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EKG Facts_Test1

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Question
Answer
Each small square is how long in seconds and how high in amplitude?   .04s and .1mV in amplitude _Each tiny box is one mm  
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Start of impulse in SA node, depolarization of RA & LA. Impulse passing thru AV junction. Usually .06-.1s   P wave (.06-.1s)  
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Begins at P wave and ends at QRS. Normally .12-2s   PR Interval _The PR segment would not include the waveform  
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Normal QRS duration   .06-.11seconds  
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Flat line that follows QRS complex   ST segment  
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Where QRS complex meets ST segment   J-point  
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From start of QRS to end of T wave. Measures ventricular depolarization AND repolarization. Normal .36-.44   QT interval _.36-.44s _Will INC as HR slows  
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As HR slows what will happen to QT interval?   Will INC  
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RA negative, LA positive   Lead 1_Bipolar Lead  
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RA negative, LL positive   Lead 2_Bipolar Lead  
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LA negative, LL positive   Lead 3_Bipolar Lead  
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Unipolar Leads: use one + electrode and a reference point which calculated by ECG machine.   Augmented Leads and Precordial Leads  
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Views BASE of heart: atria and great vessels   AVR: where RA is positive  
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Views LATERAL wall of LEFT Ventricle   AVL: where LA is positive  
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Views INFERIOR wall of LEFT ventricle   AVF: where LL (Left Foot) is positive  
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4th ICS on R of sternum (looks at R ventricle)   Precordial V1  
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4th ICS on L of sternum (looks at R ventricle)   Precordial V2  
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Located halfway between V2 and V4 (looks at septum)   Precordial V3  
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5th ICS in MCL (looks at septum)   Precordial V4  
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Anterior axillary line, same horizontal plane as V4   Precordial V5  
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Midaxillary line, same horizontal plane as V4   Precordial V6  
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Which 2 precordial leads look at the septum?   V3 and V4  
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Which 2 precordial leads look at the right ventricle?   V1 and V2  
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Why would you use precordial leads?   To see anterior & lateral heart views  
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These 2 leads provide CONTINUOUS cardiac monitoring in ER, telemetry & ICU. Place in same position as V1 or V6   Modified Chest Leads (MCL1 & MCL6)  
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Which leads show an anterior surface of the heart   V1, V2, V3, V4  
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Which leads show a lateral view of the heart?   Lead 1, AVL, V5, V6  
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Which leads show an inferior view of the heart   Lead 2, Lead 3, and AVF  
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300, 100, 75, 60, 50, 43, 38, 33   Each big box  
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Most accurate method to count EKG   1500 Method which is you count the number of small squares and then take 1500 divided by that answer.  
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Normal HR   60-100BPM  
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Mostly regular but from time to time there's irregularity   Occasionally irregular  
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Has many areas of irregularity   Very irregular  
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Pacemaker changes location from site to site producing a slightly irregular rhythm. Referred to as wandering atrial pacemaker   Slightly irregular _P wave will change depending on lead  
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Normal HR that SUDDENLY increases to a rapid rate producing an irregularity. Sudden HR acceleration   Paroxysmal Tachycardia  
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Irregular rhythm in a cyclic fashion. May see rate increasing on inspiration & decreasing during expiration.   Patterned Irregularity  
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No pattern to HR irregularity. Is typically seen in Atrial Fibrillation.   Totally Irregular "Irregularly Irregular"  
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Typical duration of P wave   .06-.1 seconds _Longer duration P wave would be sign of LAE  
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Amplitude of typical P wave   .5-2.5mm _Tall P wave would be sign of RAE  
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Amplitude of P>2.5mm seen because of R atrial pressure increase & dilation   Right Atrial Enlargement (P Pulmonale)  
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Width of P >.1s seen because of L atrial pressure & dilation   Left Atrial Enlargement (P Mitrale) _Would also see wide, notched waves.  
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Impulses arriving from atria, but NOT SA node, makes these look different   P waves _Seen with PAC, wandering atrial pacemkaer or atrial tachycardia  
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When this happens the T waves are often peaked, notched or larger than normal   Rapid HR causes P wave to be buried in T wave of preceding beat  
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Atria fires rapidly from one site at a rate of 250-350BPM. Not all atrial impulses conducted through AV node resulting in more P waves than QRS complexes.   Atrial Flutter Waves=F waves _Saw Tooth Pattern  
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Absence of discernable P waves seen when Atria fires more than 350 BPM   Fibrillatory waves  
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Occurs when P wave comes from lower R Atrium near the AV node, in the Left Atrium or the AV junction. Will result in RETROGRADE depolarization of the atria   Inverted P wave _The retrograde depolarization will cause it to deflect negatively (from bottom twds the top) instead of the normal top to bottom.  
