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Maternal Physiology : Cardiovascular system

SMF/Dept.Obstetri dan Ginekologi FK UNAIR - RSUD dr Soetomo dr. Andita Hapsari

During pregnancy and the puerperium, the heart and circulation undergo adaptation.
Changes in cardiac Function Increase Cardiac output Increases the resting pulse rate Plasma volume expansion begins and preload is increased The first 8 weeks 5 week 10 beats/min Weeks 10 and 20

Ventricular performance during pregnancy is influenced by : The decrease in systemic vascular resistance Changes in pulsatile arterial flow

Allow cardiovascular system to adjust to the physiological demands of the fetus while maintaining maternal cardiovascular integrity

The heart is displaced to the left and upward and rotated on its long axis The apex is moved laterally from its usual position

Larger cardiac silhouette on chest radiograph May increase the cardiac silhouette

Pregnant women normally have some degree of benign pericardial effusion

No characteristic electrocardiographic changes other than slight left-axis deviation

HEART

Cardiac sounds during pregnancy


(1) An exaggerated splitting of the first heart sound with increased loudness of both components (2) No definite changes in the aortic and pulmonary elements of the second sound (3) A loud, easily heard third sound (Cutforth and MacDonald (1966))

Cardiac sounds during pregnancy


A systolic murmur (90 percent disappeared shortly after delivery) A soft diastolic murmur (noted transiently in 20 percent) Continuous murmurs arising from the breast vasculature (10 percent)

The reversible morphological and functional adaptations


Cardiac plastcity is likely a continuum that encompasses physiological growth (exercise), as well as pathological hypertrophy (hypertension) -Hill and Olson, 2008
Physiological hypertrophy Never been absolutely proven

Serial Echocardiographic examination across pregnancy and postpartum in 46 healthy women 34% greater left ventricular muscle mass index during late vs early pregnancy Schannwell and associates, 2002
Derived with Echocardiographic, have not been verified with MRI

Any increased mass does not meet criteria for hypertrophy Hibbard and colleagues, 2009

Mean arterial pressure and vascular resistance

Blood volume and basal metabolic rate

Cardiac output at rest, in lateral recumbent position, beginning in early pregnancy

Cardiac Output

In lateral recumbent position

At term : increase 1.2 L/min (almost 20 percent)


a woman was moved from her back onto her left side.

Fetal oxygen saturation : 10 percent higher


a laboring woman is in a lateral recumbent > supine

Multifetal pregnancies : Singletons Maternal CO


by another almost 20% (SV 15 % and HR 3.5 %)

Left atrial diameter and left ventricular end-diastolic diameter


due to augmented preload

cardivascular reserve
due to the increased heart rate and inotropic contractility

Heart rate, stroke volume, and cardiac output Systemic vascular and pulmonary vascular resistance Colloid osmotic pressure. NSC for -Pulmonary capillary wedge pressure -Central venous pressure (between late pregnancy and the puerperium)

Cardiac output Left ventricular function (stroke work index) ~ to the nonpregnant normal range

Hemodynamic Function in Late Pregnancy

Brachial artery pressure <

Arterial pressure usually decreases to a nadir at 24 to 26 weeks Diastolic pressure decreases more than systolic Antecubital venous pressure remains unchanged

Circulation and Blood Pressure

In the supine position, femoral venous pressure rises from 8 mm Hg early in pregnancy to 24 mm Hg at term The occlusion of the pelvic veins and inferior vena cava by the enlarged uterus

The dependent edema frequently experienced Varicose veins in the legs and vulva, as well as hemorrhoids Deep-venous thrombosis
The elevated venous pressure returns to normal when the pregnant woman lies on her side and immediately after delivery

Supine compression of the great vessels by the uterus causes significant arterial hypotension, sometimes referred to as the supine hypotensive syndrome (10%).
(Kinsella and Lohmann, 1994)

Uterine arterial pressure and blood flow lower than in the brachial artery. May directly affect fetal heart rate patterns.
(Tamas and colleagues, 2007)

Occurs with hemorrhage or with spinal analgesia

Supine Hypotension

Renin-angiotensin-aldosteron Produced by the maternal kidney and the placenta Renin substrate (angiotensinogen) is produced by maternal and fetal liver. In part, from high levels of estrogen.

Renin, Angiotensin II, and Plasma Volume

Stimulation of the renin-angiotensin system is important in first-trimester blood pressure maintenance.


(August and colleagues (1995))

Nulliparas who remained normotensive became and stayed refractory to the pressor effects of infused angiotensin II.
(Gant and associates (1973))

Progesterone related. Lose the vascular refractoriness to angiotensin II within 15 to 30 minutes after the placenta is delivered. Large amounts of intramuscular progesterone given during late labor delay diminishing refractoriness.

Chamber-wall stretching

Cardiomyocytes

Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP).


Regulate blood volume natriuresis, diuresis, and vascular smooth-muscle relaxation. ANP physiological adaptations in the expansion of extracellular fluid volume The increase in plasma aldosterone concentrations

C-type natriuretic peptide (CNP), is predominantly secreted by noncardiac tissues.

Cardiac Natriuretic Peptides

Renal medullary prostaglandin E2 synthesis is increased Prostacyclin (PGI2) is increased during late pregnancy -Regulates blood pressure and platelet function. -Implicated in the angiotensin resistance

Prostaglandins

Potent vasoconstrictor Produced in endothelial and vascular smooth muscle cells Regulates local vasomotor tone Stimulated by angiotensin II, arginine, vasopressin, and thrombin. Stimulate secretion of ANP, aldosterone, and catecholamines. Endothelin receptors are in pregnant and nonpregnant myometrium. Identified in the amnion, amnionic fluid, decidua, and placental tissue Vascular sensitivity to endothelin-1 is not altered during normal pregnancy

Endothelin

Released by endothelial cells Have important implications for modifying vascular resistance during pregnancy Abnormal nitric oxide synthesis has been linked to the development of preeclampsia

Nitric Oxide

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