Rate Exam 1 Flashcards
What is one little and one big box equal to in EKG?
one little box=0.04 one big box=0.20
What are the rate for regular rhythms every large box to measure rate?
300, 150, 100, 75, 60, 50 count on the dark lines after finding the R wave centered on the dark line only if regular rhythm and R-R is the same!!! 300 boxes per minute 1/300, 2/300
How do you calculate irregular and slow rhythms
take 2 of the 3 seconds strips and mark off 6 seconds of the big boxes count the number of cycles in the boxes and multiple by 10 for the rate Might need to measure P-P and QRS-QRS to get atrial and ventricular rate
what is the P wave
atrial depolarization and it s size is proportional to the atria size (atrial contraction lasts longer though). no larger than 0.12 in precordial (1.5 mm in height normally no bigger) higher in limb leads (less than 2.5 small boxes)
QRS complex
≤ 0.11 sec ventricular depolarization begins midway down interventricular septum by left bundle branch begins left to right of septum before rest of ventricular myocardiumw/ three components (ventricular contraction lasts throughout QRST )
PR interval
beginning of P-wave to beginning of QRS wave represents the conduction from SA node to AV node
T wave
ventricular depolarization overshooting so there is a delay in the heart beat
ST wave
isoelectric segment between QRS and T wave that is a plateau and should be at the same level as the rest of the line otherwise pathological problems
P-P wave wave
between heart beats, used in rhythm identification
Describe the order of nerves in the heart and the electrolytes they use
SA node uses NA+ to K+ for depolarization nd depolarization to AV node, which uses Ca2+ conducting slower to His Bundle, which returns to using NA+ and K+ to left and right bundle branch
Where do the purkinje fibers end in the heart?
terminal filaments of the Purkinje fibers spread beneath the endocardium proceeding toward epicardium but end in endocardial lining not entering the myocardium
What does a long QT rhythm mean?
vulnerable to dangerous or even deadly rapid ventricular rhythms. QT interval should be less than half of R-to-R interval
Height or depth of EKG waves
indicator of voltage w/ upward positive cell inner overall called the amplitude
augmented limb leads design
between leads I, II, III. right hand is always negative electrode location of highest point of heart and SA node going to +/- left hand and positive foot because feet are ground lower than ventricle
AVR AVF AVL
augmented voltage right arm positive ‘’ left arm positive ‘’ foot left foot positive
positive left arm electrode records
lateral I & AVL
positive left foot electrode records
inferior II, III, AVF
chest leads positivity
V1 most negative > V6 most positive as it goes from right atrium to bottom of left ventricle, V3&4 inter-ventricular septum
Neurology of heart pace
SA node 60-100 To atrial 60-80 AV node/junctional 40-60 ventricular foci 20-40 (sensitive oxygen sensory when sensing low O2 become irritable) w/ overdrive suppression w/ any automaticity center overdrive suppress all other w/ slower inherent pacemaking rate
Arrhythmia/dysrhytmia
Abnormal/Bad rhythm
sinus arrhythmia
functions in all humans at all times caused by barely detectable rate changes in sinus pacing relating to respiration and not a true arrhythmia, may change by one small box making still regular rhythm minimal increase during inspiration (sympathetic stimulation of SA node) and minimal decrease during expiration (parasympathetic inhibition of SA node)
three conduction pathways in right atrium from SA to AV node? left atrium?
anterior, middle, and posterior internal tracts bachmann’s bundle
where are the electrodes places?
unipolar precordial leads. Electrode Placement V1 4th Intercostal space to the right of the sternum V2 4th Intercostal space to the left of the sternum V3 Midway between V2 and V4 V4 5th Intercostal space at the midclavicular line V5 Anterior axillary line at the same level as V4 V6 Midaxillary line at the same level as V4 and V5 RL Anywhere above the ankle and below the torso RA Anywhere between the shoulder and the elbow LL Anywhere above the ankle and below the torso LA Anywhere between the shoulder and the elbow
what 12 leads make up EKG?
