Electrical activity without pulse. Asystole or electrical activity without a pulse. Rhythm disturbances not requiring defibrillation

Definition: The presence of electrical activity without a palpable pulse

Causes: Hypoxia, hypovolemia, hypothermia, hypo-hyperkalemia, poisoning, pneumothorax, cardiac tamponade, thromboembolism, acidosis

Prognosis: if the cause is not treated, survival< 1%

Adrenalin

The main drug for cardiac arrest

Maximum dose: 1 mg IV, IV bone (2 mg endotracheally)

Defibrillated Rhythm

ventricular fibrillation

Heart rate: not detected (QRS complexes are not differentiated) Rhythm: fast and chaotic Causes: hypoxia, hypovolemia, hypothermia, hypo-hyperkalemia, Meaning: terminal rhythm

Better prognosis than asystole if early defibrillation is performed

Defibrillated Rhythms

Monomorphic ventricular tachycardia

Rhythm: Regular

Causes: congenital heart disease, hypoxia, hypovolemia, hypothermia, hypo-hyperkalemia, antidepressant poisoning,

Meaning: rare in children

Defibrillated Rhythms

Polymorphic ventricular tachycardia

Pirouette (Torsades de pointes)

Rhythm: QRS complexes continuously change in shape, direction, amplitude and duration

Causes: prolongation of the QT interval

Fibrillation frequency
ventricular (VF) and ventricular tachycardia
pulseless (pulseless VT)

defibrillation

4 J/kg CPR x 2 min

defibrillation

4 j/kg CPR x 2 min

adrenalin

defibrillation

CPR within 2 min

Adrenalin

CPR within 2 min

CPR x 2 min. VF/VT amiodarone

defibrillation

No pulse

Treatment of ventricular fibrillation with a monophasic and biphasic defibrillator

Monophasic Biphasic

No pulse

Other medicines

 Bicarbonate: only with prolonged cardiac arrest, severe acidosis, hyperkalemia, poisoning with antidepressants

 Lidocaine: not the first choice for VF/VT

 Glucose: only in case of hypoglycemia after restoration of blood circulation (to prevent hypo-hyperglycemia)

 Magnesium sulfate: only for hypomagnesemia or torsades de pointes ventricular tachycardia

 Vasopresin: there is not enough data for its use

C - blood circulation

Assessment of hemodynamic status

 HR and heart rate

 Systemic perfusion: skin perfusion

Peripheral and central pulse level of consciousness, diuresis

 BP

Child< 1 года: ЧСС < 80/мин или

> 180/min Child > 1 year: Heart rate< 60/мин или

> 160/min

Acidosis due to hypoperfusion causes tachypnea

RISK RR > 60 /min

Skin perfusion

Hypoperfusion of the skin is an early sign of a state of shock.

 limb temperature

 skin color (pallor, cyanosis, marbling)

 capillary refill time

 peripheral and central pulse

Capillary refill time

The time of reperfusion of the skin after pressure for 5 seconds

(norm:< 2 секунд при комнатной температуре)

Level of consciousness

Cerebral hypoperfusion = impairment of consciousness

 Hypotension is a late sign of shock and appears after compensatory mechanisms have been exhausted.

 Control and monitoring are an important element in the effectiveness of treatment

BP parameters

(minimum BP 3rd percentile)

	BP (mm/Hg st.
1 month -1 year
	70 + (2 x age in years)

Diastolic pressure = approximately 2/3 of systolic pressure

The cuff should cover 2/3 of the width of the forearm

Kidney function

Normal urine output: 1-2 ml/kg/hour

Diuresis< 1 мл/кг/час, в отсутствии почечной патологии = гипоперфузии

It is important to monitor urine output to evaluate the effectiveness of shock treatment.

Treatment of cardiogenic

priority: vascular access

peripheral vein

after 2 - 3 attempts

intraosseous access*

* alternative: central

vascular access (e.g. femoral) if the clinician is experienced

SPECIFIC SHOCK THERAPY

 Cardiogenic shock: After the first bolus, inotropic agents can be used. In cardiogenic shock, the volume of the first bolus should be no more than 5-10 ml/kg administered over at least 20 minutes.

 Hypovolemic shock: requires up to 40-60 ml / kg, within 1 hour, with bleeding

urgent need to request blood products.

