1. CARDIAC DISEASE IN PREGNANCY
Dr. Yasir Katib
MBBS, FRCSC, Perinatologest

2. Multiple Choice
When during pregnancy is peripheral vascular resistance at its lowest?
First trimester
Second trimester
Third trimester
labour

3. When during pregnancy is peripheral vascular resistance at its lowest?
First trimester
Second trimester
Third trimester
labour

4. When during pregnancy is cardiac output highest?
Second trimester
Third trimester
Labour
Postpartum

5. When during pregnancy is cardiac output highest?
Second trimester
Third trimester
Labour
Postpartum

6. Which is not a normal ECG change in pregnancy?
Q wave in lead III
Sinus tachycardia
ST-T wave changes
Prolonged QT interval

7. Which is not a normal ECG change in pregnancy?
Q wave in lead III
Sinus tachycardia
ST-T wave changes
Prolonged QT interval

8. Physiologic Changes in Pregnancy
Increased blood volume
Increases from 6-8 weeks
Max 32 wks (45%)
Increased further with multiples (70%)
?estrogen activates angiotensin-aldosterone leading to Na+ and H20 retention

9. Physiology changes cont’d
RBC mass increases by ml by term (20-30% increase)
Increased RBC due to placental somatomammotropin, progesterone
Therefore, increased demand for iron = 500mg +300mg fetus mg for daily losses = (1000mg total)

10. Physiology cont’d Increased cardiac output 30-50% increase
50% of this occurs by 8 wks
Continued rise at a slower rate to 3rd trimester
Primary reason = increased stroke volume
There is also increased heart rate (predominant in 3T)
Supine positioning leads to decreased CO by 25-30%

13. Physiology cont’d Decreased systemic vascular resistance
Decreases from 5 wks due to progesterone and prostaglandins (cause vasodilatation)
Nadir at wks then increases toward term

14. Physiology cont’d Increased venous compliance
Leads to increased stasis
Therefore, more sensitive to autonomic blockade

15. Physiology cont’d Anatomic changes:
Increased ventricular wall muscle mass (T1 only)
Increased EDV (continues through T2, T3)
These combine to cause physiologically dilated heart

16. Physiology cont’d ABG:
Tidal volume increased by 40% leading to hyperventilation and hypocapnia
Therefore, decreased PCO2 to mmHg
Partially compensated for by decreased bicarb level
Therefore, mild respiratory alkalosis with arterial pH = 7.44

17. Physiology cont’d ECG changes:
Left axis deviation (due to elevated diaphragm)
May shift to right late in pregnancy as fetus descends
Sinus tachycardia
Minor ST changes in III, aVF
Q wave in lead III
Inverted P wave in lead III

18. Intrapartum 1st stage: 12-31% increased CO owing to 22% increase in SV
2nd stage: 49% increased CO
Left side positioning decreased the amount of increase
Epidurals reduce this increase by 10%
SBP increases by 35 mmHg, DBP increases by 25 mmHg

19. Postpartum 80% increase CO within 15 min delivery
60% increase if caudal anesthesia
Increase due to:
Release of venocaval obstruction
Auto transfusion of uteroplacental blood
Rapid mobilization of extravascular fluid
All work to increase venous return and increase SV

20. Postpartum CO returns to prelabour values by 1h
C/S leads to 25-50% increase in CO
Left atrial dimensions increase days 1-3 pp, normalize within 10d
Left ventricular dimension takes 4-6 mos to decrease
SV, CO and SVR reach normal by 12 wk

21. NYHA Functional Classification
Class I: no symptoms with normal activity
Class II: symptoms with ordinary activity
Class III: symptoms with less than ordinary activity
Class IV: symptoms at rest

22. Classifying Risk of Mortality
Group 1: mortality < 1%
ASD
VSD
PDA
MS (NYHA I,II)
Pulmonic tricuspid disease
Porcine valve
Corrected TOF

