13.3.1 Premature Ventricular Complexes

Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf

Скачиваний:

Добавлен:

30.08.2026

Размер:

48 Мб

Скачать

☆

<<< < Предыдущая 25 26 27 28 29 30 31 32 33 34 35 3637 / 5037 38 39 40 41 42 43 44 45 46 47 48 49 > Следующая >>>

344

G. J. Hu and C. O’Kane

palpitations, shortness of breath, and/or syncope, all the way to the extremes of cardiac arrest and/or death. Physical and emotional stress can also precipitate VA which will often resolve once the underlying cause is addressed and rectied. The most common etiology of VA is ischemic heart disease, specically myocardial infarction [45]. Patients with acute coronary syndromes are at risk of developing VA within the rst 48h of their infarct and are known to have poorer outcomes than those without coronary artery disease [44]. Other etiologies for ventricular arrhythmias include congenital heart disease, cardiomyopathy, electrolyte disturbances, medications that prolong the QT interval, illicit drug use, and sepsis. Idiopathic presentations of VA are generally seen in patients with no structural heart disease.

13.3.1 Premature Ventricular Complexes

Premature ventricular complexes (PVCs) present as premature heartbeats followed by a full compensatory pause on an ECG (Fig.13.9). PVCs can be seen in isolation or repetitions; depending on the pattern, they can further be characterized based on the presentation (bigeminy for every other beat, trigeminy for every third beat, etc.). PVCs that present consecutively three or more times in a series are then referred to as ventricular tachycardia.

Some risk factors for PVC include male sex, older age, hypertension, African American race, and ischemic heart disease [47]. PVCs are generally self-resolving and asymptomatic, requiring no pharmacologic treatment, especially in patients with no presence of structural heart damage or ischemia and low PVC burden. However, patients may still experience symptoms like palpitations or dyspnea, and therefore common etiologies such as stimulant ingestion or electrolyte abnormalities should be investigated. If structural damage is present and/or PVC burden is high, β-blockers are considered rst-line treatment. Non-dihydropyridines are considered in symptomatic patients with no structural heart disease and high PVC burden as well. But if symptoms persist despite initiating medical therapy, catheter ablation can be pursued. Success rates for PVC resolution with catheter ablations are relatively high, particularly for unifocal or monomorphic targets. For those who may not be good candidates for ablation or experience multifocal PVCs, antiarrhythmic medications such as ecainide, propafenone, or amiodarone can be trialed but are considered off-label uses [47, 48].

Fig. 13.9 Premature ventricular complexes

Cardiac Arrhythmias

345

13.3.2 Ventricular Tachycardia

Ventricular tachycardia (VT) is dened as three or more consecutive beats at a rate greater than 100 beats per minute and a cycle length <600ms. VT can be further classied based on duration and QRS morphology and is highlighted in Table 13.5 [44, 49–51]. Electrical storm is dened as having three or more sustained episodes of a ventricular arrhythmia or appropriate shocks from an implantable cardioverterdebrillator (ICD) within 24h. In the absence of an ICD, a VT storm can be characterized as subsequent VT recurring within 5min of the cessation of the initial episode as well as sustained and non-sustained VT resulting in more ventricular ectopic beats than sinus beats over a 24-h period [52]. Electrical storm due to ventricular brillation can occur, however, less frequently than VT. Assessment of any reversible causes, such as sepsis and/or electrolyte abnormalities, should be performed as well as interrogation of patients’ ICD, if applicable. Treatment in the setting of sustained and pulseless VT with hemodynamic compromise will require initiation of ACLS. Subsequent management or VT that is not pulseless will be addressed in the Treatment Strategies section.

Table 13.5 Ventricular tachycardia denitions

Term Denition

Sustained VT lasting ≥30s or requiring interventions within 30s of hemodynamic

Non-sustained (NSVT)

Incessant Multiple, refractory VT episodes within a 24-h period despite treatment in

Bidirectional VT with beat-to-beat alternation in the QRS frontal plan axis; most

Monomorphic Uniform and stable QRS morphology (Fig.13.9) Polymorphic Multiform and variable QRS morphology (Fig.13.10)

instability VT lasting <30s and terminates spontaneously; not associated with

hemodynamic instability

hemodynamically stable patients

associated with digoxin toxicity and catecholaminergic polymorphic ventricular tachycardia (CPVT)

Fig. 13.10 Ventricular tachycardia, monomorphic

346

G. J. Hu and C. O’Kane

13.3.2.1 Torsades de Pointes

Torsades de pointes (TdP) is a form of polymorphic VT that occurs in the setting of QT prolongation. On an ECG, it presents as a gradual change in amplitude and twisting of the QRS complexes or “twisting of the points” around the isoelectric line (Fig.13.11) [44, 46, 49]. Clinical symptoms are similar to those with VT but often lead to cardiac arrest. This long QT syndrome can be congenital or acquired, with acquired QT prolongation most often being drug induced. A list of various risk factors is given in Table13.6 [46, 53]. The risk of TdP increases signicantly when multiple QT-prolonging agents are used concurrently, and therefore, prompt discontinuation of the offending agents should be performed in addition to a hemodynamic assessment to guide subsequent management.

