Rate Exam 1 Flashcards
(92 cards)
1
Q
What is one little and one big box equal to in EKG?
A
one little box=0.04 one big box=0.20
2
Q
What are the rate for regular rhythms every large box to measure rate?
A
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
3
Q
How do you calculate irregular and slow rhythms
A
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
4
Q
what is the P wave
A
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)
5
Q
QRS complex
A
≤ 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 )
6
Q
PR interval
A
beginning of P-wave to beginning of QRS wave represents the conduction from SA node to AV node
7
Q
T wave
A
ventricular depolarization overshooting so there is a delay in the heart beat
8
Q
ST wave
A
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
9
Q
P-P wave wave
A
between heart beats, used in rhythm identification
10
Q
Describe the order of nerves in the heart and the electrolytes they use
A
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
11
Q
Where do the purkinje fibers end in the heart?
A
terminal filaments of the Purkinje fibers spread beneath the endocardium proceeding toward epicardium but end in endocardial lining not entering the myocardium
12
Q
What does a long QT rhythm mean?
A
vulnerable to dangerous or even deadly rapid ventricular rhythms. QT interval should be less than half of R-to-R interval
13
Q
Height or depth of EKG waves
A
indicator of voltage w/ upward positive cell inner overall called the amplitude
14
Q
augmented limb leads design
A
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
15
Q
AVR AVF AVL
A
augmented voltage right arm positive ‘’ left arm positive ‘’ foot left foot positive
16
Q
positive left arm electrode records
A
lateral I & AVL
17
Q
positive left foot electrode records
A
inferior II, III, AVF
18
Q
chest leads positivity
A
V1 most negative > V6 most positive as it goes from right atrium to bottom of left ventricle, V3&4 inter-ventricular septum
19
Q
Neurology of heart pace
A
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
20
Q
Arrhythmia/dysrhytmia
A
Abnormal/Bad rhythm
21
Q
sinus arrhythmia
A
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)
22
Q
three conduction pathways in right atrium from SA to AV node? left atrium?
A
anterior, middle, and posterior internal tracts bachmann’s bundle
23
Q
where are the electrodes places?
A
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
24
Q
what 12 leads make up EKG?
A
3 Limb leads (bipolar 1,2, 3) + 3 Augmented Limb Leads (AVF,R,L) + 6 Precordial (Chest) Leads = 12 Lead ECG
25
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
26
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
27
paper speed
25mm/sec
28
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
29
isoelectric line
No current flow “Flatline” Reference point Obscured by very fast rhythms
30
What happens when the pathway between Sa and AV node is blocked?
then have to take route of cells causing it to be slower
31
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
32
Why is the hearts EKG show positive and negative based on side?
left ventricle has larger magnitude because of more muscle mass, creating axis
33
describe order of depolariation
septum depolarizing first with general more direction to left because of additional tilt of hear
34
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
35
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
36
dextocardia-
jheart on opposite side of body, do right sided EKG
37
purpose of lead on right leg?
right leg is the ground clearing up electrical activity
38
What do the chest leads look at?
V1 and V2 look at septum, V3 and V4 anterior part of heart, V5 and V6 lateral part of hear
39
ways to determine rate
1. Six second strip (if irregular) 2. 1500 divided by the number of small boxes (most correct) 3. 300, 150, 100, …. (regular rhythms only)
40
Unknown segments
J wave at end of QRS U wave smaller than a T after a T, can be abnormal in some conditions w/ potassium and is wider and shorter than P wave or can be normal in some cases foci can fire themselves at time of U wave too early combining U and P
41
combined vectors equal?
Leads I + III = II AvR + AvL = AvF.
42
determining rate and rhythm what do you use?
Rate, rhythm, P wave, PR segment, QRS duration
43
How do you determine rate?
First look regular or irregular if one or other have to find it out in different ways Rate fast or slow Bradycardia \<60 BPM Tachycardia \>100 BPM
44
How do you determine rhythm?
