Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Leadership > EKG Exam > Flashcards

EKG Exam Flashcards

1
Q
A
  • 2nd degree block: type 2
  • some p waves conduct, some don’t
  • rhythm regular if conduction ratio is constant; if variable, R-R interval will be irregular
  • rate atrial normal; ventricular bradycardic at 1/2, 1/3, or 1/4 of atrial
  • p wave upright, uniform, more of these than QRS complexes
  • PR interval constant but longer than normal
  • QRS normal, 0.12 sec or less
  • QT usually normal, less than 1/2 preceding R-R
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

medications for V.Tach

A
  • amiodarone 150 mg IV over 10 min
    • followed by continuous infusion
  • if unstable - cardiovert
  • torsades de pointes
    • mag sulfate 1-2g IV over 5-60 min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is this rhythm?

A

asystole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

concerns and treatment with complete heart block

A
  • concerns
    • hemodynamic compromise
    • CHB common PEA
  • treatment
    • transcutaneous pacing
    • atropine - only acts on atria
    • dopamine or epi drip - will impact both atria and ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

clinical presentation of sinus tachycardia

A
  • depends on underlying cause and individual’s ability to tolerate rapid HR
  • may be symptomatic
    • hypotension, chest pain, SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

symptoms of bradycardias

A
  • hypotension
  • poor peripheral vascular assessment
  • change in mental status
  • fatigue, lethargy, dizziness, near syncope
  • chest pain
  • SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

relative refractory period

A
  • period of time following absolute refractory period
  • heart can respond to strong stimulus, but response will be abnormal
    • R on T phenomenon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

etiology of PVCs

A
  • hypokalemia, hypomagnesemia
  • hypoxia
  • bradycardia
  • caffeine, ETOH, tobacco
  • MI
  • dig toxicity
  • exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

morphology of P wave and A:V ration in dysrrhythmia interpretation

A
  • are all P waves the same?
    • all coming from same source
  • do some look different?
    • dramatically different morphologies indicate taking different paths from atria to ventricles
  • A:V ratio is 1:1?
    • atrial activity = p wave
    • ventricular activity = QRS complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A
  • sinus tachyardia
  • rhythm regular
  • rate > 100 bpm
  • P wave for every QRS; same size and shape
  • PR interval normal, 0.10-0.20 sec
  • QRS same size and shape; duration normal (0.04-0.12 sec
  • QT interval​ normal (0.36-0.40 sec)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

causes of first degree heart block

A
  • cardiomyopathy
  • ischemia or injury to AV node
  • valvular disorders, digitalis toxicity
  • mechanical injury to AV node or junctional tissue
  • common in beta blockers
    • slows down AV node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

treatment for A.fib

A
  • rate control: meds with negative chronotropic and/or negative dromotropic properties to slow conduction speed through AV node
    • B-blockers, Ca channel blockers, amiodarone, digoxin
  • anticoagulation to prevent clot becoming thrombus
    • check with echo
    • chronic anticoag therapy (coumadin, prodaxa, xarelto)
  • cardioversion
  • EP procedures to ablate pathologic tissue
  • MAZE procedure to carve up atria to prevent abnormal foci from conducting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PR Interval

A
  • atrial to ventricular conduction time
  • time for impulse to travel through atria, through AV node, down to ventricles
  • most of delay is located in AV node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

etiologies of sinus tachycardia

A
  • non-physiologic conditions
    • exercise, caffeine, smoking, alcohol, emotions, pain, anxiety
  • physiologic stressors
    • hypovolemia, fever, anemia, early sepsis, hypermetabolic states, heart failure, allergic rxn
  • medications
    • atropine, epi, dopamine, norepi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

junctional rhythm overview

A
  • rhythm from AV junction below AV node in bundel of His
  • if conduction from SA node disrupted d/t SA or AV node damage, no impulses come down from atria in time
  • cells in junctional tissue step in has backup pacemaker to preseve life (junctional “escape” rhythm)
  • rate is less than that of SA node (40-60)
  • impulse conducted down ventricle but up atria, so P wave is late and inverted - QRS is normal
    • P waves can be before, during, or after QRS
    • lose atrial kick
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

parasympathetic stimulation

A
  • occurs through control of vagus nerve
    • vagal stimulation slows heart (valsalva maneuver)
  • only affects atria (vagal nerve innervates)
    • atropine will speed up heart via decreasing vagal suppression
    • BUT with heart block, will not conduct down to improve ventricular rate
  • atropine lifts vagal suppression and increases HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of second degree heart block: type 2

