CARDIAC DISEASE IN CARDIAC DISEASE IN PREGNANCYPREGNANCY
Dr. Yasir Katib
MBBS, FRCSC, Perinatologest
Multiple ChoiceMultiple Choice
When during pregnancy is peripheral vascular resistance at its lowest?
1. First trimester
2. Second trimester
3. Third trimester
4. labour
When during pregnancy is peripheral vascular resistance at its lowest?1. First trimester
2. Second trimester
3. Third trimester
4. labour
When during pregnancy is cardiac output highest?
1. Second trimester
2. Third trimester
3. Labour
4. Postpartum
When during pregnancy is cardiac output highest?1. Second trimester
2. Third trimester
3. Labour
4. Postpartum
Which is not a normal ECG change in pregnancy?
1. Q wave in lead III
2. Sinus tachycardia
3. ST-T wave changes
4. Prolonged QT interval
Which is not a normal ECG change in pregnancy?1. Q wave in lead III
2. Sinus tachycardia
3. ST-T wave changes
4. Prolonged QT interval
Physiologic Changes in Physiologic Changes in PregnancyPregnancy
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
Physiology changes cont’dPhysiology 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)
Physiology cont’dPhysiology 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%
Physiology cont’dPhysiology 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
Physiology cont’dPhysiology cont’d
Increased venous compliance– Leads to increased stasis– Therefore, more sensitive to autonomic
blockade
Physiology cont’dPhysiology cont’d
Anatomic changes:– Increased ventricular wall muscle mass (T1
only)– Increased EDV (continues through T2, T3)– These combine to cause physiologically dilated
heart
Physiology cont’dPhysiology 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
Physiology cont’dPhysiology 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
IntrapartumIntrapartum
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
PostpartumPostpartum
80% increase CO within 15 min delivery60% increase if caudal anesthesiaIncrease 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
PostpartumPostpartum
CO returns to prelabour values by 1hC/S leads to 25-50% increase in COLeft atrial dimensions increase days 1-3 pp,
normalize within 10dLeft ventricular dimension takes 4-6 mos to
decreaseSV, CO and SVR reach normal by 12 wk
NYHA Functional NYHA Functional ClassificationClassification
Class I: no symptoms with normal activityClass II: symptoms with ordinary activityClass III: symptoms with less than
ordinary activityClass IV: symptoms at rest
Classifying Risk of MortalityClassifying Risk of Mortality
Group 1: mortality < 1%– ASD– VSD– PDA– MS (NYHA I,II)– Pulmonic tricuspid disease– Porcine valve– Corrected TOF
Mortality cont’dMortality 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
Mortality cont’dMortality cont’d
Group III: mortality 25-50%– Pulmonary HTN– Coarctation with aortic valve involvement– Marfan’s with aortic root dilatation (>40mm)– Eisenmenger’s
Approach to PregnancyApproach 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
AntenatalAntenatal
Multidisciplinary approachIf no preconceptual visit, evaluation of status
and counselingDiscuss termination if appropriateQuestion regularly re: symptomsMonitor weight and vital signs regularlyUS: dating, anatomy, growth and well-being
Antenatal cont’dAntenatal cont’d
Fetal echo at 22wksEcho, ECG etc. every trimesterAvoid strenuous exerciseConsult re: NICU, anesthesia
Labour & DeliveryLabour & Delivery
Lateral positionClose attention to fluid balanceContinuous ECG monitoringIn high risk: invasive monitoringClose fetal surveillanceC/S for OB indications, may use operative
vag delivery to shorten 2nd stage
L&D cont’dL&D cont’d
Antibiotics:– Prosthetic valves– Previous bacterial endocarditis– Complex cyanotic heart disease– Mitral valve prolapse with regurgitation– Acquired valvar dysfunction– Hypertrophic cardiomyopathy
L&D cont’dL&D cont’d
Epidural (avoid hypotension)Avoid ergotamine
PostpartumPostpartum
Careful attention to fluid balanceWatch for failure to diureseDiscuss contraception
Well-Behaved LesionsWell-Behaved Lesions
Mitral regurgitationAortic regurgitationProsthetic valvesASDVSDPDA
Not so well behaved lesions:Not so well behaved lesions:Mitral stenosisMitral 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
Asthma in pregnancy Asthma in pregnancy
Incidence 1% in general15% of them will have an attack
Effects of pregnancy on the Effects of pregnancy on the respiratory systemrespiratory 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.
Blood gas values in pregnant Blood gas values in pregnant and non-pregnant women.and non-pregnant women.
Status pH PO2
(mmHg)
PCO2
(mmHg)
Non-
pregnant
7.4 93 35-40
Pregnant 7.4 100-106 30
Physiological changes in Physiological changes in pregnancypregnancy
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.
Physiological changes in Physiological changes in pregnancypregnancy
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.
Effect of asthma on pregnancyEffect of asthma on pregnancy
Mild: no or minimum effectSevere: increase in
1. Abortion
2. IUFD
3. IUGR
Management Management
Most will require no drug treatmentEnvirmental controlMild: B-agonist inhalersSevere: oral steroidsVaginal delivery should be anticipated