A 68-year-old woman is admitted to the neurologic intensive care unit (NeuroICU) after a fall that led to a subdural hematoma. Past medical history is remarkable for hypothyroidism, hypertension, and hyperlipidemia. Admission medications include levothyroxine, 75 μg daily; carvedilol, 6.25 mg twice daily; and aspirin, 81 mg daily. Vital signs on arrival include a heart rate of 30 bpm (beats per minute), blood pressure of 68/30 mm Hg, temperature of 98°F, respiratory rate of 18 per minute, and a pulse oximetry of 96% on room air. Physical examination reveals an elderly woman of average build who is mildly dyspneic and slow to respond to questions. Cardiac examination is remarkable for bradycardic S1 and S2 without any murmurs, rubs, or gallops. Lung examination reveals normal breath sounds with no rales or rhonchi. Extremities are cold to touch. Neurologic examination reveals no focal deficits.
This ECG demonstrates sinus bradycardia (Figure 36-1). The human heart usually beats between 60 and 100 bpm. Bradycardia is defined as a heart rate of less than 60 bpm. The sinoatrial node is usually the origin of electrical impulse, which then spreads to the rest of the heart through specialized conducting tissue including the atrioventricular node, His bundle, Bundle branches (right and left bundle) and the Purkinje network (Figure 36-2). The aforementioned tissues are all capable of generating electrical impulses independently but are usually suppressed by the higher rate of electrical firing by the sinus node which is the dominant pacemaker in the heart in normal conditions. Dysfunction of the sinus node or block in any part of the conducting tissue can lead to bradycardia.
Initial ECG of a 68-year-old woman after admission to the NeuroICU after a fall.
The conducting system of the heart.
What are the noncardiac causes of sinus bradycardia?
Bradycardia may be due to cardiac or noncardiac causes. Differentiating between the two is critical for proper management. Asymptomatic bradycardia generally requires no treatment. Well-trained athletes frequently have heart rates in the upper 30s. During sleep the heart rate can go down to the 30s, but pauses of more than 3 seconds or a heart rate in the 30s while awake are pathological. Similarly, drugs like β-blockers and calcium channel blockers can lead to marked bradycardia, necessitating withdrawal of these agents. In the NeuroICU any condition that leads to high intracranial pressure can trigger Cushing’s reflex, resulting in bradycardia, increased blood pressure, and irregular breathing. Hypothyroidism, hypoxia, hypothermia, metabolic acidosis, and hyperkalemia are other well-known causes of bradycardia due to noncardiac causes. Pain, vomiting, or spinal injuries can also cause high vagal tone, leading to bradycardia.