Regarding treatment strategies, hemodynamically unstable patients will need immediate debrillation [44]. Adjunctively, intravenous magnesium sulfate 1–2g can be given as a bolus (over 1–2min) followed by a continuous infusion to prevent recurrence; however, no benet has been shown in relation to return of spontaneous circulation (ROSC) or survival to hospital discharge [54]. In hemodynamically stable patients, magnesium can be given over 15min. It is theorized that magnesium inhibits EAD associated with TdP without shortening the QT interval; however, the exact mechanism remains unknown. Magnesium levels can be monitored with target levels ideally above >2mmol/L, but administration should occur regardless of the patient’s initial serum level. Severe magnesium toxicity can manifest as confusion, coma-like states, and even cardiac arrest; however, these are very rare presentations as magnesium has a relatively wide therapeutic threshold. A continuous infusion of isoproterenol 2–10 mcg/min may also be utilized for bradycardiaassociated and acquired TdP as it increases the heart rate while shortening the QT interval [55]. Its use is contraindicated in congenital TdP specically, as it may actually increase EAD, resulting in a further prolonged QT interval [56]. Rapid pacing through a temporary pacemaker may also be done in patients with bradycardicassociated TdP. Lastly, alkalinization with sodium bicarbonate may also be trialed, especially if patients present with TdP due to quinidine use [57]. Persistent TdP, if inadequately treated, can then quickly progress into ventricular brillation.

Fig. 13.11 Torsades de pointes, polymorphic VT with prolonged QT interval

ardiac Arrhythmias

Table 13.6 Risk factors for QT prolongation and TdP

Drug induced

Antiarrhythmics

Examples: quinidine, sotalol

Antibiotics/antifungals

Examples: voriconazole

Antidepressants

Examples:

Antiemetics

Examples: Droperidol, metoclopramide, promethazine, ondansetron

Antipsychotics

Examples: Chlorpromazine, haloperidol, olanzapine, quetiapine, risperidone, ziprasidone

Miscellaneous

Examples:

Electrolyte derangements

Examples: Hypocalcemia, h

Bradyarrhythmia

Examples: Sinus bradycardia, second- or third-de

Congenital disease

Examples: Romano-W

Coronary heart disease

Examples: Myocardial inf

Female sex Older age

Amiodarone, disopyramide, dofetilide, dronedarone, ibutilide, procainamide,

Azithromycin, clarithromycin, erythromycin, uconazole, levooxacin,

Amitriptyline, citalopram, escitalopram, sertraline, venlafaxine

Arsenic, methadone, sumatriptan, cocaine

ypokalemia, hypomagnesemia

gree AV block

ard syndrome, Jervell and Lange-Nielsen syndrome

arction, congestive heart failure

347

13.3.3 Ventricular Fibrillation

Ventricular brillation (VF) is an extremely disorganized VT with varying QRS lengths, morphology, and amplitudes and presents with a ventricular rate of more than 300 beats per minute (Fig.13.12) [44, 49]. It is one of the shockable rhythms in the ACLS algorithm and is associated with high mortality. Post-myocardial infarction, mortality was found to be signicantly higher in patients who developed early-onset VF (less than 24h) compared to those with late-onset VF [58]. VF is always sustained and life-threatening, which requires immediate debrillation and compliance with the ACLS algorithm.

13.3.4 Ventricular Arrhythmia Treatment Strategies

Acute management strategies for VA in the setting of cardiac arrest are discussed in a separate chapter. In general, proper adherence to guideline-directed ACLS therapies such as cardiopulmonary resuscitation (CPR), debrillation, and medications is crucial, with subsequent surgical interventions or revascularization procedures dependent on the underlying cause and/or presence of ischemia postarrest. The

348

Fig. 13.12 Ventricular brillation

G. J. Hu and C. O’Kane

interventions listed in this section are for patients with non-pulseless VT/VF or for secondary prevention postarrest.

