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EKG Facts_Test1
| 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 |
| Start of impulse in SA node, depolarization of RA & LA. Impulse passing thru AV junction. Usually .06-.1s | P wave (.06-.1s) |
| Begins at P wave and ends at QRS. Normally .12-2s | PR Interval _The PR segment would not include the waveform |
| Normal QRS duration | .06-.11seconds |
| Flat line that follows QRS complex | ST segment |
| Where QRS complex meets ST segment | J-point |
| 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 |
| As HR slows what will happen to QT interval? | Will INC |
| RA negative, LA positive | Lead 1_Bipolar Lead |
| RA negative, LL positive | Lead 2_Bipolar Lead |
| LA negative, LL positive | Lead 3_Bipolar Lead |
| Unipolar Leads: use one + electrode and a reference point which calculated by ECG machine. | Augmented Leads and Precordial Leads |
| Views BASE of heart: atria and great vessels | AVR: where RA is positive |
| Views LATERAL wall of LEFT Ventricle | AVL: where LA is positive |
| Views INFERIOR wall of LEFT ventricle | AVF: where LL (Left Foot) is positive |
| 4th ICS on R of sternum (looks at R ventricle) | Precordial V1 |
| 4th ICS on L of sternum (looks at R ventricle) | Precordial V2 |
| Located halfway between V2 and V4 (looks at septum) | Precordial V3 |
| 5th ICS in MCL (looks at septum) | Precordial V4 |
| Anterior axillary line, same horizontal plane as V4 | Precordial V5 |
| Midaxillary line, same horizontal plane as V4 | Precordial V6 |
| Which 2 precordial leads look at the septum? | V3 and V4 |
| Which 2 precordial leads look at the right ventricle? | V1 and V2 |
| Why would you use precordial leads? | To see anterior & lateral heart views |
| These 2 leads provide CONTINUOUS cardiac monitoring in ER, telemetry & ICU. Place in same position as V1 or V6 | Modified Chest Leads (MCL1 & MCL6) |
| Which leads show an anterior surface of the heart | V1, V2, V3, V4 |
| Which leads show a lateral view of the heart? | Lead 1, AVL, V5, V6 |
| Which leads show an inferior view of the heart | Lead 2, Lead 3, and AVF |
| 300, 100, 75, 60, 50, 43, 38, 33 | Each big box |
| 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. |
| Normal HR | 60-100BPM |
| Mostly regular but from time to time there's irregularity | Occasionally irregular |
| Has many areas of irregularity | Very irregular |
| 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 |
| Normal HR that SUDDENLY increases to a rapid rate producing an irregularity. Sudden HR acceleration | Paroxysmal Tachycardia |
| Irregular rhythm in a cyclic fashion. May see rate increasing on inspiration & decreasing during expiration. | Patterned Irregularity |
| No pattern to HR irregularity. Is typically seen in Atrial Fibrillation. | Totally Irregular "Irregularly Irregular" |
| Typical duration of P wave | .06-.1 seconds _Longer duration P wave would be sign of LAE |
| Amplitude of typical P wave | .5-2.5mm _Tall P wave would be sign of RAE |
| Amplitude of P>2.5mm seen because of R atrial pressure increase & dilation | Right Atrial Enlargement (P Pulmonale) |
| Width of P >.1s seen because of L atrial pressure & dilation | Left Atrial Enlargement (P Mitrale) _Would also see wide, notched waves. |
| Impulses arriving from atria, but NOT SA node, makes these look different | P waves _Seen with PAC, wandering atrial pacemkaer or atrial tachycardia |
| 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 |
| 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 |
| Absence of discernable P waves seen when Atria fires more than 350 BPM | Fibrillatory waves |
| 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. |
| Shows impulse was started in SA node or atria but was blocked and did NOT reach the ventricles. | More P waves than QRS |
| 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 |
| Abnormal depolarization of the ventricles caused by pacemaker sites in SA node or ectopically elsewhere can cause this | Abnormal QRS complexes _Abormal depolarization |
| Hypertrophy of venticles, an abnormal pacemaker or aberrantly conducted beat can cause this | Tall QRS |
| Seen in obese patients, HYPOthyroid pts, pericardial effusion | Low-voltage QRS complexes |
| Caused by INTRAventricular conduction defect. Typically caused by a Right or Left Bundle Branch Block. | Wide-Bizarre QRS Complex (from a Supraventricular Origin) |
| 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 |
| Shows depolarization of heart from the SA node through the Atria, AV node and His system | PR interval |
| 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 |
| A delay in impulse conduction through AV node will cause this. Can be caused by 1st degree AV block | Longer PR intervals |
| Pacemaker moves from beat to beat causing the P waves to appear difft from PR intervals | Wandering Atrial Pacemaker |
| PR intervals progressively longer until QRS is dropped then cycle repeats | 2nd Degree AV Block Type 1 |
| Absent PR intervals | Atrial Flutter & Fibrillation & 3rd degree AV block |