A
  • worsening ischemia or injury to AV node or junctional tissue
  • cardiomyopathy
  • valve disease
  • digialis toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

refractory period

A

period of time after a cell has depolarized during which it cannot depolarize again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

treatment for asystole

A
  • CPR, epi, correct underlying cause
  • meds are not rhythm specific and do not improve survival to discharge
  • check for DNR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

sympathetic stimulation

A
  • catecholamines
    • epi, norepi, dopamine
  • affects the atria and ventricles
    • can give endogenous substances via exogenous methods as code drugs (epi is #1)
  • increases HR, conduction velocity, irritability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

anticipated interventions for SVT

A
  • treat underlying cause
  • valsalva maneuvers
  • medications
    • push adenosine as close to heart as possible and elevate that extremity - will cause chest pain and anxiety
  • synchronized cardioversion if there is a pulse
    • synced to R wave to avoid R on T
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

etiologies of SVT

A
  • stress
  • metabolic dx
  • medications
  • cardiac dx
  • anemia
  • thyrotoxicosis
  • hypoxia
  • cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A
  • superior level junctional rhythm
  • upside down P waves before QRS
  • PR interval shorter than normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

P wave

A

atrial depolarization as impulse travels through atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

etiologies of sinus bradycardia

A
  • normal in athletes
  • sleep
  • vagal stimulation
  • increased parasympathetic tone d/t cerebral edema or subdural hematoma
  • decreased sympathetic tone d/t SCI
  • decreased metabolic rate d/t hypothyroidism or hypothermia
  • inferior wall MI
  • drugs such as beta blockers, calcium channel blockers, digoxin, antiarrhythmics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

PR interval in dysrrhythmia interpretation

A
  • usually between .12-.2 s (120-200 ms)
  • how long is it taking impulse to travel from atria through AV node?
  • how long is it delayed until getting to ventricle?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

clinical presentation of normal sinus rhythm

A

usually does not cause hemodynamic instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

R on T phenomenon

A
  • PVC falls on preceding initial down slop of T wave
  • may cause deterioration into unstable rhythm
    • Vf, VT, torsades de pointes
    • due to new electrical stimulus during relative refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

repolarization

A
  • return of cell’s membrane to resting state
    • positive and negative charges return to original positions
  • cells must repolarize before depolarizing again
  • sodium and calcium move out of cell, potassium back in
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
A
  • junctional rhythm
  • rate 40-60
  • rhythm regular
  • P wave inverted; immediately before/after QRS or hidden in QRS
  • PR interval short - 0.10 sec or less
  • QRS normal, 0.12 sec or less
  • QT less than 1/2 preceding R-R
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
A
  • third degree (complete) heart block
  • rhythm atria regular; ventricle regular - different
  • rate atrial rate normal; ventriclular rate slower…
    • …if junctional focus - 40-60
    • …if ventricular focus 20-40
  • p wave upright, uniform, more of these than QRS complexes
  • PR interval none, no relationship to QRS
  • QRS = 0.12 sec if junctional focus; >/= 0.12 if ventricular focus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Purkinje Fibers

