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Pericardial friction rubs
Average pulse rates at rest (beats per minute)
Determine blood pressure.
Atrial septal defect (asd)
Ventricular septal defect (vsd)
Main clinical features
Acquired heart disease
Congestive heart failure (chp)
Causes of heart failure can be classified according to the following changes
Paroxysmal nocturnal dyspnea (PND)
Bukovinian State Medical University
Department of Developmental Pediatrics
to the practical class for medical students of 3-rd years
Modul 1: Child’s development
Subject: PHYSIOLOGICOANATOMICAL PECULIARITIES OF THE HEART AND BLOOD VESSELS IN CHILDREN OF DIFFERENT AGE. SEMIOTICS OF CONGENITAL AND ACQUIRED DISEASES OF THE HEART IN CHILDREN
It is completed by:
MD, MSc, PhD Strynadko Maryna
Chernivtsy – 2007
The heart and other components of the circulatory system develop from the mesoderm beginning from the third week of gestation and are completed by the eighth week. Cardiac development parallels the embryo's increasing nutritional needs, which initially were supplied by diffusion.
During the first 3 weeks the lateral mesoderm splits to form two layers, the somatic and the splanchnic mesodermi. The somatic mesodemi eventually gives rise to limb muscle, while the splanchnic mesodemi forms two endocardial tubes that fuse to become the heart tube. At the end of 3 weeks, the heart begins to beat. The mesodermial tissue surrounding the heart tube differentiates into two layers: the endocardium and myoepicardium. Concentrations of mesenchymal cells enlarge and cause the endocardium to bulge into the lumen of the heart. These internal bulges are called endocardial cushions and eventually merge to divide the heart chambers.
The developing heart tube bulges until it finally lies in the pericardial cavity. The tube remains attached to the pericardium at its cephalic and caudal ends but is free at the mid-section. During the fifth week the midcardiac tube grows rapidly and assumes a characteristic convoluted shape with identifiable structures. These structures ultimately give rise to the chambers and vessels of the heart and include a common atrium, a common ventricle, the bulbus cordis, which eventually helps form the outflow tracts of the ventricles, the sinus venosus, which develops into the inferior and superior vena cava and coronary sinus, and the truncus arteriosus, which divides into the pulmonary artery and aorta. The formation of the internal structures of the heart, particularly the cardiac septa, takes place almost simultaneously. As this partitioning process occurs, congenital defects may result if the formation of various structures is disturbed. For a better understanding of cardiac anomalies, the embryology of each heart structure is discussed with the specific malformation.
The normal growth and development of the fetus rely on an active, independent metabolism, but they also require an efficient circulation. During fetal life the lungs are essentially nonfunctional; therefore, less blood is needed for these organs than is required after birth. The fetal brain requires the highest oxygen concentration, and the heart must pump a large amount of blood through the placenta. The characteristics of fetal circulation assure that the most vital organs and tissues receive the maximum concentration of vital materials for growth.
Blood carrying oxygen and nutritive materials from the placenta enters the fetal system through the umbilicus via the large umbilical vein (Fig. 9.1). The blood then travels upward to the underside of the liver where it separates - part of the blood enters the portal and hepatic circulation of the liver and the remainder travels directly to the inferior vena cava by way of the ductus venosus. Because of the higher pressure of blood entering the right atrium from the inferior vena cava, it is directed posteriorly in a straight pathway across the right atrium and through the foramen ovale to the left atrium. In this way the better-oxygenated blood enters the left atrium and ventricle to be pumped through the aorta to the head and upper extremities (see Fig. 9.1.).
Blood from the head and upper extremities entering the right atrium from the superior vena cava is directed downward through the tricuspid valve into the right ventricle. From here it is pumped through the pulmonary artery, where the major portion is shunted to the descending aorta via the ductus arteriosus. Only a small amount flows to and from the nonfunctioning fetal lungs. Blood is returned to the placenta from the descending aorta through the two umbilical arteries.
Before birth the high pulmonary vascular resistance created by the collapsed fetal lungs causes greater pressures iq the right side of the heart and the pulmonary arteries. At the same time the free-flowing placental circulation and the ductus arteriosus produce a low systemic vascular resistance in the remainder of the fetal vascular system. With the clamping of the umbilical cord and the expansion of the lungs at birth, the hemodynamics of the fetal vascular system undergo pronounced and abrupt changes. These changes are the direct result of cessation of the placental blood flow and the beginning of lung respiration (see Fig. 9.2).
