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Coronary Care > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

SINUS ARRHYTHMIA

A
  • may also be called ‘sinus dysrhythmia’
  • impulses originate in the SA node, but not with a regular rhythm
  • the alternating periods of slow and fast rates are due to a variance of the vagal
    influence over the SA node
  • often related to respiratory phases (faster HR with inspiration and slower HR
    with expiration)
  • patients are usually asymptomatic because the CO is satisfactory
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2
Q

SINUS ARRHYTHMIA - Interventions

A
  • if drug-induced (ie: digoxin), the medication may be discontinued
  • otherwise, no interventions are required
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3
Q

SINUS ARRHYTHMIA - Distinguishable Features

A
  • rhythm is irregular
  • all other findings are normal
  • normal atrial rate (AR = 60-100)
  • normal ventricular rate (VR = 60-100)
  • normal Ps (one before each QRS, all look the same, no extra Ps)
  • normal PR interval (0.12-0.20 seconds)
  • normal QRS complexes (narrow)
  • normal QT interval (< 0.44 seconds)
  • normal ST segments and T waves
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4
Q

SINUS BRADYCARDIA

A
  • the SA node is the original pacemaker but discharges at a rate slower than 60
    times per minute (usually 40-60)
  • a slow rate is usually secondary to PSNS (vagal) dominance over the SA node
  • the vagus nerve is excessively stimulated, slowing the SA node, and therefore
    decreasing the HR
  • threats of this rhythm include the potential for SA arrest, and allowing a faster
    ectopic focus to initiate impulses (ie: the AV junction or ventricles)
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5
Q

SINUS BRADYCARDIA - Common Causes

A
  • MI, medications (ie. beta-blockers, digoxin, morphine),
  • IICP (ie. brain tumors)
  • well toned athletes whose vagus nerve innervates the heart to pump slower
  • carotid sinus massage
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6
Q

SINUS BRADYCARDIA - Interventions

A
  • do not treat if patient is asymptomatic
  • treat only if symptomatic and showing signs of CO compromise (ie. syncope,
    hypotension, anginal pain, heart failure)
  • atropine blocks the effect of the vagus nerve on the SA node
  • cardiac pacing, if drug therapy is not effective
  • hold administration of medications causing bradycardia/slowing effects
  • monitor for worsening arrhythmias
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7
Q

SINUS BRADYCARDIA - Distinguishable Features

A
  • HR < 60 (AR and VR are the same)

- all other findings are normal

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8
Q

SINUS TACHYCARDIA

A
  • the SA node paces at a rate > 100 times per minute (usually 100-150)
  • this rhythm is reflective of overactivity of the sympathetic nervous system (SNS)
  • patients are usually asymptomatic
  • if CO decreases, symptoms can be experienced (ie. syncope, palpitations,
    dyspnea, anginal pain, hypotension)
  • tachycardia can increase the heart’s workload and O2 consumption
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9
Q

SINUS TACHYCARDIA - Common Causes

A
  • often secondary to fever, exercise, pain, fear, anxiety (SNS stimulation)
  • stimulants (ie. nicotine, caffeine, alcohol)
  • MI, heart failure, pericarditis, pulmonary embolism
  • medications (ie. atropine, bronchodilators)
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10
Q

SINUS TACHYCARDIA - Interventions

A
  • identify the underlying cause
  • remove the stimulus (ie. treat fever, stop activity, sedate for pain)
  • if unable to readily identify the rhythm’s source, be suspicious of heart failure
    (signs can include cough, congestion, orthopnea, restlessness)
  • digoxin or beta-blockers may be used if necessary
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11
Q

SINUS TACHYCARDIA - Distinguishable Features

A
  • HR > 100 (AR and VR are the same)

- all other findings are normal

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12
Q

SA BLOCK & SA ARREST (SINUS PAUSE)

A
  • SA arrest
  • the SA node fails to initiate an impulse at the expected time
  • because the impulse is absent, neither the atria nor the ventricles are
    stimulated, so an entire PQRST is missing
  • SA block
  • the impulse from the SA node originates normally, but is blocked/delayed
  • therefore, it never depolarizes the atria or the ventricles
  • again an entire PQRST is missing
  • treatment is the same for SA block and SA arrest
  • so rather than differentiate between blocks and arrests, most clinicians simply
    refer to the episode as a “Sinus Pause”
  • most patients are unaware of the missed beat
  • if missed beats occur frequently or consecutively, it is potentially dangerous as
    the HR drops
  • decreased CO is manifested as hypotension, cerebral insufficiency
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13
Q

