CARDIOLOGY - Sinus and Atrial Dysrhythmias (Week 5) Flashcards

1
Q

What are the 6 types of sinus rhythms?

A
  1. Normal Sinus Rhythm (NSR)
  2. Sinus Bradycardia
  3. Sinus Tachycardia
  4. Sinus Arrhythmia
  5. Sinus Block
  6. Sinus Arrest
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2
Q

Sinus dysrhythmias are rhythms originating from the

A

SA node

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3
Q

What are two ways in which the sinus node can “relinquish its duty” (i.e. give up its job as primary pacemaker)?

A

1. illness or death - in which another pacemaker steps in

2. Usurpation - overthrown by another pacemaker (like a king)

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4
Q

True or False. In reality, there is only one “normal” rhythm. What is it?

A

True. Normal Sinus Rhythm (NSR)

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5
Q

Describe the conduction pathway in NSR.

A

Impulse originates in sinus node. Heads down normal conduction pathway and ultimately depolarizes into ventricular muscle

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6
Q

Normal Sinus Rhythm (NSR)

Rate

Rhythm

P wave

PR Interval

QRS Complex

A

Rate: 60 - 100

Rhythm: regular R-R intervals

P wave: present. upright, regular, matching, precedes each QRS complex (may be inverted in V1)

PR Interval: 0.12 - 0.20 secs, constant from beat to beat

QRS Complex: < 0.12 seconds (can be > 0.12 sec if BBB exist)

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7
Q

Normal Sinus Rhythm (NSR)

Causes

Adverse Effects

Treatment

A

Causes: Normal

Adverse Effects: None

Treatment: None

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8
Q

Sinus bradycardia

A

looks like NSR but a lot slower (SA node is firing at a slower rate than normal)

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9
Q

Describe the conduction pathway in sinus bradycardia.

A

Impulse originates in sinus node, heads down normal conduction pathway and ultimately depolarizes into ventricular muscle

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10
Q

Sinus Bradycardia

Rate

Rhythm

P wave

PR Interval

QRS Complex

A

Rate: < 60 (THIS IS THE ONLY THING THAT IS DIFFERENT when compared to NSR)

Rhythm: regular R-R intervals

P wave: present. upright, regular, matching, precedes each QRS complex (may be inverted in V1)

PR Interval: 0.12 - 0.20 secs, constant from beat to beat

QRS Complex: < 0.12 seconds (can be > 0.12 secs if BBB exist)

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11
Q

Sinus Bradycardia

Causes

Adverse Effects

Treatment

A

Causes:

  • MI (associated with inferior MI)
  • vagal stimulation (PNS response) - Vagal maneuveres, Valsalva maneuver, carotid sinus massage)
  • Athletes - well conditioned hearts able to pump more blood with each beat and less often
  • Increased intracranial pressure - Cushing’s triad
  • Medications - calcium channel blockers, beta blockers, Digitalis toxicity
  • Disease of the SA node
  • Hypoxia
  • Post heart transplant
  • Hyper/hypokalemia
  • Hypothyroidism
  • Hypothermia

Adverse Effects:

  • Decreased cardiac output
  • dizziness
  • syncope
  • weakness
  • hypotension
  • pallor

Treatment: correct undelying cause (i.e. provide warmth, hyperventilate, etc.)

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12
Q

Sinus Tachycardia

A

looks like NSR but a lot faster (SA node firing at a faster rate than normal)

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13
Q

Describe the conduction pathway in Sinus Tachycardia

A

Impulse originates in sinus node. Heads down normal conduction pathway and ultimately depolarizes into ventricular muscle

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14
Q

Sinus Tachycardia

Rate

Rhythm

P wave

PR interval

QRS complex

A

Rate: 101 - 180

Rhythm: regular R-R interval

P wave: present, regular, upright, matching, precede each QRS complex (may be inverted in V1) & at very fast rates it may be difficult to differentiate between P waves from T waves (T wave may just look like a double hump because P wave is buried in it)