Inferior vena cava Oxygenated
Fig. 9.1. Prenatal circulation. Fig. 9.2. Postnatal circulation.
Arrows indicate direction of blood flow. RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle. NOTE: Although four pulmonary veins enter left atrium, for simplicity this diagram shows only two.
The conduction system of the heart consists of four structures:
The sinoatrial node initiates the heart's conduction system. It also possesses an intrinsic rhythm that maintains a constant heart rate. For these reasons it is called the body's pacemaker. The sinoatrial impulse spreads throughout the atria to cause depolarization. As the atria contract, impulses spread to the atrioventricular node to stimulate the ventricles. The atrioventricular node is the only normal pathway by which the impulses from the atria can be transmitted to the ventricles. The impulses then spread to the atrioventricular bundle and Purkinje fibers to cause simultaneous depolarization of the ventricles.
A cardiac cycle is composed of sequential contraction (systole) and relaxation (diastole) of both the atria and ventricles. First, the atria contract, ejecting blood into the relaxed ventricles. Then, as the atria relax, the ventricles contract to eject blood into the pulmonary artery and aorta. During the period of atrial diastole blood enters the atria from the systemic and pulmonary veins, thus completing one cardiac cycle.
Diagnosis of congenital or acquired heart disease is aided by a comprehensive history and physical examination. A variety of specific diagnostic procedures help to confirm the diagnosis. This discussion is an overview of each of these techniques. Specific positive findings are included, under the discussion of the heart defects.
Examination of the heart involves the skills of inspection, palpation, percussion, and auscultation, although the latter is the most significant. Overall assessment of cardiac function involves a comprehensive evaluation of pulse, blood pressure, respiratory function, and general physical growth and development. The doctor must be familiar with the anatomy and physiology of the normal heart in order to properly evaluate the findings.
The apex is located at the left midclavicular line and fifth intercostal space or mitral area. The heart of the infant is more horizontally positioned; therefore, the apex is higher (third to fourth intercostal space) and to the left of the midclavicular line. The apical impulse, or point of maximum impulse, is normally located at the apex.
Inspection. While examining the chest, any obvious bulging is noted, especially on the left side, which may indicate cardiac enlargement. This is best done by observing the child sitting and looking at the anterior chest wall from an angle, comparing both sides of the rib cage to each other. Normally they should be symmetric.
In children with thin chest walls, the point of maximum impulse, or apical pulse, is sometimes apparent as a pulsation. Noting the location of the impulse may give some indication of the size and positioning of the heart, especially if it deviates from the expected apical site.
Since comprehensive evaluation of cardiac function is not limited to the heart, the doctor also considers other findings, such as presence of all pulses (especially the femoral pulses), distended neck veins, peripheral cyanosis, edema, blood pressure, and respiratory status.
Palpation. Palpation is useful in determining the size of the heart by feeling for the point of maximum impulse, which ordinarily corresponds to the apex. The apex is usually at a lower interspace and more lateral in a child with cardiac enlargement. The apex is felt by placing the fingertips or the palmar aspect of the fingers and hand at the fifth intercostal space and left midclavicular line.
While feeling for the point of maximum impulse, the doctor notes the presence of vibratory thrills and pericardial friction rubs.
Thrills are palpable vibrations most commonly produced by the flow of blood from one chamber of the heart to another through a narrowed or abnormal opening, such as a stenotic valve or a septal defect. They are best felt with the ball of the hand (palmar surface at the base of the fingers) and during expiration. Thrills feel similar to the placing of one's hand on a purring cat.
^ are scratchy, high-pitched grating sounds, similar to pleural friction rubs, except that they are not affected by changes in respiration. This is a useful clue in differentiating the two rubs, because the pleural rub will cease if the child holds his breath, but the pericardial rub will not. Both thrills and rubs are abnormal and must be reported for further evaluation.
Assessing the quality and symmetry of all pulses. Pulse is examined and rate, rhythm, volume, and character are noted: alterating, large, swift, dicrotic, intermittent, labile, small, slow, soft, tense, rhythmic, rapid, pulse deficit, pulse flutter, tension of the pulse, full (weak) pulse. Comparison with other pulses is important to note radio-femoral delay. Lift the arm to feel the collapsing pulse.
The normal rate is not more then 10 % of average ^
Blood pressure, tnmHg
Physical examination. The murmur is continuous: it begins after S, peaks with S2, and trails off in diastole.
As the ductus arteriosus constricts in the neonatal period, obstruction increases at the coarctation site, leading to increased left ventricular after load with subsequent left ventricular dysfunction, pulmonary hypertension, and congestive heart failure.
