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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
334
G. J. Hu and C. O’Kane
second-degree and third-degree AV blocks in the setting of acute inferior myocardial infarctions [2]. Aminophylline is a nonselective adenosine receptor antagonist
and phosphodiesterase inhibitor. Increased adenosine production may be implicated
in the pathophysiology of AV blocks in acute inferior myocardial infarctions [2].
Aminophylline may combat this proposed mechanism to improve AV conduction,
increase ventricular rate, and improve symptoms. In refractory cases, transvenous
pacing may be considered. Goals of therapy include correcting heart rate and preventing further hemodynamic instability. Monitor heart rate, blood pressure,
electrocardiogram, symptoms, and adverse effects of interventional medications.
13.2.3 Atrial Fibrillation
Atrial brillation (AF) remains the most common cardiac arrhythmia. The estimated US prevalence of AF was 5.6million people in 2015 with 11% of these cases
being undiagnosed AF [11]. As the incidence of AF increases with advancing age,
the estimated prevalence of AF is expected to rise to 12.1million in 2030 [12]. The
overall lifetime risk of AF is 26% for men and 23% for women [13]. There are several comorbidities and risk factors that increase an individual’s risk for AF, including smoking, alcohol use, obesity, hypertension, diabetes, heart failure, coronary
artery disease, valvular heart disease, obstructive sleep apnea, and hyperthyroidism
[14]. The pathophysiology of AF is a multifactorial process that is a result of atrial
metabolic, electrical, and structural remodeling. This remodeling is a result of neurohormonal dysfunction, metabolic dysfunction, inammation, and ischemia, which
disrupts synchronized electrical signaling leading to arrhythmogenesis [14]. AF is
associated with many adverse outcomes, such as stroke, cognitive impairment,
dementia, myocardial infarction, cardiac death, heart failure, chronic kidney disease, and peripheral artery disease. For these reasons, AF is associated with higher
healthcare utilization and costs. Investigators examining health insurer data estimated that AF accounted for $28.4billion (95% CI, $24.6–$33.8billion) in healthcare spending [15]. The socioeconomic impact of AF in conjunction with chronic
cardiovascular disease cannot be understated, as hospitalization rates for AF and
AF-associated complications continue to increase.
The diagnosis of AF is suggested by irregularly irregular R-R intervals in the
absence of P waves on a 12-lead ECG (Fig.13.6) [16]. In patients with newly
Fig. 13.6 Atrial brillation
13 Cardiac Arrhythmias
Table 13.2 Stages of AF
Stage Category Description
1 At risk for AF Presence of modiable and nonmodiable risk factors associated
2 Pre-AF Evidence of structural or electrical ndings further predisposing a
3A Paroxysmal AF AF that is intermittent and terminates ≤7days of onset
3B Persistent AF AF that is continuous and sustains for >7days and requires
3C Long-standing
persistent AF
3D Successful AF
ablation
4 Permanent AF Shared decision made between patient and clinician to cease
with AF
patient to AF
intervention
AF that is continuous for >12months in duration
Freedom from AF after percutaneous or surgical intervention to
eliminate AF
attempts to restore normal sinus rhythm (NSR)
335
diagnosed AF, a transthoracic echocardiogram (TTE) to assess cardiac structure and
pertinent laboratory testing, including metabolic panel, complete blood count, and
thyroid function, should be performed to determine stroke and bleeding risk and
identify underlying conditions that may guide further management [14]. AF is a
progressive disease that requires different strategies at different stages. A summary
of stages is included in Table13.2. The foundation of optimal AF management is to
treat risk factors and enact behavioral changes. Once AF develops, there are three
important pillars that must be addressed with all patients—stroke risk assessment
and treatment, optimize all modiable risk factors, and manage symptoms using
rate- and rhythm-controlling strategies. The symptoms of atrial brillation include
palpitations, shortness of breath, lightheadedness, syncope, angina, heart failure
symptoms, fatigue, and hypotension. Many patients may be asymptomatic [15].