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Shows impulse was started in SA node or atria but was blocked and did NOT reach the ventricles.   More P waves than QRS  
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Second R or S wave that occurs after a Q(can never have more than one Q but can have multiple R/S) called   R-Prime or S-Prime  
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Abnormal depolarization of the ventricles caused by pacemaker sites in SA node or ectopically elsewhere can cause this   Abnormal QRS complexes _Abormal depolarization  
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Hypertrophy of venticles, an abnormal pacemaker or aberrantly conducted beat can cause this   Tall QRS  
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Seen in obese patients, HYPOthyroid pts, pericardial effusion   Low-voltage QRS complexes  
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Caused by INTRAventricular conduction defect. Typically caused by a Right or Left Bundle Branch Block.   Wide-Bizarre QRS Complex (from a Supraventricular Origin)  
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Occurs when electrical impuses reach bundle branch while still in refractory after having conducted a previous impulse. Results in impulse traveling down the unaffected BB first, followed by stimulation of the other bundle branch. Causes a wide QRS   Aberrant conduction  
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Shows depolarization of heart from the SA node through the Atria, AV node and His system   PR interval  
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Occurs when impulse comes from Atria close to AV junction or in the AV junction. Travels through abnormal acessory pathways to ventricles and leads to premature ventricle depolarization (pre-excitation)   Shorter PR intervals  
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A delay in impulse conduction through AV node will cause this. Can be caused by 1st degree AV block   Longer PR intervals  
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Pacemaker moves from beat to beat causing the P waves to appear difft from PR intervals   Wandering Atrial Pacemaker  
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PR intervals progressively longer until QRS is dropped then cycle repeats   2nd Degree AV Block Type 1  
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Absent PR intervals   Atrial Flutter & Fibrillation & 3rd degree AV block  
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Atria and ventricles beat independently of each other   3rd Degree AV Block  
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Overall direction of the sum of the currents   The axis  
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Normal axis of patient   Down and to the left  
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Vectors from this side of the heart are generally larger and last longer than the other side   Left>Right  
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To approximate mean QRS axis which leads should you look at?   Lead 1 and aVF _Should be between 0 and 90  
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Mean QRS between 0 and -90   Points up to L shoulder=L axis deviation  
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Mean QRS between 0 and 180   Points down to R foot=R axis deviation  
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Net upright QRS of Lead1=LeadaVF   Mean QRS=45  
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Net QRS of lead 1 positive and > than aVF   QRS lies closer to Lead 1  
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The mean axis will be 90 degrees away from any limb lead where this is isoelectric   Where QRS is isoelectric  
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Normal P wave axis   0-75 Degrees  
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Normal T wave axis   Should be close to QRS axis (0-90)  
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Left Anterior Hemiblock, Left Ventricular Hypertrophy, Q waves of inferior MI, Chronic CAD, Diffuse myocardial dz (cardiomyopathy, amyloidosis, myocarditis), HYPERkalemia, WPW with a R side accessory pathway can all cause this   Left Axis Deviation (heart is pointed upwards and to left)  
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Normal in children, tall adults. Can be caused by Right ventricle hypertrophy, chronic lung dz, anterolateral MI, Left posterior hemiblock, PE and Dextrocardia   Right Axis Deviation (heart is pointed down and to the right)  
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Tall thin ppl will have more of this type of heart with a shift in QRS towards 90   Vertical heart  
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Obese or pregnant ppl may have more of this type of heart with mean QRS shifting to the Left   Horizontal heart _"Fat or Pregnant Whores"  
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Usually caused by INC work of heart on high pressure (high BP, stenotic valve)   Hypertrophy causing thickened cardiac wall chamber  
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Usually caused by stretching of the cardiac chamber from volume overload.   Enlargement (dilation) does NOT necessarily mean hypertrophy but can exist with it  
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Atria is more likely to: dilate(enlarge) or hypertrophy?   Atria is more likely to dilate(enlarge)  
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Ventricle is more likely to: dilate(enlarge) or hypertrophy?   Ventricles are more likely to hypertrophy (work harder because of high pressure building up the cardiac wall)  
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When looking for atrial enlargement where should you look?   At the P waves (which shows how long it takes to depolarize the atria)  
