Bradycardia is a condition where your heart beats fewer than 60 times per minute, which is unusually slow. This condition may be dangerous if it keeps your heart from pumping enough blood to meet your body's needs. However, bradycardia can also happen without causing any harmful effects, especially in very physically active people.
Sinus rhythm is when your heart is beating regularly and normally. Sinus bradycardia means that your heart is beating regularly, but slower than normal. Sinus bradycardia is usually a benign arrhythmia (especially in very active people). That means while it's slower than expected, it also isn't harmful.
While bradycardia is a medical condition on its own, it often happens along with or because of other conditions. In those cases, bradycardia is often treated more like a symptom than a separate condition.
Other tests are possible if you have bradycardia, but many of these are only necessary if healthcare providers suspect you have another condition or problem. Your healthcare provider is the best person to explain the additional tests they recommend running and why.
If bradycardia is causing significant problems such as dangerously low blood pressure, an intravenous (IV) or injectable medication such as atropine can cause your heart to beat faster. Treatments like this are usually hospital-specific because people receiving these medications may need monitoring and additional care.
This involves a device with electrical contacts that touch or attach to the skin of your chest. These contacts allow a mild electrical current to enter your body and cause your heart to beat. For people who need a permanent pacemaker or whose bradycardia will likely be short-lived, temporary cardiac pacing is an effective short-term treatment.
If you receive treatment for bradycardia, you should begin to feel better as that treatment happens. Many medications that treat this condition start to work quickly (especially IV medications). If you need a pacemaker, your symptoms should get better immediately after surgery, and you should feel better overall as you recover from the procedure.
For many people, preventing bradycardia isn't possible. This is especially true when it comes to bradycardia which happens because you're in very good physical shape or bradycardia which happens naturally as you age.
Physiologically, heart rate can vary in normal adults from 40 bpm up to 180 bpm. However, a relative bradycardia may be greater than 60 bpm if that rate is too slow for the haemodynamic requirements of the patient.
It is impossible to give meaningful figures on incidence and prevalence. In most young people bradycardia is physiological and represents athletic training. The incidence of pathological bradycardia rises with age as the underlying causes become more frequent.
Bradycardia may be asymptomatic but can present with syncope, fatigue or dizziness. Ischaemic chest pain, Stokes-Adams attacks, hypoxic seizures, congestive heart failure, cardiovascular collapse and sudden cardiac death may occur, depending on the underlying cause of bradycardia.
In view of the overlap of low heart rates for pathological and physiological causes, assessment of symptoms is a critical component in the evaluation and management of bradycardia. Treatment should rarely be prescribed solely on the basis of a heart rate lower than an arbitrary cutoff or a pause above a certain duration.
The cardiovascular responses to tracheal suction were observed in 4 consecutive recently-injured tetraplegics with physiologically complete cervical spinal cord transections (C3-5) who were in spinal shock and needed artificial ventilation. In all 4 patients tracheal suction induced bradycardia and in 2 patients even cardiac arrest. The bradycardia occurred when the patients were hypoxic, and was prevented by the addition of oxygen to inspired air, or, if this was inadequate, by the administration of atropine. Two of the patients were agains studied several months later, after return of isolated spinal cord activity and spontaneous breathing. In both patients tracheal suction then caused tachycardia and increased respiratory effort. It is concluded that: 1. Tetraplegics with high cervical spinal cord transections who are in spinal shock and unable to breathe spontaneously are prone to bradycardia and cardiac arrest during tracheal suction. This is more likely to occur when they are hypoxic. 2. The bradycardia appears to be due to a vago-vagal reflex for both afferent and efferent limbs of the arc are in the vagus nerve. A number of factors play a part, including (I) absent sympathetic activity; (II) airway receptor stimulation; (III) hypoxia and (IV) the inability to breathe spontaneously (The pulmonary (inflation) vagal reflex which would normally oppose the cardio-inhibition caused by (II) and (III) is absent). 3. The bradycardia in response to tracheal suction can be prevented by adequate oxygenation, or if this cannot be achieved, by repeated atropine.