SA BLOCK & SA ARREST (SINUS PAUSE) - Common Causes

A
  • excessive vagal stimulation, carotid sinus massage
  • MI, cell ischemia in the SA node
  • medications (ie. beta-blockers, digoxin, and ASA toxicity)
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14
Q

SA BLOCK & SA ARREST (SINUS PAUSE) - Interventions

A
  • when SA arrest or SA block is infrequent, and the patient is asymptomatic, no
    treatment is needed
  • with CO compromise: treatment includes atropine, and cardiac pacing (if drug
    therapy is not effective)
  • discontinue medications that might be causing the rhythm
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15
Q

SA BLOCK & SA ARREST (SINUS PAUSE) - Distinguishable Features

A
  • entire PQRST missing amid the baseline rhythm

- all other findings are normal

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16
Q

ARRHYTHMIAS ORIGINATING IN THE ATRIA

A
  • an ectopic site in the atria replaces the SA node as pacemaker
  • this can occur for only one beat (PAC), or a continuous rhythm
  • these arrhythmias result mostly from irritability of the atrial muscle
  • can be secondary to ischemic damage or over-stretching of the atrial wall
  • remember ‘atrial kick’ from Lesson 1?…any decrease in atrial kick can result in
    decreased ventricular filling
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17
Q

PREMATURE ATRIAL CONTRACTION (PAC)

A
  • an ectopic focus in the atrium supercedes the SA node for one or more beats
  • PACs are not usually dangerous, but can be a forewarning of more serious
    atrial arrhythmias
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18
Q

PREMATURE ATRIAL CONTRACTION (PAC) - Common Causes

A
  • stimulants (ie. caffeine, alcohol, nicotine)
  • fever, fatigue, anxiety, hypoxia
  • digoxin toxicity
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19
Q

PREMATURE ATRIAL CONTRACTION (PAC) - Interventions

A
  • not necessary in most cases. Do not treat if asymptomatic
  • lifestyle counseling, sedation
  • if increasing in frequency and become cause for concern, the use of atrial
    anti-arrhythmics might be required (ie. digoxin, quinidine)
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20
Q

PREMATURE ATRIAL CONTRACTION (PAC) - Distinguishable Features

A
  • the beat with the PAC is earlier than expected (premature)
  • the PAC has a P wave that is abnormally shaped and differs from all the other P
    waves that originate from the SA node (different site of origin = different looking
    P wave)
  • the premature P might be difficult to see
  • it can be “lost” in the T wave of the beat preceding the PAC
  • the prematurity of the beat shortens the patient’s normal RR interval, causing
    an irregularity in the rhythm
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21
Q

ATRIAL FLUTTER

A
  • an irritable focus within the atria replaces the SA node as pacemaker
  • this focus stimulates the atria to contract 250-400 times per minute
  • the AV node is not capable of conducting all these impulses
  • it allows every 2nd, 3rd, 4th etc. impulse to reach the ventricles
  • symptoms are basically proportionate to the VR (ie. VR < or > 100)
  • if the ventricular rate is satisfactory, patient may be asymptomatic
  • CO can decrease with a faster VR because of the decreased stroke volume
    secondary to the short ventricular filling time
    -palpitations, dyspnea, angina can be noted with faster ventricular rates
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22
Q

ATRIAL FLUTTER - Common Causes

A
  • usually occurs as a result of ischemia or underlying heart disease
  • MI
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23
Q

ATRIAL FLUTTER - Interventions

A
  • digoxin may be administered to control the ventricular rate
  • calcium channel blockers
  • synchronized cardioversion: start with low voltage (50 joules)
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24
Q

ATRIAL FLUTTER - Distinguishable Features

A
  • VR may be fast or slow (varies on the degree of block)
  • P waves no longer exist (atria are not contracting, they are fluttering)
  • the Ps are replaced by flutter waves that appear saw-toothed or resemble
    picket fences
  • there are no P waves, therefore PR intervals cannot be calculated
  • the QRSs are normal as conduction beyond the AV node is not affected
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25
Q

ATRIAL FIBRILLATION -

A
  • ectopic foci throughout the atria emit chaotic, abnormal, uncontrolled, rapid
    impulses at a rate > 400 times per minute (can be as high as 1000)
  • atrial muscle is unable to respond to this irregular stimulation, so atrial
    contraction is disorganized
  • it results in quivering and twitching of the atria, rather than a true contraction
  • very few of these impulses reach the ventricles
  • impulses that are conducted through the AV node to the ventricles, always do
    so with an irregular rhythm
  • therefore, the ventricular rhythm is always irregular
  • controlled A Fib: VR < 100
  • uncontrolled A Fib (or A Fib with a fast ventricular response): VR > 100
  • most patients are aware of palpitations (especially if the VR is rapid)
  • loss of effective atrial contraction leads to loss of effective atrial kick
  • can lead to a possible drop in CO (↓atrial kick = ↓blood entering the ventricles)
  • there is also potential for clot formation as blood ‘swishes around’ and is not
    effectively propelled by the non-contracting atria
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26
Q

