Electrical axis and chamber enlargement, atrial dysrhythmias, ventricular dysrhythmias Flashcards
(120 cards)
1
Q
What is normal axis location
A
down and to pt left
2
Q
What are the vectors from LV like compared to RV
A
LV vectors larger and persist longer
3
Q
How do you determine QRS axis
A
4 quadrant method: Lead I and aVF
4
Q
Locations of 4 quadrants/axis
A
Axis: deg range (Lead I, Lead avF)
Normal: 0 to +90 deg (+,+)
LAD: 0 to -90 deg (+,-)
RAD: +90 to +180 (-,+)
indeterminate/extreme: -90 to -180 (-.-)
5
Q
What are the degree locations of the different leads
A
Lead I: 0 deg Lead II: 60 deg (normal quad) avF: 90 deg Lead III (+120 deg) (RAD) aVR: -150 deg (extreme) avL: -30 deg (LAD)
6
Q
if mean QRS axis is + in Lead I then you know….
A
axis is bw -90 and +90 degrees
7
Q
If mean QRS axis is + in aVF you know….
A
the axis is bw 0 and +180 deg
8
Q
If mean QRS is + in both Lead I and aVF you know
A
axis is bw 0 and +90 deg
- if net upright QRS in Lead I = Lead aVF, mean QRS axis is +45 deg
- if deflection lead I more positive than aVF, then lies closer to lead I (bw 0-45 deg) and vice versa
9
Q
If QRS complex is isoelectric in any limb lead then (positive deflection = negative deflection)
A
the axis is about 90 deg AWAY from the limb lead
10
Q
Most common causes of LAD
A
- left anterior hemiblock
- left ventricular hypertrophy
other: hyperkalemia, diffuse myocardial disease
*horizontal heart in obese or pregnant individuals
11
Q
Common causes of RAD
A
- can be normal in kids and tall thin adults (“vertical heart shifts QRS axis to +90)
- RVH
- chronic lung disease
- left posterior hemiblock
12
Q
Hypertrophy vs enlargement (*note: can exist together)
A
Hypertrophy: implies thickening of wall, usually due to increased effort against high pressure (high BP, stenotic valve)
Enlargement/dilatation: often due to stretching of cardiac chamber from volume overload (LAE due to Mitral insufficiency/MR)
13
Q
P wave: normal, RAE, LAE, biatrial enlargement
A
normal: amp 0.5-2.5 mm, 0.06-0.1 sec duration
RAE: amp >2.5 mm (p pulmonale)
LAE: duration > 0.1 sec (p mitrale)
Biatrial enlargement: increased amp and duration
14
Q
criteria/dx of RAE
A
- use Leads II and VI
- P wave > 2.5mm
- if P wave biphasic and initial component is taller than terminal component
#help: 2 to 6 hours LAEs in RAEs of sun
15
Q
Indications and clues for RAE
A
- Presence of RVH
- R wave greater than S in V1
- RAD
16
Q
Clinical conditions with RAE
A
- pulmonic stenosis
- Tricuspid stenosis
- Tricuspid regurgitation
17
Q
Criteria/dx LAE
A
*use Leads II and VI
*P wave >0.1 sec duration (usually Lead II); often with notching “P mitrale”
*terminal portion of P wave in VI is: negative, >0.04 sec duration, and >1mm deep
#help: 2 to 6 hours LAEs n RAEs of sun
18
Q
Normal QRS complex
A
amplitude: 5-30 mm
Duration: 0.06-0.11 sec
*normal Q wave duration <0.04 sec
19
Q
RVH vs LVH
A
RVH much less common, and usually due to pulmonary HTN or pulmonary stenosis
RAD occurs due to increased thickness of RV
20
Q
criteria/dx for RVH
A
- Use V1 sometimes V6
- RAD (-,+)
- R wave > S wave in V1 (R usually >7mm)
- S wave > R wave in V6 (not require)
note: starting with V1 the R waveforms take upward deflection but moving toward V6, waveforms take downward deflection
21
Q
criteria/dz LVH
A
*use V1, 2, 5, 6, AVL, Lead I, Lead III
*sum of deepest S in V1 or V2 + tallest R in V5 or 6 totals > 35mm
*R in aVL > 11mm
R in Lead I + S in Lead III >25mm
22
Q
What is a potential negative SE of sinus bradycardia if the HR slows to the point where CO drops sufficiently
A
Hypotension can result
- pt less tolerant of rates <45 bpm
- sinus bradycardia is often insignificant
23
Q
Normal sinus rhythm newborn
A
110- 150 bpm (160 in premees)
24
Q
normal sinus rhythm 2 yr
A
85-125 bpm
25
NSR 4 yr old
75-115 bpm
26
NSR 6 yr old
60-100 bpm (same as adult)
27
What is the significance of sinus tachycardia clinically
* often of no clinical significance
* can increase myocardial O2 consumption (which can aggravate ischemia --> chest pain, and infarction esp in those with CVD
28
What is sinus dysrhythmia
aka sinus arrhythmia
* same as NSR except patterned irregularity
* cycle of slowing then speeding up then slowing again
29
The beat to beat variation of sinus dysrhythmia is produced by what and corresponds with what
produced by irregular firing of the SA node; usually corresponds with respiratory cycle and changes in intrathoracic pressure (HR increases during inspiration and decreases during expiration)
30
What are some general conditions that sinus dysrhythmia can occur in..?