PR interval: 0.12-0.20 seconds, constant from beat to beat (may shorten with faster rate)

QRS complex: < 0.12 seconds (can be >0. 12 if BBB exists)

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15
Q

Sinus Tachycardia

Causes

Adverse Effets

Treatment

A

Causes:

  • MI (typical with anterior infarctions)
  • Sympathetic stimulation - maintaining HR and BP under normal conditions and “fight or flight” response)
  • CHF - abnormal condition that reflects impaired cardiac pumping
  • Shock - hypovolemic, neurogenic, anaphlyactic, septic, etc.
  • Pulmonary embolilsm - blockage of the pulmonary artery by a foreign matter
  • Drugs - cocaine, ecstasy, amphetamines, cannabis, nicotine, caffeine, etc.
  • Medications - Atropine, epinephrine, dopamine
  • Exercise
  • Pain
  • Fear and Anxiety
  • Hpoxia
  • Hyperthyroidism

Adverse Effects:

  • Decreased cardiac output
  • dizziness
  • syncope
  • weakness
  • hypotension
  • pallor

Treatment: attempt to correct the underlying cause (pain relief, reducing feer, reliveing anxiety, etc.)

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16
Q

Sinus arrhythmia (Sinus dysrhythmia)

A

Rhythm where SA node fires irregularly, which is cyclic and usually coincides with respiratory rate/breathing pattern in younger patients

Increases gradually during inspiration (R-R intervals shorten)

Decreases with expiration (R-R interval lengthens)

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17
Q

Physiologically, what is happening during sinus arrhythmia caused by breathing patterns?

A

RATE increases during inspiration: negative pressure in chest during inspiration sucks up blood from LE (causing more blood to return to RA) which ↑ HR to circulate that increased amount of blood

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18
Q

Describe the conduction pathway in sinus arrhythmia.

A

Impulse originates in sinus node, heads down the normal conduction pathway. Ultimately depolarizes in ventricular muscle.

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19
Q

Sinus Arrhythmia

Rate

Rhythm

P wave

PR interval

QRS complex

A

Rate: usually 60 - 100 (can vary due to respiratory pattern)

Rhythm: regularly irregular

  • increases during inspirations (R-R interval shortens)
  • decreases during expirations (R-R interval lengths)

P wave: present, irregular, upright, matching, precede each QRS complex (may be inverted in V1)

PR interval: 0.12-0.20 seconds (constant from beat to beat)

QRS complex: <0.12 secs (can be > 0.12 if BBB exist)

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20
Q

Sinus Arrhythmia

Causes

Adverse Effects

Treatmnent

A

Causes:

  • respiratory sinus arrhythmia:
    • normal phenomenon” - breathing pattern most commonly seen in children and <30 y.o.
  • non-respiratory sinus arrhythmia:
    • heart disease
    • MI
    • Drugs - Digitalis, Morphine

Adverse Effects: None

Treatment: None

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21
Q

Sinus block (Exit Block)

A
  • SA node fires an impulse regularly but it does not conduct (i.e. nothing wrong with the SA node but the impulse is not depolarizing to the atria)
  • The impulse is unable to “exit” into surrounding atrial tissue; impulse is NOT conducted anywhere (not to atria, not to ventricles)
  • this results in one or more beat sequences missing, creating a “pause” (length of pause will depend on how many beats are blocked)
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22
Q

In sinus block, what is unique about the pause caused by the missed beat?

A
  • The pause caused by the missed beat is the same as (or an exact multiple of) the distance between two P-P intervals of the underlying rhythm (Exactly one or more cycles will fit into the pause)
  • When the conduction of the regularly firing sinus impulse resumes, the beat returns on time at the end of the pause
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23
Q

Describe the differences between these two rhythms.

A

NSR: R-R intervals are exactly equal distances apart

Sinus Block: R-R intervals are exactly equal distance apart EXCEPT for the 6th complex

  • the SA node is firing properly but it did not depolarize the atria and therefore did not create a P wave and subsequent QRS complex
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24
Q

When interpreting a sinus block rhythm, what indications on the ECG tracing tell you that the SA node is working properly?