ATRIAL FIBRILLATION - Common Causes

A
  • MI, cardiac disorders, hypoxia, cardiac surgery

- excessive stimulants (ie. caffeine, alcohol, nicotine)

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27
Q

ATRIAL FIBRILLATION - Interventions

A
  • if A Fib is chronic, the goal is to control the ventricular rate
  • if new onset, the goal is to convert the arrhythmia to a sinus rhythm
  • drug therapy can include digoxin, calcium channel blockers, beta-blockers
  • if hemodynamically unstable: synchronized cardioversion (100 joules)
  • anti-coagulation
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28
Q

ATRIAL FIBRILLATION - Distinguishable Features

A
  • the HR varies (depending on whether it is controlled or uncontrolled)
  • the ventricular rhythm is always irregular
  • the P waves are absent (the atria are quivering, not contracting)
  • because of chaotic atrial activity, only a fibrillatory line is seen where Ps would
    normally exist
  • no P waves, therefore no PR intervals can be measured
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29
Q

PAROXYSMAL ATRIAL TACHYCARDIA (PAT)

A
  • an irritable focus within the atria originates impulses 150-250 times per min
  • impulses are fired regularly and all impulses conduct to the ventricles
  • ventricles are able to respond to each of these impulses
  • therefore, the atrial and ventricular rates are the same
  • paroxysmal means: occurs suddenly without warning, and often ends as
    suddenly as it began
  • the patient is aware of the rapid HR, and may have signs of decreased CO
  • reduction in CO results from the fast HR, which caused a shortened ventricular
    filling time. So, blood volume ejected with each beat decreases
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30
Q

PAROXYSMAL ATRIAL TACHYCARDIA (PAT) - Common Causes

A
  • stress and excessive stimulants (ie. caffeine, alcohol, nicotine)
  • MI, hypoxia, electrolyte imbalances
  • medications (ie. digoxin toxicity, bronchodilators, decongestants)
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31
Q

PAROXYSMAL ATRIAL TACHYCARDIA (PAT) - Interventions

A
  • vagal maneuvers such as - carotid sinus massage (performed by a physician)
  • valsalva maneuvers
  • facial immersion in ice water
  • verapamil (isoptin)
  • adenosine (can lead to short periods of sinister rhythms such as asystole)
  • digoxin (if the rhythm is not secondary to digoxin toxicity)
  • synchronized cardioversion (50 joules) if drug therapy is not effective
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32
Q

PAROXYSMAL ATRIAL TACHYCARDIA (PAT) - Distinguishable Features

A
  • HR is 150-250
  • the rhythm is always regular (impulses are initiated with a regular rhythm)
  • the P waves may not be visible if the HR is too fast
  • if Ps are not visible, the PR intervals cannot be measured
  • QRS complexes are usually normal (narrow) as conduction below the AV node
    and within the ventricles is not usually affected
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33
Q

ARRHYTHMIAS ORIGINATING IN THE AV JUNCTION

A
  • these are sometimes called “nodal” rhythms because at one time, it was
    thought that these impulses originated in the AV node)
  • junctional arrhythmias indicate that the SA node’s pacemaking has been
    replaced by the AV junctional tissue
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34
Q
  • all junctional arrhythmias occur for one of 2 main reasons:
A

a) the SA node fails to discharge impulses, so the junctional tissue uses
its automaticity as a safety system
b) junctional tissue initiates impulses at a faster rate than the SA node

  • all junctional impulses conduct to the atria and the ventricles
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35
Q
  • all junctional beats and rhythms have P waves manifested in one of three ways:
A

1) Inverted P because the junctional impulse can transmit upward to the atria
first, leading to atrial contraction prior to ventricular contraction (seen as an
inverted P prior to the QRS complex, due to retrograde/backward conduction)
The PR interval is usually shortened (< 0.12 seconds)
2) P wave follows the QRS because the impulse conducts to the ventricles first
3) Hidden P because the impulse conducts to the atria and ventricles
simultaneously (the smaller P would then be buried in the larger QRS)

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36
Q

PREMATURE JUNCTIONAL CONTRACTION (PJC)