SARS COV-2 infection has become a global threat. Cardiovascular manifestations associated with Covid-19 have been noted in several publications, and bradycardia related to Covid-19 is a commonly reported complication. This study reports six serial cases of bradycardia attributable to Covid-19; four of them developed complete atrioventricular block. These patients experienced clinical symptoms related to bradycardia and initially required permanent pacemaker implantation. However, one patient did not require permanent pacing later on due to spontaneous conversion to sinus rhythm. In comparison, the other two patients who developed transient sinus bradycardia experienced a self-limiting condition during their hospitalization period without requiring any cardiac pacing device or medication to increase heart rate. Complete atrioventricular block and transient sinus bradycardia in these patients, despite not having any history of bradycardia, might be due to complex processes in the systemic inflammatory response in Covid-19. Cardiac monitoring, hemodynamic evaluation, and strategy for permanent pacemaker in these patients should be treated on a case-by-case basis.
Results: Downloaded saturation and pulse rate data were available for a median of 68.3 days (interquartile range, 56.8-86.0 days). Mean percentages of recorded time with hypoxemia for the least and most affected 10% of infants were 0.4% and 13.5%, respectively. Corresponding values for bradycardia were 0.1% and 0.3%. The primary outcome was ascertained for 972 infants and present in 414 (42.6%). Hypoxemic episodes were associated with an estimated increased risk of late death or disability at 18 months of 56.5% in the highest decile of hypoxemic exposure vs 36.9% in the lowest decile (modeled relative risk, 1.53; 95% CI, 1.21-1.94). This association was significant only for prolonged hypoxemic episodes lasting at least 1 minute (relative risk, 1.66; 95% CI, 1.35-2.05 vs for shorter episodes, relative risk, 1.01; 95% CI, 0.77-1.32). Relative risks for all secondary outcomes were similarly increased after prolonged hypoxemia. Bradycardia did not alter the prognostic value of hypoxemia.
Objectives: This study sought to determine if anatomic atrial ganglionated plexus (GP) ablation leads to long-term sinus rate (SR) increase and improves quality of life in patients with symptomatic sinus bradycardia (SB).
processing.... Drugs & Diseases > Emergency Medicine Sinus Bradycardia Updated: Dec 27, 2017 Author: Mark W Livingston, MD; Chief Editor: Erik D Schraga, MD more...
Share Print Feedback Close Facebook Twitter LinkedIn WhatsApp Email webmd.ads2.defineAd(id: 'ads-pos-421-sfp',pos: 421); Sections Sinus Bradycardia Sections Sinus Bradycardia Overview Background
Pathophysiology Etiology Prognosis Show All Presentation History
Physical Examination Show All DDx Workup Laboratory Studies
Imaging Studies Show All Treatment Prehospital Care
Emergency Department Care Long-Term Monitoring Show All Medication Medication Summary
Anticholinergics Show All Questions & Answers References Overview Background Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats per minute or less. However, few patients actually become symptomatic until their heart rate drops to less than 50 beats per minute. The action potential responsible for this rhythm arises from the sinus node and causes a P wave on the surface ECG that is normal in terms of both amplitude and vector. The presence of sinus bradycardia in itself does not cause a change in the QRS complex and T wave.
The frequency of sinus bradycardia is unknown, given that most cases represent normal variants. Although the frequency of sick sinus syndrome is unknown in the general population, in cardiac patients it has been estimated to be 3 in 5000.
The pathophysiology of sinus bradycardia is dependent on the underlying cause.  Commonly, sinus bradycardia is an incidental finding in otherwise healthy individuals, particularly in young adults, athletes or sleeping patients.  Other causes of sinus bradycardia are related to increased vagal tone.
Physiologic causes of increased vagal tone include the bradycardia seen in athletes. Pathologic causes include, but are not limited to, inferior wall myocardial infarction, toxic or environmental exposure, electrolyte disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased intracranial pressure.
Sinus bradycardia may also be caused by the sick sinus syndrome,  which involves a dysfunction in the ability of the sinus node to generate or transmit an action potential to the atria. Sick sinus syndrome includes a variety of disorders and pathologic processes that are grouped within one loosely defined clinical syndrome. The syndrome includes signs and symptoms related to cerebral hypoperfusion in association with sinus bradycardia, sinus arrest, sinoatrial (SA) block, carotid hypersensitivity, or alternating episodes of bradycardia and tachycardia. 041b061a72