cardiac cycleBackground After a cavopulmonary anastomosis, the superior vena caval flow, by virtue of being the effective pulmonary blood flow, is the most important factor influencing the systemic arterial saturation. Determination of the amount of this blood flow will allow a better understanding of the physiology of the circulation after this anastomosis. The purposes of this study were to determine the volumetric flow in the superior vena cava and to evaluate its contribution to the cardiac output as children grow. Methods and Results Using two-dimensional and Doppler echocardiography, we measured the diameter of and mean flow velocities in the superior venae cavae and the pulmonary arteries of 145 healthy children. We calculated the volumetric flow in each vessel and determined the ratio of superior vena caval flow to total cardiac output. Cardiac output and superior vena caval flow increased with increasing age and body surface area. The superior vena caval flow accounted for 49% of cardiac output in newborn infants. This contribution increased to a maximum of 55% at the age of 2.5 years. Afterward, there was a slow decline in the ratio of superior vena caval–pulmonary arterial flow; it reached the adult value of 35% by 6.6 years of age. Conclusions There is a maturational change in the superior vena caval contribution to total cardiac output in children. This is most likely related to somatic growth and changes in body segment proportions. This flow maturation may explain the higher systemic saturation in infants compared with older children after cavopulmonary anastomosis.Key Words: cardiac output • regional blood flow • circulation • echocardiography • hemodynamics INTRODUCTION Fetal lamb studies showed that 22.5% of systemic venous return to the right atrium is from the superior vena cava.1 2 In human adults, 35% of the cardiac output returns through the superior vena cava; the remainder, through the inferior vena cava and the coronary sinus.3 Few data exist regarding the distribution of systemic venous return to the heart in neonates, infants, and children. There are changes in the ratio of upper to lower body segments4 and in regional body surface area5 and thus regional blood flows as the human grows from newborn to adult. For example, the newborn infant's head accounts for 19% of the total body surface area compared with only 9% in an adult.5 The Glenn6 cavopulmonary shunt and the Fontan procedure7 channel systemic venous return directly to the pulmonary circulation. These operations are used to palliate a variety of complex congenital cardiac defects. Thus, information regarding caval flow would be important in our understanding of the physiological effects of these anastomoses. Therefore, the aims of this study were to evaluate quantitatively, by Doppler echocardiography, the superior vena caval volumetric flow and to determine its relative contribution to cardiac output in infants and children. Our previous data, in infants only, demonstrated a nearly equal distribution of blood flow in the superior and inferior venae cavae.8 The goal of this study was to define this distribution over the first 6.6 years of human growth. METHODS Newborn infants (in the first week of life) were recruited from the well baby nursery of the Regional Medical Center in Memphis, Tenn. These infants were receiving standard medical care in the newborn nursery. The children were recruited from the pediatric clinics of the University of Tennessee during routine health maintenance visits. All infants and children had normal cardiovascular physical examinations and were in stable hemodynamic state. No children were acutely ill or were taking any medications at the time of the study. Children with conditions that may have caused an increase in their cardiac output, such as fever or anemia, were excluded. The protocol was approved by the University of Tennessee Institutional Review Board, and informed parental consent was obtained.Doppler Echocardiography A complete echocardiographic study was performed with a multiple-plane imaging approach; only children with normal cardiac anatomy were included. Each child was examined in the supine position. Variation in flow with changes in body position were not part of the study design, in part to maintain the same physiological conditions in all patients regardless of age. To eliminate any possible effects of sedation on the cardiac output and regional blood flows, no sedatives were used. We performed these studies on infants and children in the awake and calm state. If at any time a child became agitated, the study was stopped until the child became calm. A bottle of formula was offered at times to help soothe the child. If all failed, the study was terminated, and the subject was excluded. Only completed studies, ie, studies that recorded both the superior vena caval and pulmonary flows, were included. All ultrasound recordings were obtained with a Toshiba ultrasonoscope (model SH-140-Japan) using