METHODS OF INSPECTION, PALPATION, PERCUSSION, AUSCULTATION CARDIOVASCULAR SYSTEM

Methods of ninspection, palpation, percussion, auscultation cardiovascular system. Maiclinical pictures of cardio-vascular system disorders in children (cyanosis, nbradicardia, tachycardia)

 

1.     nBasic stages of embryogenesis of ncardiovascular system

2.     nMechanism of the heartbeat

3.     nInspection of organs of the ncardiovascular system at the children of different age (review, palpation, npercussion, auscultation)

4.     nOrganic nand non organic  murmurs

5.     nWhat is a quantity of hear nbeat  in different age group?

6.     nHeart edema

7.     nCyanosis

8.     nBradycardia

9.     nTachycardia

Embryology

The nheart and other components of the circulatory system develop from the mesoderm beginning nduring the third week of gestation and are completed by the eighth week. nCardiac development parallels the embryo’s increasing nutritional nneeds, which initially were supplied by diffusion.

During nthe first 3 weeks the lateral mesodem splits to form two layers, the somatic and the nsplanchnic mesodemi. The somatic mesodemi eventually gives rise to limb muscle, while the nsplanchnic mesodemi forms two endocardial tubes nthat fuse to become the heart tube. nAt the end of 3 weeks the heart begins to beat. The mesodemial ntissue surrounding the heart tube differentiates into two layers: the endocardium nand myoepicardium. nConcentrations of mesenchymal cells enlarge and ncause the endocardium to bulge into the lumen of the heart. These internal nbulges are called endocardial cushions nand eventually merge to divide the heart chambers.

The developing heart tube bulges until it finally nlies in the pericaidial cavity. The tube remains attached to the pericardium at nits cephalic and caudal ends but is free at the mid-section. During the fifth nweek the midcardiac tube grows rapidly and assumes a characteristic convoluted nshape with identifiable structures. These structures ultimately give rise to nthe chambers and vessels of the heart and include a common atrium, a common ventricle, the bulbus cordis, which eventually helps form nthe outflow tracts of the ventricles, the nsinus venosus, which develops into nthe inferior and superior vena cava and coronaxy sinus, and the truncus narteriosus, which divides into the pulmonary artery and aorta. The nformation of the internal structures of the heart, particularly the cardiac nsepta, takes place almost simultaneously. As this partitioning process occurs, ncongenital defects may result if the formation of various structures is ndisturbed. For a better understanding of cardiac anomalies, the embryology of neach heart structure is discussed with the specific malformation.

 

The nFetal Circulation

The human fetal circulation and its adjustments after birth are similar nto those of other large mammals, although rates of maturation differ. In the nfetal circulation, the right and left ventricles exist in a parallel circuit, as nopposed to the series circuit of a newborn or adult. In the fetus, the placenta nprovides for gas and metabolite exchange. The lungs do not provide gas nexchange, and vessels in the pulmonary circulation are vasoconstricted. Three ncardiovascular structures unique to the fetus are important for maintaining nthis parallel circulation: the ductus venosus, foramen ovale, and ductus narteriosus.

Oxygenated blood returning from the placenta flows to the fetus through nthe umbilical vein with a PO₂ of about 30–35 mm Hg. Approximately n50% of the umbilical venous blood enters the hepatic circulation, whereas the nrest bypasses the liver and joins the inferior vena cava via the ductus nvenosus, where it partially mixes with poorly oxygenated inferior vena cava nblood derived from the lower part of the fetal body. This combined lower body nplus umbilical venous blood flow (PO₂ of ≈26–28 mm Hg) enters nthe right atrium and is preferentially directed across the foramen ovale to the nleft atrium (see Fig. 421-1B ). The blood then flows into the left nventricle and is ejected into the ascending aorta. Fetal superior vena cava nblood, which is considerably less oxygenated (PO₂ of 12–14 mm Hg), nenters the right atrium and preferentially traverses the tricuspid valve, rather nthan the foramen ovale, and flows primarily to the right ventricle.

From the right ventricle, the blood is ejected into the pulmonary nartery. Because the pulmonary arterial circulation is vasoconstricted, only nabout 10% of right ventricular outflow enters the lungs. The major portion of nthis blood (which has a PO₂ of ≈18–22 mm Hg) bypasses the nlungs and flows through the ductus arteriosus into the descending aorta to nperfuse the lower part of the fetal body, after which it returns to the nplacenta via the two umbilical arteries. Thus, the upper part of the fetal body n(including the coronary and cerebral arteries and those to the upper nextremities) is perfused exclusively from the left ventricle with blood that nhas a slightly higher PO₂ than the blood perfusing the lower part of nthe fetal body, which is derived mostly from the right ventricle. Only a small nvolume of blood from the ascending aorta (10% of fetal cardiac output) flows nacross the aortic isthmus to the descending aorta.

The total fetal cardiac output—the ncombined output of both the left and right ventricles—is ≈450 mL/kg/min. nApproximately 65% of descending aortic blood flow returns to the placenta; the nremaining 35% perfuses the fetal organs and tissues. In the sheep fetus, right nventricular output is approximately two times that of the left ventricle. Ithe human fetus, which has a larger percentage of blood flow going to the nbrain, right ventricular output is probably closer to 1.3 times left nventricular flow. Thus, during fetal life the right ventricle is not only npumping against systemic blood pressure but is also performing a greater volume nof work than the left ventricle.

 

 

The Transitional Circulation

At birth, mechanical expansion of the lungs and aincrease in arterial PO₂ result in a rapid decrease in pulmonary nvascular resistance. Concomitantly, removal of the low-resistance placental ncirculation leads to an increase in systemic vascular resistance. The output from nthe right ventricle now flows entirely into the pulmonary circulation, and nbecause pulmonary vascular resistance becomes lower than systemic vascular nresistance, the shunt through the ductus arteriosus reverses and becomes left nto right. In the course of several days, the high arterial PO₂ nsignals constriction of the ductus arteriosus and it closes, eventually nbecoming the ligamentum arteriosum. The increased volume of pulmonary blood nflow returning to the left atrium increases left atrial volume and pressure nsufficiently to close the foramen ovale functionally, although the foramen may nremain probe patent.

Removal of the placenta from the circulation also results in closure of nthe ductus venosus. The left ventricle is now coupled to the high-resistance systemic ncirculation, and its wall thickness and mass begin to increase. In contrast, nthe right ventricle is now coupled to the low-resistance pulmonary circulation, nand its wall thickness and mass decrease slightly. The left ventricle, which ithe fetus pumped blood only to the upper part of the body and brain, must now ndeliver the entire systemic cardiac output (≈350 mL/kg/min), an almost n200% increase in output. This marked increase in left ventricular performance nis achieved through a combination of hormonal and metabolic signals, including nan increase in the level of circulating catecholamines and the myocardial nreceptors (β-adrenergic) through which catecholamines have their effect.

When congenital structural cardiac defects are superimposed on these dramatic nphysiologic changes, they often impede this smooth transition and markedly nincrease the burden on the newborn myocardium. In addition, because the ductus narteriosus and foramen ovale do not close completely at birth, they may remaipatent in certain congenital cardiac lesions. Patency of these fetal pathways nmay either provide a lifesaving pathway for blood to bypass a congenital defect n(a patent ductus in pulmonary atresia or coarctation of the aorta or a forameovale in transposition of the great vessels) or present an additional stress to nthe circulation (patent ductus arteriosus in a premature infant, pathway for nright-to-left shunting in infants with pulmonary hypertension). Therapeutic nagents may either maintain these fetal pathways (prostaglandin E₁) nor hasten their closure (indomethacin).

 

The Neonatal Circulation

At birth, the fetal circulation must immediately adapt nto extrauterine life as gas exchange is transferred from the placenta to the nlung. Some of these changes are virtually instantaneous with the 1st breath, nwhereas others develop over a period of hours or days. After an initial slight nfall in systemic blood pressure, a progressive rise occurs with increasing age. nThe heart rate slows as a result of a baroreceptor response to an increase isystemic vascular resistance when the placental circulation is eliminated. The naverage central aortic pressure in a term neonate is 75/50 mm Hg.

With the onset of ventilation, pulmonary vascular resistance is markedly ndecreased as a consequence of both active (PO₂ related) and passive n(mechanical related) pulmonary vasodilation. In a normal neonate, closure of nthe ductus arteriosus and the fall in pulmonary vascular resistance result in a ndecrease in pulmonary arterial and right ventricular pressures. The major ndecline in pulmonary resistance from the high fetal levels to the low “adult” nlevels in the human infant at sea level usually occurs within the 1st 2–3 days nbut may be prolonged for 7 days or more. Over the 1st several weeks of life, npulmonary vascular resistance decreases even further, secondary to remodeling nof the pulmonary vasculature, including thinning of the vascular smooth muscle nand recruitment of new vessels. This decrease in pulmonary vascular resistance nsignificantly influences the timing of the clinical appearance of many ncongenital heart lesions that are dependent on the relative systemic and npulmonary vascular resistance. The left-to-right shunt through a ventricular nseptal defect may be minimal in the 1st wk after birth when pulmonary vascular nresistance is still high. As pulmonary resistance decreases in the next week or ntwo, the volume of the left-to-right shunt through an unrestrictive ventricular nseptal defect increases and eventually leads to symptoms of heart failure.

Significant differences between the neonatal circulation and that of nolder infants include: (1) right-to-left or left-to-right shunting may persist nacross the patent foramen ovale; (2) in the presence of cardiopulmonary ndisease, continued patency of the ductus arteriosus may allow left-to-right, nright-to-left, or bidirectional shunting; (3) the neonatal pulmonary nvasculature constricts more vigorously in response to hypoxemia, hypercapnia, nand acidosis; (4) the wall thickness and muscle mass of the neonatal left and nright ventricles are almost equal; and (5) newborn infants at rest have nrelatively high oxygen consumption, which is associated with relatively high ncardiac output. The newborn cardiac output (about 350 mL/kg/min) falls in the n1st 2 mo of life to about 150 mL/kg/min and then more gradually to the normal nadult cardiac output of about 75 mL/kg/min. The high percentage of fetal nhemoglobin present in the newborn may actually interfere with delivery of noxygen to tissues in the neonate, so increased cardiac output is needed for nadequate delivery of oxygen.

The foramen ovale is functionally closed by the 3rd mo of life, although nit is possible to pass a probe through the overlapping flaps in a large npercentage of children and in 15–25% of adults. Functional closure of the nductus arteriosus is usually complete by 10–15 hr in a normal neonate, although nthe ductus may remain patent much longer in the presence of congenital heart ndisease, especially when associated with cyanosis. In premature newborinfants, an evanescent systolic murmur with late accentuation or a continuous nmurmur may be audible, and in the context of respiratory distress syndrome, the npresence of a patent ductus arteriosus should be suspected.

The normal ductus arteriosus differs morphologically from the adjoining naorta and pulmonary artery in that the ductus has a significant amount of ncircularly arranged smooth muscle in its medial layer. During fetal life, npatency of the ductus arteriosus appears to be maintained by the combined nrelaxant effects of low oxygen tension and endogenously produced nprostaglandins, specifically prostaglandin E₂. In a full-term nneonate, oxygen is the most important factor controlling ductal closure. Whethe PO₂ of the blood passing through the ductus reaches about 50 mm Hg, the ductal wall nconstricts. The effects of oxygen on ductal smooth muscle may be direct or nmediated by its effects on prostaglandin synthesis. Gestational age also nappears to play an important role; the ductus of a premature infant is less nresponsive to oxygen, even though its musculature is developed.

 

 

Heartbeat

 

The conduction system of the heart consists of four structures:

1. The sinoatrial (SA) node, nlocated within the rig atrial wall near the opening of the superior vena cava

2. The atrioventricular (AV) node, also located within the right atrium nbut near the lower end of the septum

3. The atrioventricular bundle n(bundle of His), which extends from the atrioventricular node along each nside of the interventricular septum

4. Purkinje fibers, which nextend from the atrioventricular bundle into the walls of the ventricles. The nelectric impulses from this conduction system can be recorded on aelectrocardiogram.

The sinoatrial node initiates the heart’s conduction system. It also possesses n–an intrinsic rhythm that maintains a constant nheart rate. For these reasons it is called the body’s pacemaker. The sinoatrial nimpulse spreads throughout the atria to cause ndepolarization. As the atria contract, impulses nspread to the atrioventricular node to stimulate the ventricles. The natrioventricular node is the only normal pathway by which the impulses from the natria can be transmitted to the ventricles. The impulses then spread to the natrioventricular bundle and Purkinje fibers to cause simultaneous ndepolarization of the ventricles.

A cardiac cycle is composed of sequential contraction (systole) and nrelaxation (diastole) of both the atria and ventricles. First, the atria ncontract, ejecting blood into the relaxed ventricles. Then, as the atria relax, the nventricles contract to eject blood into the pulmonary artery and aorta. During nthe period of atrial diastole blood enters the atria from the systemic and pulmonary veins, thus completing one ncardiac

 

 

 

 

DIAGNOSTIC EVALUATION

 

Diagnosis of congenital or acquired heart disease is aided by a comprehensive history and physical examination. A variety of nspecific diagnostic procedures help confirm the diagnosis. nThis discussion is an overview of each of these techniques. Specific positive nfindings are included, under the discussion of the nheart defect.

 

Gathering complaints

The child of older age capresent his/her complaints by himself/herself:

•           nPain on the area of heart . In this case it is necessary to specify:

•           nCharacter of pain – sharp, blunt, burning, stabbing.

•           nTime when it appears – at night, in the afternoon, constant, after nneuro-psychological stress or physical exercises or in a state of connection of npain with position of the patient – change in pain while getting up, iposition on the left or right side.

•           nIrradiation of the pain – especially to the left hand.

•           nProbable change after taking medicines , ect.

•           nCardiac dyspnea which leads to take deep breath, stop during climbing n,sometimes with groaning.

•           nPerceptible heartbeat (in a state of rest or during physical excretion).

•           n Complaints of general character: nrise in temperature, fatigue, weakness, headache, loss of memory, loss of nappetite , loss of body weight, ect.

•           nWhen younger children and especially  nchildren of the breast feeding are ill, gathered complaints are less ninformative as parents usually notice

•           nAttentive relatives can specify certain is orders such as:

•           nSudden shout, anxiety of child , which alternates with long periods of nflaccidity , flabbiness and pallor.

•           nImproper sucking:

•           nA child starts sucking  breast , nbut after short time baby stops.

•           nSigns of weariness and dyspnea.

•           nAfter resting for a while child again starts sucking, but for a short ntime.

•           nWhile gathering anamnesis of disease it is necessary to ask the parents nin details about the dynamics of disease from the moment it started: when and nwhich symptoms appeared first , how they changed (for example if the parents nknow about presence of noise , it is  nnecessary to ascertain its features- time of appearance, what noise , nits changes, ect.), what are the additional symptoms.

 

 

 

Anamnestic:

-A complete history is essential regardless of the type of heart defect. nThe major categories to investigate include a history of:

– Poor weight gain, poor feeding habits, and fatigue during feeding

– Frequent respiratory infections and difficulties

– Cyanosis with or without clubbing of fingers

– Evidence of exercise intolerance in addition,

– A history of previous defects in a sibling,

– Maternal rubella infection during npregnancy, or associated chromosomal abnormalities, nsuch as Turner’s or Down’s syndrome

 -In rheumatic fever a history of na previous streptococcal infection is of primary importance.

 

Physical nexamination

Physical examination of ncardiovascular patients allows to establish various manifested symptoms of npathological origin. To manifest them, it is necessary to focus the following nparameters.

Consciousness.

Dyspnea

Facial expression (especially in children of nearly age.

(a)Widely opened eyes of a nchild indicating fear, and suffering are signs of severe cardiac pain;

(b)if patient’s face expresses napathy, it nindicates dyspnea.

 

There are several characteristic positions in bed:

·        nIn diseases with insufficient blood ncirculation, the patient acquires a compelled position that makes patients ncondition better half sitting or sitting, lowering legs, leaning with patients nback to pillows (orthopneic nposture). Such position directs flow of blood to the lower limbs, reduces nblood stagnation in lesser ncirculation and nimproves excursion of diaphragm.

