Arrhythmias
Cardioversion
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“timed” for ventricular depolarization: On the QRS
HAS to be synched!
Atrial complications
Anticoagulation
Sedation
Voltage varies
Take safety: Standard power outlet is 120 – 140 joules; Men with hairy chest —> remove
hair
takes less electricity
Protocol for atrial dysrhythmia: start with 50-100 joules
Not going to deliver impulse; will delay until right at QRS
AFib/A Flutter: risk of clots
- Strokes and pulmonary emboli can result
HR high but controlled
Still need to be on anticoagulation (warfarin)—> less stress, blood can move more freely
Conduction system of the heart: Sinoatrial node depolarizes/contracts by sending electrical
impulses to the atrioventricular node via internodal pathways; this is the PR interval (0.12-0.2
seconds → the electrical impulses initiate ventricular contraction (depolarization) by traveling
through bundle of His → down the bundle branches → through Purkinje fibers and up the
myocardium
The electrical impulse quickly travels from the SA node through the atria to the atrioventricular
(AV) node; this process is known as conduction. The electrical stimulation of the muscle cells of
the atria causes them to contract. The structure of the AV node slows the electrical impulse,
giving the atria time to contract and fill the ventricles with blood. This part of atrial contraction is
frequently referred to as the atrial kick and accounts for nearly one third of the volume ejected
during ventricular contraction. The electrical impulse then travels very quickly through the bundle
of His to the right and left bundle branches and the Purkinje fibers, located in the ventricular
muscle.
The electrical stimulation is called depolarization, and the mechanical contraction is called
systole. Electrical relaxation is called repolarization, and mechanical relaxation is called diastole.
The process from sinus node electrical impulse generation through ventricular repolarization
completes the electromechanical circuit, and the cycle begins again.
To calculate HR from ECG, find R that aligns with bold line and count backwards on each line
(300, 150, 100, 75, 60, 50) until
Atrial Arrhythmias
Atrial Flutter: conduction defect in atrium
Rhythm: typically sinus
Atrial Rate: 280-320
Ventricular rate: 90
No P waves; saw toothed “F waves”
QRS shape and duration: usually normal but can also be abnormal or absent
PR: many indiscernible P waves cannot confirm PR interval
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Remains low because impulse from SA node is blocked at AV node, preventing the
conduction of atrial impulses; this would cause ventricular tachycardia
Heart’s electrical signals spread through the atria in a fast but regular rhythm instead of
irregularly (Afib)
“Birds in the attic (atria) are fluttering their wings in sequence and unison”
Conduction begins outside SA node in other part of atria
Causes
1. Lung Problems (COPD) 2. Cardiac Problems (Pulm. HTN/Left Side HF; fluid backs up in
lungs, placing pressure on the heart) (Valvular Disease → ex: mitral stenosis which is a
disease of the valve doors) (Thyrotoxicosis/Excess thyroid hormone → hyperthyroidism
crisis (thyroid storm) 3. Cardiac Surgery (CABG and birth defect repairs)
- Atria are not squeezing properly so less cardiac output → *less oxygen in the body*
Signs/Symptoms
COLLAPSED: Chest Pain, Oxygen SPO2 Lower, Low BP, Lethargy, Anxiety, Palpitations (racing
heart/gallops), SOB, Even HR/rhythm, Dizziness (syncope)
Patient Goals
1. Slow the HR and restore normal electrical conduction at the SA node
2. Effective/organized pump in those atria
3. Prevent clots
i.
Anticoagulants - high risk for bleeding so ensure INR ranges from 2.5-3.5
1. Maintain typical intake of leafy greens that have Vitamin K which
blocks the effectiveness of warfarin
ii.
Beta Blockers - slow HR
iii.
Cardiac Ablation - burning/freezing erratic atria cells
iv.
Digoxin- cardiac glycoside that produces deeper contractility (positive
inotropic) and decreases HR (negative chronotropic)
1. Hold if apical pulse (fifth intercostal space) is less than 60 bpm
2. Toxicity is 2.0 or more; symptom is seeing green/yellow halos;
hypokalemia due to diuretics (furosemide, hydrochlorothiazide)
puts the patient at risk for toxicity
v.