a 2.5-, 3.75-, or 5-MHz transducer and were recorded on super VHS videotape for later analysis. Color-flow, pulse-wave, and continuous-wave Doppler studies were used to assess intracardiac flows. Pulmonary arterial flow velocities were interrogated by color-flow Doppler to exclude infants or children with patent ductus arteriosus. Pulmonary arterial blood flow velocities were recorded from the parasternal short-axis view. The pulse-wave Doppler sample volume was placed in the middle of the main pulmonary artery distal to the pulmonary valve and proximal to the pulmonary artery bifurcation. The transducer was angled until the maximal frequency shift was obtained. Superior vena caval flow velocities were recorded from the subxyphoid sagittal view. The pulse-wave Doppler sample volume was placed in the superior vena cava just proximal to the cavoatrial junction. The Doppler beam was angled in a similar fashion to achieve the maximal frequency shift. We found this approach easier to use than the suprasternal notch window, especially in young children. In addition, it provided higher superior vena caval flow velocities than the suprasternal notch view. To time flow events, a simultaneous ECG was recorded with the Doppler flow velocities. Flow profiles were displayed as the frequency shift versus time at 50-mm/s sweep speed. The RR interval was measured from the same beats used to assess the velocity integral. The pulmonary artery ID was measured in the parasternal short-axis view distal to the pulmonary valve (ie, the distance between the luminal bright edges of the pulmonary artery) from a midsystolic frame. The superior vena caval ID was measured from the subxyphoid sagittal view in most children. In some older children, because of the long distance between the transducer and the superior vena caval orifice, the diameter was assessed from a right parasternal view to obtain a more accurate measurement. The superior vena caval diameter was measured at the right atrial–superior vena caval junction. To eliminate any possible respiratory or cardiac cycle effects, superior vena caval diameter was measured from several different frames. Previous studies on chronically instrumented dogs demonstrated that the average change in the superior vena caval diameter secondary to cardiac pulsation was approximately 2% of the diameter.9 In addition, during thoracotomy in humans, the superior vena caval diameter looked roughly unchanged during positive pressure ventilation.10 These minimal changes cannot be distinguished with current echocardiographic measurement devices. The mean velocity of blood flow was calculated from the integral of the Doppler velocity tracings. Flow time and heart rate were measured from the same beat. Because superior vena caval flow occurs throughout the cardiac cycle, its flow time was equal to the cardiac cycle. Pulmonary arterial flow time was equal to the time from the beginning to the end of the pulmonary arterial flow profile. Five or more cardiac cycles were analyzed for each patient. Because all infants and children were in normal hemodynamic state and fully hydrated during the echocardiographic study, we assumed that both the pulmonary artery and the superior vena cava had completely circular cross sections. The equations used for flow were as follows: cardiac output=pulmonary flow=pulmonary artery cross-sectional areaxmean flow velocity in the main pulmonary artery (as recorded during the ejection phase of the cardiac cycle)xright ventricular ejection timexheart rate; superior vena caval flow=superior vena caval cross-sectional areaxmean superior vena caval flow velocityx60 (beat durationxheart rate=60 for superior vena caval flow). Body surface area was calculated according to the method of Haycock et al.11 Statistics Data analysis was performed off-line with a Dextra-200 digitizer (Micro Five, model 5.000, Samsung Electronics Co Ltd). Statistical analyses were performed on a VAX mainframe with the SAS REG procedure. Multiple regression analyses were used to determine the best predictor equation for the superior vena cava to pulmonary arterial flow ratio, with age, height, weight, body surface area, sex, and race as independent variables. Log and power transformations of the independent variables were included in the statistical models in an attempt to define the best fit. A value of P=.05 was used to determine significance. Data are presented as mean±SD.rESULTS A total of 145 infants and children had complete data. Their mean age was 1.6±2.0 years (range, 1 day to 6.6 years). Their mean weight was 9.7±6.8 kg (range, 2.6 to 32.5 kg); their mean height was 73.3±24.0 cm (range, 32.0 to 136.5 cm). The mean body surface area was 0.44±0.23 m2 (range, 0.17 to 1.11 m2). All subjects had normal growth parameters. Pulmonary artery anterograde flow occurred only during systole. On the superior vena caval flow pattern, there were three distinct waveforms during each cardiac cycle (Fig 1 ). The initial positive