Scribd Logo
Upload

Welcome to Scribd!

  • Cardiac

    Uploaded by

    Usman AR Vaince
    6 views10 pages

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    Report this Document

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    6 views10 pages

    Cardiac

    Uploaded by

    Usman AR Vaince

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    of 10
    iy Cardiac disease in pregnancy Rog “The most striking cardiovascular change in early pregnancy is a marked decreaein peripheral resistance, which fllsby up 30% of it prepregnancy valve (1) Tiss most likely de tothe changes in maternal hormone levels (particularly progesterone, slain, pros- tacydlin, and prolactin) brought about by the developing concepts, stimulated in part byt secretion of human chorionic gonadotropin (similar in structure to luteinizing hormone) although exactly how these hormones act to do this remains uncertain (2)-Itis probably mediated in part by the sneeases in nize oxide production in the «endothelium (3), and by increased resistance othe effects of angi tensin II and norepinephrine (noradrenaline). As pregnancy pro- sreses, the placental circulation is established, and its blood flow ‘of up to 700 ml. per minute bythe third trimester (bout 10% of ‘cardiac output) acts a low resistance shunt which contsbutes to the loss of peripheral resistance (4). These changes would produce ‘a marked decreae im blood presse if ther ellct was not coun teraced by the increase in circulating blood volume of upto 50% (there i large increase in plasma volume and a somewhat smaller inexease in the ctculating red cell mass, resulting in a decrease in Ihsemoglobin concentration—the ‘physiological anaemia of preg- nancy’) This increase occurs because the decreas in blood pres- sure stimulates the production of renin inthe kidney leading tthe {formation of angiotensinogen and angiotensin I, which s thea con- verted into angiotensin If by a converting enzyme (2) This would normally produce vasoconstriction, but this action is blocked by the hhormone changes described carr. However is effects on the ad- scnal cortex and kidney arenotblocked,revulingin a three-‘ofour- fold increase in aldosterone level, causing cumulative sodium and ‘water retention which expands the circulating volume and restores ‘cardiac preload. The overall net change is up to 50% increase in resting cardiac output, which peaks between 26 and 36 weeks of pregnancy, and which represents a considerable challenge to anyone ‘with impaired cardiac function Clisealy, these changes are manifested by a small (about 10 mig) decrease in blood pressure as pregnancy progresses, reaching 8 nadir between 26 and 34 weeks of gestation, and then rising slowly thereafter back tothe prepregnancy level by bout 40 ‘weeks (5), Resting heart rate increases by about 15-20 bests per mic saute (bpm) bythe early tied wimester: esting heart ratof 90-100 ‘bpm is common but rates higher than this shouldbe investigated. Both cardia oulput and blood pressure can decrease in pregnant ‘women who are allowed to lie on their back in late pregnancy, be- ‘cause the weight ofthe ulerus compresses the inferior vena cava and obstructs Venous return, This can cause the woman to fel faint and may i prolonged led to a reduction n placental perfusion and {etalhypoxis the supine position should therefore be avoided in late pregnancy and labour especally ifthe mother ha an epidural an- aesthetic (which also encourages venous pooling inte legs). ‘The sess and pain ofabour also places an increased demand on, the heart (6), which can largely be avoided by the use of regional an- aesthetic for pain relief Because rapid onset af sympathetic blockade ‘an decrease blood pressure acutely, itis wsul to administer such a blockade very slowly with careful monitoring Congenital cardiovascular malformation is the single commonest ‘group of congenital abnormalities seen in newborn children, ‘occurring about 0.8-1% (7), Before the introduction of open heart surgery in the 1960s (requiring the development of heart-lung by- pass technology, and the use of hypothermia), about two-thirds of flected babies died in the ist year of life (8). Accordingly, the majority of women with cardiac disease becoming pregnant before the 1960s had acquired disorders, mostly secondary to theumatic fever. Mitral stenosis (caused by autoimmune damage to the valve