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Cardio/Pulm > Electrocardiographic Assessment > Flashcards

Electrocardiographic Assessment Flashcards

1
Q

Be able to describe the specific ions responsible for cardiac contraction, conduction through the heart, repolarization of the heart and conduction through the AV node.

A
  • Phase 0: Rapid depolarization (inflow of Na+)
    Phase 1: Partial repolarization (inwards Na+ current deactivated, outflow of K+)
  • Phase 2: Plateau (slow inward Ca++ current)
  • Phase 3: Repolarization (Ca++ current inactivated, K+ outflow)
  • Phase 4: Pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) Autorhythmicity

Refractory period: Phases 1-3

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2
Q

Which leads assess the heart in the frontal plane** versus the **horizontal plane?

A
  • *Limb leads**: Frontal plane. Used for determining axis.
  • *Precordial leads**: Horizontal plane.
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3
Q

What is the concern with a prolonged QT?

A

Prolonged QT is associated with risk of developing Torsade’s de pointes – Ventricular fibrillation (deadly dysrhythmia)

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4
Q

What are causes of prolonged QT?

A

Hypomagnesemia
Hypokalemia
Antidepressants
Antipsychotics
Antifungals
Antibiotics
Fluoroquinolone
Antiarrhytmics
Digitalis (Foxglove)

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5
Q

What are automaticity foci?

A

Pacemaker sites within the heart. Helpful when SA node fails to pace or there is a block somewhere in the conduction system that does not allow electrical activity to be conducted.

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6
Q

What are causes of increased foci irritability that increases one’s susceptibility to a dysrhythmia?

A

Sympathetic stimulation (drugs, caffeine, alcohol), inflammation, infection, dehydration/electrolyte abnormalities, stress, atrial enlargement/ventricular hypertrophy, beta blockers, calcium channel blockers

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7
Q

What are symptoms of a dysrhythmia?

A

Palpitations, syncope, sudden death, angina

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8
Q

What labs might one order to assess a dysrhythmia?

A

CBC, comprehensive metabolic panel, TSH

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9
Q

What “imaging” might one consider to assess a dysrhythmia?

A

ECG, Holter monitor, ambulatory telemetry monitoring, implant event recorders, echo

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10
Q

What is sudden cardiac death and what is the most common cause?

A

SCD is an unexpected death from cardiac causes either without symptoms or within 1-24 hours of symptom onset. Most common cause = Coronary artery disease (80-90%)

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11
Q

What is the definition of bradycardia versus tachycardia?

A
  • *Bradycardia**: <60 bpm
  • *Tachycardia**: >100 bpm
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12
Q

Describe the autonomic nervous system’s role in the regulation of heart rate, contractility, and irritability.

A
  • *Sympathetic**:
  • (NE) β-1 adrenergic receptors -> stimulate cardiac activity
  • Also stimulates α-1 adrenergic receptors on arteries
  • Affect on atria and junctional foci; minimal effect on ventricular foci
  • *Parasympathetic**
  • (vagus nerve) ACh -> cholinergic receptors -> inhibit cardiac activity
  • Affect on atrial and junctional foci; no effect on ventricular foci

These two branches also have an effect on systemic arteries to control blood flow and pressure

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13
Q

Be able to describe the theory behind the acetylcholine protocol, the supplements used, and in which patients it may be indicated and contraindicated for treatment.

A

MAP treatment is to give 2 essential nutrient precursors for endogenous production of Ach

(Choline + pantetheine)

  • *Indications**: Any tachydysrhythmias, any ectopic dysrhythmias
  • *Contraindicated**: Any bradydysrhythmias, any AV blocks
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14
Q

Be able to describe the views of the heart from each of the leads.