A

The following P wave and QRS complex after the pause resumes exactly a certain number of cycles apart (depending on pause duration)

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25
Q

Sinus Block

Rate

Rhythm

P wave

PR Interval

QRS complex

A

Rate: can occur at any rate (usually 60 - 100 BPM)

Rhythm: occasionally irregular (due to pause(s) caused by sinus block); pause is the same distance between two other P-P intervals

P wave: normal sinus P’s before AND after the pause

PR Interval: 0.12-0.20 seconds, constant from beat to beat

QRS complex: <0.12 seconds (can be > 0.12 if BBB exist)

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26
Q

Sinus Block

Causes

Adverse Effects

Treatment

A

Causes:

  • MI
  • Vagal stimulation
  • CAD (building up atherosclerotic plaque)
  • Myocarditis
  • CHF
  • Hypoxia
  • Medications - eg. Digitalis, Quinidine, Procainamide

Adverse Effects: frequent or very long sinus blocks can cause decreased cardiac output

Treatment: attempt to correct the underlying cause

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27
Q

Sinus Arrest (Sinus Pause)

A

SA node stops firing impulses regularly (aka SA node is not working) and ultimately the heart begins beating after one more missed beats

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28
Q

What’s happening to the SA node in sinus arrest?

A
  • SA node suddenly stops firing for a brief period - result is one or more beat sequences missing, creating a “pause”
  • EITHER
    • 1) sinus node eventually resumes functioning after missing one or two beats OR
    • 2) other pacemaker may continue as the new pacemaker and possibly create a new rhythm
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29
Q

Describe the conduction pathway in sinus arrest

A

SA node does NOT generate an impulse so no impulse heads down the normal conduction pathway

30
Q

Describe the differences between these two rhythms.

A

Sinus Block: R-R intervals are exactly equal distance apart EXCEPT for the 6th complex

Sinus Arrest: R-R intervals are exactly equal distance apart EXCEPT for anything after 5th complex

  • An ectopic beat follows which confirms another pacemaker (purkinje fibers) assumed responsibility for pacing the heart (heart MUST continue to beat!)

note that the underlying rhythm has to be regular to be able to distinguish between the two

31
Q

Sinus Arrest

Rate

Rhythm

P wave

PR interval

QRS complex

A

Rate: Can occur at any rate

Rhythm: Occasionally irregular due to the pause(s) - always measure a pause in seconds

  • P-P interval may vary after the pause depending on whether SA node regains pacemaker control

P wave: Normal sinus P’s before the arrest

PR interval: 0.12-0.20 seconds (before the pause); may be shorter or absent after the pause

QRS complex: <0.12 (can be > 0.12 if BBB exist) before the pause

  • On escape beats, if:
    • Junctional escape beat: <0.12 secs if AV node escapes as pacemaker (with appropriate P wave characteristics)
    • Ventricular escape beat: >0.12 secs if Purkinje fibers escape as pacemaker (with NO P waves)
32
Q

Sinus Arrest

Causes

Adverse Effects

Treatment

A

Causes:

  • Myocardial ischemia or infarction
  • Vagal stimulation
  • Sinus node ischemia
  • hypoxia
  • hyperkalemia
  • Medication (Digitalis toxicity, beta blockers, calcium channel blockers)

Adverse Effects: ​Frequent/very long sinus arrest can cause decreased cardiac output

Treatment: attempt to correct underlying cause

33
Q

All of the following rhythms can lead to decreased cardiac output except:

a) sinus tachycardia
b) sinus block
c) sinus arrest
d) sinus arrhythmia

A

d) sinus arrhythmia

34
Q

Types of atrial dysrhythmias

A
  1. Premature Atrial Complex
  2. Wandering Atrial Pacemaker
  3. Supraventricular Tachycardia
    1. Atrial trachycardia
    2. AV Nodal Re-entrant tachycardia (SVT)
  4. Atrial Flutter with block ratio
  5. Atrial Fibrillation
    1. Slow Atrial Fibrillation
    2. Atrial Fibrillation
    3. Rapid Atrial Fibrillation
    4. Uncontrolled Atrial Fibrillation
35
Q

In atrial dysrhythmias, the rhythm originates in the:

A

atria

36
Q

What happens during atrial dysrhythmias?

