INTRODUCTION
Arrhythmias are a common issue in pregnancy presenting both in women with a structurally normal as well as abnormal heart, with or without arrhythmias that preexisted and including those with congenital heart diseases.[123] Women with congenital heart disease, structural heart disease, and preexisting arrhythmias are at the highest risk of developing the same.[123] They may, however, present with such symptoms and signs for the first time in pregnancy.[2]
Several hemodynamic changes occur during normal pregnancy, including an increase in blood volume and cardiac output, decreased systemic vascular resistance (SVR), and blood pressure. There is an increase in heart rate (HR) by 25% due to increased adrenergic activity. Preload increases as a result of increased circulating volume and afterload decreases due to decreased SVR.[4] All these factors increase cardiac output. Hormonal changes include increased estrogen, beta-human chorionic gonadotropin, and adrenergic activity. Autonomic activity, mostly sympathetic activity, increases.
The exact etiology of arrhythmias that occur in pregnancy is unclear, but hormonal, hemodynamic, and autonomic changes are postulated to play a part.[4] Increased intravascular volume increases preload stretching cardiac chambers, thereby activating stretch-activated channels resulting in membrane depolarization, shortened refractory period, slowed conduction, and a mismatch of depolarization and refractoriness.[5] There is also an increase in adrenergic activity and autonomic stimuli that are proarrhythmic in nature.
Women suspected of arrhythmias present most often with palpitations, dizziness, and syncope and less often breathlessness or chest pain. Others are detected during evaluation of a murmur. Sudden cardiac death is very rare. The investigation of such a pregnant woman for a possible arrhythmia is the same as in the nonpregnant woman. A thorough history and clinical examination are nevertheless always essential. Laboratory investigations including full blood count, coagulation, electrolytes, glucose, thyroid function tests, Electrocardiogram (ECG), and an Echocardiogram (two-dimensional [2D] echo) to detect underlying structural heart disease should be performed. Holter monitoring may also be beneficial but has a low yield, whereas stress testing runs the risk of fetal bradycardia.[5]
The electrocardiogram (ECG) represents graphically the electrical activity of the heart recorded from the surface. ECG is no doubted the technique of choice in the study of patients with chest pain, syncope, palpitations, and acute dyspnea and is crucial for the diagnosis of cardiac arrhythmias, conduction disturbances, preexcitation syndromes, and channelopathies. It is also very important for assessing the evolution and response to treatment of all types of heart diseases and other diseases and different situations such as electrolytic disorders, drug administration, athletes, and surgical evaluation.[6]
During pregnancy, about 4%–14% of women develop nonspecific ST-segment and T-wave changes that are most commonly seen in the left precordial leads, which typically resolve after delivery. These changes often recur with subsequent pregnancies. With the increased HR of pregnancy, the PR and QT intervals shorten.[7] There may also be a slight leftward or rightward axis deviation due to rotation of the heart from elevation of the diaphragm and/or the gravid uterus. Stretch of the chambers, particularly the left atrium, produces cardiac conduction abnormalities. Supraventricular tachycardias and ventricular extrasystoles are common. T-wave inversion and Q-waves may occur inferiorly.[7]
As arrhythmias in pregnancy are common and may cause concern for the well-being of both the mother and the fetus, understanding the physiologic changes and the types of arrhythmias that occur during pregnancy can help the practitioner identify when further interventions are necessary. The present study was thus conducted to determine electrocardiography changes and cardiac arrhythmias in normal pregnancy.
MATERIALS AND METHODS
A hospital-based prospective observational study was conducted at the department of medicine of a tertiary care hospital from December 2015 to September 2017. Pregnant Women aged 20-25 years in early pregnancy, irrespective of the parity, attending the antenatal clinic of the tertiary care hospital comprised the study group.