A
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15
Q

Define: Arrhythmia/dysrhythmia

A

Abnormal cardiac rhythm – any disturbance in rate, regularity, site or origin, or conduction of the cardiac electrical impulse

Arrhythmia: without rhythm

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16
Q

What is the amplitude of a wave

A

Amplitude of a wave is the magnitude of deflection and is a measure of voltage

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17
Q

Segment vs Interval

A

Segment: straight line between two waves

Interval: a straight line + at least one wave

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18
Q

Sinus bradycardia symptoms

A

Asymptomatic

Presyncope/syncope

Unexplained falls

Fatigue

Exercise intolerance

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19
Q

Sinus bradycardia labs

A

Comprehensive metabolic panel

TSH

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20
Q

Sinus bradycardia pathophsiology

A
  • Normal during sleep
  • Medications (beta blockers, non-dihydropyridine calcium channel blockers, opioids)
  • Hypothyroidism
  • Anorexia nervosa
  • Parasympathetic excess (athletes at rest)
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21
Q

Sinus tachycardia sxs

A

Palpitations

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22
Q

Sinus tachycardia pathophysiology

A
  • Fever
  • Hypovolemia
  • Anemia
  • Pain
  • Anxiety
  • Caffeine/nicotine
  • Amphetamines
  • Hyperthyroidism
  • Sympathetic stimulation (exercise)
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23
Q

Sinus tachycardia labs

A
  • CBC
  • Comprehensive metabolic panel
  • TSH
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24
Q

Sinus arrhythmia

A

Rate increases with inspiration and decreases with expiration

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25
Q

Name these rhythms:

A

Sinus tachycardia

Sinus bradycardia

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26
Q

Define Premature Atrial Complexes (PAC)

A

Early beat typically due to an irritable focus in the atrium.

PAC may come at a time when the ventricles have yet to be repolarized, resulting in a longer PR interval

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27
Q

Define Premature Junctional Complexes (PJC)

A

P waves inverted as the atria depolarize via retrograde conduction

P wave can come before or after the QRS complex, or can be lost entirely within QRS complex. If visible, P wave will be inverted.

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28
Q

Premature beats: Identify (PAC or PJC)?

A

PJC - No P wave at 4th beat

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29
Q

Premature beats: Identify (PAC or PJC)?

A

PAC - 3rd beat premature

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30
Q

Premature beats: Identify (PAC or PJC)?

A

PAC - 3rd is a premature beat

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31
Q

Premature beats: Identify (PAC or PJC)?

A

PJC - 3rd beat is premature. No P wave

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32
Q

Premature beats:

  • Pathophysiology
  • SXS
  • Treatment
A
  • Pathophysiology:
    • Structural heart disease - Valvular disease (mitral stenosis)
    • Hypertrophic cardiomyopathy
    • Smoking/alcohol/coffee
  • SXS
    • Asymptomatic
    • Skipping sensation
    • Irregular rhythm palpitated at radial pulse
  • Treatment
    • Often benign do not need tx
    • Frequent PACs may degenerate intro atrial fibrillation:
    • Avoid triggers/beta blockers/ nervine herbs
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33
Q

Define: Atrial flutter

A

Impulses travel in circular course in atria, setting up regular, rapid (220-300/min) flutter (F) waves without any isoelectric baseline.

An irritable focus initiates an impulse that is conducted in a repetitive, cyclic pattern, creating atrial waves with sawtooth appearance called flutter waves.

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34
Q

Atrial Flutter with Block

A

Regularly irregular

  • With the heart rate this rapid, the ventricles do not have adequate time to fill:
    • AV node prevents this from occurring by blocking some impulses from reaching ventricles
    • The AV node doesn’t have enough time to repolarize; therefore not all atrial depolarizations are conducted to the ventricles
    • Observe that not every flutter wave is followed by a QRS complex
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35
Q

Atrial Fibrillation

A

Multiple atrial foci firing at >350x/min the AV node allows ventricular depolarization at variable intervals - often producing a irregularly irregular rhythm

•https://www.youtube.com/watch?v=1pOVk1hZjv8

Most common sustained dysrhythmia. Increased prevalence with age. Over 8% in pt over 80YO

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36
Q

Tachycardia induced cardiomyopathy

(bpm) Atria to ventricles ratio:

A

Atria to ventricles ratio 2:1

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37
Q

(T or F) There are no discernable P waves in atrial fibrillation, and conduction is irregularly irregular.