^ develops during the first year of infant's life with irritability, lethargy, poor feeding, inadequate growth.
Physical examination includes ashen color of skin, its mottling, decreased or absent lower extremity pulse, gallop rhythm, single loud S2, a nonspecific and often low-pitched systolic murmur, and hepatomegaly.
The clinical manifestation of this syndrome is slow weight gain and frequent lower respiratory infections.
Physical examination. Right ventricular heave is present. A systolic ejection murmur in the pulmonic area and a mid-diastolic rumble murmur in the lower right sternal area reflect the increased flow across the pulmonary and tricuspid valves. S2 is widely and constantly split.
VSD may be single or multiple and may be found anywhere along the septum, it is most common in the membranomuscular portion. As long as pulmonary vascular resistance is lower than systemic resistance, the shunt is left-to-right. If pulmonary vascular resistance rises above systemic resistance, the shunt reverses.
^ are growth failure, congestive heart failure, shortness of breath, chest pain, cyanosis.
Physical examination. A left-to-right shunt produces turbulence during isovolumic contraction, and the murmur begins with SL The murmur usually is harsh and is best heard at the midsternal or lower left sternal border. It ends in middiastole in case of small defects and extends to the S2 in large left-to-right shunts.
Acquired heart disease, as opposed to congenital heart disease, occurs as a result of a previously existing disease, defect or as a complication of an acute disease. The most common condition classified as acquired heart disease is congestive heart failure, usually as a complication of congenital heart disease. Cor pulmonale is the term applied to congestive failure that results from pulmonary hypertension associated with chronic lung disease, principally cystic fibrosis.
Congestive heart failure is inability of the heart to pump an adequate amount of blood to the systemic circulation to meet the body's metabolic demands.
Degree of heart failure
4. High cardiac output demands, in which the body's need for oxygenated blood exceeds the cardiac output (even though the volume may be normal), such as in obstructive lung disease, hyperthyroidism and severe anemia.
In children CHF occurs most frequently secondary to structural abnormalities that result in increased blood volume and pressure. It is a symptom caused by an underlying cardiac defect, not a disease in itself, since it is usually the result of an excessive workload imposed on a normal myocardium. The majority of children, who experience CHF, are infants, and more than 50% are younger than 1 month of age.
Heart failure is often separated into two classifications: right-sided or left-sided failure. In right-sided failure the right ventricle is unable to pump blood into the pulmonary artery, resulting in less blood being oxygenated by the lungs and increased pressure in the right atrium and systemic venous circulation. Systemic venous hypertension causes edema on the extremities. In left-sided failure the left ventricle is unable to pump blood into the systemic circulation, resulting in increased pressure in the left atrium and pulmonary veins. The lungs become congested with blood, causing elevated pulmonary pressures and pulmonary edema.
Although each type produces different systemic/pulmonary artery alterations, clinically it is unusual to observe solely right- or left-sided failure. Since both sides of the heart are dependent on adequate function of the other side, failure of one chamber causes a reciprocal change in the opposite chamber. For example, in left-sided failure increase in pulmonary vascular congestion will cause increased pressure in the right ventricle, resulting in right ventricular hypertrophy, decreased myocardial efficiency, and eventually pooling of blood in the systemic venous circulation.
CHF is actually failure of compensatory mechanisms to increase cardiac function in accordance with metabolic requirements. Since most of the signs and symptoms result from decompensation, one must first look at the compensatory processes that attempt to preserve cardiac function.
Sympathetic stimulation. When the cardiac output falls, the atrial and venous stretch receptors and the aortic and carotid baroreceptors stimulate the sympathetic nervous system, which exerts two major effects. It increases the force and rate of myocardial contraction, resulting in a more efficient pumping action. It also increases venous return by increasing the tone of blood vessels and decreasing peripheral circulation to the limbs, splanchnicbed (viscera), and kidneys.
Stimulation of the sympathetic cholinergic fibers in the skin causes increased sweating, which is especially prominent on the scalp during periods of exertion, such as crying or feeding.
Renal system. Reduced renal blood flow from sympathetic stimulation has a profound effect on kidney function and results in changes aimed at increasing venous return through increased blood volume. First, there is an increase in aldosterone production in response to increased renin secretion from decreased renal blood flow and sympathetic stimulation. Aldosterone increases the rate of sodium reab-sorption by the distal tubules, promoting osmosis of water into the blood. The absorbed sodium increases the osmotic concentration of the extracellular fluid, stimulating release of antidiuretic hormone from the hypophysis, which promotes increased water reabsorption by the tubules.
