Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 911 - файл
.pdf
376
https://t.me/medicina_free
CONCLUSION
Acute MI during pregnancy is rare, but carries signicant
risk for both maternal and fetal morbidity and mortality.
Physiologic changes during normal pregnancy can make
diagnosis of AMI dicult and may impact maternal recovery and prognosis. Timing and mode of delivery as well as
treatment options should be determined on a case- by- case
basis, and anesthesia providers should be involved in multidisciplinary care discussions for these complicated patients.
CASE- BASED LEARNING DISCUSSION
1. What is your dierential diagnosis for this patient?
2. What clinical signs and symptoms are meaningful to
elicit in this scenario?
3. What testing might be useful to narrow your
dierential diagnosis?
4. What are the treatment options for this patient?
5. How do you counsel this patient about labor and
delivery and anesthetic implications?
6. How would you discuss this patient’s prognosis?
REFERENCES
1. Kealey A. Coronary arter y disease and myocardial infarction in preg-
nancy:a review of epidemiolog y, diagnosis, and medical and surgical
management. Canandian Journal of Cardiology. 2010;26:185– 9.
2. Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarc-
tion in pregnancy and the puerperium:a population- based study.
Obstetrics and Gynecology. 2005;105:480– 4.
3. James AH, Jamison MG, Biswas MS, et al. Acute myocardial
infarction in pregnancy: a United States population- based study.
Circulation. 2006;113:1564– 71.
4. Karpati PC, Rossignol M, Pirot M, et al. High incidence of myo-
cardial ischemia during postpartum hemorrhage. Anesthesiology.
2004;100:30– 36.
5. Roth A, Elkayam U. Acute myocardial infarction associated
with pregnancy. Journal of the American College of Cardiology.
2008;52:171– 81.
6. Heeschen C, Dimmeler S, Hamm CW, etal. Pregnancy- associated
plasma protein- A levels in patients with acute coronary syndromes:comparison with markers of systemic inammation, platelet activation, and myocardial necrosis. Journal of the American
College of Cardiology. 2005;45:229– 37.
7. Iadanza A, Del Pasqua A, Barbati R, etal. Acute ST elevation myo-
cardial infarction in pregnancy due to coronary vasospasm:a case
report and review of literature. International Journal of Cardiology.
2007;115:81– 5.
8. Elkayam U, Jalnapurkar S, Barakkat MN, et al. Pregnancyassociated acute myocardial infarction:a review of contemporary
experience in 150 cases between 2006 and 2011. Circulation.
2014;129:1695– 702.
9. Shade GH, Ross G, Bever FN, et al. Troponin I in the diagnosis of acute myocardial infarction in pregnancy, labor, and
postpartum. American Journal of Obstetrics and Gynecology.
2002;187:1719– 20.
10. ygesen K, Alpert JS, Jae AS, et al. ird universal denition of myocardial infarction. Journal of the American College of
Cardiology. 2012;60:1581– 98.
11. Rubin PC. Current concepts: beta- blockers in pregnancy. New
England Journal of Medicine. 1981;305:1323– 26.
12. Butters L, Kennedy S, Rubin PC. Atenolol in essential hypertension
during pregnancy. British Medical Journal. 1990;301:587– 9.
13. Turrentine MA, Braems G, Ramirez MM. Use of thrombolytics
for the treatment of thromboembolic disease during pregnancy.
Obstetrics and Gynecology Surveys. 1995;50:534– 41.
14. CLASP collaborative group. Low dose aspirin in pregnancy and
early childhood development: follow up of the collaborative low
dose aspirin study in pregnancy. British Journal of Obstetrics and
Gynaecology. 1995;102:861– 8.
15. Hauth JC, Goldenberg RL, Parker CR, Cutter GR, Cliver SP.
Low- dose aspirin: lack of association with an increase in abruptio placentae or perinatal mortality. Obstetrics and Gynecology.
1995;85:1055– 58.
16. Henck JW, Cra WR, Black A, Colgin J, Anderson JA. Pre- and
postnatal toxicity of the HMG- CoA reductase inhibitor atorvastatin in rats. Toxicology Science. 1998;41:88– 89.
