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Cardiac Physiology

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Cardiac Physiology Cardiac Physiology Gia Marzano, AC PNP Pediatric Cardiac Surgery Rush Center for Congenital Heart Disease Rush University Medical Center Objectives Part 1 • Fetal Circulation • Transition to Postnatal Circulation • Normal Cardiac Anatomy • Ductal Dependence and use of PGE1 Objectives Part 2 • Basic principles of cardiac physiology • Basic categories of congenital heart disease based on pathophysiology • Application of physiology to your bedside management 1 Fetal Circulation Few Concepts • Fetal heart starts developing during the 3rd week of life • By the 3rd month of development, all major blood vessels are present and functioning. • Pulmonary Blood Flow is Low • Gas Exchange (Oxygen) occurs in placenta More Concepts • Pulmonary Resistance is High – Lungs are still underdeveloped – Small pulmonary arteries have a thicker smooth muscle layer than similar arteries in adults. Fetal Circulation Overview • Umbilical Circulation: – Pair of umbilical arteries carry deoxygenated blood & wastes to placenta. – Umbilical vein carries oxygenated blood and nutrients from the placenta. • Placenta facilitates gas and nutrient exchange between maternal and fetal blood. 2 Fetal Circulation Overview • Oxygenated blood from placenta is transported to the fetus through the Umbilical Vein Fetal Circulation Overview • Most of the oxygenated blood bypasses the liver through the Ductus Venosus and mixes with De-Ox Blood from IVC Fetal Circulation Overview • Blood travels from the IVC and enters the RA 3 Fetal Circulation Overview • 40 % of oxygenated blood from the IVC bypasses the RV and is shunted to the LA via the Foramen Ovale • The rest mixes with De-ox blood from the SVC and enters the RV Fetal Circulation Overview • Blood then travels to the LV and is distributed through the aorta mainly to the coronaries and upper body (carotid and subclavian arteries) • Only 1/3 of this volume goes to the lower body Fetal Circulation Overview • Most blood from the IVC (60%) mixes with SVC blood and enters the RV from the RA • Because the lungs are non-functional, most (90%) will be shunted away from the pulmonary arteries through the Ductus Arteriosus to the Descending Aorta and Placenta for oxygenation 4 Fetal Circulation Overview • Blood circulates to the body and returns to the placenta via the umbilical arteries Fetal Circulation Overview • Placenta re- oxygenates blood returning from the umbilical arteries • New fetal cardiac cycle… Fetal Circulation Overview • Parallel circulation with shunts (PFO and PDA) allows various lesions to provide adequate transport of blood to placenta for oxygenation and deliver it to the tissues • RV performs ~ 2/3 cardiac work RV larger and thicker at birth 5 Transitional and Post-Natal Circulation • What happens at birth ?? • The change from fetal to postnatal circulation happens very quickly. • 2 major events: – Changes initiated by baby’s first breath. – Elimination of the placenta Transitional Circulation • Clamping of the umbilical cord: – Eliminates the low resistance placental circulation peripheral vascular resistance increases – decreases blood volume returning to the heart from IVC Transitional Circulation • With initiation of pulmonary ventilation: – Increased alveolar O2 pressure vasodilates the pulmonary arteries – Pulmonary vascular resistance decreases significantly 6 Transitional Circulation Increase Drop in in systemic + pulmonary Vascular Vascular resistance resistance Pulm Blood flow increases 8-10 X Transitional Circulation • Increased pulmonary blood flow increased pulmonary venous return into LA LAP >RAP the greater LAP (and lower IVC flow) closes the valve of the foramen ovale, preventing right-to-left shunting. Transitional Circulation • PDA: changes from R2L conduit of blood to the descending aorta to a L2R conduit of blood to the lungs • Ductus arteriosus constricts and closes functionally within several hours after birth, largely in response to the increase in oxygen tension. 7 Transitional Circulation • PFO closure • Ductus arteriosus closure • These events result in the effective separation of the systemic and pulmonary circulations after birth. Ductal Dependence The Ductus Arteriosus • In fetus: – large channel that allows blood to bypass the lung circulation to the Dao and placenta for oxygenation – as big as the Dao ! (10mm) – allows equalization of Ao and pulm arterial P The Ductus Arteriosus Role of O2 • Thick muscular layer • Towards late gestation, the muscle layer thickens and the lumen becomes smaller • After birth, increased arterial O2 causes more constriction of the ductus • Constriction decreases PO2 in the muscle severe hypoxia cell destruction and fibrosis • Functional closure within 10-15 hrs after birth • Complete