waveform (S in Fig 1 ) represented anterograde flow during ventricular systole, ie, the X descent on the normal jugular venous waveform during atrial diastole. The second positive waveform of anterograde flow (D) occurred during ventricular diastole and represented the Y descent on the jugular venous waveform; it coincided with the rapid ventricular filling phase. The third, a negative waveform (A), represented the retrograde flow during atrial systole, ie, the "a" wave on the jugular venous tracing.12 We were unable to demonstrate an H wave (an anterograde flow wave in late diastole before the retrograde A flow wave) in infants, presumably because of their high heart rates. In older children with slower heart rates, however, the H wave was demonstrable. The amplitude of the superior vena caval flow pattern, and hence the amount of venous return, varied with respiration. We did not attempt to quantify these variations. We attempted to correct for the respiratory influence on flow velocity by averaging consecutive beats whenever possible from the tracings for both the pulmonary artery and the superior vena cava.
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Cardiac Output and Blood Pressure I. Cardiac OutputA. Function of heart pumping ability1. Beats per minute (cardiac rate)2. Volume of blood pumped per beat (stroke volume)3. Cardiac output = cardiac rate X stroke volume (ml/min) (beats/min) (ml/beat)5.5 L per minute4. Total blood volume = 5.5 LB. Regulation of cardiac rate1. SA node - 70 bpma. Increased by sympathoadrenal stimulationb. Decreased by the effects of parasympathetic fibers2. Cardiac control centerMedulla oblongataBaroreceptorsC. Regulation of stroke volume1. The Frank-Starling law of the hearta. End-diastolic volume influences the contraction strength of the myocardium and thus the stroke volumeb. Myocardial sarcomeres not optimally stretched at restGreater the distance between Z lines, the greater the force of contractionc. Preload lengthens sarcomeres and increases force of contraction2. Total peripheral resistanceArterial blood pressure, provides an afterload that acts to reduce the stroke volume.3. Contractility or strength of ventricular contractionsa. Strength of contraction is increased by sympathoadrenal stimulationNorepinephrine from sympathetic nervesEpinephrine from adrenal medullaD. Venous return1. Determines end-diastolic volume2. Dependent on total blood volume and mechanisms that improve flow of blood in the veins.a. The total blood volume is regulated by the kidneys60-70% of blood in veinsb. Venous flow aided by the action of skeletal muscle pumps and the effects of breathingSkeletal muscles pump by squeezingDiaphragm contraction creates partial vacuum in thoracic cavityII. Blood VolumeA. Body water1. 2/3 contained in cells2. 1/3 extracellulara. 80% interstitial fluidb. 20% blood plasmaB. Distribution of water between blood and tissues1. Balance between blood pressure filtration and osmotic pressure2. Normally in dynamic equilibriuma. The hydrostatic pressure of the blood forces fluid from the arteriolar ends of capillaries into the interstitial spaces of the tissuesb. Colloid osmotic pressure of plasma is greater than tissue fluid, water returns by osmosis to the venular ends of capillariesc. Excess tissue fluid is returned to the venous system by lymphatic vesselsd. Edema occurs when there is an accumulation of tissue fluidC. Regulation of blood volume by kidneys1. Kidneys control the blood volume by regulating the amount of filtered fluid that will be reabsorbed180 L/ day filtered 1.5 L/day excreted as urine 2. Antidiuretic hormone (ADH or vasopressin)a. Stimulates reabsorption of water from the kidney filtrateb. Released from posterior pituitary in response to dehydrationHypothalamus contains osmoreceptors and stimulates release of ADH3. Aldosteronea. Promotes retention of salt (Na+ and Cl-)Water is retained indirectlyb. Released from adrenal cortexReleased in response to angiotensin II4. Renin-angiotensin systema. Increases blood volumeb. A decrease in blood flow through the kidneys activatesJuxtaglomerular apparatus secretes reninRenin converts angiotensinogen to angiotensin IAngiotensin I converted to angiotensin II in lung by angiotensin-converting enzyme (ACE)Angiotensin II stimulates vasoconstriction and the secretion of aldosterone by the adrenal cortex.III. Vascular Resistance and Blood FlowA. Blood flow equal to rate of venous returnB. Poiseuille's law1. Blood flow is directly related to the pressure difference between the two ends of a vessel and is inversely related to the resistance to blood flow through the vessel2. Total peripheral resistanceSum of all vascular resistanceOrgans arraigned in parallelIncreased resistance of one organ affects resistance in that organVasodilation of a large organ can have system wide effectsC. Extrinsic regulation of vascular resistance1. Provided by the sympathetic nervous system and endocrine2. Sympathetic nervesa. Affect arteriole