17. Costantine MM, Cleary K, Hankins G, et al. For the Eunice
Kennedy Shriver National Institute of Child Health and
Human Development Obstetric- Fetal Pharmacology Research
Units Network. Pravastatin for the prevention of preeclampsia in high- risk pregnant women. Obstetrics and Gynecology.
2013;121:349– 53.
18. Boztosun B, Olcay A, Avci A, Kirma C. Treatment of acute myocardial infarction in pregnancy with coronary artery balloon angioplasty and stenting:use of tiroban and clopidogrel. International
Journal of Cardiology. 2008;127:413– 6.
19. Kamran M, Suresh V, Ahluwalia A. Percutaneous transluminal coronary angioplasty (PTCA) combined with stenting for acute myocardial infarction in pregnancy. Journal of Obstetrics and Gynaecolog y.
2004;24:701– 2.
20. Al- Aqeedi RF, Abdulrahman D. Drug- eluting implantation for
acute myocardial infarction during pregnancy with use of glycoprotein IIb/ IIIa. Journal of Invasive Cardiology. 2008;20:146– 9.
21. Arimura T, Mitsutake R, Miura S, Nishikawa H, Kawamura A, Saku
K. Acute myocardial infarction associated with pregnancy successfully treated with percutaneous coronary intervention. Internal
Medicine. 2009;48:1383– 86.
22. De SM, Cesari E, Nobili E, Straface G, Cavaliere AF, Caruso A.
Radiation eects on development. Birth Defects Res C Embryo
Today. 2007;81:177– 82.
23. Conti CR. Cardiovascular studies and the radiation dose. Clinical
Cardiology. 2009;32:56– 57.
24. Davies G, Herbert W. Ischemic heart disease and cardiomyopathy in pregnancy. Journal of Obstetrics and Gynaecology Canada.
2007;29:575– 79.
25. Arnoni RT, Arnoni AS, Bonini RC, et al. Risk factors associated
with cardiac surgery during pregnancy. Annals of oracic Surgery.
2003;76:1605– 8.
26. Wassing JG, Polak PE, de Groot CJ, Roos- Hesselink JW. Acute
coronary syndrome during pregnancy. Netherlands Heart Journal.
2005;13:360– 65.
376 SECTION B. CARDIAC CRISES
https://t.me/medicina_free
377
27. Burchill LJ, Lameijer H, Roos- Hesselink JW, etal. Pregnancy risks
in women with pre- existing coronary artery disease, or following
acute coronary syndrome. Heart. 2015;101:525– 9.
28. Jeejeebhoy FM, Zelop CM, Lipman S, et al. On behalf of the
American Heart Association Emergency Cardiovascular Care
Committee, Council on Cardiopulmonary, Critical Care,
Perioperative and Resuscitation, Council on Cardiovascular
Diseases in the Young, and Council on Clinical Cardiology. Cardiac
arrest in pregnancy:a scientic statement from the American Heart
Association. Circulation. 2015;132:1747– 73.
VESSELS:CORONARY ARTERY DISEASE AND PERIPARTUM ACUTE CORONARY SYNDROME 377
378
https://t.me/medicina_free
53.
VOLTAGE DISTURBANCES DURING PREGNANCY
Heather C.Nixon
CASE
Brid observed the ECGs of 50 parturients during their
second and third trimesters.2 A signicant number of the
A 23- year- old G1P0 at 37 weeks and 4days estimated gestational age is admitted to the labor and delivery oor in
active labor. She is 4cm dilated and contracting regularly.
On interview, you learn that she experienced palpitations
at the beginning of her third trimester and was seen by a
cardiologist. Holter monitor workup at that time revealed
one brief, self- limiting episode of supraventricular tachycardia (SVT) without symptoms. Her transthoracic echo was
normal. e patient states she was not placed on any medication and had no further palpitations or lightheadedness
during her pregnancy.