A
  • bundle branches terminate in this network branching of fibers
  • conduction through Purkinje fibers is extremely rapid
    • spreads throughout inner surface of both ventricles
  • fibers contain pacemaker cells with inherent rate of 20-40 times/minute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

anticipated interventions for normal sinus rhythm

A

no treatment is usually necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q
A
  • electricity flows from upper right to lower left
  • right arm negative; left leg positive
  • as electricity flows through heard and down towards left leg
    • towards positive lead
    • positive ECG deflection
  • flow towards negative lead = negative deflection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

concerns with V.tach

A
  • response varies
  • asymptomatic –> pulseless
  • bad CO, bad pumping
  • no diastolic filling
  • no perfusion of heart b/c no diastole
    • why rapid deterioration is imminent - V.fib
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
A
  • accelerated junctional rhythm
  • rate 60-100; > 100 = tachycardia
  • P wave same as junctional escape
  • PR interval short, if measurable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

atrioventricular node

A
  • impulse passes from internodal tracts through AV node to reach ventricles
  • located at top of interventricular septum in right atrium near coronary sinus
  • cardiac impulse is delayed here to allow for ventricular filling during atrial contraction (atrial kick is 25% of ventricular filling, occurring after diastolic filling)
  • acts as gatekeeper by controlling number of atrial impulses reaching ventricles
    • normally no more than 180 impulses/minute
  • AV node does NOT possess pacemaker cells - surrounding junctional tissue does
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

overview of supraventricular tachycardia

A
  • fast rhythms originating above ventricles
    • atria, junctional tissue, sometimes sinus node
  • usually paroxysmal, but may sustain in some cases
  • rhythms that cannot be identified as atrial tachycardia, junctional tachycardia, sinus tachycardia, or atrial flutter are all grouped into this classification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q
A
  • sinus bradycardia
  • rhythm regular
  • rate < 60 bpm
  • P wave for every QRS; all same size and shape
  • PR interval normal, 0.10-0.20 sec
  • QRS all same size and shape; duration normal - 0.04-0.12 sec
  • QT interval normal: 0.36-0.40 sec
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

causes of asystole

A
  • untreated Vtach or Vfib
  • electrocution
  • profound electrolyte or acid-base imbalance
  • MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
A
  • asystole
  • rate none
  • rhythm none
  • p wave none
  • PR interval none
  • QRS none
  • QT interval none
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

internodal tracts & Bachman’s bundle

A
  • carry cardiac impulse from SA node
  • 3 tracts
    • anterior
    • middle (Wenkebach)
    • posterior (Thorel’s)
  • Bachman’s bundle
    • interatrial pathway facilitating transmission from the right to left atrium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q
A
  • normal sinus rhythm originating from SA node
  • regular atrial and ventricular rhythm
  • 60-100 bpm
  • p wave for every QRS; p waves same size and shape
  • PR interval normal: 0.10-0.20 sec
  • QRS waves same size and shape; duration normal - 0.04-0.12 sec
  • QT interval normal: 0.36-0.40 sec
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

etiologies of atrial fibrillation

A
  • hypoxia
  • ischemia/infarction
  • electrolyte disturbances
  • cardiac surgery
  • excessive adrenergic stimulation
    • catecholamine surge from stress, surgery
  • cardiomyopathy
  • CHF
  • pericarditis
  • alcohol withdrawal
  • hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

etiology, causes, and treatment of ventricular escape rhythm

A
  • etiology: failure of SA and AV nodes to pacemake
  • causes:
    • ischemia, infarction
    • severe acid-base disturbances
    • cardiomyopathy
    • dig toxicity
  • treatment
    • transcutaneous pacing
    • dopamine or epi drip
    • DO NOT SUPPRESS VENT ESCAPE RHYTHM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

causes of third degree heart block

A
  • untreated digitalis toxicity
  • worsening ischemia/injury
  • cardiomyopathy
  • valvular disease
  • mechanical trauma to AV node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

QT interval

A

time from start of depolarization of the ventricles to end of the relative refractory period

beginning of QRS complex to end of T wave

48
Q

sinoatrial node

A
  • posterior wall of the right atrium
  • “natural pacemaker” of the heart
  • inrinsic rate of 60-100 times/minute
49
Q
A
  • mid-level junctional rhythm
  • P waves during QRS - drowned out by much bigger QRS
50
Q

what is pulseless electrical activity?