Despite compensatory mechanisms, the heart may be unable to maintain an adequate cardiac output. Decreased blood flow to the kidneys continues to stimulate sodium and water reabsorption, leading to hypervolemia, increased workload on the heart, and congestion in the pulmonary and systemic circulations. Because these hemodynamic changes occur at different times, the signs and symptoms can vary.
Impaired myocardial function. One of the earliest signs of compensation and decompensation is tachycardia (sleeping heart rate above 160 beats/minute in infants), as a direct result of sympathetic stimulation. It is elevated even during rest but becomes markedly rapid during the slightest exertion.
Increased blood volume causes the ventricles to dilate, stretching the myocardial fibers until they are no longer as contractile. Ventricular dilation results in extra heart sounds, S3 or S4. The addition of these extra sounds to S,S2 produces a gallop rhythm. S3 is believed to be caused by vibrations against the ventricle walls as blood flow is abruptly stopped when the dilated ventricles can no longer accommodate the volume. It is heard immediately after the second heart sound (ventricular diastolic gallop). S4 is believed to be caused by atrial contraction in response to ventricular resistance during filling of the ventricles. It occurs just before the first heard sound (atrial presystolic gallop). The presence of S3 and S4 is called a summation gallop. Each is best heard at the apex.
Variations in the strength of ventricular contraction result in pulsus alternans, regular alternation of one strong beat and one weak one. It is best detected by palpating the pulse while taking the blood pressure. The increased pressure from the inflated cuff occludes the weak beats, so that only the stronger beats are counted. As a result, the pulse is half the actual rate.
Cardiomegaly results from dilation of the ventricle to accommodate increasing volumes of blood and from hypertrophy, as a result of persistent lengthening and thickening of the myocardial fibers. Although hypertrophy decreases the contractility of the fibers, it is partially compensated by an increase in muscle mass.
Decreased cardiac output results in poor peripheral perfusion, which is manifested by cold extremities, weak pulses, low blood pressure, mottled skin, and eventually growth retardation.
^ As the left ventricle fails, blood volume and pressure increase in the left atrium, pulmonary veins, and lungs.
Eventually the pulmonary capillary pressure exceeds the plasma osmotic pressure, forcing fluid into tissues, causing pulmonary edema. The increased pressure also decreases the compliance (expansion) of the lungs.
Dyspnea is the earliest signs of failure and is thought to be caused by a decrease in the distensibility of the lungs, as a result, additional muscles must be used for respiration, causing costal retractions. Initially dyspnea may only be evident on exertion but may progress to the point that even slight activity results in labored breathing. In infants dyspnea at rest is a prominent sign and may be accompanied by flaring nares.
Tachypnea (respiratory rate above 60 breaths /minute in infants) occurs in response to decreased lung compliance. Inability to feed with resultant weight loss is primarily a result of tachypnea and dyspnea on exertion.
Orthopnea (dyspnea in the recumbent position) is caused by increased blood flow to the heart and lungs from the extremities. It is relieved by sitting up, because blood pools in the lower extremities, decreasing venous return. In addition, this position decreases pressure from the abdominal organs on the diaphragm. In infants orthopnea may be evident in their inability to lie supine and their desire to be held upright.
^ is a severe shortness of breath that occurs shortly after falling asleep. It is a result of reabsorption of fluid (from dependent edema), which increases blood volume, producing more severe pulmonary congestion.
Edema of the bronchial mucosa may produce cardiac wheezing from obstruction to airflow. Mucosal swelling and irritation result in a persistent, dry, hacking cough. As pulmonary edema increases, the cough may be productive from increased secretions. Pressure on the laryngeal nerve results in hoarseness. A late sign of heart failure is gasping and grunting respirations. An uncommon sign in infants is rales.
Cyanosis may occur without a right-to-left shunt and is the result of impaired respiratory gas exchange. On exertion, such as crying or feeding, the infant may experience mottling of the skin or generalized transient duskiness. Extreme pallor or persistent duskiness is an ominous sign of CHF.
^ Systemic congestion is a primary consequence of right-sided failure due to the inability of the right ventricle to eject blood into the pulmonary circulation, resulting in increased pressure and pooling of blood in the venous circulation. As was explained earlier, it can result as a late consequence of left-sided failure.
Hepatomegaly is usually the earliest sign of failure and occurs from pooling of blood in the portal circulation and transudation of fluid into the hepatic tissues. The liver may be tender on palpation and its size is an indication of the course of heart failure.