Two hours into her labor, she complains of chest
pain, nausea, and lightheadedness. e nurse calls you
emergently because “the patient’s heart rate is really
fast.” Electrocardiogram shows the following rhythm
subjects in both the second and third trimesters demonstrated le deviation of the QRS axis and Q waves in leads
II, III, and aVF. In addition, many patients also had inverted
T- waves, especially in leads III, and V1- V3. Goloba et al. also
found that the T and QRS axes shi signicantly during
second and third trimesters of pregnancy and subsequent
deliveries.3 e authors concluded that as many obstetric
patients are young, healthy, and asymptomatic, interpretation of ECG changes in pregnant patients should be done
with caution. Finally, pregnancy typically lengthens the QT
interval, which, while not typically causing clinical manifestations, may inuence medication choices during both pregnancy and delivery. Patients diagnosed with prolonged QT
syndromes may improve during pregnancy, and QT interval
typically returns to baseline around three days postpartum.
4
(Figure53.1).
ELECTROCARDIOGRAM INPREGNANCY
ELECTROCARDIOGRAM INTHE
PERIPARTUMPERIOD
Electrocardiogram (ECG) alterations during pregnancy are
common. Although few young and healthy parturients will
have baseline ECGs, variations in expected “normal” patterns
are not necessarily predictive of cardiac distress. e cardiovascular changes observed during pregnancy are thought
to be both anatomical and physiologic, all of which contribute to dicult interpretation of ECG in the parturient.
Early increases in cardiac outow during pregnancy result
in le displacement of the heart secondary to le ventricular loading.1 Other anatomical changes include the upward
displacement of the heart due to the growing uterus and the
concentric hypertrophy of the heart, especially the le ventricle, secondary to increased cardiac output and increased
intravascular volume. Hormonal and autonomic inuences
including increased circulating progesterone and epinephrine may also inuence the electrical conducting system.
378
Due to the rapidly changing hemodynamics of labor and
both vaginal and surgical delivery, the peripartum period
can be a time where demands on the cardiac system and
hormonal inuences may result in profound alterations in
cardiac rhythms.
DURING LABOR AND DELIVERY
Little is known about ECG alterations that may occur during labor and vaginal delivery as healthy parturients rarely
have cardiac monitoring during this period.
DURING CESAREAN DELIVERY
Up to 60% of parturients may demonstrate ST segment
depressions with accompanying tachycardia that are
https://t.me/medicina_free
379
Figure53.1 This gure illustrates an example of SVT in a parturient.
morphologically consistent with myocardial ischemia during cesarean delivery.5 Many of the patients in this study also
reported chest pain, nausea, and dyspnea concurrent with
the ECG changes. is may be the result of rapid changes in
cardiac output, uid shis secondary to uterine autotransfusion or aggressive oxytocin use. Zakowski etal. prospectively observed 170 consecutive cesarean deliveries using
Holter monitors. In addition, 30 patients in this study also
were examined with transthoracic two- dimensional echocardiograms.6 Although no wall motion abnormalities were
reported, 160 events with ST segment depression or elevation were observed in 44 patients, most of which occurred
aer the induction of anesthesia with either lumbar epidural catheter or spinal anesthesia. Creatinine kinase measurements failed to show evidence of myocardial damage.
Spinal anesthesia has also been associated with the
development of arrhythmia during cesarean delivery. In a
prospective study of spinal anesthesia in 254 parturients for
cesarean delivery, 3.5% of patients developed rst- degree
atrioventricular (AV) block, 3.5% developed second- degree
AV block, and 6.7% developed severe bradycardia (HR <
50 bpm).7 erefore, neuraxial anesthesia may contribute
to the incidence of arrhythmia during cesarean delivery.
cardiac defects or structural abnormalities.8 Luckily, the
development of life- threatening dysrhythmias in parturients is very rare.
9,10
e potential for the development of
arrhythmia is increased by pregnancy and especially during
labor and delivery for several reasons. First, there is an upregulation of both hormones and catecholamines that may
promote myocardial irritability. e increased resting heart
rate typically seen in pregnancy may foster irregular electrical conduction.11 Increased blood volume and resultant
cardiac output can activate myocardial atrial stretch receptors and promote arrhythmia via ion channel activation
and depolarization.
12– 14
Finally, a relative hypokalemia of
pregnancy may predispose patients to arrhythmias.15 Other
etiologies including pulmonary embolism, peripartum cardiomyopathy, and hyperthyroidism should also be considered as possible contributing factors.