A
  • an ectopic focus in the AV junction discharges an impulse before the onset of
    the next expected impulse from the SA node
  • patients are rarely aware of the ectopic beat
37
Q

PREMATURE JUNCTIONAL CONTRACTION (PJC) - Common Causes

A
  • MI. Ischemia or injury in the junctional area. Digoxin toxicity
38
Q

PREMATURE JUNCTIONAL CONTRACTION (PJC) - Interventions

A
  • do not treat if asymptomatic. Hold next dose of digoxin, assess serum dig level
39
Q

PREMATURE JUNCTIONAL CONTRACTION (PJC) -

A
  • P is either inverted (with shortened PR), buried, or follows the QRS
40
Q

JUNCTIONAL ESCAPE RHYTHM

A
  • may also be called “passive junctional rhythm”
  • a focus in the AV junctional tissue replaces the SA node as pacemaker
  • the SA node is either too slow at generating impulses or it completely fails
  • the AV junction serves as pacemaker by using its property of automaticity
  • the AV junction initiates impulses at a rate of 40-60 times per minute
  • the impulses are spread both upward to the atria and down to the ventricles
  • the rhythm seldom produces symptoms, unless the HR is very slow
  • if symptoms develop, it is due to the low CO, secondary to the slow HR
    (remember: HR x SV = CO)
  • this arrhythmia can be dangerous for 2 reasons:
    1. an ectopic focus with a faster rate can take over as pacemaker leading
    to junctional tachycardia or ventricular tachycardia
    2. a slow ventricular rhythm can develop, if the pacemaker ‘displaces’
    downward to the ventricles
41
Q

JUNCTIONAL ESCAPE RHYTHM - Common Causes

A
  • excessive vagal activity (excessive slowing by the vagus nerve)
  • MI, ischemia of the SA node
  • digoxin toxicity
42
Q

JUNCTIONAL ESCAPE RHYTHM - Interventions

A
  • there is no specific drug therapy to revert the actual rhythm
  • atropine can be used if the HR is too slow and producing symptoms
  • pacemaker (if patient is compromised and drug therapy is not effective)
  • hold next dose of digoxin and obtain serum digoxin level
  • observe for downward displacement to the ventricles (PVCs can develop if the
    rate becomes too slow)
43
Q

JUNCTIONAL ESCAPE RHYTHM - Distinguishable Features

A
  • HR is 40-60 (the junction initiates 40-60 impulses / minute
  • the rhythm is regular (the junctional pacemaker fires at a regular rate)
  • P waves are either inverted, after the QRS or absent/buried in the QRS
  • PR intervals <0.12 seconds (if P waves occur prior to the QRSs)
44
Q

ACCELERATED JUNCTIONAL RHYTHM

A
  • an irritable ectopic focus in the junctional tissue replaces the SA node as
    pacemaker and initiates impulses a little faster (60-100 impulses / minute)
45
Q

ACCELERATED JUNCTIONAL RHYTHM - Common Causes

A
  • MI, enhanced automaticity of the AV node
  • digoxin toxicity, hypokalemia
  • advanced CHF
  • cardiogenic shock (the rhythm represents a stage of downward displacement of
    the SA node’s pacemaker in a severely damaged heart)
  • if the rhythm is due to digoxin toxicity, and there are no signs of circulatory
    failure, there are usually no symptoms
  • in the absence of digoxin toxicity, the arrhythmia might…
  • indicate extensive myocardial damage
  • lead to downward pacemaker displacing (to the ventricles)
  • decrease CO, mostly due to the decrease in atrial kick
  • be associated with high mortality rates following an MI,
    because of the underlying myocardial damage
46
Q

ACCELERATED JUNCTIONAL RHYTHM - Interventions

A
  • treatment of the underlying cause
  • verapamil or adenosine might be administered, but are not often effective
  • cardiac pacing can be attempted if the threat of downward pacemaker
    displacement exists
  • if the rhythm is due to digoxin toxicity, discontinue digoxin, treat dig toxicity and
    monitor serum digoxin
47
Q

ACCELERATED JUNCTIONAL RHYTHM -Distinguishable Features

A
  • HR is 60-100
  • the rhythm is regular (the junction fires impulses with a regular pattern)
  • P waves are either inverted, buried or follow the QRS complex
  • the PR interval is < 0.12 seconds (if a P wave precedes the QRS)
  • QRS is narrow, due to normal conduction beyond the AV junction
48
Q