Can occur naturally in athletes, children and older adults
| Also: pt with HD or inferior wall MI, medications ie digitalis and morphine, increased intracranial pressure
31
What is the clinical significance and sx of sinus dysrhythmia?
Usually none and has no sx
| Some pt and conditions are assoc with palpitations, dizziness and syncope
32
What is sinus arrest and what does it cause?
SA node transiently stops firing
| Causes short periods of cardiac standstill until lower level pacemaker d/c or SA node resumes normal function
33
What is the exact dx for a sinus pause? a sinus arrest?
Sinus pause: 1-2 beats dropped
| Sinus arrest: 3 or more beats dropped
34
What is the most prominent characteristic of a sinus arrest? What usually follows?
A pause in ECG rhythm producing irregularity
| *rhythm usually resumes normal appearance after pause unless escape pacemaker resumes the rhythm
35
What are some different names for sinus node dysfunction and what is it/who does it affect?
"sick sinus syndrome" or "brady-tachy syndrome"
* primarily elderly due to degeneration of SA node
* periods of bradycardia, tachycardia, prolonged pauses or alternating brady and tachy
36
What is tx for sinus node dysfunction/ sick sinus syndrome
tx may require pacemaker for slow rhythms and meds for fast rhythms
37
Where do atrial dysrhythmias originate
atrial tissue or internodal pathways DUH :)
38
What types of atrial dysrhythmias are common
PAC, a Flutter, a fib, a. tachy, wandering atrial pacemaker, multifocal atrial tachycardia
39
What 3 mechanisms are believed to cause atrial dysrhythmias?
Automaticity
Triggered activity
Reentery (pathways that go both ways not just down)
40
What effect on heart contraction and circulation/perfusion can atrial dysrhythmias have
atrial dysrhythmias can affect ventricular filling time and diminish strength of atrial contraction/kick
Can lead to decreased CO and thus tissue perfusion
41
What are some key characteristics to look for on EKG strip to distinguish atrial dysrhythmias
1. P waves that different in appearance from normal sinus P waves
2. abnormal, shortened, or prolonged PR intervals
3. narrow or normal QRS complex
42
What is a wandering Atrial pacemaker and how does it show on an EKG
Pacemaker site shifts bw SA node, atria and/or AV junction
*produces P waves that change in appearance
(norm rate, rhythm slightly irregular, changing P wave, normal QRS, PR interval varies)
43
What is the cause and clinical significance of a wandering atrial pacemaker?
Usually caused by inhibitory vagal effect of respiration on SA node and AV junction
* norm in children, older adults and well conditioned athletes; usu not significant
* may be related to organic HD and drug toxicity, specifically digitalis/digoxin
44
What are PACs?
early ectopic beats originating outside SA node
(irregular rhythm, P waves different (upright in lead II but diff morphology), QRS norm, PR varies)
noncompensatory pause
45
what makes PACs unique?
* *p waves FOLLOWED BY NONCOMPENSATORY PAUSE
| * this is diff from PVC which have a compensatory pause
46
what exactly is a noncompensatory pause?
Pause where there are less than 2 full R-R intervals bw R wave of normal beat which preceds the PAC and the R wave of the first normal beat that follows it (doesn't stay on track; tip of caliper fails to line up with next R wave)
47
How should we address PAC's in pt with healthy hearts
isolated PACs in pt with healthy hearts are considered insignificant
*asymp pt usually only require obs
48
How should we address PAC's in pt with HD
Be aware that PAC's in pt with HD may predispose pt to more serious atrial dysrhythmias
- a tachycardia
- a flutter
- a fib
49
What can PACs indicate in pt experiencing acute myocardial infarction
early indicator of electrolyte imbalance or CHF in pt experiencing acute myocardial infarction
50
what types of PACs might you see on EKG strip?