3 Limb leads (bipolar 1,2, 3) + 3 Augmented Limb Leads (AVF,R,L) + 6 Precordial (Chest) Leads = 12 Lead ECG
Monitoring LeadsRhythm Strips
Allow for continuous assessment versus “snapshot” same time for everything in that column only Commonly Lead II Most have capability to switch to others Should be limited to determination of rate and rhythm 12 Leads required for further interpretation
12 Lead ECG
Trace of electrical activity versus time in 12 leads Snapshot views Some will be simultaneously recorded Pick the best view Commonly have rhythm strip across the bottom
paper speed
25mm/sec
time of boxes
1 small box = 0.04 sec 1 large box = 0.2 sec 5 large boxes = 1 sec 300 large boxes = 1 min 1500 small boxes = 1 min *Paper speed at 25mm/sec
isoelectric line
No current flow “Flatline” Reference point Obscured by very fast rhythms
What happens when the pathway between Sa and AV node is blocked?
then have to take route of cells causing it to be slower
purkingje fibers
can’t see activity on EKG too minimal fibers Right under endocardum depolarizing surface of heart to anterior and =osterior fasicle (back and bottom) depolarizing them
Why is the hearts EKG show positive and negative based on side?
left ventricle has larger magnitude because of more muscle mass, creating axis
describe order of depolariation
septum depolarizing first with general more direction to left because of additional tilt of hear
Describe what limb leads laook at what not he ehart
Leads II & III lookalike’s t bottom part of heart, Lead 1 lateral part of heart. they are bipolar using both to measure current and are positive in the general right/downward direction
How do AVL< AVF, and AVR leads form
unipolar leads w/ EKG sending positive charges to each electrode to measure current in respons. AVR reading is usually negative, AVL usually positive these look at left and right of hear
dextocardia-
jheart on opposite side of body, do right sided EKG
Sinus pause
Delay of activation within the atria of 1.7 to 3 seconds. Measure from P wave to P wave
is a time period when there is no sinus pacemaker working. will have normal rhythm and then it just stopped, pause wasn’t big enough for anything else to take over. Regular just with an event Rate: Varies Regularity: Irregular during pause/arrest. Underlying may be regular. P wave: Present except in areas of pause/arrest P:QRS ratio: 1:1 PR interval: Normal QRS width: Normal Grouping: None Dropped beats: Yes, no P wave (and so no QRS)
Sinus Arrest
Delay of activation within the atria of 3 seconds or more. SA node ceases pacing because it is absent overdrive suppression by SA node, automaticity focus w/ inherent pacing rate escapes to become an active pacemaker since it has fastest inherent rate overdrive suppresses all foci below to become dominant pacemaker. Occurs when a very sick SA node ceases pacemaking completely, heart’s efficient, failsafe mechanism provides 3 seperate levels of automaticity foci for backup pacemaking. Can perhaps make an escaped beat happen asystole anyplace in heart could jump in to get it going junctional and ventricular escape beat. If atria beat would be PQRS but not be an escaped beat.
sinus block
Sinoatrial block occurs in some multiple of the P-P interval. The pathology involved is a nonconducted beat from the normal pacemaker. Sinoatrial Block Rate: Varies Regularity: Irregular during block. Underlying may be regular. P wave: Present except in areas of dropped beats P:QRS ratio: 1:1 PR interval: Normal QRS width: Normal Grouping: None Dropped beats: Yes, no P wave. Same thing we just saw except it will start where it should have came, shows up where it should have. Can miss one to a few beats but so long as it starts when it is supposed to Sinoatrial block occurs in some multiple of the P-P interval. The pathology involved is a nonconducted beat from the normal pacemaker.
An atrial premature contraction (APC)
PAC, APC, APB
Rate: 60 – 100; Depends on underlying rate
Rhythm: May be slightly irregular during event. Underlying regular.
P wave: differs from normal P wave, may be subtle difference
Rate: 60 – 100
Depends on underlying rate
Rhythm: May be slightly irregular during event. Underlying regular.
P wave: differs from normal P wave, may be subtle difference
occurs when some other pacemaker cell in the atria fires at a rate faster than that of the SA node. Beat from atrium coming early, underlying rhyth and atrium decides to fire early than it was supposed too. Part that got excited was ectopic exited making P look different If ectopic beat sits close to SA node looks similar,.
Blocked APB P and T combined and was too early ventricules couldn’t fire because of depolarizing so nothing happened, blocked PAC making T wave look weird. Or notched with T then notching with a P wave
Beat from atrium coming early, underlying rhyth and atrium decides to fire early than it was supposed too. Part that got excited was ectopic exited making P look different
If ectopic beat sits close to SA node looks similar,.
An atrial premature contraction (APC) occurs when some other pacemaker cell in the atria fires at a rate faster than that of the SA node.
