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ECG > Electrical axis and chamber enlargement, atrial dysrhythmias, ventricular dysrhythmias > Flashcards

Electrical axis and chamber enlargement, atrial dysrhythmias, ventricular dysrhythmias Flashcards

1
Q

What is normal axis location

A

down and to pt left

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2
Q

What are the vectors from LV like compared to RV

A

LV vectors larger and persist longer

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3
Q

How do you determine QRS axis

A

4 quadrant method: Lead I and aVF

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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 (-.-)

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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)
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6
Q

if mean QRS axis is + in Lead I then you know….

A

axis is bw -90 and +90 degrees

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7
Q

If mean QRS axis is + in aVF you know….

A

the axis is bw 0 and +180 deg

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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
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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

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10
Q

Most common causes of LAD

A
  1. left anterior hemiblock
  2. left ventricular hypertrophy
    other: hyperkalemia, diffuse myocardial disease

*horizontal heart in obese or pregnant individuals

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11
Q

Common causes of RAD

A
  1. can be normal in kids and tall thin adults (“vertical heart shifts QRS axis to +90)
  2. RVH
  3. chronic lung disease
  4. left posterior hemiblock
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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)

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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

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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
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15
Q

Indications and clues for RAE

A
  1. Presence of RVH
  2. R wave greater than S in V1
  3. RAD
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16
Q

Clinical conditions with RAE

A
  1. pulmonic stenosis
  2. Tricuspid stenosis
  3. Tricuspid regurgitation
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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

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18
Q

Normal QRS complex

A

amplitude: 5-30 mm
Duration: 0.06-0.11 sec
*normal Q wave duration <0.04 sec

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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

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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

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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

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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
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23
Q

Normal sinus rhythm newborn

A

110- 150 bpm (160 in premees)

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24
Q

normal sinus rhythm 2 yr

A

85-125 bpm

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25
Q

NSR 4 yr old

A

75-115 bpm

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26
Q

NSR 6 yr old

A

60-100 bpm (same as adult)

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27
Q

What is the significance of sinus tachycardia clinically

A
  • often of no clinical significance
  • can increase myocardial O2 consumption (which can aggravate ischemia –> chest pain, and infarction esp in those with CVD
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28
Q

What is sinus dysrhythmia

A

aka sinus arrhythmia

  • same as NSR except patterned irregularity
  • cycle of slowing then speeding up then slowing again
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29
Q

The beat to beat variation of sinus dysrhythmia is produced by what and corresponds with what

A

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)

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30
Q

What are some general conditions that sinus dysrhythmia can occur in..?

A

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

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31
Q

What is the clinical significance and sx of sinus dysrhythmia?

A

Usually none and has no sx

Some pt and conditions are assoc with palpitations, dizziness and syncope

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32
Q

What is sinus arrest and what does it cause?

A

SA node transiently stops firing

Causes short periods of cardiac standstill until lower level pacemaker d/c or SA node resumes normal function

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33
Q

What is the exact dx for a sinus pause? a sinus arrest?

A

Sinus pause: 1-2 beats dropped

Sinus arrest: 3 or more beats dropped

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34
Q

What is the most prominent characteristic of a sinus arrest? What usually follows?

A

A pause in ECG rhythm producing irregularity

*rhythm usually resumes normal appearance after pause unless escape pacemaker resumes the rhythm

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35
Q

What are some different names for sinus node dysfunction and what is it/who does it affect?

A

“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
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36
Q

What is tx for sinus node dysfunction/ sick sinus syndrome

A

tx may require pacemaker for slow rhythms and meds for fast rhythms

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37
Q

Where do atrial dysrhythmias originate

A

atrial tissue or internodal pathways DUH :)

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38
Q

What types of atrial dysrhythmias are common

A

PAC, a Flutter, a fib, a. tachy, wandering atrial pacemaker, multifocal atrial tachycardia

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39
Q

What 3 mechanisms are believed to cause atrial dysrhythmias?

A

Automaticity
Triggered activity
Reentery (pathways that go both ways not just down)

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40
Q

What effect on heart contraction and circulation/perfusion can atrial dysrhythmias have

A

atrial dysrhythmias can affect ventricular filling time and diminish strength of atrial contraction/kick

Can lead to decreased CO and thus tissue perfusion

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41
Q

What are some key characteristics to look for on EKG strip to distinguish atrial dysrhythmias

A
  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
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42
Q

What is a wandering Atrial pacemaker and how does it show on an EKG

A

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)

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43
Q

What is the cause and clinical significance of a wandering atrial pacemaker?