Pregnant women with cardiovascular disease, metabolic disease like diabetes, renal disease, thyrotoxicosis, history suggestive of any congenital heart disease, valvular heart disease, sickle cell disease, anemia with a packed cell volume <0.3, prepregnancy hypertension, and diseases with any other chronic medication or any other condition likely to affect the cardiovascular system, and hence, ECG was also excluded [Flow Chart 1]. Twin pregnancies detected in the first trimester USG were excluded as their hemodynamic status would be different.
Sample size
We consecutively enrolled 590 cases coming to our hospital during the study period fulfilling eligibility criteria. After applying inclusion and exclusion criteria, the final sample came as 450.
METHODOLOGY
All patients fulfilling the inclusion criterion were interviewed for symptoms suggesting preexisting cardiovascular disease. All these patients underwent thorough clinical examination and a baseline 12-lead electrocardiogram which was recorded on Schiller Cardiovit AT-102 plus machine at the first visit after giving 5 min of rest. All the patients also underwent echocardiogram using Siemens Acuson SC2000 machine to exclude preexisting structural heart disease and left ventricular dysfunction. All the standard echocardiographic views were performed and documented as per preformed pro forma. At each interview, a complete physical examination was carried out to rule out heart disease.
The women without any clinical or echocardiographic evidence of heart disease with a baseline normal ECG of the first trimester of pregnancy were thus included. These women were followed up closely and reviewed with a repeat ECG in the second (24 weeks) and third (32 weeks) trimesters along with 24 h Holter studies using Mortara during 20–24 weeks of gestation.
Repeat 2D echo was done after 32 weeks to assess for left ventricular dysfunction. The first ECG findings after detection of pregnancy or any prepregnancy ECG (if available) were taken as the baseline ECG for future comparison. The ECG was analyzed, and various axes, intervals, and segments were recorded as per planned pro forma. Therefore, three ECGs, in each trimester, followed by 2D echo in the first and last trimesters and a second trimester Holter, were carried out for each patient.
Statistical analysis
Data were analyzed using Statistical Package for the Social Sciences. Appropriate statistical tests were used to determine the significance of the results as per type and distribution of data.
RESULTS
Most of the participants in our study group were between 21 and 30 years of age (83.3%). Out of the total 450 females, 35.8% were primipara, whereas 64.2% were multipara. The mean HR was 86.53/min at the time of enrollment which increased to 95.72/min at 22–24 weeks and to 100.54/min at 32 weeks. The rate of increasing HR was statistically significant [Figure 1].
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Figure 1: Mean comparison of heart rate
All the ECG parameters were compared between observations made at the time of enrollment, at 22–24 weeks, and at 32 weeks. No difference was observed between P-axis wave and PR interval. P-duration was significantly less at the second term in comparison to the third term and at the time of enrollment. QRS axis decreased significantly from 35.67 at the time of enrollment to 26.99 at 22–24 week. QRS duration decreased from 82.76 ms at the time of enrollment to 81.44 ms at 22–24 weeks, but the difference was statistically nonsignificant (P = 0.055). QTc interval increased significantly during the course of pregnancy from enrollment to 22–24 weeks to 32 weeks (417.3 vs. 424.6 vs. 430.35; P < 0.01) [Table 1].
Table 1: Mean comparison of electrocardiograph parameters
No ST/T-wave changes were seen in any of the cases at the time of enrollment, whereas during the ECG monitoring at 22–24 weeks and at 32 weeks, T-wave inversion in one of the leads was observed in 8.2% of females. The most common leads involved were LIII (30/37 cases) and V1–V2 (10/37 cases) [Figure 2].
Figure 2: Prevalence of T-wave changes
At the time of enrollment, none of the females had any rhythm disturbances, whereas by 22–24 weeks, 2.67% of females developed rhythm disturbances which increased to 2.9% at 32 weeks. The most common rhythm disturbance was ventricular premature contractions (1.8%), followed by atrial fibrillation (AF, 0.7%) [Table 2]. A significant association was seen between rhythm disturbances with advancing age and development of pregnancy-induced hypertension (PIH) (P < 0.05). All the cases of AF (3/3) and 5 out of 8 cases of ventricular premature complex (VPC) were seen in females above 30 years of age. Out of 9 cases of PIH, 1 had AF (11.1%) and 2 had VPC (22.2%).