 Septic shock:sometimes an injection is required 150-200 ml/kg for 1 hour

 Obstructive shock: diagnose the cause and treat it, pneumothorax, cardiac tamponade

 Anaphylactic shock: infusion therapy + adrenaline +

antihistamines

(anti-H1 and anti-H2) + steroid drugs

Pharmacotherapy of arrhythmias in emergency pediatrics

A drug		Indications and contraindications		Dose and route of administration
	Indications
adenosine
		Drug of choice for supraventricular
		tachycardia		While monitoring the ECG IV, rapidly inject 100 mcg/kg
		Effective in supraventricular		(first dose not to exceed 6 mg)
		tachycardia arising from the mechanism		After 15-30 seconds recovery is possible
		entrina at the level of the atrioventricular node		sinus rhythm
		May be useful in differential diagnosis		In case of inefficiency, repeaton is administered at a dose
		inter-superventricular tachycardia		200 mcg/kg up to a maximum of 12 mg. Etadoza
		atrial flutter		preferred when adenosine is administered in
		Not effective for flutter		peripheral veins.
		atrial fibrillation and tachycardia
		not caused by the mechanism of circulation	Mode of application
		excitation at the level		Takkaku adenosine very short period
		atrioventricular node		half-life (less than 10 seconds), entered as
				as soon as possible
	Mechanism of action			The drug is rapidly metabolized
		Short-term atrioventricular		erythrocyte endotheliocytes
		blockade (approx. 10 sec)		To speed up the delivery of the drug to the point
				applications in the heart, then quickly injected
	Warnings			10-15 ml of saline.
		Short-term (10 - 15 sec) bradycardia,		Adenosine can be administered intraosseously.
		3rd degree atrioventricular block or
		asystole is not a contraindication
		for repeated administration of adenosine

Amiodarone

Indications

Effective

at various

atrial and

With unstable hemodynamics, as with

ventricular tachyarrhythmias

supraventricular, but with ventricular

Applies

hemodynamically

tachycardia initial dose of amiodarone 5

stable

supraventricular

tachycardia

mg/kg (maximum 300 mg) given over

refractory to techniques that stimulate

20 - 60 min. Since the introduction

vagus nerve and adenosine.

amiodarone possible decrease

Safe

effective

myocardial contractility and development

hemodynamically

unstable

ventricular tachycardia

slower drug administration

tachyarrhythmia, unwelcome with

Mechanism of action

resuscitation after

Inhibits

alpha and beta adrenergic

cardiac arrest.

receptors

causes

vasodilation,

A repeat dose of 5 mg/kg may be given up to

slows down

atrioventricular

maximum daily dose of 15 mg/kg (not

conductivity

exceeding the maximum dose for

Lengthens the QT interval, QRS

adults2.2 g/day)

Warnings

Mode of application

interval

increases

Rapid administration of amiodarone results in

development

polymorphic

ventricular

vasodilation and arterial hypotension.

tachycardia (torsades de pointes)

develop

Rare but significant complications

atrioventricular

amiodarone

are

bradycardia,

polymorphic ventricular tachycardia.

hypotension

polymorphic

ventricular

blood pressure monitoring

tachycardia.

introductions

amiodarone.

warnings

non-invasive

blood pressure measurements are required

relevance

hepatic

frequent measurements

insufficiency

a joint

amiodarone use of other agents,

prolonging the QT interval (eg.

procainamide)

Procainamide

Indications

Effective

atrial

ventricular

arrhythmias,

supraventricular

ventricular

tachycardia.

stop

supraventricular Method of application

resistant

others

antiarrhythmics

Can be used for cupping

hemodynamically

stable

supraventricular

tachycardia

refractory to vagal influences and

adenosine

frequent measurements

Effective

flutter

Application

procainamide,

atrial fibrillation

amiodarone,

increases

apply

ventricular tachycardia

Mechanism of action

Prolongs the effective refractory period of the atria and ventricles, disrupts conduction

By slowing down intraventricular conduction, it prolongs the QT interval,

Procainamide

Warnings

A loading dose of 15 mg/kg is injected into

Maybe

paradoxical

shortening

within 30-60 minutes with ECG monitoring

effective

refractory

atrioventricular

acceleration

passing through the node. This

beHow to use

mechanism

explanatory

increase

Infusion should be carried out slowly

cardiac

cuts

to avoid blockages, arterial

the use of procainamide for the treatment

hypotension and prolongation of the QT interval,

ectopic atrial tachycardia.

which increases the risk of ventricular

May cause hypotension

tachycardia or torsades de pointes

due to vasodilating effect

Non-invasive blood pressure measurements require

Metabolites

procainamide

frequent measurements

accumulate in the body and cause

Application

procainamide,

renal dysfunction

amiodarone,

increases

polymorphic ventricular tachycardia.