JUNCTIONAL TACHYCARDIA

A
  • called “paroxysmal junctional tachycardia (PJT) when the rhythm develops
    suddenly
  • an irritable focus in the junctional tissue repeatedly discharges impulses more
    rapidly than the SA node
  • the AV junction assumes the role of pacemaker, firing at a rate of 100-200
  • all impulses are conducted to the ventricles, therefore the VR is100-200
  • symptoms are the same as with any rhythm with a fast rate and a decrease in
    CO (ie. dyspnea, ischemic chest pain, cerebral insufficiency)
  • the rhythm can predispose to LVF, myocardial or cerebral ischemia
  • the threat of the rhythm is directly related to the duration of the tachycardia
  • can be a sinister and lethal rhythm, can deteriorate into Ventricular Tachycardia
49
Q

JUNCTIONAL TACHYCARDIA - Common Causes

A
  • MI, digoxin toxicity, hypokalemia, ischemia in the junctional tissue
50
Q

JUNCTIONAL TACHYCARDIA - Interventions

A
  • discontinue digoxin, and monitor serum digoxin level
  • treatment of the underlying cause
  • drug therapy might include verapamil, adenosine, lidocaine
  • synchronized cardioversion, if the patient is compromised due to low CO
51
Q

JUNCTIONAL TACHYCARDIA - Distinguishable Features

A
  • HR is 100-200
  • the rhythm is regular (junctional rhythms are regular)
  • P waves are either inverted, buried or follow the QRS complex
  • the PR interval is < 0.12 seconds (if a P wave precedes the QRS)
  • QRS is narrow, due to normal conduction beyond the AV junction
52
Q

SUPRAVENTRICULAR TACHYCARDIA (SVT)

A
  • if junctional tachycardia cannot be differentiated from PAT or atrial flutter
    because the HR is so rapid that it becomes difficult to determine if P waves are
    present, the term SVT can be used
  • the term SVT can be used for any rhythm originating above (supra) the level of
    the ventricles (ventricular), at a rapid rate (tachycardia)
53
Q

ARRHYTHMIAS ORIGINATING IN THE VENTRICLES

A
  • so far, all the arrhythmias we have examined originated from areas above the level of
    the ventricles
  • as such, they can all be referred to as supraventricular rhythms
  • when the heart’s pacemaker originates from within the ventricular conduction system,
    the impulses only depolarize the ventricles
  • atrial depolarization and contraction does not occur, leading to loss of atrial kick
54
Q

Distinguishable Features of all Ventricular Beats and Rhythms

A
  • absent P wave (there is no atrial depolarization)
  • absent PR interval (PR intervals cannot be measured without P waves)
  • the QRS complex is always widened, distorted and bizarre in appearance
  • the T wave deflects in the opposite direction of the QRS
  • complete compensatory pause: the time interval from the normal beat preceding the PVC
    to the beat following the PVC, is equal to the time interval of two normal beats
55
Q

PREMATURE VENTRICULAR CONTRACTION (PVC)

A
  • an irritable focus within the ventricles discharges before the arrival of the next
    anticipated impulse from the SA node
  • patients are often aware of the PVC and describe their “heart skipping a beat”
  • the following PVCs represent more irritability and become more cause for concern
    because they may warn of an impending serious sustained ventricular rhythm:
  • when they begin to occur frequently
  • when they occur in pairs/couplets (2 in a row) or triplets (3 in a row)
  • when every 2nd or 3rd beat is a PVC (ventricular bigeminy or trigeminy)
  • when they are multifocal (originating from different ectopic foci,
    thereby producing different looking PVCs)
  • when there is R on T phenomena (PVC strikes on preceding T wave)
56
Q

PREMATURE VENTRICULAR CONTRACTION (PVC) -Common Causes

A
  • electrolyte imbalances (ie. hypokalemia), MI, ischemia, hypoxia
  • drug intoxication (ie. cocaine), excessive stimulants (ie. stress, caffeine, nicotine)
57
Q

PREMATURE VENTRICULAR CONTRACTION (PVC) - Interventions

A
  • if not symptomatic, may not require treatment
  • lidocaine suppresses the ventricular ectopic foci
  • procainamide (pronestyl) or amiodarone can be attempted
  • if PVCs are secondary to hypokalemia, initiating an IV with K+ is effective
58
Q

PREMATURE VENTRICULAR CONTRACTION (PVC) - Distinguishable Features

A
  • all beats are normal, except for the PVC (the PVC features are as noted above)
59
Q

VENTRICULAR TACHYCARDIA (VT)