Table 2: Distribution of cases as per rhythm disturbances
DISCUSSION
Electrocardiography is one of the basic tools in the investigation of cardiovascular diseases. The electrocardiogram during normal pregnancy may show a wide variation from the normal accepted. Most of the ECG changes that occur during pregnancy can be explained by the physiological adaptations in response to pregnancy. The changes in Electrocardiogram during pregnancy may be due to changed spatial arrangement of the chest organs, changed electrical properties of the myocardium due to changes in both the sympathetic and hormonal (epinephrine and progesterone) variations during pregnancy.
In the present study, we aimed to determine electrocardiography changes and cardiac arrhythmias in normal pregnancy. ECG changes observed during progression of pregnancy in the present study were as follows: reduction in QRS axis, T-wave inversion in lead III and V1–2, and prolonged QTc. The overall prevalence of rhythm disturbances was low, with VPC being the most common pathology.
As the cardiac output increases by 50% during pregnancy, the HR speeds up from a normal prepregnancy rate of about 70 bpm to 80 or 90 bpm.[891011] In the present study, the mean HR increased from 86.53 bpm to 100.54 bpm as the pregnancy advanced. In similar, such studies conducted by Silversides and Colman[4] proved an increase in HR as the pregnancy advances as a direct consequence to an increase in cardiac output and other hemodynamic changes associated with pregnancy.[10] The electrocardiogram in normal pregnancy as studied by Carruth et al. concluded that the HR increased in pregnancy when compared to the control group, which was significant.[7] Sinus tachycardia is maximum in the third trimester which compensates for the fall in stroke volume in the third trimester occurring due to caval compression.
The P-wave signifies atrial depolarization. The normal sinus P-wave demonstrates depolarization from the right to the left atrium. The amplitude and duration of the wave are analyzed on an ECG to determine left and right atrial enlargement. In the present study, no significant difference was found during the course of pregnancy. The study conducted by Parthasarathy et al.[12] did not show any P-wave changes and variation in PR interval in 150 pregnant women studied from a 20- to 34-week period of gestation. Although the exact mechanism of increased incidence and the severity of arrhythmias in pregnancy are unknown, the probable mechanisms are increased plasma volume, increased sympathetic activity, and hormonal changes. Estrogen increases the excitability in uterine muscles. It may also show similar effects on myocardial cells by increasing alpha-adrenergic receptors.[10] Similar results were also obtained from another study conducted on women of Nigerian origin[13] where ECG showed a normal PR interval and no changes as the pregnancy advanced. In a study by Sonam Chaudhary et al.,[14] the ECG showed a decrease in PR interval associated with pregnancy, which was highly significant.
The QRS axis is a measure of the overall direction of depolarization of the ventricles. In this study, the results showed that the QRS axis decreased significantly, i.e., left axis deviation with the course of pregnancy. The change in electrical axis can be attributed to rising of diaphragm as pregnancy advances[15]. Changes in left ventricular size and mass with associated increased volume may cause the apical impulse to be displaced to the left. Elevation and rotation of heart resulting from the enlarging uterus and increased blood volume also contribute to the displacement[16] and increased left ventricular load.[17] In the study by Singh et al.[15] and Misra et al.,[17] it was observed that a significant left axis deviation occurred as the pregnancy progressed which they attributed to the rising of the diaphragm. Misra et al. even concluded that the increase in left ventricular load due to increase in blood volume by about 50% also contributed significantly to the results obtained. Similar observations were also made by Lechmanova et al.[18] in their study when the group observed a changed spatial position of the heart during the last trimester of pregnancy leading to left axis deviation. Carruth et al. also made similar conclusions.[7] A significant deviation of QRS axis toward left with progression of pregnancy was also observed in the studies by Nandini et al.,[19] Madras and Challa,[20] Chaudhary et al.,[21] and Sunitha et al.[22] The results obtained in this study confirm the results of various such studies as noted above which shows the significant left axis deviation that is noted as the pregnancy advances.