Edema forms as the sodium and water retention cause systemic vascular pressure to rise. The earliest sign is weight gain. However, as additional fluid accumulates, it leads to swelling of soft tissue that is dependent and favors the flow of gravity, such as the sacrum and scrotum when recumbent and loose periorbital tissues. In infants edema is usually generalized and difficult to detect. Gross fluid accumulation may produce ascites and pleural effusions.
^ and peripheral veins, which are uncommon in infants, result from a consistently elevated central venous pressure. Normally neck and hand veins collapse when the head or hands are raised above the level of the heart, since the blood drains by gravity back to the heart.
However, when the venous pressure is high, it prevents the back flow of blood, causing the veins to remain distended.
Diagnosis is made on clinical symptoms such as dyspnea (especially when at rest), flaring nares, moist grunting respirations, subcostal retractions, tachycardia, activity intolerance (particularly during feeding), excessive sweating, and unexplained weight gain from edema. Since the signs of pulmonary congestion from heart failure resemble respiratory infections, it is imperative to differentiate between the two. Signs selectively indicative of CHF are cardiac enlargement, edema, sweating, hepatomegaly, and auscultatory findings such as tachycardia, gallop rhythm, and pulsus alternans.
The objectives of nursing care are to (1) assist in measures to improve cardiac function, (2) decrease cardiac demands, (3) reduce respiratory distress, (4) maintain nutritional status, (5) assist in measures to promote fluid loss, and (6) provide emotional support. Although the objectives are the same, the interventions differ depending on the child's age, especially with infants as compared to older children. Assist in measures to Improve cardiac function. The doctor's responsibility in administering digitalis includes observing for signs of toxicity, calculating the correct dosage, and instituting parental teaching regarding drug administration at home.
Clinical manifestation: apnoea, absence of pulse, loss of consciousness, dilatation of pupils, areflexia and cyanosis. The duration of the clinical death depends on the time, during which the brain is without blood supply, and the body temperature. When the body temperature is normal - effective resuscitation is possible during 5 min; at the body temperature 36-32 °С - the resuscitation will be effective during 8 min, 32-28 °С - 15 min, 28-18 °С - 45 min.
I. To provide upper respiratory tract passage.
^ of the lungs is carried out either by mouth to mouth respiration, or by mouth to nose, or with the help of breathing pump.
After making deep breath in, inhale the air to the mouth of the child through the cotton mask. Nose of the child must be closed.
The rate of inhalation is 40 per min for newborn, for infants -30; for children over 5 years - 25; 6-14 years - 20 and for elder -16-18 per 1 min.
Artificial ventilation of the lungs is connected with indirect massage of the heart.
In the children of the first 3 month of life massage is done by thumb. In the children from 3 months till 3 years - by 3 fingers, in children over 5 years - by two hands which are put in cross position on the lower part of the sternum. Press on the sternum to compress the heart between the sternum and vertebral column. In newborns sternum should be pressed down on 1-1.5 cm, in children 2 month-3 years - on 2.5 cm, in children 5-15 years - on 3-4 cm.
The frequency of compression is 60-100 times per 1 minute, depending on age. During 1 inspiration should be made 4 compression on sternum.
The manifestations of effective resuscitation are appearance of pulse on carotids, renewal of breathing, constrictions of pupils and decreasing of cyanosis.
Putting ice or bags with cold water around the head helps to prolong time f effective resuscitation. If it's possible you can make intubation of trachea.
Make a general conclusion on a theme of a class №1 and conducted practical work.
1. Nursing care of Infants and Children / editor Lucille F. Whaley and I. Wong. Donna L. - 2nd ed. - The C.V. Mosby Company. - 1983. - 1680 p.
2. Nykytyuk S.O. et al. Manual of Propaedeutic Pediatrics. – Ternopil: TSMU, 2005. – P. 6-22.
3. Pediatric Nurse Practitioner Certification Review Guide / editor, Virgina layng Milloing: contributing authors, Ellen Rudy Clore and all. - 2nd ed. - Health Leadership Associates,Inc.,1994. - 628 p.
4. Nelson Textbook of Pediatrics / edited by Richard E. Behrman, Robert M. Kliegman, Ann M. Arvin; senior editor, Waldo E. Nelson - 15th ed. - W.B.Saunders Company, 1996. - 2200 p.
5. Whaley L.F., Wong D.L.: Nursing care of infants and children, St. Louis, Toronto, London, 1983.
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