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Circulatory Physiology

Circulatory Physiology. AnS 536 Spring 2014. Development of the Circulatory System. 1st functional organ system – heart is functional when embryo is 2 mm in size Heart rate peaks at 9 weeks, and slows to ~145 beats at term

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Circulatory Physiology

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  1. Circulatory Physiology AnS 536 Spring 2014

  2. Development of the Circulatory System • 1st functional organ system – heart is functional when embryo is 2 mm in size • Heart rate peaks at 9 weeks, and slows to ~145 beats at term • Huge increase in cardiac output postnatally but limited ability to increase further • Increase in thyroid hormone prenatally matures myocardium in preparation for increased postnatal requirements

  3. Development of the Circulatory System • The heart functions partly in parallel and dominated by right ventricular function • Parallel function allows the shunts to be more effective and the foramen ovale to not compromise cardiac output • Heart functions in series postnatally with equal ventricular function • Blood volume ~11% in fetus (7.5% in adults) because of amount of placental blood

  4. VIDEO BREAK http://www.youtube.com/watch?v=K4B5fFQ8OGw&feature=player_detailpage

  5. The Fetal Circulatory System Pathways of the fetal heart and representative oxygen saturation values (in numbers). The via sinistra (red) directs well oxygenated blood from the umbilical vein (UV) through the ductus venosus (DV) (or left half of the liver) across the inferior vena cava (IVC), through the foramen ovale (FO), left atrium (LA) and ventricle (LV) and up the ascending aorta (AO) to join the via dextra (blue) in the descending AO. Deoxygenated blood from the superior vena cava (SVC) and IVC forms the via dextra through the right atrium (RA) and ventricle (RV), pulmonary trunk (PA) and ductus arteriosus (DA). The isthmus aortae (arrow) and the section of the left portal vein between the main stem (P) and the DV (striped area) represent watershed areas during hemodynamic compromise. CCA, common carotid arteries; FOV, foramen ovale valve; LHV, left hepatic vein; MHV, medial hepatic vein; PV, pulmonary vein; RHV, right hepatic vein

  6. Foramen ovale Shunts blood from the right atrium to the left atrium Ductus arteriosus Shunts blood from the pulmonary artery to the ascending aorta Bypasses pulmonary circulation Ductus venosus Shunts blood from the umbilical vein to the inferior vena cava Separates the hepatoportal and systemic circulation Physiology Fetal blood passes from the placenta  umbilical vein  fetal heart Left ventricle shunts blood to the cranium Advantages of shunts Bypasses normal “flow patterns” to allow most oxygenated blood (left ventricle) to reach the fetal brain Unsaturated blood (from the right ventricle) is diverted to the trunk and lower body of the fetus Fetal Circulatory Shunts

  7. Blood coming from the placenta (umbilical veins) is 80% saturated with oxygen Enters right atrium via inferior vena cava Half of venous return bypasses portal circulation via ductusvenosus Because ductusvenosus has small diameter, blood accelerates and is more likely to push though foramen ovale into left atrium and to “upper circulation” From right atrium to left atrium via foramen ovale (now 65% saturated) Pumped to carotid artery and to brain (most oxygen rich blood) Oxygen Tension Levels

  8. Foramen Ovale Flow distribution at the foramen ovale. The edge of the atrial septum (crista dividens) divides the ascending flow in two arms, to the right and left atrium (RA and LA). The horizontal diameter between the foramen ovale valve and the atrium (broken line) represents the restricting area into the LA. Position, direction and kinetic energy of the flow from the ductusvenosus makes it predominantly enter the left atrium (dark gray). Conversely, blood from the inferior vena cava (IVC) enters the RA (light gray). Ao, aorta; PA, pulmonary trunk; PV, stem of the portal vein (From Kiserudand Rasmussen, 2001)

  9. Blood coming from the superior vena cava is directed primarily through tricuspid valve into right ventricle (50% saturated with oxygen) Enters aorta, provides lower levels of oxygen to caudal half of body and then enters the umbilical arteries to be re-oxygenated in the placenta Once oxygenated, returns to body as fully oxygenated blood via umbilical veins Oxygen Tension Levels

  10. DuctusArteriosus • Factors involved in closure • PGE2 helps maintain patency and nitic oxide will cause relaxation (indomethacin will induce closure anytime during latter half of third trimester through postnatal life) • Increased PO2 of arterial blood postnatally causes spasms of the ductus • Fetus has low-resistance circulation from the placenta during gestation • Parturition, umbilical cord rupture, and initiation of respiration increase resistance