13.2.3.1
oke Risk Assessment andBleeding Risk Assessment
Str
AF increases the risk of ischemic stroke and systemic embolism. The risk of stroke
can be assessed by calculating the CHA
-VASc score or other validated clinical
2DS2
risk scores such as Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA)
and Global Anticoagulant Registry in the Field-Atrial Fibrillation (GARFIELD-AF)
[14]. The CHA2DS2-VASc is most commonly used in clinical practice and recommended for use with the most updated guidelines. The CHA2DS2-VASc score
assigns one point each to congestive heart failure, hypertension, diabetes mellitus,
history of vascular disease, age ≥65years, and female sex and two points each to
age ≥75years and history of stroke or transient ischemic attack (TIA). For patients
with AF and an estimated annual thromboembolic risk of ≥2% per year (CHA
2DS2
VASc score ≥2in men and ≥3in women), anticoagulation is recommended to prevent stroke and systemic thromboembolism [14]. Risk scores are equally benecial
in quantifying bleeding risk in AF.The HAS-BLED score assigns one point each to
-
336
G. J. Hu and C. O’Kane
hypertension, abnormal liver function or renal function, history of stroke, history of
bleeding, labile international normalized ration (INR), age >65years, concomitant
antiplatelet or nonsteroidal anti-inammatory drugs (NSAIDs), and alcohol use
[14]. A score ≥3 indicates a high bleeding risk. Other validated bleeding risk scores
that are recommended by guidelines include HEMORR2HAGES and
ATRIA. Bleeding risk scores should not be used in isolation to determine the eligibility for anticoagulation but identify and modify bleeding risk factors.
13.2.3.2 Anticoagulation
For patients with AF and an estimated annual thromboembolic risk of ≥2% per year
(CHA
-VASc score ≥2 in men and ≥3 in women), anticoagulation is recom-
2DS2
mended to prevent stroke and systemic thromboembolism [14]. For patients with
AF and an estimated annual thromboembolic risk of ≥1% but <2% per year (equivalent to a CHA2DS2-VASc score of 1in men and 2 in women), anticoagulation is
reasonable to prevent stroke and systemic thromboembolism. Direct oral anticoagulants (DOACs) are preferred over warfarin for stroke prevention in the setting of AF
due to convenience of xed doses, minimal monitoring parameters, and superior
safety proles [17]. Warfarin (target INR 2–3) remains an option for select patients
with AF such as those with moderate to severe mitral stenosis, rheumatic mitral
stenosis, or mechanical heart valves [14]. A detailed comparison between warfarin
and DOAC can be found in Table 13.3. Additionally, oral anticoagulation recommendations and preferences for select patient populations can be found in
Table13.4 [14].
For hemodynamically stable patients undergoing cardioversion, therapeutic anticoagulation should be established before cardioversion and continued for at least
4 weeks afterwards without interruption to prevent thromboembolism [14]. For
patients that have been on uninterrupted therapeutic anticoagulation for at least
3weeks, then they may proceed with cardioversion without imagining for intracardiac thrombus. For patients who were not receiving uninterrupted therapeutic anticoagulation, then it is recommended to undergo imaging to assess the patient for
intracardiac thrombi including device-related thrombi prior to cardioversion. This
remains a reasonable approach even for patients with left atrial appendage occlusion
(LAAO) who are no longer actively on anticoagulation. If intracardiac thrombus is
identied on imaging, then treatment with therapeutic anticoagulation for at least
3–6weeks is recommended before cardioversion. It is also recommended to repeat
imaging before cardioversion.