Bigeminal (PAC every other R wave)
Trigeminal (2 normal R waves in bw each PAC)
Quadrigeminal (3 normal R waves in bw each PAC)
51
When can PACs be confused with PVCs
bc may have wide QRS complexes when seen with abnormal ventricular conduction
*called "PACs with aberrant ventricular conduction"
52
How can we distinguish the PACs with aberrant ventricular conduction (aka wide QRS) from PVCs
the PACs will have noncompensatory pause and PVCs will have compensatory pause
53
what are the characteristics of atrial tachycardia
rapid dysrhythmia (150-250 bpm) arising from atria
* rate is so fast it overrides SA node
* P waves will be different
54
What is the PR interval like in atrial tachycardia
*PR interval can be normal, shorter than 0.12 sec if impulse from lower right atrium or upper part of AV junction, or unmeasureable if can't distinguish from preceding T waves
55
what will P waves look like in a tachy
upright or inverted; appear diff than underlying rhythm and can be hidden in preceding T wave
56
How can atrial tachycardia occur?
in short bursts or sustained
* short bursts = paroxysmal atrial tachycardia PAT
* short bursts well tolerated in healthy people
57
In atrial tachycardia, what is the risk with sustained rapid ventricular rates
risk: ventricular filling may not be complete during diastole; can comprimase CO in pt with underlying HD bc fast HR increases O2 requirement
* may increase myocardial ischemia and potentially lead to MI
58
How does Multifocal Atrial tachycardia (MAT) present?
pathological condition presenting with changing P wave morph and HR 120-150
* irregular rhythm due to multiple foci
* same features as wandering atrial pacemaker but faster rate (changing P waves, variable PR)
59
what might MAT (multifocal atrial tachycardia) be confused with
atrial fibrillation
of Wandering atrial pacemaker (but faster rate than WAP)
60
What is Supraventricular Tachycardia (SVT)
Arises from above ventricles but cannot be defined as atrial or junctional tachy bc P waves cannot be seen sufficiently
61
What types of SVT are there
Paroxysmal SVT
nonparoxysmal atraial tachycardia
MAT (multifocal atrial tachycardia)
62
what is atrial flutter and how does it appear on EKG strip?
rapid depolarization of SINGLE FOCUS in the atria at a rate of 250-350 bpm
*p waves absent, instead saw tooth flutter "F" waves present; PR and QT intervals unmeasurable
63
What is the tolerance for atrial flutter? How do you determine the ventricular rate in atrial flutter?
* often well tolerated
* # impulses conducted through AV node determines ventricular rate (ex 3:1 conduction ratio)
* slower ventricular rates 150 bpm can compromise CO
64
What is atrial fibrillation
Chaotic, asynchronous firing of multiple areas within the atria at >350 bpm resulting in totally irregular rhythm with no discernible P waves. Chaotic baseline of f waves. (get QRS complexes every so often when signal manages to get through AV node)
65
What are characteristics of Atrial fibrillation
chaotic baseline, rate >350, totally irregular, absent P waves, unmeasurable PR and QT intervals
66
What effect does atrial fibrillation have on the heart
a fib leads to loss of atrial kick decreasing CO up to 25% --> pt may dev intra atrial emboli as atria not contracting and blood stagnates in atrial chambers forming clot *predisposes pt to systemic emboli/stroke
67
A fib increases pt risk for what due to stagnant blood in the atria?
predisposes pt to systemic emboli/stroke due to blood forming a clot in the atria
68
What is a junctional dysrhythmia?
