not well elucidated. From some studies, estradiol and progesterone are proarrhythmic. Estrogen augments the number of adrenergic receptors in the myocardium, and adrenergic responsiveness seems to be greater in pregnancy (Enriquez, 2014). Perhaps the normal but mild hypokalemia of pregnancy and/or the physiological rise in heart rate serves to induce arrhythmias. Alternatively, detection of arrhythmias may be greater because of the frequent visits typical of routine prenatal care.
Slow heart rhythms, including complete heart block, are compatible with a successful pregnancy outcome (Keepanasseril, 2015). Some women with complete heart block have syncope during labor and delivery, and occasionally temporary cardiac pacing is necessary (Hidaka, 2006). In our experiences and from others, women with permanent artificial pacemakers usually tolerate pregnancy well (Hidaka, 2011; Jafe, 1987). With ixed-rate devices, cardiac output apparently is increased by augmented stroke volume.
Patients with pacemakers or other electrical implants require special precautions during surgery. Stray current may be interpreted as an intracardiac signal by the implanted device and lead to pacing changes. In addition, myocardial burns may result from conduction of current through the pacing electrode rather than through the grounding pad (Pinski, 2002). With these devices, preventive steps include cardiology consultation; bipolar electrosurgery or Harmonic scalpel use rather than mono polar current; if needed, minimal monopolar settings; continuous cardiac and pulse oximetry monitoring; contingency plans for arrhythmias; and close proximity of electrosurgery active and return electrodes (Crossley, 2011).
The most common arrhythmia seen in reproductive-aged women is paroxysmal SVT. The prevalence during pregnancy is 24 cases per 100,000 hospital admissions, and approximately 20 percent will experience symptomatic exacerbations during pregnancy (Enriquez, 2014). Interestingly, the mean heart rate of pregnant women with paroxysmal SVT is faster compared with nonpregnant women-184 versus 166 bpm, respectively (Yu, 2015). From Hungary, BGnhidy and associates (2015) found that approximately half of women with paroxysmal SVT had an initial onset during pregnancy. Notably, maternal paroxysmal SVT was associated with a twofold greater risk of septal cardiac defects, particularly secundum atrial septal defects, in their ofspring.
In contrast, rarely do atrial ibrilation and atrial lutter present for the irst time during pregnancy. Indeed, new-onset atrial ibrillation should prompt a search for underlying etiologies that include cardiac anomalies, hyperthyroidism, pulmonary embolism, drug toxicity, and electrolyte disturbances (DiCarloMeacham, 2011). Major complications include embolic stroke, and when associated with mitral stenosis, pulmonary edema may develop in later pregnancy if the ventricular rate is increased.
For acute treatment, vagal maneuvers, which include Valsalva maneuver, carotid sinus massage, bearing down, and immersion of the face in ice water, raise vagal tone and block the atrioventricular node (Link, 2012; Page, 2015). Intravenous adenosine is a short-acting endogenous nucleotide that also blocks atrioventricular nodal conduction. Our experiences are similar to those of others in that adenosine is safe and efective for cardioversion in hemodynamically stable gravidas (Page, 2015; Robins, 2004). Transient fetal bradycardia has been described with adenosine (Dunn, 2000).