• Shuffle
Toggle On
Toggle Off
• Alphabetize
Toggle On
Toggle Off
• Front First
Toggle On
Toggle Off
• Both Sides
Toggle On
Toggle Off
• Read
Toggle On
Toggle Off
Reading...
Front

### How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

Play button

Play button

Progress

1/40

Click to flip

### 40 Cards in this Set

• Front
• Back
 how might you calculate the the voltage criteria in LVH (left ventricular hypertrophy) look at S in V1 and R in V5 and if it is over 35 then you probably have LVH what kind of AV block involves a prolonged PR interval and continuously declining frequency of QRSs first degree what happens in LV hypertrophy to the ST segment ST strain hypertophy produces ST segment depression (subendocardial hypoxia in the hypertophied ventricle) why might you get an enlarged P wave's negabie component in V1 with LVH due to left atrial enlargement (LAE) it is defined if the P wave is negative in V1 at least 1mm deep and at least .04 seconds long) if the you have RVH then the initial (positive component) of the P wave would be larger. remember diphasic P waves are a sign of hypertrophy what happens to the QRS duration in LVH it is greater than .09 seconds each criteria for LVH is assigned points. There are 6 criteria. what are they and how many points is assigned to each 1. voltage criteria - 3pts 2. ST depressoin - 3 pts 3. LAE - 3 pts 4. L axis devation - 2 pts 5. QRS duration over .09 sec - 1 pt 6. intrinsicoid deflection - 1 point if points are over 4 is probable LVH and if its 5 pts - it is definated as LVH what kind of deviation do you get with RVH Right axis deviation (negative QRS in lead I) how do evaluate the voltage in RVH you compare the relative sizes os R and S waves in V1 and V6. the waves will be great in right leads should be greater what is the right ventricular "strain" pattern ST-T depression in right sided leads explain what is meant by a Q wave infarction a pathological Q wave is one that is at least .04 seconds wide and at least 1/4the the magnitude of the remaining R wave. An infarct large enough to produces this is called a Q wave infarction or an transmural infarction. a small infarct is called a non-Q wave or nontransmural infarction. an Anterior MI (Left anterior descending artery) will produce pathological Q waves in what leads V1 - V4 An inferior MI involves what artery and produces pathological Q waves in what leads posterior descending artery pathological Q waves in II, III, aVF A lateral MI involves what artery and produces pathological Q waves in what leads I,aVL, V5, V6 how does infarcted muscle versus ischemic muscle affect an ECG differently infarcted muscle is dead - it has large Q wave and possible St elevation. ischemic mscle is still viable and will show depression of the ST (also in subendocardial infarct) 5 causes for spontaneous depolarization of the His Purkinje fibers (fast fibers) 1. Increased Sympathetic Tone (drugs, anxiety, etc) 2. Hypolalemia 3. Hypoxia or ischemia 4. Digitalis toxicity 5. Atrial Enlargement what ST segment characterisitic is seen in someone with typical angina ST-depression - sign of subendocardial ischemia. T wave inversion happens when? with ischemia (symmetrical) LVH (assymetrical) how do you check for a BBB look for RR' in right (v1,v2)and left chest leads (v5,v6) what is the first sign of transmurel ischemia a peaked symmetrical T wave also seen in hyperkalemia a q wave indicating necrosis would have what measurements on an ECG at least 1 mm wide and 1/3 the amplitude or more of the QRS what EKG characterisitics persist after an infarction T wave inversion disappears over months and Q waves remain as evidence of prior infarction W/ a LBBB you would see a wide positive QRS (>.12 seconds)with RR' in what chest leads V5 and V6 for a RBBB you would look for this in V1 and V2 LBBB can mimic on the EKG what other three differential diagnosis LVH anterior infarction inferior infarction so these diagnosis cannot be made in the presense of LBBB in order to make the diagnosis of a BBB you need a QRS that is at least how many squares wide 3 (.12 secs) what chest lead do you want to check first if you suspect hypertrophy v1 P waves for atrial H R waves for RVH S waves depth in V1 + R wave in V5 for LVH what are the two left chest leads V5 and V6 If there is a R,R' in the right chest leads V1 and V2 then there probably is a Right Bundle Branch Block The EKG pattern for RBBB and LBBB can often be confused with what other EKG detectable pathology the ventricular complexes in Ventricular tachycardia if the P wave is diphasic then we know there is atrial enlargement or even if the P wave is not diphasic if it is higher than 2.5 mm if the initial componenet of diphasic P wave in lead V1 is larger than the terminal portion then what atria is enlarged right if the terminal portion is larger in V1 then its left atrial enlargment In V1 - which is larger the S wave or the R wave S (pointing down). The R wave is small. Of course if you have Right ventricular hypertrophy you will have a large R wave pointing up what does Reentry mean premature stimulus reaches two pathways of differing excitability. In pts with Wolff-Parkinson-White (WPW) syndrome what two pathways are present and which one is slow vs fast and shoter vs longer refractory 1. A-V node (slow conduction velocity and shorter refractory period) 2. Bundle of Kent is fast conduction and longer refractory period what does the "delta wave" represent? in pts with WPW. the bundle of kent conducts fast and the A-V node conduction follows shortly after via the normal His Purkinje route the two wave fronts merge, producing a "fusion beat" what is the most common trigger of WPW circuit atrial premature beat APB how might the impulse in WPW go back to conducting down the right pathway if when the impulse arrives at the A-V node the bypass tract is still in a refractory period (it does have a longer refractory period) then the abnormal impulse will be forced to travel back through the A-V node. if then the normal impulse which is slower reaches the Av node (which is now in repolarization) it will propagate retrogradely back to the atrium why might you see an inverted P wave in lead II in pts with WPW backward depolarization of the atrium. the slow normal impulse reaches the AV node but the AV node is still in the refractory period due to early depolarization by the faster abnormal impulse which has reached the node first. t Why is PSVT sustainable over days (150-250) slow AV nodal conduction makes the re-entrant tachycardia possible because it allows enough time for each part of the circuit to recover excitability before the impulse reaches it. - three conditions for all re-entrant tachycardias 1. anatomically distinct pathways 2. slow conduction 3. Diff refractory periods how might you terminate an AV nodal reentrant tachycardia? carotid massage drugs (AV nodal blockers) which usually work by shortening the refractory period