Lidocaine	Indications		Dose / route of administration
		Alternative remedy for	Loading dose 1 mg/kg lidocaine
		cupping hemodynamically
		stable ventricular tachycardia	mcg/kg/min
			If there is a delay of more than 15 minutes
	Not used for supraventricular		between the first bolus and
	arrhythmia with a narrow QRS complex		start of continuous infusion
	Mechanism of action		bolus administration at a dose of 0.5 - 1.0 mg / kg for
		Sodium channel blocker, reduces	recovery of therapeutic
		automatism and suppresses ventricular	concentration of lidocaine.
		wide QRS complex arrhythmias

Warnings

An overdose of lidocaine may occur in patients with low cardiac output, with renal or hepatic insufficiency.

	Indications
	Use in the treatment	25 - 50 mg / kg IV, intraosseously
	tachycardiatorsadesdepointesand	(maximum 2 g), injected 10-
	ventricular tachycardia	20 min (faster when stopped
	phonohypomagnesemia.	heart due to tachycardia
		torsades de pointes

Testing on the topic "Violation of the heart rhythm and conduction at the prehospital stage"

QUESTION N 1. What nonspecific symptoms can be observed with rhythm disturbances?

1. Collapse

2.Violation of consciousness

3. Shock with hypotension and peripheral hypoperfusion

4. Respiratory distress/respiratory failure, pulmonary edema

5. All of the above symptoms

Correct answer 5

Nonspecific symptoms in tachyarrhythmias:

The patient may experience weakness, palpitations, dizziness, fainting and fainting. In young children, tachyarrhythmia may go unrecognized for a long time, especially at home, until symptoms of congestive heart failure appear.

Symptoms indicating an unstable state with tachyarrhythmias:

respiratory distress/respiratory failure, pulmonary edema

shock with hypotension and peripheral hypoperfusion

disturbance of consciousness

sudden collapse with rapid pulse

Nonspecific symptoms in bradyarrhythmias:

Shock with hypotension Impaired perfusion of organs and tissues Impaired consciousness

Collapse

QUESTION N 2. Does bradycardia occur in healthy people?

1. Yes

2. No

Correct answer 1

Sinus bradycardia occurs in healthy people, especially at a young age; during sleep, in athletes, the so-called sports bradycardia.

QUESTION N 3. Name the possible causes of pathological sinus bradycardia

1. Hypoxia

2. Side effects of drugs

3. Poisoning

4. Electrolyte disorders

5. Hypoglycemia

6. intracranial hypertension

7. All of the above reasons

Correct answer 7

The causes of pathological sinus bradycardia are hypoxia, poisoning, electrolyte disturbances, infections, sleep apnea, drug effects, hypoglycemia, hypothyroidism, intracranial hypertension.

QUESTION N 4. The cause of bradycardia can be:

1.hypokalemia

2.hyperkalemia

3.hypocalcemia

4. hypomagnesemia

5. all of the above reasons

Correct answer 2.

The normal level of potassium in the blood serum is 3.4 - 4.7 mmol / l; Hypokalemia is accompanied by tachycardia, with hyperkalemia, bradycardia occurs. An increase in serum potassium above 6 mmol/l may be the cause of asystole.

QUESTION N 5. What changes on the ECG can be recorded with bradycardia?