A

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
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44
Q

What are PACs?

A

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

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45
Q

what makes PACs unique?

A
  • *p waves FOLLOWED BY NONCOMPENSATORY PAUSE

* this is diff from PVC which have a compensatory pause

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46
Q

what exactly is a noncompensatory pause?

A

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)

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47
Q

How should we address PAC’s in pt with healthy hearts

A

isolated PACs in pt with healthy hearts are considered insignificant
*asymp pt usually only require obs

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48
Q

How should we address PAC’s in pt with HD

A

Be aware that PAC’s in pt with HD may predispose pt to more serious atrial dysrhythmias

  • a tachycardia
  • a flutter
  • a fib
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49
Q

What can PACs indicate in pt experiencing acute myocardial infarction

A

early indicator of electrolyte imbalance or CHF in pt experiencing acute myocardial infarction

50
Q

what types of PACs might you see on EKG strip?

A

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
Q

When can PACs be confused with PVCs

A

bc may have wide QRS complexes when seen with abnormal ventricular conduction
*called “PACs with aberrant ventricular conduction”

52
Q

How can we distinguish the PACs with aberrant ventricular conduction (aka wide QRS) from PVCs

A

the PACs will have noncompensatory pause and PVCs will have compensatory pause

53
Q

what are the characteristics of atrial tachycardia

A

rapid dysrhythmia (150-250 bpm) arising from atria

  • rate is so fast it overrides SA node
  • P waves will be different
54
Q

What is the PR interval like in atrial tachycardia

A

*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
Q

what will P waves look like in a tachy

A

upright or inverted; appear diff than underlying rhythm and can be hidden in preceding T wave

56
Q

How can atrial tachycardia occur?

A

in short bursts or sustained

  • short bursts = paroxysmal atrial tachycardia PAT
  • short bursts well tolerated in healthy people
57
Q

In atrial tachycardia, what is the risk with sustained rapid ventricular rates

A

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
Q

How does Multifocal Atrial tachycardia (MAT) present?

A

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
Q

what might MAT (multifocal atrial tachycardia) be confused with

A

atrial fibrillation

of Wandering atrial pacemaker (but faster rate than WAP)

60
Q

What is Supraventricular Tachycardia (SVT)

A

Arises from above ventricles but cannot be defined as atrial or junctional tachy bc P waves cannot be seen sufficiently

61
Q

What types of SVT are there

A

Paroxysmal SVT
nonparoxysmal atraial tachycardia
MAT (multifocal atrial tachycardia)

62
Q

what is atrial flutter and how does it appear on EKG strip?

A

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
Q

What is the tolerance for atrial flutter? How do you determine the ventricular rate in atrial flutter?

A
  • 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
Q

What is atrial fibrillation

A

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
Q

What are characteristics of Atrial fibrillation

A

chaotic baseline, rate >350, totally irregular, absent P waves, unmeasurable PR and QT intervals

66
Q

What effect does atrial fibrillation have on the heart

A

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
Q

A fib increases pt risk for what due to stagnant blood in the atria?

A

predisposes pt to systemic emboli/stroke due to blood forming a clot in the atria

68
Q

What is a junctional dysrhythmia?

A

originate in AV junction (area around AV node and bundle of His)

69
Q

What are key characteristics of Junctional Dysrhythmias? specifically regarding P waves and QRS complex

A
  • 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
Q

What is a premature junctional complex PJC

A

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
Q

What is a junctional escape rhythm

A

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
Q

What are accelerated junctional rhythms

A

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
Q

What is junctional tachycardia

A

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
Q

What did Dr. Pearl say about junctional tachycardia and surgery

A

it is common for patient to experience junctional tachycardia during surgery bc operating near AV node

75
Q

When do Ventricular dysrhythmias occur

A

when the atria, AV junction or both are unable to initiate an electrical impuse –> enhanced automaticity of the ventricular myocardium

76
Q

What are some key features of Ventricular dysrhythmias

A

Wide >0.11 sec, bizarrre QRS complex
T waves in opposite direction of R
Absent P waves

77
Q

What are some types of Ventricular dysrhythmias

A 
Premature ventricular complex (PVC)
Ventricular escape complex
Ventricular tachycardia
Ventricular fibrillation
Asystole
78
Q

What is the prognosis for Ventricular Dysrhythmias

A

can be benign or potentially life threatening (bc ventricles are responsible for CO)

79
Q

Distinguishing characteristic of PVC??