  11. DuctusArteriosus • Physiological changes • Lungs become the organ of respiration • Oxygen tension increases • Right ventricular outflow passes into the lungs instead of the ductus • Ductus constriction begins shortly after birth • Closure occurs 24-48 hours after birth

  12. Factors involved in closure Liver pressure and resistance Gestational age and weight at birth Premature neonates will have delayed closure Drugs Promote closure Antenatal corticosteroids Delay closure Prostaglandins and nitroxide distend diameter of ductus DuctusVenosus

  13. VIDEO BREAK http://www.youtube.com/watch?v=SUP1K4gPw4s&feature=player_detailpage

  14. Physiologic changes Functional closure initially after birth Umbilical vein constricts reducing supply of shunted blood Ductusvenosus becomes ligamentumvenosum Blood enters liver through hepatic sinuoids DuctusVenosus

  15. Foramen Ovale • Factors contributing to closure • Pulmonary and vascular resistance increase • Physiological changes • Increased quantity of blood into the left atrium • Causes left atrial pressure to rise above that in the right atrium • Closes the flap of this one-way valve preventing blood flow across the septum • Anatomical closure takes months or years

  16. VIDEO BREAK http://www.youtube.com/watch?v=wsDwQw1JjTU&feature=player_detailpage http://www.youtube.com/watch?v=ZOtk_FSfHpw&feature=player_detailpage

  17. Persistent (Patent) DuctusArteriosus • Failure of closure of the vessel that joins the pulmonary artery to the aorta • Effects • Depend on size of shunt and degree of pulmonary hypertension • Small to moderate shunts • Easy to fatigue, dyspnea on exertion and exercise intolerance later in life • Large shunts • Poor growth and development • Frequent episodes of pneumonitis and development of congestive heart failure • Life expectancy is markedly reduced – these individuals often die in their second or third decade

  18. Persistent (Patent) DuctusArteriosus • Potential causes • Hypoxia and acidosis will increase pulmonary vascular resistance and increase right-to-left shunting • Higher incidence when infants are born at high altitudes (>10,000 ft) • Twice as common in females vs. males • Frequency increased in preterm infants • Fail to close spontaneously • Closure induced with cyclooxygenase inhibiting drugs in premature babies ONLY • COX-1 and COX-2 are enzymes in arachidonic acid metabolism producing producing prostaglandins, prostacyclins and thromboxanes • COX inhibitors are NSAIDS (ibuprofen or indomethacin)

  19. VIDEO BREAK http://www.youtube.com/watch?v=g_zQEQBLv_g&feature=player_detailpage

  20. Persistent Pulmonary Hypertension • Occurs when pulmonary vascular resistance fails to decrease • Treatments • Mechanical hyperventilation • Inhaled nitric oxide • Ventilation • Extracorporeal membrane oxygenation (ECMO) • Free radical scavengers (SOD)

  21. Mechanical hyperventilation Results in alkalosis Improves condition as systemic pH rises over 7.55 to 7.6 Problems can occur if too vigorous or sustained too long Inhaled nitric oxide Mimics endothelium-derived relaxing factor Promotes pulmonary vasodilatation Poorly sustained response in most infants Persistent Pulmonary Hypertension

  22. Ventilation High oscillatory Effective with severe associated lung disease ECMO Infants placed on blood bypass pump Blood exits the right atrium passes through a membrane oxygenator and returns to the aortic arch Lungs are essentially at rest When hypertension improves – infants are weaned off Problems Used as a last resort Neurodevelopmental disorders can occur Persistent Pulmonary Hypertension

  23. Factors involved Chemical Bradykinins Epinephrine Seratonin Mechanical Increase in PO2 Humoral Thromboxane Histamine If constriction does not occur Persistent bleeding leading to hemorrhage and severe blood loss Potential for infection Surgical intervention may be needed Umbilical Vessel Constriction

  24. Transfer of blood from the placenta to the fetus at birth Dependent upon timing of umbilical clamping (1-5 minutes) after birth Late clamping Increases blood volume and RBC’s of neonate (20-50%) Can increase bilirubin concentrations Early clamping Decreases blood volume  anemia Foals Early clamping leads to barker syndrome, temporary blindness, and dummy foal syndrome Increased frequency of death Placental Transfusion

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