A

True

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38
Q

Who is she?

A

A fib

  • Irregularly irregular
  • P waves are lost and replaced by fibrillatory waves
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39
Q

Atrial Fibrillation pathophysiology

A
  • Often associated w history of rheumatic heart disease affecting mitral valve (structural abnormalities)
  • Hyperthyroidism
  • Obstructive sleep apnea (low O2 irritates atria)
  • Post-op inflammation, oxidative stress, fibrosis
40
Q

(T or F) Post-op for a fib is significantly associated with increased risk of neurocognitive disorders and septicemia

A

True

41
Q

______ supplementation was associated with a significantly reduced risk of post-op a fib in coronary artery bypass graft surgery.

A

Vitamin C

42
Q

Labs for a fib

A
  • CBC
  • Comprehensive metabolic panel
  • TSH
43
Q

Imaging for a fib

A
  • Transthoracic echocardiogram
  • Transesophageal echocardiogram (evaluate for presence of a left atrial thrombus prior)
44
Q

Complications of a fib

A
  • Atrial remodeling
  • Tachycardia induced cardiomyopathy
  • As atria fibrillate, blood pools in the atria and a clot may form increasing the risk of embolic stroke
45
Q

Types of a fib (3)

A
  • Paroxysmal: Episodic and resolve spontaneously or with intervention within 7 days
  • Persistent: Lasts >7 days
  • Permanent: Attempts to restore or maintain normal sinus rhythm have been discontinues. (Causes atrial remodeling)
46
Q

Treatment of A fib

A
  • Cardioversion
  • Rate control (beta blockers)
  • Anticoagulation
  • Ablation therapy
  • Left atrial appendage obliteration (LAA)
47
Q

What is Virchow’s Triad?

A

Factors important in the development of thrombosis.

  • Abnormal blood flow (stasis/turbulence)
  • Endothelial injury (inflammation/hypercholesterolemia)
  • Hypercoagulability (inherited/acquired)
48
Q

Supraventricular tachycardia (SVT)

A
  • Heart rates are so fast that the p wave often is not visible as it may be hidden in the preceding T wave:
    • Rates: 150-250 beats-per-minute
    • Rhythm: regular without visible p waves
  • Often called paroxysmal supraventricular tachycardia PSVT as a very irritable focus suddenly paces very rapidly and the termination is abrupt
  • Typically SVT is due to AV node reentrant tachycardia (above the ventricles)
  • Technically atrial flutter and atrial fibrillation are considered SVT but it is more precise to call them by their respective names
49
Q

SXS and triggers of SVT

A

Sudden (paroxysmal) onset of symptoms: (Start and stop quickly vs gradual onset of sinus tachycardia)

  • Palpitations
  • Dyspnea
  • Presyncope/syncope
  • Chest discomfort
  • Anxiety

Triggers: Caffeine, stress, exercise

50
Q

SVT: Wolff-Parkinson-White Syndrome

A

Abnormal accessory AV conduction pathway

  • Delta wave
  • Short PR interval
51
Q

Atrial tachycardia

A
52
Q

SVT treatment

A
  • Valsalva maneuver
  • Adenosine (short acting AV node blocking agent)
  • Beta blockers (metoprolol)
  • Non-dihydropyridine calcium channel blockers (varapamil, diltiazem)
  • Cardioversion (if unstable)
  • Chronic setting: Pharm agent or catheter ablation (95% success rate)
53
Q

Premature Ventricular Complexes (PVCs)

A

Ventricles made irritable by low O2

54
Q

PVC (unifocal or multifocal) ?

A

Unifocal

55
Q

PVC (unifocal or multifocal) ?