A
  • defined by 4 or more consecutive PVCs occurring at a rapid rate, >100
  • an ectopic focus in the ventricles uses its property of automaticity and becomes the
    pacemaker
  • the focus discharges all beats from within the ventricles at >100 times per minute
  • VT can occur in short unsustained runs, leaving the patient without symptoms
  • VT can develop spontaneously without warning, and can be a forerunner to V Fib
  • most patients are immediately aware of the rapid HR and signs of CO drop
  • hypotension and heart failure develop quickly due to the poor CO (low CO is due lack
    of atrial kick and a shortened ventricular filling time)
  • seizures and unconsciousness will quickly follow if the rhythm is not corrected
  • if VT is sustained and becomes an established rhythm, the patient very quickly shows
    signs of decreased CO, heart failure, cardiogenic shock, cerebral insufficiency
  • VT can quickly and easily change to V Fib, leading to death
60
Q

VENTRICULAR TACHYCARDIA (VT) - Common Causes

A
  • MI, and all causes similar to PVCs (but more severe)

- severe drug intoxication (ie. cocaine, digoxin)

61
Q

VENTRICULAR TACHYCARDIA (VT) - Interventions

A
  • this arrhythmia is an emergency and can require preparation for a cardiac arrest
  • if the patient has a pulse:
  • quickly assess level of consciousness & clinical state (ie. symptoms)
  • lidocaine
  • procainamide (pronestyl) or amiodarone may sometimes be tried
  • synchronized cardioversion (start with 100 joules)
  • if hypokalemic, MD might order IV potassium
  • if the patient is pulseless:
  • CPR
  • defibrillation (200, 300, then 360 joules if needed)
62
Q

VENTRICULAR TACHYCARDIA (VT) - Distinguishable Features

A
  • the VR is >100 (usually 150-250)
  • the rhythm is usually regular, but some irregularity can be noted
  • no P waves are present, and no PRs are measurable
  • the QRS complexes are wide and bizarre, typical of repetitive PVCs
63
Q

VENTRICULAR FIBRILLATION (VF)

A
  • VF is the most common cause of sudden death in patients with CAD
  • it is usually triggered by PVCs or VT, but can occur spontaneously
  • there are many chaotic, irritable foci discharging impulses in the ventricles, simultaneously
  • the muscle fibers twitch and quiver, but do not contract
  • the ventricles are repeatedly stimulated at a rate so extremely fast, that the ventricular
    recovery period disappears
  • there is no proper propelling of blood from the ventricles, leading to a major drop in CO
    and inadequate tissue oxygenation
  • therefore, the patient convulses and loses consciousness almost instantly
  • VS, heart sounds, BP, peripheral pulses are all absent
  • pupils dilate rapidly due to immediate cerebral anoxia
  • cyanosis develops quickly
  • death is inevitable and occurs within a few minutes if the rhythm is not terminated
64
Q

VENTRICULAR FIBRILLATION (VF) - Common Causes

A
  • trauma, hypoxia, severe hypothermia
  • acute MI with extensive myocardial damage
  • severe electrolyte imbalances
  • electrical shock
65
Q

VENTRICULAR FIBRILLATION (VF) - Interventions

A
  • this is a cardiac arrest situation…CPR
  • defibrillation is the first treatment (200, 300, then 360 joules if needed)
  • the sooner the shock is delivered, the greater the chance for recovery
  • continuous prophylactic ventricular anti-arrhythmic drips are maintained afterward to
    prevent the recurrence of VF (ie. lidocaine, amiodarone, procainamide)
66
Q

VENTRICULAR FIBRILLATION (VF) - Distinguishable Features

A
  • rapid repetitive series of chaotic waves
  • fibrillatory line with no regular uniformity or pattern
  • cannot differentiate any PQRSTs, as there are no atrial or ventricular contractions
67
Q

IDIOVENTRICULAR RHYTHM (IVR)

A
  • the ventricles exercise their property of automaticity, becoming the heart’s pacemaker
  • ventricular automaticity causes 20-40 impulses to be discharged per minute
  • this rhythm occurs when the higher pacing centers fail or when conduction through to the
    ventricles is blocked
  • it is a protective safety mechanism to ensure that the ventricles contract and is referred to
    as an ‘escape rhythm’
  • unless the HR is very slow, patients may not be symptomatic
  • the ventricles are propelling enough blood to adequately perfuse the system
  • accelerated IVR (AIVR) occurs when the HR is 40-100
68
Q

IDIOVENTRICULAR RHYTHM (IVR) - Common Causes

A
  • MI, myocardial ischemia
  • conduction disturbances when the AV node does not conduct impulses to the ventricles
    (the ventricles do not receive impulses, so they ‘create’ their own)
  • reperfusion following thrombolytic therapy
  • metabolic imbalances
69
Q