A
  • any rhythm w/o pulse
    • except asystole, VF, VT
  • dissociation between the electrical and mechanical functions of heart
  • always ask: is there a pulse?
    • CPR if no pulse
    • large bore IV access (better for circulation)
    • epi 1mg IVP q3-5 min
51
Q

what are PVCs?

A
  • early beats from ventricle
  • make ventricular rhythm irregular
  • can be in individual complexes, pairs, triplets
    • bigeminy, trigeminy, quadrageminy
    • unifocal or multifocal
  • conduction from cell to cell instead of rapidly across tissue
  • precursors to V.tach and V.fib
52
Q

treatment for VTach

A
  • pulseless - defibrillate
  • pulse with serious S/Sx - synchronized cardioversion
  • pusle without serious S/Sx - medication trials
53
Q

treatment of bradycardias

A
  • treated only when symptomatic
  • atropine 0.5 mg q3-5 min (total 0.03-0.04 mg/kg)
  • transcutaneous pacing as bridge therapy
  • dopamine infusion 2-10 ug/kg/min
  • epi infusion 2-10 ug/min
    • epi and dopamine have more general response if atropine not working
54
Q

overview of ventricular escape rhythm

A
  • potentially lethal - requires immediate assessment and appropriate intervention
  • presentations very from asymptomatic to complete cardiac arrest
  • likely to result in decreased CO, decreased perfusion
    • discomfort, anxiety, fear
55
Q
A
  • low-level junctional rhythm
  • upside down P waves after QRS
    • sort of hidden in T wave
56
Q

causes of V.fib

A
  • untreated V.tach
  • MI
  • electrolyte imbalances
  • acid-base disturbances
  • hypoxia
  • cardiac trauma
  • electrical shock
57
Q
A
  • ventricular escape rhythm
  • rhythm regular
  • rate below 40 bpm
  • PR interval immeasurable
  • QRS greater than .12 sec, uniform morphology
  • QT interval difficult to discern from T-wave - less than 1/2 R-R if measurable
58
Q

anticipated interventions for sinus tachycardia

A
  • beta-blockers, calcium channel blockers
  • if HR exceeds 150bpm with serious S/Sx
    • tachycardia should be cardioverted
    • sinus tachycardia will not respond to cardioversion
      • need to treat underlying problem
59
Q

what type of PVC is this?

A

couplet - two PVCs in a row (uniform or multiform)

also known as “pair”

60
Q
A
  • atrial fibrillation
  • rhythm: atrial - chaotic; ventricular - irregularly irregular
  • rate: atrial 350-700 bpm; ventricular > 100 bpm if uncontrolled; < 100 bpm if controlled
  • P waves: fibrillatory waves or “f” waves (coarse or fine)
  • PR interval: unable to measure
  • QRS: narrow, should be same: 0.04-0.12 sec
61
Q

why is there a pause after a PAC?

A

compensatory pause - occurs b/c heart is expecting to go back to underlying rhythm

62
Q

what is this rhythm?

63
Q

clinical presentation of SVT

A
  • palpitations, angina
  • dyspnea, anxiety
  • not enough passive diastolic fill time of ventricles
64
Q

concerns for second degree heart block: type 1

A
  • hemodynamic implications based on HR
  • individual symptoms vary
  • watch for progression of block
65
Q

treatments for accelerated junctional rhythms

A
  • remove underlying cause
  • control HR
  • meds to limit automaticity of junction
    • B blockers
    • amiodarone
    • Ca channel blockers
66
Q

T wave

A

ventricular repolarization as ventricules return to resting electrical state

67
Q

treatment for atrial flutter

A
  • similar to A.fib
  • rate control - med with negative chronotropic and/or negative dromotropic properties to slow conduction speed through A/V
    • B-adrenergic blockers
    • calcium channel blockers
    • amiodarone
    • digoxin
  • anticoagulation - coumadin, prodaxa, xarelto
  • often cardioversion
  • EP procedures - tissue ablation
  • MAZE - carve up atria to prevent abnormal conduction
68
Q

concerns and treatments for 1st degree heart block

A
  • concerns:
    • nothing major
    • hemodynamically stable if asymptomatic
    • watch for progression to further block
  • treatment
    • not required
69
Q

etiologies of junctional rhythms

A
  • infarction, ischemia
  • drug toxicity
    • digoxin, digitalis, CA channel blockers, beta blockers
70
Q

causes of 2nd degree heart block: Type 1

A
  • inferior MI
  • cardiomyopathies
  • digitalis toxicity
  • valvular disease
71
Q

what type of PVC is this?