16
In a retrospective review of patients with a history
of tachyarrhythmia, the risk of recurrence during pregnancy was 44%, and in 20% of these patients, arrhythmia
was thought to contribute to adverse fetal outcomes.17
erefore, women with known or treated arrhythmias who
become pregnant should be advised to follow regularly with
a cardiologist and may require consultation with a maternal
fetal medicine physician.
ARRHYTHMIAS INPREGNANCY
Arrhythmias during pregnancy can occur in patients with
no previously documented cardiac disorders, although they
more frequently are seen in parturients with underlying
VOLTAGE DISTURBANCES DURING PREGNANCY 379
ATRIAL AND VENTRICULARECTOPY
During pregnancy, many women (50%– 60%) experience benign premature atrial or ventricular beats.
18,19
Subjectively, the patient may experience palpitations,
380
https://t.me/medicina_free
lightheadedness, and dyspnea, which may prompt formal
cardiac evaluation. In most cases, no treatment is necessary
and supportive care with periodic monitoring is recommended. However, if persistent ectopy exists, beta- blocker
therapy may be instituted. Shen etal. found that following
spinal anesthesia during cesarean delivery 8% and 18% of
patients developed premature ventricular contractions and
premature atrial contractions, respectively.7 Initial workup
on women complaining of ectopy symptoms should include
electrolyte evaluation, as hypokalemia and hypomagnesemia may exacerbate ectopy.
resolution of the arrhythmia. In the case of hemodynamically stable spontaneous SVT that is nonresponsive to vagal
manipulation, antiarrhythmic therapy is warranted. For
AVNRT, IV adenosine is the rst- line agent, with a reported
ecacy of >90% for termination of the tachyarrhythmia25
(see Table 53.1). Metoprolol, sotalol, or verapamil may also
be used as second- line agents in women in whom adenosine
is not eective.26 If the patient is unstable, emergent direct
current cardioversion with 50– 100 joules is indicated in the
synchronized mode. If the arrhythmia is recurrent, ablation
therapy of the slower pathway may be necessary, but potential benet of this intervention during pregnancy must be
SUPRAVENTRICULAR TACHYCARDIA— NARROW
QRS COMPLEX
Types of supraventricular arrhythmias include paroxysmal supraventricular tachycardia, Wol- Parkinson- White
(WPW syndrome), atrial utter and atrial brillation.
Supraventricular tachycardia (SVT) rst manifesting in
pregnancy is rare, but carries an overall incidence of 4% in
pregnant patients.20 e diagnosis requires a QRS less than
0.12 msec and usually a range of 180– 240 bpm, although it
may be higher.21 In patients with preexisting SVT, the rate
of recurrence is high (22%), indicating that physiological
changes and anatomic changes of pregnancy can exacerbate
preexisting arrhythmias.
20
weighed against the fetal exposure to radiation during the
procedure and the risks to the mother.
WOLFF- PARKINSON- WHITE SYNDROME
9,27
Wol- Parkinson- White (WPW) syndrome is another category of SVT, where an accessory or alternative pathway,
called the bundle of Kent, transmits between the atrium
and ventricle. Also known as preexcitation syndrome or
AV reentrant tachycardia (AVRT), WPW can result in
very high heart rates, as the conduction pattern is not tempered by the AV node.28 Characteristic ECG patterns demonstrate a delta wave (slurred upstroke of QRS complex)
and a short PR interval. Procainamide or amiodarone may
be the agents of choice for patients with WPW syndrome.
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
Paroxysmal supraventricular tachycardia (PSVT) is generally a reentry tachycardia, where electrical current con-
Verapamil and digoxin should not be used, as these may
increase the risk of the rapid accessory path conduction due
to AV node suppression.9 Cardiac ablation may be required
for denitive treatment.
ducted to the ventricle then reenters the atria, leading to
inappropriately rapid heart rate. e most common form of
SVT is AV nodal reentrant tachycardia (AVNRT), where
the impulse is carried to the ventricle via the AV node and
then transmitted via an accessory pathway within or next to
the AV node back to the atria. In AVNRT, there is a characteristic retrograde P- wave on the ECG that follows the
narrow QRS complex, indicating the reentry of the conduction to the atria. e incidence of PSVT in pregnancy is
estimated to be 24 per 100,000 patients.