IDIOVENTRICULAR RHYTHM (IVR) - Interventions

A
  • if the HR is adequate and the patient is asymptomatic: observe closely
  • if symptomatic:
  • atropine
  • cardiac pacing

NEVER ADMINISTER LIDOCAINE or any other anti-arrhythmic drug because these drugs suppress ventricular foci and abolish automaticity, leading to no impulse formation at all

70
Q

IDIOVENTRICULAR RHYTHM (IVR) - Distinguishable Features

A
  • the VR is 20-40 (or 40-100 with AIVR)
  • the rhythm is regular
  • P waves are not usually seen and no measurable PR intervals
  • the QRS complexes are wide, distorted, bizarre
  • the T waves are in opposite deflection to the QRS complexes
71
Q

So far, the arrhythmias we have explored were caused by a disturbance in impulse formation, such as…..

A
  • an abnormal site of impulse origin
    ie. ) impulses originate somewhere other than the SA node
  • an abnormal mechanism of impulse formation
    ie. ) too fast, too slow or irregular impulse formation
72
Q

ARRHYTHMIAS DUE TO CONDUCTION DISTURBANCES (AV HEART BLOCKS)

A
  • these result when there is interference or abnormal delay in the conduction of impulses
    from the SA node through to the ventricles
  • the SA node initiates impulses normally, but they are blocked/delayed at the AV node
  • their classification is based on the extent/severity of conduction delay or block
73
Q

FIRST DEGREE HEART BLOCK

A
  • impulses originate normally in the SA node and conduct normally to the AV node
  • they are abnormally delayed by the AV node before reaching the ventricles
  • this arrhythmia is not serious, but can be a warn of impending higher degree of block
  • usually, there are no symptoms with first degree AV block
74
Q

FIRST DEGREE HEART BLOCK - Common Causes

A
  • ischemia or injury of the AV node or junctional area
  • MI
  • increased parasympathetic activity (increased vagal/slowing activity)
  • medications (ie. digoxin toxicity, beta-blockers)
75
Q

FIRST DEGREE HEART BLOCK - Interventions

A
  • treatment is seldom required because the patient is usually asymptomatic
  • observe for any development of higher degree of block
  • withhold medications with a slowing effect (ie. digoxin, beta-blockers)
  • if the HR is slow and causing decreased CO, atropine might be administered
76
Q

FIRST DEGREE HEART BLOCK - Distinguishable Features

A
  • the rhythm is regular
  • P waves are normal and there is a P wave preceding each QRS complex
  • PR intervals are constant (always the same length), but prolonged (> 0.20 sec)
    because impulses are delayed by the AV node
  • QRS complexes are narrow (there is no disturbance beyond the AV junction)
77
Q

SECOND DEGREE BLOCK, TYPE I (WENCKEBACH)

A
  • impulses originate normally in the SA node, activate the atria and produce P waves, and
    reach the AV area normally
  • conduction through the AV node becomes progressively longer and more difficult with
    each impulse, until one impulse takes so long that it doesn’t to get through the AV node,
    and hence, it doesn’t reach the ventricles
  • then, the sequence starts over again
  • symptoms depend on the ventricular rate
  • patients are not usually aware of this arrhythmia, unless the rate is very slow
  • the rhythm can be potentially dangerous, as it can lead to a higher degree of block
78
Q

SECOND DEGREE BLOCK, TYPE I (WENCKEBACH) - Common Causes

A
  • MI
  • ischemia or injury in the junctional area
  • medications (ie. digoxin toxicity, beta-blockers)
  • increased parasympathetic activity (increased slowing activity)
79
Q

SECOND DEGREE BLOCK, TYPE I (WENCKEBACH) - Interventions

A
  • this arrhythmia is usually transient, requiring no treatment
  • withhold slow-rate-causing medications (ie. digoxin, beta-blockers)
  • atropine might be used, if the HR is too slow, causing symptoms due to low CO
  • cardiac pacing is sometimes (but rarely) necessary
80
Q

SECOND DEGREE BLOCK, TYPE I (WENCKEBACH) - Distinguishable Features

A
  • the AR is that of the SA node
  • the VR is slower than the AR (because some Ps don’t reach the ventricles)
  • the rhythm is always irregular
  • the P waves are normal in configuration, but there are more P waves than QRS complexes
    because some impulses are blocked at the AV node and do not reach the ventricles, so
    the ventricles do not contract
  • the PR interval is variable
  • the PR interval progressively lengthens until an impulse is completely blocked at the AV
    node and does not reach the ventricles, which produces a missing QRS complex
  • then, a new PR interval sequence of lengthening begins again
  • QRS complexes are narrow if conduction within the ventricles is normal
81
Q

