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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
HEART
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
Cardiac Output
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
Arterial pressure usually decreases to a nadir at 24 to 26 weeks Diastolic pressure decreases more than systolic Antecubital venous pressure remains unchanged
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)
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.
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
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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