13.3.4.1 ICD Implantation

For primary prevention of SCD due to life-threatening VT/VF, numerous studies have shown that ICD insertion compared to conventional medication therapies alone improved survival in patients with signicant coronary artery disease and ischemic cardiomyopathy, especially those with severe left ventricle systolic dysfunction [59–61]. Secondary prevention with ICD therapy has also shown similar mortality benets [62–64]. Therefore, the 2017 AHA/ACC/HRS Guidelines recommend ICD therapy for these select patients [44]:

1. Primary prevention in patients with ischemic heart disease:

(a) Left ventricular ejection fraction (LVEF) ≤40%, receiving guideline-

directed medical therapies, and at least 40days post-myocardial infarct and 90days post-revascularization with meaningful survival

(b) LVEF ≤30–35% with NewYork Heart Association (NYHA) classes I–III

heart failure

advanced cardiac therapies

2. Secondary prevention

(a) Patients with ischemic heart disease:

(i) Cardiac syncope and LVEF ≤35% (ii) Cardiac syncope with inducible ventricular arrhythmia during electro-

physiological studies

(iii) Resuscitated patients post-cardiac arrest or sustained spontaneous

monomorphic VT who do not need revascularization of their ischemia but are good candidates for ICD placement

(b) Patients with nonischemic cardiomyopathy:

(i) Resuscitated patients post-cardiac arrest or sustained spontaneous

monomorphic VT who are appropriate ICD candidates

(ii) LVEF ≤35% and NYHA classes II–III heart failure

13 Cardiac Arrhythmias

349

Other high-risk conditions such as hypertrophic cardiomyopathy, cardiac sarcoidosis, Brugada syndrome, and long QT syndrome may also warrant ICD therapy. It is always important to evaluate for any reversible causes for VT/VF, as these would preclude patients from ICD placement. Other contraindications to therapy include meaningful survival time of less than a year and patients with NYHA class IV heart failure who are not candidates for advanced therapies such as transplantation or mechanical circulatory devices.

13.3.4.2 Pharmacologic Treatments

There are numerous antiarrhythmic agents that can be used to control ventricular arrhythmias, which are listed in Table 13.7. β-Blockers are considered rst-line agents in VA and provide mortality benet in structural heart disease states such as myocardial infarction and systolic heart failure. β-Blockers such as nadolol and propranolol can also be initiated in patients with long QT syndrome. Sodium channel blockers are not typically utilized in VT since specic agents such as propafenone and ecainide have shown increased mortality risk in patients with structural heart disease. However, patients with structural heart disease who present with monomorphic VT and are hemodynamically stable may sometimes receive procainamide as superior outcomes were shown with its use over amiodarone and lidocaine [65, 66]. In the setting of cardiac arrest, both amiodarone and lidocaine can be utilized in pulseless VT/VF. Other specic arrhythmias such as congenital long QT syndrome and Brugada syndrome may also utilize agents with sodium channel blockade like mexiletine and quinidine, respectively [44]. Amiodarone and sotalol may also be trialed in patients with ischemic heart disease presenting with refractory VA due to increased success rates of VT termination, but patient-specic factors, such as having a severely reduced EF (<20%) and/or prolonged QTc interval, may preclude its use. Lastly, non-dihydropyridine calcium channel blockers are only initiated for the treatment of idiopathic interfascicular reentrant left VT. Otherwise, this antiarrhythmic class should not be given for VT management, especially in the setting of systolic heart failure.

13.3.4.3 Catheter Ablation

Catheter ablations can be done for both atrial arrhythmias and ventricular arrhythmias, especially for patients with symptomatic, idiopathic VT. Once cardiac mapping is performed to determine areas of highest arrhythmogenic foci, various energy sources like direct current, radiofrequency, or cryothermal can then be delivered to cardiac tissue to terminate the arrhythmia. Guidelines recommend catheter ablations as adjunctive treatments in patients with structural heart disease who have VT/ VF storm despite ICD placement and antiarrhythmic therapy because of the various positive outcomes associated such as lower rates of composite death, VT storm, and ICD shock [44, 67]. Patients with nonischemic cardiomyopathy may also receive a

350

Drug of choice for AF with RVR and WPW

Active metabolite

NAPA (metabolite) causes QTc prolongation

Accumulates in heart failure, renal dysfunction, and hepatic

dysfunction

Early signs of lidocaine toxicity are tremor or sedation

Accumulates in heart failure, renal dysfunction, and hepatic

Infusion-related

hypotension

Lupus-like reactionsVTTdP

GI distress

Bradycardia

Hypotension

G. J. Hu and C. O’Kane

dysfunction

Therapeutic monitoring may be performed in patients who are

on therapy for >24h (typically for analgesia indication):