22
First- line management of PSVT includes the use of
vagal maneuvers including carotid sinus massage, gagging,
Valsalva maneuvers, and the dive reex. Valsalva maneuvers
may eectively terminate up to 25% of arrhythmias.
23,24
Carotid massage may result in vagal stimulation with
resultant hypotension and bradycardia. erefore, careful
monitoring of the mother and fetus is necessary during that
technique. If the patient is hypotensive secondary to anesthetic intervention, correction of hypotension may result in
ATRIAL FIBRILLATION AND ATRIAL FLUTTER
Atrial brillation (AF) and utter (AFL) originate in an
ectopic center in the atria and, if atrial beats are conducted
to the ventricle in high ratio, may result in signicant tachycardia. Atrial utter typically originates in the right atrium
and conducts at either a 2:1 or 4:1 atrial:ventricular bpm
ratio leading to a ventricular heart rate of 150 or 75, respectively. Atrial brillation is created by disorganized atrial
electrical activity, and rates vary widely based on AV conduction of the sensed atrial beats. During pregnancy, both
AF and AFL occur more commonly in patients with underlying cardiac structural abnormalities such as valvular disorders and surgically corrected congenital cardiac disease. e
incidence of both is much less common than SVT during
pregnancy, with recorded rates of 2 patients per 100,000.
Sustained or chronic AF may increase the risk of throm-
boembolism and stroke. Pregnant patients are considered to
22
380 SECTION B. CARDIAC CRISES
https://t.me/medicina_free
381
TABLE53.1 DRUG TREATMENTS FORSUPRAVENTRICULAR TACHYCARDIA
Drug
Adenosine Adenosine
Metoprolol Beta blocker Category C IV:1 mg/ min— up to 10 mg total Implications of intrauterine growth
Procainamide Sodium channel
Propranolol Beta blocker Category C IV:1- 3 mg slow IVP repeat ever y 2- 5
Quinidine Sodium channel
Verapamil Calcium
Drug Type FDA Pregnancy Classication Dose
Category C IV:6 mg rapid bolus followed by 20 mL
receptor agonist
Category C IV (initial dose):20- 50 mg/ min until
blocker
Category C Oral:200- 400 mg every 6 hours Rare complications:
blocker and
muscarinic
antagonist
Category C IV:10 mg over 3 min or
channel blocker
rapid saline ush
Repeat if necessary with 12 mg IV
bolus
QRS widens or 100 mg every 5 min
Maintenance IV:1- 4 mg/ min
min up to 5 mg
5 mg in pts on beta blockers
Fetal Concerns
Little known fetal effect, possibly due to
short half- life (10- 15 sec)
retardation, neonatal hypoglycemia and
hyperbilirubinemia
Rare complications:drug- induced lupus
erythematous
Implications of intrauterine growth
retardation, neonatal hypoglycemia and
hyperbilirubinemia
uterine contractions, neonatal
thrombocytopenia
8th cranial nerve injury
Toxic doses:Spontaneous abortion
Possible ischemia secondary to maternal
hypotension, possible risk of fetal
bradycardia
31– 33
34
be hypercoagulable, and therefore antithrombotic prophylactic therapy is recommended if sustained AF is diagnosed.
If the rhythm is prolonged greater than 48 hours, or for an
unknown period of time, transesophageal echocardiogram
(to identify thrombus) or therapeutic anticoagulation for 3
weeks should be undertaken prior to any medical or electrical conversion of the rhythm, as the risk of cerebral systemic
embolus increases at that timepoint.
Considerations for teratogenicity, uterine perfusion,
and eects on labor and delivery must be taken into account
whenever caring for a pregnant patient.10 All current antiarrhythmic drugs cross the placenta and therefore have the
potential to impact the fetus.25 e risk of teratogenicity
markedly decreases aer the organogenesis period (roughly
aer 8 weeks), but antiarrhythmic medications may still
inuence fetal growth.29 Most commonly used antiarrhythmic drugs are classied by the FDA as classC, indicating
TREATMENTS
Management of SVT arrhythmias in pregnant patients is
very similar to that in nonpregnant patients. In line with
advanced cardiac life support (ACLS) guidelines, in stable patients, medical conversion can be attempted with
beta blockers, calcium channel blockers, or adenosine.