1. Sinus rhythm

2. Ectopic rhythm

3.Sinoatrial blockade

4. Atrioventricular block

5. All of the above

Correct answer 5

With bradycardia, a rare sinus rhythm can be recorded on the ECG - sinus bradycardia. With sinus rhythm and slowing of atrioventricular conduction (prolongation of the pQ interval above the age norm) - may

register atrioventricular blockade of the 1st degree. Atrioventricular blockades of the 2nd and 3rd degree can be registered (the pQ interval lengthens gradually, and after the QRS complex is lost, it is shortened, up to a normal value in the Mobitz variant 1; and may be normal or prolonged in the Mobitz variant 2). At 3 degrees of atrioventricular blockade, the pQ interval is not evaluated. Ectopic rhythms - atrial, nodal, ventricular, if these are not accelerated ectopic rhythms, are always less often than the sinus rhythm normal for age. Sinoatrial blockade can also be accompanied by bradycardia.

QUESTION N6. What element on the ECG reflects the speed of atrioventricular conduction?

1. P wave

2. QRS wave

3. T wave

4. pQ interval

5. QT interval

Correct answer: 4

The time of impulse conduction from the sinus node through the atria and the atrioventricular node to the ventricles is reflected by the pQ interval. Normally, the pQ interval is not more than 0.15 seconds in children under 2 years old; 0.16 sec in children aged 3-10 years; 0.18 sec - in children 11 - 15 years old; in adults no more than 0.2 sec.

QUESTION N7. How is the pQ interval measured?

1. from the end of the P wave to the beginning of the Q wave

2. from the beginning of the P wave to the beginning of the Q wave

3. from the end of the P wave to the end of the Q wave

4. from the beginning of the P wave to the beginning of the R wave

5. 2 and 4 are correct answers

Correct answer: 5

The pQ or pR interval is measured, in the absence of a Q wave, in the 2nd standard lead from the beginning of the P wave, to the beginning of the Q or R wave.

QUESTION N 8 At what length of the pQ interval in children of the first 2 years of life can we talk about atrioventricular blockade?

1. pQ more than 0.15 sec

2. pQ more than 0.16 sec

3. pQ more than 0.18 sec

4. pQ more than 0.2 sec

5. pQ less than 0.1 sec

Correct answer: 1

QUESTION N 9. At what length of the pQ interval in children aged 3-10 years of life can we talk about atrioventricular blockade?

1. pQ more than 0.15 sec

2. pQ more than 0.16 sec

3. pQ more than 0.18 sec

4. pQ more than 0.2 sec

5. pQ less than 0.1 sec

Correct answer: 2

Normally, the pQ interval is not more than 0.15 seconds in children under 2 years old; 0.16 sec in children aged 3-10 years; up to 0.18 sec - in children 11 - 15 years old; in adults no more than 0.2 sec. If the duration of the pQ interval exceeds the specified value, it indicates an atrioventricular block.

QUESTION N 10. At what length of the pQ interval in children aged 11 - 15 years life it is possible to speak about an atrioventricular blockade?

1. pQ more than 0.15 sec

2. pQ more than 0.16 sec

3. pQ more than 0.18 sec

4. pQ more than 0.2 sec

5. pQ less than 0.1 sec

Correct answer: 3

Normally, the pQ interval is not more than 0.15 seconds in children under 2 years old; 0.16 sec in children aged 3-10 years; up to 0.18 sec - in children 11 - 15 years old; in adults no more than 0.2 sec. If the duration of the pQ interval exceeds the specified value, it indicates an atrioventricular block.

QUESTION N 11. At what length of the pQ interval in children of the first year of life can we speak of a shortening of the pQ interval?

1. pQ less than 0.15 sec

2. pQ less than 0.12 sec

3. pQ less than 0.11 sec

4. pQ less than 0.1 sec

5. pQ less than 0.08 sec

Correct answer: 5

QUESTION N 12. At what length of the pQ interval in children aged 1 to 3 years of life can we speak of a shortening of the pQ interval?

1. pQ less than 0.15 sec

2. pQ less than 0.12 sec

3. pQ less than 0.11 sec

4. pQ less than 0.1 sec

5. pQ less than 0.08 sec

Correct answer: 4

Normally, the pQ interval is at least 0.08 seconds in children under 1 year old; 0.1 sec in children aged 1–3 years; 0.11 sec - in children 3 - 6 years old; from 7 years and older at least 0.12 sec. A shorter pQ interval indicates an acceleration of the atrioventricular

conduction, which may be due to the presence of additional pathways, in the presence of which the risk of supraventricular tachyarrhythmias increases.

QUESTION N13. At what length of the pQ interval in children aged 3 to 6 years of life can we speak of a shortening of the pQ interval?