Electro Cardioversion (50-200) joules to reset SA node; usually done after
TTE (transthoracic echocardiogram), which is used to rule out presence of
blood clots
Medical Management
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Adenosine: causes sympathetic block and slowing of conduction through the AV node
- Used to end the tachycardia
- Ideally used for visualization for dx reasons
- Given by rapid IV administration immediately followed by a 20 mL saline flush and
elevation of the arm to promote circulation of medicine
- Atrial flutter is treated with antithrombotic therapy, rate control, and rhythm control
in the same manner as atrial fibrillation
- Cardioversion
Junctional Rhythm aka idionodal rhythm
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When SA node/pacemaker sites fail, the AV Junction is left with pacemaker responsibility.
Sinus node slows or when the impulse can’t be conducted through the AV node → AV
node discharges an impulse automatically
Originates from the junctional area (mostly AV node, bundle of His, and bundle branches)
that will generate a signal to pace the heart when the SA node is not working
ECG Characteristics (if rhythm is not caused by complete heart block)
- Ventr. rate: 40-60 bpm
- Atrial rate: 40-60 bpm if P waves are visible
- Heart Rate: 40 - 60 BPM
- Ventricle/Atrial rhythm: regular
- QRS shape/duration: usually normal but can be abnormal
- P wave may be: absent, after/before QRS complex, or inverted especially in lead II
- PR: <0.12 seconds; may be inverted, hidden in QRS, or following QRS (retrograde)
May produce S/S of reduced cardiac output; tx is then the same as for bradycardia
Ventricular Dysrhythmias (Amiodarone is most commonly used for ventricular problems)
Ventricular Tachycardia
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Three or more consecutive PVCs > 100 bpm
Patient is nearly always unresponsive and pulseless
Ventricular and atrial rate: ventricular: 100-200 bpm; atrial depends on underlying rhythm
(e.g., sinus rhythm)
Ventricular and atrial rhythm: ventricular is usually regular and atrial is sometimes regular
QRS shape/duration: 0.12 seconds or more; bizarre, abnormal shape
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P wave: very difficult to see; atrial rate and rhythm may be indeterminable
PR interval: very irregular, if P waves can be seen
P:QRS Ratio: difficult to determine but if P waves are present, there are usually more QRS
complexes than P waves
Medical Management
- Initial treatment is determined by: identifying rhythms as either mono/polymorphic,
determining existence of prolonged QT interval before TV initiation, any comorbidities, and
verifying patient’s heart function (normal/decreased)
- Antiarrhythmic medications include: procainamide, amiodarone, sotalol, and lidocaine
(based upon type of VT, clinical presentation, and patient comorbidities)
- Cardioversion is tx of choice for monophasic VT in a symptomatic patient
- Defibrillation is tx of choice for pulseless VT
- Patient with VT who is unconscious and pulseless is treated in SAME MANNER as V Fib
→ immediate defibrillation
- EF >35% may be managed with antiarrhythmic medication
- EF <35% should be considered for an implantable cardioverter defibrillator
Torsades de Pointes
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Polymorphic VT preceded by prolonged QT interval (congenital or acquired)
Common causes: CNS disease; medications (cipro, erythromycin, haloperidol, lithium,
methadone), hypokalemia, hypocalcemia, or hypomagnesemia, congenital QT prolonged
interval
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Rhythm is likely to cause the patient to deteriorate and become pulseless; immediate
treatment is required, which include: electrolyte correction, IV magnesium, IV
isoproterenol, or pacing if bradycardic
Hard to regulate, NO PULSE!