A

ventricular bigeminy - ever other beat is a PVC

72
Q
A
  • first-degree block
  • conduction thru SA node delayed, lengthening PR interval
  • rhythm regular
  • rate underlying rhythm, atrial and ventricular usually same
  • P wave sinus, normal, upright
  • P interval prolonged, greater than 0.20 sec and constant
  • QRS normal, 0.12 sec or less
  • QT interval usually normal
73
Q

treatment for V.fib

A
  • CPR when pulselessness is established
  • defibrillate ASAP
  • first meds:
    • epi 1mg IVP q3-5 min
    • antiarrhythmic med - amiodarone
74
Q

treatment of PVCs

A
  • treat underlying cause
  • limited to those with severe Sx
  • meds to suppress ventricular ectopy suppress protective vent escape rhythms
    • pro-arrhythmic properties
  • treatment is cost-benefit anaysis
75
Q
A
  • PVCs
  • rhythm may interrupt underlying rhythm
  • rate at any HR and with any underlying rhythm
  • P wave may not be present or immediately after; unrelated to PVCs
  • PR interval immeasurable
  • QRS wide, bizarre, 0.12 sec or longer
  • T wave frequently extends in opposite direction of QRS
76
Q

absolute refractory period

A

immediately following depolarization - heart cannot respond to another stimulus regardless of stimulus strength

77
Q

etiologies of PAC’s

A
  • stress, fatigue
  • caffeine, alcohol, tobacco
  • may be associated with:
    • MI, CHF
    • infection
    • hypoxia
    • hypokalemia, hypomagnesemia
  • may precede deterioration into A-f or AFc
78
Q

clinical presentation of complete heart block

A
  • serious and life-threatening
  • not tolerated d/t low heart rate (decreased CO)
  • hemodyanmic instability
    • dyspnea, HF, hypotension, syncope, chest pain
  • can progress to ventricular standstill with little/no warning
79
Q

P wave/QRS complex in dysrrhythmia interpretation

A
  • P wave in front of every QRS complex?
  • every QRS complex with a preceding P wave?
  • if YES - electrical activity coming from atria
    • but NOT necessarily the SA node
  • if NO - QRS complex w/o preceding P wave
    • electrical activity originated in ventricle
80
Q
A
  • wandering atrial pacer
  • rate usually 60-100, if over 100 - multiple atrial tachycardia
  • rhythm regular or irregular
  • P wave 3+ morphologies, A:V ratio 1:1
  • PR interval varies on location of ecotpic atrial sites (some may be less than .12sec)
  • QRS less than 0.12 sec
  • QT interval less than 1/2 preceding R-R interval
81
Q

regular or irregular HR in dysrrhythmia interpretation

A
  • regular, regularly irregular, or irregularly irregular?
    • ex: a.fib is irregularly irregular
  • does the abnormality appear on a regular basis or irregular basis?
  • pattern in the abnormality or abnormalities?
82
Q

what type of PVC is this?

A

ventricular trigeminy - every third beat is a PVC

83
Q
A
  • ventricular fibrillation
  • rate immeasurable
  • rhythm chaotic
  • p wave chaotic, no AV ratio
  • PR interval immeasurable
  • QRS absent
  • QT interval absent
  • will NEVER be a perfusing rhythm
84
Q

atrial fibrillation overview

A
  • chaotic electrical activity originating from irritable atrial tissue
  • cause atrial muscle to quiver ineffectively, losing atrial kick
  • only some of atrial impulse conduct thru AV junctional tissue thru ventricular conduction system
  • CO can be compromised by 5-30%
  • gatekeeping fxn of AV node important
    • only lets the strongest of the 300+ atrial impulses thru/minute
85
Q