Hemodynamically unstable patients should receive electrical cardioversion.
If the patient is hemodynamically stable, quinidine and
procainamide may be administered to convert the rhythm.
that there are not enough studies in pregnant women and
animal studies are nonconclusive for teratogenicity.
30
During pregnancy, increased intravascular volume,
increased volume of distribution, increased renal clearance, and decreased serum protein binding may make antiarrhythmic dosing more challenging.21 It is advisable to
closely monitor therapy in this patient population.
For hemodynamically unstable patients or planned
cardioversion, synchronized electrical cardioversion may
be attempted with 120– 200 joules in biphasic devices for
patients in atrial brillation and 50– 100 joules in biphasic
devices for patients with atrial utter.
It may be advisable to administer pretreatment with betablocking drugs to mitigate the vagolytic eect of quinidine.21 If the rhythm is not converted, rate control may be
attempted with digoxin, beta blockers, or calcium channel
blockers.
VENTRICULAR TACHYCARDIA— WIDE COMPLEX
Ventricular tachycardia in pregnancy is also a rare phenomenon (2 cases per 100,000 hospital admissions).19 In patients
VOLTAGE DISTURBANCES DURING PREGNANCY 381
382
https://t.me/medicina_free
TABLE53.2 DRUG TREATMENTS FORVENTRICULAR TACHYCARDIA
Drug
Amiodarone Potassium- blocking
Digoxin Inhibitor of Na + / K +
Lidocaine Sodium- blocking agent Category C IV:0.5- 1.5 mg/ kg May increase myometrial tone, decreased
Magnesium
sulphate
Metoprolol Beta- blocker Category C Oral:50- 100 mg Implications of intrauterine growth retardation,
Procainamide Sodium- blocking agent Category C IV:20- 30 mg/ min,
Propranolol Beta- blocker Category C IV (initial dose):
Quinidine Sodium channel
Drug Type FDA Pregnancy
Classication
Category D Loading dose:150 mg IV
agent
Category C Loading dose:
ATPase
Magnesium receptor
agonist
blocker and muscarinic
antagonist
Category D Loading dose:1- 2 gm IV Depression of FHT tracing, low calcium levels and
Category C Oral:200- 400 mg every 6
Dose
over10min
Maintenance IV:1 mg/ min ×
6 hours
0.5- 1 mg
up to 17 mg/ kg
20- 50 mg/ min until QRS
widens or 100 mg every
5 min
Maintenance IV dose:
1- 4 mg/ min
hours
Fetal Concerns
Fetal hypothyroidism, fetal goiter, growth
retardation, prematurity
Digitalis toxicity may contribute to fetal death
placental blood ow, fetal bradycardia
bone changes with prolonged use
neonatal hypoglycemia and hyperbilirubinemia.
Rare complication:drug- induced lupus
erythematous
Intrauterine growth delay, fetal bradycardia, fetal
hypoglycemia, polycythemia, hyperbilirubinemia
Rare complications:
uterine contractions, neonatal thrombocytopenia
8th cranial nerve injury
Toxic doses:Spontaneous abortion
29
29
34
without structural heart disease, physical and/ or mental
stresses may contribute to the development of usually monomorphic ventricular tachycardia.8 Parturients with underlying structural heart disease have a higher rate of ventricular
tachycardia (approximately 10 per 1,000 pregnancies).
e treatment of choice will depend on the patient’s hemodynamic stability. In stable patients, pharmacologic agents
may be administered (Table 53.2). In patients with torsades
de pointes, magnesium sulfate therapy is indicated. Patients
who are hemodynamically unstable require emergent direct
peers. However, consideration should always be given to
weeks of gestation and the risk of maternal hemodynamic
instability, which may compromise uterine blood ow. It
is advisable that mothers and fetuses should be monitored
31,32
during therapy initiation as hemodynamic alterations
may impact fetal well- being. Although no antiarrhythmic
medication is proven safe in pregnant women, severe complications from therapy are very rare. If the patient is hemodynamically unstable, cardioversion with electrical current
is recommended.
current cardioversion with 50– 100 J.If recurrent ventricular arrhythmia occurs, an implantable internal cardioverterdebrillator (ICD) should be considered.