Treatment
CPR first
Early defibrillation
EPI
Magnesium
Ventricular Fibrillation
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Most common arrhythmia in patients with cardiac arrest
Rapid, disorganized ventricular rhythm that causes ineffective quivering of ventricles
Always characterized by absence of audible heartbeat, palpable pulse, respirations
No coordinated activity → cardiac arrest and death are imminent if not corrected
Early defibrillation with immediate CPR until defibrillation is available
No atrial activity on ECG
Most common cause is coronary artery disease and resulting acute MI
Other causes: unsuccessfully treated VT, cardiomyopathy, valvular heart disease,
proarrhythmic medications, acid-base and electrolyte imbalances, electrical shock,
Brugada syndrome (patient frequently of Asian descent has a normally structured heart,
few/no risk factors for coronary artery disease, and family hx of sudden cardiac death
Medications: Amiodarone, Epinephrine
ECG Characteristics
- Ventricular rate is > 300 BPM
- Ventricular rhythm: extremely irregular with no specific pattern
- QRS shape and duration: irregular, undulating waves with changes amplitudes
- *NO recognizable QRS complexes*
Idioventricular Rhythm
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Ventricles “last call” before things stop
Ventricles move more slowly than normal
<50 BPM
Usually don’t see it unless patient has actively been in cardiac arrest
No pulse —> EPI
Compressions and EPI will treat
Not shockable
Atrial Fibrillation
Rhythm: irregular
Atrial rate: ≥ 350; other rate usually over 100 bpm
No PR intervals
No P waves, “fib waves” instead; atria is not contracting
QRS is normal
RR, QRS, and QT intervals are analyzed to verify effectiveness of antiarrhythmics
First goal is rate control, then cardioversion
Cardizem is commonly used
Anticoagulation is needed
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AV node blocks most of the rapid misfires from the SA node, protecting the ventricles
**Increased risk of HR, MI, and embolic events (e.g. PE, CVA, DVT)**
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Rapid and irregular ventricular response → reduced time for ventricular filling → lower
stroke volume
Atria are not squeezing blood out to body → less cardiac output = lower oxygen to the
body
Atrial kick (last part of diastole & ventricular filling, which accounts for 25-30% of cardiac
output) is lost due to absence of AV synchrony
Some patients are asymptomatic while other experience palpitations and manifestations
of HF, including SOB, hypotension, dyspnea, and fatigue
High ventricular rate: greater than 80 bpm
- Can lead to mitral valve dysfunction, regurgitation, intraventricular conduction
delays, and dilated ventricular cardiomyopathy
Pulse deficit (difference between apical and radial pulses)
- Shorter diastole → ventricles not adequately filling → less time available for
coronary artery perfusion → increases risk of MI with onset of chest pain
Promotes thrombi formation, especially in left atrium
Most common origin of embolisms that result in a stroke in those with nonvalvular afib
(arrhythmia caused by HTN, stress, etc) is the left atrial appendage (LAA)
LAAO (left atrial appendage occlusion):
Paroxysmal: sudden onset with spontaneous termination or an intervention; lasts ≤7 days
and may recur
Persistent: continuous, lasting more than 7 days
Long-standing persistent: continuous, lasting more than 12 months
Permanent: persistent, but decision has been made not to restore or maintain sinus
rhythm
Nonvalvular: absence of moderate-to-severe mitral stenosis or mechanical heart valve
Causes
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Recovering from open heart surgery can place stress on the heart
HTN adds pressure on the heart
Alcohol (Holiday Heart Syndrome) is a full episode of AFib
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Hyperthyroidism can increase your metabolism, causing added heart stimulation
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Diastole: ventricles are relaxed and filling with blood (relax and refill)
Systole: heart contracts and pumps blood out from arteries
Assessment/Dx
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Evaluation should include history and exam that identifies onset, nature, frequency,
duration, any precipitating factors, and response to medications
Risk Factors: Increasing age, Hypertension, Diabetes, Obesity, Valvular heart disease, Heart
failure, Obstructive sleep apnea, Alcohol abuse, Hyperthyroidism, Myocardial infarction,
Smoking, Exercise, Cardiothoracic surgery, Increased pulse pressure, European ancestry,
Family history
12 lead ECG to confirm the arrhythmia and to identify presence or absence of left ventricular
hypertrophy, bundle branch block, prior MI, or other arrhythmias
TTE (transesophageal echocardiogram) can identify valvular heart disease, provide info about
ventricle size/function, RV pressure to identify pulmonary hypertension, LV hypertrophy, and
presence of atrial thrombi
Blood tests are used to screen for diseases that are risks for atrial fibrillation (thyroid, renal,
hepatic) when it is a recent onset or when ventricular rate is hard to control
Signs/Symptoms
COLLAPSED: Chest Pain, Oxygen SPO2 Lower, Low BP, Lethargy, Anxiety, Palpitations (racing
heart/gallops), SOB, Elevated ventricle or heart rate, Dizziness (syncope)
What are the main patient outcome goals?
1. SLOW the heart rate and RESTORE normal electrical conduction at the SA NODE
2. Effective/organized PUMP in those ATRIA
3. Prevent CLOTS
Nursing Interventions
A. Anticoagulants (warfarin) to prevent clots but caution for bleeding
i.
Monitor INR; 2.5-3.5 is therapeutic range
ii.