A

Multifocal

56
Q

Who is she? Name this pattern of PVC

A

Unifocal bigeminy

57
Q

PVC labs and imaging

A
  • CBC
  • Comprehensive metabolic panel
  • TSH
  • Echocardiogram
58
Q

(T or F) You should be concerned if there are > 6 PVC/min.

A

True. >10% of beats = pathologic

> 3 PVCS in a row = ventricular tachycardia

59
Q

Ventricular Tachycardia presents on an ECG as _______.

A

Tombstones

60
Q

Ventricular Tachycardia (VT) pathophysiology and SXS

A
  • Ischemia/infarction
  • Structural heart disease
  • Heart failure
  • Electrolyte imbalance

SXS:

  • Palpitations
  • Dyspnea
  • Chest pain
  • Presyncope/syncope
61
Q

Who is she?

A

Ventricular Tachycardia

4+ beats = V tach

> 30 seconds = sustained v tach

62
Q

Ventricular Fibrillation definition and treatment

A

Chaotic depolarization in the ventricle causes loss of organized QRS complexes and loss of organized ventricular contractions

  • circulatory arrest begins within second
  • Cause of most sudden cardiac deaths

Treatment: Defibrillation and CPR

63
Q

Asystole

A

No detectable cardiac activity on ECG

64
Q

Atrial flutter

A

P wave without a QRS, regular, 2:1 block, 3:1 block, 4:1 block (2 flutter 1 QRS)

65
Q

Atrial Fibrillation

A

Irregularly irregular rhythm, no P wave

66
Q

What are the signs and symptoms of atrial flutter or atrial fibrillation?

A

Asymptomatic, palpitations, dyspnea, heart failure, stroke

67
Q

What are common conditions associated with atrial fibrillation?

A
  • Epicardial, myocardial, and endocardial disease
  • Lactogenic conditions
  • Structural heart disease
  • Electrolyte abnormalities
  • Illicit drugs
  • Sleep apnea
  • Hyperthyroidism
68
Q

What are appropriate blood tests and imaging for evaluating someone with atrial fibrillation?

A
  • CBC
  • CMP
  • TSH
  • Transthoracic echocardiogram
  • Transesophageal echocardiogram
69
Q

What are complications of atrial fibrillation?

A

Atrial remodeling

Tachycardia induced cardiomyopathy

Embolic stroke

70
Q

What is the left atrial appendage?

A

Small pouch shaped like a windsock found in the L atrium which can fill with blood and form a clot that can lead to a stroke

71
Q

What are CHADsVASC and HASBLED scoring systems used for?

A

CHADsVASc is used for measuring stroke risk

HAS-BLED is used for measuring bleeding risk

72
Q

How do patients typically describe their symptoms when they have SVT?

A

Sudden (paroxysmal) onset of:

  • Palpations
  • Dyspnea
  • Presyncope/syncope
  • Chest discomfort
  • Anxiety
73
Q

What is the pathophysiology of SVT?

A

AV node depolarizes down the alpha pathway once it reaches the bottom of AV node it travels retrograde and renters the AV node via the beta pathway

74
Q

What are the treatments used to abort an acute episode of SVT?

A
  • Valsalva maneuver
  • Medication: adenosine, beta blockers, non-dihydropyridine calcium channel blockers
  • Cardioversion
75
Q

Why are ventricular rhythms concerning?

A

Ventricles don’t have enough time to fill, and the brain is deprived of oxygen

76
Q

What is the definition of ventricular tachycardia?

A

When the ventricles beat too fast to pump enough oxygenated blood to the body

77
Q

What is the pathophysiology and causes of VT and VF?

A

VT:

  • Ischemia/infarction
  • Heart failure
  • Electrolyte imbalances
  • Structural heart disease
  • Cardiomyopathies:
    • Hypertrophic cardiomyopathy
    • Dilated cardiomyopathy
    • Infiltrative cardiomyopathy

VF:

  • Chaotic depolarization in ventricle causes los of organized QRS complexes and loss of organized ventricular contractions, VT lasting >30 seconds
  • Ischemia/infarction
  • Heart failure
  • Electrolyte imbalances
  • Structural heart disease
  • Cardiomyopathies
    • Hypertrophic cardiomyopathy
    • Dilated cardiomyopathy
    • Infiltrative cardiomyopathy
78
Q

At what point is ventricular tachycardia considered sustained and at risk of ventricular fibrillation?