·       nIn exudative pericarditis, the patient lies ndown or sits icompelled knee-elbow ( Bozeman’s) position that reduces cardiac pain.

·       nWhen a child suffers from dyspneic cyanotic nparoxysms (in CHD pentalogy of Fallot — French doctor of the 19^m-20^w ncenturies), another compelled nposition is observed with a knee-chest position (when his/her knees are npressed to the chest).

·        nAt vascular insufficiency (collapse), the nacquired position is passive npatient just lies down.

Physical nand neuro-psychological development of a child:

·        nSlow nrate of development is often seen in children of younger age; the ngreater the deficiency in gaining weight and growth is, the older the disease.

·        nOne of the pathognomonic features of coarctation (i.e. narrowing) of aorta nis the disproportion of trunk, when the child of school age (I) has a wide neck nand large upper limbs, but underdeveloped pelvis and lower limbs.

 

Skin color;

1.    nPallor n(collapse, heart diseases with arteriovenous shunt).

2.    nCyanosis n— the syndrome is caused by hypoxemia, however if in respiratory ndisease, cyanosis of skin is of respiratory origin, in cardiovascular pathology, nit is of circulatory genesis. In the latter case, cyanosis is caused by ndestruction of hemodynamics. Its classic variation is heart diseases with nvenous-arterial shunt:

·          nCyanosis can be general or local.

·          nThe color during cyanosis can be of different nshades — violet, blue, etc., it depends on the defect of heart. One factor for noccurrence of cyanosis is coarctation of aorta and patent ductus arteriosus n(opened Botallo’s duct) below the place of stenosis; thus there is a flow of nvenous blood from the duct into aorta that results in supplying the lower half nof the trunk with mixed blood and causes cyanosis of skin.

Different kinds of rashes on skin are symptoms of rheumatic nfever.

 

Cardiac edema:

·        nFirst appears on the feet.

·        nIn young children and seriously ill patients nif they fie nin a horizontal position, then edema can also appear in the lumbar and nsacral areas, i.e. in the lower part of the trunk,

·        nBoys may have scrotal edema,

·        nIf a patient’s condition gets worse, edema is nalso observed on shins, hips, puffiness of face occurs, ascites and hydrothorax ndevelop: anasarca — general edema of whole body — arises.

·        nPlace of edema depends on position of patient n— if the patient lies on the same side for a long time, edema is located in the nlower part of the body

·        nCardiac; edema have to be differentiated from nrenal edema:

ü nCardiac edema is accompanied by cyanosis of nskin. Increases after physical work, seen at the end of the day and decreases nafter sleep; edema is dense (hollow formed, by pressing restores its form nslowly); skin is often cold when touched; if the body position changes, shift nof edema is unlikely to occur: if conditions gets worse, edema spreads upward, ni.e. first they appear on feet and then they spread lo the legs and trunk.

ü nRenal edema develops on the base of paleness, nfirst symptom is the edema around the eyes which occurs in the morning] during nday, it decreases or disappears; it’s not dense (edema easily pits opressure); skin is often cold when touched; if the body positiochanges if the body position changes; if condition gets worse, renal edema nspreads downward, i.e. first they appear around the eyes and then they spread nto lower parts of the trunk

Apex beat (apical thrust) is the thrust of nheart apex against a small area of thoracic wall during each systole. Apex beat ncan be visually determined in the form of weak pulsation in almost all the nchildren, Sometimes, when the intercostal space s are narrow, when the nsubcutaneous adipose tissue is significantly thick in obese children, or wheapex beat is positioned at the rib, it is. not determined visually. On the ncontrary: under condition of hypertrophy and emaciation, after physical nexercises or during emotional activation, the beat may exist as a strong npulsation.

During examination, the following criteria nare established:

(a) Location of apical thrust according to nthe horizontal line — normally before the age of 1.5 years, it lies in the IV nand later on In the V intercostal space.

(b) Location of apical thrust according to nthe vertical line:

·        nTill the age of 2 years, it lies 1-2 cm lateral to the left nmedioclavicular line.

·        n2-7 nyears — 1 ncm lateral to it.

·        n7-12 nyears — on left medioclavicular line,

·        nIn children more than 12 years — 0.5 cm to the middle from the nleft medioclavicular tine.

(c)     Area nof apex beat is not more than 1*1 cm and in an older child it can be 2*2 cm.

Change of these borders occurs when patient suffers nfrom cardiac disease, pathology of respiratory organs and the gastrointestinal ntract, etc. Cardiac thrust is fluctuating movements of large area of the thorax nin the projection of the heart or beyond its limit, which occurs when walls of nventricles (not apex only) push thorax wall during each systole.

Cardiac thrust is normally not identified visually. nIts presence during examination indicates substantial growth in heart size and nits contraction force (mostly during CHD). It might be due to emphysema of the nlungs, mediastinal tumors, which brings the heart closer to the thorax.

 

Cardiac hump is bulging of thorax in the form of ndeformation on the area of heart that is determined visually (symptom of nprolonged cardiac defect). The hump is formed mainly in children of younger nage. In older child with fairly solid bones, for the formation of the hump, a long ntime is necessary. Localization of the hump in relation to sternum indicates nthe part of heart with hypertrophy: closer to the sternum means that the right npart is defected; far from it means that the defect is on the left part.

 

Pulsation of peripheral vessels:

(a) ‘Carotid shudder’ is pulsation of carotid narteries, visually observed in front of the sternocleidomastoid muscle (itrigonum carolicus), which specifies insufficiency of aortal valves and naneurysm of aorta (duct is open wide). In this condition, the head might nod naccording to the cardiac contractions. This is called Mussets sign (French poet nof the 19^lh century, who suffered of insufficiency of aortal nvalves). Mechanism of this phenomenon lies in significant fluctuation of blood npressure. Weak pulsation can sometimes be observed in healthy children, but it nis possible only in horizontal position.

(b) As for cervical veins, which are located behind nsternocleidomastoid muscle, normally their pulsation is not visually ndetermined. It is very nweak and it does not coincide with pulsation of carotid arteries. nBulging and pulsation of cervical veins, which coincide with pulsation of ncarotid arteries are called positive venous pulse which is the symptom of ntricuspid insufficiency. Mechanism of this phenomenon is nregurgitation during systole, from the right ventricle to the right atrium that ndecreases its filling with blood and increases the pressure in cervical veins.

(c) Pulsation in epigastrium happens nnormally sometimes when diaphragm is situated low. Pathologically, such npulsation manifests itself under the following conditions:

·               nRight nventricle hypertrophy — noticeable, especially at the end of ninspiration.

·               nDuring structural pathologies of aorta — pulsation is visualised nduring expiration.

 

Palpation

While examining cardiovascular system by palpating, nthe condition of npulse (frequency, rhythm, tension, filling and size) is nestablished, palpatioof heart area is performed; presence of edema is established.

 

Pulse rate (PR) is determined by palpating peripheral big vessels. nHeart rate (HR) is established by palpating apex beat or nduring auscultation of the heart.

In healthy children, pulse rate is equal to heart nrate. Thus, having determined the pulse rate, it is possible to know heart rate nand vice versa.

However, there are diseases with deficiency of pulse, i.e. after a few cardiac ncontractions pulse wave does not spread through the vessels. In this case, the npulse rate will be less than the heart rate. Thus, during the first examinatioof child, it is necessary to determine and compare pulse rate and heart rate.

Rules for determination of pulse rate:

·        nThe most accurate data can be obtained in the nmorning right after sleep, on an empty stomach.

·        nA child should be calm, as excitation and nphysical exercises may result in increase of heart rate.

·        nA child sits or lies down.

·        nAt first, the pulse is palpated on both hands nby the second and third fingers on radial artery in the area of radiocarpal joint. During this procedure, ndoctor’s thumb surrounds back part of a child’s hand. If the pulse on both nhands is identical, i.e. synchronous on both hands, further determination of npulse may be carried out on one hand.

·        nThis method is hardly applicable in childreof breast feeding age. It is more convenient to determine their heart rate by nauscultation of the heart or palpating the apex beat (Attention! n1 pulse = 1 heart beat = 1 napex beat = 2 heart sounds), In the case history, it is nwritten — b.p.m. n(beats per minute).

·        nPoise can be read during 15 or 20 seconds, nand then the figure obtained should be multiplied by 4 or 3 respectively.

·        nIn case of a substantial increase of heart nrate in children of early age and to make the process of calculation simple, it nis possible to count two heart beats (= four sounds) as one, count them during none minute and then multiply this number by two.

·        nIf nit is necessary, pulse in a. temporalis, a. carotis, a. ulnaris, a. femoralis, a. popliteal, na. tibialis posterior and a. dorsalis pedis is determined by palpation.

 

 

Average pulse rates at rest (per minute)

 

 

As the heart rate decreases, duratioof cardiac cycle increases with the age of child from 0.4 sec to 0.8 sec.

There are some physiological deviations from the average normative nparameters of heart rate:

• ± 10 % fluctuation is considered acceptable.

• Female pulse rate per minute is 3-5 beats nmore than that of male.

• During puberty age, the rate per minute cabe 10-12 beats more than the norm.

• In healthy children, pulse rate increases when they nare scared or excited and after physical exercises; in calm condition this frequency should restore in 2-3 minutes.

 

As the child grows pulse rate per minute decreases:

As nconsidered earlier, when a child gets older there is reduction in pulse nrate. Let’s remember that breathing rate reduces simultaneously. However ratio between breathing rate and pulse rate in children depends on age and nis:

·     nIewborn babies — 1 : 2-2.5

·     nBreast feeding period — 1 ; 2.5-3

·     nPreschool age — 1 : 3.5—4

·     nSchool age — 1 : 4-5

 

Pulse nrhythm is determined simultaneously during palpation, nPulse can be rhythmic (Lati— Pulsus reaularis) and irregular (Latin — Pulsus irregularis). Normally the pulse is nrhythmic.

It is interesting, that in healthy children from 2 to 11 years, respiratory arrhythmia may be seen when the pulse nrate increases during inspiration, and decreases during expiration. For differential diagnosis nof arrhythmia of respiratory and pathological genesis, the following test may nbe carried out in such a way: stop breathing with closed mouth and nose — nrespiratory arrhythmia disappears,

 

Tensioof pulse is determined by the force, which is necessary to stop the pulse in the artery. There can be distinguished npulse of normal pressure, hard pulse (Latin — Pulsus duros) and soft pulse (Latin — Pulsus mollis).

 

Filling nof pulse is the filling of palpated artery with blood during systole. This criteria is determined ithe following way: proximally located finger presses the artery so that the npulse disappears, at the same time the distally located finger feels how the nartery is filled with blood. Filling of pulse first of all depends on stroke volume nand volume of circulating blood. There can be distinguished pulse of satisfactory filling, full nfilling (Lati— Pulsus olenus) and less or low filling {Latin — Pulsus vacuus).

 

Size nof pulse — conclusion on this parameter, which ncorresponds to the degree of artery expansion caused by npulse waves, is nmade by the doctor on the basis of tension and filling of pulse. There ncan be distinguished pulse of a normal size, high (Latin — Pulsus maanus s. altos), small or low (Latin — Pulsus parvus s. humilis) weak or thread (Latin — Pulsus filiformis).

 

Apex nbeat and cardiac thrust are determined by palpation on the heart area

Technique of palpation:

·       nPatient on supine position.

·       nDoctor sits at the right side of the child.

·       nThe palm of the right hand is in completely nflat position on the left half of chest in the area of the heart with the base nof wrist towards the sternum, fingers are placed along intercostal space ntowards anterior axillary line, This is how cardiac thrust  is determined.

·       nTo find apex beat, the last phalanges of the nfingers of the same hand are moved along the intercostal space from the outside ninwards in the direction of sternum till the maximum force of beat is felt. nConfirmation of apex beat location and its features are performed by lips of nthe second and third fingers,

When apex beat is examined, the following criteria are estimated:

(a) Localization of apex beat — this parameter depends on age of nthe child, and also according to the position of patient. If the patient lies non the left or the right side, apex beat is displaced to the similar side, the ndisplacement to the left is more significant (in older nchildren — up to 2 cm), displacement to the right is insignificant as left lobe nof the liver is on the way and prevents it. Localization of apex beat also ndepends on the stage of respiration: during inspiration it descends and during nexpiration it rises up.

(b) Extension (area) — normal area of napex beat is 1*1 cm, but in elder children it is 2*2 cm

(c) Magnitude (height) — of apex beat is estimated ntaking into consideration amplitude of fluctuations of intercostal intervals nduring systole. Besides the condition of cardiac muscles, the height also ndepends on the thickness of thorax. Normally, apex beat is of moderate height. The increase of the parameter in a healthy nchild is observed when he/she is excited or cries,

(d) Resistance (force) of apex beat is nsubjectively determined by the amount of force which has to be applied to nprevent pulsation of thoracic wall during systole (it is the pressure which is nfelt by the doctor’s finger while palpating). This parameter depends on the nforce of contractions of ventricles, distances between the finger and apex of nheart and thickness of thoracic wall. Normally the apex beat is of moderate nforce.

When cardiac thrust is examined, the following criteria are estimated:

·        nExtensio— corresponds to the size of ventricles.

·        nForce (it is determined in a similar was as nthe force of apex beat).

Thus, apex beat is when the nheart’s apex hits against the thoracic wall (small area), and the cardiac beat nis when the heart’s ventricles hit against the thoracic wall as well (larger narea). Nevertheless, during hypertrophy of right ventricle, the whole heart or nincrease of cardiac thrust, it may be difficult to distinguish apex beat from ncardiac thrust.

 

Symptomatological ndisorders determined by palpating

 

Pulse nrate

Increase nin frequency by 10% and more than the norm indicates tachycardia, which is one of the first nindications of nintoxication of nvarious organs during various diseases of bacterial and viral etiology. Increase in temperature for every ndegree above 37*C accelerates pulse rate by ten-fifteen beats per minute in younger nchildren, and approximately by eight beats in older children.

Besides, tachycardia accompanies cardiovascular ndiseases (circulatory insufficiency, vegetovascular dystonia), and also such nendocrinal pathology like hyperthyroidism, such pathology of blood as anemia, netc. If under this condition, pulse suddenly rises more than 180 per minute, it nis referred to as paroxysmal tachycardia.

Decrease in pulse rate by 10% and more than the norm indicates bradycardia — happens imyocarditis, neglected hypotrophy, hypertensions and while recovering after nscarlet fever (Scarlelatinal pulse) and other infectious

diseases.

Bradycardia may be normal and may be present isportsmen and healthy prematurely born babies.

Basic signs of arrhythmic pulse are:

·          nCiliary arrhythmia ( cardiac fibrillation) as a clinical feature oj nstenosis of the mitral valve occurs when rhythm is chaotic in frequency and nheight and often with a deficiency of pulse; fluttering is caused by malfunction of nthe cardiac conductive system,

·          nExtrasystole (in pathologies of cardiac ngenesis, infectious diseases, etc), when one (sometimes two) extraordinary ncardiac contractions with a compensatory pause are registered after nregistration of normal pulse.

Additional positive differential sign of these two nkinds of arrhythmic pulse can be done by assigning the child some light nphysical exercise: cardiac fibrillation is characterized by increase ideficiency of pulse; extrasystole is characterized by its reduction or absence.

 

Asymmetric (when pulse rate at the left nand right hands are unequal or when pulse is late). Causes are due to:

·        nStenosis of left AV valves f pay attention to the mechanism: hypertrophied left atrium npushes the left subclavian artery, especially when the child is on left side).

·        nCompressing the arteries by tumor or lymph nnodes.

In many respiratory and cardiovascular diseases, nthe ratio between breath rate and pulse rate can change considerably. nMalfunction will depend on the system damaged.

 

Pulse pressure

Hard pulse (Latin — Pulsus durum) and soft pulse (Latin — Pulsus mollis) are indicators of high and nlow blood pressure respectively.