13.2.3.3 Rate vs. Rhythm Control
The primary goal of treatment of AF is to reduce symptoms, such as palpitations
and shortness of breath, with rate- or rhythm-controlling strategies. The optimal
strategy remains debated, and neither strategy confers denitive mortality benet
Cardiac Arrhythmias
13
337
Table 13.3
Drug Warfarin Dabigatran Apixaban Edoxaban Rivaroxaban
Class Vitamin K
Metabolism S-isomer:
Excretion 92% renal
Half-life (h) 20–60 12–17 12 10–14 5–9
Renal dose
adjustments
Hepatic dose
adjustments
CYP3A4
inhibitors/
P-gp
inhibitors
Dose
adjustments
CYP3A4
inhibitors/
P-gp
inducers
Dose
adjustments
Comparison of oral anticoagulation for
antagonist
CYP2C9
R-isomer:
CYP1A2,
CYP2C19,
CYP3A4
(only
metabolites)
None CrCl
Adjust dose
based on INR
trends
Adjust dose
based on INR
trends
Adjust dose
based on INR
trends
Direct thrombin
inhibitor
Minimal
P-glycoprotein
(P-gp) substrate
80% renal 27% renal
15–30mL/min:
75mg twice
daily
Child-Pugh B
(moderate): Use
with caution
Child-Pugh C
(severe): Avoid
use
Yes Yes No Ye s
Avoid use Avoid use Avoid use Avoid use
AF [18–22]
Factor Xa inhibitor
CYP3A4
P-gp substrate
73% biliary and
intestinal
If any 2 of the
following—
Age ≥80years,
body weight
≤60kg, SCr
≥1.5mg/day:
2.5mg twice
daily
Child-Pugh B
(moderate): Use
with caution
Child-Pugh C
(severe): Avoid
use
50% renal
50% liver,
biliary, and
intestinal
CrCl
15–50mL/
min: 30mg
daily
Child-Pugh
B
(moderate):
Use with
caution
Child-Pugh
C (severe):
Avoid use
CYP3A4/5
P-gp substrate
66% renal
28% feces
CrCl
15–50mL/
min: 15mg
daily
Child-Pugh B
(moderate)
and childPugh C
(severe):
Avoid use
338
Table 13.4 Anticoagulation recommendations in select populations [14]
Specic population Recommendations
AF complication acute
coronary syndrome or
percutaneous coronary
intervention (PCI)
Chronic coronary disease Oral anticoagulation monotherapy is recommended over
Peripheral artery disease Oral anticoagulation monotherapy is recommended over
Chronic kidney disease
(CKD) including end-stage
renal disease (ESRD)
Valvular heart disease Rheumatic mitral stenosis: Warfarin
Obesity Obesity (body mass index ≥40kg/m
a
Dose-adjusted DOAC=labeled dose adjustments (see Table13.3)
b
Dose-adjusted apixaban=evidence-based dosing included 2.5mg or 5mg twice daily (stroke and
bleeding risk assessment should be performed to guide dosing)
DOACs are preferred over warfarin for most patients with AF
who undergo PCI
Early discontinuation of aspirin (within 1–4weeks) and
continuation of dual-antithrombotic therapy with oral
anticoagulant and P2Y12 inhibitor are preferred over triple
therapy (aspirin, oral anticoagulant, and P2Y12 inhibitor)
combination therapy (oral anticoagulant and antiplatelet) for
patients with AF and chronic coronary disease beyond 12months
after last revascularization
combination therapy (oral anticoagulant and antiplatelet) for
patients with AF and stable peripheral artery disease
CKD stage 3: Dose-adjusted DOAC
CKD stage 4: Dose-adjusted DOAC
ESRD with or without dialysis: Dose-adjusted apixaban
warfarin
Moderate-to-severe mitral stenosis: Warfarin
Mechanical heart valve: Warfarin
All other valvular heart disease: DOAC preferred over warfarin
apixaban are reasonable to select over warfarin
Obesity following bariatric surgery: Warfarin may be reasonable
to choose over DOAC due to concerns for drug absorption
G. J. Hu and C. O’Kane
a
or warfarin
a
or warfarin
2
): Rivaroxaban and
b
or
compared to the other. Earlier studies comparing the two approaches did not show
differences in efcacy endpoints when evaluating cardiovascular death or incidence
of adverse cardiovascular outcomes, such as the development of heart failure, or
adverse cerebrovascular outcomes, such as incidence of stroke or transient ischemic
attack (TIA) [23–25]. Additionally, some of these studies demonstrated that there
may be a higher risk for hospitalizations related to AF or incidence of adverse outcomes to treatment with a rhythm-based treatment. However, recent literature suggests that a rhythm-controlling strategy with antiarrhythmic medications, catheter
ablation, or cardioversion may confer a reduction in cardiovascular death, stroke,
and hospitalizations related to AF [26]. This may be due to advances in rhythmcontrolling strategies, increased use of catheter ablation, and availability of newer
antiarrhythmic medications with closer monitoring.
For the reasons mentioned above, rate control and rhythm control are both reasonable approaches for managing patients with AF.However, rate control is often
the initial strategy for patients with AF due to familiarity and safety of the drugs.
Antiarrhythmic medications should be considered if patients remain symptomatic.