A
  • impulse originates in one or more irritable foci (location) in the atria, depolarizes the atria and heads down the conduction pathway towards the ventricles
  • remember: atria is NOT considered “inherent” (like SA node, AV node, Purkinje fibers), yet acts like another pacemaker of the heart
  • a rhythm that begins in the atria will have P waves that are differently shaped from the P waves that begin in SA node
    • because remember that P waves reflect atrial depolarization
37
Q

Ectopic atrial impulse is the result of:

A

1) Altered automaticity

OR

2) Re-entry

38
Q

Enhanced Automaticity - what is it, what causes it

A

Caused by an acceleration in depolarization (ussually results from high Na+ leakage into cell)

One of the following occurs:

  1. cardiac cells that are NOT associated with pacemaker function begin to depolarize spontaneously
  2. A pacemaker site other an SA node increases it firing rate beyond which is considered normal
39
Q

What occurs in altered automaticity, and what cells can this event occur in?

A
  • cells initiate an impulse BEFORE the SA node impulse
  • can occur in both normal pacemaker cells and contractile cells (that do not normally function as pacemaker sites)
40
Q

Re-entry

A
  • Reactivation of myocardial tissue for the 2nd or subsequent time by the same impulse
  • Occurs when an impulse is DELAYED, BLOCKED or BOTH in one or more segments in the conduction system
  • The propagation of the impulse fails to end and continues activating excitable tissue which have just become polarized
41
Q

Premature Atrial Complex (PAC)

A
  • impulse originates from an irritable atrial focus before the next sinus beat is due (i.e PACs occur early before the next expected beat)
  • is NOT the entire rhythm - it is a single beat occuring in an underlying rhythm
    • ex. Sinus tachycardia with a PAC (5th complex)
42
Q

PAC P wave morphology

A
  • if the irritable site is close to the SA node, the atrial P wave will look similar to P wave initiated by SA node BUT WILL BE DIFFERENT
  • morphology may look:
    • 1) biphase, “notched”, pointed, flattened
      OR
    • 2) buried in the preceding T wave (T wave may have an extra “hump” suggestting presence of hidden P wave)
43
Q

The PAC is followed by a pause before the underlying rhythm returns. What are the two different types of pauses that can follow a premature complex?

A

Compensatory (complete) pause

OR

Non-compensatory (incomplete) pause

44
Q

Compensatory (complete) pause

A
  • pause is compensatory if the normal beat following PAC occurs WHEN IT IS expected
  • if you measure from R wave of complex BEFORE the PAC to the R wave of the complex AFTER the PAC, the period between the complex before and after the premature beat is the same as two normal R-R intervals
45
Q

Describe the difference between these two rhythms.

A

NSR: two R-R intervals are exactly equal distance apart

NSR with PAC (3rd complex):

  • Two R-R intervals that are unequal distance apart
  • The distance before and after the PAC IS equal to two normal R-R intervals and therefore considered compensatory (complete)
46
Q

Non-compensatory (incomplete) pause

A
  • pause is non-compensatory if the normal beat following the PAC occurs BEFORE it was expected
  • Measure from R wave of complex before the PAC to the R wave of the complex AFTER PAC (i.e. the period between the complex before and after the premature beat is less than normal R-R interval)
47
Q

Describe the difference between these two rhythms.

A

NSR: Two R-R intervals are exactly equal distance apart

NSR with a PAC (3rd complex): two R-R intervals that are unequal distance apart; the distance before and after the PAC is NOT equal to two normal R-R intervals and therefore considered non-compensatory (incomplete) as it’s actually shorter than two normal R-R intervals

48
Q

PACs may also be non-conducted. True or False.

