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pathophysiology > Chapter 3 Arrhythmias > Flashcards

Chapter 3 Arrhythmias Flashcards

1
Q

what is the term that describes a normal heart rate?

A

normal sinus rhythm

Anything else is called arrhythmia or dysrhythmia

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2
Q

what are palpitations?

A

feelings or sensations that your heart is pounding or racing

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3
Q

decreased cardiac output causes?

A

light-headedness and syncope (fainting)

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4
Q

rapid arrhythmias can cause?

A

angina (chest pain) as the increased heart rate can increase the oxygen demands of the myocardium.

The sudden onset of an arrhythmia in a patient with underlying cardiac disease can also precipitate congestive heart failure.

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5
Q

what greatly increases the risk of arrhythmic sudden death?

A

acute myocardial infraction, which is why these patients are taken to the CCUs (cardiac care units) where their heart can be constantly monitored.

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6
Q

what are the causes of arrhythmia?

mnemonic HIS DEBS.

A
  • H-hypoxia: pulmonary disorders (pulmonary embolus)
  • I-ischemia and irritability (myocardial infraction, myocarditis)
  • S-sympathetic stimulation (hyperthyroidism, exercise, nervousness)
  • D-drugs
  • E-electrolyte disturbances (hypokalemia and hyperkalemia + calcium and magnesium imbalance)
  • B-bradycardia
  • S-stretch (enlargement and hypertrophy of the atria and ventricles)
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7
Q

A heart rate cycle that repeats itself once every 5 large squares represents (BPM?)

A

1 beat per second, or a heart rate of 60 beats per minute.

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8
Q

3 step process of calculating heart rate easily?

A
  1. find an R wave that falls on, or nearly on, one of the heavy lines.
  2. Count the number of large squares until the next R-wave.
  3. Determine the rate in beats per minute as follows:
    - If there are two large squares between successive R waves, then each R wave is separated by 0.4 seconds. Therefore, over the course of 1 full second, there will be 2.5 cycles of cardiac activity (1 second divided by 0.4 seconds) and over 1 minute 150 cycles (2.5 x 60 seconds)/ The heart rate is therefore 150 beats per minute.

same answer can be done by dividing 300 by the number of large square between R-waves (300/2 = 150BPM).

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9
Q

5 basic types of arrhythmias?

A
  1. Arrhythmia of sinus origin. If the normal path of electrical activity is followed but the depolarization of the sinus node is too fast, too slow, or irregular.
  2. Ectopic rhythms; electrical activity originates from a focus other than the sinus node
  3. Reentrant arrhythmias
  4. Conduction blocks
  5. Preexciations syndromes (short circuit, bypassing normal conduction pathway.
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10
Q

what is considered sinus tachy and bradycardia? And what could cause it?

A

over 100BPM is sinus tachycardia and below 60 is called sinus bradycardia. (SA node is firing faster or slower)

Exercise and rest can cause both of these but they can also be pathological; congestive heart failure or severe lung disease or hyperthyroidism in elderly.

Bradycardia can be caused by medications: Beta-blockers, calcium channel blockers and opioids.
Enhanced vagal tone can cause fainting.

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11
Q

Describe sinus arrhythmia?

A

variations in heart rate that accompanies inspiration and expiration.
inspiration accelerates heart rate, expiration decreases it.

there may be a prolonged separation of each P-wave from its ensuing QRS complex (prolonged PR interval) this is a 1st degree AV-block.

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12
Q

what is sinus arrest, asystole and escape beats?

A

Sinus arrest = SA node stops firing
asystole = prolonged electrical inactivity.
Escape beats = SA node stops firing so another part of the heart stimulates electrical activity.

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13
Q

what is a nonsinus pacemaker?

A

The sinus node fires between 60-100 times each minute, other potential pacemakers cells of the heart have their own intrinsic rhythm.

  • Atrial pacemakers: discharge at 60-75 bpm
  • Pacemakers near the AV node called functional pacemakers fire at 40-60 bpm.
  • ventricular pacemaker cells usually discharge at 30-45 bpm
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14
Q

what would a functional escape look like on an ECG?

A

depolarization originates near the AV node, and the usual pattern of atrial depolarization does not occur. A normal P-wave is not seen. A retrograde P wave may be seen representing atrial depolarization moving backward from the AV node into the atria.

Normal P-wave is upright in Lead II and inverted in lead aVR
RETROGRADE P-wave is inverted in lead II and upright in lead aVR. Retrograde P-wave can occur before, after or during the QRS complex.

