Sick Sinus Syndrome

Description

Sick sinus syndrome (SSS) is characterized by abnormalities in the generation of cardiac impulses from the sinoatrial node (SAN).
- Sinus bradycardia
- Sinus arrest
- Sinus exit block
- SA and AV conduction disturbances
- Chronic atrial tachyarrhythmias
- Alternating episodes of atrial bradyarrhythmias and tachyarrhythmias (tachy-brady syndrome).
SSS is categorized into etiologies that are intrinsic or extrinsic to the SAN.

Epidemiology

Incidence

Overall incidence has not been quantified
Accounts for at least 50% permanent pacemaker placement in the US.

Prevalence

Increases with age (mean age = 68 years)
Occurs equally in both genders and without predominance in any one race

Morbidity

Its association with advanced cardiovascular (CV) disease may carry a variety of coexisting conditions.
Associated with thromboembolism and/or stroke; chronic atrial fibrillation (a-fib), AV block; and complications of therapeutic anticoagulation

Mortality

Increased risk of sudden cardiac death
Following permanent pacemaker placement, 1–year mortality is 5–10% and 5–year mortality is 25–30%. This is, in part, attributable to comorbid CV disease.
Ventricular pacing is associated with higher mortality than atrial pacing alone.
Pacemakers in patients with tachy-brady syndrome have been shown to ameliorate symptoms of bradycardia and frequency of a-fib, but not improve survival.
Patients with only bradycardia have a better prognosis; their mortality is similar to that of the general population (1).

Etiology/Risk Factors

Intrinsic etiologies – Most commonly caused by fibrosis of nodal tissue
- Idiopathic (most common cause)
- Cardiac: Chronic ischemia, infarction, myocarditis, pericarditis, cardiomyopathy
- Autoimmune: Amyloid, sarcoid, SLE
- Genetic: Familial SAN disorders, Friedreich's ataxia, hemochromatosis
- Infectious: Chagas, diphtheria, rheumatic disease
- Neoplasm: Leukemia, metastatic disease
- Pediatric: Congenital abnormalities
Extrinsic etiologies
- Iatrogenic: Digitalis, calcium channel blockers, beta-blockers, sympatholytics, antiarrhythmics
- Hypoxia
- Electrolyte imbalance: Hyper/hypokalemia, hypoglycemia
- Hyper/hypothyroid

Physiology/Pathophysiology

Idiopathic fibrosis of the SAN is the most longstanding hypothesis; however, other general mechanisms have been proposed and researched primarily in animal models. Intrinsic dysfunction is the result of failure to generate a sinus impulse and/or diminished travel of an impulse to surrounding myocardium.
Age-related remodeling of the cardiac extracellular matrix can affect cellular ionic currents and channels.
Familial condition has been linked to genetic mutations in genes that encode ion channels, such as the Na⁺ channel (SCN5A), funny current (HCN4), and Ca²⁺ channel = (CASQ2).
Acute inferior wall myocardial ischemia/infarction is associated with a transient alteration of neurologic rhythm control.
Heart failure has demonstrated down regulation of funny current channels.
Extreme physical conditioning can result in intrinsic changes to the SAN and the cardiac conduction system from dilation and hypertrophy (2).

Anesthetic GOALS/GUIDING Principles

Medical therapies and coexisting medical conditions should be optimized.
Device interrogation and appropriate preoperative reprogramming should be performed.
The anesthetic plan should aim for hemodynamic stability, rate control, and adequate ventricular filling/ejection.
Preoperative therapeutic anticoagulation must be optimized. Chronic anticoagulation is recommended in tachy-brady syndrome and chronic atrial fibrillation. Preoperative therapeutic anticoagulation must be optimized.

Diagnosis ⬆ ⬇

Symptoms

Syncope, dizziness, or lightheadedness
Palpitations
Fatigue, poor exercise tolerance
Dyspnea, orthopnea

History

History of dysfunction and type
Coexisting conditions and risk factors
- CAD is common
Functional status

Signs/Physical Exam

CV exam
- Irregular rhythm on auscultation or palpation of pulses, bradycardia/tachycardia, JVD, orthostatic hypotension
- Carotid massage: A sinus pause >3 seconds should elicit concern for SSS.
- A Valsalva maneuver will not cause an increase in the HR (3)
Extremities
- Cyanosis: Thromboembolism
- Edema from congestive heart failure
Neurologic
- Focal deficits: Stroke

Treatment History

Permanent pacemaker +/– defibrillator placement. Patients with any form of tachycardia-related SSS may require rate control with beta-blockers and appropriate prevention of bradycardia with pacing.

