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Preclerkship > EKGs & arrhythmia > Flashcards

EKGs & arrhythmia Flashcards

1
Q

Sinus rhythm if….

A

P wave followed by QRS (+vv)
P wave upright in leads I/II (also sometimes aVF/III but they’re beyond 75 degrees)
PR interval 0.12-0.2 seconds (3-5 small boxes)

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2
Q

Irregularly irregular rhythm is almost always…

A

AFib

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3
Q

HR = ___/small boxes or ___/large boxes

A

1500/small

300/large

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4
Q

Rates always refer to ____

A

Ventricular

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5
Q

Normal PR interval

A

0.12-0.2 seconds (3-5 small boxes)

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6
Q

Normal QRS interval

Normal QRS amplitude

A

<=0.1 seconds (<=2.5 small boxes)
Amp > 0.5 mV in at least 1 standard lead, >1.0 mV in at least one precordial lead
Upper limit of amp = 2.5-3 mV

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7
Q

Normal QT interval

A

Corrected QT <=0.44 sec (male) <=0.46 (female)

If HR normal (60-100), QT <50% interval between QRS complexes is okay

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8
Q

Normal mean QRS axis

A

-30 –> +90

positive deflection of leads I/II

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9
Q

What is the isoelectric complex? What can occur in the T wave following this?

A

Upward/downward deflections of QRS complex are equal magnitude
(T wave may cancel itself out)

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10
Q

Voltage calibration: 1 mm vertical =

A

0.1 mV

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11
Q

Decrease PR interval: 2 differentials

A

Preexcitation syndrome

Junctional rhythm

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12
Q

Increased PR interval differential

A

1st-degree AV block

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13
Q

Increased QRS interval: 4 differentials

A

BBBs
Ventricular ectopic beat
Toxic drug effect (e.g. certain antiarrhythmic drugs)
Severe hyperkalemia

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14
Q

Decreased QT interval: 2 differentials

A 
Hypercalcemia
Tachycardia (QT interval varies with HR (shorter for faster) so need to correct based on RR interval)
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15
Q

6 differentials for increased QT interval

A 
Hypocalcemia
Hypokalemia (QU interval)
Hypomagesia
Myocardial ischemia
Congenital prolongation of QT 
Toxic drug effect
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16
Q

What is a U wave

A

small, rounded deflection sometimes seen after the T wave (see Fig. 2-2). As noted previously, its exact significance is not known. Functionally, U waves represent the last phase of ventricular repolarization. Prominent U waves are characteristic of hypokalemia

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17
Q

What quick check automatically tells you that the QRS axis is normal?

A

Primarily upward in leads I & II

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18
Q

If leads I/II aren’t primarily upward, how do you determine the mean axis? (2 steps)

A

Perpendicular to the lead with the most isoelectric complex

Then if it’s primarily up then the mean axis points to the + pole of that lead, and vice versa

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19
Q

Is the R or L side of the heart more anterior

A

R

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20
Q

Which atrium depolarizes first?

A

RA (helpful for differentiating RA vs LA enlargement when the P wave isn’t smooth)

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21
Q

In V1 what does the P wave look like

A

Small positive then negative deflection
Positive = RA (anterior)
Negative = LA (posteriod)

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22
Q

d. Solkolow-Lyon criteria: add the S wave in V1 plus R wave in V5 or V6; if sum > 35…

A

LVH is present! (too high amplitude)

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23
Q

R axis deviation could indicate…

A

RV hypertrophy or acute right heart strain

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24
Q

What happens to QRS in an incomplete/complete BBB?

A

Incomplete: 0.1-0.12 sec
complete: >0.12 sec

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25
Q

RBBB EKG diagnostic criteria (3)

A

QRS duration > 120ms
RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)

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26
Q

LBBB ECG diagnostic criteria (5 things)

A

QRS duration > 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Absence of Q waves in lateral leads
Prolonged R wave peak time > 60ms in leads V5-6

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27
Q

LBBB vs RBBB - which one starts normally in the QRS?