 

Size nof pulse

High pulse — of non cardiac genesis is a sign of nhigh temperature caused by intoxication and indicates hyperthyroidism; high npulse of cardiac genesis occures due to an open Sotallo’s duct (PDA — patent nductus arteriosus) and insufficiency of aortal valves.

Small pulse (Latin — Pulsus parvus) till approaching thready nindicates stenosis of the mitral and aortal valves and cardiovascular ninsufficiency.

Alternating pulse (Latin — Pulsus alternans) is characterized by stable nalternation of high and low pulsations. It occurs during damage of myocardium.

Paradoxical pulse (Latin — Pulsus paradoxus) is weakening or complete ndisappearance of pulse waves during inspiration. Paradoxical pulse is due lo nreduction in filling the heart, which results in reduction in filling and size nof pulse. The reasons of such destructions are exudative and adhesive npericarditis, severe exudative pleuritis, mediastinal tumors and bronchial nasthma. In adhesive pericarditis the pulse can disappear completely during ninspiration as there is a significant extension of heart muscles, adhesion of npericardium with thoracic .wall, diaphragm and vertebral column.

Paradoxical pulse can be of exlracardial origiwhen the chest, which rises during inspiration, compresses the subclaviaartery between the first rib and the clavicle. In this case, paradoxical pulse nis fell either in one or in both hands, and (Attention!) it is not present in lower nlimbs.

Sometimes, paradoxical pulse is present in healthy nchildren wheegative pressure in thorax at the peak of inspiration prevents nfrom filling the left atrium of heart and vessels of the greater circulatiowith blood.

 

Additional parameters

Corriagan’s symptom (Irish doctor of the 1century) nis a sign of insufficiency of aortal valves, when putse waves are frequent, and nalso high and fast while increasing and decreasing (Latin — Pulsus celer et altus).

The capillary pulse of Quincke or Quincke’s svmotom n(a German therapist of the 19-20 centuries) is also of great diagnostic nimportance: the tip of a nail is slightly pressed till a white spot appears iits centre. Normally. while the nail is pressed, the spot remains white all nthis time. In the case of insufficiency of aortal valves, the stain turns red nand pale with systole and diastole respectively.

 

Apex beat

 

Location:

·        nDisplacement to the left indicates the nexpansion of left ventricle or the whole heart; it also happens during nhypertension, right pneumothorax, right hemothorax and exudative pleurisy,

·        nDisplacement to the right occurs at left nexudative pleurisy, pneumothorax or hemothorax; and also in a very rare nabnormality of development when a larger part of the heart is displaced in the nthoracic cavity to the right side from the median line, i.e. in dextrocardia.

·        nDisplacement downwards is observed during ndilatation of left ventricle, insufficiency of aortal valves and pulmonary nemphysema,

·        nDisplacement upwards happens at atelectasis nof lungs, it is a symptom of highly elevated diaphragm during meteorism and nascites (it is simultaneously displaced to the left).

 

Extension:

·        nExpansion of apex beat to the area of more nthan 1 «1 cm, and In older nchildren — more than 2*2 cm or if it is palpable in 2 or more intercostal nspaces is considered expanded; expanded beat is a symptom of expansion and left nventricular hypertrophy (heart defect).

·        nLimited apex be at may be observed iexudative pericarditis, pulmonary emphysema and a descended diaphragm n(phrenoptosia).

 

Height (magnitude):

(a) The apex beat can be high during the increase nin force and speed of heart contraction, hypertrophy of left ventricle and also nduring significant approaching of heart apex to the wall of thorax (deep nexhalation, weight toss, elevated diaphragm, tumor in posterior mediastinum).

(b)     Apex nbeat is low. during deep inspiration, nadiposity, pericarditis, left sided pleurisy with exudative and pulmonary nemphysema; sometimes idifficult conditions it may not be determined at all.

(c)     Apex nbeat is called negative when the thoracic wall is pulled inside during

systole instead of bulging out (symptom of MacKenzie — an English doctor of the n19-20 centuries).

This symptom occurs in adhesive pericarditis whepericardium sticks to anterior wall of the thorax.

 

Resistance n(fores)

(a)     Apical nthrust is said to be resistant nwhen while palpating, the pressure or the force is felt more than the nnormal force; it is seen in LVH patient’s.

(b)     The nreasons for weak apex beat are similar to the reasons of low apex beat

 

Cardiac thrust

Extension — expanded cardiac thrust is spread over a large area and, nbesides normal place of location, it can be displaced in axillary and nepigastric regions (heart diseases).

Force — if strong beat is felt in the area of more than 1*1 cm (in older children — more than 2*2 cm), it is regarded as a force ndisorder of ncardiac thrust.

The causes of cardiac thrust disorder is similar to nthat of the apex beat disorders.

 

Additional ndata

Symptom ‘purr of cat’ is trembling of the chest wall nwhich is determined during placing the palm or fingers on the heart. It nreminds the purring of a cat. This symptom may occur:

·     nDuring nsystole (coinciding with cardiac thrust) in the second intercostal interval to the right of nthe sternum (it is sign of aortic stenosis) or to the left of the sternum (it is sign of open Botallo’s duct, rarely of the pulmonary artery nstenosis).

·     During diastole in the I point (between cardiac ncontractions) — it is a sign of mitral valve stenosis.

Cardiac nedema specifies the weakness of cardiac activity and nstagnation of fluid.

 

Percussion

 

Percussion of the heart is a method for ndetermination of its borders and size. Only a small internal part of anterior nsurface of the heart directly adjoins the thorax. Limits of this zone are ncalled borders of absolute heart dullness. The other part of anterior surface nof heart is covered with lungs. Location of limits of this zone, i.e. true size nof heart, is an establishment of borders of relative heart dullness. Ichildren, especially in younger ones, absolute heart dullness is determined nrarely, so practically, the main diagnostic parameter is the borders of nrelative heart dullness.

Rules and techniques of percussion:

·        nThe doctor stands to the right side of the npatient.

·        nThe best way to examine the patient is whehe/she is in vertical position with the hands down. Severe cases or children of nvery young age are examined in horizontal position (the results obtained will nbe a little bit higher).

·        nIt is possible to use direct (more often ichildren of early age) and indirect ways of percussion.

·        nPercussion is carried out along the nintercostal intervals in the direction from pulmonary tissues to heart.

·        nPlessimeter-finger is placed parallel to the nrequired border of heart.

·        nThe order of percussion — right, upper and nleft borders of relative cardiac dullness;

·        nDetermining of the right border: first, place nthe piessimeter-finger into the right II-III intercostal intervals parallel to nthe ribs. The inferior border of right lung is found by percussion from the top nto the bottom along the medioclavicular line. After that, rising one nintercostal interval above and having placed the finger parallel to right nborder of heart (i.e. perpendicular to the ribs), percussion is performed from noutside inwards as the sound changes from vesicular resonance to decrease iresonance. Appearance of decrease in resonance specifies that the nplessimeter-finger is on the border of heart. Percussion stops and the border of nheart is marked on the external edge of the finger.

·        nLocation of the upper border: the nplessimeter-finger is placed in the first intercostal interval parallel to the nribs along the medioclavicular line in young children and on the parasternal nline in older children. Percussion is carried out from the top to the bottom ntill the decrease in resonance appears The border of heart is marked above nupper edge of the finger,

·        nLocation of the left border: first the nlocation of apex beat is defined by palpating, the finger is moved along the nsame intercostal interval to the anterior axillary line and percussion is ncarried out in the same intercostal interval. If the apex beat is not found by npalpation, percussion is carried out in the intercostal interval where the beat nshould be situated depending on the age — IV or V. The so-called northopercussion method is the most accurate one for locating the left border of nrelative heart dullness: in the defined intercostal interval on the same level nwith anterior axillary line, the plessimeler-finger is placed almost parallel nlo the required border in such a way, lhat it completely touches the skiot nwith its palmar surface of finger’s phalanxes but mainly with the lateral nsurface. The hit of plessor-finger in the place of auscultation in this way is ndirected from the front to the back (perpendicular to sagittal plane). I.e., if nin all methods of percussion studies earlier the angle between the finger and nskin from both sides was 90°, in orthopercussion the internal angle between the nfinger and skin of the chest is less than 90” (it is designated as angle a), nand between the finger and skin on an external side — more than 90° (it is ndesignated as angle (3). Percussion is carried out in intercostal inlervals nfrom outside inwards till the sound changes from vesicular .esonance lo ndecrease in resonance: the border is marked on the external edge of the finger.

 

Border’s of hearts relative dullness

 

 

Border’s of hearts absolute dullness

 

 

 

Symptomatological npercussional disorders

Changes or deviation in borders of the relative cardiac ndullness may occur both in the direction of expansions or in the direction of nshrinking.

The most common reasons of expansion of borders of relative heart dullness are:

·        nCongenital and acquired heart diseases .

·        nMyocarditis.

·        nFibroelastosis.

·        nThe horizontal position of heart and thus nexpansion of mostly left border may be caused by diseases of other organs and nsystems, Such as — meleorism, ascites, alonia of diaphragm, mediastinal tumors, nright pneumothorax and hemothorax, exudative pleurisy, etc.

Reductioof borders of the relative heart dullness is rarely observed:

·        nEmphysema of lungs.

·        nLeft pneumothorax.

·        nAsthenic constitution of body.

 

Auscultation is an art that improves with practice. The diaphragm of the stethoscope nis placed firmly on the chest for high-pitched sounds; a lightly placed bell is noptimal for low-pitched sounds. The physician should initially concentrate othe characteristics of the individual heart sounds and their variation with nrespirations and later concentrate on murmurs. The patient should be supine, nlying quietly, and breathing normally. The 1st heart sound is best heard at the apex, whereas the 2nd heart sound should be evaluated at nthe upper left and right sternal borders. The 1st heart sound is caused by nclosure of the atrioventricular valves (mitral and tricuspid); the 2nd sound is ncaused by closure of the semilunar valves (aortic and pulmonary). During ninspiration, the decrease in intrathoracic pressure results in increased nfilling of the right side of the heart, which leads to an increased right nventricular ejection time and thus delayed closure of the pulmonary valve; nconsequently, splitting of the 2nd nheart sound increases during inspiration and decreases during nexpiration.

Often, the 2nd heart sound seems to be single during expiration. The npresence of a normally split 2nd sound is strong evidence against the diagnosis of natrial septal defect, defects associated with pulmonary arterial hypertension, nsevere pulmonary valve stenosis, aortic and pulmonary atresia, and truncus narteriosus. Wide splitting is noted in atrial septal defect, pulmonary nstenosis, Ebstein anomaly, total anomalous pulmonary venous return, and right nbundle branch block. An accentuated pulmonic component of the 2nd sound with nnarrow splitting is a sign of pulmonary hypertension. A single 2nd sound occurs nin pulmonary or aortic atresia or severe stenosis, truncus arteriosus, and, noften, transposition of the great arteries.

A 3rd heart sound is best nheard with the bell at the apex in mid-diastole. A 4th sound occurring in conjunction with atrial contraction may be nheard just before the 1st heart sound in late diastole. The 3rd sound may be nnormal in an adolescent with a relatively slow heart rate, but in a patient nwith the clinical signs of heart failure and tachycardia, it may be heard as a ngallop rhythm and may merge with a 4th heart sound, a finding known as a nsummation gallop. A gallop rhythm is attributed to poor compliance of the nventricle, and exaggeration of the normal 3rd sound is associated with nventricular filling.

Ejection clicks, which are heard in early systole, may be related to dilatation of the naorta or pulmonary artery or to a mildly to moderately stenotic semilunar nvalve. They are heard so close to the 1st heart sound that they may be mistakefor a split 1st sound. Aortic ejection clicks are best heard at the left middle nto right upper sternal border and are constant in intensity. They occur iconditions in which the aortic valve is stenotic or the aorta is dilated n(tetralogy of Fallot, truncus arteriosus). Pulmonary ejection clicks, which are nassociated with mild to moderate pulmonary stenosis, are best heard at the left nmiddle to upper sternal border and vary with respirations, often disappearing nwith inspiration. Split 1st heart sounds are usually heard best at the lower nleft sternal border. A midsystolic click heard at the apex, often preceding a nlate systolic murmur, suggests mitral valve prolapse.

 

Auscultation involves listening for heart sounds with the stethoscope, similar nto the procedure used in assessing breath sounds.

Origin of heart sounds. The heart sounds are produced by the opening and nclosing of the valves and the vibration of blood against the walls of the heart nand vessels. Normally two sounds – S₁ and S2 – are heard, which ncorrespond  respectively to the familiar n”lub dub” often used to describe the sounds. S₁ is caused nby the closure of the tricuspid and mitral valves (sometimes called the natrioventricular valves). Right ventricular contraction follows tricuspid valve nclosure, and left ventricular contraction follows mitral valve closure. The ncontractions (systole) occur almost simultaneously, although the mitral valve n(left side) closes slightly before the tricuspid valve (right side). Normally nthis split of the sounds is so close that it is not audible, except noccasionally at the apex of the heart.

S₂ is the result of the closure of the pulmonic and aortic nvalves (sometimes called semilunar valves). Aortic valve closing (left side) noccurs slightly before pulmonic valve closing (right side). The flow of blood ninto the aorta and pulmonary artery occurs following closure of their nrespective valves. The interval between S₂ and S₁ is ndiastole, or relaxation, of the heart. Normally the split of the two sounds iS₂ is distinguishable and widens during inspiration, since ninspiration prolongs right ventricular filling and delays pulmonic valve nclosure. “Physiologic splitting” is a significant normal finding that nshould be elicited. “Fixed splitting”, in which the split in S₂ ndoes not change during inspiration, is an important diagnostic sign of atrial nseptal defect.

.

 

The points of auscultations of heart.

 

Two other heart sounds – S₃ and S₄ – may be nproduced. S₃ is the result of vibrations produced during ventricular nfilling. It is normally heard only in some children and young adults, but it is nconsidered abnormal in older individuals. S₄ is caused by the recoil nof vibrations between the atria and ventricles following atrial contraction, at nthe end of diastole. It is rarely heard as a normal heart sound; usually it is nconsidered indicative of further cardiac evaluation.

Another important category of heart sounds is murmurs, which are nproduced by vibrations within the heart chambers or in the major arteries from nthe back and forth flow of blood.

 

Murmurs are classified as: 1. Innocent, noccurring in individuals with no anatomic or physiologic abnormality.

2. Functional, occurring in individuals with no anatomic cardiac defect nbut with a physiologic abnormality such as anemia.

3. Organic, occurring in individuals with a cardiac defect with or nwithout a physiologic abnormality. The description and classification of nmurmurs are skills that require considerable practice and training. In general nthe doctor should be able to recognize murmurs as distinct swishing sounds that noccur in addition to the normal heart sounds. The following information should nbe found:

1.  Location of the area of the nheart where the murmur is heard best.

2.  Time of the occurrence of the nmurmur within the S₁ S₂ cycle.

3.  Evaluation of its intensity irelationship to the child’s position.  

 4.  Estimation of its loudness

Although the doctor consults with a physician whenever a murmur is nidentified, the following guidelines can be used in distinguishing betweeinnocent and organic murmurs. Innocent murmurs generally are:

1.  Systolic, that is, they occur nwith or after S_1.

2.  Of short duration and have no ntransmission to other areas of the heart.

3.  Grade III or less in intensity nand do not increase over time.

4.  Usually loudest in the npulmonic area (second or third intercostal space along the left sternal nborder).

5.  Variable in relationship to nposition, respiration, and activity (for example, audible in the supine nposition but absent in the sitting position; may be louder with exercise, nfever, anxiety, or anemia).

6.  Not associated with any nphysical signs of cardiac disease.  

7.  Usually of a low-pitched, nmusical, or groaning quality.

 

 

 

 

Sequence of auscultating heart sounds

 

 

 

Heart murmurs are divided into two ncategories: (1) nonorganic or physiologic murmurs, also called ninnocent, functional, or benign murmurs; and (2) organic or pathologic murmurs. Innocent murmurs are ncommon during childhood, pregnancy, febrile episodes, anemia, and sepsis. They ndevelop in gravid women because of increased blood volume and in childrebecause of increased blood flow rate through the heart. Innocent murmurs nrepresent a nonpathologic state and arc most frequently heard during systole. nIn children and gravid women, the murmur usually disappears after puberty or nafter childbirth, respectively.