1.5–5.0 mcg/mL (therapeutic)

Check levels 8–10h after the start of infusion, each dose

AV block

Tremors

titration, or if toxicity concern is present

Delirium

Psychosis

Seizure

GI distress

dysfunction

Tinnitus

Dyspnea/bronchospasm

See above (lidocaine) Accumulates in heart failure, renal dysfunction, and hepatic

Indications:

AF, AVRT (including WPW), VT

Loading dose (IV)

10–17mg/kg (IBW)

1000mg ONCE

Maintenance dose (IV)

1–4mg/min

Indications:

VF, VT

Loading dose (IV), ACLS (IV/IO)

1–1.5mg/kg (IBW), 0.5–0.75mg/kg as second dose; max

3mg/kg

Maintenance dose (IV): 1–4mg/min

illiams W

Vaughan-

classication Indications and dosing Adverse effects Additional comments

Sodium

channel

blockers

Drug

Table 13.7 Select antiarrhythmic drugs [69–84]

Procainamide Ia

Lidocaine Ib

Sodium

channel lockers

Ventricular arrhythmias, PVC

Maintenance dose (oral)

150–200mg every 8–12h, increase by increments of

50–100mg every 2–3days; max 1.2g/day

Mexiletine Indications:

13 Cardiac Arrhythmias

Do not use in patients with structural heart disease, prolonged

QRS, or bundle branch blocks

Should be used in combination with β-blocker or non-DH

CCB to reduce the risk for atrial utter

Dizziness

Visual disturbances

Tremor

Dyspnea

HF exacerbations

AV block

Atrial utter

See above (ecainide)

Taste disturbances

Dizziness

GI distress

Angina

HF exacerbations

AV block

Atrial utter

Titrate rate no faster than every 4min

Due to uid volume, may consider alternative therapy in HF

Hypotension

Bradycardia

Hyperkalemia

Extravasation

Fluid overload

IV to PO conversion: 1:2.5mg

Hypotension

Bradycardia

Masking hypoglycemia

None

Hypotension

Bradycardia

351

(continued)

Indications:

Vaughan-

classication Indications and dosing Adverse effects Additional comments

Williams

Drug

Flecainide Ic

AF, SVT, PVC, ventricular arrhythmias (with no

structural heart disease)

Acute cardioversion (oral)

300mg ONCE (weight≥70kg)

200mg ONCE (weight<70kg)

Maintenance dose (oral)

Sodium

channel

blockers

50mg every 12h, max 400mg/day

AF, SVT, PVC, ventricular arrhythmias (with no

structural heart disease)

Acute cardioversion (oral IR)

600mg once (weight≥70kg)

450mg once (weight<70kg)

Maintenance dose (oral)

Propafenone Indications:

IR: 150mg every 8h, max 900mg/day

ER: 225mg every 12h, max 900mg/day

Indications:

AF with RVR, SVT, VT

Loading dose (IV)

500 mcg/kg bolus

Maintenance dose (IV)

β-blockers

Esmolol II

50 mcg/kg/min continuous infusion, max 300 mcg/kg/

min

AF, SVT, NSVT

Acute rate control (IV)

IR: 2.5–5mg every 5min; max 15mg

Maintenance dose (oral)

IR: 12.5–50mg every 6–12h; max 400mg/day

ER: 50–200mg every 12–24h; max 400mg/day

AF, SVT, NSVT

Maintenance dose (oral)

3.125–25mg oral twice daily

Metoprolol Indications:

Carvedilol Indications:

352

Should reserve use for patients who cannot take alternative

antiarrhythmic therapies due to toxicities associated with

long-term use

Many drug-drug interactions due to inhibition of CYP3A4,

CYP2D6, and CYP2C9

Pulmonary brosis

Hepatotoxicity

Photosensitivity

Thyroid dysfunction

Corneal deposition

AV block

Hospital initiation required

Many drug-drug interactions via CYP3A4 and renal tubular

secretions (e.g., hydrochlorothiazide)