SECOND DEGREE HEART BLOCK, TYPE II (MOBITZ II)

A
  • impulses originate normally in the SA node, activate the atria to produce P waves, and
    reach the AV node normally
  • the AV node then blocks the impulses at regular intervals
  • so, only certain impulses reach the ventricles (ie. every 2nd, 3rd, 4th, etc)
  • this rhythm is often referred to as having 2:1 block, 3:1 block, 4:1 block, etc
  • this means there are 2 Ps for each QRS, 3 Ps for each QRS, 4 Ps for each QRS, etc
  • symptoms are related to the ventricular rate
  • higher degrees of block (ie. 4:1 block) cause a slower ventricular rate, and therefore
    present a higher risk of decreased CO
  • symptoms include the usual signs of decreased CO due to the slow HR
    (remember…HR x SV =CO)
  • higher degrees of block also increase the risk of deterioration to 3rd degree block
82
Q

SECOND DEGREE HEART BLOCK, TYPE II (MOBITZ II) - Common Causes

A
  • MI, severe CAD
83
Q

SECOND DEGREE HEART BLOCK, TYPE II (MOBITZ II) - Interventions

A
  • monitor for CO compromise
  • withhold slow-rate-causing medications
  • if CO is compromised… - atropine might be attempted
    - cardiac pacing (to stop progression to 3rd degree block)
84
Q

SECOND DEGREE HEART BLOCK, TYPE II (MOBITZ II) - Distinguishable Features

A
  • the AR is that of the SA node
  • the VR is 2, 3, 4 times slower than the AR
  • the rhythm is regular because the block occurs at regular intervals
  • the P waves are normal, but there are 2, 3 or 4 more P waves than QRSs
  • the PR intervals are constant (always the same length)
  • PR interval may be normal in length or can be prolonged, but it’s constant
  • PR intervals only exist with every 2nd, 3rd, 4th ventricular beat (where Ps exist)
  • the QRS complexes are usually narrow, but can be slightly widened
  • the width of the QRS basically determines the location of the block
  • if the QRS complex is narrow, the block is at the AV nodal area
  • if the QRS complex is widened, the block is sub-junctional, and can more easily
    advance to 3rd degree block
  • therefore, the wider the QRS complex, the more serious the block
85
Q

THIRD DEGREE HEART BLOCK or COMPLETE HEART BLOCK (CHB)

A
  • all impulses from the SA node blocked at the AV node, and never reach the ventricles
  • ventricles use their automaticity to initiate their own impulses, at a rate of 20-40 / min
  • the atria are paced by the SA node
  • the ventricles are paced by their own automaticity
  • the atria and ventricles beat independently of each other
  • the heart now has 2 separate pacemakers
  • there is no synchrony between the atrial and the ventricular contractions
  • the independent ventricular pacemaker is not very dependable
  • it can cease abruptly, leading to ventricular standstill
  • it can also be replaced by a faster ventricular focus, leading to VT or VF
  • these patients have very low CO (due to the slow VR and lack of atrial kick)
  • low stroke volume from the ventricles decreases the CO, and can lead to myocardial
    ischemia, heart failure and cerebral hypoxia
86
Q

THIRD DEGREE HEART BLOCK or COMPLETE HEART BLOCK (CHB) - Common Causes

A
  • MI, CAD, medications (ie. digoxin toxicity, beta-blockers)
87
Q

THIRD DEGREE HEART BLOCK or COMPLETE HEART BLOCK (CHB) - Interventions

A
  • repeatedly monitor mental status and CO
  • atropine is sometimes used until a pacemaker can be inserted
  • the treatment of choice is cardiac pacing (pacemaker)
  • observe closely for ventricular ectopi in the form of PVCs, as they can be a forewarning
    of impending VT or VF
  • a defibrillator must be closely available, because of possible progression to VT or VF
88
Q

THIRD DEGREE HEART BLOCK or COMPLETE HEART BLOCK (CHB) - Distinguishable Features

A
  • the AR is that of the SA node (60-100) and the VR is 20-40
  • both atrial and ventricular rhythms are regular, but independent of each other
  • the P waves are normal and occur regularly, but there are more P waves than
    QRS complexes (some Ps may be hidden in QRS complexes)
  • the PR interval is variable and totally erratic
  • because the atria and ventricles have independent pacemakers, there is no relationship
    between the Ps and the QRSs, and therefore a variable PR interval is present
  • QRS complexes are usually wide and distorted, but can be relatively narrow if the
    ventricular impulses originate nearer to the AV node

Coronary Care (8 decks)

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