2. Rhythm regular or irregular If irregular, is it: Regularly irregular (some form of regularity to the pattern Regular irregular if there is pattern or irregularly) Irregularly irregular (no pattern at all)
45
What do you look for in a P wave?
If P waves start something else, if don’t have same shape can be coming from someplace else even if they are not the same could be a spot next to it. SA at top if ectopic beat of foci up near it will look the same, AV at bottom may be upside down will fire different PR should be same. 3. P wave present or absent Are all P waves identical? Identical P waves are generated by same pacemaker site Should have identical PR intervals Are P waves not identical? Two possible causes: Additional pacemaker cell firing Another component of complex superimposed on P wave Does each QRS complex have a P wave? Abnormal number of P waves suggests AV nodal block
46
What do you look for in a PR, QRS interval?
4. PR interval 5. QRS duration If P waves and QRS same number but not associated with each other can have tract between that is closed w/ each happening at one pace. Is QRS falling where it should or before or after If QRS wide had ectopic foci and had to travel cell to cell making it slower Are P waves and QRS complexes associated with one another? If yes: Entire complex is a normal beat. Entire complex is a premature beat. Are QRS complexes narrow or wide? Narrow indicates impulses usually found in supraventricular rhythms. Wide indicates impulses transmitted by direct cell-to-cell contact. Are QRS complexes grouped or not grouped? Useful in determining: Recurrent premature complexes Are there any dropped beats? Dropped beats occur in: AV nodal blocks Sinus arrest QRS bunch fire at a time every second or third beat must notice pattern if coming early, blocked beats and then no QRS Sinus arrest no p waves
47
Sinus bradycardia
everything else normal just a rate below 60. The origin of sinus bradycardia may be in the SA node or in an atrial pacemaker. Medications like beta blockers can cause this rhythm. The origin of sinus bradycardia may be in the SA node or in an atrial pacemaker. Medications like beta blockers can cause this rhythm.
48
Sinus tachycardia
everything else normal just a rate above 100. can be caused by medications or conditions that require increased cardiac output (exercise, hypovolemia, hemorrhage). Sinus tachycardia can be caused by medications or conditions that require increased cardiac output (exercise, hypovolemia, hemorrhage). If faster can adjust speed of paper from 25 mm/sec to 50 mm/sec Supraventricular tachycardia- above the ventricle tachycardia don’t know what it is and cant slow it down so it is SVT, which is general name but can be more specific if you can see P waves
49
Sinus arrhythmia
is a normal respiratory variation. It becomes slower during exhalation and faster upon inhalation. Random PQRS all over the place, if like accordion it is a most likely breathing Rate increases with inspiration decreases with expiration Rhythm Can be only slightly irregular to greater irregularity, varies with respiration Think accordion everything else normal
50
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)
51
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.
52
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.
53
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.
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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
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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.
56
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.
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Multifocal Atrial Tachycardia (MAT)
Rate: \>100 BPM Regularity: Slightly irregular P wave: different morphologies P:QRS ratio: 1:1 PR interval: May be variable QRS width: Normal Grouping: None Dropped beats: None Irregular rhythm, P’ wave shape varies, faster WAP particularly found in COPD patients because three or more atrial foci are involved irregular ventricular rhythm caused by signal “wandering to nearby atrial automaticity Foci producing cycle length variation and changes in shape of P waves w/ high rate because they are not taking turns or behaving Multifocal atrial tachycardia (MAT) is simply a tachycardic WAP. Treatment is difficult and should be aimed at correcting the underlying problem. WAP over 100 this is a type of SVT faster than 100 comes so fast cant tell what Ps are regular or irregular,
58
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
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"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.
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concerns for afib
Cardioconvert someone before blood thinner, thin before converting conversions may not stick.
Feel faint, tired, if not high enough ventricle rate pacemaker to just pace ventricles, or synchronized for ventricular and atrial can fill ventricle.