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When looking for ventricle hypertrophy where should you look?   At the QRS complex which will show how long it takes for ventricles to become depolarized  
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Would see a P wave >.1 seconds and >2.5mm in this condition   Biatrial enlargement  
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If P is biphasic and the first part is taller than the second what should you think?   Right atrial enlargement (P Pulmonale) since the first half of the P wave shows the right atria  
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Which leads should you look at to dx Atrial enlargement?   Leads 2 and V1  
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Presence of R ventricle hypertrophy (R axis deviation), an R wave >S in V1 can all be signs of this   Right Atrial Enlargement (P Pulmonale) _Effects pulmonary/tricuspid side  
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Pulmonic stenosis, tricuspid stenosis, and tricuspid regurgitation can all cause this   Right Atrial Enlargement (P Pulmonale) _Effects pulmonary/tricuspid side  
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If second half of P wave in V1 is negative, >.04s or >1mm in depth suspect this   Left Atrial Enlargement (P Mitrale)  
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Normal size of QRS   .06-.11  
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Normal size of Q wave   <.04s  
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Ventricle depolarizes DOWN, to LEFT and POSTERIOR in the direction of this   Thicker Left ventricular muscle _This is the normal pattern: Down, Left, Posterior  
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Often caused by pulmonary HTN, stenosis, can see R axis deviation because of the increased thickness of this   Right Ventricle Hypertrophy  
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Right Axis Deviation+ R wave>S in V1 (~7mm) S wave>R in V6 (not required)   Use to dx Right Ventricle Hypertrophy  
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Commonly caused by HTN & valvular heart dz, best to look at precordial leads for this dx   Left Ventricle Hypertrophy  
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Sum of DEEPEST S in V1 or V2 + Tallest R in V5 or V6=value >35 R in AVL>11mm   Dx of Left Ventricle Hypertrophy  
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"Working cells of the heart" with contractile ability. Branch into a syncytium containing actin/myosin fibers   Myocardial Cells  
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Pacemaker cells of the heart that conduct electricity (bundle branches & Purkinje fibers)   Conducting Cells  
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Permit rapid conduction in intercalated disks to allow for electrical impulses to pass   Gap junctions  
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Cardiomycyte's membrane called this   Sarcolemma  
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Hold myocytes together during contraction   Desmosomes  
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Normal cardiac output (blood ejected)   60-100cc=HR x SV  
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Amt of blood ejected from ventricles during systole   Stroke Volume  
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Cardiac Output x Peripheral Vascular Resistance determines this   Blood Pressure  
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SNS releases NE and Epi for flight or fight to INC HR & myocardial contraction. What's also called?   SNS=Cardioaccelerator _INC pacemaker, impulse conduction, force of contraction & coronary vasoDILATION  
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PNS works via the stimulation of Vagus which releases ACh to slow heart & electrical conduction   PNS=Cardioinhibitor _DEC rate of SA node pacemaker, and rate of conduction through AV node  
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If BP too low, which is activated, cardioaccelerator (SNS) or inhibitor (PNS via Vagus)   DEC BP-->CardioACCELERATOR _Constrict peripheral blood vessels and INC hr, contraction to INC CO and INC BP  
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If BP too low, which is activated, cardioaccelerator (SNS) or inhibitor (PNS via Vagus)   INC BP-->CardioINHIBITOR _Slows heart so blood pressure is lowered  
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Ability of certain cells to produce an electrical impulse without nerve stimulation   Automaticity  
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Ability of cell to respond to electrical stimulus   Excitability  
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Ability of cell to transmit an electrical stimulus from cell to cell   Conductivity  
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Ability of cell to contract when stimulated   Contractility  
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Have ability to spontaneously cause an impulse (depolarize) at a certain rate   Pacemaker Cells  
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Carry the electrical impulses to the right regions of the heart   Electrical Conducting Cells  
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Heart's primary pacemaker is the SA node. What is its intrinsic rate?   SA Node 60-100BPM  
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Pathway for impulses to reach ventricles occurs through this which is located in the low Right Atrium. Acts as gatekeeper for impulses reaching the ventricles since it conducts more slowly.   AV Node 40-60BPM  
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What is the intrinsic rate of the purkinje fibers   20-40BPM (Pacemaker of last resort)  
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The heart is normally in this state (non polar, polar or depolar)?   Polarized (resting state) _Negative ions in, positive out  