closure within 5-7 days, can be up to 21 days 8 Ductus Arteriosus Role of Prostaglandins • Produced by the wall of the ductus and placenta • 2 types: PGI2 and PGE2 • Relax the ductus arteriosus smooth muscle • Metabolized in the lungs • After birth, ↓↓ PG ductal closure Ductus Arteriosus in Congenital Heart Disease • In many CHD cases (mainly cyanotic), ductus does not close normally after birth: – TA/PA/TGA: arterial O2 remains low after birth lower stimulus for constriction – Left-sided lesisons (Ao atreasia, coarctation): arterial O2 increases after birth but the high PAP/flow keeps ductus patent Ductus Arteriosus in Congenital Heart Disease Ductal Dependency • Normally, ductus carries ~ 60 % of combined C.O from the PA to the DAo • If LV outflow tract is obstructed (e.g. aortic valve atresia, coarctation, interruption): – larger portion of combined C.O crosses the ductus (~90%) larger Ductus 9 Ductus Arteriosus in Lt sided lesions Ductal Dependency – After birth: need the ductus to provide most of systemic blood flow (from PA to Ao) Ductus Arteriosus in Congenital Heart Disease • If RV outflow is narrow (e.g. pulmonary atresia, tricuspid atresia) – minimal blood from RV to ductus small ductus Ductus Arteriosus in Rt sided lesions Ductal Dependency • After Birth: Need the ductus to maintain pulmonary blood flow 10 Prostaglandin Therapy • Indomethacin: inhibits PG production • PGE1: – relaxes the ductus arteriosus smooth muscle cells. – Effective within the first 7-10 days after birth – Dose: 0.05-0.1 mcg/kg/min – IV/PO Prostaglandin Therapy Side Effects • Apnea • Fever • Flushing • Hypotension • Thrombocytopenia • Seizure • Pyloric gastric outlet obstruction Questions? 11 Part 2 • Basic principles of cardiac physiology including Flow and pressure relationships Oxygen delivery Determinants of blood pressure and cardiac output Let’s start with a case… • You are admitting a 4 day old female who had no prenatal care and presented to the ED with poor feeding, respiratory distress, lethargy and poor urine output. PGE infusion was started in the ED. • On exam, she is floppy with grunting respirations and her skin appears gray. Let’s start with a case… • VS:T 97 P 190 R 70 BP 40/P SpO2 92% • PE: Chest: coarse BS with retractions Heart: tachycardic, no murmur Abd: soft, liver 4cm below RCM Ext: gray, cool, cap refill 5 sec, poor distal pulses 12 Let’s start with a case… • Labs: WBC 8.2 Hg 11 Hct 33 Plt 189 Lytes:Na132/K5/Cl103/CO8/BUN13/Cr0.9 ABG: 6.99/32/54/8/-16/85% CXR: cardiomegaly, increased PVM ECHO: critical CoA Questions… • A nursing student asks “why is that baby gray?” How will you answer? • Then she asks why the baby is so hypotensive. You explain… • The MD decides to transfuse prbc and asks you to get consent from the parents. What will you tell them is the reason for the transfusion? Flow and Pressure Relationship (all you really need to know to understand any concept in cardiac critical care….seriously!) 13 Ohm’s Law Pressure change (dP) Flow (Q) = __________________ Resistance (R) Increased P Increased Q Increased R Decreased Q Cardiac Physiology • What is the purpose of the heart? O2 Cardiac Physiology Delivery of oxygen (DO2) is a direct function of the cardiac output (CO) and the arterial oxygen content (CaO2) DO2 = CO x CaO2 14 Cardiac Physiology Oxygen Delivery DO2 = CO x CaO2 Cardiac Output (CO) Arterial Oxygen Content (CaO2 art Rate (HR) x Stroke Volume (Hgb(SV) x 1.39 x SaO2) + (0.003 x PaO roke Volume is directly related to: Preload Afterload Contractility Cardiac Physiology • What are we trying to achieve? Maximize O2 delivery Provide adequate end organ perfusion Maintain BP Determinants of blood pressure 15 Ohm’s Law BP = Flow(Q) x Resistance(R) What is Blood Pressure? BP CO SVR (Afterload) Heart rate Stroke Volume Intravascular Volume Contractility (Preload) Maintaining Blood Pressure • Derrangement in: – Volume status – Cardiac function BP – Vascular tone – Heart rate CO SVR HR SV Preload Contractility 16 Preload • Derrangement in: – Volume status – Cardiac function BP – Vascular tone – Heart rate CO SVR HR SV Preload Contractility Determinants of Cardiac Output • Preload -“Resting fiber length before contraction” -End diastolic ventricular volume -If preload is increased, SV and capability for pressure generation are increased. • Frank-Starling Mechanism -Compliance dependent CVP • CVP: Central venous pressure – Transduced via RA lines or CVL – Reflects the intravascular volume status of the patient and the filling pressure of the ventricle – Relationship between CVP and BP is important 17 Afterload (SVR) • Derrangement in: – Volume status – Cardiac function BP – Vascular tone – Heart rate CO SVR HR SV Preload Contractility Afterload • Any factor that resists the ejection of blood from the heart (SVR or obstruction) • With increasing
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