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15
Q

what is sinus arrest/sinus exit block?

A

the SA node cannot transmit its signal to the surrounding tissue

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16
Q

what is missing during functional escape?

A

the P-wave, which could be inverted or masked by the QRS complex.

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17
Q

describe ectopic rhythms?

A

ectopic rhythms are abnormal rhythms that arise from elsewhere than the sinus node. The arise from enchanced automaticity (intrinsic pacemaker activity) of a nonsinus node site, either a single focus or a roving one. (overdrive suppression)
Some of the causes of enhanced automaticity are: digitalis toxicity, beta adrenergic stimulation (inhaler therapies to treat asthma and COPD), caffeine and alcohol, cocaine and amphetamines.

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18
Q

what are the 2 major causes of nonsinus arrhythmias?

A
  • ectopic rhythms

- reentrant rhythms

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19
Q

Describe reentrant rhythms?

A

Reentry represents a disorder of impulse transmission (vs enhanced automaticity = disorder of impulse transmission)

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20
Q

what does a normal P-wave look like?

A

upright in lead II and inverted in aVR.

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21
Q

what are the 4 questions for assessing a rhythm disturbance on EKG?

A
  1. Are normal P-waves present? (+ in lead II and - in aVR)
  2. Are the QRS complexes Narrow (<0.12 seconds) or wide (>0.12 seconds)? wide QRS means the origin of ventricular depolarization lies within the ventricles themselves. Short QRS means depolarization is following the normal efficient path of conduction.
  3. what is the relationship between the P waves and the QRS complexes? (AV dissociation; condition where the atria and ventricles depolarize and contract independently of each other) IS THERE A P-WAVE BEFORE EACH QRS?
  4. Is the rhythm regular or irregular?
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22
Q

Describe atrial and functional premature beats?

A
  • Atrial premature beats: single ectopic supraventricular beats originating in the atria
  • junctional premature beats: single ectopic supraventricular beats originating from the vicinity of the AV node.
23
Q

how can an atrial premature beat be distinguished from a normal sinus beat?

A

by the contour of the P-wave and by the timing of the beat;

  • an atrial premature beat originates at the site distant from the sinus node, the axis of the P-wave differs. (contour) (PAC = premature atrial contractions)
  • an atrial premature beat comes too early. (timing)
24
Q

describe the ECG appearance of a junctional premature beats?

A
  • P-wave may not be present

- sometimes a retrograde P wave may be seen

25
Q

what is the difference between a junctional premature beat and a junctional escape beat?

A

they look exactly alike
junctional premature beat: occurs early
junctional escape beat: occurs late FOLLOWED by a pause when the sinus node has failed to fire.

26
Q

name the 6 types of sustained supraventricular arrhythmias?

A
  1. AV nodal reentrant tachycardia (AVNRT) (paroxysmal supraventricular tachycardia)
  2. Atrail flutter
  3. Atrail fibrillation
  4. Multifocal atrial tachycardia (MAT)
  5. Paroxysmal atrial tachycardia (PAT), also called ectopic atrial tachycardia
  6. AV reciprocating tachycardia (we’ll hold on discussing this one until Chapter 5, since it is uniquely associated with a particular kind of cardiac condition called preexciation)
27
Q

describe AVNRT (AV nodal reentrant tachycardia)

A

Very common and has a sudden onset initiated by a premature supraventricular beat (atrial or junctional), and is terminated just as fast. Can occur in normal healthy hearts with no underlying disease.
Symptoms: palpitations, shortness of breath, dizziness or syncope.
Can be caused by: alcohol, coffee, or just sheer excitement can elicit this rhythm disturbance.

AVNRT: is NORMAL rhythm that is about 150-250bpm

28
Q

what causes AVNRT?

A

reentrant circuit looping within the AV node (retrograde P waves may sometimes be seen in leads II or III.
Look at lead V1 for an pseudo-R (a little blip in the QRS complex that represents the superimposed retrograde P wave.
QRS is narrow (normal) and sometime the P-wave is masked by the QRS.

29
Q

AVNRT can be treated by?

A

Carotid Massage. it can help diagnose and terminate AVNRT.
the vagus reflex slows down the rate for SA node firing and slows conduction through the AV node.
Left carotid artery = AV node
Right carotid artery = SA node

  • Interrupts the reentrant circuit and thereby terminate the arrhythmia
  • At the very least, slow the arrhythmia so that the presence or absence of P waves can be more easily determined and the arrhythmia diagnosed.
30
Q

how to perform a carotid massage?