An up-front rhythm-controlling strategy may be attempted to restore and maintain
13 Cardiac Arrhythmias
339
NSR in patients with a recent diagnosis of AF to prevent atrial remodeling. Patient
factors and preferences should be considered before electing to pursue one strategy
over the other. Rate-controlling strategies may be preferred in older patients with
longer histories of AF, those with less symptom burden, those with easily controlled
heart rates, and those with less left ventricular (LV) or valvular dysfunction [14]. A
rhythm-controlling strategy may be preferred in younger patients with newer histories of AF, those with many symptoms of AF, those for whom it is difcult to control
heart rate, and those with LV dysfunction or valvular dysfunction [14].
Treatment withRate Control
Previous recommendations for rate control suggested a heart rate (HR) goal
<80beats/min at rest in symptomatic patients and <110beats/min at rest in asymptomatic patients [27]. However, more recent literature suggests that lenient HR
goals are comparable to strict HR goals [28]. The updated recommendation is that
rate control should be guided by underlying patient symptoms, in general aiming for
a resting HR <100–110beats/min [14]. The initial rate control strategy involves a
gradual titration of β-blockers or non-dihydropyridine calcium channel blockers
(non-DHP CCB) until the HR is adequately controlled and symptoms are manageable. Both classes of medications are equally efcacious at acutely controlling HR
[29]. β-Blockers are preferred in patients with a history of HFrEF.Non-DHP CCBs
are avoided in this population due to their negative inotropic effects. In patients with
heart failure with preserved ejection fraction (HFpEF), a strategy of either diltiazem
or β-blockers is acceptable. These agents are initiated during the episode of AF in a
hospital or ambulatory care setting. Hemodynamically unstable patients with AF
and rapid ventricular rate response (AF with RVR) should undergo emergent cardioversion to restore NSR.Rate control in a hospital setting can be complicated by
hypotension or heart failure, precluding the use of a high dose of β-blockers or nonDHP CCB. In these situations, intravenous amiodarone or digoxin may be a reasonable approach. A combination of the agents can be used to achieve adequate rate
control. Medications used for rate control are described in Table13.7.
AV nodal ablation followed by permanent pacemaker placement may be considered in select patients with refractory AF with rapid ventricular rate in whom rateand rhythm-controlling strategies are not ideal or have been unsuccessful [14].
Considerations to consequences of lifelong pacemaker implantation with respect to
age and comorbidities are imperative before electing this type of strategy for rate
control.
Treatment withRhythm Control
After the decision to pursue rhythm control is established, patients must rst be
converted to NSR with electrical or pharmacological cardioversion. Pharmacological
cardioversion is a reasonable alternative to electrical cardioversion for those
340
G. J. Hu and C. O’Kane
individuals who are hemodynamically stable or in situations where electrical cardioversion cannot be performed [14]. As previously discussed, appropriate anticoagulation should be established before cardioversion and continued after to reduce
the incidence of stroke and systemic embolism. For patients undergoing electrical
cardioversion, an initial electrical shock of at least 200 joules (J) should be delivered
synchronized to the QRS interval to reduce the risk of inducing ventricular brillation [14]. In patients with longer duration AF or unsuccessful initial shock, using
higher energy and pretreatment with antiarrhythmic medications can facilitate the
success of electrical cardioversion. Patients should be adequately sedated prior to
electrical cardioversion. For acute pharmacological cardioversion, ibutilide and
intravenous amiodarone are usual options [14]. Ibutilide works rapidly but is associated with severe adverse effects such as QT interval prolongation and torsades de
pointes, particularly in patients with HFrEF.For this reason, it should be avoided in
patients with known HFrEF and those with long QT syndromes. Intravenous amiodarone requires a longer time for AF cardioversion (8–12h) compared to ibutilide.
Procainamide may also be considered for pharmacological cardioversion of AF but
was considered less effective than ibutilide [30, 31]. Outside of the hospital, ecainide and propafenone demonstrated efcacy to support their use in pharmacological cardioversion using the pill-in-the-pocket approach [32]. Dofetilide, oral
amiodarone, and oral sotalol can be used for pharmacological cardioversion of AF
but require several days and are not practical for acute conversion of AF to NSR
[14]. Intravenous sotalol is not supported for pharmacological cardioversion of AF.