A

True

49
Q

Non-conducted PACs

A
  • PACs that are very premature which will NOT be conducted to the ventricle because it will arrive during the ventricle’s absolute refractory period
  • P waves may or may not be followed by a QRS depending on how premature the PAC is
  • occur because the AV junction is still refractory to stimulation and is unable to conduct an impulse to the ventricles thus no QRS complex
50
Q

Morphology/signs on rhythm strip where you may suspect non-conducted PAC

A
  • P waves may or may not be followed by a QRS depending on how premature the PAC is (may occur very early and close to the T wave of the preceding beat so only P wave seen)
  • always be suspicious when T waves change shape suddently! if one T wave is different, there’s probably a P wave hiding in it

*NOTE: non-conducted PACs may be confused with sinus block or sinus arrest (especially if P wave of PAC happens early enough to be hidden in the preceding T wave)

  • to differentiate between the, look and compare T wave contours (in sinus block/arrest, no P wave is producted so the T wave remains the same morphology; in non-conducted PAC, an early abnormal P wave of the PAC will distort preceding T wave)
51
Q

Premature Atrial Complex

Rate

Rhythm

P wave

PR interval

QRS complex

A

Rate: Can occur at any rate

Rhythm: occasionally irregular

P wave: Shaped different from sinus P waves; can be upright and pointed or inverted depending on its origin (premature P waves may be hidden in T wave and if so may deform T wave - in these cases, compare the T waves preceiding each PAC with those of the underlying rhythm)

PR interval: 0.12-0.20 secs

QRS complex: <0.12 secs (or will be absent if it’s a non-conducted PAC)

52
Q

Premature Atrial Complex

Causes

Adverse Effects

Treatment

A

Causes:

  • Acute Coronary Syndromes (ACS) - eg. STEMI, non-STEMI, unstable angina
  • CHF
  • Atrial enlargement
  • Valvular heart disease
  • Emotion stress
  • Electrolyte imbalance
  • Hyperthyroidism
  • Medication - Digitalis toxicity
  • Drugs - cocaine, tobacco, caffeine

Adverse Effects: frequent PACs may be an early sign of heart failure or atrial fibrillation

Treatment: reduce stress, reduce stimulants

53
Q

Wandering Atrial Pacemaker

A
  • Transient pacemaker shifting from SA node to another pacemaker site in the atria or AV junction
  • size, shape and direction of P waves vary, sometimes from beat to beat
54
Q

Describe the conduction pathway of wandering atrial pacemaker.

A
  • impulse originates in at least 3 different foci (location) in the atria (the difference in the look of P waves is the result of pacemaker shifting between the SA node, atria and AV junction)
  • heads down the normal conduction pathway and ultimately depolarizes the ventricular muscle
55
Q

Wandering Atrial Pacemaker

Rate

Rhythm

P wave

PR Interval

QRS complex

A

Rate: <100 (usually 50s - 60s)

Rhythm: regular, BUT may be irregular as pacemaker site shifts from SA node to ectopic locations

P wave: _at least 3 different shape_s (hallmark sign); some beats may have no visible P waves

PR Interval: varies (because P wave varies)

QRS complex: < 0.12 secs (can be > 0.12 if BBB exist)

56
Q

Wandering Atrial Pacemaker

Causes

Adverse Effects

Treatment

A

Causes:

  • may occur in healthy individuals (eg. athletes, during sleep)
  • heart disease
  • medication (Digitalis toxicity)

Adverse Effects: usually no ill effects

Treatment: usually none needed; typically resolves on its own

57
Q

Supraventricular Tachycardia (SVT)

A
  • A fast, regular and narrow dysrhythmia originate somewhere above the ventricles (“supra” meaning above)
  • Its exact location of origin can not be identified due to the absence of P waves (P waves may be buried in QRS complex)
  • can also be used to describe an “umbrella” of tachycardias that originate above the ventricles in either SA node, atria, or AV junction
  • 3 main types of SVT:
    • atrial tachycardia (AT)
    • AV nodal re-entrant tachycardia (AVNRT)* what paramedics call SVT
    • AV re-entrant tachycardia (AVRT)
58
Q

