EKG 2 Flashcards by Steph Nicolette

11 step method

-1. standardization- make sure settings are correct, check pt name and other input information
-2. heart rate
-3. intervals…PR and QT intervals, QRS width
-4. axis
-5. rhythm:
-normal P waves
-QRS wide or narrow
-relationship between P and QRS
-rhythm regular or irregular
-6. AV block?
-7. bundle branch or hemi block
-8. pre-excitation?
-9. enlargement or hypertrophy
-10. ischemia or infarction?
-11. utter confusion?…think of your non-cardiac or unusual conditions

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AV block

-signal is blocked between the sinus node and the terminal purkinje fibers
-first degree
-second degree
-third degree

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bundle branch block

-a block below the bundle of his
-conduction is blocked in one or both ventricular branches
-if only portion of branch is blocked it is called fascicular block or hemiblock
-tissue has electrical disturbance

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first degree AV block

-prolonged delay at level of AV node
-normal sinus signal held longer at AV node
-PR interval greater than 200ms (one big box) -> prolonged PR interval
-every P waves gives a QRS -> all beats conducted but delayed
-every impulse arrive regularly
-the PR interval is increasingly prolonged until it drops

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second degree AV block

-not every impulse arrives to the ventricles
-Two Types!
-1. Mobitz type I second degree AV block (Wenckebach Block):
-Block is within the AV node
-PR interval delay is increasing with each beat then drop
-Longer and longer PR interval then drop and reset of PR interval!
-No intervention needed

-1. Mobitz type II second degree AV block:
-Block below the AV node in the His bundle
-No lengthening PR interval, just drop QRS!
-Evidence of progressive severe conduction system disease requiring a Pacemaker implant

-2:1 when you don’t have PR intervals to compare -> usually make exercise to see a change and identify the issue

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third degree AV block

-no communication between atrial and ventricular conduction
-Site can be AV node or below
-Atria are at the sinus rhythm 60-100 bpm.
-Ventricles will give escape rhythm around 30-40 bpm
-AV dissociation**
-Requires Pacemaker if not reversible
-p waves are regular with each other, QRS are regular -> BUT there is no P:QRS correlation
-atrial rhythm is normal

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bundle branch blocks

-conduction block in either right or left bundle branch
-ventricular conduction should be less than 100 ms with a leftward axis (0-90)
-when width of QRS is greater than 120 ms and the configuration is changed you have a bundle branch block

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right bundle branch block

-Right depolarization is delayed.
-QRS greater than 120 ms
-In V1 see the initial R wave then a second R wave as the delayed right ventricle depolarizes.
-“R-S-R prime”… Rabbit ears.
-In left precordial leads a late deep S wave

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left bundle branch block

-Left depolarization is delayed
-QRS greater than 120ms
-Leads overlying left ventricle have a broad or notched R wave. Lead over the right ventricle have broad deep S wave.
-Left axis deviation may be present

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is that ischemia I see? Nope!

-with RBBB the right precordial leads will show ST segment depressions and T wave inversions
-with LBBB the ST segment and T wave inversion will be seen in left lateral leads
-so cant use ST or T wave dx for ischemia with BBB
-cant use hypertrophy dx rules when BBB

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who gets BBB

-RBBB- diseased conduction or normal phenomenon
-LBBB- rarely normal -> seen in underlying cardiac disease degenerative or ischemic
-critical rate: BBB:
-things only become abnormal when they are doing strenuous activity -> normal otherwise
-BBB can be intermittent or fixed
-sometimes only appears at faster rate “critical rate” -> so normal QRS at slow rate and wide (BBB) at faster rate
-rate related bundle

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hemi-blocks (dont need to know)

-just 1 of 3 fascicles are blocked:
-septal
-left anterior fascicle
-left posterior fascicle

-QRS not wide, no ST segment or T wave changes

-left anterior:
-axis is redirected upward and to the left -> left axis
-tall R waves in left lateral leads and deep S waves in inferior leads

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hemi-block: left posterior

-usually in a diseased heart
-reverse occurs
-current runs superior to inferior and left to right
-right axis deviation

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hemiblock: are we concerned?

-when combined with a RBBB we are concerned!
-together called bifascicular block
-with a disease RBBB and a hemi block only one fascicile is supply both ventricles
-see EKG below for combined LAFB and RBBB

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who needs a Pacemaker?