sphinctersb. Adrenergic sympathetic fibersNorepinephrineVasoconstrictionc. Cholinergic sympathetic fibersAcetylcholineVasodilation (primarily skeletal muscles)D. Intrinsic control of vascular resistance1. Allows organs to autoregulate their own blood flow rates.a. Myogenic regulation occurs when vessels constrict or dilate as a direct response to a rise or fall in blood pressure.b. Metabolic regulation occurs when vessels dilate in response to the local chemical environment within the organ.III. Blood Flow to the Heart and Skeletal MusclesA. Heart normally respires aerobicallyBecause of its high capillary supply, myoglobin content, and enzyme content.B. When the heart's metabolism increasesIntrinsic metabolic mechanisms stimulate vasodilation of the coronary vessels and thus increase coronary blood flow.C. Skeletal muscle1. Just prior to exercise and at the start of exercise2. Blood flow through skeletal muscles increases due to vasodilation caused by cholinergic sympathetic nerve fibers3. During exercise, intrinsic metabolic vasodilation occursD. Cardiac output can increase by a factor of five or more during exercise1. Heart and skeletal muscles receive an increased proportion of a higher total blood flowa. Cardiac rate increases due to lower activity of the vagus nerve and higher activity of the sympathetic nerveB. Venous return is greater because of higher activity of the skeletal muscle pumps and increased breathingC. Increased contractility of the heart, combined with a decrease in total peripheral resistance, can result in a higher stroke volumeIV. Blood Flow to the Brain and SkinA. Cerebral blood flow is regulated both myogenically and metabolically1. Cerebral vessels automatically constrict if the systemic blood pressure rises too high2. Metabolic products cause local vessels to dilate and supply more active areas with more blood.B. Cutaneous blood flow1. Skin has unique arteriovenous anastomosesCan shunt the blood away from surface capillary loops2. Cold temperaturesThe activity of sympathetic nerve fibers causes constriction of cutaneous arterioles and arteriovenous anastomoses3. Warm temperaturesIncreased cutaneous blood flow and increased flow through surface capillary loopsSweat glands stimulated if temperature continues to increaseV. Blood PressureA. Regulation1. Blood volume (stroke volume)2. Total peripheral resistance3. Cardiac rateB. Baroreceptors1. In aortic arch and carotid sinuses2. Stretch receptors3. Affect, via the sympathetic nervous system, the cardiac rate and the total peripheral resistance.4. Baroreceptor reflexa. Maintains pressure when an upright posture is assumedb. This reflex can cause a lowered pressure when the carotid sinuses are massagedC. Atrial Stretch Reflexes1. Stimulate reflex tachycardia2. Inhibit ADH release3. Promotes atrial natriureic factor secretionIncreases urinary salt and water excretionD. Measurement of blood pressure1. Measured indirectly by auscultation of the brachial arterya. First sound of Korotkoffi. Caused by turbulent flow of blood through a constriction in the arteryii. Occurs when the cuff pressure equals the systolic pressureb. Last sound of KorotkoffHeard when the cuff pressure equals the diastolic blood pressure2. Pulse pressurea. Difference between systolic and diastolic pressureb. Expansion of artery by blood ejected from ventricle3. Mean arterial pressurea. Represents the driving force for blood flow through the arterial systemb. Mean arterial pressure = diastolic pressure + 1/3 pulse pressure.E. Hypertension (high blood pressure)1. Primary hypertension (essential hypertension)a. May be the result of the interaction of many mechanisms that raise the blood volume, cardiac output, and/or peripheral resistanceb. Systolic pressure greater than 140 mmHg or 90 mmHg2. Secondary hypertensionResult of known, specific diseases3. Dangers of hypertensiona. Vascular damageb. Increased afterload increasing ventricular workc. Damage to cerebral vessels (stroke)d. Contributes to atherosclerosis4. Treatmenta. Modification of lifestyleCessation of smoking, drinking and weight reductionb. Diuretics to reduce blood volumec. Beta blockers reduce cardiac rated. ACE inhibitors and vasodilatorsF. Shock1. Inadequate delivery of oxygen to the organs of the body.2. Hypovolemic shocka. Low blood volume causes low blood pressureb. May progress to an irreversible state.c. Fall in blood volume and pressure stimulates various reflexes that produceRise in cardiac rate Shift of fluid from the tissues into the vascular system Decrease in urine volume Vasoconstriction. 3. Septic shocka. Results from sepsis (infection)b. Endotoxin that promotes vasodilation4. Anaphylactic shocka. Severe allergic reactionb. Widespread release of histamineCauses vasodilationG. Congestive heart failure1. Occurs when the cardiac output is insufficient to supply the blood flow required by the body2. Congestive describes the increased venous volume and pressure that results3. Left ventricle failure leads to pulmonary edema