A

RBBB because L always depolarizes first

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28
Q

Bundle blocks are typically detected in the ___ leads

Fasicular blocks are typically detected in the ___ leads

A

BBBs - chest (precordial)

Fasicular - Limb leads

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29
Q

Fasciular blocks aka?

Can markedly alter ___ but don’t significatly alter ___

A

Change QRS axis but don’t significantly widen QRS

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30
Q

Evidence of past STEMI can include ____

Or if it was posterior infarction could be ____ on ___ leads

A

Pathological Q waves

Tall R wave on V1/V2

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31
Q

What changes on EKG happen ~1 day after stemi

A

Elevation disappears
T wave inversion begins
Q wave deepens

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32
Q

NSTEMI and unstable angina typically cause ST segment depressions, which are frequently accompanied by ….

A

inverted or flat T waves

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33
Q

T wave inversion in lead III is…

A

a normal variant (unless suddenly new)

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34
Q

T wave deflection should be in the same direction as the QRS complex in at least…

A

5/6 limb leads

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35
Q

T wave should be ___ in leads V2-V6, ___ in aVR

A

Upright in V2-V6

Inverted in aVR

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36
Q

T wave should have amplitude of at least _ mV in leads V3 and V4 and at least __mV in leads V5 and V6

A

V3/V4: 0.2 mV

V5/V6: 0.1 mV

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37
Q

• isolated T wave inversion in an asymptomatic adult is generally…

A

a normal variant

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38
Q

Hyperkalemia leads to what T wave alteration?

A

Tall “peaked” T wave
(K+ is involved in repolarization. Lots of potassium  total flux will increase (net amount of K moving)  Peaked T wave)

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39
Q 
R wave becomes progressively taller from V1 --> V6
Transition lead (where height R > depth S) is usually which?
A

V3 or V4

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40
Q

Normal ejection fraction = __/___ = ___%

A

SV/EDV = ~55%

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41
Q

Name 5 pacemakers of heart (native/latent) and their bpm

A

SA node = 60-100 bpm
Atria = <60
AV node, bundle of His = 50-60
Purkinje = 30-40

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42
Q

Parasympathetic (vagal) tone impacts ___ most, then ___, then ___
o Mod vagal stim –> ____
o Strong vagal stim —> _____

A

Parasympathetic (vagal) tone impacts SA node most, then AV, then ventricular system
o Mod vagal stim –> AV node becomes pacemaker
o Strong vagal stim —> ventricular escape rhythm

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43
Q

Escape beat/rhythm vs ectopic beat/rhythm

A

Escape beat/rhythm= initiated by latent pacemaker because SA firing slowed
Ectopic beat/rhythm = latent pacemaker develops intrinsic rate > SA
(rhythm = many beats)

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44
Q

Possible causes of ectopic rhythms

A

High catecholamines, ischemia/hypoxemia, drug toxicities, electrolyte imbalance

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45
Q

Cardiac injury can lead to leaky cell membranes which can lead to…

A

Gradual depolarization in cells that don’t have pacemaker channels –> abnormal automaticity –> ectopic rhythms (if rate of depol > SA node)

46
Q

_____ is more likely in conditions that prolong AP duration/QT interval; can be self-perpetuating –> tachyarrhythmia
Example:

A

Early afterdepolarization

Torsades de pointes (polymorphic ventricular tachycardia)

47
Q

2 varieties of conduction blocks

A

Functional (refractory period)

Fixed (fibrosis, ischemic scarring)

48
Q

Wolff-Parkinson-White syndrome involves the presence of _____
Leading to what EKG appearance and why?

A

Congenital accessory bypass tract (Bundles of Kent) b/w A & V
EKG has PR <0.12 (“preexcited ventricles”) & wide QRS w/ delta wave because impulse passed both through AV/purkinje system and myocardium via bypass tract

49
Q

WPW sets up ideal conditions for…

A

Anatomic reentry + monomorphic tachycardia

Premature beat can trigger the reentry circuit

50
Q

Polymorphic ventricular tachycardia can result from what type of re-entry? Can lead to ___ if very disorganized

A

Functional reentry w/ spiral waves

can lead to AFib or VFib

51
Q

The heart block poem

A

If the R is far from P, then you have a first degree
Longer, longer, longer, drop! Then you have a Wenckebach (Mobitz I)
If some Ps don’t get through, then you have a Mobitz II
If Ps and Qs don’t agree, then you have a 3rd degree!