SVT: Atrial Tachycardia (AT)

A
  • usually caused by altered automaticity (irritable site in the atria fires at a rate of 100-250 times per minute)
  • often precipitated by a PAC
  • heads down the normal conduction pathway and ultimately depolarizes into ventricular muscle
  • typically present when 3 or more PACs occur in a row of >100 BPM
  • hard to different between sinus tach and atrial tach (you’d have to see a long ECG tracing and the rhythm that precedes atrial tach to call it atrial tach)
59
Q

Atrial Tachycardia

Rate

Rhythm

P wave

PR interval

QRS complex

A

Rate: 100 - 250 beats/min

Rhythm: regular

P wave: upright P wave in Lead II

  • if rhythm originated in lower portion of atrium, P’s will be negative in Lead II)
  • matching and precede each QRS complex (P wave looks different from those seen when the impulse is initiated from the SA node)

PR interval: may be shorter or longer than normal

QRS complex: <0.12 seconds (can be >0.12 seconds if BBB exists)

60
Q

Atrial Tachycardia

Causes

Adverse Effects

Treatment

A

Causes:

  • can occur in person’s with normal heartbeats
  • Myocardial Infarction (MI)
  • Acute illness with catecholamine release
  • Electrolyte imbalance
  • Infection
  • Medications - albuterol, theophylline
  • Drugs - caffeine, cocaine, etc.

Adverse Effects: decreased cardiac output secondary to rapid HR

Treatment: None

61
Q

SVT: AV nodal Re-entrant Tachycardia (AVNRT)

A
  • most common type of SVT
  • impulse originates from an irritable side above the Bundle of His
  • exact location of origin CANNOT be identified because P waves are not discernable
  • P waves may be hidden in T wave of preceding complex
  • heads down normal conduction pathway and ultimately depolarizes in ventricular muscle
  • usually caused by a PAC
  • impulse is stuck in a re-entry loop as it enters the AV node
  • impulse re-enters the normal electrical pathway with each pass of the circuit
62
Q

SVT: AV nodal Re-entrant Tachycardia (AVNRT)

Rate

Rhythm

P wave

PR interval

QRS complex

A

Rate: >100 (generally >150)

Rhythm: regular

P wave: no P waves (P waves are non-discernable)

PR interval: n/a (because no P waves)

QRS complex: <0.12 secs (narrow)

63
Q

SVT: AV nodal re-entrant tachycardia (AVNRT)

Causes

Adverse Effects

Treatment

A

Causes: typically occurs:

  • later in life for unknown reason not determined (30s-40s)
  • in individual with no structural heart disease AND triggered due to hypoxia, stress, anxiety, caffeine, smoking, sleep deprivation and medications
  • women more than men
  • in persons with COPD, CAD, valvular heart disease, CHF, and Digitalis toxicity

Adverse Effects: decreased cardiac output secondary to rapid HR

Treatment: None

64
Q

Paroxsymal Supraventricular Tachycardia (PSVT)

A
  • SVT that starts and ends suddenly
  • “paroxsymal” can describe a rhythm that starts and stops suddenly
  • you have to witness the SVT starting to be able to call it PSVT (otherwise it’s just SVT)
65
Q

Atrial flutter (A flutter) with block ratio

A
  • A rapid re-entry circuit caused by an irritable focus within the atria
  • so rapid that “flutter” wave are produced instead of P waves
  • usually saw shaped and no P waves
  • typically would not see isoelectric line because the flutter waves affect the whole baseline so much
66
Q

Describe the conduction pathway of atrial flutter.