| Atria and ventricles beat independently of each other | 3rd Degree AV Block |
| Overall direction of the sum of the currents | The axis |
| Normal axis of patient | Down and to the left |
| Vectors from this side of the heart are generally larger and last longer than the other side | Left>Right |
| To approximate mean QRS axis which leads should you look at? | Lead 1 and aVF _Should be between 0 and 90 |
| Mean QRS between 0 and -90 | Points up to L shoulder=L axis deviation |
| Mean QRS between 0 and 180 | Points down to R foot=R axis deviation |
| Net upright QRS of Lead1=LeadaVF | Mean QRS=45 |
| Net QRS of lead 1 positive and > than aVF | QRS lies closer to Lead 1 |
| The mean axis will be 90 degrees away from any limb lead where this is isoelectric | Where QRS is isoelectric |
| Normal P wave axis | 0-75 Degrees |
| Normal T wave axis | Should be close to QRS axis (0-90) |
| 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) |
| 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) |
| Tall thin ppl will have more of this type of heart with a shift in QRS towards 90 | Vertical heart |
| 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" |
| Usually caused by INC work of heart on high pressure (high BP, stenotic valve) | Hypertrophy causing thickened cardiac wall chamber |
| Usually caused by stretching of the cardiac chamber from volume overload. | Enlargement (dilation) does NOT necessarily mean hypertrophy but can exist with it |
| Atria is more likely to: dilate(enlarge) or hypertrophy? | Atria is more likely to dilate(enlarge) |
| 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) |
| When looking for atrial enlargement where should you look? | At the P waves (which shows how long it takes to depolarize the atria) |
| 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 |
| Would see a P wave >.1 seconds and >2.5mm in this condition | Biatrial enlargement |
| 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 |
| Which leads should you look at to dx Atrial enlargement? | Leads 2 and V1 |
| 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 |
| Pulmonic stenosis, tricuspid stenosis, and tricuspid regurgitation can all cause this | Right Atrial Enlargement (P Pulmonale) _Effects pulmonary/tricuspid side |
| If second half of P wave in V1 is negative, >.04s or >1mm in depth suspect this | Left Atrial Enlargement (P Mitrale) |
| Normal size of QRS | .06-.11 |
| Normal size of Q wave | <.04s |
| Ventricle depolarizes DOWN, to LEFT and POSTERIOR in the direction of this | Thicker Left ventricular muscle _This is the normal pattern: Down, Left, Posterior |
| Often caused by pulmonary HTN, stenosis, can see R axis deviation because of the increased thickness of this | Right Ventricle Hypertrophy |
| Right Axis Deviation+ R wave>S in V1 (~7mm) S wave>R in V6 (not required) | Use to dx Right Ventricle Hypertrophy |
| Commonly caused by HTN & valvular heart dz, best to look at precordial leads for this dx | Left Ventricle Hypertrophy |
| 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 |
| "Working cells of the heart" with contractile ability. Branch into a syncytium containing actin/myosin fibers | Myocardial Cells |
| Pacemaker cells of the heart that conduct electricity (bundle branches & Purkinje fibers) | Conducting Cells |
| Permit rapid conduction in intercalated disks to allow for electrical impulses to pass | Gap junctions |
| Cardiomycyte's membrane called this | Sarcolemma |
| Hold myocytes together during contraction | Desmosomes |
| Normal cardiac output (blood ejected) | 60-100cc=HR x SV |
| Amt of blood ejected from ventricles during systole | Stroke Volume |
| Cardiac Output x Peripheral Vascular Resistance determines this | Blood Pressure |
| 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 |
| 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 |
| 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 |
| If BP too low, which is activated, cardioaccelerator (SNS) or inhibitor (PNS via Vagus) | INC BP-->CardioINHIBITOR _Slows heart so blood pressure is lowered |
| Ability of certain cells to produce an electrical impulse without nerve stimulation | Automaticity |
| Ability of cell to respond to electrical stimulus | Excitability |
| Ability of cell to transmit an electrical stimulus from cell to cell | Conductivity |
| Ability of cell to contract when stimulated | Contractility |
| Have ability to spontaneously cause an impulse (depolarize) at a certain rate | Pacemaker Cells |
| Carry the electrical impulses to the right regions of the heart | Electrical Conducting Cells |
| Heart's primary pacemaker is the SA node. What is its intrinsic rate? | SA Node 60-100BPM |
| 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 |
| What is the intrinsic rate of the purkinje fibers | 20-40BPM (Pacemaker of last resort) |
| The heart is normally in this state (non polar, polar or depolar)? | Polarized (resting state) _Negative ions in, positive out |
| Change in charge that occurs when Na enters the cardiocyte and depolarizes the membrane | Potential Voltage |