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Change in charge that occurs when Na enters the cardiocyte and depolarizes the membrane   Potential Voltage  
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What causes repolarization of the cells   Positive ions leaving the interior of the cell so it may become more negative again  
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Following depolarization, unable to be further depolarized during this state. Keeps wave of depolarization moving fwd, and prevents spasm of continued contraction in one area   Absolute refractory period  
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Frontal Leads   Limb Leads 1,2,3, aVR and aVF  
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Horizontal Leads   Unipolar Precordial Chest Leads V1-V6  
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Occurs when atria, AV junction or both are unable to start an electrical impulse. Will cause enhanced automaticity of ventricel myocardium   Overall Ventricle Dysrhythmia  
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Wide (>.11s) bizarre QRS, T waves in opposite direction of R waves, and absence of P waves all seen here   Ventricle Dysrhythmia  
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Early ectopic beats that start from an irritable focus in the ventricle conduction system/muscle tissue   PVC  
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MI, enlarged ventricles, CHF, myocarditis, drug intoxication, Hypoxia , INC SNS stimulation, decreased Mg/Ca/K can all cause this   PVC  
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2 PVCs in a row, show extremely irritable ventricles   Couplet  
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PVS that fall inbetween 2 regular complexes but do not interrupt the cardiac cycle   Interpolated PVCs  
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R-on-T PVCs (PVCs which occur on or near previous T wave) may start before this   Ventricular Tachycardia or Fibrillation  
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Slow ventricle dysrhythmia of 20-40BPM   Idioventricular Rhythm  
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Idioventricular dysrhythmia of 40-100BPM (this actually EXCEEDS the intrinsic rate of the ventricles   Accelerated Idioventricular Rhythm _40-100  
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Fast Idioventricular dysrhythmia of 100-250BPM. Presence of 3 or more PVCs in a row   Ventricular Tachycardia _100-250 _Can occur with or WITHOUT pulses. May be stable/unstable  
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May come in bursts of 6-10 complexes or may persist at this idioventricular rate of 100-250BMP   Sustained Ventricular Tachycardia  
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Appearance of each QRS complex is similar in this type of ventricular tachycardia (100-250BPM)   Monomorphic Ventricular Tachycardia  
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Appearance of each QRS complex is different in this type of ventricular tachycardia (100-250BPM)   Polymorphic Ventricular Tachycardia  
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Unique variant of polymorphic ventricular tachycardia (100-250BPM) that may be associated w/INC QT interval. Can be drug induced or caused by electrolyte imbalance   Torsades de Pointes (twisting about the points)  
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How would you treat a patient with Torsades de Pointes (pleopmorphic ventricular tachy=100-250BPM)   If NOT in cardiac Arrest: MgSO4 If in cardiac Arrest: DEFIBRILLATION needed  
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Caused by chaotic firing of multiple ventricular sites that causes heart to quiver rather than contract properly. No effection contraction occurs and CO will decrease   Ventricular Fibrillation (300-500 unsync'd pulses per minute)  
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MOST common cause of prehospital cardiac arrest in patients   Ventricular Fibrillation _Death often occurs if don't do Defibb quickly  
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Absence of any cardiac activity=Flat line. Stops all cardiac output   Asystole _Terminal rhythm with low chance of recovery & poor resuscitation attempts  
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Has organized electrical rhythm on ECG (which should produce a pulse) but cannot feel a pulse and pt not breathing. Usually caused by underlying heart dz. Reversible if caused by HYPOvolemia, pericardial tamponade, tension pneumo, massive acute MI,drug OD   Pulseless Electrical Activity  
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Ischemia, myocardial necrosis, degenerative dz of conduction system, congenital defects and drugs like Digitalis can all cause this   Heart Blocks  
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Not a true heart block, just a consistent delay of conduction at AV node. See INCREASED PR interval(>.2s)   1st Degree AV Block  
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Intermittent block at AV node where have transiently INC PR interval till QRS is dropped. Cycle then repeats   2nd Degree AV Block=Wenckebach _Usually transient/reversible _Can occur if healthy  
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Intermittent block at bundle of His/bundle branches causing atrial impulses that are NOT conducted to ventricles. PR interval is prolonged but remains the same, more P waves than QRS   2nd Degree AV Heart Block, Type 2 _Mobitz Type 2 _Seriously malignant!!! -->dec CO, hypoperfusion, can lead to severe heart block & ventricle asystole  
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What's more serious a second degree heart block: Type 1 or Type 2?   Type 2 is more serious because there is whole block to the ventricles when this occurs.  