associated with the immuune response to rheumatic fever caused by. streptococcal infections) was the commonest lesion, and in 1957 the maternal mortality due to acquired heart disease was approxi- rately 5 per 100,000 maternities. However the widespread use of penicillin greatly reduced the incidence of rheumatic fever, and by 1990 the maternal mortality rate due to acquired disease had fallen tw only 0.38 per 100,000 maternities. In contrast, by the 1990s two. thirds of women with congenital heart disease were surviving into their 208 and were therefore eligible to become parents themeelves SECTION 2 Fetomaternal Medicine 1999 2002 2005, 2008 Figure 12.1 Cardiac deste 1 Source dts rom Caml 8 Chaan-rockT Cooper, Dasion A Ore) Carae Data Sarng Votes ves evening mater aexhs'9 mace meieho0e ‘ler 2005808 The tpn Repo ae Cenenes Ensis Vs] Desh Inte Unvea Kngéom S105 201,18 Supp 1-203 (8); and they now accounted for half of maternal deaths due to car- diac disease (also 0.38 per 100,000 maternities). However, since that time, in the United Kingdom, the rate of death due to acquired heart disease has increased again—it has almost trebled, to 2.18 per 100,000 maternities in 2008, while those due to congenital hear dis- case had fallen to 0.13 per 100,000 maternities (Figure 121) (9). The ‘United Kingdom Confidential Enquiries into Maternal Deaths and ‘Morbidity report for the triennisim 2009-2011 confirmed the fact that cardiac disease now represents the single most common cause ‘of maternal death related to pregnancy (10) (Figure 12.2). What ies bbehind this worrying increase? ‘Currently, one-third of maternal deaths from cardiac disease are ‘the result of myocardial infarction/iechaemic heart disease, This sin part due to the growing number of women having babies ater in life. ‘Figure 12.3 illustrates the changing age distribution of maternal age in the United Kingdom from 1938 through 2013. The most striking {feature isa more than halving ofbirths to women under the age of25 since the eatly 1970s, paralleled by a mote than fourfold increase in 5 i [-Hyperenion | + Haemorrhage Sepsis | thrombosis Jecardine > a we SS oP Fo oS 8 Pe PPS Figure 12.2 Numer of ceths by cause by yar Sve dan fon MOIACE=K sa hes mpeg Mabe’ Creel Seams vreomeadsininenne onepeniee pte seas “prom pene roxtoeeraani ate births to women aged 35 and over. This iea trend seen in most devel- ‘oped countries, and has resulted in a major increase in age-related complications such ashypertension, diabetes, and obesity (11), all of ‘which contribute tothe aetiology of ischaemic heart disease ‘A further third of deaths are associated with cardiomyopathy. “This comprises a variely of conditions, the commonest being hypertrophic cardiomyopathy and the specific pregnancy-related condition of peripartu cardiomyopathy, as well as less common conditions such as restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and let ventricular non-compaction. ‘The overall prevalence of dilated cardiomyopathy is difficult to de- fine because many affected individuals ae apparently healthy: about a third of cases are familial (12). The common feature in all cases is left ventricular dilatation and systolic dysfenction in the ab- sence of any obvious cause such as hypertension. The aetiology of peripartam cardiomyopathy remains conjectural, but may include genetic susceptibility, viral myocarditis, immunologically mediated damage, and the antiangiogenic 16 kDa fragment of the hormone prolactin (13) Rheumatic heart disease, congenital heart disease, and pul ‘monary hypertension are currently each responsible for about 5~ 10% of deaths. Implications for the baby Fetal growth is very dependent upon efficient placental perfusion snd gas nd nutrient exchange. Thien tur is determined party by maternal cardiac output atfectng the maternal blood supply tothe placenta), the structure and function ofthe placenta itself (ineuding the microvasculature), and the efiiency ofthe etal circulation. In ‘women with heart disease, even when apparently normal cardiac cpt ie maintained, there ssa tendency for babies to be smaller than average (Figure 12.4), The reasons for this are not cleat, but sight in some cases be associated with duced maternal stature, impaired nutetion, or genetic effects. Easier to understand is @ greater reduction in mean centile birboeeight when there is reduced

    You might also like