originate in AV junction (area around AV node and bundle of His)
69
What are key characteristics of Junctional Dysrhythmias? specifically regarding P waves and QRS complex
* potentially inverted P wave with short PR interval or absent P waves buried in QRS complex, or P waves that follow QRS
* QRS usually normal unless intraventricular conduction defect, aberrancy or preexcitation
70
What is a premature junctional complex PJC
single early electrical impulse that arises from AV junction
*irregular rhythm due to early beat, P wave of PJC inverted and may be before, buried in, or after QRS; if present PR interval shorter than 0.12
71
What is a junctional escape rhythm
arises from AV junction rate 40-60 BPM
*regular rhythm, P waves inverted and before, during or after QRS, shorter PR if present
note: accelerated junctional rhythm 60-100 bpm; junctional tachycardia is 100-180
72
What are accelerated junctional rhythms
arise from AV junction at rate of 60-100 BPM
| *P waves are inverted, may appear before, during or after ARS, if present PR interval is short <0.12
73
What is junctional tachycardia
fast ectopic rhythm that arises from bundle of His at 100-180 BPM
*regular rhythm, P wave inversted and are before, during or after QRS, normal QRS, PR shorter if present
74
What did Dr. Pearl say about junctional tachycardia and surgery
it is common for patient to experience junctional tachycardia during surgery bc operating near AV node
75
When do Ventricular dysrhythmias occur
when the atria, AV junction or both are unable to initiate an electrical impuse --> enhanced automaticity of the ventricular myocardium
76
What are some key features of Ventricular dysrhythmias
Wide >0.11 sec, bizarrre QRS complex
T waves in opposite direction of R
Absent P waves
77
What are some types of Ventricular dysrhythmias
```
Premature ventricular complex (PVC)
Ventricular escape complex
Ventricular tachycardia
Ventricular fibrillation
Asystole
```
78
What is the prognosis for Ventricular Dysrhythmias
can be benign or potentially life threatening (bc ventricles are responsible for CO)
79
Distinguishing characteristic of PVC??
Compensatory Pause - tipc of right caliper leg lines up with next R wave
80
What is a PVC
early ectopic beats that interrupt normal rhythm. Originate from irritable focus in ventricular conduction or m tissue.
81
Characteristics of PVC
Irregular rhythm, P waves unrelated to QRS,
wide and bizzare QRS complex,
T waves in opposite direction of R wave,
PR absent, QT usually prolonged
82
PVCs that all look the same are called...
unifocal/uniform
83
PVCs that look different from each other are called
multifocal/multiform
84
What types of PVC's are there
```
Bigeminal PVC (1 normal QRS in bw PVC)
Trigeminal PVC (2 normal QRS bw)
Quadrigeminal PVC (3 normal QRS bw)
```
85
what are 2 PVCs in a row and what do they represent
2 PVCs in a row are called a couplet and indicate extreme irritable ventricles
86
What are interpolated PVCs
PVCs that fall bw 2 regular complexes and do not disrupt normal cardiac cycle
87
PVCs occurring on or near previous T wave (R on T PVCs) may come before what?
R on T PVCs may precipitate ventricular tachycardia or fibrillation
88
What is an idioventricular rhythm
slow dysrhythmia (20-40 BPM) with wide QRS complexes that arise from the ventricles
* P waves not visible bc hidden in QRS complexes (if present, not related to QRS complex)
* T waves in oppositve direction of R wave, PR interval absent, prolonged QT interval
89
Accelerated Idioventricular rhythm
idioventricular rhythm that exceeds the inherent rate of the ventricles (40-100bpm)
* P waves hidden in QRS (if present, not related to QRS complex)
* QRS wide and bizarre, T waves opposite of R
* PR absent, QT prolonged
90
Ventricular tachycardia (VT)
fast dysrhythmia (100-250 bpm) that arises from the ventricles
* arises from single site in ventricles
* p waves hidden in QRS complex (if present, not related to QRS), QRS wide and bizarre, T in opposite direction of R, PR interval absent
91
When can we determine VT is present
V tachycardia when there are 3 or more PVCs in a row; brief episode = run, burst or salvo of ventricular tachycardia
* may come in bursts of 6-10 PVC complexes or persist (sustained VT)
* if QRS present, not related to QRS complex
92
How is VT related to pulses and patient stability?
VT can occur with or without pulses
| VT pt may be stable or unstable
93
What is a monomorphic VT
appearance of each QRS complex is similar
94
What is a polymorphic VT
appearance of QRS varies considerably
95
What is Torsades de Pointes and what is it associated with?
"twisting about the points"; a unique variant of polymorphic VT
*may be associated with prolonged QT interval, drug induced or assoc with electrolyte abnormalities
96
What is an easy way to identify Torsades de Pointes on an EKG strip?
the outline looks like a party streamer!!
97
How should you treat Torsades de Pointes?
If pt not in cardiac arrest, infusion of MgSO4- helps
If in cardiac arrest must defibrillate pt
98
What causes ventricular fibrillation and what effect does v fib have on the heart?
* V fib results from chaotic firing of mult sites in the ventricles 300-500 bpm
* causes heart muscle to quiver rather than contract efficiently --> no effective contraction and no CO
99
What are characteristics of V fib found on EKG strip?