52
Q

A Mobitz I heart block would be what kind of rhythm?

A

Regularly irregular

53
Q

Mobitz I and Mobitz II blocks are usually issues with __ and ___ respectively

A

Mobitz I = AV node issue

Mobitz II = usually distal to AV node (His/Purkinje, e.g. LBBB/RBBB)

54
Q

An AV block where multiple Ps in a row are not followed by QRS

A

“High grade” AV block (Mobitz II)

55
Q

What is the rate like in a complete heart block? Width of QRS?

A

Depend on source of escape rhythm
Often slow (lightheadedness/syncope)
If block is in AV node, escape pacemaker may be in distal AV or common Bundle of His before bifurcation –> normal QRS + not super slow

56
Q

SVT is characterized by ___ QRS. Why?

A

Narrow because His-Purkinje system normal (originates in AV node or above)

57
Q

Treatment for atrial premature beats?

A

If symptomatic, can use B-blockers; otherwise treatment not necessary (common in healthy hearts)

58
Q

2 pharmalogical classes used to treat bradyarrhythmias + examples

A

1) Anticholinergics (e.g. atropine) - decrease vagal effect via competitive inhibition of muscarinic receptors
2) B1-receptor agonists (isoproterenol) - mimic catecholamines

(both are IV, not suitable long-term)

59
Q

What does carotid sinus massage do?

A

Triggers baroreceptor reflex –> increased vagal tone, decreased symp tone –> reduce SA node activity + AV blocking “unmasks” atrial activity, SVT termination

60
Q

Adenosine blocks what?

A

Nodes, NOT accessory pathways (so don’t use when the issue is an accessory pathway)
Totally stops heart temporarily, have cardiac resus ready

61
Q

Cardioversion is synced to _____. If that’s not present (e.g. ____), then perform ____

A

QRS complex

Not present in VFib –> external defibrillation (asynchronous)

62
Q

Sick Sinus Syndrome =

A

Intrinsic SA node dysfunction –> bradycardia

63
Q

cell’s automaticity is decreased when the cell is driven to depolarize more frequently than its intrinsic discharge rate
- Increases hyperpolarizing current of Na/K-ATPase

What is this called?
Example of arrhythmia where this is seen in action?

A

Overdrive suppression

Bradycardia-tachycardia syndrome

64
Q

Junctional escape rhythms come from where? About how many bpm? Wide or narrow QRS?

A

AV node or bundle of His
40-60
Narrow QRS

65
Q

A pacemaker for AFlutter could do what?

A

Burst pacing (rapid atrial stimulation)

66
Q

Cardiac glycosides: mechanism/effects, example

A

Digoxin
Inhibit Na/K ATPase
–> positive inotropic effect (increased contractility),
–> negative chronotropic effect (SA node depression, reduced HR)
–> negative dromotropic effect (reduced velocity of conduction via AV node depression)

67
Q

Visual disturbance common in digoxin overdose

A

Blurry vision + yellow tint/halos

68
Q

Digoxin has a ___ therapeutic index

A

Narrow

69
Q

Main indications for digoxin treatment:

A

Afib

Treatment-resistant heart failure

70
Q

Atrial fibrillation has a _____ ______ rhythm

A

Regularly irregular

71
Q

AFib is associated w/ atrial ___ e.g.

A

atrial enlargement

HF, hypertension, CAD, pulmonary disease

72
Q

Examples of paroxysmal supraventricular tachycardias (PSVTs)

A

AVNRT = AV nodal reentrant tachy

AVRT (bypass tract, e.g. WPW syndrome)

73
Q

WPW syndrome usually leads to ___ AVRT. What’s the other type. EKGs?