CONCLUSION
Arrhythmias during pregnancy are rare and generally well
tolerated in healthy young parturients. Many electrical
disturbances are benign and secondary to the many physiological changes of pregnancy. In most cases, parturients
can be treated with the same medications as nonpregnant
33
CASE- BASED LEARNING DISCUSSION
1. What rhythm is shown on this ECG? Is this normal
for a pregnant patient? If not, what changes during
pregnancy predispose this patient to developing this
arrhythmia? What other information or vital signs do
youwant?
2. What are initial steps of treatment for this patient? Are
you able to have the parturient perform any maneuvers
382 SECTION B. CARDIAC CRISES
https://t.me/medicina_free
383
that may correct this rhythm? What medications do
you want to prepare if the blood pressure is 120/ 70?
How would your therapy change if the blood pressure
were 70/ 45? What if the rhythm appeared irregular?
What if the rhythm was irregular and the patient reveals
she has had this issue for 2– 3years?
3. What if the ECG instead showed a QRS with duration
0.3 sec? What type of arrhythmia might the patient
have in that case? What are your therapeutic options?
REFERENCES
1. Misra J DB, Ganguly D. Electrocardiographic study in pregnant
women in normal and toxemia of pregnancy. Journal of Obstetrics
and Gynecology India. 1986;1968(18):635– 8.
2. Sunitha M, Chandrasekharappa S, Brid SV. Electrocradiographic
QRS axis, Q wave and T- wave changes in 2nd and 3rd trimester of normal pregnancy. Journal of Clinical and Diagnostic
Research:JCDR. 2014;8(9):Bc17– 21.
3. Goloba M, Nelson S, Macfarlane P. e electrocardiogram in pregnancy. Computing in Cardiology 2010;37:693– 6.
4. Baumert M, Seeck A, Faber R, Nalivaiko E, Voss A. Longitudinal
changes in QT interval variability and rate adaptation in pregnancies with normal and abnormal uterine perfusion. Hypertension
Research. 2010;33(6):555– 60.
5. Palmer CM, Norris MC, Giudici MC, Leighton BL, DeSimone
CA. Incidence of electrocardiographic changes during cesarean
delivery under regional anesthesia. Anesthesia and Analgesia.
1990;70(1):36– 43.
6. Zakowski MI, Ramanathan S, Baratta JB, etal. Electrocardiographic
changes during cesarean section:a cause for concern? Anesthesia
and Analgesia. 1993;76(1):162– 7.
7. Shen CL, Ho YY, Hung YC, Chen PL. Arrhythmias during spinal anesthesia for cesarean section. Canadian Journal of
Anaesthesia=Journal Canadien d’Anesthesie. 2000;47(5):393– 7.
8. Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac
arrhythmias in pregnancy:clinical and therapeutic considerations.
International Journal of Cardiology. 2003;88(2– 3):129– 33.
9. Enriquez AD, Economy KE, Tedrow UB. Contemporary management of arrhythmias during pregnancy. Circulation: Arrhythmia
and Electrophysiology. 2014;7(5):961– 7.
10. Ferrero S, Colombo BM, Ragni N. Maternal arrhythmias
during pregnancy. Archives of Gynecology and Obstetrics.
2004;269(4):244– 53.
11. Soliman EZ, Elsalam MA, Li Y. e relationship between high
resting heart rate and ventricular arrhythmogenesis in patients
referred to ambulatory 24 h electrocardiographic recording. Europace: European Pacing, Arrhythmias, and Cardiac
Electrophysiology. 2010;12(2):261– 5.
12. Adamson DL, Nelson- Piercy C. Managing palpitations and
arrhythmias during pregnancy. Heart (British Cardiac Society).
2007;93(12):1630– 6.
13. Franz MR, Cima R, Wang D, Prott D, Kurz R. Electrophysiological
eects of myocardial stretch and mechanical determinants of
stretch- activated arrhythmias. Circulation. 1992;86(3):968– 78.
14. Wang Y, Joyner RW, Wagner MB, Cheng J, Lai D, Crawford
BH. Stretch- activated channel activation promotes early
aerdepolarizations in rat ventricular myocytes under oxidative
stress. American Journal of Physiology. Heart and circulatory physiology. 2009;296(5):H1227– 35.