A

Compensatory Pause - tipc of right caliper leg lines up with next R wave

80
Q

What is a PVC

A

early ectopic beats that interrupt normal rhythm. Originate from irritable focus in ventricular conduction or m tissue.

81
Q

Characteristics of PVC

A

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
Q

PVCs that all look the same are called…

A

unifocal/uniform

83
Q

PVCs that look different from each other are called

A

multifocal/multiform

84
Q

What types of PVC’s are there

A 
Bigeminal PVC (1 normal QRS in bw PVC)
Trigeminal PVC (2 normal QRS bw)
Quadrigeminal PVC (3 normal QRS bw)
85
Q

what are 2 PVCs in a row and what do they represent

A

2 PVCs in a row are called a couplet and indicate extreme irritable ventricles

86
Q

What are interpolated PVCs

A

PVCs that fall bw 2 regular complexes and do not disrupt normal cardiac cycle

87
Q

PVCs occurring on or near previous T wave (R on T PVCs) may come before what?

A

R on T PVCs may precipitate ventricular tachycardia or fibrillation

88
Q

What is an idioventricular rhythm

A

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
Q

Accelerated Idioventricular rhythm

A

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
Q

Ventricular tachycardia (VT)

A

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
Q

When can we determine VT is present

A

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
Q

How is VT related to pulses and patient stability?

A

VT can occur with or without pulses

VT pt may be stable or unstable

93
Q

What is a monomorphic VT

A

appearance of each QRS complex is similar

94
Q

What is a polymorphic VT

A

appearance of QRS varies considerably

95
Q

What is Torsades de Pointes and what is it associated with?

A

“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
Q

What is an easy way to identify Torsades de Pointes on an EKG strip?

A

the outline looks like a party streamer!!

97
Q

How should you treat Torsades de Pointes?

A

If pt not in cardiac arrest, infusion of MgSO4- helps

If in cardiac arrest must defibrillate pt

98
Q

What causes ventricular fibrillation and what effect does v fib have on the heart?

A
  • 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
Q

What are characteristics of V fib found on EKG strip?

A

300-500 bpm ventricular unsynchronized impulses, totally chaotic, absent P waves, wavy and chaotic line without logic, absent PR and QT intervals

100
Q

What is the prognosis for patients in V fib?

A

Death is not promptly defibrillated

Most common cause of prehospital cardiac arrests in adults

101
Q

What is Asystole and how does it appear

A

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
Q

What is the prognosis for Asystole

A

Terminal rhythm, chances of recovery extremely low, poor response to attempts at resuscitation

103
Q

What is PEA (pulseless electrical activity)

A

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
Q

What is PEA (pulseless electrical activity) usually associated with

A

assoc with underlying HD

105
Q

What are some reversible causes of PEA (pulseless electrical activity)

A

hypovolemia, pericardial tamponade, tension pneumothorax, massive acute MI, drug OD etc

106
Q

What is a Heart Block

A

partial delay or complete interruptions in cardiac conduction pathway bw atria and ventricles
*deg of block defines type and classification of heart block

107
Q

What are some common causes of heart block

A

Ischemia, Myocardial necrosis, Degenerative disease of conduction system, congenital anomalies, drugs, surgery

108
Q

What are all the possible heart blocks

A

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
Q

clinical significance of 1st deg AV heart block

A

often little or none bc all impulses conducted (just delayed)
*can progress to higher deg block, esp in inferior wall MI

110
Q

EKG of 1st deg AV heart block would show

A

longer than 0.2 sec PR interval

111
Q

What is a 2nd deg AV heart block Type I

A

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
Q

What are some EKG characteristics of 2nd deg AV heart block type I (wenckebach)

A

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
Q

When does a 2nd deg AV heart block Type I take place (wenckebach) and what may this block progress to

A

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
Q

What is a 2nd deg AV heart block type II

A

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
Q

What are some EKG characteristics of 2nd degree AV heart block Type II “Mobitz”

A

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
Q

What is the clinical significance/outlook for pt with 2nd deg type II “Mobitz” AV block

A

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
Q

What is 3rd deg AV heart block

A

COMPLETE block of conduction at or below the AV node; impulses from atria cannot reach ventricles (“escape” QRS complexes)

118
Q

What is a 3rd deg AV heart block also known as? Characterize atrial pacemaker and ventricular pacemaker

A

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
Q

What EKG findings indicate 3rd deg AV heart block

A

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
Q

What are clinical outcomes/prognosis for pt with 3rd deg AV heart block?

A

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

ECG (3 decks)

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