In an instant, your body betrays you. You feel you are floating, but you are dropping, powerless, to the ground. That’s how Mrs. Moy, in vehement Cantonese, described the most unsettling sensation of her life. Now, hooked up to cardiac, blood pressure, and oxygenation monitors, with an external pacemaker’s oversize pads gummed to her chest, she felt safe. But she refused to sit up, much less walk.
"No, no," she gestured. "Dizzy . . . so dizzy."
She had been sent from her cardiologist’s office, the first stop after a fainting episode at home. His note read, "67 y.o. with syncope and bradycardia. Diagnosis: Sick sinus syndrome. Admit for pacemaker insertion." Syncope means faint and bradycardia means slow heart rate. Sick sinus syndrome is a grab-all diagnosis that implies the heart’s own pacemaker, a nubbin of cells in the right atrium called the sinus node, can’t keep time because of disease or old age.
But this is the United States in the late 1990s, where bradycardia is more likely to be inflicted by a doctor than nature. Drug companies have unleashed a swarm of cardiovascular drugs, each one touted better and more potent than the last. My emergency room at New York University Downtown Hospital sees medication-induced bradycardia so often that young doctors in training aren’t allowed to think the words sick sinus syndrome until they first hunt down every drug a patient is taking.
On the overhead monitor, Mrs. Moy’s heartbeat trudged along in the mid-30s; 60 to 100 is normal. Her P-waves, the small blips made when the sinus node fires, had disappeared; a natural backup pacemaker, nestled at the junction of the atria and the ventricles, had taken over. But when this backup timer takes over, the rate is slow and fixed; it won’t speed up to compensate for low blood pressure. And Mrs. Moy’s was now ominously low.
