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EKG Use and Interpretation > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Results in “short circuits” or shortcuts from the Sinoatrial (SA) node to the Ventricles.

A

Preexcitation Syndromes

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2
Q

Accessory Atrioventricular (AV) conduction pathway.

A

Preexcitation Syndrome

  • Essentially the opposite of an AV-Block
  • The A-V current happens quicker than normal.
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3
Q

How are preexcitation syndromes diagnosed?

A

By using a 12-Lead EKG

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4
Q

What are two major Preexcitation Syndromes that we focused on?

A
  1. Wolff-Parkinson-White Syndrome
  2. Lown-Ganong-Levine Syndrome
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5
Q

Pathophysiology

  • Accessory pathway via “bundle of Kent”.
  • Impulse skip the AV node and go directly from Atria to Ventricle.

What syndrome?

A

Wolff-Parkinson-White (WPW) Syndrome

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6
Q

What syndrome is predisposed to tachycardia syndromes such as AVNRT, Atrial Fibrillation, and Ventricular Fibrillation?

A

Wolff-Parkinson-White (WPW) Syndrome

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7
Q

What is the treatment for Wolff-Parkinson-White Syndrome?

Stable/Unstable/Unstable n

A

Stable - Adenosine

Unstable - Cardiovert

Definitive - Radiofrequency Ablation

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8
Q

EKG Finding:

  • PR Interval appears short (< 0.12s)
  • Presence of Delta wave

Note:

  • Cannot accurately diagnose Axis, Bundle Branch Block, Hypertrophy
A

Wolff-Parkinson-White Syndrome

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9
Q

What does a Delta wave look like?

A

Wide QRS base with upslope into the R wave.

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10
Q
  • Access an accessory pathway via “James Bundle”.
    • Passes from the Sinoatrial (SA) node to the Right and Left Bundle Branches by skipping the Atrioventricular (AV) node and the Bundle of His.
A

Lown-Ganong-Levine (LGL) Syndrome

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11
Q

What is the clinical course/treatment for Lown-Ganong-Levine (LGL) Syndrome?

Stable/Unstable/Definitive

A
  • Beware of rapid arrhythmias.
  • Stable - Adenosine
  • Unstable - Cardioversion
  • Definitive - Radiofrequency Ablation
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12
Q

EKG Finding:

  • Short PR Interval (<0.12s)
  • No Delta Wave
A

Lown-Ganong-Levine (LGL) Syndrome

*The only difference between Wolff-Parkinson-White (WPW) Syndrome and Lown-Ganong-Levine (LGL) Syndrome is that WPW does not have a Delta wave.

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13
Q
  • Resting sinus bradycardia and 1st degree AV block.
  • Criteria for LVH is met.
    • RVH is less common, but possible.
  • Nonspecific ST-T wave changes (such as early repolarization/ST elevation in precordial leads).
  • Right Bundle Branch Block is often seen.
  • All findings are normal in the absence of underlying cardiac disease.
A

Athlete’s Heart

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14
Q
  • Familial condition predisposing to sudden cardiac death.
  • Young Asian males are more commonly affected.
A

Brugada Syndrome

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15
Q

What is the definitive treatment for Brugada Syndrome?

A

Electrophysiology Studies

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16
Q

What is the treatment for Brugada Syndrome?

A

Beta-Blockers and Implantable Cardiac Defibrillator (ICD)

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17
Q

EKG Findings:

  • Right Bundle Branch Block, with downsloping R’ (RSR’).
  • T-wave inversion in V1 and/or V2.
  • ST Elevation V1, V2, V3.
A

Brugada Syndrome

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18
Q
  • Produces low voltage in all leads.
  • Often accompanied by:
    • Right Axis Deviation (RAD).
    • Poor R wave progression.
    • Multifocal Atrial Tachycardia
A

Chronic Pulmonary Obstructive Disease (COPD)

  • Voltage appears low because of air trapping in lungs.
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19
Q

What is the treatment for Chronic Obstructive Pulmonary Disorder (COPD)?

A

Treat the underlying pulmonary disease.

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20
Q

What is the pathophysiology for Pulmonary Embolus (PE)?

A

Blood clot lodged in the pulmonary vasculature.

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21
Q

EKG Findings:

  • Classic Findings (Classic S1Q3T3):
    • S wave in Lead I
    • Q wave in Lead III
    • Inverted T wave in Lead III
  • Most common finding is Sinus Tachycardia
  • Other Findings:
    • May or may not show T wave inversion in V1-V4.
    • May or may not show Right Bundle Branch Block (complete or incomplete).
A

Pulmonary Embolus (PE)

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22
Q

What is the range of potassium for cardiac conduction cycle at the cellular level?

A

3.5-5 mEq/L

mEq/L = milliequivalents per Liter

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23
Q

Abnormal levels of potassium cause:

A

Cardiac Arrhythmias

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24
Q

EKG Finding

  • Tall, peaked T Waves
A

Hyperkalemia

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25
Q

As the levels of potassium increase, the P wave flattens, while the QRS wave, which can progress to:

A

Ventricular Tachycardia

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26
Q

What is the treatment for Hyperkalemia?

A
  • The goal is to force excess K+ into the cells and out of the serum.
27
Q

What is the EKG Progression for Hyperkalemia? (3 Steps)

A
  1. Tall, peaked T waves
  2. PR-Interval prolongs and the P-Wave flattens
  3. QRS begins to widen, which can progress to Ventricular Fibrillation
28
Q

Which is a better measure of clinically significant K+ toxicity?

EKG changes associated with hyperkalemia or serum K+ levels.

A

EKG changes associated with hyperkalemia.

