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FA - Cardiovascular > Cardio - Physio (ECG Concepts) > Flashcards

Cardio - Physio (ECG Concepts) Flashcards

Pg. 276-279 in First Aid 2014 Pg. 261-263 in First Aid 2013 Includes sections: -Electrocardiogram -Torsades de pointes -Wolff-Parkinson white syndrome -ECG Tracings

1
Q

What does the P wave signify?

A

Atrial depolarization

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2
Q

Why isn’t atrial repolarization seen on ECG?

A

Masked by QRS complex

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3
Q

What does the PR interval represent? What is a normal PR interval?

A

Time from start of atrial depolarization to start of ventricular depolarization; Normally < 200 mec

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4
Q

What does the QRS complex signify? How long is it normally?

A

Ventricular depolarization; Normally < 120 msec

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5
Q

What does the QT interval represent?

A

Mechanical contraction of the ventricles

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6
Q

What does the T wave signify?

A

Ventricular repolarization

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7
Q

What might a T wave inversion indicate?

A

Recent MI

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8
Q

What is a key feature of the ST segment? What state are the ventricles in during this period?

A

Isoelectric; Ventricles depolarized

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9
Q

What can cause a U wave to appear on ECG?

A

(1) Hypokalemia (2) Bradycardia

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10
Q

List major parts of the heart’s conduction pathway(s) in order of decreasing speed of conduction.

A

Purkinje > Atria > Ventricles > AV node

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11
Q

What are the pacemakers of the heart (in order of use/importance in the divine design of failsafe options for pacemaker activity)?

A

SA > AV > bundle of His/Purkinje/ventricles

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12
Q

What is the order of the conduction pathway?

A

SA node –> Atria –> AV node –> Common bundle –> Bundle branches –> Purkinje fibers –> Ventricles

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13
Q

What is key to remember about SA node in terms of how it compares to other pacemakers?

A

Inherent dominance with slow phase of upstroke

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14
Q

What is key to remember about AV node in terms of timing?

A

100-m sec delay = atrioventricular delay = allows time for ventricular filling

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15
Q

Graph an ECG, labeling the following: (1) P (2) QRS Complex (3) T (4) U (5) PR interval (6) ST segment (7) QT interval (8) Isoelectric line.

A

See p. 261 - graph in middle on right

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16
Q

Draw the heart, labeling the following parts of the conduction pathway: (1) Sinoatrial node (2) Internodal pathways (3) Atrioventricular node (4) Bundle of His (5) Right bundle branch (6) Left bundle branch (7) Purkinje system (8) Left anterior fascicle (9) Left posterior fascicle.

A

See p. 261 - illustration in middle on left

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17
Q

In general, what is Torsades de pointes? More specifically, what characterizes it on ECG? To what can it progress?

A

Polymorphic ventricular tachycardia; Characterized by shifting sinusoidal waveforms on ECG; Can progress to ventricular fibrillation

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18
Q

What can predispose someone to Torsades de pointes?

A

Long QT interval predisposes to torsades de pointes

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19
Q

How is Torsades de pointes treated?

A

Treatment includes magnesium sulfate

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20
Q

What are at least 3 general causes of Torsades de pointes?

A

Caused by (1) drugs, (2) low K+, (3) low Mg2+, other abnormalities

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21
Q

Name 7 drugs that can prolong QT.

A

(1) Sotalol (2) Risperidone (antipsychotics) (3) Macrolides (4) Chloroquine (5) Protease inhibitors (-navir) (6) Quinidine (class Ia; also class III) (7) Thiazides; Think: “Some Risky Meds Can Prolong QT”

22
Q

What kind of disorder is congenital long QT syndrome, and what causes it?

A

Inherited disorder of myocardial repolarization, typically due to ion (cardiac sodium or potassium) channel defects

23
Q

What risk does congenital long QT syndrome increase?

A

Increase risk of sudden cardiac death due to torsades de pointes

24
Q

What are 2 types of Congenital long QT syndromes?