Instruct patient to maintain their normal intake of leafy greens; they contain
Vitamin K, which blocks warfarin’s effectiveness
B. Beta Blockers to slow the heart rate
C. Cardiac Ablation: burn/freeze erratic atria cells
D. Digoxin (cardiac glycoside) increases contractility (inotropic) & decreases HR (negative
chronotropic); slower but more effective movement of the heart
i.
HOLD if heart rate is <60 bpm; listen to apical pulse in 5th intercostal space
ii.
Side note: chrono = time → rate
iii.
Toxic level: ≥ 2
iv.
S/S include patient reports of seeing green or yellow halos and
hypokalemia from diuretics (hydrochlorothiazide, furosemide)
E. Electro Cardioversion (50-200 joules) given to reset SA node; usually done after TTE (used
to rule out blood clots in the atria
- Defibrillation (200-360 joules) is usually only given with deadly rhythms (VFib, pulseless V
Tach)
Premature Ventricular Complex (PVC)
- Impulse that begins in a ventricle and is conducted through ventricles before the next
normal sinus impulse (premature beat of QRS)
- Can occur in healthy people, especially those who use nicotine, caffeine, or alcohol
- May be caused by cardiac ischemia, infarction, increased workload on heart (HF and
tachycardia), digitalis toxicity, hypoxia, acidosis, or electrolyte imbalances (hypokalemia)
- Unifocal: PVCs look the same; we can pinpoint where issue is occurring in cardiac cycle
- Multifocal: PVCs have at least two different morphologic appearances
Bigeminy: every other complex is a PVC
Trigeminy: every third complex is a PVC
Quadrigeminy: every fourth complex is a PVC
- QRS either accelerates/rebounds or widens out
- Ventricular/Atrial rate: depends on underlying rhythm
- Ventricular/Atrial rhythm: irregular due to early QRS, creating one RR interval that is
shorter than the others; the PP interval may be regular, indicating that the PVC did not
depolarize the SA node
- QRS shape/duration: duration is ≥ 0.12 seconds, shape is bizarre/abnormal;
- P wave: visibility depends on timing of PVC; may be absent (hidden in QRS or T wave) or in
front of the QRS; if P wave follows the QRS, its shape may be different
- Patients feel that their “heart is skipping a beat”
- Effect depends on its timing in cardiac cycle and how much blood was in the ventricles
when they contracted
- Common occurrence and may increase in frequency with age
- Initial tx: aimed at correcting the cause
Medical Management
- PVCs that are frequent and persistent may be treated with amiodarone or beta blockers
- Long-term pharmacotherapy is not usually indicated
- Association with adverse outcomes: patients may need to be evaluated for underlying
causes (ischemic heart disease and LV dysfx)
Premature Atrial Contraction
- Premature contraction/beat of P wave
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Atria did not wait on depolarization after T wave (electrical impulse starts in atrium before
next normal impulse of SA node)
- QRS look the same
- Early P wave
- Less likely to be symptomatic
- Can be caused by caffeine, alcohol, nicotine, stretched atrial myocardium (hypervolemia),
anxiety, hypokalemia, hypermetabolic states (pregnancy), atrial ischemia, injury, or
infarction
- Often seen with sinus tachycardia
- If infrequent, no tx necessary
- If frequent (more than 6/min) this may signal a worsening state or onset of more serious
arrhythmia (AFib)
- Management is directed towards treating underlying state
Premature Junctional Contraction
- Impulse that starts in AV node area before the next normal sinus impulse reaches the AV
node
- Less common than PACs
- Causes: digitalis toxicity, HF, CAD
- P wave may be absent, may follow QRS, or may occur before QRS but with a PR interval of
< 0.12 seconds
- Rarely produces symptoms
Treatment
- If infrequent, no tx necessary
- If frequent (more than 6/min) this may signal a worsening state or onset of more serious
arrhythmia
- Management is directed towards treating underlying state
Heart Block (1st degree AV block)
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Occurs when all atrial impulses are conducted through the AV node into the ventricles at a
slower rate
- PRI = > 20 seconds
- PR interval: > 0.20 seconds; PR interval measurement is consistent
Heart Block (2nd Degree Type I AV Block) Winckebacke
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Occurs when there is a repeating pattern in which all but one of a series of atrial impulses
are conducted through the AV nose into the ventricles (e.g., every ⅘ atrial impulses are
conducted)
Each atrial impulse takes a longer time for conduction than the one before, until one
impulse is fully blocked
AV node is not depolarized by the blocked atrial impulse → AV node has time to fully
repolarize so that the next atrial impulse can be conducted within the shortest amount of
time
Ventricular and atrial rate: Depends on the underlying rhythm, but the ventricular rate is
lower than the atrial rate
Ventricular and atrial rhythm: The PP interval is regular if the patient has an underlying
normal sinus rhythm; the RR interval characteristically reflects a pattern of change.