etiology of normal sinus rhythm

A

normal pacemaker rate

86
Q
A
  • 2nd degree heart block: type 1 (Wenckebach)
  • rhythm irregular
  • rate atrial normal; ventricular slower b/c not all beats conduct
  • P wave upright, uniform, some now followed by QRS
  • PR interval progressively longer until no conduction
  • QRS normal, 0.12 sec or less
  • QT usually normal, less than 1/2 preceeding R-R
87
Q

causes of PEA

88
Q

depolarization

A
  • electrical excitation across the myocardial cell membrane
  • spreads from cell to cell through conduction system and muscle cells
  • sodium and calcium move into cell, potasssium out
  • provides stimulus for ocntraction
89
Q
A
  • sinus arrhythmia - from SA node irregularly in relation to respiration
    • variations in breathing d/t fluctuations in parasympathetic vagal tone
  • rhythm irregular
  • rate speeds up during inspiration, slows during expiration
  • P wave for every QRS, same size and shape
  • PR interval normal, 0.10-0.20 sec
  • QRS same size and shape; normal duration (0.04-0.12 sec)
90
Q

what is this rhythm?

91
Q
A
  • supraventricular tachycardia (SVT)
  • rhythm may be regular
  • rate 150-250 bpm
  • p wave usually hidden in preceding T wave
  • PR interval immeasurable d/t hidden P waves
  • QRS narrow, less than 0.12, all the same
92
Q

overview of atrioventricular conductiondisorders (aka blocks)

A
  • delay through bundle of His = PR interval
    • time to allow atria to complete contract and impart “kick” in pressurizing ventricles to prepare (stretch) them for power of stroke contraction (Starling’s Law)
  • problems arise when conduction through AV node is slowed (1st), delayed to prevention (2nd T1), intermittent (2nd T2), completely blocked (3rd)
  • reaches a point where more passive filling of RA won’t impact CO (too much delay)
    • dysfxn, fewer ventricular complexes, fewer ventricular contractions, negative impact on CO
93
Q

conduction system of the heart

94
Q

QRS interval in dysrrhythmia interpretation

A
  • less than .12 s (120 ms)
  • QT normally less than 1/2 of proceeding R-R interval
95
Q

concerns and treatments with 2nd degree heart block: type 2

A
  • concerns
    • bradycardia common
    • often progresses to complete heart block
  • treatment
    • transcutaneous pacing
96
Q

QRS wave

A
  • ventricular depolarization as impulse travels through both ventricles
  • width of QRS wave indicates intraventricular conduction time
97
Q

etiologies of atrial flutter

A
  • after open heart surgery
  • MI
  • mitral or tricuspid valvular disease
  • PE
  • chronic atrial flutter d/t organic heart dx
  • ischemia
98
Q

EKG

A

graphic recording of the electrical current produced by depolarization and repolarization of the heart

99
Q

overview of third degree (complete) heart block

A
  • total block at AV node, so no conduction of SA node impulses through AV node
  • atria and ventricles dissociated from each other
    • funtion independently, using intrinsic mechanisms to pace themselves
100
Q

causes of ventricular tachycardia

A
  • MI, CHF, cardiomyopathy
  • electrolyte disturbances
  • acid-base disturbances
  • R on T
  • direct stimulation of myocardium
  • profound hypokalemia
101
Q

isoelectric line

A
  • EKG machine’s stylus producing a straight line on the paper when unconnected from the patient’s electrodes
  • all electrical forces are equal
  • also asystole - no electrical activity
  • flow towards positive electrode = upright waveform
  • flow towards negative electrode = downward waveform
102
Q

HR in dysrrhythmia interpretation

A
  • normal = 60-100
    • origin likely from SA node
  • dramatic changes in HR without changes in SV will change CO
103
Q
A
  • ventricular tachycardia
  • rate 140-250 bpm
  • rhythm regular
  • p wave no discernable p waves
  • QRS >0.12 sec, morphology can be identical or vary
  • QT interval usually immeasurable
    • subcategory of VT called polymorphic, prolonged QT, ventricular tachycardia b/c of QT of underlying rhythm
  • can be brief/nonsustained (30 sec or less) or sustained (>30 sec)
104
Q

what type of PVC is this?