15. Cox JL, Gardner MJ. Treatment of cardiac arrhythmias during pregnancy. Progress in Cardiovascular Diseases. 1993;36(2):137– 78.
16. Moore JS, Teefey P, Rao K, Berlowitz MS, Chae SH, Yankowitz
J. Maternal arrhythmia:a case report and review of the literature.
Obstetrical and Gynecological Survey. 2012;67(5):298– 312.
17. Silversides CK, Harris L, Haberer K, Sermer M, Colman JM, Siu
SC. Recurrence rates of arrhythmias during pregnancy in women
with previous tachyarrhythmia and impact on fetal and neonatal
outcomes. American Journal of Cardiology. 2006;97(8):1206– 12.
18. Kron J, Conti JB. Arrhythmias in the pregnant patient: current
concepts in evaluation and management. Journal of Interventional
Cardiac Electrophysiology. 2007;19(2):95– 107.
19. Shotan A, Ostrzega E, Mehra A, Johnson JV, Elkayam U. Incidence
of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope. American Journal of Cardiology.
1997;79(8):1061– 4.
20. Lee SH, Chen SA, Wu TJ, et al. Eects of pregnancy on rst
onset and symptoms of paroxysmal supraventricular tachycardia.
American Journal of Cardiology. 1995;76(10):675– 8.
21. Trappe HJ. Acute therapy of maternal and fetal arrhythmias during
pregnancy. Journal of Intensive Care Medicine.2006;21(5):305– 15.
22. Li JM, Nguyen C, Joglar JA, Hamdan MH, Page RL. Frequency
and outcome of arrhythmias complicating admission during pregnancy:experience from a high- volume and ethnically- diverse obstetric service. Clinical Cardiology. 2008;31(11):538– 41.
23. Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison
of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Annals of Emergency Medicine.
1998;31(1):30– 35.
24. Smith GD, Dyson K, Taylor D, Morgans A, Cantwell K.
Eectiveness of the Valsalva manoeuvre for reversion of supraventricular tachycardia. Cochrane Database of Systematic Reviews.
2013;3:Cd009502.
25. Trappe HJ. Emergency therapy of maternal and fetal arrhythmias
during pregnancy. Journal of Emergencies, Trauma, and Shock.
2010;3(2):153– 9.
26. Dennis AT, Gerstman MD. Management of labour and delivery in
a woman with refractory supraventricular tachycardia. Int J Obstet
Anesth. 2014;23(1):80– 85.
27. Manjaly ZR, Sachdev B, Webb T, Rajappan K. Ablation of arrhythmia in pregnancy can be done safely when necessary. European
Journal of Obstetrics, Gynecology, and Reproductive Biology.
2011;157(1):116– 7.
28. Kounis NG, Zavras GM, Papadaki PJ, Soufras GD, Kitrou MP,
Poulos EA. Pregnancy- induced increase of supraventricular arrhythmias in Wol- Parkinson- White syndrome. Clinical Cardiology.
1995;18(3):137– 40.
29. Chow T, Galvin J, McGovern B. Antiarrhythmic drug therapy
in pregnancy and lactation. American Journal of Cardiology.
1998;82(4a):58i- 62i.
30. Rakusan K. Drugs in pregnancy: implications for a cardiologist.
Experimental and Clinical Cardiology. 2010;15(4):e100– 103.
31. Siu SC, Sermer M, Harrison DA, et al. Risk and predictors for
pregnancy- related complications in women with heart disease.
Circulation. 1997;96(9):2789– 94.
32. Braverman AC, Bromley BS, Rutherford JD. New onset ventricular
tachycardia during pregnancy. International Journal of Cardiology.
1991;33(3):409– 12.
33. Miyoshi T, Kamiya CA, Katsuragi S, et al. Safety and ecacy of
implantable cardioverter- debrillator during pregnancy and aer
delivery. Circulation Journal. 2013;77(5):1166– 70.
VOLTAGE DISTURBANCES DURING PREGNANCY 383
384
https://t.me/medicina_free
https://t.me/medicina_free
385
SECTIONC
PULMONARY/ AIRWAYCRISES
Соседние файлы в папке @xirurgi_2025