A

Orthodromic (down the AV node, retrograde up bypass tract)
vs antidromic (vv)
*both EKGs have retrograde P waves
Orthodromic has narrow QRS, antidromic has widened QRS

74
Q

First-line long-term treatment for WPW

A

Catheter ablation of accessory pathway

75
Q

What is the specific treatment consideration for WPW syndrome (ventricular preexcitation) & tachyarrhythmia

A

AV node blocking agents or vagal maneuvers–> unrestricted ventricular conduction of rapid atrial impulses through accessory pathway –> Vtach (BAD)

Rhythm control (cardioversion, IV procainamide = Na-blocker) are safer

76
Q

EKG shows irregular rhythm, each QRS preceded by P wave of varying morphology
Pt has severe COPD
Atrial rate > 100

Probable arrhythmia =

A

Multifocal atrial tachycardia

77
Q

What is bigeminy? Trigeminy? What happens after that?

A

Every 2nd beat is a Ventricular Premature Beat
every 3rd beat
3+ consecutive VPBs = ventricular tachycardia

78
Q

Atrial flutter is usually ___ over a _______ circuit

A

Reentry over a large, fixed circuit

79
Q

Polymorphic VT w/ varying QRS amplitude =
Results from ____
Risk factor?

A

Torsades de pointes
Early afterdepolarizations
RF = long WT interval

80
Q

3 EKG characteristics of VTach

A

Change in axis
Change in QRS morphology (often wide)
AV dissociation

81
Q

Why is the change in QRS axis a more convincing feature of VTach than wide QRS?

A

SVT can cause wide QRS if aberrant conditions (e.g. BBB)

Change in axis of QRS means the SOURCE of conduction has changed

82
Q

Vtach such as torsades de pointes can degenerated into….

A

Vfib + Cardiac arrest

83
Q

Ventricular Fib –> ____ if not quickly reversed

A

CO cessation + death

84
Q

Characteristics of pulse in Vfib?

A

PULSELESS

85
Q

Name 2 shockable rhythms & 2 NONshockable rhythms

A

Shock: Vfib, pulseless Vtach

Nonshockable: Ventricular asystole, pulseless electrical activity

86
Q

CPR: ratio of compressions:breaths

A

30:2

87
Q

Describe pulseless electrical activity

A

Although an electrocardiographic rhythm is present, there is no meaningful ventricular activity (also referred to as electromechanical dissociation).

88
Q

Amiodarone blocks ___ and is used to treat ____ and ___ after unsuccessful defib and ___ long-term

A

Blocks VG K+ channels –> prolonged repolarization

Vtach + Vfib

AFib long-term

89
Q

Lung fibrosis & chronic interstitial pneumonitis are rare but serious side effects of…

A

amiodarone

90
Q

Beta blockers = class ___ antiarrhythmic

A

II

91
Q

Metoprolol, atenolol, esmolol,, bisoprolol = ___ beta blockers

A

Cardioselective (B1 only)

92
Q

Mnemonic for CAUSAL factors of arrhythmia

A 
HIS DEBS
Hypoxia (pulmonary disorders)
Ischemia
Sympathetic stimulation
Drugs (incld anti-arrhythmics!)
Electrolyte disturbances (hypokalemia, Ca/Mg imbalances)
Bradycardia
Stretch
93
Q

Recommended drugs for rate control in AFib

A

Beta-blockers
ND-CCBs
Digoxin
Amiodarone (rare)

94
Q

What is “Pill-in-the-Pocket” Antiarrhythmic drug therapy?

Who is this indicated for?

A

Symptomatic patients w/ sustained AF episodes (>2hrs) that occur <1/month
No severe/disabling Sx during episodes
Can reliably comply w/ med instructions

Basically use immeidate release oral AV nodal blocker (ND-CCB or BB) followed by class Ic antiarrhythmic (Flecainide, propafenone)

95
Q

We recommend ____ of AF in patients who remain symptomatic after an adequate trial of antiarrhythmic drug therapy and in whom a rhythm control strategy remains desire

A

catheter ablation

96
Q

Most patients should receive ____ for anticoagulation rather than _____

A

DOAC (apixaban, rivaroxaban, dabigatran, edoxaban) rather than warfarin
(at least as effective + less bleeding complications, easier to dose

97
Q

Stable vascular disease and AF in patients at high risk of stroke/systemic thromboembolism –> treatment?

