Transcript HEART DISEASE IN PREGNANCY

HEART DISEASE IN
PREGNANCY
The incidence of cardiac lesion is less than 1% among hospital
deliveries. The commonest cardiac lesion is of rheumatic origin
followed the congenital ones.
Rheumatic valvular lesion predominantly includes mitral stenosis
(80%)
The marked hemodynamic changes by pregnancy have a profound
effect on underlying heart disease. During pregnancy cardiac
output is increased by as much as 50%
Almost half the increase occurs by 8 weeks and it is maximized by
mid pregnancy.
The early increase can be attributed to augmented stroke volume
that results from decreased vascular resistance. Later in
pregnancy, resting pulse increases, stroke volume increases even
more, presumably because of increased diastolic filling from the
expanded blood volume. Because significant hemodynamic
alterations are apparent early in pregnancy, women with severe
cardiac dysfunction may experience worsening of heart failure
before midpregnancy. In others heart failure develops after 28
weeks, when pregnancy induced hypervolumia is maximal. In
majority, however heart failure develops peripartum when the
physiological capability for rapid changes in cardiac output may be
overwhelmed in the presence of structural cardiac disease
History in cardiac disease aims at
Diagnosing the heart disease
To clinically classify the heart disease
Clinical indicators of heart disease
during pregnancy
History of progressive dyspnoea/orthopnoea
Nocturnal cough
Hemoptysis
Syncope
Chest pain
Palpitations
Clinical classification: 1928 by New York Heart
Association (NYHA)
Class I: Uncompromised - No limitation of
physical activity
Class II: Slight limitation of physical activity.
Women are comfortable at rest
But if ordinary physical activity is undertaken
discomfort results in the form of excessive
fatigue, palpitation, dyspnoea or chest pain
Class III: Marked limitation of physical activity
Women are comfortable at rest, but less than
ordinary activity causes fatigue, palpitation,
dyspnoea and chest pain
Class IV: Severely compromised - Symptoms
even at rest
Past History
History of cardiac failure in past
pregnancy in multi
History of rheumatic fever/arthritis/ RHD
History of CHD
History of Surgery before or in present
pregnancy
Drug therapy like anticoagulants or
penidure prophylaxis
Personal History
History of alcohol or smoking should be
asked
Examination - Patient may be uncomfortable at rest
Temperature may be increased due to secondary infection
Cyanosis: Peripheral or central
Clubbing
Pulse – Rate: Tachycardia
Rhythm: Irregularly irregular pulse-AF, ectopic beats
Volume High volume pulseAortic regurgitition
Thyrotoxicosis
Associated anaemia
Low volume - Mitral stenosis
Collapsing pulse – Aortic regurgitition
Respiratory rate increased, orthopnoea may be present
B.P.: May reveal associated PIH
Wide pulse pressure as in aortic regurgitition
Patient in failure: JVP is raised
Pedal oedema
Tender hepatomegaly
Associated
Anaemia
Thyroid enlargement
Dental caries
Cardiac examination in detail
Inspection: Precordial bulge
Abnormal pulsations - Parasternal heave - Right
ventricular hypertrophy
Forceful Apical impulse - left ventricular enlargement
Palpation: Mitral area - apical impulse location and quality
Pulmonary area - Palpable II heart sound
Palpation of thrill
Percussion: Cardiac borders to be located
Auscultation: Mitral area- Opening snap
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Mid diastolic murmur } MS
Loud S1
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Pansystolic murmur - MR VSD
Aortic area - Ejection systolic murmur conducted to
carotids –Aortic stenosis
Early Diastolic murmur Aortic regurgitition
Pulmonary area - Loud second sound - Pulmonary
hypertension
Split fixed second sound - ASD
Tricuspid area - Pansystolic murmur more during
inspiration - TR
Abdominal examination
Hepatomegaly
Ascitis
Fundal Height May be less than expected
because of IUGR
To rule out CPD as there is no place for trial
of labour
Respiratory system
Basal crepitations - Pulmonary oedema
Associated Infections