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Complete block of conduction at or below AV node. Atrial impulses won't reach ventricles and so each will be firing at own rates   3rd Degree Heart Block=Complete Heart Block _Atria will fire @60-100BMP _From AV junction will fire @40-60BPM _From ventricles will fire @20-40BPM  
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Can you handle a 3rd Degree AV heart block?   Well tolerated as long as escape rhythm is fast enough to generate a sufficient CO to keep ok perfusion. Can result though in DEC CO because atria & ventricles not synchronized and ventricle rate is slow.  
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Can result if HR slows to a point where CO drops enough.   Caused by sinus bradycardia  
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Can INC myocardial O2 consumption which can worsen ischemia(causing chest pain) & MI   Sinus Tachycardia  
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What will happen when patient breathes in with dysrhythmia   Breathe IN=HR INC  
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What will happen when patient breathes out with dysrhythmia   Breathe OUT=HR dOwn  
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Occurs naturally in kids, athletes elderly, but can also occur when have heart dz, inferior wall MI, digitalis, INC intracranial pressure   Sinus Dysrhythmia _May cause palpitations, dizzy, syncope  
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Occurs when SA node randomly stops firing until a lower level pacemaker turns on or SA node resumes   Sinus Arrest  
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Dz in elderly caused by degeneration to SA node. Bouts of bradycardia, tachycardia & prolonged pauses or alternating brady/tachy   Sinus Node Dysfunction _Sick Sinus Syndrome  
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Probs w/automaticity, triggered activity and reentry all cause this   Atrial Dysrhythmia _Can eventually lead to DEC CO, tissue perfusion  
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Generally caused by inhibitory vagal effect of breathing on SA/AV nodes. Normal in kids, elders, athlets, digitalis. Causes changes in looks of P waves.   Wandering Atrial Pacemaker  
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Early ectopic beats that start from outside SA node   Premature Atrial Complexes (PACs) _Usually followed by NONcompensatory pause  
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Pause where less than 2 full R-R intervals btwn R wave of normal beat which precedes the PAC and R wave of first normal beat after   Noncompensatory Pause  
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Isolated PAC in asymptomatic patient   Only need observation but may predisposes to tachycardia, flutter, fib. Serves as early sx of electrolyte imbalance or CHF in ppl having acute MI  
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How would you distinguish a wide PAC from a PVC?   A wide PAC will NOT be compensated while a PVC will be compensated. _"PACs with aberrant ventricular conduction"  
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Atrial tachycardia (150-200) which occurs in short bursts. Normally well tolerated in otherwise normally healthy people but can compromise CO in pt's with underlying heart dz.   Paroxysmal Atrial Tachycardia  
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Why might fast heart rates increase MI risk and ischemia?   Because requires INC oxygen needs  
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Pathologic Atrial Tachycardia (120-150BPM) where IRREGULAR rhythm is seen. P wave changes and it looks like wandering atrial pace maker at a fast rate.   Multifocal Atrial Tachycardia _Falls under supraventricular tachy  
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Arises from above the ventricles but cannot definitely define as atrial or junctional tachycardia because CANNOT SEE P WAVE.   Supraventricular Tachycardia _Includes: Paroxysmal Supraventricular Tachy _Nonparoxysmal atrial tachy _Multifocal Atrial Tachy  
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Rapid atria depolarization at 250-350BPM   Atrial Flutter  
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Chaotic non-synchronized firing of multiple atrial areas. Will see a QRS occur with this. >350BPM   Atrial Fibrillation _Lose CO by up to 25%  
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Patients with this may devo intra-atrial emboli as atria are not contracting and blood stays in atrial chambers forming clots. Predisposes to sytolic emboli (stroke)   Atrial Fibrillation  
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Dysrhythmias that arrise from AV junction, have no/inverted P wave & normal QRS   Junctional Dysrhythmia  
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Single early electrical impulse from AV junction with no/inverted P, normal QRS   PJC  
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Impulses from AV junction with no/inverted P, normal QRS at rate of 40-60BPM   Junctional Escape Rhythm(40-60BPM)  
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Impulses from AV junction with no/inverted P, normal QRS at rate of 60-100BPM   Accelerated Junctional Rhythm(60-100BPM) _Now firing higher than intrinsic rate of AV node (40-60BPM)  
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Fast ectopic impulses from AV junction with no/inverted P, normal QRS at rate of 100-180BPM   Junctional Tachycardia(100-180BPM) _Now firing higher than intrinsic rate of AV node (40-60BPM)  
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