APBs are very common. They may occur with a normal heart or virtually any type of organic heart disease. Thus the presence of APBs does not imply that an individual has cardiac disease. In normal people these premature beats may be seen with emotional stress, hyperthyroidism, excessive intake of caffeine, or the administration of sympathomimetic agents (epinephrine, isoproterenol, theophylline). APBs may produce palpitations; in this situation, patients may complain of feeling a skipped beat or an irregular pulse. APBs may also be seen with various types of structural heart disease. Frequent APBs are sometimes the forerunner of atrial fibrillation or other atrial tachyarrhythmias.
Atrial bigeminy
in which each sinus beat is followed by an atrial premature beat (or premature atrial complex). irritable automaticity focus fires premature atrial beat (p’_ that couples to end of normal cycle, and repeated process coupling PAB to end of each successive normal cycle. Group beating, each premature stimulus depolarizes and resets AV node proceeding clear baseline between couplets w/ widened aberrant QRS after each P’ PAB originates suddenly in irritable atrial automaticity focus procucing P’ wave earlier than expected. atrial depolariziation from focus near SA node produces upright P’ wave whereas focus in lower atrium depolarizes in atria in bottom-upwards retrograde fashion recording an inverted P’ wave Double hump T and P wave beat PAC coming early every other one, called atrial bigeminy, could have ventricle bigeminy Trigemy, quadreminy This rhythm strip shows sinus rhythm with three atrial premature beats. The first two (marked ) are conducted with right bundle branch block aberrancy (rSR in lead V1 ). The third atrial premature beat ( ) is conducted with normal ventricular activation. Notice how the first two premature P waves come so early in the cardiac cycle that they fall on the T waves of the preceding sinus beats, making these T waves slightly taller. Abbherent beat- bundle branch block because not completely repolarized and colliding with a blockage
what do the rhythm strips for APC show
Notice the atrial premature beat (APB) after the fourth sinus beat (arrow). B, Notice also the blocked atrial premature beat, again after the fourth sinus beat (arrow). The premature P wave falls on the T wave of the preceding beat and is not followed by a QRS complex because the atrioventricular node is still in a refractory state.
1st page- This rhythm strip shows sinus rhythm with three atrial premature beats. The first two (marked ) are conducted with right bundle branch block aberrancy (rSR in lead V1 ). The third atrial premature beat ( ) is conducted with normal ventricular activation. Notice how the first two premature P waves come so early in the cardiac cycle that they fall on the T waves of the preceding sinus beats, making these T waves slightly taller.
Wandering Atrial Pacemaker (WAP
Rhythm not an event, not a sinu rhythm What’s pacing the atria is wandering, so all parts of heart taking turns jumping in taking over, sinus rhythm but not sinus node causing rhythm, and sending signal out varying rate less than 100, 3 different looking Ps WAP,Irregular rhythm, P’ wave shape varies, atrial rate less than 100, irregular ventricular rhythm caused by signal “wandering to nearby atrial automaticity Foci producing cycle length variation and changes in shape of P waves w/ normal rate they are taking their turn and behaving WAP could be going faster than SA node and whatever comes first depolarizers, so SA node could be broken or be working.
Rate: varies, <100 Regularity: Slightly irregular P wave: Different morphologies, at least 3 P:QRS ratio: 1:1 PR interval: May be variable depending on focus QRS width: Normal Grouping: None Dropped beats: None Wandering atrial pacemaker (WAP) is created by multiple atrial pacemakers each firing at its own pace. This results in an ECG with different P wave morphologies. If each pace were firing from a different distance, with a different P wave axis, then the longer the distance, the longer the PR interval.
A-Fib
Rate atrial >350, unable to count ventricular varies Rhythm “irregularly irregular” P waves not discernible PR interval not measurable QRS normal Atrial fibrillation is the firing of numerous pacemaker cells in a haphazard fashion. Caused by continuous rapid-firing of multiple atrial automaticity foci. No single impulses depolarizies atria completely and only occasional, random atrial depolarization reaches AV node, conducted to ventricles producing irregular rhythm causing tiny erratic spikes. Result of multiple “irritable” atrial foci suffering from entrance block and pacing rapidly multiple are parasystolic insensitive to overdrive suppression. cause stroke by incorrect contraction of heart
“fine” vs. coarse Afib
Rapid undulation of the baseline due to fibrillatory (f) waves. No true P waves are present, and the ventricular rate is irregular.