The choice of antiarrhythmic drugs to maintain NSR is based upon the patient’s
underlying comorbidities. Comorbidities of importance include coronary artery disease (CAD), HFrEF, chronic obstructive pulmonary disorders (COPDs), renal dysfunction, and long QT syndromes. In patients with CAD, sodium channel blockers
(Vaughan-Williams class I antiarrhythmics) are contraindicated due to increased
mortality [33]. Alternative therapies include sotalol, dofetilide, amiodarone, and
dronedarone. In patients with HFrEF, sodium channel blockers (Vaughan-Williams
class I antiarrhythmics) are also contraindicated due to increased mortality, negative
inotropic effects, and increased risk for ventricular arrhythmias [16]. Dronedarone
use has been associated with increased mortality in this population, especially with
decompensated heart failure, thus leaving dofetilide, sotalol, and amiodarone as
options for the maintenance of NSR [34]. Sotalol also possesses β-blocking properties and is often avoided in HFrEF to maintain higher doses of β-blockers as part of
guideline-directed medical therapy. Therefore, dofetilide and amiodarone remain
preferred options in patients with HFrEF.The choice between dofetilide and amiodarone is based on age, renal function, baseline-corrected QT (QTc) interval, and
presence of pulmonary disease [16]. For patients without underlying cardiac comorbidities, sodium channel blockers, particularly the class Ic medications ecainide
and propafenone, are commonly used. Once the antiarrhythmic drug is chosen, the
patient should be monitored for recurrence of AF and adverse effects. A review of
rhythm-controlling medications may be found in Table13.7. If a patient experiences
an adverse event, especially proarrhythmias, the offending agent should be withdrawn. Consideration of an antiarrhythmic drug from a different class may be
13
Cardiac Arrhythmias
341
considered if contraindications are not present, as can catheter-based or surgical
ablation.
AF is a disease continuum that requires a variety of strategies at different stages
targeting lifestyle and risk factor modication, increased screening, and initiating
therapy when necessary. The three important pillars for atrial brillation management include thromboembolism assessment and treatment, optimizing modiable
risk factors, and managing symptoms of AF using rate- and/or rhythm-controlling
strategies.
13.2.4 Atrial Flutter
Atrial utter (AFL) is an easily treatable atrial tachycardia related to atrial brillation. In fact, the updated guidelines for the management of atrial brillation classify
atrial utter under stage 2 pre-AF [14]. ECG ndings are consistent with a narrow
QRS complex tachycardia with an irregular “sawtooth” pattern (Fig.13.7). Atrial
utter is an electrical abnormality usually as a result of structural changes in the
heart. Atrial utter typically originates from the right atrium. It typically involves a
large circuit around the area of the tricuspid valve, which gives it the name “typical
AFL” [35]. Other circuits that form in the right atrium or left atrium resulting in
AFL are less common and termed “atypical AFL.” Symptoms are similar to those
seen in atrial brillation. For that reason, treatment modalities are similar to management principles described in atrial brillation with regard to rate/rhythm control
and anticoagulation. However, many patients are treatable with catheter ablation,
specically cavotricuspid isthmus (CTI) ablation [36]. This is a routine and straightforward procedure used to treat typical AFL.
13.2.5 Supraventricular Tachycardia (SVT)
Supraventricular tachycardia (SVT) is a broad term used to describe tachyarrhythmias originating above the ventricles of the heart. The estimated incidence of SVT
is 35 per 100,000 person-years [37]. Examples of these tachyarrhythmias include
AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT,
Fig. 13.7 Atrial utter
342
G. J. Hu and C. O’Kane
including Wolff-Parkinson-White [WPW]), atrial tachycardia, inappropriate sinus
tachycardia, and junctional tachycardia. The most common forms of SVT include
AVNRT (60% of cases) and AVRT (30% of cases). ECG ndings typically show a
regular rhythm (may be irregular in some cases), rate between 120 and 220beats/
min, narrow QRS complex, and absent P waves (Fig.13.8). Some forms of SVT
present with wide QRS complex like WPW syndrome. Signs and symptoms of SVT
include a pounding sensation in the neck, palpitations, dizziness, lightheadedness,
weakness, syncope, and polyuria due to the release of atrial natriuretic factor which
increases diuresis [38].
Reentry refers to an action potential that propagates in a closed-loop-like manner. Reentry may occur within the AV node itself or through an accessory pathway.