What is the treatment of sustained VT and VF?

A

VT lasting >30 seconds

Treatment: Implantable cardioverter defibrillator

79
Q

What does axis assess on ECG?

A

Direction of movement of depolarization through the heart

80
Q

What leads are used to assess axis?

A

Limb leads

81
Q

What are the causes of axis deviation?

A

Ventricular hypertrophy and infarction

82
Q

What is a hemiblock? How does a left anterior versus left posterior hemiblock impact axis?

A

Hemiblock is a block in either the left anterior or posterior fascicle

Left anterior hemiblock: shifts the axis to the left

Left posterior hemiblock: shifts the axis to the right

83
Q

What is the differential diagnosis of left axis deviation versus right axis deviation?

A

Left axis deviation:

  • Left ventricular hypertrophy:
  • Hypertension
  • Aortic stenosis
  • Left anterior hemiblock

Right axis deviation:

  • Right ventricular hypertrophy:
  • Chronic obstructive pulmonary disease
  • Pulmonary emboli
  • Certain types of congenital heart disease
  • Pulmonary hypertension
  • Left posterior hemiblock
84
Q

How does right atrial enlargement versus a left atrial enlargement appear on ECG? What are respective causes of right atrial enlargement and left atrial enlargement?

A

Right atrial enlargement: Tall narrow P wave in leads, II, III, and aVF

  • Chronic obstructive pulmonary disease
  • Pulmonary emboli
  • Pulmonary hypertension
  • Pulmonary valve disease
  • Some congenital disorders
  • Tricuspid stenosis
  • Tricuspid regurgitation

Left atrial enlargement: Wide and notched P wave in I, II, and aVL

  • Mitral stenosis
  • Left ventricular failure
  • Aortic valve disease
  • Systemic hypertension
  • Mitral regurgitation
85
Q

How does right ventricular hypertrophy versus left ventricular hypertrophy appear on ECG?

A

Right ventricular hypertrophy R >S in V1 or deep S in I, aVL, V5, V6

Left ventricular hypertrophy: deep S waves V1 or V2 and large R waves V5 and V6

86
Q

What ECG manifestation is associated with ischemia

A

ST Depression

87
Q

What ECG manifestation is associated with injury

A

ST Elevation

88
Q

What ECG manifestation is associated with infarction

A

Deep Q Wave

89
Q

What ST abnormality is associated with a transmural infarct versus a subendocardial infarct?

A

Transmural: ST segment is shifted toward the epicardial layer, ST elevation

Subendocardial infarction: no Q wave, ST depression

90
Q

How do you assess for ST elevation or depression?

A

Find the S wave go two small boxes over and then look to see if the segment is elevated or depressed compared to baseline

91
Q

Rank from most specific to least specific the ST segment depression morphology associated with ischemia.

A

Least to most

92
Q

What are some examples of non-ischemic causes of ST depression?

A

Right and left ventricular hypertrophy

Right and left bundle branch blocks

93
Q

What are some examples of non-infarction causes of ST elevation?

A

Early repolarization

Pericarditis

94
Q

What are tall T waves associated with?

A

Acute MI, hyperkalemia, injury

95
Q

How might potassium levels impact the T wave?

A
96
Q

What is the criteria for a Q wave to be significant?

A

Greater than one small box or more, Q wave dominates the R wave

97
Q

What is the pathophysiology for a Q wave after an infarct?

A

When infarct tissue is dead it can no longer depolarize, so only one side is being shown on the EKG and shown as a negative deflection creating a bigger Q wave

Cardio/Pulm (6 decks)

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