Clinical meaning
Sinus bradycardia and sinus tachycardia originate from the sinoatrial (SA) node — they represent sinus rhythm at abnormal rates. SINUS BRADYCARDIA: SA node fires at <60 bpm. The rhythm is regular with normal P waves, normal PR interval, and narrow QRS — all parameters normal except the rate. The SA node firing rate is influenced by autonomic tone: increased parasympathetic (vagal) tone slows the SA node. Causes include: physiologic (well-conditioned athletes, sleep), pharmacologic (beta-blockers, calcium channel blockers, digoxin, amiodarone), pathologic (hypothyroidism, increased intracranial pressure with Cushing's triad, inferior MI affecting SA node blood supply, hypothermia, obstructive sleep apnea, sick sinus syndrome). Clinical significance depends on symptoms — many patients tolerate rates in the 40s–50s. Symptomatic bradycardia causing hemodynamic compromise requires treatment. Sick sinus syndrome (SSS) refers to SA node dysfunction causing alternating bradycardia and tachycardia (tachy-brady syndrome), sinus pauses, or sinus arrest. SINUS TACHYCARDIA: SA node fires at >100 bpm (typically 100–160 bpm, can reach 200 in extreme exercise). It is a RESPONSE to a physiologic stimulus, not a primary arrhythmia. The rhythm is regular with normal P waves, normal PR (may shorten slightly at high rates), and narrow QRS. Causes include: physiologic (exercise, anxiety, pain), compensatory (hypovolemia, hemorrhage, dehydration, heart failure, sepsis, PE, anemia), pharmacologic (stimulants, anticholinergics, thyroid hormone excess), and pathologic (fever — HR increases ~10 bpm per 1°F above 98.6°F, hyperthyroidism, pheochromocytoma). Sinus tachycardia is never treated by targeting the heart rate — the underlying cause must be identified and addressed.