23. Mortality cont’d Group II: mortality 5-15% MS with atrial fibrillation
Artifical valve
MS (NYHA III,IV) AS
Uncorrected TOF
Marfan’s with normal aorta
Coarctation of aorta
Previous MI

24. Mortality cont’d Group III: mortality 25-50% Pulmonary HTN
Coarctation with aortic valve involvement
Marfan’s with aortic root dilatation (>40mm)
Eisenmenger’s

25. Approach to Pregnancy Prepregnancy:
Prior to D/C contraception, counseling should be done
Assess maternal disease status
Optimize medical management
Counsel re: risk of fetal anomaly
Switch prosthetic valves to heparin
Assess re: need for surgery prior to pregnancy

26. Antenatal Multidisciplinary approach
If no preconceptual visit, evaluation of status and counseling
Discuss termination if appropriate
Question regularly re: symptoms
Monitor weight and vital signs regularly
US: dating, anatomy, growth and well-being

27. Antenatal cont’d Fetal echo at 22wks Echo, ECG etc. every trimester
Avoid strenuous exercise
Consult re: NICU, anesthesia

28. Labour & Delivery Lateral position Close attention to fluid balance
Continuous ECG monitoring
In high risk: invasive monitoring
Close fetal surveillance
C/S for OB indications, may use operative vag delivery to shorten 2nd stage

29. L&D cont’d Antibiotics: Prosthetic valves
Previous bacterial endocarditis
Complex cyanotic heart disease
Mitral valve prolapse with regurgitation
Acquired valvar dysfunction
Hypertrophic cardiomyopathy

30. L&D cont’d
Epidural (avoid hypotension)
Avoid ergotamine

31. Postpartum Careful attention to fluid balance
Watch for failure to diurese
Discuss contraception

32. Well-Behaved Lesions Mitral regurgitation Aortic regurgitation
Prosthetic valves
ASD
VSD
PDA

33. Not so well behaved lesions: Mitral stenosis
State of fixed cardiac output – avoid hypotension and tachycardia
Left atrial and pulmonary pressures are increased
Can go into pulm. HTN if longstanding disease
Issues for antenatal care:
Watch re: symptoms of right heart failure
Beta-blockers can be used to control rate
Watch for arrhythmia

34. Asthma in pregnancy Incidence 1% in general
15% of them will have an attack

35. Effects of pregnancy on the respiratory system
Ribs flare out, subcostal angle increases as transverse diameter of chest increases by 2cm and diaphragm rises by 4cm.
Minute ventilation increases while the respiratory rate remains the same.
Progesterone stimulates brain centers to produce hyperventilation which decreases alveolar CO2 tension and the arterial PCO2 producing respiratory alkalosis.

36. Blood gas values in pregnant and non-pregnant women.
Status pH
PO2
(mmHg)
PCO2
Non-
pregnant
7.4 93
35-40
Pregnant 30

37. Physiological changes in pregnancy
We must remember that a PO2 < 70 in a pregnant woman with acute asthma represents severe hypoxemia, and a PCO2 > 35 represents acute respiratory failure.
Normal alkalosis in pregnancy can be aggravated by acute asthma and lead to significant decreases in placental blood flow
If hypoxemia is present, it is more severe in the fetus.

38. Tidal volume remains same. Decrease in: FRC, RV, ERV, TLC.

39. Physiological changes in pregnancy
Although assessing FEV1 and FVC is important clinically to monitor efficacy of treatment it requires spirometry.
PEFR (peak expiratory flow rate) requires only an inexpensive portable flow meter and changes in a pregnant asthmatic with SOB are likely caused by asthma and not by physiological change in pregnancy.
Thus educating the patient is key to proper Mx.

40. Effect of asthma on pregnancy
Mild: no or minimum effect
Severe: increase in
Abortion
IUFD
IUGR

41. Management Most will require no drug treatment Envirmental control
Mild: B-agonist inhalers
Severe: oral steroids
Vaginal delivery should be anticipated