AVNRT refers to a reentry pathway that occurs in the AV node, while AVRT is usually a result of an accessory pathway. For AVNRT, there will be one impulse that
divides into two pathways within the AV node—the fast pathway and the slow pathway [39, 40]. During sinus rhythm, electrical impulses travel down both pathways
simultaneously. With discordance of these impulses and refractory periods, impulses
can continually cycle around the two pathways activating the bundle of His from
above and the atria from below within the AV node. For AVRT, there will be one
impulse generated from the sinoatrial node that travels through two pathways—the
AV nodal pathway and an accessory pathway [39, 40]. A premature atrial impulse
will occur and reach the accessory pathway while it is still refractory. The impulse
will also travel through the AV nodal pathway but will take longer, so it will reach
the ventricle in an excitable state and conduct the impulse back to the atrium, thus
creating a reentry circuit.
Patients who present with SVT will be assessed for hemodynamic stability and
underlying cardiac-related causes of arrhythmia. If patients have regular rhythms
and are hemodynamically stable, then AV nodal stimulation should be considered
using vagal maneuvers such as having the patient cough, gag, instruct them to bear
down using the Valsalva maneuver, carotid massage, and using cold stimulation
[38]. Increased vagal stimulation causes bradycardia at the level of the AV node. It
prolongs the refractoriness of the nodal tissue and disrupts the reentry circuit. If
patients do not convert to NSR, then adenosine should be considered. Adenosine is
a miscellaneous antiarrhythmic that exerts its activity on purinergic adenosine
receptors located in the AV node. Usual dosing of adenosine 6mg intravenous bolus
should be performed, followed by up to two 12mg intravenous bolus if unresponsive. Initial lower doses of adenosine 3mg intravenous bolus may be considered
when administering via a central venous catheter rather than peripheral venous
Fig. 13.8 Supraventricular tachycardia
13 Cardiac Arrhythmias
343
catheters [41, 42]. Adenosine administration is usually recommended to be given
through a two-syringe system or stopcock system to administer a 0.9% sodium
chloride ush solution following adenosine. However, some observational data suggests that adenosine 6mg may be diluted in 18 milliliters (mL) of 0.9% sodium
chloride solution (20mL total) and pushed via intravenous bolus using a singlesyringe administration method [43]. For narrow QRS complex tachycardia,
β-blockers or non-DH CCB may be considered. However, for wide QRS complex
tachycardia, procainamide, amiodarone, or sotalol should be considered [38]. You
may still use adenosine in wide QRS complex tachycardia as long as the rhythm is
regular and monomorphic. For WPW syndrome, preferred agents are ibutilide or
procainamide. Adenosine, β-blockers, non-DHP CCB, digoxin, and amiodarone
should be avoided as they may accelerate antegrade conduction down the accessory
pathway and increase ventricular rate in patients leading to serious ventricular
arrhythmias. Prevention of SVT recurrence may include performing catheter ablation if the patient is considered a good candidate or using rate/rhythm-controlling
strategies similar to those seen in the management of atrial brillation. Goals of
therapy include terminating SVT and restoring NSR, preventing the recurrence of
SVT, and avoiding adverse effects from medication therapies.
13.3 Ventricular Arrhythmias
Ventricular arrhythmias (VAs) are dened as any abnormal rhythm originating from
below the AV node. All ventricular arrhythmias are characterized by a wide QRS
complex, greater than or equal to 120ms in duration, and often require immediate
intervention. It is one of the leading causes of sudden cardiac death (SCD) and is
estimated to account for 30–75% of all out-of-hospital cardiac arrests [44]. In the
United States, around 300,000 deaths annually from SCD are caused by VA [45].
The prognosis is poor as signicant anoxic brain injury is often seen in patients with
prolonged downtime resulting in lack of oxygenation and perfusion to the brain. In
the setting of hemodynamic instability and cardiac arrest, the American Heart
Association Advanced Cardiac Life Support (ACLS) algorithm for pulseless ventricular tachycardia and ventricular brillation should be initiated and followed.
Treatments for non-pulseless ventricular tachycardia and ventricular brillation will
be discussed later in this section.
Electrical reentry is the most common mechanism for VA in patients with structural heart disease due to the cardiac remodeling that results from myocardial scar
tissue. Other mechanisms include enhanced automaticity between the Purkinje
bers and myocytes in the ventricles that occurs often around the area of ischemic
damage as well as triggered activity from delayed afterdepolarizations of the action
potential [44]. Conversely, early afterdepolarization (EAD) is the most common
mechanism for torsades de pointes [46]. Some VAs, such as premature ventricular
complexes and non-sustained ventricular tachycardias, can be asymptomatic and
self-limiting. But if symptoms are present, they can range widely in severity, from