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CARDIAC DISEASE IN PREGNANCY

CARDIAC DISEASE IN PREGNANCY. Dr. Yasir Katib MBBS, FRCSC, Perinatologest. Multiple Choice. When during pregnancy is peripheral vascular resistance at its lowest? First trimester Second trimester Third trimester labour.

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CARDIAC DISEASE IN PREGNANCY

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  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 4700-6200ml @ 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 250-400ml by term (20-30% increase) • Increased RBC due to placental somatomammotropin, progesterone • Therefore, increased demand for iron = 500mg +300mg fetus + 200 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%

  11. Physiology cont’d • Decreased systemic vascular resistance • Decreases from 5 wks due to progesterone and prostaglandins (cause vasodilatation) • Nadir at 14-24 wks then increases toward term

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

  13. 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

  14. Physiology cont’d • ABG: • Tidal volume increased by 40% leading to hyperventilation and hypocapnia • Therefore, decreased PCO2 to 28-31 mmHg • Partially compensated for by decreased bicarb level • Therefore, mild respiratory alkalosis with arterial pH = 7.44

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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

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

  21. 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

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

  23. 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

  24. 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

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

  26. 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

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

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

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

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

  31. 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

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

  33. 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.

  34. Blood gas values in pregnant and non-pregnant women.

  35. 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.

  36. 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.

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

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

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