Organic heart murmurs are the result of a nvalvular disorder. They are most often heard during diastole and do not ndisappear with time. An organic heart murmur may be caused by a noncompliant n(stenotic) valve that reduces the size of the orifice between heart chambers, nor it may be caused by regurgitation of blood from endocardial fibro­sis that nresults in a floppy, incompetent valve. Most organic murmurs are a combinatioof regurgitant and stenotic. The valves of the left side of the heart are more ncommonly affected than those of the right side. The mitral valve is most nfrequently affected, followed by the aortic valve, tricuspid valve, and npulmonic valve. Causes of organic heart murmur include congenital heart defects n(e.g., mitral valve prolapse), infections such as rheumatic heart disease, nconnective tissue disease (e.g.. osteogenesis imperfecta), and autoimmune ndisease (e.g., systemic lupus erythematosus ).

 

Murmurs should nbe described according to their intensity, pitch, timing (systolic or ndiastolic), variation in intensity, time to peak intensity, area of maximal nintensity, and radiation to other areas. Auscultation for murmurs should be ncarried out across the upper precordium, down the left or right sternal border, nand out to the apex and left axilla. Auscultation should also always be nperformed in the right axilla and over the back. Systolic murmurs are nclassified as ejection, pansystolic, or late systolic according to the timing nof the murmur in relation to the 1st and 2nd heart sounds. The intensity of nsystolic murmurs is graded from I to VI: I, barely audible; II, medium nintensity; III, loud but no thrill; IV, loud with a thrill; V, very loud but nstill requiring positioning of the stethoscope at least partly on the chest; nand VI, so loud that the murmur can be heard with the stethoscope off the nchest. Systolic ejection murmurs nstart a short time after a well-heard 1st heart sound, increase in intensity, npeak, and then decrease in intensity; they usually end before the 2nd sound. Ipatients with severe aortic or pulmonary stenosis, however, the murmur may nextend beyond the 1st component of the 2nd sound, thus obscuring it. Pansystolic or holosystolic murmurs nbegin almost simultaneously with the 1st heart sound and continue throughout nsystole, on occasion becoming gradually decrescendo. It is helpful to remember nthat after closure of the atrioventricular valves (the 1st heart sound), a nbrief period occurs during which ventricular pressure increases but the nsemilunar valves remain closed (isovolumic contraction). Thus, pansystolic nmurmurs (heard during both isovolumic contraction and the ejection phases of nsystole) cannot be caused by flow across the semilunar valves because these nvalves are closed during isovolumic contraction. Pansystolic murmurs are ntherefore related to blood exiting the contracting ventricle via either aabnormal opening (a ventricular septal defect) or atrioventricular (mitral or ntricuspid) valve insufficiency. Systolic ejection murmurs usually imply nincreased flow or stenosis across one of the ventricular outflow tracts (aortic nor pulmonic). In infants with rapid heart rates, it is often difficult to ndistinguish between ejection and pansystolic murmurs. If a clear and distinct n1st heart sound can be appreciated, the murmur is most likely ejection inature.

A continuous murmur is a nsystolic murmur that continues or “spills” into diastole and indicates ncontinuous flow, such as in the presence of a patent ductus arteriosus or other naortopulmonary communication. This murmur should be differentiated from a nto-and-fro murmur, which indicates that the systolic component of the murmur nends at or before the 2nd sound and the diastolic murmur begins after semilunar nvalve closure (aortic or pulmonary stenosis combined with insufficiency). A nlate systolic murmur begins well beyond the 1st heart sound and continues until nthe end of systole. Such murmurs may be heard after a midsystolic click ipatients with mitral valve prolapse and insufficiency.

Several types of diastolic nmurmurs (graded I–IV) can be identified. A decrescendo diastolic murmur nis a blowing murmur along the left sternal border that begins with S₂ nand diminishes toward mid-diastole. When high-pitched, this murmur is nassociated with aortic valve insufficiency or pulmonary insufficiency related nto pulmonary hypertension. When low-pitched, this murmur is associated with npulmonary valve insufficiency in the absence of pulmonary hypertension. A nlow-pitched decrescendo diastolic murmur is typically noted after surgical nrepair of the pulmonary outflow tract in defects such as tetralogy of Fallot or nin patients with absent pulmonary valves. A rumbling middiastolic murmur at the nleft middle and lower sternal border may be due to increased blood flow across nthe tricuspid valve, such as occurs with an atrial septal defect or, less noften, because of actual stenosis of this valve. When this murmur is heard at nthe apex, it is caused by increased flow across the mitral valve, such as noccurs with large left-to-right shunts at the ventricular level (ventricular nseptal defects), at the great vessel level (patent ductus arteriosus, naortopulmonary shunts), or with increased flow because of mitral insufficiency. nWhen an apical diastolic rumbling murmur is longer and is accentuated at the nend of diastole (presystolic), it usually indicates anatomic mitral valve nstenosis.

The absence of a precordial murmur does not rule out significant ncongenital or acquired heart disease. Congenital heart defects, some of which nare ductal dependent, may not demonstrate a murmur if the ductus arteriosus ncloses. These lesions include pulmonary or tricuspid valve atresia and ntransposition of the great arteries. Murmurs may seem insignificant in patients nwith severe aortic stenosis, atrial septal defects, anomalous pulmonary venous nreturn, atrioventricular septal defects, coarctation of the aorta, or anomalous ninsertion of a coronary artery. Careful attention to other components of the nphysical examination (growth failure, cyanosis, peripheral pulses, precordial nimpulse, heart sounds) increases the index of suspicion of congenital heart ndefects in these cases. In contrast, loud murmurs may be present in the absence nof structural heart disease, for example, in patients with a large noncardiac narteriovenous malformation, myocarditis, severe anemia, or hypertension.

Many murmurs are not associated with significant hemodynamic nabnormalities. These murmurs are referred to as functional, normal, ninsignificant, or innocent (the preferred term). During routine random nauscultation, more than 30% of children may have an innocent murmur at one time nin their lives; this percentage increases when auscultation is carried out nunder nonbasal circumstances (high cardiac output because of fever, infection, nanxiety). The most common innocent nmurmur is a medium-pitched, vibratory or “musical,” relatively short nsystolic ejection murmur, which is heard best along the left lower and nmidsternal border and has no significant radiation to the apex, base, or back. nIt is heard most frequently in children between 3 and 7 yr of age. The nintensity of the murmur often changes with respiration and position and may be nattenuated in the sitting or prone position. Innocent pulmonic murmurs are also ncommon in children and adolescents and originate from normal turbulence during nejection into the pulmonary artery. They are higher pitched, blowing, brief nearly systolic murmurs of grade I–II in intensity and are best detected in the n2nd left parasternal space with the patient in the supine position. Features nsuggestive of heart disease include murmurs that are pansystolic, grade III or nhigher, harsh, located at the left upper sternal border, and associated with aearly or midsystolic click or an abnormal 2nd heart sound

 

A venous hum is another nexample of a common innocent murmur heard during childhood. Such hums are nproduced by turbulence of blood in the jugular venous system; they have no npathologic significance and may be heard in the neck or anterior portion of the nupper part of the chest. A venous hum consists of a soft humming sound heard iboth systole and diastole; it can be exaggerated or made to disappear by nvarying the position of the head, or it can be decreased by lightly compressing nthe jugular venous system in the neck. These simple maneuvers are sufficient to ndifferentiate a venous hum from the murmurs produced by organic cardiovascular ndisease, particularly a patent ductus arteriosus.

The lack of significance of an innocent murmur should be discussed with nthe child’s parents. It is important to offer complete reassurance because nlingering doubts about the importance of a cardiac murmur may have profound neffects on child-rearing practices, most often in the form of noverprotectiveness. An underlying fear that a cardiac abnormality is present nmay negatively affect a child’s self-image and subtly influence personality ndevelopment. The physician should explain that an innocent murmur is simply a n“noise” and does not indicate the presence of a significant cardiac defect. nWhen asked, “Will it go away?” the best response is to state that because the nmurmur has no clinical significance, it therefore does not matter whether it n“goes away.” Parents should be warned that the intensity of the murmur might nincrease during febrile illnesses, a time when, typically, another physiciaexamines the child. With growth, however, innocent murmurs are less well heard nand often disappear completely. At times, additional studies may be indicated nto rule out a congenital heart defect, but “routine” electrocardiographic, nchest roentgenographic, and echocardiographic examinations should be avoided iwell children with innocent murmurs

 

Blood pressure, mmHg

 

 

 

Any disturbance in the distribution of the fluid inside the vessels and nthat outside the vessels ( Extra and Intra vascular fluids ) may lead to edema n, which is a common presentation in the children and adults at any age . There nare 5 main general causes of edema which are :

 

1-Renal : the cause here is a kidney disease leading to disturbance igetting red of the fluids inside the body causing generalized edema , Nephrotic nsyndrome as an example is a very common cause of the renal pathology , the nedema here begins in the eyelids , the upper respiratory distress . Other ncauses of renal edema is Nephritic syndrome , edema here is mild and may not be nrecognized by the mother .

2-Cardiac : any cardiac pathology lead to decrease the force of ncontraction of the blood to all the body will lead to edema , as the blood and nfluids returning to the heart will not be pumped well to the whole body . nCardiac pathology in childhood may be congenital anomaly which when progress nmay cause heart failure leading to generalized edema an example of the heart ncongenital anomalies is VSD ( ventricular septal defect ) , here there is a ndefect in the septum between the left and the right ventricle , if left with nout treatment may cause recurrent chest infections , failure to thrive and nheart failure . There are many other defects in the heart can progress to cause nheart failure as Atrial septal defect and Patent ductus arteriosus whuch are ncommon causes of congenital anomalies .

3-Allergic : exposure to allergen as certain types of food , bites or ncertain types of drinks can stimulate the inflammatory cells and inflammatory ntransmitters leading to dilatation in the vessels of the body and generalized nedema .

 

 

“pitting” edema

 

 

Additional methods of investigation

 

Laboratory test

Common blood analysis-increased ESR, leucocytosis; nincreases in the erythrocyte count, hemoglobilevel, and hematocrit.

Biochemical blood analysis-elevated level of glycoproteins, seromucoid, protein’s fractions n(α-1 and α-2-globulins), kreatininephosphokinase, fibrinogen, nmucoproteins.

Serological-elevation of antistreptolysin O (AS-O, antidesoxyribonuclease B, antihyaluronidase).

Bacteriological – culture of group A streptococcus is the gold standard evidence of the nprevious infection.In children with cyanosis, nblood gas analysis and laboratory tests for hemostasis.

In children with cyanotic heart disease, a number of hemostatic abnormalities are common, including thrombocytopenia and low levels of prothrombin and factors V, nVII, and IX.

 

 

Functional tests

Orthostatic test of Martinet (French therapist of the 19ⁱⁿ-20^lh ncenturies): The npulse rate and BP are determined En children in lying, and then — in vertical position.

Normally, when the patient ngets Lip, the pulse rate does not increase more than 10 per nminute, and the systolic BP — not more than 5 mmHg.

The cardiovascular npathology are accompanied by great increase in the pulse rate and decrease of nthe maximal BP,

 

Shalkov’s test (native doctor of the n20^ century}: First, the npulse rate and BP are measured. Using the formula of Erlanger-Guker (Edanger — U,S, nphysiologist of the 20^lh century), the minute volume (CO) of blood is calculated, which = pulse pressure * pulse rate.

For example: BP = 110/60 mmHg. Pulse rate – 70 per nminute. CO =(110 -60) * 70 -3500 ml.

After that, the patient is nasked to carry out some exercises which depend on the regime of the child:

·        nBed rest regime — change of the lying nposition to sitting one 3 times, then 5 and 10 times.

·        nHatf-bed¹, nambulant regime and practically healthy children — sit-ups 5 times in to 10 nsec, then 10 times in 20 sec. and 20 times in 30 sec.

After the exercises, the nmentioned parameters (pulse rate and BP) are determined after 3, 5 and 10 minutes later. Test is considered positive (or adequate), i.e. physical exercise did nnot result to any problems in the functioning of heart, if:

·     nExercise did not cause exhaustion of the nchild.

·     nPufse rata and minute volume of blood rises nno! more than 25%.

·     nSystolic nBP raises nno more than by 10 mmHg.

·     nDiastolic nBP does nnot change or decreases a little.

·     All parameters return to the figures which were nreceived in quiet condition, within 3 minutes

According to the list, there are 6 exercises. A patient, who is on bed nrest regime, should change his/her horizontal posture to the sitting one 3 ntimes during the first inspection. If the test is negative (pulse rate increased nby 35%, systolic BP increased by 25 mmHg, the parameters normalize in 15 nminutes, etc.), after a while (2, 3 days and more) the child again is appointed nthe same lest (as in the first case). If the test is positive, then during the nnext inspection the following exercise is used — the second changing horizontal nposture to the sitting one 5 times, etc.

Thus, each subsequent exercise is appointed to the patient as the change nof treatment and inspection, when the result of the previous exercise was npositive. It is the criteria for the patient to change to next regime (for nexample, from bed rest regime to half-bed).

The pathology of cardiovascular system is accompanied by significant changes in Shalkov’s test — the npulse rate and minute volume of blood increase by 40-50% and more, systolic npressure — by 15-20 mmHg and more, the restoration is achieved in 5-10 minutes nand later.

 

Electrocardiography

 

 

Electrocardiogram n(ECG): A record usually graphically displayed or electrically recorded activity nproduced by the biological tissues of heart.

Today we use twelve nstandard (bipolar limb, bipolar extremity) leads: three standard ones n(classic), three unipolar (monopolar) limb leads and six unipolar precordial n(chest, semidirect) leads.

Three nstandard leads from limbs were suggested by Einthoven (Dutch nphysiologist of the 19^,h-20′” centuries). In the leads, nindicated by Romaumbers I, II and III, differences in potentials are nregistered between:

·         nRight and left hands — in the I lead.

·         nRight hand and left foot — in the II lead.

·         nLeft hand and left foot — in the III lead.

In three unipolar leads from the limbs (according to Goldberger — nU.S. cardiologist of the 20¹” century), indicated as aVR (AVR), aVL (AVL) and aVF (AVF), letter a’ means naugmented, ‘V means voltage, and the third letter specifies the location of aactive electrode: R — on the right hand, L — on the left hand and F — on the nleft foot.

Six nunipolar precordial leads are indicated Ly letter ‘V. Position of active nelectrode is indicated in small numbers near this letter:

·       V. stands for IV nintercostal space at right sternal edge

·        nindicates IV intercostal space at left nsternal edge

·       V, shows location on the nmiddle of a line between II and IV leads.

·      nV_t npoints at the place of intersection of V intercostal Space and left nmedioclavicular line,

·      V₅ locates at nthe intersection of the left anterior axillary lire and a horizontal line thai nruns through point V„.

·      nV locates at the intersection of the left nmedial axillary line and a horizontal line that goes through point V₄.

Rules of registering the nelectrocardiogram:

·      Device should be earthed or nthe cabinet should be shielded.

·      Recording is carried out ia warm room

·      nECG nare performed in an empty stomach or at least two hours after food.

·      Recording, especially a nmultiple one, is carried out in the same position of patient. It is better if npatient is in a supine position for 15-20 minutes before the recording starts.

·      nIts necessary to convince the young childrethat the procedure is safe, recording should be done in the presence of their nmother; if the child is worried, it may be difficult to carry out the recording nso first, you may try to do this procedure on a relaxed child in the presence nof the worried child.

·      nRegistration of electrocardiogram ipediatrics should be performed quickly.

·      Before the procedure, the nchild should not take strong and sedative medicines.

·        nRecording cannot bo carried out after hydro nand physiotherapeutic procedures.

·        nMaximum speed of tape movement, which is nfrequently applied, is 50 mm/sec,

 

Common rules to read electrocardiogram

Elements of normal electrocardiogram suggested by nEinthoven:

·      Six waves (P, Q, R, S_t nT and U).