QTc interval in electrocardiogram reflects the time taken for depolarization and repolarization in the ventricular myocardium. The QT interval when corrected for HR is QTc. It must be emphasized that the surface electrocardiographic QTc interval reflects complex and interrelated aspects of cardiac electrophysiology, cardiac geometry, torso shape, tissue impedance, and biological signal processing. In the present study, there was a statistically significant increase in QTc interval in the second and third trimesters of pregnancy when compared to the first trimester. An increase in the QTc interval may be due to increase in HR. This could be linked to changes in ventricular depolarization and repolarization patterns during pregnancy. This must be considered as a complex consequence of changes in the various regulatory mechanisms occurring during normal pregnancy.[23] Similar reports were given in previous studies by Carruth et al.[7] and Lechmanova et al.[23] Lechmanova et al.[23] in their study found an increase in QT interval as well as prolongation of QTc interval during late pregnancy. They also opined that these prolonged QT and QTc intervals should be interpreted simply as“an unspecific sign of changed course of repolarization.” Nandini et al.[19] in their study also observed a statistically significant increase in QTc interval in the first, second, and third trimesters of pregnancy when compared to the control group. There was also a statistically significant increase in QTc interval in the second and third trimesters when compared to the first trimester of pregnancy and also in the third when compared to the second trimester of pregnancy. Similar observations were also made by Oram and Holt,[24] Madras and Challa,[20] and Chaudhary et al.[21]
In the present study, inverted T-waves were seen in 8.2% of cases during the second and third trimesters. Inversion was predominantly observed in lead III and chest leads V1–V3. These finding may be attributed to the increased workload on heart due to temporary increased blood volume during pregnancy which may cause a temporary ischemia, represented by T-wave inversion.[17] Misra et al. in their study setting observed a negative T-wave in lead III in 70% of participants of normal pregnancy. The T-wave abnormalities in the normal pregnant women their study was detected in almost all the chest leads.[17] A study by Oram and Holt found that S-T changes in the ECG were a common finding that affected both the limb and chest leads but a few of them at one time. The common finding was ST-segment sagging that caused a depression to a depth of 0.5–1.0 mm. The left side precordial leads V3 to V6 were the most affected.[24] T-wave inversion in V2 which was noted in the study by Veille et al. was more frequent in the pregnant than in the nonpregnant patients. Two cases in their study had marked T-wave peaking, and one had a biphasic T-wave in V2 out of the total cases studied.[25] These results obtained in the current study are in conformity with the studies showing significant T-wave inversion noted in pregnant women.
Another very common symptom in pregnancy is palpitations which can be explained by HR increases by almost 25%, thus leading to sinus tachycardia, ectopic beats, and nonsustained arrhythmia. These findings are more common in the last trimester and can be present in more than 50% of pregnant women.[26]
In the present study, the incidence of rhythm disturbances such as ventricular premature contractions and ventricular bigeminy was observed as 1.8% and 0.4% of cases, whereas AF was seen in 0.7% of cases. A significant association was seen between rhythm disturbances with advancing age (P < 0.01). As the age increases, so does the risk for AF. The prevalence becomes almost ten times higher with advancing age.[2728] The results in the study conducted by Lee et al. observed that the odds of having an AF increased dramatically with age.. The odds ratio (OR) of AF was 4.1 in women aged 30–34 years, 4.9 in women aged 35–39 years, and 5.2 in women aged ≥40 in comparison to women <25 years of age. Odds of AF were steadily higher in the third trimester as compared to the first and second trimesters (OR, 3.2; 95% confidence interval: 1.5–7.7). Similar results were also observed by Shotan et al.[10] and Gowda et al.[11] which are comparable to this study showing the various arrhythmias that start appearing as the pregnancy advances.