Medications

Medical treatment is utilized in accordance with specific symptoms or rhythm disturbance.
- Warfarin therapy particularly in tachy-brady syndrome
- Negative chronotropic medications (beta-blockers, calcium channel blockers, digitalis) may be used in select patients with a tachycardic component, but may cause excess bradycardia, block or arrest and should be used judiciously as chronic treatment. Pacemaker placement may aid with maximizing therapy.
- Rhythm conversions with procainamide or quinidine are uncommon and unpredictable.
- Theophylline therapy may be employed with dual-chamber pacing (1,3).

Diagnostic Tests & Interpretation

Labs/Studies

Electrolytes, INR, PTT
EKG: May demonstrate pacing or a variety of manifestations in untreated patients
Cardiac enzymes in the setting of recent onset arrhythmias
Pacemaker device interrogation. The type, setting, and manufacturer of the pacemaker should always be determined. Device interrogation may be appropriate if not performed recently or there are concerns of malfunction based on the patient's symptoms.
Preoperative consultation with cardiology/EP care team does not typically require a full workup, provided that the patient is regularly followed in clinic.

CONCOMITANT ORGAN DYSFUNCTION

CV (as described above)
Neurologic: Focal deficits as well as generalized CNS deficits related to cerebral hypoperfusion
GI and renal dysfunction also as a result of organ hypoperfusion

Classifications

Generally SSS is classified by the distinct rhythm and or rate disturbance that is specific to each patient's condition.
Intrinsic versus extrinsic causes (4)

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Implanted pacemakers allow for rate control with beta-blockers and Ca⁺ channel blockers in the case of tachyarrhythmias. If a pacemaker device is not present, these medications may exacerbate the underlying conduction disturbance and should be utilized cautiously. Similar disturbances may result from sympatholytic medications such as clonidine or methyldopa (1,5).

INTRAOPERATIVE CARE

Choice of Anesthesia

Dictated by the procedure and comorbidities, with consideration given to sympatholytic activity or effect that may uncover or worsen bradycardias.
Regional and neuraxial methods may be contraindicated in the setting of anticoagulation therapy.
- Neuraxial techniques may blunt the cardioaccelerator fibers (T1–T4).

Monitors

Standard ASA monitors with EKG
Noninvasive BP monitor may be acceptable in hemodynamically stable patients, but the threshold for arterial catheter placement should be lowered.
Central venous line and transesophageal echocardiography may also be considered

Induction/Airway Management

No specific induction agents/methods have been established. The sympatholytic effects of induction agents can produce transient or sustained bradyarrhythmias (5).
IV lidocaine administration may interrupt sinus node activity causing arrest or severe bradycardia (6)
Sympathetic discharge associated with laryngoscopy may elicit tachyarrhythmias in patients with tachycardia related SSS (5).
In asymptomatic patients, SSS may be unmasked and require halting the procedure pending workup.

Maintenance

General anesthesia with either IV or inhalational administration may be acceptable.
New onset bradycardia may initially be treated with beta-agonists or antimuscarinics.

Extubation/Emergence

Minimize sympathetic simulation
Balanced titration of reversal agents

Follow-Up ⬆ ⬇

Bed Acuity

Routine postoperative care in hemodynamically stable patients with uncomplicated course
Step down or ICU bed for any hemodynamic instability or new onset sinus node dysfunction

Medications/Lab Studies/Consults

Anticoagulation as indicated, beta or calcium channel blocker for control of tachyarrhythmias
Electrolytes, cardiac enzymes where indicated by new onset sinus dysfunction
Device reprogramming, cardiology/EP follow-up

Complications

Myocardial ischemia
Cardiac arrhythmias
Systemic hypoperfusion/ischemia
Thromboembolism versus bleeding

References ⬆ ⬇

Adan V , et al. Diagnosis and treatment of sick sinus syndrome. Am Fam Physician. 2003;67:1725–1732.
Monfredi O , et al. The anatomy and physiology of the sinoatrial node-a contemporary review. Pacing Clin Electrophysiol. 2010;33(11):1392–1440.
Brignole M. Sick sinus syndrome. J Clin Geriatr Med. 2002;18:211–227.
Epstein AE , et al. ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities: Executive summary: A report of the American College of Cardiology/American Heart Association Task force on Practice Guidelines. Circulation. 2008;117(21):2820–2840.
Atlee JL. Perioperative cardiac dysrhythmias. Anesthesiology. 1997;86(6):1397–1424.
Kim KO , et al. Profound bradycardia with lidocaine during anesthesia induction in a silent sick sinus syndrome patient. J Clin Anesth. 2011;23(3):227–230.

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Special Concerns for Informed Consent

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