·      Intervals (P-Q. QRS, ST, nQ-T. T-P, R-R).

·      nTwo complexes (atrial—P and P-Q; nventricular—QRST -QRS+ST +T; shown at Fig. 183 as I and nII respectively); sum of two complexes — cardiac cycle.

·        nSometimes segment PQ is also defined.

To read an electrocardiogram, the following nparameters of elements should be established:

·      nPresence.

·       Duration.

·        nAmplitude of waves.

·        nForm of waves.

·        nDirection of waves in relation to isoelectric nline.

Duration of elements (sec) and amplitude of waves n(mm.) are defined with the help of a ruler or a grid which is drawn on aelectrographic paper. Distance between horizontal and thin vertical lines othe grid is 1 mm. One interval between thin vertical lines, when tape moves nwith a speed of 50 mm/sec, is covered for 0.02 seconds. After every 5 thivertical lines, there appears one thick vertical line. Distance between two nthick lines equals 002 sec. × 5 = 0.1 sec.

Duration of intervals is ngenerally measured in the II standard lead.

Wave that goes upward from isoelectric line is positive n(upward), if it goes downward, it is negative (downward, inverted).

 

Besides frequency of cardiac contraction, ntheir rhythm as well as electric I axis of heart nare other very important parameters of electrocardiogram.

 

Heart has a conducting system. Excitation begins isinoatrial node (SA node) which is located in right atrium near to superior nvena cava and characterized by automatism. This moment of excitation is not nreflected in the electrocardiogram and coincides with isoelectric line. Then the nprocess of excitation (depolarization) spreads to muscles of atrium.

 

P wave appears on ECG, P wave represents atrial ncomplex. Its first half till its peak indicates excilalion of right atrium, the nsecond half after its peak indicates excitation of left atrium. In most of the nleads, it is positive (+). i.e. located higher, than the isoelectric line. nDuration of P wave depends on the age of children. Normally it does not exceed 0.09-0,10 sec. Amplitude of P wave is nnot higher than 3 mm.

 

Interval nP-Q characters the time required for the impulse to go from the beginning of atrial excitation to the nbeginning of ventricular excitation, i.e. it includes both the time of ndistribution of impulse through the atrium and its physiological delay iatrioventricular node. It is measured starting from the beginning of P wave to nthe beginning of Q wave. If the latter is absent, it is measured to the beginning nof R wave. Duration of the P-Q interval depends on the frequency of cardiac ncontractions, age and sex of the child. Normal fluctuations are 0.11-0.18 sec.

 

Segment nPQ is a part of interval P-Q from the end of P wave to the beginning of Q wave (interval P-Q minus P nwave).

After that, depolarization takes place in the ventricle and it is registered in the nECG as ventricular ncomplex QRST which reflects:

•  Process of spreading nexcitation in ventricles (QRS — process of depolarization lasts for 0.04-0.09 sec),

•  Process of fading of ventricular nexcitation — process of repolarizatio(S-T and T).

 

Q wave nis always negative n(-), i.e. it is located lower than isoelectric line, it is variable and reflects nelectrodynamic force of interventricular septum and partially reflects nelectrodynamic force of the apex of right ventricle Its duration is 0.01-0.02 sec. to form a ncomplex.

 

R wave nis always positive n(+), It reflects electrodynamic force of left and right ventricular nmyocardial walls. Duration of this wave is 0.03-0.05 sec. nto form complex QRS.

Normally, the R waves relate to the standard leads nin the following way: R nII > R III > R I. By determining the height of R wave in I and 111 leads, obtained ECG could be classified in the following nway: if the namplitude is higher in the III lead, it is called the deviation of the nelectrical axis to the right (Rill > Rll > Rij, if It is higher in the I lead, it is called the deviation of the electrical axis to the nleft (Rt > Rll > Rill).

 

To find out the most accurate type of nECG, it is necessary to know the sum of amplitudes R {+} and S (-) in the I nstandard lead and the sum of amplitudes R (+) and 5 (-) in the III standard lead. nSo the conclusions as for the type of ECG can be made with the help of nthe following results:

·       nIf the sum of amplitudes in the I and III standard nleads is positive, the tvoe of ECG can be defined after comparing nthe obtained numbers: if it is greater in the 111 lead. ECG is rightcardiocram <RIII>RII>RlUnd if it is greater in the I lead nECG is leftcardiogram fRI>RII=>RIH).

·       nif the sum is positive in the III lead nand negative in the I lead. ECG is dextrogram

·       nIf the sum positive in the I lead and nnegative in the III lead, ECG is leftcardiogram.

 

S wave is always negative (-). changeable and nreflects electrodynamic force of the myocardium of basal parts of the heart; it nis 0.06-0,07 sec.

During the full scope of ventricular nagitation, the potential difference disappears and isoelectric line is nregistered in ECG, which reflects the period of early nrepolarization — interval ST. It is measured from the end of S wave to the beginning of T wave. nIts duration does not exceed 0.15 sec. Usually the interval nis on the isoline. It can move 1 mm upwards or 0.5 mm downwards.

 

T wave is characterized by the process of fast nventricular repolarization, Le. the end of their activation. Its normal nduration is 0.12-0,18 nsec. This wave is often positive, but it can also be negative in the III nlead. The amplitude of the wave in different leads varies greatly. In standard nleads, greater size of R wave corresponds to the greater amplitude of T wave. nTherefore, it is considered as norm to take into account not the real size of T nwave but its relation to R wave. On the average it is 1:3, 1:4.

 

In approximately 8% of children of pre-preschool nage and in 1/3 of children of preschool and school age, positive U wave may occur after the T nwave. The amplitude of the U wave ia 1.5 mm. It is usually found at nbradycardia. Genesis of this wave is not yet established.

 

Q-T interval is a part of an electrocardiogram that nbegins from the beginning of Q wave and lasts to the end of T wave. It shows depolarizatioand repolarization of ventricles. Duration of the interval depends on different nparameters: heart rate, age and sex. Its average size is 0.26-0.34 sec.

 

T-P interval corresponds to absence of potential ndifference on the body surface, i.e. heart is in the condition of rest — ndiastolic period.

 

R-R interval is duration of one cardiac cycle. Its nrate is taken into account when frequency of cardiac contraction (beats per nminute is determined.

Variations in length of different R-R intervals make nit possible to evaluate whether the function of cardiac rhythm is right: if nthey do not exceed 10%, the rhythm is correct, regular. If they exceed 10%, ncardiac contraction is arrhythmic. In such situation, we will calculate the naverage duration of intervals from greater number of cycles.

 

Electrical axis of heart n(EAH) — is a total value of cardiac electric field.

To define direction and nsize of EAH, a geometric construction should be done in Einthoven’s ntriangle  using a two-standard lead.

 

Normal age nparameters of duration ofECG elements in children (sec.)

 

 

 

 

 

Position and deviations of EAH depending on α nangle

 

 

Direction of EAH depends othe age of child and position of heart in thorax. In healthy children before they nturn three, EAH is within the following limits: (+100°), at the age betweethree and fourteen years — (+30°)-(+70°). Changes of parameters are seen during ncardiac hypotrophy, conductive disorders, etc.

Features of ECG in children (caused by age changes n— positions of heart in thorax. size of muscles of right and left ventricles, nendocrinal functions, etc):

Digital ndifferences. ■ D extra gram prevails.

·       Tendency to tachycardia,

·       Shorter duration of waves and intervals of nelectrocardiogram which is caused by fast transferring of nexitation or activation through conducting system and myocardium: the younger nthe children, the shorter the period of transferring exitation the more the nrhythm often occurs.

·        nSize of waves in electrocardiogram is not of ngreat practically importance, their relation to one another is more important,

·        nArrhythmic ndisorders of functional etiology occur quite often.

·        nQ nwave, which is poorly defined, is less informative.

·        nIn 25% of healthy children of the first three nyears of life, QRS complex is split (jagged, notched), which indicates nincomplete blockade of the right branch of atrioventricular fascicle.

 

Symptomatological of ECG disorders

 

Rhythmic ndisorders

 

1.     Sinus tachycardia — is an increase in frequency nof cardiac contractions up to 200 per minute (b.p.m.) in children of early age nand up  to 150 cardiac contractions n(b.p.m.) in grown-ups.

2.     Sinus bradycardia is a reduction ifrequency of cardiac contractions up to 100 and less per minute in children of nbreast feeding

age and less than 80-60 cardiac contractions iolder children.

3. Sinus arrhythmia: R-R interval is sometimes shorter nand sometimes longer that exceeds mean rate for more than 10%.

 

Conductive disorders (blocks)

1. Sinoatrial (sinuatrial, sinus) block — transference of sinus impulse from SA node nto the ventricles is blocked in the heart. In electrocardiogram, you ncan observe periodic loss of one cardiac cycle after few normal cycles. Thus, a npause between two cardiac cycles is approximately twice as long as the usual ninterval between R-R or P-P waves.

2. nAtrioventricular heart blocks are disorders of conducting electric impulse from natriums to ventricle. They are divided into incomplete (among them nblocks of I and II degrees) and complete (blocks of III degree).

 

A. nFirst degree (incomplete) atrioventricular heart block is characterized by delay in atrioventricular conduction or lengthening natrioventricular delays. It is characterized by the nfollowing ECG criteria;

·       Correct rhythm.

·       Presence of all atrial and nventricular complexes.

·       P-Q interval is lengthened.

And lengthening is also possible only due to PQ nsegment (Fig. 191 – B) — more than 0.20 sec. (usually does not exceed 0,40 nsec). Thus, first degree (incomplete) atrioventricular block has 2 forms — natrial and nodular.

 

B. nSecond degree {incomplete) atrioventricular block is characterized by periodic block of supraventricular impulse which leads to the fact nthat some impulses from sinus node or atriums do not reach ventricles. It nresults in arrhythmia and bradycardia.

There are 2 types of second ndegree atrioventricular blocks.

Second ndegree atrioventricular block, type I (Wenkaaach’s heart block, Mobitz type I of atrioventricular block (German doctor of the 20 ncentury) — is characterized by the following disorders of nelectrocardiogram;

 

Second ndegree atrioventricular block, type II (drop beat, Mobitz type II of atrioventricular block) differs from block type I nbecause there is no gradual lengthening of P-Q interval in electrocardiogram (it was nbefore atrioventricular block and loss of ventricular complex). Disorders nconducting impulse occur below atrioventricular node (AV-node), not so often, nthey occur in the node. The following attributes are registered in ECG;

 

C. nThird degree (complete) atrioventricular heart block is characterized by independent contractions of atriums and nventricles. Ventricular rhythm is supported by the rhythm nfrom atrioventricular node, His’ bundle or Purkinje’s fibers. Characteristic nparameters of electrocardiogram  nincludes:

·      P waves are shorter irhythm, which is more often, than ventricular rhythm.

·      QRST complex appears in its nrhythm.

·      P-P intervals (0.7 sec, — n3-8 in the figure) and R-R (1,6 sec. — 1-2 in the figure) are constant,

·      P-P interval is shorter: nR-R is longer,

·      P-Q intervals are different n(P wave it is not connected with QRS),

 

Extrasystole

Extrasvstole nis a premature unexpected heart contraction caused by getting an impulse from ectopic focus. Depending on location of nfocus in heart, there are different forms of extrasystole: atrial, natrioventricular and ventricular.

1. nAtrial extrasystole: Changes in electrocardiogram depend on the atrium where npathological center of agitation is located (right or left}, and also in which npart of the atrium (top, middle or at the bottom part).

When ectopic focus is located in an atrium. ECG shows the following nimpairments:

·        nUnexpected occurrence of extrasystolic P wave nand then occurrence of QRST complex.

·       P wave is positive, if nfocus is located in the upper third of atrium, or negative, if it is located ithe lower third.

·       If extrasystole arises ithe middle third of atrium, deformed P wave occurs.

·       Shortening or lengthening nof P-Q interval.

·       Incomplete compensating npause after extrasystole.

 

2. Disorders of nelectrocardiogram in case of atrioventricular extrasystole (= premature beats) ndepend on the place in the node where ectopic focus is located.

The basic ECG features, if the focus is located ithe middle third of atrioventricular node are:

·       Absence of P wave as it ncoincides with QRS complex.

·       Incomplete compensating npause after extrasystole.

 

Location of the focus in the lower third of natrioventricular node i.e. is closer to ventricles, will be shown in ECG by the nfollowing basic features:

·        nP waves goes after QRS complex.

·       P wave is negative.

·       Incomplete compensating npause after extrasystole

 

3. Right and left ventricular extrasystole will be nshown in electrocardiogram by the following basic nchanges:

·       Absence of P wave before nventricular extrasystole,

·       nDeformation and widening of QRS complex, nwhich occurs unexpectedly.

·       nLocation of ST interval and T wave of nextrasystole is discordant to the direction of basic QRS complex (i.e., see nFig. 200, in V, R is lower than isoline, and ST and T wave is higher than it; nin V₆ it is vice versa). By the way, at left ventricular nextrasystole the data in V_n and in V₆ are opposite.

·        nComplete compensating pause after nextrasystole.

 

If changes in electrocardiogram come after each nnormal contraction, it is called bigeminy, if it occurs after every nsecond contraction, it is called trigeminy, if it occurs after every nthird contraction, it is called — quadrigeminy, etc.

 

Electrocardiographic Holter monitoring

Electrocardiographic Holler nmonitoring – is a method of functional diagnosis of the heart’s work by ncontinuous daily record of ECG in several leads. The method is named in honor nof the American scientist Norman Holler, who developed ECG monitoring in 1961.

ECG is carried out ncontinuously during 24 hours. Registration is done by means of a small worapparatus, which is mounted on the patients wist or arm. Leads are placed orelevant sectors of the thorax.

A child carries the machine non himself all the time. The big advantage of this method is that, during the nstudy the patient does not experience discomfort, he/she leads a normal life n(in school, walking). ECG is recorded continuously, regardless of the positioof the subject for all the various events. With this method, you can set Holter ncardiac arrhythmias that are provoked by domestic, social and school factors ichild’s daily life, to reveal the intensity of their impact on the functioning nof the heart, which is impossible with standard disposable ECG. The method is very simple for nthe patient; it does nnot  require any special ntraining, the machine patient nis installed in some minutes, after which the machine siliently records nthe electrocardiogram. After 24 hours, the machine is nremoved. The information about the daily work of the heart of the child is ntransferred to a computer.

 

Every patient, during nHolter’s monitoring is given a special diary. In it, the child or parents nreport possible complaints, discomfort on the part of the heart (with time and ncircumstances of their occurrence), overall health, the type of work and nphysical activity, taking of medicines, lime of wakefulness and sleep, etc. As na result, during analyzing of received information, the doctor compares the ndata of ECG with records in patient’s diary.

The nmain indications for the use of Holter’s monitoring (primarily in the ncomplexity of diagnosing the disease) include:

·        nComplaints of the patient of palpilalion and nintermittence of the heart,

·       Recurrent fainting of unknowetiology.

·       nRecurrent vertigo.

·       nSupervision of an artificial pacemaker, the nevaluation of the pacemaker.

·       Identification of nasymptomatic arrhythmias.

·       Transient arrhythmias and nconduction.

·       Assessment of the severity nof arrhythmias.

·        nVegetal-vascular dystonia with frequent ncrisis.

·        nRational choice antiarrhythmic therapy.

·       Evaluation of treatment nefficacy.

In some cases (high and low nblood pressure, etc.), a combined apparatus of monitoring of ECG and BP is nused. Registration is done at specific intervals of lime (usually every 15-30 nminutes during the day and every 30-60 minutes at night),

Contraindications for such examination are nabsent-Currently, Holler’s monitoring in pediatrics is one of the best and most npopular methods of diagnosing cardiac arrhythmias. Analysis of the records nallows us to determine asymptomatic arrhythmia, to characterize all of its nforms, most accurately determine the cause of disease and diagnosis, and also nincrease the efficiency of treatment of pathology of the cardiovascular system.