1. pQ less than 0.15 sec

2. pQ less than 0.12 sec

3. pQ less than 0.11 sec

4. pQ less than 0.1 sec

5. pQ less than 0.08 sec

Correct answer: 3

Normally, the pQ interval is at least 0.08 seconds in children under 1 year old; 0.1 sec in children aged 1–3 years; 0.11 sec - in children 3 - 6 years old; from 7 years and older at least 0.12 sec. A shorter pQ interval indicates an acceleration of atrioventricular conduction, which may be due to the presence of additional conduction pathways, in the presence of which the risk of developing supraventricular tachyarrhythmias increases.

QUESTION N 14. At what length of the pQ interval in children aged 7 to 14 years of life can we speak of a shortening of the pQ interval?

1. pQ less than 0.15 sec

2. pQ less than 0.12 sec

3. pQ less than 0.11 sec

4. pQ less than 0.1 sec

5. pQ less than 0.08 sec

Correct answer: 2

Normally, the pQ interval is at least 0.08 seconds in children under 1 year old; 0.1 sec in children aged 1–3 years; 0.11 sec - in children 3 - 6 years old; from 7 years and older at least 0.12 sec. A shorter pQ interval indicates an acceleration of atrioventricular conduction, which may be due to the presence of additional conduction pathways, in the presence of which the risk of developing supraventricular tachyarrhythmias increases.

QUESTION N 15. How is the QT interval measured?

1. from the beginning of the Q wave to the beginning of the T wave

2. from the beginning of the Q wave to the top of the T wave

3. from the beginning of the Q wave to the end of the T wave

Correct answer: 3

The duration of the QT interval is measured from the beginning of the Q wave to the end of the T wave in standard lead 2.

QUESTION N 16 An extended QT interval in children of the first year of life is considered if its corrected value exceeds:

1. 0.3 sec

2. 0.35 sec

3. 0.4 sec

4. 0.45 sec

5. 0.47 sec

Correct answer: 5

An extended interval is considered if the corrected QT (QTc) in children of the first year of life exceeds 0.47 seconds

QUESTION N 17 An extended QT interval in children aged 1 to 8 years of life is considered if its corrected value exceeds:

1. 0.3 sec

2. 0.35 sec

3. 0.4 sec

4. 0.45 sec

5. 0.47 sec

Correct answer: 4

An extended interval is considered if corrected QT (QTc) in children in

ages 1 to 8 years life exceeds 0.45 sec

QUESTION N 18 An extended QT interval in young men is considered if its corrected value exceeds:

1. 0.3 sec

2. 0.35 sec

3. 0.4 sec

4. 0.45 sec

5. 0.47 sec

Correct answer: 4

An extended interval is considered if the corrected QT (QTc) in young men exceeds 0.45 sec.

QUESTION N 19 An extended QT interval in girls is considered if its corrected value exceeds:

1. 0.3 sec

2. 0.35 sec

3. 0.4 sec

4. 0.45 sec

5. 0.47 sec

Correct answer: 5

An extended interval is considered if the corrected QT (QTc) in girls exceeds 0.47 seconds

QUESTION N 20 What can cause prolongation of the QT interval?

1. congenital long QT syndrome

2. acquired long QT syndrome

3. All answers are correct

Correct answer: 3

The reasons for the prolongation of the QT interval are diverse: genetic defects that are the causes of channelopathy. The causes of acquired long QT syndrome are electrolyte disturbances (hypomagnesemia, hypokalemia, hypocalcemia); increased intracranial pressure, ischemia

myocardial infarction, inflammatory diseases of the myocardium, taking antiarrhythmics IA, IC and III classes, tricyclic antidepressants, calcium channel blockers, phenothiazines, macrolide and fluoroquinolone antibiotics, some antihistamines.

QUESTION N 21 What are the reasons for the acquired prolonged QT interval?

1. electrolyte disturbances

2. intracranial hypertension

3. overdose of certain drugs

4. myocarditis

5. All answers are correct

Correct answer: 5

The causes of QT prolongation are varied. The causes of acquired long QT syndrome are electrolyte disturbances (hypomagnesemia, hypokalemia, hypocalcemia); increased intracranial pressure, myocardial ischemia, inflammatory myocardial diseases, taking class IA, IC and III antiarrhythmics, tricyclic antidepressants, calcium channel blockers, phenothiazines, macrolide and fluoroquinolone antibiotics, some antihistamines.