In this present study, a significant association was also seen between rhythm disturbances and PIH (P < 0.01). Out of 9 cases of PIH, 1 had AF (11.1%) and 2 had VPC (22.2%), the results being comparable to observations made by Lee et al.[26] who also observed a significant association of obstetric complications such as preeclampsia with rhythm disturbances. The induced electrophysiological effects in the atrium which may be attributed to increased inflammatory response and adrenergic state and stimulation of rennin angiotensin pathway due to preeclampsia can lead to an increase in arrhythmia susceptibility.[293031]
CONCLUSION
ECG changes such as reduction in QRS axis, T-wave inversion in lead III and V1–2, and prolonged QTc were observed in pregnant women. The overall prevalence of rhythm disturbances was low, with VPC being the most common pathology. Thus, our observations showed that ECG parameters do alter during pregnancy. Although minor electrocardiographic changes were found at rest, these should be considered normal unless associated with significant symptoms. The interpretation of ECG during the antenatal period should be done with caution. Further studies should be done, especially longitudinal studies to provide more information about the changes that take place in a particular woman during the entire period of pregnancy and their reversal after delivery. Since the patient can present with very vague symptoms that are a common presentation during pregnancy, such as, palpitations, breathlessness, easy fatiguability, presyncope, and syncope, it is imperative that a clinician should take all these symptoms seriously to pick up cardiac disorders and early intervention may decrease both morbidity and mortality in such cases. Patients presenting with cardiac arrhythmias may have underlying heart disease or systemic disorders such as thyroid dysfunction, pulmonary embolism, infections, and inflammatory conditions which may have precipitated it. Congenital conditions such as mitral stenosis may present for the first time during pregnancy. Patients with congenital abnormalities who have undergone surgical corrections in childhood and are completely asymptomatic now are particularly vulnerable during pregnancy.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
REFERENCES
1. Siu SC, Sermer M, Colman JM, Alvarez AN, Mercier LA, Morton BC, et al Prospective multicenter study of pregnancy outcomes in women with heart disease Circulation. 2001;104:515–21
2. Lee SH, Chen SA, Wu TJ, Chiang CE, Cheng CC, Tai CT, et al Effects of pregnancy on first onset and symptoms of paroxysmal supraventricular tachycardia Am J Cardiol. 1995;76:675–8
3. Drenthen W, Boersma E, Balci A, Moons P, Roos-Hesselink JW, Mulder BJ, et al Predictors of pregnancy complications in women with congenital heart disease Eur Heart J. 2010;31:2124–32
4. Silversides CK, Colman JMOakley C, Warnes CA. Physiological changes in pregnancy Heart Disease in Pregnancy. 1st. 20072nd Malden Blackwell Publishing
5. Ninio DM, Saint DA. The role of stretch-activated channels in atrial fibrillation and the impact of intracellular acidosis Prog Biophys Mol Biol. 2008;97:401–16
6. Goloba M, Nelson S, Macfarlane P. The Electrocardiogram in pregnancy In: Computing in Cardiology. 2010;37:693–6
7. Carruth JE, Mivis SB, Brogan DR, Wenger NK. The electrocardiogram in normal pregnancy Am Heart J. 1981;102:1075–8
8. Turner AS, Watson OF, Adey HS, Cottle LP, Spence R. The prevalence of disturbance of cardiac rhythm in randomly selected New Zealand adults N Z Med J. 1981;93:253–5
9. Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ, et al ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias – Executive summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias) Developed in collaboration with NASPE – Heart Rhythm Society Eur Heart J. 2003;24:1857–97