Starting from the RR that is the longest, the RR interval gradually shortens until there is
another long RR interval
“long, longer, longer, DROP”
QRS shape and duration: Usually normal, but may be abnormal
P wave: In front of the QRS complex; shape depends on underlying rhythm.
PR interval: The PR interval becomes longer with each succeeding ECG complex until
there is a P wave not followed by a QRS. The changes in the PR interval are repeated
between each “dropped” QRS, creating a pattern in the irregular PR interval measurements
Heart Blocks (2nd degree Type II AV Block)
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Occurs when only some of the atrial impulses are conducted through the AV node into the
ventricles
Generally a little slower than type 1 and patient becomes more symptomatic
Random P wave but no QRS with it
Ventricular and atrial rate: Depends on the underlying rhythm, but the ventricular rate is
lower than the atrial rate
Ventricular and atrial rhythm: The PP interval is regular if the patient has an underlying
normal sinus rhythm. The RR interval is usually regular but may be irregular, depending on
the P:QRS ratio
QRS shape and duration: Usually abnormal, but may be normal
P wave: In front of the QRS complex; shape depends on underlying rhythm
PR interval: The PR interval is constant for those P waves just before QRS complexes
P:QRS ratio: 2:1, 3:1, 4:1, 5:1, and so forth
- 2, 3, 4… P waves to every
Heart Blocks (3rd degree AV Block)
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QRS
Occurs when no atrial complex is conducted through the AV node into the ventricles
Two impulses stimulate the heart: one stimulates the ventricles (QRS complex), and one
stimulates the atria (P wave)
P wave may be seen, but atrial electrical activity is not conducted down into the ventricles
to initiate the QRS complex, the ventricular electrical activity
Having two impulses stimulate the heart results in a condition called AV dissociation,
which may also occur during VT
Ventricular and atrial rate: Depends on the escape rhythm (idionodal or idioventricular) and
underlying atrial rhythm, but the ventricular rate is lower than the atrial rate
Ventricular and atrial rhythm: The PP interval is regular and the RR interval is regular, but
the PP interval is not equal to the RR interval
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QRS shape and duration: Depends on the escape rhythm; with junctional rhythm, QRS
shape and duration are usually normal; with idioventricular rhythm, QRS shape and
duration are usually abnormal
P wave: Depends on underlying rhythm
PR interval: Very irregular
Sporadic P waves & sporadic QRS
P:QRS ratio: More P waves than QRS complexes
P wave is basically firing whenever it wants
Atrial rate is typically in the 30s
Dizziness, fatigue, palpitations, possible chest discomfort
Transcutaneous pacemaking (defibrillation pads applied —> hit “pacer” function on
crash cart)
Increase pacing by 10 millivolts until desired rate is reached
Usually stabilized short-term quickly after pacing
atropine makes HR go up (works on SA) but all it will do is increase atrial rate and
place patient at risk for MI
P and QRS miscommunication
Bundle Branch Blocks
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QRS is the issue
Blockage in heart where impulse will split
Widening on would cause ventricular (bad)
TX
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document; can’t do anything about it
Watch every 6 months
Chest pain, SOB, syncope episodes
Do not use BB
MI, cardiomyopathy, advanced heart disease, stimulant abuse
Medical Management of Conduction Abnormalities
Based on the cause of the AV block and the stability of the patient, treatment is directed toward
increasing the heart rate to maintain a normal cardiac output. If the patient is stable and has no
symptoms, no treatment may be indicated or it may simply consist of decreasing or eliminating
the cause (e.g., withholding the medication or treatment). If the causal medication is necessary
for treating other conditions and no effective alternative is available, pacemaker implantation may
be indicated. The initial treatment of choice is an IV bolus of atropine, although it is not effective in
second-degree AV block, type II, or third-degree AV block. If the patient does not respond to
atropine, has advanced AV block, or has had an acute MI, temporary transcutaneous pacing may
be started. If the patient has no pulse, treatment is the same as for ventricular asystole (Link et al.,
2015; Soar et al., 2018). A permanent pacemaker may be necessary if the block persists (see later
discussion).
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