QUESTION N 22. Name the factors predisposing to pirouette tachycardia:

1. Long QT Syndrome

2. Hypomagnesemia

3. Overdose of antiarrhythmics (class IA: quinidine, procainamide, disopramide; class IC: encainide, flecainide; class III: sotalal, amiodarone)

4. Overdose of other drugs: tricyclic antidepressants, calcium channel blockers, phenothiazines, macrolide and fluoroquinolone antibiotics, some antihistamines)

5. All answers are correct.

Correct answer: 5

The reasons for the prolongation of the QT interval are diverse: genetic defects that are the causes of channelopathy. The causes of acquired long QT syndrome are electrolyte disturbances (hypomagnesemia, hypokalemia, hypocalcemia); increased intracranial pressure, myocardial ischemia, inflammatory myocardial diseases, taking class IA, IC and III antiarrhythmics, tricyclic antidepressants, calcium channel blockers, phenothiazines, macrolide and fluoroquinolone antibiotics, some antihistamines. In addition, some patients may develop pirouette tachycardia, the cause of which is not always possible to establish.

QUESTION N 23. The development of what tachyarrhythmia is most expected with a prolonged QT interval?

1. Supraventricular tachycardia

2. Pirouette ventricular tachycardia

Correct answer: 2

With a prolonged QT interval of a congenital or acquired nature

there is a high risk of developing such a variety of polymorphic ventricular tachycardia as pirouette ventricular tachycardia (Torsades de pointes)

Ventricular tachycardia can be monomorphic, when all the QRS complexes on the ECG are the same in shape, and polymorphic, when the QRS complexes differ from each other in their shape. Tachycardia Torsades de pointes (pirouette tachycardia) is a separate form of polymorphic ventricular tachycardia. With it, the QRS complexes continuously change in shape, direction, amplitude and duration: as if they are dancing around the isoline. The heart rate is in the range of 150 - 250 per minute. It develops with a significant lengthening of the QT interval, both congenital and acquired. The duration of the QT interval is estimated in sinus rhythm and cannot be determined during tachycardia. On a short tape, prolongation of the QT interval may be recorded, and not episodes of torsades de pointes because they are of short duration.

QUESTION N24. At what length of the corrected QT interval can one speak of short QT interval syndrome?

1. if QTc is less than 0.35 sec

2. if QTc is less than 0.37 sec

3. all answers are correct

Correct answer: 3

There are 2 degrees of shortening of the QT interval. At grade 1, QTc is less than 0.35 sec, at grade 2, it is less than 0.33 sec.

QUESTION N 25. For supraventricular paroxysmal tachycardia in children of the first year of life, a sudden increase in

heart rate over:

1. 250 bpm

2. 220 bpm

3. 150 bpm

4. 100 bpm

5. all answers are correct

Correct answer: 2

Rhythm significantly exceeding the norm in frequency with a source of occurrence in the supraventricular structures. The most common mechanism of occurrence is re-entry with the involvement of additional pathways (atrioventricular, intranodal). Also, supraventricular tachycardia occurs when active ectopic foci appear in the atria. Supraventricular tachycardia is the most common type of tachyarrhythmia in infants.

		Missing or inverted
pQ (pR) interval
			shortened	with ectopic	atrial
		tachycardia
RR interval		Equal duration
QRS complex
				supraventricular	paroxysmal

tachycardia in children older than 1 year of age is characterized by a sudden increase in heart rate more than:

1. 250 bpm

2. 220 bpm

3. 180 bpm

4. 150 bpm

5. all answers are correct

Correct answer: 3

ECG signs of sinus tachycardia:

Supraventricular tachycardia

Rhythm significantly exceeding the norm in frequency with a source of occurrence in the supraventricular structures. The most common mechanism of occurrence is re-entry with the involvement of additional pathways (atrioventricular, intranodal). Also supraventricular tachycardia

occurs when active ectopic foci appear in the atria. Supraventricular tachycardia is the most common type of tachyarrhythmia in infants.