 

Ultrasound: examination of heart— Ultrasound ncardiography (USG)

 

 

Fundamentals nof the method: Ultrasonic examination is comparatively n’young’. Its been in use for half a century, In 1954, the Swedish scientists Ed nHer and Hertz used reflections of Ultrasound wave impulses for studying nventricular walls and anterior shutters of mitral valve. And since then, the nbloodless method of ultrasonic examination is as highly informative and nauthentic as X-rays and an electrocardiogram.

 

The basis of all ultrasonic devices (which are nimproved constantly), including the third generation of them, is the piezocrystal. Under the influence of the nvariable electric field, it changes its size accordingly and thus sends nultrasonic waves into the examined body. In reply to it, the piezocrystal nreceives the reflected impulses and transforms them into electric signals. nThese signals go to the special device, and then — to the register for a ngraphic representation of the record. The used frequency of fluctuations (2-3 MHz) nenables to distinguish the structures of heart located at the distance of 0,7 nmm and more from each other,

The gauge of the device is fixed on the body of the nchild. During the examination, it is necessary to observe the following nobligatory rules:

·        nUltrasonic waves on the way to the heart npasses through different types of tissues, but they all should have similar nultrasonic resistance. For example, the gauge should not be fixed in such a way nthat the ultrasonic waves passes through the lung tissues filled with air, nTherefore, it is necessary to ftx it in the zone of the ‘ultrasonic window’ nwhich corresponds to the area of the absolute heart dullness. On this site of nthe thorax, its soft tissues are nearest to the heart.

·       For ihe same reason, the nskin on which the gauge is fixed, nis applied with some glycerin. Vaseline or special gel (vacuum is created).

·       The exact places of nlocation of the gauge are the II, lit, IV and V intercostal intervals, 2-3 cm lateral to the left edge of sternum. The gauge should nnot be fixed further than 3 cm from the sternum, as it is the area of relative nheart dullness, where it is unsuitable to examine the heart as there is lung ntissue between the heart and the gauge.

 

During the time of EchoCG, nthe record of an ECG is simultaneously carried out. Now 2 kinds of nechocardiography are used: M-mode and two-dimensional.

 

M-mode nechocardiography

The position of the patient; mostly lying on the nback and the head end of the couch is raised approximately by 30°. If the heart nof the examined patient is considerably covered by lung tissues, it is possible nto apply the following kinds of position:

·       nIncrease the angle of the head end of the ncouch.

·       nCarry out Ihe procedure in the silting nposition.

·        nLateral position of the patient — on the left nside.

 

The gauge is fixed in the area of one of the specified points (usually in ll-IV nintercostal intervals) 2-3 ncm lateral nto the nleft edge of the sternum. n

Then, for the passage of ultrasonic wave through different layers of heart, it should be specially inclined using different angles.

 

The allowable features of the place of fixing of nthe gauge are:

·        nFor patients with asthenic constitution and nvertical position of heart. The gauge is located in IV-V intercostal intervals nleft — lateral to the sternum.

·        nFor patients with hypersthenic constitution, na short thorax and a horizontal position of the heart, the gauge is located iII-III intercostal intervals left — lateral to the sternum.

·        nFor patients with low located diaphragm, the ngauge is possible to put on epigastrium.

·       For children of early aoe. nthe gauge can be located on the rib or on the sternum.

·       nUnder some indications, the gauge is located nin other sites (in the right hypochondrium, at the right edge of a sternum). nContra-indicalions to echocardiography nare absent.

 

To understand the material better, please pay nattention to the sagittal dissection of the heart and major vessels structure nthrough the left edge of the sternum. Specify, through which sites the nultrasonic beam passes in 4 basic standard positions. These 4 variants of beams n’are formed’ by an inclination of the gauge and are designated in the figure by ndotted lines and the Roman figures from I up to IV. For example: in positioII, the beam passes through the right ventricle, inter ventricular septum, nanterior and posterior cusps of the mitral valve, and also through posterior nwalls of the left ventricle.

 

In 4 standard positions, the condition of the ncertain sites of the heart and vessels is determined.

 

Position I — the character of movement and nthickness of inter-ventricular septum (IVSS and posterior wall of the left nventricle, the dimension of the left and right ventricular cavitv. and also the ncharacter of movement of chordae tendinae of mitral valve. The position I is very ninformative. Its main parameters are:

·        nDuring systole, the inter-ventricular septum nand the walls of ventricle move concordantly. i.e. together: the changes iconcordant movements are the sign of volumetric overload of the left ventricle,

·        nThe change in thickness of the posterior wall nof the left ventricle and inter-ventricular septum are the parameter of nhypertrophy of the myocardium,

·        nBesides, during diastole, the correlation of nthe thickness of interventricular septum to the thickness of posterior wall of nthe left ventricle = 1.3; this parameter changes nduring cardiomyopathy,

·        nThe thickening of chordae tendinae of the nmitral valve is the sign of fibrosis.

 

Position II — the shutters of mitral valve, is in form nof the letter ‘M’ in the echocardiogram, and also its kinetic parameters. nDuring the syslole of ventricles, on the record of ultrasonic examination, the nshutters of mitral valve are connected. Then, when diastole comes, the ntwo-stage opening of the shutters is registered; at the beginning of diastole nand finally — at the end of it-

The parameters of positioII are important at:

·          nInsufficiency, stenosis, prolapse of the nmitral valve — i.e. during its distruction.

·          nCongenital heart diseases, cardiomyopathy — ni.e..during those diseases which cause the disorders in the movement of the nvalve.

 

Positions III—IV — aortic knuckle and aortic valve, nand also in position IV — the left atrium.

For getting the data about condition of the ntricuspid valve. The gauge in position II should be inclined medially and a nlittle downwards, and the valve of the pulmonary artery — the gauge in positioIV is displaced a little upwards and laterally.

As it became clear from the listed results of the nechocardiography, it is especially difficult to find out the condition of the nright atrium.

 

 

During two-dimensional echocardiography, it is possible to determine:

·        nMovement of blood during the systole and ndiastole of the left ventricle.

·        nPrecise contours of the left atrium.

·        nPapillary muscles of the left ventricle.

·        nMutual correlation of bicuspid valve and ninterventricular septum with vessels.

·        nA cross-section view of the root of an aorta, nleft ventricle and mitral valve at different levels, etc.

Ail received data of ntwo-dimensional echocardiography allows us lo distinguish the normative nparameters from pathological infringements and lo make the exact diagnosis on the basis of il.

 

Dopplerography

Doppler Effect (Austrian astronomer and physicist nof the 20^lh century) is a change of frequency of vibration of the nwaves in the process of the movement of their source and the observer as nregards to each other. For this purpose, in modern devices, the methods of nconstant or impulse emission of ultrasound are used. i. e., ultrasonic dopplerography is expressed as the shift nof the frequency of the sent ultrasonic signal in the process of its reflectiofrom the particles namely from the blood cells. This method is non-invasive and ncompletely safe for the patient.

Combined method of a two-dimensional nechocardiography, with simultaneous investigation of the linear speed of blood nflow according lo Doppler Effect is widely used as well.

 

In cardiology, the device for impulse Doppler nmethod can determine:

·       nVisualization of defects of interatrial and ninterventricular septum, and also the volume of the shunted blood.

·       nMeasurement of the pressure in pulmonary nartery system, the gradient pressure above the valves {the specified researches have special value ipediatrics}.

·       Pulsation of vessels.

·       nPermeability of the peripheral vessels, speed nand direction of the blood flow in them.

·       nBlood flow in deeply located vessels — iaorta, veins, vessels of internal bodies, etc.

·        nThe presence of thrombs in vessels.

·       Mobility of the valves and walls nOf the heart.

·       The cardiac function of a nfetus during delivery, etc.

Due to Doppler method, it is possible to determine nthe quantitative characteristic of blood circulation in vessels.

 

Cardiac nCatheterization/Angiogram

A cardiac ncatheterization is a diagnostic procedure that provides detailed, x-ray npictures of the heart and its blood vessels. The pictures taken with contrast ndye during this procedure are called angiograms. Interventional procedures to correct problems that are found cabe performed at the same time. A cardiac catheterization is performed by a nspecially trained cardiologist, ncalled an interventional ncardiologist. 

These procedures are performed at a hospital in a special room called the catheterization laboratory, or “cath lab.” The cath lab is equipped nwith an x-ray camera and a TV monitor (screen) on which the cardiologist views nthe child’s heart and arteries.

A pediatric or adult congenital catheterization procedure typically takes nlonger than an adult coronary catheterization procedure – generally about 2–3 nhours. The patient is given medications nfor sedation by mouth or by injection prior to starting the procedure. nSometimes, an IV (intravenous line) is placed into a vein in the patient’s arm. nThe IV allows the patient to receive fluids and medications easily. If your nchild becomes anxious during the catheterization, he or she will receive more nmedications to help relax. 

The patient may be sedated but awake (in the “twilight”) throughout the nprocedure or may be completely asleep under general anesthesia, depending othe procedure to be done. After the child has relaxed, the doctor will use a nsmall needle to inject lidocaine, na local anesthetic, to numb the areas where the vessels will be entered. This ninitial needle prick could be the only discomfort experienced throughout the nprocedure. The procedure is typically painless. The heart itself does not ncontain pain receptors.

The femoral vein and artery in the groin – near where the leg bends from nthe hip – are the vessels doctors most commonly use to insert a catheter (a flexible tube that is nsmaller than the vessels) and thread it through the vessels to the heart, veins nand peripheral arteries to perform the procedure. Sometimes a vein under the ncollar bone (subclavian vein) or in the neck (internal jugular) is used. 

From this “access” point, nthe catheter is threaded through the veins and arteries to the nheart. Because there are no nerves in the arteries, the patient will not nfeel the catheter or any pain during the catheterization procedure. A wide nvariety of specialized catheters in different sizes are available to be used nfor patients of all sizes – from newborn babies to adults.

The x-ray camera helps the nphysician guide the catheter to the heart. When the catheter is properly positioned, nthe cardiologist injects a contrast dye n(radiographic contrast agent) through the catheter into the heart and its narteries. Most people do not feel the dye injection. However, some may feel a nsensation of warmth in the chest, typically lasting only a few seconds. A few nmay feel lightheaded or nauseous.

When the x-ray beam passes through the dye, the arteries appear in black nsilhouette on a white background. The x-ray camera records a “movie” of the nheart’s pumping chamber and arteries – a movie that can be recorded as a ndigital image or on 35mm film. This move of the heart provides critical ninformation about the structure and functioning of the child’s heart.

 

CT/MRI

A computed tomography (CT) scan is a scan that nuses x-rays to take detailed cross-sectional images of the body, including the narteries and beating heart. A contrast dye is injected into a nvein. As this dye moves through the heart and blood vessels, the CT scan will ntake detailed pictures. These pictures can then be used to create a 3-D nreconstruction of the heart and major blood vessels. Your doctor can use these nimages to identify problems with the heart or blood vessels and develop a ntreatment plan if necessary.

cMRI (cardiac MRI) is a scan that provides pictures nof the heart and blood vessels inside the body using a magnetic field and npulses of radio wave energy. Unlike a CT scan, it does not use x-ray radiation. nThe MRI generates images of the heart and blood vessels, which can help your ndoctor assess the heart’s structure and function. In addition to providing ninformation on anatomy, cardiac MRI can also provide information on how blood nflows through the heart and vessels, how well the heart valves are functioning, nhow well the heart muscle is being supplied with blood, and if scars have nformed within the heart muscle. Some kinds of stress testing can be performed nwith a cMRI as well. A cMRI scan takes longer to perform than a cardiac CT nscan.

 

Exercise/Stress Testing

There are different ntypes of “stress ntests” that can be used to evaluate the heart. The simplest is nan exercise test, which is performed on a treadmill or stationary bicycle for npeople with suspected or known heart disease. The test records heart rate and nblood pressure. Sticky electrodes are attached to the chest, shoulder and hip nand are connected to a machine that records heart rate and blood pressure while nyour child is exercising. An echocardiogram [link to section oEchocardiogram above] may also be performed during and immediately after nexercising (stress echocardiogram). Some problems with the heart are not seewhen the heart is at a calm, resting state. Exercise testing allows doctors to n“work” the heart and evaluate it during times of activity and stress. This is a nnon-invasive ntest, meaning nothing is put into the body during the test. nSince the purpose of the test is to have your child exercise, it is important nto have your child dress appropriately, including comfortable clothes and shoes nmeant for activity.

Other types of n“stress testing” include giving medications by vein while performing aechocardiogram or cardiac MRI to make the heart work harder. Sometimes nabnormalities may be more easily identified if the heart is made to nintentionally work harder. 

Occasionally, cardiac nuclear perfusiotesting is performed in children. In this test, a small amount nof radioactive compound is injected by vein and pictures of the heart are taketo see how well blood is being provided to the heart itself. These kinds of ntests are only ordered after a detailed evaluation by your child’s ncardiologist.

Electrophysiology n(EP) Study (Ablation Procedure)

An electrophysiology (EP) nstudy is an invasive test to assess the heart’s electrical npathways. It is used to identify causes of abnormal heart rhythms n(arrhythmias) and to provide therapies (called an ablation) to fix nabnormalities in the electrical system of the heart. 

An EP study is nperformed in the cardiac catheterization lab in a hospital. In this safe and ncontrolled setting, your doctor intentionally will try to reproduce the nabnormal rhythm. Special catheters (thin, flexible tubes) are inserted into the nvessels in the leg and neck. These catheters sense the small electrical ncurrents within the heart. Special ablation catheters can heat or freeze the nabnormal areas of heart tissue to alter the ability of these areas to create narrhythmias. If successful, many children will no longer need to take nmedications to control their abnormal heart rhythms after an ablatioprocedure. Typically, an EP study is performed as an outpatient procedure and nchildren will be able to go home the same day as their procedure.

 

 

Pulse Oximetry Screening

A pulse noximetry screen is a noninvasive (and painless) test performed on all nnewborn babies to determine the level of oxygen in their blood. This test uses nrays of light of different wavelengths to measure the percent of hemoglobin (the part of blood that ncarries oxygen) that is filled with oxygen. Normally, a newborn baby should nhave an oxygen saturation level that is greater than 95%. Screening using pulse noximetry can detect some infants with congenital nheart disease who otherwise may go undetected for a while. There are nsome congenital heart defects that cause a newborn baby to have lower oxygesaturation in the blood after birth. It often can be difficult to determine if na baby has cyanosis (bluish ndiscoloration of the skin due to poor oxygen content of the blood) just by nlooking at him or her after birth.

 

How Is a Pulse nOximetry Test Performed?

The pulse noximeter has a lighted probe that is temporarily attached to the baby’s nfinger, ear lobe, or foot. Once the baby’s finger is attached to the probe n(usually by a sticker), the red light of the probe reads the amount of oxygecarried by the blood. The oxygen level is tested in both arms and both feet. Isome kinds of congenital heart disease, the numbers can be different in the narms compared to the legs. It also helps to validate the test to do it in all nof the extremities. The time required to complete this test is approximately 1 nto 5 minutes.

 

Is Pulse Oximetry nTesting Safe?

Yes. There are no known risks associated with npulse oximetry testing. This is not a blood test so it does not require a nneedle stick. There is no radiation involved with this test as well. It simply ntemporarily shines a light through the skin to test how much of the blood ncontains oxygen.

 

Why Is Pulse Oximetry nTesting Important?

Some congenital heart defects do not show signs withithe first days or even weeks of life. Sometimes babies with significant ncongenital heart disease may not have a murmur nafter birth. Therefore, some babies may not show signs of significant ncongenital heart disease until after they become very sick. If healthcare nproviders discover a heart problem before a baby becomes ill, then the baby nwill have a better chance to do well with any necessary surgeries or procedures. Early diagnosis of the heart problem may nalso prevent damage to other organs that may occur when a baby becomes sick due nto congenital heart disease.

While pulse oximetry screening cannot rule out nall forms of congenital heart disease, it is a good starting point for nevaluating many serious types of congenital heart defects. In 2011, the U.S. nDepartment of Health and Human Services recommended the pulse oximetry nscreening should be included in the routine evaluation that all newborn babies nundergo before they are discharged from the hospital after birth. More and more nstates are adopting this test as a routine procedure to be done on all newborbabies before they go home from the hospital.

 

 

Main clinical symptoms in patient with ncardiovascular disorders

a)     nCardialgies,

b)    ntachycardia,

c)     ndyspnea, nabdominal pains, heart enlargement,

d)    ndecrease of tones’ nsonority,

e)     nrigidity of ncardiac rhythm,

f)      nrhythm of ngallop,

g)     napical systolic nmurmur,

h)    nconsiderable  cardiomegaly,

i)       nsubstantial ndecrease of myocardial contractile ability,

j)       nblood ncirculation’s insufficiency ,

k)    nstability or nslow progress of heart disturbances,

l)       ncombined  ECG-disorders , ,

m)  echocardiographic disorders (the disorders of nautomatism, conductivity, excitability, processes of de-and repolarization);

n)    ndecreased of nmyocardium contractive ability, objectively confirmed by the instrumental ninvestigations,

o)    n mitral or aortic configuration of the heart at nX-ray of the chest.

 

Congenital heart disease (CHD)

 

The exact incidence of congenital heart disease. In children is napproximately 8:1000 to 10:1000 live births. CHD is the major cause of death ithe first year (other than prematurity). Depending on the defect, the sexes are naffected differently. Heart defects are found in a much higher percentage of stillbirths, spontaneous abortions, and nlow-birth-weight infants, especially those small for age. The most common heart nanomaly is ventricular septal ndefect.

Etiology. The etiology of nmost congenital heart defects is not known. However, several factors are nassociated with a higher thaormal incidence of the disease. These include nprenatal factors such as maternal rubella or other viruses, such as coxsackievirus, during pregnancy, poor nutrition ithe mother, maternal alcoholism, maternal age over 40 years, maternal insulin-dependent ndiabetes, and maternal ingestion of lithium salts.

Several genetic factors are also implicated in CHD. There is aincreased risk of congenital heart disease in the child who has siblings with a nheart defect, has parents with congenital heart disease, has a chromosomal aberration, such as Down’s syndrome, or is nborn with other noncardiac congenital anomalies.

 

Types of defects

Congenital heart defects are usually divided ninto two types, based on the alteration in circulation: acyanotic, nin which there is no mixing of unoxygenated blood nin the systemic circulation. Cyanotic, in which unoxygenated blood enters the systemic ncirculation, regardless if cyanosis is clinically evident.

Clinical manifestations depend on the severity of the defect and the namount of pulmonary blood flow. In acyanotic defects no associated signs and nsymptoms may be apparent if the defect is small and the heart is able to ncompensate for the extra workload.

 

Altered hemodynamic. To nunderstand the physiology of heart defects, it is necessary to review the role nof pressure gradients and flow resistance to blood circulation. Blood flows as na result of pressure gradients existing in different parts of the body. Like nany fluid, blood flows from an area of high pressure to one of low pressure. nThe rate of flow is directly proportional to the pressure gradient (that is, nthe higher the pressure gradient, the greater the rate of flow) and inversely nproportional to the resistance (that is, the higher the resistance, the less nthe rate of flow). Normally the pressure on the right side of the heart is nlower than on the left side, and the resistance in the pulmonary circulation is nless than in the systemic circulation. Likewise, vessels entering or exiting nfrom these chambers have corresponding pressures. Therefore, if there is aabnormal connection between the heart chambers, such as a septal defect, blood nflows from an area of higher pressure (left side) to one of lower pressure n(right side). This directional flow of blood is termed a left-to-right shunt. If the hole is small, the amount nof blood shunted to the atrium or ventricle may be nminimal. In this instance no unoxygenated blood nflows directly into the left side of the heart, therefore, the term acyanotic defect .

Severe acyanotic defects are potentially cyanotic as a result of npulmonary vascular changes. Eisenmeng’s complex n(syndrome) refers to the clinical situation in which a left-to-right shunt nbecomes a right-to-left shunt because of progressive increase in pulmonary nvascular resistance. With increasing pulmonary vascular thickening the nresistance in the pulmonary circulation can exceed that in the systemic circulation, causing a reversal of blood flow from the nright to the left ventricle.

Cyanotic heart ndefects may be the result of anomalies that cause a change in pressure so that nthe blood is shunted from the right to the left side of the heart, hence the nterm right-to-left shunt, because of neither increased pulmonary vascular resistance or obstruction to blood flow nthrough the pulmonic valve/artery. Cyanosis nmay also occur because of a defect that allows direct communication between the npulmonary and systemic circulations, such as truncus arteriosus or ntransposition of the great vessels.

 

Physical consequences

The general effects of heart malformation may be summarized as (1) increased workload in terms of systolic or diastolic noverloading of the chambers, (2) pulmonary hypertension (increased vascular nresistance), and (3) in cyanotic defects arterial unsaturation from shunting of nunoxygenated blood directly into the systemic circulation. The principal physical consequences of these changes, nwhich may vary in severity, are growth retardation, decreased exercise ntolerance, recurrent respiratory infections, dyspnea, ntachypnea, tachycardia, cyanosis, and tissue hypoxia.

Growth retardation and decreased exercise tolerance nare direct consequences of inadequate nutrient intake, feeding difficulties, nand increased caloric requirements resulting from tachypnea and tachycardia. nFailure to gain weight, even during the neonatal period, is a consistent nfinding. Exercise intolerance is usually first nnoted by the parent during feedings when the infant nis too fatigued to consume the entire formula.

Recurrent respiratory infection is the result of pulmonary vascular congestion as large namounts of blood pool in the lungs, compromising pulmonary compliance. Dyspnea also occurs from increased npulmonary resistance as the lungs are unable to noxygenate adequate supplies of blood, resulting in “air hunger.” If nmay be associated with tachypnoe as the nlungs try to compensate through an increased respiratory effect. Tachycardia is the heart’s attempt to nincrease cardiac output by increasing the number of beats per minute.

Cyanosis is the result of deoxygenated hemoglobin in the skin blood vessels, nespecially in the capillaries. In polycy-themia, ncyanosis appears more readily because of the large namount of hemoglobin. Cyanosis reflects inadequate arterial blood oxygesaturation. Any event that increases metabolism and thus causes demand for additional oxygen may result in a more severe degree nof cyanosis in the presence of a fixed intracardiac right-to-left shunt.

Persistent hypoxia may result in tissue changes anywhere in the body. A ncharacteristic finding in cyanotic cardiac lesions nis clubbing of the fingers, a thickening and flattening of the distal nphalanges. Although the exact cause is unknown, some theories include soft ntissue fibrosis and hypertrophy from anoxia and nformation of increased numbers of capillaries to enhance blood supply.

 

Overview of Congenital Heart Disease

According to the March of Dimes, one in 125 babies born in the United nStates has a congenital (present at birth) heart defect – a problem that noccurred as the baby’s heart was developing during pregnancy, before the baby nis born. Congenital heart defects are the most common birth defects. 

 

A baby’s heart begins to develop at conception, but is completely formed by neight weeks into the pregnancy. Congenital heart defects happen during this crucial nfirst eight weeks of the baby’s development. Specific steps must take place iorder for the heart to form correctly. Often, congenital heart defects are a nresult of one of these crucial steps not happening at the right time, leaving a nhole where a dividing wall should have formed, or a single blood vessel where ntwo ought to be, for example.

 

What causes congenital nheart disease?

The vast majority of congenital heart defects have no known cause. Mothers nwill often wonder if something they did during the pregnancy caused the heart nproblem. In most cases, nothing can be attributed to the heart defect. Some nheart problems do occur more often in families, so there may be a genetic link nto some heart defects. Some heart problems are likely to occur if the mother nhad a disease while pregnant and was taking medications, such as anti-seizure nmedicines. However, most of the time, there is no identifiable reason as to why nthe heart defect occurred.

 

Congenital heart problems range from simple to complex. Some heart problems ncan be watched by the baby’s physician and managed with medicines, while others nwill require congenital heart surgery, sometimes as soon as in the first few nhours after birth. A baby may even “grow out” of some of the simpler nheart problems, such as patent ductus arteriosus (PDA) or atrial septal defect n(ASD), since these defects may simply close up on their own with growth. Other nbabies will have a combination of defects and require several operations nthroughout their lives.

 

What are the different ntypes of congenital heart defects?

We can classify congenital heart defects into several categories in order nto better understand the problems the baby will experience. They include:

• problems that cause too much blood to pass through the lungs. These defects allow oxygen-rich blood that should be traveling to the body to re-circulate through the lungs, causing increased pressure and stress in the lungs.

• problems that cause too little blood to pass through the lungs. These defects allow blood that has not been to the lungs to pick up oxygen (and, therefore, is oxygen-poor) to travel to the body. The body does not receive enough oxygen with these heart problems, and the baby will be cyanotic, or have a blue coloring.

• problems that cause too little blood to travel to the body. These defects are a result of underdeveloped chambers of the heart or blockages in blood vessels that prevent the proper amount of blood from traveling to the body to meet its needs.

n

Again, in some cases there will be a combination of several heart defects, nmaking for a more complex problem that can fall into several of these ncategories.

 

Some of the problems that cause too much blood to pass through the lungs ninclude the following:

• patent ductus arteriosus (PDA) -this defect, which normally occurs during fetal life, short circuits the normal pulmonary vascular system and allows blood to mix between the pulmonary artery and the aorta. Prior to birth, there is an ope passageway between the two blood vessels, which closes soon after birth. When it does not close, some blood returns to the lungs. Patent ductus arteriosus is often seen in premature infants.

n

Anatomy of a heart with a patent ductus arteriosus

 

• atrial septal defect (ASD) – in this condition, there is an abnormal opening between the two upper chambers of the heart – the right and left atria – causing a abnormal blood flow through the heart. Some children may have no symptoms and appear healthy. However, if the ASD is large, permitting a large amount of blood to pass through the right side, symptoms will be noted.

n

Anatomy of a heart with an atrial septal defect

 

• ventricular septal defect (VSD) – in this condition, a hole in the ventricular septum (a dividing wall between the two lower chambers of the heart – the right and left ventricles) occurs. Because of this opening, blood from the left ventricle flows back into the right ventricle, due to higher pressure in the left ventricle. This causes an extra volume of blood to be pumped into the lungs by the right ventricle, which can create congestion in the lungs.

n

Anatomy of a heart with ventricular septal defect

 

• atrioventricular canal (AVC or AV canal) – atrioventricular canal is a complex heart problem that involves several abnormalities of structures inside the heart, including atrial septal defect, ventricular septal defect, and improperly formed mitral and/or tricuspid valves.

n

Atrioventricular Canal Defect

Some of the problems that cause too little blood to pass through the lungs ninclude the following:

• tricuspid atresia (TA) – in this condition, there is no tricuspid valve, therefore, no blood flows from the right atrium to the right ventricle. Tricuspid atresia defect is characterized by the following:

• a small right ventricle

• a normal left ventricle

• diminished pulmonary circulation

• cyanosis – bluish color of the skin and mucous membranes caused from a lack of oxygen.

• A surgical shunting procedure is ofteecessary to increase the blood flow to the lungs.

n

Anatomy of a heart with tricuspid atresia

 

• pulmonary atresia (PA) – a complicated congenital defect in which there is abnormal development of the pulmonary valve. Normally, the pulmonary valve is found between the right ventricle and the pulmonary artery. It has three leaflets that function like a one-way door, allowing blood to flow forward into the pulmonary artery, but not backward into the right ventricle.

• With pulmonary atresia, problems with valve development prevent the leaflets from opening, therefore, blood cannot flow forward from the right ventricle to the lungs.

n

 

• transpositio of the great arteries (TGA) – with this congenital heart defect, the positions of the pulmonary artery and the aorta are reversed, thus:

• the aorta originates from the right ventricle, so most of the blood returning to the heart from the body is pumped back out without first going to the lungs.

• the pulmonary artery originates from the left ventricle, so that most of the blood returning from the lungs goes back to the lungs again

n

Anatomy of a heart with transposition of the great arteries

 

• tetralogy of Fallot (TOF) – this condition is characterized by the following four defects:

n

1.     an abnormal opening, or nventricular septal defect, that allows blood to pass from the right ventricle nto the left ventricle without going through the lungs

2.     a narrowing (stenosis) at or njust beneath the pulmonary valve that partially blocks the flow of blood from nthe right side of the heart to the lungs

3.     the right ventricle is more nmuscular thaormal and often enlarged

4.     the aorta lies directly over nthe ventricular septal defect

Tetralogy of Fallot results in cyanosis (bluish color of the skin and nmucous membranes due to lack of oxygen).

Anatomy of a heart with tetralogy of Fallot

 

• double outlet right ventricle (DORV) – a congenital heart defect (one that occurs as the heart is forming during pregnancy) in which both the aorta and the pulmonary artery are connected to the right ventricle.

n

• truncus arteriosus – the aorta and pulmonary artery start as a single blood vessel, which eventually divides and becomes two separate arteries. Truncus arteriosus occurs when the single great vessel fails to separate completely, leaving a connection between the aorta and pulmonary artery.

n

Anatomy of a heart with truncus arteriosus

Some of the problems that cause too little blood to travel to the body ninclude the following:

• coarctatio of the aorta (CoA) – in this condition, the aorta is narrowed or constricted, obstructing blood flow to the lower part of the body and increasing blood pressure above the constriction. Usually there are no symptoms at birth, but they can develop as early as the first week after birth. If symptoms of high blood pressure and congestive heart failure develop, surgery may be considered.

n

Anatomy of a heart with a coarctation of the aorta

• aortic stenosis (AS) – in this condition, the aortic valve between the left ventricle and the aorta did not form properly and is narrowed, making it difficult for the heart to pump blood to the body. A normal valve has three leaflets or cusps, but a stenotic valve may have only one cusp (unicuspid) or two cusps (bicuspid).
  Although aortic stenosis may not cause symptoms, it may worsen over time, and surgery may be needed to correct the blockage – or the valve may need to be replaced with an artificial one.

n

An Example of Aortic Stenosis

A complex combination of heart defects known as hypoplastic left heart nsyndrome can also occur.

• hypoplastic left heart syndrome (HLHS) – a combination of several abnormalities of the heart and the great blood vessels. In hypoplastic left heart syndrome, most of the structures on the left side of the heart (including the left ventricle, mitral valve, aortic valve, and aorta) are small and underdeveloped. The degree of underdevelopment differs from child to child. The functional ability of the left ventricle can be reduced to the extent of not being able to pump an adequate blood volume to the body. Hypoplastic left heart syndrome ca be fatal without treatment.

n

Hypoplastic Left Heart Syndrome

Who treats congenital nheart defects?

Babies with congenital heart problems are followed by specialists called npediatric cardiologists. These physicians diagnose heart defects and help manage nthe health of children before and after surgical repair of the heart problem. nSpecialists who correct heart problems in the operating room are known as npediatric cardiovascular or cardiothoracic surgeons.

 

A new subspecialty within cardiology is emerging as the number of adults nwith congenital heart disease (CHD) is now greater than the number of babies nborn with CHD, as a result of the advances in diagnostic procedures and ntreatment interventions that have been made since 1945.

 

In order to achieve and maintain the highest possible level of wellness, it nis imperative that those individuals born with CHD who have reached adulthood ntransition to the appropriate type of cardiac care. The type of care required nis based on the type of CHD a person has. Those persons with simple CHD cagenerally be cared for by a community adult cardiologist. Those with more ncomplex types of CHD will need to be cared for at a center that specializes iadult CHD.

 

For adults with CHD, guidance is necessary for planning key life issues nsuch as college, career, employment, insurance, activity, lifestyle, ninheritance, family planning, pregnancy, chronic care, disability, and end of nlife. Knowledge about specific congenital heart conditions and expectations for nlong-term outcomes and potential complications, and risks must be reviewed as npart of the successful transition from pediatric care to adult care. Parents nshould help pass on the responsibility for this knowledge and accountability nfor ongoing care to their young adult children to help ensure the transition to nadult specialty care and optimize the health status of the young adult with nCHD.

 

 

 

 

CYANOSIS

 

 

 

Cyanosis is the abnormal blue discoloration of the skin and mucous nmembranes, caused by an increase in the deoxygenated haemoglobin level to above n5 g/dL. Patients with anaemia do not develop cyanosis until the oxygesaturation (SaO₂) has fallen to lower levels than for patients with nnormal haemoglobin levels, and patients with polycythaemia develop cyanosis at higher noxygen saturation levels.^[1] Cyanosis can be divided into either ncentral or peripheral.

 

Central cyanosis:

o        nCentral cyanosis nis caused by diseases of the heart or lungs, or abnormal haemoglobi(methaemoglobinaemia  or nsulfhaemoglobinaemia).

o        nCyanosis is seein the tongue and lips and is due to desaturation of central arterial blood nresulting from cardiac and respiratory disorders associated with shunting of ndeoxygenated venous blood into the systemic circulation.

o        nPatients who are ncentrally cyanosed will usually also be peripherally cyanosed.

o        nAssociated nfeatures of central cyanosis depend on the underlying cause and include ndyspnoea and tachypnoea, secondary polycythaemia, and bluish or purple ndiscolouration of the oral mucous membranes, fingers and toes. The hands and nfeet are usually normal temperature or warm, but not cold unless there is aassociated poor peripheral circulation.

Peripheral cyanosis:

• Peripheral cyanosis is caused by decreased local circulation and increased extraction of oxygen in the peripheral tissues.

• Isolated peripheral cyanosis occurs in conditions associated with peripheral vasoconstriction and stasis of blood in the extremities, leading to increased peripheral oxygen extraction, eg congestive heart failure, circulatory shock, exposure to cold temperatures and abnormalities of the peripheral circulation.

• Features of peripheral cyanosis therefore include peripheral vasoconstriction and bluish or purple discoloration of the affected area, which is usually cold. Peripheral cyanosis is most intense iail beds and may resolve with gentle warming of the extremity. The mucous membranes of the oral cavity are usually spared.

n

Unless the cause is already established, episodes of central cyanosis nrequire urgent assessment, especially infants and young children, who require nurgent admission.

Differential diagnosis

• Central cyanosis i neonates:

• Transient cyanosis after delivery: central cyanosis should clear within a few minutes of the birth. Peripheral cyanosis clears within a few days. Increased sensitivity of the peripheral circulation to cold temperature may persist well into infancy.

• Cardiac and circulatory causes include:

• Transposition of the great arteries.

• Fallot’s tetralogy.

• Stenosis or atresia of the pulmonary valve or tricuspid valve.

• Total anomalous pulmonary venous return (all 4 pulmonary veins drain into systemic veins or the right atrium, associated with a right-to-left shunt through an atrial septal defect.

• Hypoplastic left heart.

• Truncus arteriosus (a single great artery leaves the heart and divides into the pulmonary artery and the aorta).

• Persistent fetal circulation (blood continues to be shunted through the foramen ovale and a patent ductus arteriosus).

• Respiratory causes include:

• Respiratory distress syndrome.

• Birth asphyxia, birth injury or haemorrhage.

• Transient tachypnoea of the newborn.

• Pneumothorax.

• Meconium aspiration.

• Pulmonary oedema.

• Congenital diaphragmatic hernia.

• Tracheo-oesophageal fistula.

• Pleural effusion.

• Obstruction of the upper respiratory tract, for example in Pierre Robin’s syndrome or choanal atresia.

• Other causes include infection, seizures and metabolic abnormalities, eg hypoglycaemia, hypomagnesaemia.

n

Causes of peripheral cyanosis:

• All causes of central cyanosis cause peripheral cyanosis.

• Reduced cardiac output, eg heart failure, shock.

• Peripheral vascular disease, eg thrombosis, atheroma or embolism.

• Vasoconstriction:

• Cold exposure.

• Raynaud’s phenomenon.

• Acrocyanosis: benign, caused by spasm of smaller skin arteries and arterioles, causing hands and feet to be cold and mottled.

• Erythrocyanosis: usually affects young women; blotches of cyanosis occur in the lower legs.

• Betablocker drugs.

• Venous obstruction, eg lower limb deep vein thrombosis ca occasionally produce a painful blue leg (phlegmasia cerulea dolens). Obstruction of the superior vena cava can cause cyanosis, venous engorgement and oedema affecting the face.

n

Symptoms

• Age and nature of onset:

• Cyanosis due to congenital heart disease causing anatomical right-to-left shunts may have been present since birth or the first few years of life.

• Acute onset of cyanosis may be due to pulmonary emboli, cardiac failure, pneumonia or asthma.

• Patients with COPD develop cyanosis over many years and associated polycythaemia may exacerbate the degree of cyanosis.

• The description may be typical of Raynaud’s phenomenon.

• Past history: cyanosis can result from any lung disease of sufficient severity.

• Drug history: certai drugs may cause methaemoglobinaemia (eg nitrates, dapsone) or sulfhaemoglobinaemia (eg metoclopramide).

• Associated symptoms:

• Chest pain: cyanosis associated with pleuritic chest pains may be due to pulmonary emboli or pneumonia. Pulmonary oedema may cause dull, aching chest tightness.

• Dyspnoea: sudden onset of dyspnoea can occur with pulmonary emboli, pulmonary oedema or asthma.

n

Signs

• Temperature: pneumonia and pulmonary emboli may be associated with pyrexia.

• Inspection:

• Central cyanosis produces a blue discoloration of the mucous membranes of the lips and tongue as well as the extremities.

• Peripheral cyanosis affects the extremities and the skin around the lips but not the mucous membranes.

• The combination of clubbing and cyanosis is frequent in congenital heart disease and may also occur in pulmonary disease (lung abscess, bronchiectasis, cystic fibrosis) and pulmonary arteriovenous shunts.

• The jugular venous pressure is elevated with congestive cardiac failure.

• Respiratory examination:

• Poor chest expansion occurs with chronic bronchitis, and asthma. Unilateral reduced chest expansion may occur with lobar pneumonia.

• Dullness to percussion occurs over an area of consolidation.

• Localised crepitation may be heard with lobar pneumonia. Crepitation is more widespread with bronchopneumonia and pulmonary oedema. Air entry may be poor with COPD and asthma. Bronchial breathing may be auscultated over an area of consolidation, and wheezing may be heard with asthma.

• Heart sounds may be abnormal or added heart murmurs may suggest a cardiac origin.

• Localised features suggesting an aetiology of peripheral cyanosis, such as oedema in venous insufficiency or absent peripheral pulses and ischaemia in arterial occlusion.

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Investigations

• Arterial blood gases: oxygen saturation for patients with central cyanosis is usually below 85%. If the oxygen saturation does not increase to above 95% while the patient inhales 100% oxygen then there is likely to be pulmonary intravascular shunting of blood bypassing the alveoli (eg right-to-left intracardiac shunt or pulmonary arteriovenous fistulae).

• FBC: haemoglobin level is increased with chronic cyanosis. White cell count is increased i pneumonia and pulmonary embolism.

• ECG: features of myocardial infarction; nonspecific ST abnormalities with pulmonary emboli.

• CXR: pneumonia, pulmonary infarction, cardiac failure.

• Sputum and blood cultures: pneumonia.

• Ventilation-perfusio scan – ‘VQ scan’, or pulmonary angiography: pulmonary embolus.

• Echocardiography: cardiac defects.

• Haemoglobi spectroscopy: methaemoglobinaemia, sulfhaemoglobinaemia.

• Digital subtractio angiography: acute arterial occlusion.

• Duplex Doppler or venography: acute venous occlusion.

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Management

• Oxygen therapy for patients who are hypoxic.

• Treatment of the underlying cause

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BRADYCARDIA

Definition

Bradycardia is defined by a heart rate less than the lower limit of nnormal for age.

Guidelines for bradycardia based on a 12-lead ECG recorded during the nawake state are as follows:

• 0 – 3 years: <100 bpm

• 3 – 9 years: < 60 bpm

• 9 – 16years: < 50 bpm

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Guidelines for bradycardia based on 24-hour Holter monitoring are as nfollows:

• 0 – 2 years: < 60 bpm while asleep, < 80 while awake

• 2 – 6 years: < 60 pbm during sleep or awake

• 6 – 11 years: < 45 bpm during sleep or awake

• Older than 11 years: < 40 bpm during sleep or awake

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Background

Bradycardia can be caused by intrinsic dysfunction of or injury to the nheart’s conduction system, or by extrinsic factors acting on a normal heart. nBoth intrinsic and extrinsic factors can affect any part of the heart’s nconduction system, including the SA node, AV node or bundle of His.

Sinus bradycardia can be defined as a nsinus rhythm with a resting heart rate of 60 beats per minute or less. However, nfew patients actually become symptomatic until their heart rate drops to less nthan 50 beats per minute. The action potential responsible for this rhythm narises from the sinus node and causes a P wave on the surface ECG that is nnormal in terms of both amplitude and vector. These P waves are typically nfollowed by a normal QRS complex and T wave.

History

• Sinus bradycardia is most often asymptomatic. However, symptoms may include the following:

• Syncope

• Dizziness

• Lightheadedness

• Chest pain

• Shortness of breath

• Exercise intolerance

• Pertinent elements of the history include the following:

• Previous cardiac history (eg, myocardial infarction, congestive heart failure, valvular failure)

• Medications

• Toxic exposures

• Prior illnesses

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Physical

• Cardiac auscultation and palpation of peripheral pulses reveal a slow, regular heart rate.

• The physical examination is generally nonspecific, although it may reveal the following signs:

• Decreased level of consciousness

• Cyanosis

• Peripheral edema

• Pulmonary vascular congestion

• Dyspnea

• Poor perfusion

• Syncope

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Causes

• One of the most common pathologic causes of symptomatic sinus bradycardia is the sick sinus syndrome.

• The most common medications responsible include therapeutic and supratherapeutic doses of digitalis glycosides, beta-blockers, and calcium channel-blocking agents.

• Other cardiac drugs less commonly implicated include class I antiarrhythmic agents and amiodarone.

• A broad variety of other drugs and toxins have been reported to cause bradycardia, including lithium, paclitaxel, toluene, dimethyl sulfoxide (DMSO), topical ophthalmic acetylcholine, fentanyl, alfentanil, sufentanil, reserpine, and clonidine.

• Sinus bradycardia may be seen in hypothermia, hypoglycemia, and sleep apnea.

• Less commonly, the sinus node may be affected as a result of diphtheria, rheumatic fever, or viral myocarditis.

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TACHYCARDIA

Background

Tachycardia is an abnormal rapidity of heart actiothat usually is defined as a heart rate more than 100 beats per minute (bpm) iadults. In children, the normal heart rate is age dependent, and the definitioof tachycardia varies, as shown below.

·         nAge 1-2 days – n123-159 bpm

·         nAge 3-6 days – n129-166 bpm

·         nAge 1-3 weeks – n107-182 bpm

·         nAge 1-2 months – n121-179 bpm

·         nAge 3-5 months – n106-186 bpm

·         nAge 6-11 months n- 109-169 bpm

·         nAge 1-2 years – 89-151 nbpm

·         nAge 3-4 years – n73-137 bpm

·         nAge 5-7 years – n65-133 bpm

·         nAge 8-11 years – n62-130 bpm

·         nAge 12-15 years n- 60-119 bpm

Clinical nPresentation

·         nChest pain

·         nPalpitations

·         nSyncope

·         nDizziness

·         nShortness of breath

·         nDiaphoresis (for infants—while feeding)

·         nColor changes

·         nNeurologic changes (mental status, motor/sensory deficits)

·         nDecrease in intake and output

·         nTrauma

·         nPain

·         nFever

·         nOnset/duration of illness

·         nRelationship to exercise, meals, and stress

·         nMedical history, especially history of tachycardia or other cardiac nproblems

·         nMedications – Amphetamines, cocaine, caffeine, ephedrine, antihistamines, nphenothiazines, antidepressants, theophylline, appetite suppressants, albuterol n

·         nAllergies

·         nFamily history of sudden death, deafness (Jervell-Lange Nielsen syndrome) nor cardiac disease

Physical

·         nGeneral appearance

·         nTemperature

·         nHeart rate

·         nRespiratory rate

·         nBlood pressure

·         nOxygen saturation

·         nAssessment of pain

·         nDecreased level of consciousness, decreased level of activity

·         nJugular venous distention

·         nNeck mass

·         nDyspnea, increased work of breathing, retractions

·         nCrackles, wheezing

·         nCardiac gallop

·         nCardiac murmur

·         nIncreased liver size

·         nAbdominal mass

·         nDecreased urine output

·         nPoor peripheral perfusion (delayed capillary refill >2 sec, cool nextremities, pallor)

·         nCyanosis

·         nEdema

Causes

Tachycardia can be ndue to a physiologic response of the heart to noncardiac stimuli or to a true ndysrhythmia.

·         nHyperdynamic ncardiac activity

o    nIncreased heart nrate and contractility are physiologic responses to catecholamine release.

o    nCatecholamine nrelease may occur with stress or anxiety, exercise, fever or infection, pain, nanemia, seizure, hypovolemia, hypoxia, drugs or medications/stimulants (eg, namphetamines, cocaine, caffeine, ephedrine, antihistamines, phenothiazines, nantidepressants, tobacco, theophylline, general anesthesia), vasodilation (eg, nanaphylaxis), oncologic mass (pheochromocytoma, neuroblastoma), hypoglycemia, nhyperthyroidism, or acidosis.

·         nTrue ndysrhythmias

o    nSupraventricular ntachycardia (SVT)

§  nDrug induced n(eg, amphetamines, cocaine, caffeine, ephedrine, antihistamines, nphenothiazines, antidepressants, tobacco, albuterol, theophylline, general nanesthesia)

§  nWolff-Parkinson-White nsyndrome (WPW)

§  nHyperthyroidism

§  nCongenital heart ndisease

§  nPostoperative ncardiac repair

§  nAtrial ectopic ntachycardia

o    nAtrial nfibrillation or atrial flutter

§  nDrug induced

§  nWolff-Parkinson-White nsyndrome (WPW)

§  nPostoperative ncardiac repair

§  nCongenital or nrheumatic mitral disease

§  nHyperthyroidism

o    nJunctional nectopic tachycardia (JET) – Postoperative cardiac repair

o    nVentricular ntachycardia (VT)

§  nDrug induced n(eg, tricyclics, phenothiazines, antiarrhythmics, chloral hydrate, norganophosphates, hydrocarbons, digoxin, amphetamines, cocaine, arsenic)

§  nProlonged Q-T nsyndrome/torsades de pointes

§  nMyocarditis

§  nRheumatic fever

§  nMitral valve nprolapse

§  nCardiomyopathy

§  nMyocardial nischemia

§  nPostoperative ncardiac repair

§  nHyperkalemia n(peaked T waves, prolonged QRS and QT intervals)

§  nHypocalcemia n(increased QT intervals secondary to ST-segment prolongation)

§  nHypokalemia n(especially in association with digoxin use due to its synergistic effects oautomaticity and conduction)

§  nHypomagnesemia n(associated with hypocalcemia and hypokalemia)

§  nCardiac tumors

§  nArrhythmogenic nright ventricular dysplasia

References

а) Basic

 

1. Manual of Propaedeutic nPediatrics / S.O. Nykytyuk, N.I. Balatska, N.B. Galyash, N.O. Lishchenko, O.Y. nNykytyuk – Ternopil: TSMU, 2005. – 468 pp.

2. Kapitan T. nPropaedeutics of children’s diseases and nursing of the child : [Textbook for nstudents of higher medical educational institutions] ; Fourth edition, updated nand  translated in English / T. Kapitan – nVinnitsa: The State Cartographical Factory, 2010. – 808 pp.

3. NelsoTextbook of Pediatrics /edited by Richard E. Behrman, Robert M. Kliegman; nsenior editor, Waldo E. Nelson – 19^th ed. – W.B.Saunders Company, n2011. – 2680 p.

 

b) Additional

1.  www.bookfinder.com/author/american-academy-of-pediatrics 

2. nwww.emedicine.medscape.com

3. nhttp://www.nlm.nih.gov/medlineplus/medlineplus.html