A

(1) Romano-Ward syndrome (2) Jervell and Lange-Nielsen syndrome

25
Q

What kind of syndrome is Romano-Ward syndrome? What kind of inheritance does it have?

A

Congenital long QT syndrome; Autosomal dominant

26
Q

What kind of syndrome is Jervell and Lange-Nielsen syndrome? What kind of inheritance does it have?

A

Congenital long QT syndrome; Autosomal recessive

27
Q

What is the distinguishing phenotype of Romano-Ward syndrome?

A

Pure cardiac phenotype (no deafness)

28
Q

What is the distinguishing phenotype of Jervell and Lange-Nielsen syndrome?

A

Sensorineural deafness

29
Q

Compare/Contrast the 2 types of congenital long QT syndrome in terms of mode of inheritance and associated symptoms.

A

(1) Romano-Ward syndrome: Autosomal dominant, Pure cardiac phenotype (no deafness) (2) Jervell and Lange-Nielsen syndrome: Autosomal recessive, Sensorineural deafness

30
Q

What is the most common type of ventricular pre-excitation syndrome?

A

Wolff-Parkinson-White syndrome

31
Q

What is the mechanism of Wolff-Parkinson-White syndrome? What ECG finding does this cause?

A

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG.

32
Q

What arrhythmia may result from Wolff-Parkinson-White syndrome, and why?

A

May result in reentry circuit => supraventricular tachycardia

33
Q

Describe the ECG tracing of Atrial fibrillation.

A

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes

34
Q

What condition can result from Atrial fibrillation, and why?

A

Can result in atrial stasis and lead to thromboembolic stroke

35
Q

What are 3 components are included in the treatment of Atrial fibrillation?

A

Treatment includes rate control, anticoagulation, and possible pharmacological or electrical cardioversion

36
Q

Describe the ECG tracing of Atrial flutter.

A

A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves

37
Q

What are the treatments for Atrial flutter in each of the following ways: (1) Pharmacologic conversion to sinus rhythm (2) Rate control (3) Definitive?

A

(1) Pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmics (2) Rate control: Beta-blocker or calcium channel (3) Definitive treatment is catheter ablation

38
Q

Describe the ECG tracing of Ventricular fibrillation.

A

A completely erratic rhythm with no identifiable waves.

39
Q

What is the treatment/management approach to Ventricular fibrillation, and why?

A

Fatal arrhythmia without immediate CPR and defibrillation

40
Q

Describe the ECG tracing of 1st degree AV block.

A

The PR interval is prolonged (> 200 msec)

41
Q

How does 1st degree AV block affect the patient? What treatment is required?

A

Benign and asymptomatic; No treatment required

42
Q

Describe the ECG tracing of 2nd degree Mobitz type I (Wenckebach) AV block.

A

Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex).

43
Q

How does 2nd degree Mobitz type I (Wenckebach) AV block usually affect the patient?

A

Usually asymptomatic

44
Q

What is another name for 2nd degree Mobitz type I AV block?

A

Mobitz type I (Wenckebach)

45
Q

Describe the ECG tracing of 2nd degree Mobitz type II AV block. How is it often found?

A

Dropped beats that are not preceded by a change in the length of the PR interval (as in type I). It is often found as a 2:1 block, where there are 2 or more P waves to 1 QRS response.

46
Q

To what condition may 2nd degree Mobitz type II AV block progress?

A

May progress to 3rd-degree block.

47
Q

How is 2nd degree Mobitz type II AB block often treated?

A

Often treated with pacemaker

48
Q

In general, what causes/characterizes 3rd degree (complete) AV block?

A

The atria and ventricles beat independently of each other.

49
Q

Describe its ECG tracing, especially in terms of waves present and contrasting rates.

A

Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate.

50
Q

What is usually used to treat 3rd degree AV block?

A

Usually treated with pacemaker

51
Q

What disease can result in 3rd degree heart block?

A

Lyme disease can result in 3rd-degree heart block

FA - Cardiovascular (18 decks)

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