A
  1. do no perform the massage if there is evidence of significant carotid disease.
  2. the patient should lie down, extend the neck and rotate the head slightly away from you
  3. palpate the carotid artery and apply pressure for 10-15 seconds
  4. NEVER compress both arteries
  5. Right carotid has a higher rate of success.
  6. have and EKG setup to see if the massage works.
31
Q

Describe atrial flutter.

A

less common than AVNRT, can occur in normal hearts. Just like in AVNRT the atrial activation is normal but even more rapid. P waves appear at a rate of 250 to 350 bpm.
Caused by a reentrant circuit that runs largely around the annulus of the tricuspid valve.
“saw tooth pattern” is seen in EKG.
There is an AV block because not all atrial signals can get through. A 2:1, 3:1 and 4:1 pattern may be seen.
Carotid massage may change a 2:1 block to a 4:1 block making it easier to diagnose but will NOT terminate the flutter.

32
Q

describe atrial fibrillation?

A

unlike atrial flutter where a single constant reentrant circuit is creating a saw-toothed pattern on the EKG, atrial fibrillation the atrial activity is completely chaotic and the AV node may be bombarded with more than 500 impulses per minute.
Multiple tiny reentrant circuits whirl around in totally unpredictable fashion.
NO true P-wave is seen.
The P-waves appear flat and occasionally the AV node allows for an impulse to pass.
RESULT: irregularly irregular rhythm.

33
Q

Describe multifocal atrial tachycardia (MAT) and wandering atrial pacemakers.

A

MAT is an irregular rhythm occurring at a rate of 100-200bpm resulting from a random firing of several different ectopic atrial foci.
less then 100bpm the arrhythmia is called wandering atrial pacemaker.
MAT is common in patients with severe lung disease. carotid massage has NO effect. Wandering atrial pacemaker can be seen in normal healthy hearts.

34
Q

what does MAT (multifocal atrial tachycardia) look like on ECG?

A

P waves originating from multiple sites in the atria will vary in shape and the interval between the different P waves and the QRS complexes may vary as well.
Try to identify 3 different P-wave morphologies.

In contrast to wandering atrial pacemaker (similar to MAT) the P-wave will appear normal for 2-3 beats before a new site for the P-wave is located. NOT a tachyarrhythmia since the rate is between 60-100 bpm.

35
Q

describe PAT (paroxysmal atrial tachycardia)?

A

a regular rhythm with a rate of 100-200bpm.
Can result from enhanced automaticit of an ectopic atrial focus or from a reentrant circuit within the atria.
the automatic type typically displays a warm-up period when it starts, during which the rhythm appears somewhat irregular and a similar cool-down period when it terminates.
Less common reentrant from starts abruptly with atrial premature beat. (atypical atrial flutter).

36
Q

how to tell the difference between PAT and AVNRT?

A

PAT: has a warm-up and cool-down period
AVNRT: can be fixed with carotid massage whereas the massage has no effect on PAT.

37
Q 
what would you see with:
sinus tachycardia:
AVNRT:
Paroxysmal atrial tachycardia:
atrial flutter with a regular block:
A

sinus tachycardia: Normal P wave for every QRS complex
AVNRT: No P-waves or retrograde P waves and faster than average sinus tachycardia.
Paroxysmal atrial tachycardia (PAT): similar to AVNRT but more with a warm-up and cool-down.
atrial flutter with a regular block:flutter waves

38
Q

what are ventricular arrhythmias?

A

rhythm disturbances arising below the AV node.

39
Q

what does a premature ventricular contraction (PVC) look like on ECG?

A

the QRS complex of PVC appears wide and bizarre since the normal conduction pathway is not followed by the depolarization. retrograde P-wave may sometimes be seen (more common to not see a P-wave at all).
A compensatory pause may follow a PVC, or less commonly a PVC may occur between two normally conducted beats withou compensatory pause called (interpolated PVCs)

40
Q

under what conditions can a PVC (premature ventricular contraction) occur?

A

isolated PVCs are common in normal hearts and rarely require treatment an isolated PVC in the setting of an acute myocardial infraction could trigger ventricular tachycardia or ventricular fibrillation. Both of which are life threatening.

41
Q

in terms of PVCs what is bigeminy and trigeminy?