Decreased Cardiac Output
Hemodynamically the most significant effect of AF is decreased cardiac output, which is especially marked in patients with underlying cardiac impairment and in elderly people, who appear to be more dependent on atrial contraction for filling of the ventricles. In addition, the amount of this decreased output depends on the ventricular rate with AF. The faster the rate, the more decreased the cardiac output becomes. Thus the patient with AF at a rate of 180 beats/min is more likely to be hypotensive or in congestive heart failure (CHF) than is the patient with a rate of 100 beats/min. In patients with coronary artery disease this rapid ventricular rate can cause myocardial ischemia and even infarction.
Atrial Thrombi and Embolization
The second significant effect of AF, resulting from the stagnation of blood, is a tendency in some patients for atrial thrombi to develop and dislodge into the arterial circulation, causing peripheral embolism. The thrombi can produce a cerebrovascular accident, occlusion of the blood supply to the legs, and other complications.
The risk of thrombus formation and embolization is highest in patients with chronic AF related to rheumatic mitral valve disease. However, thrombi and embolization also occur in patients with AF from other causes (so-called nonrheumatic atrial fibrillation). Indeed, atrial fibrillation is a major substrate for embolic strokes, particularly in the elderly.
61
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.
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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.
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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
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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.
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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.
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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).
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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
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interpolated
Sometimes a ventricular premature beat (X) falls between two normal beats, in which case it is interpolated. DOESNT RESET TIMING.
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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.
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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
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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.
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Variations of QRS
RS, R, QR, Q, RSr'
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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
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What is a regular sinus rhythm?
aka RSR, NSR Rate 60 to 100 Rhythm regular P wave 1 for each QRS PR interval Normal 0.12-0.2 QRS Normal = 0.11
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Irregular rhythm
Rhythms that lack a constant duration between paced cycles w/ no predictable recurring cycles. Caused by (parasystolic)- structural pathology or hypoxia where an incoming depolarization is blocked, “protecting them” from passive depolarization by any other source. Cannot be “over-drive supressed while automaticity is conducted to surrounding tissue insensitive to passive depolarization. Ex. Wandering pacemaker, multiracial atrial tachycardia, atrial fibrillation
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Escape rhythm
Automaticity focus escapes overdrive suppression to pace at its inherent rate ex. Atrial escape rhythm, junctional escape rhythm, ventricular escape rhythm. If SA node pacing ceases entirely, an automaticity focus will escape to pace at its inherent rate producing this.
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Escape beat
Automaticity focus transiently escapes overdrive suppression to emit one beat ex. Atrial escape beat, junctional escape beat, ventricular escape beat. If pause in pacing is brief missing only one cycle an automaticity focus may escape to emit beat before normal rhythm returns. a transient sinus block makes SA node miss one cycle producing a pause so the atrial automaticity focus escapes overdrive suppression w/ long enough pause longer than inherent pacing cycle length of focus focus will escape SA node's overdrive suppression
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Escape
brief pause in SA Node’s regular pacing overdrive-suppresses all automaticity foci permits an automaticity foci to escape overdrive suppression
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Ventricular escape rhythm
occurs when a ventricular automaticity focus is not regularly stimulated by paced depolarizations from above, so it escapes overdrive suppression to emerge as ventricular pacemaker w/ an inherent rate between 20-40/min. results from: 1) conduction block high in ventricular conduction system but below AV node ventricular foci are not stimulated from above a a ventricular focus escapes to pace ventricles or 2) total failure of SA node and all automaticity above ventricles (downward displacement off pacemaker) w/ ventricles becoming final futile pace to attempt o sustain life. causing decreased blood flow to brain to unconsciousness creating Stokes-Adams syndrome
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atrial escape rhythm
a kind of sinus arrest where atrial focus quickly escapes overdrive suppression to become the dominant pacemaker at its inherent rate. originates in an atrial automaticity focus, so the P' waves are not identical to the previous P waves that were produced by the SA node. active atrial automaticity focus overdrive suppresses all lower, slower foci to become dominant pacing at own rhythm slower than previous sinus rate.
