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EKG Facts_Test1

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)
Created by: glittershined