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
As the levels of potassium increase, the P wave flattens, while the QRS wave, which can progress to:
Ventricular Tachycardia
26
What is the treatment for Hyperkalemia?
* The goal is to force excess K+ into the cells and out of the serum.
27
What is the EKG Progression for Hyperkalemia? (3 Steps)
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
Which is a better measure of clinically significant K+ toxicity? EKG changes associated with hyperkalemia or serum K+ levels.
EKG changes associated with hyperkalemia.
29
Serum K+ levels \> 5 mEq/L
Hyperkalemia
30
Serum K+ level \< 3.5 mEq/L
Hypokalemia
31
Hypokalemia - EKG changes typically when serum K+ level is ...
\< 2.5 mEq/L
32
EKG Finding * Flattened T waves * Development of U waves
Hypokalemia
33
A wave appearing after the T wave and before the next P wave.
U-wave
34
What is the treatment for hypokalemia?
* Oral Potassium * IV Potassium
35
What is a bigger issue hypercalcemia or hypocalcemia? Why?
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
Core body temperature \< 95° F
Hypothermia
37
EKG Findings * J-Wave or Osborn Wave * Bradycardia Note: * Artifiact may be seen as the patient shivers.
Hypothermia
38
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
Osborn Wave or J-wave
39
What is digitalis?
Antiarrhythmic It's not used much anymore due to the narrow therapeutic window.
40
EKG Finding * Scooped ST Segment * Expected.
Digitalis Effect
41
EKG Finding * Induce Sinus and/or AV Block, cause new onset PAC or PVCs.
Digitalis Toxicity
42
Inflammation of the pericardium. Can be acute or chronic. It's commonly associated with virus.
Pericarditis
43
EKG Findings * Diffuse ST Elevations
Acute Pericarditis \*Diffuse ST Elevations means that it is occuring through most, if not all, leads - except aVR.
44
EKG Findings * T-wave Inversion
Chronic Pericarditis
45
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.
Pericarditis
46
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.
STEMI
47
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".
Pericardial Effusion
48
EKG Finding * *Electrical Alternans:* Results in varying amplitude (alternating large and small) of EKG beats.
Pericardial Effusion
49
Congenital condition leading to hypertrophy of the heart wall.
Hypertrophic Cardiomyopathy (HCM)
50
What are the three classifications for Hypertrophic Cardiomyopathy?
Obstructive Dilated Restrictive
51
What pathology is associated with heart failure signs and symptoms in young?
HCM
52
Can cause sudden cardiac death in young athletes.
HCM
53
A typical type of Cardiomyopathy what is induced from stress/catecholamine. Also known as, broken heart syndrome. Acute Chest Pain and Shortness of Breath
Tako-Tsubo
54
EKG Findings: * ST elevations * Deep anterior T-wave inversions
Tako-Tsubo Presents just like an acute MI, but on cardiac angiography, vessles are patent.
55
Most common in post-menopausal women. Considered an example of myocardial "stunning". Stunning and shape changes usually resolve spontaneously in 4 weeks.
Tako-Tsubo
56
What is the defining test for Tako-Tsubo?
Echocardiogram
57
What is the immediate treatment for Tako-Tsubo?
The same as Myocardial Infarction. ABC; MONA (No nitroglycerin in Inferior Wall Myocardial Infarction). Antiplatelets, Beta-Blockers, Anticoagulants, Morphine, Oxygen, Nitroglycerin, Aspirin
58
Associated with cerebrovascular accident. (Not diagnostic)
Cerebral T Waves
59
EKG Findings * Large, deeply inverted T-waves in many leads. * U-waves possible. * Sinus bradycardia is common.
Cerebral T Waves Changes seen are a result of disruption in the autonomic nervous system.
60
What is the concern of Long QT?
R-on-T phenomenon; which leads to Polymorphic Ventricular Tachycardia
61
Causes of Long QT:
GAAPAAE * Genetic Abnormalities * Antiarrhythmics * Amiodaraone * Antifungals * Ketoconazole * Psychotropics * Haloperidol * Antibiotics * Macrolides * Fluoroquinolones * Antidepressants * Tricyclic Antidepressants * Amitrypilines * SSRI * Citalopram * Fluoxetine * Electrolytes
62
QT intervals vary with HR. Therefore, the corrected QT interval is used (QTc):
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