10. Shotan A, Ostrzega E, Mehra A, Johnson JV, Elkayam U. Incidence of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope Am J Cardiol. 1997;79:1061–4
11. Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac arrhythmias in pregnancy: Clinical and therapeutic considerations Int J Cardiol. 2003;88:129–33
12. Parthasarathy S, Sripriya R, Krishnaveni N. A study of the electrocardiographic changes in normal pregnant women RJPBCS. 2015;6:604–9
13. Akinwusi PO, Oboro VO, Adebayo RA, Akintunde AA, Adeniji AO, Isawumi IA, et al Cardiovascular and electrocardiographic changes in Nigerians with a normal pregnancy Cardiovasc J Afr. 2011;22:71–5
14. Revathi M, Sujatha V, Sunitha K, Venkatachalam M. A Comparative Study of electrocardiographic changes in pregnant and non-pregnant women IOSR J Dent Med Sci. 2015;14:2279–861
15. Singh AD, Devi L, Singh L, Devi R, Singh J. Electrocardiograpic findings at term, labour and immediate postpartum J Obstet Gynecol India. 1986;36:316–9
16. Chia P, Chia H, Subramanian R. A clinical approach to heart disease in pregnancy part 1. General considerations in management Obstet Gynecol. 2002;4:162–8
17. Misra J, Dutta B, Ganguly D. Electrocardiographic study in pregnant women in normal and toxemia of pregnancy J Obstet Gynecol India. 1986;36:635–8
18. Lechmanova M, Parizek A, Halaska M, Slavicek J, Kittnar O. Changes of the electrical heart field and haemodynamic parameters in 34
th to 40
th weeks of pregnancy and after delivery Arch Gyneol Obstet. 2002;266:145–51
19. Nandini BN, Shivakumar DG, Manjunath A, Sreepadma S. Occurrence of Q wave, QTC interval and QRS frontal axis during different trimesters of Pregnancy A cross sectional study Int J Curr Res Aca Rev. 2014;2:79–88
20. Madras V, Challa N. Electrocardiographic variations during three trimesters of normal pregnancy Int J Res Med Sci. 2015;3:2218–22
21. Chaudhary S, Saha C, Sarkar D. Electrocardiographic Changes During Pregnancy at Third Trimester: A Comparative Study Medical Journal of Shree Birendra Hospital. 2016 14. 41. 10.3126/mjsbh.v14i2.13367
22. Sunitha M, Chandrasekharappa S, Brid SV. Electrocradiographic qrs axis, q wave and T-wave changes in 2
nd and 3
rd trimester of normal pregnancy J Clin Diagn Res. 2014;8:BC17–21
23. Lechmanová M, Kittnar O, Mlcek M, Slavícek J, Dohnalová A, Havránek S, et al QT dispersion and T-loop morphology in late pregnancy and after delivery Physiol Res. 2002;51:121–9
24. Oram S, Holt M. Innocent depression of the ST segment and flattening of the T-wave during pregnancy J Obstet Gynecol. 1961;68:765–70
25. Veille JC, Kitzman DW, Bacevice AE. Effect of pregnancy on electrocardiogram in healthy subjects during strenuous exercise Am J Obstet Gynecol. 1996;175:1360–4
26. Lee MS, Chen W, Zhang Z, Duan L, Ng A, Spencer HT, et al Atrial fibrillation and atrial flutter in pregnant women – A population-based study J Am Heart Assoc. 2016;5:e003182.
27. Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, et al Prevalence of diagnosed atrial fibrillation in adults: National implications for rhythm management and stroke prevention: The an ticoagulation and risk factors in atrial fibrillation (ATRIA) Study JAMA. 2001;285:2370–5
28. Shen AY, Contreras R, Sobnosky S, Shah AI, Ichiuji AM, Jorgensen MB, et al Racial/ethnic differences in the prevalence of atrial fibrillation among older adults – A cross-sectional study J Natl Med Assoc. 2010;102:906–13
29. Redman CW, Sargent IL. Latest advances in understanding preeclampsia Science. 2005;308:1592–4
30. Granger JP, Alexander BT, Bennett WA, Khalil RA. Pathophysiology of pregnancy-induced hypertension Am Heart J. 2001;14:178S–85
31. Healey JS, Baranchuk A, Crystal E, Morillo CA, Garfinkle M, Yusuf S, et al Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: A meta-analysis J Am Coll Cardiol. 2005;45:1832–9