Premature Junctional Contraction(PJC)
Rate Depends on underlying rhythm Rhythm slightly irregular due to event. Underlying may be regular. P wave absent, inverted, retrograde PR interval when an irritable automaticity focus in AV junction suddenly fires premature stimulus that is conducted to, and depolarizes, ventricles (and atria in retrograde). as ventricle depolarize, one bundle branch may depolarize slower than other so too-early depolarization from PJB may conduct through one bundle branch but impulse is delayed in the other creating widened QRS complex w/ aberrant ventricular conduction. originates in an irritable junctional focus w/in the AV node. expect such a premature stimulus to conduct to the ventricles, may depolarize atria retrograde fashion records as inverted P’ w/ upright QRS. PJB produces retrograde atrial depolarization may record inverted P’ wave immediately before premature QRS complex the P’ disappears w/in QRS when atrial and ventricular depolarization occur simultaneously resetting SA node creating gaps of empty baseline between couplets. irritable focus in AV junction initiateing a premature junctional beat after each normal (SA node generated cycle) PJB coupled with two consecutive, normal cycles in a repeating series of these couplets.
Atrioventricular junctional (nodal) beats
produce P waves that point upward in lead aVR and downward in lead II; this is just the opposite of what is seen with sinus rhythm. The P wave may just precede the QRS complex (A), follow it (B), or occur simultaneously with it (C). In the last instance no P wave is visible.
Junctional Escape Beat
An escape beat occurs when the normal pacemaker fails to fire and the next available pacemaker in the conduction system fires in its place. If PR interval is present, it does NOT represent atrial stimulation of the ventricles. when a junctional automaticity focus escapes overdrive suppression because of an SA node missed cycle producing normal QRS complex recording no P wave or may cause retrograde backwards P wave. Rate: Depends on underlying rhythm Regularity: Irregular due to event P wave: Variable (none, antegrade, or retrograde) P:QRS ratio: None; or 1:1 if antegrade or retrograde PR interval: None, short, or retrograde QRS width: Normal Grouping: None Dropped beats: Yes
junctional rhythm
Rate 40 – 60 Rhythm regular P wave absent, inverted, retrograde PR interval
Junctional rhythm at 60 beats/min. Note the negative P waves “hidden” at the end of the ST segments.
junctional escape rhythm
This rhythm strip shows a slow junctional escape rhythm at about 40 beats/min. No P waves are visible, and the baseline between QRS complexes is flat. Junctional rhythm at 60 beats/min. Note the negative P waves “hidden” at the end of the ST segments. a kind of sinus arrest where w/ absent regular pacing stimuli from above, an automaticity in the AV junction may escape overdrive suppression to become an active pacemaker producing a junctional escape rhythm between 40-60/min. junctional focus escapes influence of overdrive suppression if there is a sinus arrest, and atrial foci also fail to function or if there is a complete conduction block in proximal end of AV node. conducting mainly to the ventricles producing series of lone QRS complexes except in cases of retrograde atrial depolarizing sending signal back up to atria causing upside down p wave reporting immediately before QRS, after QRS, or within one.
Premature Ventricular Contraction (PVC, VPC, VPB)
Rate Depends on underlying rhythm Rhythm slightly irregular due to event P wave absent in PVC PR interval absent in PVC QRS >.18, distorted, wide originates suddenly in irritable ventricular automaticity focus producing a giant ventricular complex on EKG. premature ventricular contraction and pulse beat weaker than normal because not filled. irritable may fire stimulus producing premature ventricular complex on EKG, occurring early in cycle recognized by great width and enormous aptitude (height and depth) usually opposite polarity of normal QRS’s PVCs downward (contraction) weaker than normal not completely filled causing one area of ventricular wall to begin to depolarize before rest of ventricle before other ventricle depolarizes producing an enormously wide ventricular complex producing unopposed deflections of immense amplitude, wider, taller & deeper than normal pause and can see well-timed but useless P wave in PVC. only polarize ventricles not SA node discharging on schedul. if left ventricular depolarization in leftward direction counterbalances right ventricular minimizing amplitude in remote such as PVC spreads without opposite slow course causing pause because P wave fires while ventricles are still refractor allowing depolarizing pause to next sinus generated. PVCs heart warning sign always respond. With ventricular premature contractions (VPCs), the ventricles do not contract at their normal time because they are in a refractory state, are not yet repolarized, and are unavailable to fire again. However, the underlying pacing schedule is not altered, so the beat following the VPC will arrive on time. This is called a compensatory pause. VPBs are not uncommon in normal adults of all ages although they occur more frequently with advancing age. Young adults, for example, may have VPBs because of anxiety or excessive caffeine intake. Certain drugs used in asthmatics (e.g., epinephrine, isoproterenol, and aminophylline) can provoke VPBs in normal hearts. Nevertheless, if a patient has frequent VPBs, you should search carefully for underlying cardiac disease (heart murmurs, abnormal echocardiographic findings, etc.) and also obtain a careful drug history. Occasional or even frequent isolated VPBs in an otherwise healthy person without organic heart disease are not usually a source of concern. VPBs are also common with mitral valve prolapse, and they may be seen with virtually any type of heart disease. VPBs are the most common arrhythmia seen with acute MI. VPBs may be seen in patients with electrolyte disturbances such as hypokalemia or hypomagnesemia and in patients with lung disease or hypoxemia from any cause. 1 A ventricular premature beat (VPB) is recognized because it comes before the next normal beat is expected and it has a wide aberrant shape. Notice also the long PR interval in the normal sinus beats, indicating first-degree atrioventricular block. Notice that the same ventricular premature beat (marked X) recorded simultaneously in three different leads has different shapes. Notice the wide aberrant shape of a ventricular premature beat (VPB) compared to the QRS complexes of an atrial premature beat (APB), which generally resembles the sinus QRS complexes. can be in the same lead Two ventricular premature beats (V) are referred to as a pair or a couplet. They also show the “R on T” phenomenon ( P, P wave; T, T wave).
