The sinoatrial node (SA) is the default pacemaker and therefore a crucial component of the hearts conduction system. It is located subepicardially and is crescent in shape. In an average adult, a sinoatrial node is 13.5 millimeters in length and is innervated by vagus and sympathetic nerves. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases it comes off the left circumflex coronary artery. Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node generating less than 60 beats per minute (bpm). Diagnosis of sinus bradycardia requires visualization of an electrocardiogram showing a normal sinus rhythm at a rate lower than 60 bpm. Where a normal sinus rhythm has the following criteria:
In clinical practice, adults over the age of 65 and young athletes of both sexes are commonly known to present with sinus bradycardia. One in 600 adults over the age of 65 has sinus node dysfunction, but more research needs to be done to collect epidemiologic data within the United States and globally for patients with sinus bradycardia.
Sinus bradycardia as any of the other bradyarrhythmias is caused by a multitude of intrinsic and extrinsic factors which may compromise the integrity of the sinus node. These factors can cause failure of the impulse formation at the sinus node, impulse conduction at the atrioventricular node or bundle of His-Purkinje fibers.
Majority of patients with sinus bradycardia do not have symptoms. Healthy young adults and athletes tend to have an increased vagal tone which keeps them in sinus bradycardia at rest. Also, patients above the age of 65 tend to have sinus bradycardia during sleep secondary to the aging of the sino-atrial node. Using history to relate to the symptoms of a patient with sinus bradycardia on an electrocardiogram is essential to come to the correct diagnosis. Those who present with symptoms may present with fatigue, exercise intolerance, lightheadedness, dizziness, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure or cognitive slowing. When taking a history a health care provider must include relevant questions which help narrow down the differential. Such as any recent medication changes, medication overdoses, chest pain, shortness of breath, history of prior myocardial infarction, symptoms of intermittent palpitations, history of chest trauma, rash or recent tick bite, current or past diagnosis of streptococcus pharyngitis, family history of sinus bradycardia, family history of muscular dystrophy. Moreover, physical exam findings should be correlated with the history given by the patient to help narrow the differential diagnosis, such as any murmur heard during the physical exam or any skin exam findings of a developing rash.
The most significant component of evaluation for a patient who presents with signs and symptoms of sinus bradycardia is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate) and an electrocardiogram. During evaluation it should be established whether the patient is hemodynamically unstable, evaluation for this includes high blood pressure, altered mental status or difficulty breathing. If the patient is healthy, athletic and has no symptoms than no further medical intervention is required. On the contrary, in older individuals, sinus bradycardia may point towards an unhealthy sinus node. Patients with congestive heart failure often have sinus bradycardia. These patients may have compromised blood supply from the right coronary artery or left circumflex artery to the sinus node secondary to some underlying ischemic heart disease.
A patient in sinus bradycardia should be evaluated for hemodynamic instability. If found to be hemodynamically unstable patient can be treated with intravenous (IV) atropine 0.5 mg push every 3 to 5 minutes up to 3 mg total. If the patient's symptoms and heart rate do not improve, the patient is a candidate for a temporary pacemaker. If the patient on arrival is hemodynamically stable but has signs and symptoms of acute myocardial infarction, they should be treated for an acute myocardial infarction appropriately. If there are no signs or symptoms of acute myocardial infarction in a hemodynamically stable patient, then workup should be initiated for an infectious etiology (including chest x-ray, blood cultures, urinary analysis, viral panel) together with thyroid function tests. If a patient is found to have an infectious etiology or a thyroid abnormality, the patient should be appropriately treated for these underlying etiologies and re-evaluated. Upon re-evaluation, if this patient is no longer symptomatic and his heart rate returns to within normal limits patient could be evaluated for a possible sick sinus syndrome or a long-term implantable loop recorder. While management decisions are being made for a patient with sinus bradycardia patient's medication list should also be reviewed for possible causes of bradycardia, and those medications should be withdrawn if possible. If a patient has comorbid conditions that require him to be on certain medications which may be causing his sinus bradycardia than in that case-patient may be a candidate for a permanent pacemaker. In cases where medication can be withdrawn than medication, withdrawal is made and if symptoms and heart rate still do not improve than the patient may be evaluated for a permanent pacemaker.
Differentiation of sinus bradycardia from other bradyarrhythmias is done by establishing a relationship between P waves and QRS complexes on an electrocardiogram. Nondiscernible P waves are associated with junctional or ventricular escape rhythms. Whereas, second or third degree AV blocks will have more than 1-to-1 relationship between P waves and QRS complexes.
Rhythms on the differentials are:
Prognosis is good when the rhythm is promptly identified by a healthcare provider.
If not identified promptly symptomatic complications such as syncope, fatigue or dizziness can occur.
Multiple resources are available for providers to help educate patients about this rhythm and its potential symptomatic complications. A patient who comes to the hospital or a clinic and has this rhythm identified should be provided with educational pamphlets if they are available at the facility.
