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