A

OAC therapy

98
Q

AF patients at higher risk of stroke undergoing elective PCI without high-risk features for thrombotic CV events –> treatment?

A

Dual therapy: OAC + P2Y12 (clopidogrel)

99
Q

AF patients at higher risk of stroke undergoing PCI for ACS or elective PCI with high-risk features –> treatment

A

Triple therapy (OAC + ASA + P2Y12) for up to 1 month, then dual therapy for up to 12 months

100
Q

In what AF patients is therapeutic OAC for 3+ weeks REQUIRED before cardioversion?

A
  1. Valvular AF (any duration), or
  2. NVAF Duration <12 hours and recent stroke/TIA, or 3. 3. NVAF Duration 12-48 hours and CHADS2≥2, or
  3. NVAF Duration >48 hours
101
Q

Alternative to 3 weeks of anticoagulation before cardioversion in hemodynamically stable AF patients?

A

TEE to rule out thrombus

102
Q

2 circumstances where cardioversion may be performed w/out preceding anticoagulation

A

i) patients with non-valvular AF who present with a clear AF onset within 12 hours in the absence of recent stroke or TIA;
ii) patients with non-valvular AF and a CHADS2 score 0 (men) or 0-1 (women) who present after 12 hours but within 48 hours of AF onset.

103
Q

In the absence of strong contraindication, all patients who undergo cardioversion of AF should receive____ afterward for ____ long

A

Anticoagulation for at least 4 weeks

104
Q

In what context would a patient w/ AF and CAD be NOT put on OAC? what would they be put on?

A

ASA only if they have stable CAD and CHADS2 = 0

105
Q

What do you do in an unstable patient with Afib >48hrs

A

Don’t delay electrical cardioversion but anticoagulate w./ heparin/DOAC ASAP

106
Q

Validated scoring system for assessing risk of stroke in nonvalvular Afib

A 
CHA2DS2-VASc
Congestive HF or LV dysfunction
Hypertension
Age 75+ (2)
Diabetes
Prior stroke/TIA/TE (2)
Vascular disease
Age 65-74
Sex: female
107
Q

Scoring system used to assess risk of bleeding in patients starting anticoagulation

A 
HAS-BLED
Hypertension uncontrolled (1 pt)
Abnormal renal/liver function (1 each)
Stroke Hx (1)
Bleeding Hx (1)
Labile INR (1) (in therapeutic range <60% of time)
Elderly (>65, 1)
Drugs predisposing to bleeding or alcohol use (1 each)
0 = low risk, 1-2 = mod, 3+ = high
108
Q

When is heparin indicated as an anticoagulant in AFib/AFlutter? (2)

A

Pregnancy

Anticoagulation prior to immediate unplanned cardioversion (may also use DOACs in this case)

109
Q

We suggest that, in the absence of a strong contraindication, ALL patients who undergo cardioversion of AF ______ after cardioversion

A 
We suggest that, in the absence of a strong contraindication, all patients who undergo cardioversion of AF receive at least 4 weeks of
therapeutic anticoagulation (adjusted-dose VKA or a DOAC) after cardioversion
110
Q

Does Mobitz I or Mobitz II have a worse prognosis?

A

Mobitz II because tends to progress to 3rd degree

Mobitz 1 generally doesn’t progress to a more advanced block

111
Q

What is a high-grade Mobitz II?

A

Sequential QRS complexes are blocked

112
Q

What is the most common EKG finding during pulmonary embolism? What is a very characteristic finding but that only one occurs in 10-20% of patients?

A

Most common = sinus tachycardia

~10% = S1Q3T3 (wide S in lead 1 + Q and inverted T in lead III) = McGinn-White Sign

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