A

Bigeminy: 1 normal sinus beat to one PVC
trigeminy: 2 normal sinus beats for every one PVC

42
Q

what are the rules of malignancy for PVC?

A

certain circumstances PVCs pose an increase risk fro triggering ventricular tachycardia, ventricular fibrillation and death.

  1. frequent PVCs
  2. runs of consecutive PVCs especially three or more in a row
  3. multiform PVCs in which the PVCs vary in their site of origin and hence in their appearance
  4. PVCs falling on the T wave of the previous beat, called the R-on-T phenomenon. The T wave is a vulnerable period in the cardiac cycle, and the PVC falling there is more likely to set off ventricular tachycardia.
  5. Any PVC occurring in the setting of an acute myocardial infraction.
43
Q

Describe ventricular tachycardia?

A

3 or more consecutive PVCs is called ventricular tachycardia (120-200bpm)
unlike AVNRT, it may be somewhat irregular.
The ventricular tachycardia may be uniform or polymorphic; changing appearance from beat to beat.
Polymorphic ventricular tachycardia is more commonly associated with acute coronary ischemia infraction, profound electrolyte disturbances.
Uniform ventricular tachycardia is more often seen with healed infractions (scarring myocardium provides the substrate for reentrant ventricular tachycardia.

44
Q

describe ventricular fibrillation?

A

a pre-terminal event, seen almost solely in dying hearts.

45
Q

what are some of the common precipitants of ventricular fibrillation?

A
  • myocardial ischemia/infraction
  • heart failure
  • hypoxemia or hypercapnia
  • hypotension or shock
  • electrolyte imbalances
  • Overdoses of stimulants, especially when used in combination.
46
Q

describe accelerated idioventricular rhythm?

A

a benign rhythm that is sometimes seen during an acute infraction during the 1st few hours following a re-perfusion.
when the rhythm falls below 50bpm it is called idioventricular rhythm
This is not dangerous.

47
Q

Describe torsade de pointes? (twisting of the points)

A

a unique form of ventricular tachycardia that is seen in patients with prolonged QT intervals (time from beginning of ventricular depol to end of repol.)
Prolonged QT can be caused by?
- congenital (ion channel mutation)
- electolyte distrubances
- medications/drugs
since a prolonged T-wave can cause this, if a PVC falls on the larger T-wave a torsade de pointes can occur.

48
Q

what does a torsade de pointes look like on an ECG?

A

similar to a ventricular tachycardia but the QRS complexes spiral around the baseline changing their axis and amplitude.

49
Q

how to differentiate between a supraventricular versus ventricular arrhythmias?

A

supraventricular: narrow QRS
ventricular: wide QRS
except for the following condition (ABERRANCY): if the atrial depolarization occurs when the ventricle is still repolarizing, and since the right bundle branch is more sluggish in repolarizing the signal may go down the left bundle branch and then be conducted across from the left bundle branch to the right one, forming a bizarre wide QRS.

50
Q

how to tell AVNRT and ventricular tachycardia apart?

clinical clues

A
  1. ventricular tachycardia occur in diseased hearts, AVNRT can occur in normal hearts
  2. Carotid massage can terminate AVNRT but no effect on ventricular tachycardia
  3. most cases of ventricular tachycardia is accompanied by AV dissociation. If atria contract against the closed valves, backflow into jugular veins, a classic cannon A waves are produced which are not seen in AVNRT.
51
Q

how to tell AVNRT and ventricular tachycardia apart?

ECG clues

A
  1. the P-waves appear independent in ventricular tachycardia, while in AVNRT the retrograde P-waves are seen before each QRS
  2. Fusion beats; seen only in ventricular tachycardia only. It occurs when an atrial impulse manages to slip through the AV node at the same time that an impulse of ventricular origin is spreading across the ventricular myocardium. (larges amplitude on ECG)
  3. AVNRT QRS deflection occurs in the normal direction while in ventricular tachycardia its in the opposite direction.
52
Q

describe the ashman phenomenon?

A

commonly seen in patients with atrial fibrillation.
a wide aberrant conducted supraventricular beat occurring after a QRS complex that is preceded by a long pause.
the bundle branches reset their rate of repolarization according to the length of the preceding beat. If there is a long pause after a beat the bundles will repolarize slowly. Then if a signal enters the AV node before repolarization occurs a wide bizarre QRS will be seen.

53
Q

what condition could predispose someone to torsade de pointes?

A

a long QT interval which should normally make up just 40% of the cardiac cycle.

pathophysiology (7 decks)

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