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atrial escape beat
transient sinus block of one cycle by SA node and sufficient pause atrial automaticity foci escape overdrive suppression making an escape beat making P' wave differ from sinus generated caused by transient sinus block
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ventricular escape beat
originates in a ventricular automaticity focus that is no longer overdrive suppressed by regular pacing stimuli from above producing enormous ventricular QRS complex. ventricular automaticity foci escape suppression when not stimulated for at least one up to two cycles and is quite common. cardiac parasympathetic innervation inhibits SA node and atrial and junctional foci but not ventricular. Bursts of excessive parasympathetic activity depress SA node producing pause as well as atrial and junctional foci leaving only ventricle to respond and is usually transient.
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premature beat
an irritable focus spontaneously fires single stimulus spontaneously producing beat earlier than expected in rhythm ex. premature atrial beat, junctional beat, and ventricular beat. very irritable atrial or junctional focus may fire series of rapid pacing impulses to become dominant pacemaker, overdrive suppressing rest
84
atrial and junctional foci becomee irritable because of
adrenaline (epinephrine) released by adrenal glands; increased sympathetic stimulation; presence of caffeine, amphetamines, cocaine, or other B1 receptor stimulants; excess digitalis, some toxins, occasionally ethanol; hyperthyroidism, direct stimulation plus heart oversensitive to adrenergic stimulants; stretch- and to some extent, low O2. substances that activate adrenergic receptors, adrenergic chemicals that mimic substances or conditions that release epinephrine or norepinephrine
85
Pacemaking resets
all centers of automaticity reset rhythm when depolarized by a premature stimulus, so its pacemaking activity rests in step w/ premature beat. next pacing stimulus it generates is one cycle length from premature beat (stimulus) continues one cycle length from in step w/ P' w/ same pacing rate and first cycle after PAB lengthened due to parasympathetic effect on SA node resumé's;ing pace during systole ; however, it has to be depolarized to reset
86
aberrant ventricular conduction
ventricular conduction system is usually receptive to being polarized by PAB, but one branch may not have repolarized and is still in refractory when other is receptive producing slightly widened QRS for premature cycle only.
87
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
88
Ventricular focus can be made irritable by
low oxygen ex. airway obstruction, absence of air ((near-drowning or suffocation), air w/ poor O2 content, minimal blood oxygenation in lungs (pulmonary embolus or pneumothorax), reduced cardiac output (hypovolemic or cariogenic shock), poor to absent coronary blood supply (coronary insufficiency or infarction); low potassium ex. reduced serum potassium (hypokalemia); pathology ex. mitral valve prolapse, stretch, myocarditis and adrenergic stimulants. a very irritable ventricular focus may be so excessively provoked by hypoxia or ischemia that it fires a series of rapid impulses overdrive-suppressing sinus rhythm becoming heart's dominant pacemaker. cocaine causes coronary spasm, making ventricular foci hypoxic and irritibale can cause dangerous.
89
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.
90
Mitral valve prolapse
Barlow syndrome. MVP causes PVCs including runs a VT and multifocal PVCs but it is benign. Mitral valve is floppy and billows into the left atrium during ventricular systolic more common in females slender body slight chest a foreman he experienced dizzy spells and Anxiety exhibit after age 20. during ventricular systole. The billowing valves pull on the chordae that tether them to the papillary muscles in the left ventricle. This traction on the papillary muscles causes localized and ischemia irritating adjacent ventricular automatically having a mid systolic click with a descrendo murmur on auscultation
91
R on T phenomenon
If a PVC falls on a T wave in a situation of hypoxia or low serum potassium it occurs during a vulnerable. And dangerous arrhythmias may result. T Wave takes longer to repolarize because of ischemia
92
Semgmebt versus interval
Segment does not include wave