There is a growing clinical consensus to lower the diagnosis threshold of sinus bradycardia to less than 50 bpm as there is a significant population size with a resting heart rate between 50 to 60 bpm. At present, the diagnostic consensus remains at a rate lower than 60 bpm with only the American College of Cardiology/American Heart Association/American College of Physicians–American Society of Internal Medicine (ACC/AHA/ACP–ASIM) Task Force recommending that it be diagnosed at 50 bpm.
Educating patients at risk for this rhythm and making a closed loop communication between them and their providers can help further improve the management of these rhythms.
|||Pathology of sinoatrial node. Correlations with electrocardiographic findings in 111 patients., Thery C,Gosselin B,Lekieffre J,Warembourg H,, American heart journal, 1977 Jun [PubMed PMID: 871100]|
|||Reconstruction of the human sinoatrial node., Truex RC,Smythe MQ,Taylor MJ,, The Anatomical record, 1967 Dec [PubMed PMID: 5586287]|
|||Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined., Spodick DH,, American heart journal, 1992 Oct [PubMed PMID: 1529897]|
|||ACC/AHA clinical competence statement on electrocardiography and ambulatory electrocardiography. A report of the ACC/AHA/ACP-ASIM Task Force on Clinical Competence (ACC/AHA Committee to Develop a Clinical Competence Statement on Electrocardiography and Ambulatory Electrocardiography)., Kadish AH,Buxton AE,Kennedy HL,Knight BP,Mason JW,Schuger CD,Tracy CM,Boone AW,Elnicki M,Hirshfeld JW Jr,Lorell BH,Rodgers GP,Tracy CM,Weitz HH,, Journal of the American College of Cardiology, 2001 Dec [PubMed PMID: 11738321]|
|||Cardiac involvement in the muscular dystrophies., Silvestri NJ,Ismail H,Zimetbaum P,Raynor EM,, Muscle & nerve, 2017 Nov 11 [PubMed PMID: 29130502]|
|||Friedreich's ataxia (FA) associated with diabetes mellitus type 1 and hypertrophic cardiomyopathy: analysis of a FA family., Gucev Z,Tasic V,Jancevska A,Jordanova NP,Koceva S,Kuturec M,Sabolic V,, Medicinski arhiv, 2009 [PubMed PMID: 19537671]|
|||Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel., Milanesi R,Baruscotti M,Gnecchi-Ruscone T,DiFrancesco D,, The New England journal of medicine, 2006 Jan 12 [PubMed PMID: 16407510]|
|||Cannabinoids and Symptomatic Bradycardia., Heckle MR,Nayyar M,Sinclair SE,Weber KT,, The American journal of the medical sciences, 2018 Jan [PubMed PMID: 29289259]|
|||Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia., Nof E,Luria D,Brass D,Marek D,Lahat H,Reznik-Wolf H,Pras E,Dascal N,Eldar M,Glikson M,, Circulation, 2007 Jul 31 [PubMed PMID: 17646576]|
|||Cardiac involvement in myotonic dystrophy: The role of troponins and N-terminal pro B-type natriuretic peptide., Valaperta R,De Siena C,Cardani R,Lombardia F,Cenko E,Rampoldi B,Fossati B,Brigonzi E,Rigolini R,Gaia P,Meola G,Costa E,Bugiardini R,, Atherosclerosis, 2017 Dec [PubMed PMID: 29121498]|
|||Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease., Brodsky M,Wu D,Denes P,Kanakis C,Rosen KM,, The American journal of cardiology, 1977 Mar [PubMed PMID: 65912]|
|||Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve., Sanders P,Kistler PM,Morton JB,Spence SJ,Kalman JM,, Circulation, 2004 Aug 24 [PubMed PMID: 15302799]|
|||New insights into pacemaker activity: promoting understanding of sick sinus syndrome., Dobrzynski H,Boyett MR,Anderson RH,, Circulation, 2007 Apr 10 [PubMed PMID: 17420362]|
|||Structure, function and clinical relevance of the cardiac conduction system, including the atrioventricular ring and outflow tract tissues., Dobrzynski H,Anderson RH,Atkinson A,Borbas Z,D'Souza A,Fraser JF,Inada S,Logantha SJ,Monfredi O,Morris GM,Moorman AF,Nikolaidou T,Schneider H,Szuts V,Temple IP,Yanni J,Boyett MR,, Pharmacology & therapeutics, 2013 Aug [PubMed PMID: 23612425]|
|||Survey of cardiac pacing in the United States in 1989., Bernstein AD,Parsonnet V,, The American journal of cardiology, 1992 Feb 1 [PubMed PMID: 1734644]|
|||Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care., Neumar RW,Otto CW,Link MS,Kronick SL,Shuster M,Callaway CW,Kudenchuk PJ,Ornato JP,McNally B,Silvers SM,Passman RS,White RD,Hess EP,Tang W,Davis D,Sinz E,Morrison LJ,, Circulation, 2010 Nov 2 [PubMed PMID: 20956224]|