| What causes repolarization of the cells | Positive ions leaving the interior of the cell so it may become more negative again |
| 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 |
| Frontal Leads | Limb Leads 1,2,3, aVR and aVF |
| Horizontal Leads | Unipolar Precordial Chest Leads V1-V6 |
| Occurs when atria, AV junction or both are unable to start an electrical impulse. Will cause enhanced automaticity of ventricel myocardium | Overall Ventricle Dysrhythmia |
| Wide (>.11s) bizarre QRS, T waves in opposite direction of R waves, and absence of P waves all seen here | Ventricle Dysrhythmia |
| Early ectopic beats that start from an irritable focus in the ventricle conduction system/muscle tissue | PVC |
| MI, enlarged ventricles, CHF, myocarditis, drug intoxication, Hypoxia , INC SNS stimulation, decreased Mg/Ca/K can all cause this | PVC |
| 2 PVCs in a row, show extremely irritable ventricles | Couplet |
| PVS that fall inbetween 2 regular complexes but do not interrupt the cardiac cycle | Interpolated PVCs |
| R-on-T PVCs (PVCs which occur on or near previous T wave) may start before this | Ventricular Tachycardia or Fibrillation |
| Slow ventricle dysrhythmia of 20-40BPM | Idioventricular Rhythm |
| Idioventricular dysrhythmia of 40-100BPM (this actually EXCEEDS the intrinsic rate of the ventricles | Accelerated Idioventricular Rhythm _40-100 |
| 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 |
| May come in bursts of 6-10 complexes or may persist at this idioventricular rate of 100-250BMP | Sustained Ventricular Tachycardia |
| Appearance of each QRS complex is similar in this type of ventricular tachycardia (100-250BPM) | Monomorphic Ventricular Tachycardia |
| Appearance of each QRS complex is different in this type of ventricular tachycardia (100-250BPM) | Polymorphic Ventricular Tachycardia |
| 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) |
| 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 |
| 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) |
| MOST common cause of prehospital cardiac arrest in patients | Ventricular Fibrillation _Death often occurs if don't do Defibb quickly |
| Absence of any cardiac activity=Flat line. Stops all cardiac output | Asystole _Terminal rhythm with low chance of recovery & poor resuscitation attempts |
| 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 |
| Ischemia, myocardial necrosis, degenerative dz of conduction system, congenital defects and drugs like Digitalis can all cause this | Heart Blocks |
| Not a true heart block, just a consistent delay of conduction at AV node. See INCREASED PR interval(>.2s) | 1st Degree AV Block |
| 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 |
| 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 |
| 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. |
| 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 |
| 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. |
| Can result if HR slows to a point where CO drops enough. | Caused by sinus bradycardia |
| Can INC myocardial O2 consumption which can worsen ischemia(causing chest pain) & MI | Sinus Tachycardia |
| What will happen when patient breathes in with dysrhythmia | Breathe IN=HR INC |
| What will happen when patient breathes out with dysrhythmia | Breathe OUT=HR dOwn |
| 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 |
| Occurs when SA node randomly stops firing until a lower level pacemaker turns on or SA node resumes | Sinus Arrest |
| 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 |
| Probs w/automaticity, triggered activity and reentry all cause this | Atrial Dysrhythmia _Can eventually lead to DEC CO, tissue perfusion |
| 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 |
| Early ectopic beats that start from outside SA node | Premature Atrial Complexes (PACs) _Usually followed by NONcompensatory pause |
| 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 |
| 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 |
| 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" |
| 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 |
| Why might fast heart rates increase MI risk and ischemia? | Because requires INC oxygen needs |
| 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 |
| 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 |
| Rapid atria depolarization at 250-350BPM | Atrial Flutter |
| Chaotic non-synchronized firing of multiple atrial areas. Will see a QRS occur with this. >350BPM | Atrial Fibrillation _Lose CO by up to 25% |
| 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 |
| Dysrhythmias that arrise from AV junction, have no/inverted P wave & normal QRS | Junctional Dysrhythmia |
| Single early electrical impulse from AV junction with no/inverted P, normal QRS | PJC |
| Impulses from AV junction with no/inverted P, normal QRS at rate of 40-60BPM | Junctional Escape Rhythm(40-60BPM) |
| 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) |
| 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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