ventricular hegemony ventricular trigemini
A, Ventricular bigeminy, in which each normal sinus impulse is followed by a ventricular premature beat (marked X). B, Ventricular trigeminy, in which a ventricular premature beat occurs after every two sinus pulses. emanate from same ventricular focus, warning that focus is irritable because of poor state of oxygenation w/ 6 or more considered pathological. suggest poor oxygenation of single ventricular focus because blood supply to focus is diminished. can have coronary blood flow but poorly oxygenated blood as in drowning, pneumothorax, pulmonary embolus or obstruction or low serum potassium adrenergic stimulants can aggravate situation
interpolated
Sometimes a ventricular premature beat (X) falls between two normal beats, in which case it is interpolated. DOESNT RESET TIMING.
Ventricular Tachycardia
Rate 140-220 or faster Rhythm regular P wave none PR interval none QRS >.18 run of thee or more PVCs in rapid succession w/ oxygen decreased further especially problematic in patients w/ acute myocardial infarction. if lasts longer than 30 seconds it is sustained found in severe cardiac hypoxia, desperation measure produced by multiple, exceptionally irritable (hypoxic) ventricular foci each produces its own unique, identifiable PVC every time it fires indicating imminent trouble. Ventricular tachycardia is a very fast ventricular rate that is usually dissociated from an underlying atrial rate. The irregularities are the underlying sinus beats. Blue dots indicate sinus beats. Arrows pinpoint the irregularities.
Idioventricular Rhythm
Rate less than 40 Rhythm regular P wave absent PR interval none QRS greater than .20 Idioventricular rhythm occurs when a ventricular focus acts as the primary pacemaker for the heart.
Should be less than 40 and start walking heart rate will go up called accelerate atrioventricular rhythm. Fix it otherwise asystole start pacing them. If it sped up under 100 idioventricular slow Vtach
Accelerated Idioventricular Rhythm
Rate: 40–100 BPM Regularity: Regular P wave: None P:QRS ratio: None PR interval: None QRS width: Wide (≥0.12 sec), bizarre appearance Grouping: None Dropped beats: None Accelerated idioventricular rhythm is a faster version of idioventricular rhythm.
Why do we treat the patient and not the monitor?
if someone scratches the heart monitor person’s leads could fall off and could be because of screen if the baseline is waving could be from external environment etc… don’t worry about it
non-conducted premature atrial beat
when AV node is still in refractory phase beat is shown w/ no QRS-T response just a premature beat, but does depolarize SA node resetting pacemaking one cycle length looking like some-kind-kind-of-block
ventricle parasystole
produced by ventricular automaticity focus suffers form entrance block (not irritable). paraystolic focus not vulnerable to overdrive suppression, so it paces at inherent rate and ventricular complexes that generates poke through dominant sinus rhythm.solitary ventricular focus suffering from entrance block is parasystolic can’t be oveerdrive suppressed (insulating it from others) can deliver pacing stimuli at its inherent rate. parasystolic ventricular focus suffers from entrance block insulating it from depolarizing by outside sources. absent overdrive suppression, pacing its inherent rate dual rhythm pacing from SA node and ventricular focus. dual rhythm pacing from two sources, PVCs coupled to long series of normal cycles. not always consistent interval.