29
Q

Serum K+ levels > 5 mEq/L

A

Hyperkalemia

30
Q

Serum K+ level < 3.5 mEq/L

A

Hypokalemia

31
Q

Hypokalemia - EKG changes typically when serum K+ level is …

A

< 2.5 mEq/L

32
Q

EKG Finding

  • Flattened T waves
  • Development of U waves
A

Hypokalemia

33
Q

A wave appearing after the T wave and before the next P wave.

A

U-wave

34
Q

What is the treatment for hypokalemia?

A
  • Oral Potassium
  • IV Potassium
35
Q

What is a bigger issue hypercalcemia or hypocalcemia? Why?

A

Hypocalcemia becuase it can cause a long QT interval.

A long QT interval creates an R-on-T phenomena, which can lead to Polyventricular Tachycardia or Torsades de Pointes.

36
Q

Core body temperature < 95° F

A

Hypothermia

37
Q

EKG Findings

  • J-Wave or Osborn Wave
  • Bradycardia

Note:

  • Artifiact may be seen as the patient shivers.
A

Hypothermia

38
Q

Present, typically in the leads facing the left ventricle*. It is a narrow positve deflectrion closely attached to the end of the R or S wave of the QRS complex, at the point where the QRS complex joins the ST segment - J point.

*Lead II, III, aVF, V5, V6

A

Osborn Wave or J-wave

39
Q

What is digitalis?

A

Antiarrhythmic

It’s not used much anymore due to the narrow therapeutic window.

40
Q

EKG Finding

  • Scooped ST Segment
    • Expected.
A

Digitalis Effect

41
Q

EKG Finding

  • Induce Sinus and/or AV Block, cause new onset PAC or PVCs.
A

Digitalis Toxicity

42
Q

Inflammation of the pericardium.

Can be acute or chronic. It’s commonly associated with virus.

A

Pericarditis

43
Q

EKG Findings

  • Diffuse ST Elevations
A

Acute Pericarditis

*Diffuse ST Elevations means that it is occuring through most, if not all, leads - except aVR.

44
Q

EKG Findings

  • T-wave Inversion
A

Chronic Pericarditis

45
Q

STEMI or Pericarditis?

  • ST-segment and T-wave changes tend to be diffuse.
  • The ST-segment is typically concave upward (saddle shaped).
  • T-wave inversion usually occurs only after the ST segments have returned to baseline.
  • Q-wave formation does not occur.
A

Pericarditis

46
Q

STEMI or Pericarditis?

  • ST-segment and T-wave changes tend to be focal and localized.
  • ST elevation “tombstones”.
  • T-wave inversion usually precedes normalization of the ST segments
  • Q-waves may form.
A

STEMI

47
Q

Fluid collection within an enclosed pericardial sac.

Electrical axis of the heart varies with each beat due to the heart “floating in fluid-filled sac”.

A

Pericardial Effusion

48
Q

EKG Finding

  • Electrical Alternans: Results in varying amplitude (alternating large and small) of EKG beats.
A

Pericardial Effusion

49
Q

Congenital condition leading to hypertrophy of the heart wall.

A

Hypertrophic Cardiomyopathy (HCM)

50
Q

What are the three classifications for Hypertrophic Cardiomyopathy?

A

Obstructive

Dilated

Restrictive

51
Q

What pathology is associated with heart failure signs and symptoms in young?

A

HCM

52
Q

Can cause sudden cardiac death in young athletes.

A

HCM

53
Q

A typical type of Cardiomyopathy what is induced from stress/catecholamine.

Also known as, broken heart syndrome.

Acute Chest Pain and Shortness of Breath

A

Tako-Tsubo

54
Q

EKG Findings:

  • ST elevations
  • Deep anterior T-wave inversions
A

Tako-Tsubo

Presents just like an acute MI, but on cardiac angiography, vessles are patent.

55
Q

Most common in post-menopausal women.

Considered an example of myocardial “stunning”.

Stunning and shape changes usually resolve spontaneously in 4 weeks.

A

Tako-Tsubo

56
Q

What is the defining test for Tako-Tsubo?

A

Echocardiogram

57
Q

What is the immediate treatment for Tako-Tsubo?

A

The same as Myocardial Infarction.

ABC; MONA (No nitroglycerin in Inferior Wall Myocardial Infarction).

Antiplatelets, Beta-Blockers, Anticoagulants, Morphine, Oxygen, Nitroglycerin, Aspirin

58
Q

Associated with cerebrovascular accident. (Not diagnostic)

A

Cerebral T Waves

59
Q

EKG Findings

  • Large, deeply inverted T-waves in many leads.
  • U-waves possible.
  • Sinus bradycardia is common.
A

Cerebral T Waves

Changes seen are a result of disruption in the autonomic nervous system.

60
Q

What is the concern of Long QT?

A

R-on-T phenomenon; which leads to Polymorphic Ventricular Tachycardia

61
Q

Causes of Long QT:

A

GAAPAAE

  • Genetic Abnormalities
  • Antiarrhythmics
    • Amiodaraone
  • Antifungals
    • Ketoconazole
  • Psychotropics
    • Haloperidol
  • Antibiotics
    • Macrolides
    • Fluoroquinolones
  • Antidepressants
    • Tricyclic Antidepressants
      • Amitrypilines
    • SSRI
      • Citalopram
      • Fluoxetine
  • Electrolytes
62
Q

QT intervals vary with HR.

Therefore, the corrected QT interval is used (QTc):

A

QTc > 500ms = long

QTc > 550ms = Bundle Branch Block

The formula is most accurate between 50-120 bpm.

Upper level of noraml may vary by source. We will use 500 and 550 ms in this class for consistency.

63
Q
A

EKG Use and Interpretation (5 decks)

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