300-500 bpm ventricular unsynchronized impulses, totally chaotic, absent P waves, wavy and chaotic line without logic, absent PR and QT intervals
100
What is the prognosis for patients in V fib?
Death is not promptly defibrillated
| Most common cause of prehospital cardiac arrests in adults
101
What is Asystole and how does it appear
asystole = absence of any cardiac activity, appearing as a flat or nearly flat line on EKG
*complete cessation of cardiac output (get light headed, pass out and die)
102
What is the prognosis for Asystole
Terminal rhythm, chances of recovery extremely low, poor response to attempts at resuscitation
103
What is PEA (pulseless electrical activity)
condition where there is an organized electrical rhythm on ECG monitor (which should produce a pulse) but pt is pulseless and apneic
*electrical activity but no cardiac output
104
What is PEA (pulseless electrical activity) usually associated with
assoc with underlying HD
105
What are some reversible causes of PEA (pulseless electrical activity)
hypovolemia, pericardial tamponade, tension pneumothorax, massive acute MI, drug OD etc
106
What is a Heart Block
partial delay or complete interruptions in cardiac conduction pathway bw atria and ventricles
*deg of block defines type and classification of heart block
107
What are some common causes of heart block
Ischemia, Myocardial necrosis, Degenerative disease of conduction system, congenital anomalies, drugs, surgery
108
What are all the possible heart blocks
1st deg AV: consistent delay in conduction thru AV
2nd deg AV block type I (wenckebach): block at AV node, progressive lengthening of PR interval
2nd deg AV block type II: intermittent block at the bundle of His, some atrial impulses not conducted
3rd deg AV: complete block of conduction at or below AV, impulses cant reach ventricles
109
clinical significance of 1st deg AV heart block
often little or none bc all impulses conducted (just delayed)
*can progress to higher deg block, esp in inferior wall MI
110
EKG of 1st deg AV heart block would show
longer than 0.2 sec PR interval
111
What is a 2nd deg AV heart block Type I
intermittent block at the level of the AV node
also referred to as "wenckebach"
*PR interval progressively longer until a QRS complex is dropped then cycle begins again
112
What are some EKG characteristics of 2nd deg AV heart block type I (wenckebach)
more P waves than QRS
* patterned irregularity
* PR interval progressively increases/lengthens until QRS dropped
* after dropped beat, the next PR interval is shorter, cycle repeats
113
When does a 2nd deg AV heart block Type I take place (wenckebach) and what may this block progress to
may occur in otherwise healthy people; usually transient and reversible
* may progress to more serious blocks (particularly if it occurs early in MI)
* if dropped ventricular beats occur freq, pt may show s/sx of decreased CO
114
What is a 2nd deg AV heart block type II
2nd deg AV block type II = "Mobitz"
*intermittent block at bundle of His or bundle branches resulting in atrial impulses that are not conducted to the ventricles
115
What are some EKG characteristics of 2nd degree AV heart block Type II "Mobitz"
More P waves than QRS
PR interval is prolonged, duration of PR interval is constant
Intermittently a P wave occurs and is not followed by a QRS complex (conduction to ventricles is blocked)
116
What is the clinical significance/outlook for pt with 2nd deg type II "Mobitz" AV block
This is a serious dysrhythmia, usually considered "malignant" in emergency setting
*can result in decreased CO and produce s/sz of hypoperfusion
may progress to more severe heart block and ventricular systole
117
What is 3rd deg AV heart block
COMPLETE block of conduction at or below the AV node; impulses from atria cannot reach ventricles ("escape" QRS complexes)
118
What is a 3rd deg AV heart block also known as? Characterize atrial pacemaker and ventricular pacemaker
Also called "Complete Heart Block"
Atrial pacemaker site is the SA node (atrial rate 60-100 bpm)
ventricular pacemaker site is an escape rhythm (from AV junction rate 40-60 bpm) (from ventricles rate 20-40 bpm)
119
What EKG findings indicate 3rd deg AV heart block
upright and round P waves "MARCH RIGHT THROUGH THE QRS complexes"
= no association bw P waves and QRS complex
*atrial rhythm and ventricular rhythms are reg but not related
*QRS complexes are normal if escape focus is junctional and widened f escape focus inventricular
120
What are clinical outcomes/prognosis for pt with 3rd deg AV heart block?
well tolerated as long as the escape rhythm is fast enough to gen enough CO for adequate perfusion
*Can result in decreased CO bc of asynchronous action of the atria and ventricles and if ventricular rate is slow