A
  • impulse originates in a irritable atrial focus AND rapidly circles a round a larger area of tissue continuously (eg. entire RA and arrives back at the same point)
  • AV node is bombarded with impulses and allows some to go through and blocks others (protects the ventricles from extremely fast impulses)
  • heads down the normal conduction pathway and ultimately depolarizes into ventricular muscle
  • the irritable focus typicall depolarizes at a rate of 300/min BUT AV node can’t conduct faster than 180 impulses/min due to its intrinsic conduction rate (otherwise if impulse was transmitted to ventricles, ventricular rate would be 300/min)
67
Q

Atrial Flutter

Rate

Rhythm

P wave

PR Interval

QRS Complex

A

Rate: Atrial rate - 250 - 350; ventricular rate - 60 -100

  • ventricular rate depends on number of impulses the AV node conducts (eg. if AV node conducts 1 impulse every 2 atrial contractions, conduction block/ratio would be 2:1 block/ratio) - i.e. two flutter waves for every 1 QRS
  • Three flutter waves for every one QRS: 3:1 block/ratio
  • Four flutter waves for every one QRS: 4:1 block/ratio
  • Five flutter waves for every one QRS: 5:1 block/ratio
  • If block/ratio is inconsistent, it is referred to as “variable block/ratio”

Rhythm: regular if conduction ratio is constant; irregular if conduction ratio varies

P wave: NO P waves; flutter waves present (hallmark signs) - “saw tooth”, “picket fence”, V-shaped, upside down V-shaped

  • 2 or more flutter waves to each QRS
  • some flutter waves may be hidden inside QRS and T waves even though you can’t see flutter waves, they still count (count those inside the these components)

PR Interval: n/a (since no real P waves)

QRS Complex: < 0.12 seconds (can be >0.12 if BBB exist)

68
Q

Atrial Flutter

Causes

Adverse Effects

Treatment

A

Causes: commonly associated with

  • CHF
  • cardiomyopathy
  • cardiac hypertrophy
  • myocarditis
  • pericarditis
  • hypoxia

Adverse Effects: can be well tolerated at normal ventricular rates; at higher rates, may see signs of decreased cardiac output

Treatment: None

69
Q

Atrial Fibrillation (A Fib)

A
  • Increased irritability causes many sites/foci in the atria to initiate an electrical impulse at the same time (seen as a wavy line)
  • caused by enhanced automaticity or re-entry
70
Q

Describe conduction pathway of atrial fibrillation.

A
  • atria depolarizes in section instead of a unit causing a “wiggle” or quiver (fibrillate) instead of a contraction - like a bag of worms
  • AV node is bombarded with impulses (some are allowed through, but blocks others)
  • at irregular intervals, one electrical impulse is conducted
  • heads down the normal conduction pathway and ultimately depolarizes into ventricular muscle
71
Q

Atrial Fibrillation

Rate

Rhythm

P wave

PR Interval

QRS complex

A

Rate: atrial rate of 250-750

  • Slow atrial fibrillation: ventricular rate of <60
  • Atrial fibrillation: ventricular rate 60 -100
  • Rapid atrial fibrillation: ventricular rate of >100
  • Uncontrolled atrial fibrillation: ventricular rate of >150

Rhythm: irregularly irregular, completely unpredictable

  • atrial depolarization occurs very irregularly which results in irregular ventricular depolarization

P wave: Fibrillatory waves are present, NO P waves (if there are P waves, the rhythm is NOT atrial fibrillation)

PR Interval: n/a (not measured since no real P waves)

QRS complex: <0.12 secs (can be >0.12 if BBB exist)

72
Q

Atrial Fibrillation

Causes

Adverse Effects

Treatment

A

Causes:

  • Idiopathic (no clear cause)
  • Advanced age
  • HTN
  • heart disease and MI
  • Pericarditis
  • Lung Disease
  • Pulmonary Embolism
  • CHF
  • WPW
  • Hyper/hypothyroidism, hypokalemia, hypoxia, hypoglycemia
  • Infection
  • Sympathomimetics
  • Electrocution
  • Stress, etc.

Adverse Effects:

  • Blood clots collecting in a sluggish atria causing MI and strokes (so that’s why they are on blood thinners - the blood clots can circulate to the brain)
  • Decreased cardiac output secondary to rapid HR

Treatment: None