Headache

Dizziness

Insomnia

G. J. Hu and C. O’Kane

Avoid use in patients with prolonged QTc and discontinue

therapy if QTc >500ms

Avoid use in patients with prolonged QT intervals, HFrEF,

and those with hypokalemia and hypomagnesemia

Avoid in patients with permanent AF as many patients will

Angina

TdP

Headache

GI distress

Lupus-like reactions

revert back to AF after pharmacological cardioversion

BradycardiaVTTdP

Avoid use in patients with prolonged QT intervals, HFrEF,

and patients with permanent AF

Discontinue therapy if QTc >500ms

AV block

Pulmonary brosis

Hepatotoxicity

AV block

Hospital initiation required

Avoid use in patients with prolonged QTc and discontinue

therapy if QTc >500ms

Bradycardia

Fatigue

Dizziness

Dyspnea

AV block

HF exacerbations

Pulmonary edema

TdP

Vaughan-

classication Indications and dosing Adverse effects Additional comments

Williams

Drug

Table 13.7 (continued)

Indications:

AF, SVT, PVC, VT, VF

ACLS (IV, IO)

300mg bolus, followed by 150mg for second dose, if

needed

Loading dose (IV, oral)

IV: 150mg bolus, then 1mg/min for 6h, then 0.5mg/

min

Potassium

channel

blockers

Amiodarone III

Oral: 400mg every 8–12h

(target loading dose—6–10g)

Maintenance dose (oral)

200–400mg daily

AF, SVT

Maintenance dose (oral)

Dofetilide Indications:

500mg every 12h

*Dose adjust based on renal function

Loading dose (IV)

0.01mg/kg (weight<60kg)

1mg (weight≥60kg)

Ibutilide Indications:

Dronedarone Indications:

Maintenance dose (oral)

400mg every 12h

AF, SVT, VT

Maintenance dose (oral)

Sotalol Indications:

80mg twice daily; max 320mg/day*

13 Cardiac Arrhythmias

Conversion IV to PO:

5mg/h=180mg/day

10mg/h=200–260mg/day

15mg/h=480mg/day

Hypotension

Bradycardia

Peripheral edema

Acute decompensated HF

None

Hypotension

Bradycardia

Peripheral edema

Acute decompensated HF

Useful in patients with hypotension since it is

hemodynamically neutral

Less effective in patients with sepsis or increased sympathetic

tone

Therapeutic drug monitoring—Digoxin concentrations

0.5–1.2ng/mL considered therapeutic for AF

GI distressVTAnorexia

Altered mentation

AV block

Yellow-colored vision

353

Indications:

Williams

Vaughan-

classication Indications and dosing Adverse effects Additional comments

Drug

Diltiazem IV

AF, SVT, NSVT

Loading dose (IV)

0.25mg/kg bolus (may repeat 0.35mg/kg bolus after

15min)

Maintenance dose (IV, oral)

IV: 5–15mg/h continuous infusion

Oral (IR): 30–60mg every 6h

Oral (ER): 120–480mg every 12–24h

AF, SVT, NSVT

Loading dose (IV)

0.075–0.15mg/kg IV bolus over 2min, may give an

additional 10mg after 30min if no response

Maintenance dose (IV, oral)

IV: 0.005mg/kg/min continuous infusion

Calcium

channel

blockers

Verapamil Indications:

Oral (ER): 180–480mg daily

AF, SVT

Loading dose (IV, oral)

8–12 mcg/kg (IBW) given as 50% total dose followed by

25% total dose every 6h for 2 doses

Maintenance dose (oral)

Oral: 62.5–250 mcg daily

Digoxin Miscellaneous Indications:

premature ventricular contractions, RVR rapid ventricular response, TdP torsade de pointes, VF ventricular brillation, VT ventricular tachycardia, WPW Wolff-

AFatrial brillation, AVRT atrioventricular reentry tachycardia, AV atrioventricular, GI gastrointestinal, HF heart failure, HFrEF heart failure with reduced

ejection fraction, IBW ideal body weight, IO intraosseous, NA PA -acetylprocainamide, Non-DHP CCB non-dihydropyridine calcium channel blocker, PVC

Parkinson- White *Dose adjust based on renal function

<<< < Предыдущая 25 26 27 28 29 30 31 32 33 34 35 3637 / 5037 38 39 40 41 42 43 44 45 46 47 48 49 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
30.08.202652 Мб0Книга_5847_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202650 Мб0Книга_5848_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202649 Мб0Книга_5849_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202675 Мб0Книга_585_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202649 Мб0Книга_5850_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202648 Мб0Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202647 Мб0Книга_5852_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202646 Мб0Книга_5853_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202645 Мб0Книга_5854_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202645 Мб0Книга_5855_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202644 Мб0Книга_5856_Библиотеки_им_академика_М_И_Перельмана.pdf