A

triplet - three PVCs in a row (uniform or multiform)

105
Q
A
  • premature atrial contractions
  • impulse from atria that is earlier than next expected sinus beat d/t irritable, ectopic focus in atrial tissue
  • rhythm underlying may be regular, overall irregular d/t PAC
  • rate of underlying rhythm
  • P wave different morphology from SA node p wave; may be hidden in preceding T wave
  • PR interval between .10 and .20 seconds - different fro the ectopic beat
  • QRS narrow, same, less than .12 sec
  • QT interval less than 1/2 preceding R-R
106
Q

overview of second degree heart block: type 1

A
  • aka Wenckebach
  • SA node impulses progressively delayed until one impulse is not conducted
    • then cycle repeats
  • longer, longer, longer drop. Now I know my Wenkebach
107
Q

six questions for dysrrhythmias interpretation

A
  1. HR: fast, slow, normal?
  2. regular or irregular?
  3. morphology of p waves and A:V ratio
  4. PR interval
  5. QRS measurement
  6. P wave for every QRS?
    1. QRS after every P wave?
108
Q

treatments for second degree heart block: type 1

A
  • based on symptoms of bradycardia
  • transcutaneous pacing
  • atropine
  • dopamine or epi drip
  • permanent pacemaker may be indicated if Wenckebach persists
109
Q

polarized

A
  • resting cell’s electrical charges are balanced
  • cell is ready for action
110
Q

atrial rhythms - overview

A
  • result of electrical impulse originating from atrial tissue that is NOT SA node - ectopic impulse
  • occurs when atrial rate faster than sinus rate and overrides SA node to generate depolarization
  • unusual P waves - notched, flattened, peaked or biphasic
    • d/t slower, atypical impulse conduction thru atria
  • impulse travels thru AV junctional tissue and ventricular conduction pathways terminating in Purkinje fibers
  • supraventricular rhythms create narrow (normal) QRS wave - no problem in ventricle
111
Q

etiologies of accelerated junctional rhythms

A
  • usually transient
  • enhanced autorhythmicity of junction
    • digitalis or theophylline toxicity
    • catecholamien surge from stress, stimulants
    • acid base imbalances
112
Q

digitalis

A
  • increases contractility of heart indirectly by actingon AV node to make it less irritable and slow conduction
  • allows for more ventricular filling
  • rate control in A.fib
  • things to check
    • therapeutic levels - narrow therapeutic range (renally cleared)
    • apical HR
113
Q

Bundle of His and Bundle branches

A
  • divides into right and left Bundle branches which descends on either side of interventricular septum
  • left bundle branch divides into 2 fascicles (anterior and posterior)
    • conduction speed in left bundle is faster than right
  • Bundle of His is a pacemaker site with inherent rate of 40-60 times/minute
114
Q

what type of PVC is this?

A

ventricular quadrigeminy - every fourth beat is a PVC

115
Q

basic electrophysiology of EKG

A
  • electrocardiography cannot detect mechanical performance of the heart
  • beware of pulseless electrical activity (PEA)
    • aka electromechanical dissociation
  • expert level dysrhythmia interpretation does not replace expert level patient assessment
116
Q

concerns with atrial fibrillation

A
  • most common dysrhythmia - patients can live with it chronically
  1. rate control
  2. prevent clot formation
  3. loss of CO from atrial kick
117
Q
A
  • atrial flutter
  • rhythm atrial regular, ventricular variable (depends on A:V)
  • rate atrial 250-400, ventricular variable
  • P wave fast “saw tooth” or “picket fence” flutter waves that are uniform; AV ratio can be fixed w/ regular ventricular rhythm or variable
  • PR interval immeasurable
  • QRS duration less tahn 0.12 sec, identical morphology
  • QT interval less than 1/2 preceding R-R interval (normal)

Leadership (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions