MINISTRY OF HEALTH OF UKRAINE

Zaporizhzhya state medical university

ADOPTED
by methodical conference
of faculty pediatrics department
________________________
Head of the chair professor Nedel'ska S.M.
"___" ___________ 2017__

Methodical recommendations for students

Educational discipline Pediatrics

Module №1 Pediatrics
Substantial module #2 Differential diagnostics of circulatory disorders in
children . Emergency in cardiac diseases.
Topic of lesson #7 Differential diagnostics of arrhythmia and conductivity
in children. Emergency in paroxysmal rhythm
disorders and Morganie-Adams –Stocks syndrome.
Course 6
Faculty Medical

Zaporizhzhуa 2017
Actuality of the topic:

The American Heart Association's principles of emergency management of

pediatric dysrhythmias should be reviewed periodically by all health care
providers. In an emergency situation, the dysrhythmia should be classified simply
as “slow” or “fast.” Undue time and effort spent refining the specific diagnosis of a
compromising tachycardia or bradycardia may jeopardize a child's recovery from
the event.

The decision to intervene and treat a pediatric dysrhythmia chronically depends

somewhat on the assessment of associated myocardial structure and function. In
general, in a child with an abnormal heart, seemingly trivial dysrhythmias such as
premature beats may have prognostic significance different from that of an
identical rhythm disturbance in a child with a normal heart. Conversely,
asymptomatic pathologic sustained tachycardias may sometimes be monitored
without treatment in certain pediatric scenarios in which the underlying cardiac
structure and function are optimal. Assessing the importance of a specific
dysrhythmia in terms of the underlying cardiac structure or function may be
important in defining the risk of sudden cardiac death (SCD) associated with the
dysrhythmia. Although rhythm disturbances causing SCD in the pediatric
population are rare, the clinical context (similar to its adult counterpart) may
involve a rhythm disturbance in a child with an associated abnormality in cardiac
structure or function.

Because the potential for SCD in most children with dysrhythmias is low,
treatment is frequently instituted to avoid bothersome symptoms. In older children,
dysrhythmia symptoms are reported in familiar terms, such as palpitations,
dizziness, racing heart, and so forth. In younger children, particularly infants,
symptoms may be harder to elicit or may be expressed in more obtuse terms (e.g.,
“chest pains”). Because a younger child may not always be reliable in reporting
symptoms, prophylactic treatment of certain rhythm disturbances is sometimes
instituted to avoid the consequences of a prolonged, unrecognized, sustained
arrhythmia that could result in significant morbidity. Conversely, in an older child,
symptoms of dysrhythmias are more reliably reported, so treatment on an as-
needed basis may be an effective alternative.

Two different treatment modalities may be used for dysrhythmias. The traditional
treatment option involves antiarrhythmic medications. Drugs can be taken every
day to avoid dysrhythmia symptoms or can be taken as needed when symptoms
occur. Very few antiarrhythmic agents are officially formulated for pediatric use.
Only a small number of well-controlled studies outline the effective use of specific
antiarrhythmic agents in children. In certain cases, antiarrhythmic agents
manufactured only in tablets or capsules have to be modified by pharmacies to a
suspension form for use in children. Powerful antiarrhythmic agents such as
amiodarone, flecainide, sotalol, and procainamide are examples of such drugs.
Thus advanced pharmacologic treatment of childhood dysrhythmias can be quite
challenging.

Since 1990, nonpharmacologic treatment options have revolutionized the approach

to the treatment of rhythm disturbances in adults and children. In the 1970s and
1980s, open heart surgical ablation procedures that “cured” tachycardias were
reserved for severe, life-threatening cases. In the 1990s, the venue for dysrhythmia
ablation procedures changed from the operating room to the catheterization
laboratory. A variety of tachycardias that previously needed daily antiarrhythmic
therapy can now be eliminated by radiofrequency catheter ablation procedures
performed in the catheterization laboratory. These procedures were first performed
on adult patients and then applied to the pediatric population. Common
dysrhythmias such as supraventricular tachycardia (SVT) secondary to an
accessory bypass tract can be “cured” with a 90% to 95% success rate and a low
(less than 1%) complication rate in the context of a 24-hour hospital admission.
Initially, in the early 1990s, the indication for these procedures in children involved
dysrhythmias with excessive symptoms or life-threatening potential. Throughout
the 1990s, as experience with this modality in children increased, indications for
catheter ablation changed so patient/parental choice became the most common
reason for performing a pediatric catheter ablation. Many parents elect to have
their child's dysrhythmia addressed with this procedure when confronted with the
alternative of chronic long-term antiarrhythmic medication therapy.

The use of other nonpharmacologic therapies, such as implantation of pacemakers

and defibrillators, has increased in the pediatric population. Implantation of such
devices is usually reserved for the control of pediatric dysrhythmias with life-
threatening consequences, such as advanced atrioventricular (AV) block
(pacemakers) and ventricular tachycardia (VT)/ventricular fibrillation
(defibrillators). Once again, most of these implantable devices were designed
originally to treat adult disease processes. Their application in pediatric patients
sometimes involves unique technical and programming adaptations.

The other consideration in the treatment of pediatric dysrhythmia is the

prescription of a proper activity profile commensurate with the child's rhythm
disturbance. For a well-controlled dysrhythmia in a child with normal heart
structure, the goal is to prescribe unlimited activity, including participation in
competitive sports. Dysrhythmias exacerbated by exercise and with associated
symptoms generally require some activity restrictions. Such restrictions may be as
mild as allowing the child to “rest at will” during the physical activity. However,
rhythm disturbances that are sustained and exacerbated by physical activity need
“control” before prescription of unlimited physical activity. Also, even minor
asymptomatic dysrhythmias (e.g., premature ventricular contractions) in patients
with cardiac structure or function abnormalities may require activity restriction
because of the concern for SCD. In addition, certain rhythm disturbances that have
life-threatening consequences, even though they occur rarely (e.g., the long QT
syndrome), require some limitation of physical activities (competitive sports). For
children and their parents, these physical limitations are sometimes the most
stringent and obtrusive portion of the dysrhythmia treatment plan. Chronic
treatment options for commonly encountered pediatric dysrhythmias are reviewed
next.

1. Goals:

1. To indicate etiologic and pathophysiologic factors at premature contraction at

paroxysmal tachycardia, atrial flutter, atrial fibrillation, atrioventricular block,

Morganie-Adam-Stocks syndrom.
2. To indicate etiologic and pathophysiologic factors at cardiac arrhythmia in children.
3. To classify, analyze typical clinics of the cardiac arrhythmia.
4. To make list of the examination and to analyze data of the laboratory and
instrumental examination at cardiac arrhythmia.
5. To prescribe treatment, rehabilitation, prophylaxis of the paroxysmal tachycardia,
atrial flutter, atrial fibrillation, atrioventricular block, Morgainie-Adam-Stocks
syndrom.
6. To diagnose and to give the first medical aim at cardiac arrhythmia: paroxysmal
tachycardia, atrial flutter, atrial fibrillation, atrioventricular block, Morganie-Adam-
Stocks syndrom.
7. To perform differential diagnostic of cardiac arrhythmia in children
8. To make prognosis at cardiac arrhythmia.
9. To demonstrate knowledge of moral and deontological principles and
principles of professional subordination in child's cardioreumatology.
3. Base level of training, skills and knowledge.
Discipline Skills which must be got by students
Anatomy, To know the anatomo-physiological features of
Physiology organs of the heart.
Path. аnatomy, To define the indexes of organs of the
cardiovascular system, functions of organs of the
Path. рhysiology cardiovascular system. To know the etiology and
pathogenesis aspects acute heart failure in
children.
Introduction to the child's To own a research method and semiotics of diseases
diseases of organs of the cardiovascular system, leadthrough of
laboratory methods of research (clinical blood,
clinical and biochemical blood tests; coagulogram;
immunological data of 1 level; electrocardiogram,
X-ray, ultrasound heart research); instrumental and
functional methods of research.
X-ray To own the X-ray methods of diagnostics of organs
of the heart. To appoint and estimate the results of
X-ray methods of inspection.
Pharmacology To write preparations: glicosides, antyarrhythmici,
adrenoblockers, preparations of potassium,
magnesium.
To study indications, to prescribe and write recipes
with the proper remedies.

4. Organization contents of educational material

Cardiac Dysrhythmias

Key Concepts
▪ The cornerstone of effective therapy for a specific pediatric dysrhythmia first
involves obtaining an accurate diagnosis.
▪ More harm can be done by assuming a pathologic dysrhythmia exists solely
on the basis of the clinical history and thus adopting a specific therapy that is
either ineffective or unnecessary.
▪ It is most important to attempt to record and diagnose the dysrhythmia (via
surface electrocardiography, Holter monitor, event recorder, electrophysiology
study, or a combination of these modalities) before initiating therapy.
▪ Documenting the diagnosis before treatment is the foundation of accurate
 therapy for pediatric dysrhythmia.

In the emergency treatment of a pediatric rhythm disturbance, it is best to “think

simple.” If a child is suspected of having pathologic bradycardia or tachycardia
causing hemodynamic compromise (loss of consciousness or no recordable blood
pressure), it is sometimes proper to institute emergency therapy before recording
and obtaining a specific diagnosis. In the presence of bradycardia causing
hemodynamic collapse, simple principles of cardiopulmonary resuscitation
(airway, breathing, circulation) are used effectively to treat most situations. In the
event a pathologic tachycardia causes significant hemodynamic compromise
(regardless of its origin), cardioversion or defibrillation is indicated.

General practitioners are diagnosing dysrhythmias in children with greater

frequency. This increase in diagnosis reflects a greater awareness by health-care
providers of the existence of pediatric rhythm disturbances, as well as
technological advances that make high-fidelity recordings of such dysrhythmias
possible, even in the youngest of children. Once a pediatric dysrhythmia is
diagnosed, a wide range of treatment strategies are available, including
nonintervention, pharmacologic therapy, device implantation, and surgical/catheter
ablation treatments. This chapter discusses the principles of therapeutics for
commonly encountered pediatric rhythm disturbances.
 Supraventricular Tachycardia

SVT is the most common sustained dysrhythmia encountered in children. More

than 95% of cases of SVT encountered in younger children are re-entrant in nature,
usually secondary to an accessory AV connection. If this accessory connection is
manifested on the surface electrocardiogram during sinus rhythm, the condition is
termed Wolff-Parkinson-White (WPW) syndrome. Children with WPW syndrome
have a small risk for malignant arrhythmias and SCD as a result of rapid antegrade
conduction across their accessory connection. In children with accessory
connection re-entrant tachycardia (with or without WPW syndrome), the most
common circuit for their SVT is antegrade down the AV node with retrograde
conduction up the accessory connection. This tachycardia circuit is responsible for
most of the paroxysmal events of SVT seen in the majority of children
(orthodromic SVT). Acute termination of this SVT can be accomplished with vagal
maneuvers (Valsalva) or intravenous adenosine (starting dose, 50 to 100 mcg per
kg by rapid intravenous push). In very rare cases, with hemodynamic collapse, re-
entrant SVT needs to be cardioverted (1 J/kg). Intravenous verapamil (0.15 mg per
kg over a period of 15 to 20 minutes) may also be used to terminate SVT acutely,
but its use in children is frequently complicated by hypotension, and it is now
supplanted by adenosine. Intravenous verapamil is associated with hemodynamic
collapse in infants, so it should be avoided in this population and cautiously used
in older children.

If SVT is successfully terminated acutely, prophylactic treatment with a chronic

oral antiarrhythmic agent can be chosen to prevent recurrences. If no clear
preexcitation is apparent on the surface electrocardiogram, oral digoxin is the drug
of choice (10 mcg/kg/day divided twice a day). If WPW syndrome is manifestly
present, oral β-blockers are frequently used (propranolol, 2 to 6 mg/kg/day divided
three or four times daily, or atenolol, 25 to 50 mg per day in older children
weighing more than 25 kg). If WPW syndrome is present and the child has
syncope or hemodynamic collapse, catheter ablation of the accessory connection is
the treatment of choice. For children with frequent recurrences of orthodromic
SVT despite therapy with digoxin, propranolol, or both, catheter ablation is a
reasonable therapy, especially if the child is older than 5 years, because natural
history studies indicate that SVT could become a chronic problem.

If SVT is initially encountered in a preadolescent or adolescent, the tachycardia

circuit is commonly secondary to AV node re-entry tachycardia (AVNRT). This
tachycardia is commonly responsible for SVT in the adult population and often
first seen in young teenagers. Treatment principles (acutely and chronically) are
similar to those for SVT caused by an accessory AV connection. The sudden death
potential of AVNRT is small. Many patients choose a catheter ablation procedure
for chronic treatment of AVNRT because of its high efficacy and low complication
rate.

On rare occasions, SVT in children is recalcitrant to termination with adenosine or

verapamil or to cardioversion (or to both modalities). This situation usually
necessitates admission to the intensive care unit, intravenous invasive blood
pressure monitoring, and the use of powerful intravenous antiarrhythmic agents for
termination of the tachycardia (procainamide or amiodarone). After conversion,
catheter ablation of the SVT can be considered in view of the recalcitrant nature of
the acute rhythm disturbance. If catheter ablation is not feasible, the use of digoxin,
propranolol, or more powerful antiarrhythmic agents (e.g., sotalol, amiodarone,
flecainide, procainamide) should be considered. The use of antiarrhythmic
medications beyond digoxin or propranolol invokes issues of proarrhythmia, which
usually necessitates monitoring of the initiation of therapy in a controlled hospital
setting.

SVT encountered in infancy deserves special mention. Natural history studies

indicate that infantile SVT caused by an accessory connection has a good chance
(60% to 70%) of resolving by the age of 1 year. Medications used to control SVT
in this age group can frequently be discontinued at 1 year of age without
recurrence of SVT. Although SVT in infancy may resolve, many infants with SVT
initially have significant symptoms of congestive heart failure and, on occasion,
shock with poor cardiac function. This situation arises because SVT in infancy
may have subtle symptoms; the infant can be in incessant SVT for days or weeks,
and the ultimate manifestation can be dramatic. Thus control of SVT in infancy by
medications must be rigorously verified so a repeat scenario is avoided.

Finally, certain rarer SVTs from arrhythmia mechanisms confined to the atria
(atrial flutter, atrial ectopic tachycardias [AETs]) can occur in children. Atrial
flutter usually occurs at birth or during early infancy. Once the arrhythmia is
terminated (cardioversion or spontaneously), the need for chronic treatment
(digoxin or propranolol) beyond 1 year of age is rare. AET is an incessant
tachycardia in children that is difficult to treat with antiarrhythmic agents. It is
frequently manifested as a cardiomyopathy because of its incessant nature.
Treatment of AET may involve the use of β-blockers, class I or III antiarrhythmic
agents, or catheter ablation. Success rates for catheter ablation of AET are lower
than with re-entrant SVTs because of a high recurrence rate and the possibility of
multiple foci causing the AET.
Ventricular Tachycardia
VT is a rare but important dysrhythmia in the pediatric population because of the
implication involving SCD. In reality, most VTs encountered in children are
associated with normal cardiac structure and function; treatment strategies in this
scenario usually involve mitigating bothersome symptoms rather than attempting
to decrease the incidence of SCD. In contrast, when ventricular arrhythmias are
encountered in children with heart disease (postoperative congenital heart disease,
cardiomyopathies), treatment is primarily directed at preventing SCD. In most
pediatric cardiac disease entities associated with VTs, no pharmacologic or
nonpharmacologic therapies are rigorously proved to decrease the incidence of
SCD. Also, with the issues of proarrhythmia magnified in children with structural
heart disease, more consideration is being given to defibrillator implantation rather
than antiarrhythmic therapy to mitigate the risk of SCD caused by ventricular
arrhythmias in this patient population. These trends, however, are based on
extrapolation of data involving adult SCD caused by VT secondary to coronary
artery disease.

Experience is growing with the use of implantable defibrillators in various

pediatric cardiac disease states in which SCD secondary to VT is a reality. Such
diseases include hypertrophic cardiomyopathy, dilated cardiomyopathy,
postoperative congenital heart disease, and the long QT syndrome. The decision to
use these devices is sometimes clear cut when an older child has recorded
ventricular arrhythmias with a witnessed aborted SCD episode. The decision
becomes murkier when implantation is considered for younger children whose
initial VT and SCD episode is not well documented but whose cardiac structure or
function is abnormal and nonsustained VT is present after the event.
Acute treatment of VT is guided by the clinical context. If the child has
hemodynamic collapse, cardioversion or defibrillation (or both) is the treatment of
choice. In an emergency situation in which a sustained, hemodynamically stable
VT is encountered, intravenous antiarrhythmics can also be used. Lidocaine,
procainamide, and amiodarone can be given intravenously to help terminate
ventricular irritability. Intravenous use of these medications may have various
unwanted deleterious electrophysiologic effects, so the ability to cardiovert,
defibrillate, or pace for bradycardia should be available.

Chronic treatment of ventricular arrhythmias involves the use of medications,

catheter ablation, defibrillator placement, or a combination of these modalities.
Antiarrhythmic medication is generally used to treat sustained VTs in children with
normal heart structure. Two types of sustained VT are commonly encountered in
children with normal hearts. One emanates from the right ventricular outflow tract;
this VT can be exercise sensitive and may respond to β-blocker therapy. The other
VT encountered in children with normal cardiac structure entails a re-entry circuit
involving the Purkinje network of the posterior fascicle in the left ventricle
(posterior fascicular VT). This tachycardia can be terminated acutely with
intravenous verapamil and can be prevented with chronic oral verapamil therapy.
In children with normal hearts, both these tachycardias may also be cured with
catheter ablation, which is a reasonable alternative to chronic drug therapy.

Chronic treatment of VTs in children with abnormal cardiac structure and function
usually involves the use of therapies that can prevent SCD. In the past, ventricular
arrhythmias encountered in such disease states as dilated cardiomyopathy,
hypertrophic cardiomyopathy, and postoperative congenital heart disease were
treated with antiarrhythmic medications such as procainamide, flecainide, sotalol,
and amiodarone. However, concern about the lack of efficacy and the
proarrhythmic potential of these medications made chronic pharmacologic therapy
a less attractive alternative for these conditions. The use of device therapy
(defibrillation implantation) to prevent SCD in the pediatric population has
increased. However, these devices are not always pediatric friendly, and their use
in the pediatric population has a unique set of problems.

Two pediatric disease states in which ventricular arrhythmias are common deserve
special mention. The first is the long QT syndrome, a genetic condition in which
disorders of either sodium or potassium myocardial ionic channels cause
repolarization abnormalities and the propensity for malignant ventricular
arrhythmias (torsades de pointes). SCD is a frequent outcome in this condition.
The initial treatment of long QT syndrome involves the use of a β-blocker
(propranolol) and activity restriction. Second-line therapy includes the use of
mexiletine (class I antiarrhythmic agent), cardiac sympathectomy, or defibrillator
implantation.
VT occurring in infancy is another unique arrhythmia. Similar to SVT, when VT is
encountered in infancy, it may be characterized by symptoms of cardiogenic shock
as a result of its incessant, unrecognized nature. The substrate underlying
ventricular arrhythmias in infancy is usually hamartomatous lesions (plaques) on
the ventricular myocardium that exhibit abnormal automaticity and cause
ventricular irritability. These hamartomas usually resolve by 5 years of age, and the
VT subsides. Until they resolve, these VTs in infancy may require very powerful
class I or III antiarrhythmic agents alone or in combination to avoid severe
symptoms. On occasion, for medically recalcitrant infantile VT, ablation (either
surgical or catheter) therapy is needed to avoid severe mobility or mortality.
However, despite the severe initial symptoms, most children with this condition
become free of tachycardia without the necessity of any therapy by 4 to 5 years of
age.

Finally, the use of catheter ablation techniques to cure VTs in children is

increasing. With special three-dimensional mapping systems, more and more
complex re-entrant VTs are amenable to cure with catheter ablation techniques.
Success rates, however, are lower than those with pediatric SVTs and, depending
on the mechanism of the VT, range from 33% to 90%.

Premature Beats

Premature beats from the atrium, ventricle, or AV junction are encountered

frequently in children. If the child has a normal heart and the beats are not
exacerbated by exercise, treatment is not usually indicated. If the premature beats
cause intolerable symptoms (palpitations), they can sometimes be suppressed with
β-blocker therapy.

Premature beats (especially from the ventricle), when encountered in children with
abnormal cardiac structure, function, or both, may be of concern because of issues
involving prevention of SCD. Although these beats may not require any specific
treatment, re-examination of the underlying cardiac substrate may be necessary. A
new onset of cardiac ectopy sometimes indicates a cardiac substrate that is
changing for the worse. In addition, some restriction of activity in children with
cardiac structural disease and new-onset ectopy may at times be warranted.

Bradycardia
Bradyarrhythmias encountered in children that are significant enough to need
treatment are extremely rare. If significant sinus bradycardia is encountered in a
child with a normal heart, most likely the cause of this arrhythmia is not cardiac. A
workup of noncardiac reasons for bradycardia is imperative and includes ruling out
apnea, intracranial pathology, endocrine abnormalities, and other systemic
diseases. Because the only reliable cardiac treatment of chronic, hemodynamically
significant sinus bradycardia is permanent cardiac pacing, searching for other
causes of the bradycardia is crucial.

Bradycardia secondary to a high-grade or complete AV block is encountered in

children with normal myocardial structure and function (congenital complete AV
valve block) and in children who have undergone correction of a congenital heart
lesion (surgical AV block). Treatment of both these conditions is permanent cardiac
pacing. Pacemakers can be implanted via the epicardial or transvenous route. As
pacemaker systems become more miniaturized, the transverse approach is
becoming more feasible in younger children. Indications for pacemaker insertion in
children with bradyarrhythmias are outlined in the American College of
Cardiology/American Heart Association guidelines.
ADAMS-STOKES SYNDROME

1. recurrent sudden attacks of unconsciousness caused by impaired conduction of

the impulse that regulates the heartbeat

Familiarity information: ADAMS-STOKES SYNDROME used as a noun is very

rare.

Meaning:

Recurrent sudden attacks of unconsciousness caused by impaired conduction of the

impulse that regulates the heartbeat

Classified under:

Nouns denoting stable states of affairs

Synonyms:

Adams-Stokes syndrome; atrioventricular block; heart block; Stokes-Adams syndrome.

6. Additions. Controlling of knowledges
Tests 1.
1.A child of 6 yrs while observation ,on the ECG it was found that fibrillation of
the ventricles, what is first medicine supposed to give?
A. Electrical defibrillation
B. Injection of epinephrine
C. Injection of glucocorticosteroids
D. Injection of cardiac glucosides

2.A child of 7yrs suffering from the age of 4 yrs from pneumonia,a complication of
pulmonary heart is developed, what are the characteristic indication of this on
the ECG?
A. high P wave
B. Leftgram
C. Lower P wave
D. ST on the isolinea
E. Low T wave

3.A child was admitted in the hospital with infectious –allergic myocaditis, in
the 2nd day there he faced attack of paroxysmal tachycardia, which of the
following drugs is used to avoid attacl?
A. Nor epinephrine
B. Cardiac glycosides
C. Morphine
D. Finoptin(Isoptin)
E. Hinidine

4.A 8 mo old baby is suffering from adenoviral infection, with high t. the PS is
220\min, after 6 hrs the condition got worsened, child became pale, irritable,
increased tachypnoea. Abdomen is soft, liver +2.5cm from the costal edges, On
ECG-paroxysmal supra ventricular tachychadia. Which of the the tactics is the
most suitable?
A. TO complete Valsalva manuever
B. cooling the Face with ice block
C. Drink cold water
D. IV injection of Lidocaine
E. Per oral Anaprilin

5. There is a 14 yrs old girl with diagnosis of vegetative disfunction with tonus
of sympathetic part of the vegetative NS, what is the most suitable diet?
A. Addition of protein and fat
B. Control of protein and carbohydrates
C. Control of protein and fat
D. Addition of fat and carbohydrates

6. A girl of 11 years, while observation was found that deepened inspiration

with incomplete expiration, attack of dyspnoea in the night time, without
snores,diskinesia of gall bladder, enures in the night time. Pregnancy time of
the mother faced serious hystose, What clinico-morphological form is that
disfunction?
A. Vegetative-visceral
B. Neuro circular
C. Vegetative bronchial
D. Paroxysmal vegetative
E. Vegetatve-vascular

7. Boy of 3yrs.Is discharged from cardiology, where he was admitted due to often
attack of cyanotic dispnoea with a Teetrad Fallow, which of the following drug
is most suitable to take as prophylaxis?
A. Curantil
B. Relanium
C. Digoxin
D. Obzidan
E. Cordaron

8.A child of 5 years, diagnosed with rheumatoid endocarditis . On ECG -

elongation of the PQ. Intervals up to 0.22, inversion of T wave, in the thoracic
abduction. Which of the of the function of the myocard is disturbed?
A. Stimulation
B. Automatism
C. Contracting ability
D. Conduction

9.A baby of 4,5m, is admitted in order to detect the congenital abnormalities of

the heart, The mother complaints that there is no addition of body weight ,
dyspnoea and cyanosis, which is increased with physical work, Condition of
the baby suddenly worsened, increased dyspnoea and cyanosis, uncalm, systolic
sound decreased, What is the 1st aid that should be given?
A. IV of promedol, Anaprilil
B. IV of Strophantin
C. IV of Euphillyn
D. IV of Prednisolon
E. IV of Furosemid
10.In nursery while playing the boy was found with some tablets ,suddenly
the 3yrs. Old boy faced change in gait, conversation, the face was reddish,
observation- tachycardia, decrease of BO, up to 42\20mmHg.Dialation of the iris,
IN ECG- dialated QRS complex, interval Q-T, suddenly started convulsion ,
Poisoning with which drugs will give those symptoms?
A. Barbiturates
B. Diazepam
C. Phosphor-organic substances
D. Tricyclic anti depressant

Tests 2.
1. A 5yrs. Old child suddenly had an attack of palpitation, accompanied with
nausea, headache and weakness, On ECG – tachycardia of 220\min. ventricular
complex fixed and widened, P waves is absent, what drug will you give first?
A. Lidocaine
B. Izoptin
C. Seduxin
D. Novocainamide
E. Strophanthin

2.Mother of 1,5yrs. baby complaints of anorexia, weakness, pale skin,

acrocyanosis, oedema on the knee. US scan- defect of interventricular septum,
13mm, What is the most suitable drug?
A. Euphillyn
B. Prednisolon
C. Digoxin
D. Lasix
E. Papaverin

3. a boy of 7yrs. Is having congenital defect of the heart , for the last time
there is an increased paleness of the skin, peri-oral acrocyanosis in the time of
rest, BR:36\min, HR=PS=102\min, oedema on the legs, liver +6cm, what type
cardiac insufficiency is observed?
A. Total cardiac insufficiency
B. Chr. Left ventricular incompetence IIB
C. Chronic right ventricular in sufficiency
D. Chronic right ventricular incompetence IIA
E. Chr. Right ventricular insufficiency IIA

4. A baby of 13 yrs with rheumatoid mitral valve incompetence, when got

ARVI, got dyspnoea, weakness, pain in the chest, dry cough, position of half
sitting , cyanosis of the lips,PS-150, in the lungs moist snores of different
caliber, liver –on the level of the ribs, what complication has taken place?
A. Acute leftventrcular incompetence
 B. Acute rt.tventrcular incompetence
C. Acute total incompetence
D. Chronic leftventrcular incompetence
E. Acute vascular incompetence

5. A boy of 14yrs after high physical exercise got an attack of palpitation, In

ECG- Tachycardia 180\min, widened QRS complex, which drug is must in the
case of emergency?
A. Etacicin
B. Isoptin
C. Digoxin
D. Lidocaine
E. Cordaron

Questions
1To indicate etiologic and pathophysiologic factors at premature contraction at
paroxysmal tachycardia, atrial flutter, atrial fibrillation, atrioventricular block, Moraine-
Adam-Stocks syndrom.
2To indicate etiologic and pathophysiologic factors at cardiac arrhythmia in children.
1. Determination paroxysmal tachycardia, atrial flutter, atrial fibrillation,
atrioventricular block, Moraine-Adam-Stocks syndrom.
2. Classification cardiac arrhythmia in children.

3. What causes paroxysmal tachycardia, atrial flutter, atrial

fibrillation?
4. What causes atrioventricular block, Moraine-Adam-Stocks syndrom?
5. Clinical manifestations. Diagnosis.

6. Can medicine treat cardiac arrhythmia in children?

7. Will medicine drag help paroxysmal tachycardia, atrial flutter, atrial
fibrillation, atrioventricular block, Moraine-Adam-Stocks syndrom?
8. Rational treatment.
9. Rehabilitation and prevention therapy.
8. Literature.
1. Pediatrics: Manual on Faculty Pediatrics for Foreign Students/Y.V. Odynets,
A.F. Ruchko, I.N. Poddubnaya. – Kharkov: «Kruk», 2003.-224p.
2. Pediatric clinical methods/Kaushal Singh. – SAGAR PUBLICATIONS,
2006. – 333p.
3. Basic Clinical Pediatrics/Mohammed El-Naggar. – National library, 2006. –
84p.
4. Ferri FF. Glomerulonephritis, acute. In: Ferri's Clinical Advisor 2007:
Instant Diagnosis and Treatment. 9th ed. Philadelphia, PA: Mosby, An
Imprint of Elsevier; 2007.
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