-sick sinus syndrome- sinus node broken
-mobitz 2- unreliable heart beat
-3rd degree AV block- ventricles and atria arnt talking to each other
-bifascicular block -> RBBB and 1 fascicle (dont need to know this for quiz 1)

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pacemaker on EKG

-straight up and down line
-a straight vertical line is never natural
-vertical line before p wave -> atrial paced beat
-vertical line before QRS -> ventricular paced beat
-vertical line before p and qrs -> AV paced beat

pre-excititation

-an accessory pathway exists that conducts faster than AV node
-less than 1% of the population
-two major syndromes:
-Wolff-Parkinson White (WPW)
-Lown- Ganong- Levine

Pre-excititation: Wolff-Parkinson White (WPW) -> ALWAYS ON THE BOARDS

-Bundle of Kent- the piece of tissue that brings the signal down
-Short PR interval <120 ms with QRS >100 ms
-Slurred upstroke, delta wave
-P and then up slope -> never hits the isoelectric line
-no pause in AV node
-you get this tissue ablated (burned off) -> bc if they go into a fib (most people do when they get older) -> it will rapidly conduct

pre-excititation: Lown-Ganong-Levine (dont need to know)

-James fiber, intra-nodal
-No delta because uses the usual conduction system past AV node. Normal QRS
-Only short PR

MI and ischemia

-MC -> narrowed coronary arteries lead to restricted (ischemia) and then no blood flow -> infarction
-superimposed thrombosis initiated by plaque rupturei
-evolving changes noted on EKG while troponin levels are waiting from the lab

ischemia

-angina is typical chest pain associated with coronary artery disease
-assoc changes with strenuous work
-ST segment depression or T wave inversions*
-segment return to baseline after relief of symptoms
-T wave inversions seen in ischemia
-nonspecific
-can be normal variant in young person in V3-V4
-observed EKG during stress testing

myocardial infarction

-evolving EKG changes
-T wave peaking -> then T wave inversion
-ST segment elevation- injury to myocardium -> Reversible if quick intervention
-appearance of new Q waves
-you never have MI and ischemia at the same time -> it look like it bc the MI is taking blood from a diff area

myocardial infarction: pathological Q waves

-Irreversible myocardial cell death.
-Appear within several hours to several days when ST segment has returned to baseline.
-Caused from electrically silent dead tissue.
-Don’t forget sometimes Q waves are a normal finding from left to right depolarization of the septum.
-Infarction Q waves are greater than 40 ms and depth at least 1/3 of the height of the R wave in the same complex. (Except aVR)

reciprocals

-during an MI there are other leads that have ST depressions
-these areas are known

myocardial infarction: identify posterior infarction (dont have to know posterior MI)

-Right coronary artery -Conventional leads not over posterior -Reciprocal changes in anterior leads -> look for ST segment depression and tall R waves in V1 -Mirror image of an anterior wall MI -RCA also supplies inferior wall so often ST elevation noted in inferior leads -anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium -Because posterior electrical activity is recorded from anterior side of heart -> typical injury pattern of ST elevation and Q waves becomes inverted: -ST elevation becomes ST depression -Q waves become R waves -Terminal T-wave inversion becomes an upright T wave

MI: posterior information

-Posterior infarction accompanies 15-20% of STEMIs -> usually occurring in context of inferior or lateral infarction -Isolated posterior MI is less common (3-11% of infarcts). -Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death. -Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed. -Be vigilant for evidence of posterior MI in any pt with an inferior or lateral STEMI

posterior leads

-Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram below): -V7 – Left posterior axillary line, in the same horizontal plane as V6. -V8 – Tip of the left scapula, in the same horizontal plane as V6. -V9 – Left paraspinal region, in the same horizontal plane as V6

non-Q wave infarction

-T wave inversion and ST segment depressions -> Not elevation! -Lower risk of initial mortality. High risk for a further infarction and mortality. -Think of as a small, incomplete infarction -Prevent the next MI, with aggressive management -not the whole wall -> just small parts -troponin leak -> they will have MI eventually

ischemia: printzmetal angina (not on quiz 1)

-ST segment elevation -Can occur at anytime -Coronary artery spasm* -Returns quickly to baseline with anti-anginal medication, nitroglycerin

hyperkalemia

-progressive evolution -leads to ventricular fibrillation if not corrected -T waves start to PEAK in ALL LEADS -if progresses QRS widens until it merges with T wave then VF -ST segment depression -> flattening of T wave with QT prolongation and U wave -U wave is more prominent than T wave -U wave best seen in the anterior lead -uncontrolled -> torsade -sharp t waves -> prick finger

calcium

-hypocalcemia prolonged QT interval -concerns for torsade de pointes -hypercalemia shortened QT interval

hypothermia

-sinus bradycardia -all segments prolonged -special ST segment elevation seen -> osborn wave osborn wave- abrupt ascent with a plunge to baseline

pericarditis

-Diffuse ST-Segment and T wave changes -A large effusion can cause low voltage and electrical alternans -sinus tach -large s wave in lead 1 deep q in 3, T wave inversion in lead 3

acute pulmonary embolism: board question

-large S wave in lead 1 and deep Q wave in lead 3 -> S1Q3 -T wave inversion in 3 -> S1Q3T3

central nervous system

-CVA events such as subarachnoid bleed or cerebral infarction can produce diffuse T wave inversions and prominent U waves. -Sinus bradycardia often seen.

check for infarction before ischemia