complete heart block)
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No P waves are conducted
Atrium and Ventricle have their own separate rhythms with no connection to each other (AV dissociation) |
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QRS interval
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All that matters (to you guys at this point) is whether the QRS is normal or wide. Exact measurement is unnecessary
Use the lead with the widest QRS for measurement If the QRS is wider than three small boxes (>120 ms) then it’s wide |
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Importance of assessing intervals early
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Wide QRS prevents assessment of chamber enlargement (hypertrophy)
Wide QRS makes ST changes much more difficult to interpret -Left Bundle Branch Block can obscure an underlying ST elevation MI |
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Right bundle branch block
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Initial activation normal, then right bundle is delayed, so next is left ventricle alone, then finally right ventricle alone (slow muscle conduction, no His/purkinje system)
Only care about leads I, V1, and V6 "Rabbit ears" in V1, RsR' -may vary, most important component is significant R wave I and V6 show scooped out S |
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Left bundle branch block
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LBBB – initial septal activation is abnormal – Right septum is
activated first, starts to send current toward left. Right ventricle is activated normally, but is overshadowed by beginnings of Left ventricular depolarization. Then slowly depolarizing Left ventricle takes over. Right ventricular component is never really seen. In effect, the whole process goes toward the left. Only care about leads I, V1, and V6 -V1 is deep, wide, all negative -I and V6 are all positive |
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Wolff-Parkinson-White EKG
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Three characteristics:
-Wide QRS -Delta wave -Short PR interval Can be confused with BBB |
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QT interval
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Rule of thumb: QT is prolonged if it is more than half the R-R interval
-For measurements: exact cutoff values a bit fuzzy, but if QT > 500, then definitely prolonged Rule of thumb and absolute measurements only work if HR < 100 -For HR >100, need “corrected” QT (QTc) |
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Causes of acquired long QT
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Drugs
-Class IA and III antiarrhythmics, TCA’s, phenothiazines, quinolones and apparently, Methadone Electrolytes -Hypo-K+, Hypo-Mg++, Hypo-Ca++ Neurologic -CVA, intracerebral hemorrhage, coma Bundle Branch Block (by lengthening the QRS interval, which is part of the QT interval) Myocardial ischemia / infarction |
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Coronary artery dominance
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Posterior descending artery (PDA)
-In 85% of people, the PDA is a branch of the right coronary artery (RCA) --Heart is called “right dominant” -In 15%, PDA arises from the Left Circumflex Artery (LCx) --Heart is called “left dominant |
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Posterior descending artery
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Supplies the inferior surface of the left ventricle
-So, an “inferior myocardial infarction” means there has been damage in the area supplied by the posterior descending artery Level of occlusion can be within the PDA itself, or could be “upstream” -If the patient is right dominant, then upstream damage is within the RCA -If the patient is left dominant, then upstream damage is within the LCx (left circumflex) |
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Basic lead groups, heart locations, and arteries involved
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Inferior:
Leads -II, III, aVF Arteries -PDA (85% from RCA, 15% from LCx) Septal: Leads -V1, V2 Arteries -Always LAD Anterior: Leads -V2, V3, V4 Arteries -Always LAD Anterolateral: Leads -V5, V6 Arteries -Nearly always LCx Lateral: Leads -I, aVL Arteries -LCx Posterior: Leads -Inverse of V1, V2, V3 Arteries -Usually LCx |
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Normal Q waves
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Some leads normally have big Q waves
-Would otherwise meet criteria as pathologic Q waves if present in other leads -aVR – who cares? -V1 and III – very common to have big Q waves, on a normal EKG -aVF and aVL – occasionally… This is one reason why it helps to have the same pattern in 2 anatomically contiguous leads: -Q wave in I and aVL? Probably lateral MI -Q wave in II and III? Probably inferior MI -Q wave only in III? Probably nothing |
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ST segment changes
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ST elevation means acute transmural injury at the part of the heart evaluated by that EKG lead
ST depression means active ischemia -Some exceptions, though… |
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T wave inversion
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Can be a sign of ischemia
-But can also be seen in LVH and some other things -Notice in all these cases, the T wave is going in the opposite direction of the QRS and the QRS is not wide – so they’re all abnormal |
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Normal T wave inversion
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V1 has an inverted T wave in most normal EKGs
Lead III and aVR also frequently have inverted T waves in normal EKGs |