ECG signs of supraventricular tachycardia:

	There is no rhythm variability.
		more than 220 minutes in children under 1 year
		more than 180 minutes in children older than 1 year
	Missing or inverted
pQ (pR) interval		Impossible to determine in the absence of a P wave;
		shortened in ectopic atrial
	tachycardia
RR interval	Equal duration
QRS complex	Narrow (more than 90% of cases), less than 0.09 sec

QUESTION N 27. What is the heart rate in case of ventricular paroxysmal tachycardia in children?

1. frequency close to the age norm

2. ranges from close to the age norm to 200 beats per minute

3. above 200 beats per minute

4. all answers are correct

Correct answer: 4

With ventricular tachycardia with a pulse, the frequency of ventricular contractions varies from a frequency close to normal to 200 and above. With a frequent ventricular rhythm, the stroke volume and cardiac output decrease, the pulse disappears, that is, there is a place to be ventricular tachycardia without a pulse.

QUESTION N 28. What is the duration of the paroxysm of non-sustained tachycardia?

1. less than 30 seconds

2. less than 1 minute

3. less than 30 min

4. less than 6 hours

5. less than 1 day

Correct answer: 1

A paroxysm of unstable tachycardia is considered a paroxysm of ventricular or supraventricular tachycardia with a duration not exceeding 30 seconds.

QUESTION N 29. What is the duration of the paroxysm of sustained tachycardia?

1. at least 30 seconds

2. at least 1 minute

3. at least 30 min

4. at least 6 hours

5. at least 1 day

Correct answer: 1

A paroxysm of sustained tachycardia is considered a paroxysm of ventricular or supraventricular tachycardia with a duration exceeding 30 seconds.

QUESTION N 30. What is the minimum number of ectopic ventricular or supraventricular complexes recorded in a row, which allows us to consider this episode as an episode of paroxysmal

tachycardia?

1. 200

2. 100

3. 30

4. 10

5. 3

Correct answer: 5

Three consecutive or more ectopic complexes with a high frequency are considered to be a paroxysm of tachycardia.

QUESTION N 31 Tachycardia with a narrow QRS complex is usually:

1. supraventricular tachycardia

2. ventricular tachycardia

Correct answer: 1.

With supraventricular tachycardia, as a rule, the QRS complex is narrow, does not exceed 0.09 sec. A wide QRS complex in supraventricular tachycardia occurs with aberrant intraventricular conduction (either pre-existing or frequency dependent). In addition, a wide QRS complex is observed in atrioventricular antidromic tachycardia, when the impulse from the atria to the ventricles is conducted along an additional path, and returns to the atria through the atrioventricular node.

QUESTION N 32 Tachycardia with a wide QRS complex is usually:

1. supraventricular tachycardia

2. ventricular tachycardia

Correct answer: 2.

With ventricular tachycardia, as a rule, the QRS complex is wide, exceeding 0.09 seconds. Also, a wide QRS complex can be associated with supraventricular tachycardia and is observed with aberrant intraventricular conduction (preexisting or frequency dependent). In addition, a wide QRS complex is observed in atrioventricular antidromic tachycardia, when the impulse from the atria to the ventricles is conducted along an additional path, and returns to the atria through the atrioventricular node.

In some cases, when the ectopic focus of excitation is located in the cells of the bundle of His before dividing it into legs, the QRS complex in ventricular tachycardia may be narrow.

QUESTION N 33. What is the value of the duration of the QRS complex, which allows you to draw a line between a wide and narrow QRS complex in paroxysmal tachycardia?

1.0.08 sec

2.0.09 sec

3. 0.1 sec

4. 0.11 sec

5. 0.12 sec

Correct answer: 2

According to the ILCOR 2010 recommendations for tachycardia, the criterion for a narrow QRS complex is its duration not more than 0.09 seconds, the criterion for a wide QRS complex is its duration exceeding 0.09 seconds. The previous ILCOR 2005 recommendations recommended that the border value between the narrow and wide QRS complex be considered as 0.08 sec.

QUESTION 34. What tachycardia should be suspected in infants, children and adolescents in the first place with a wide QRS tachycardia?

1. supraventricular tachycardia with aberrant conduction

2. ventricular tachycardia

Correct answer: 1

Supraventricular tachycardia is the most common type of tachyarrhythmia in children. In infants, children, and adolescents with wide-complex tachycardia, supraventricular tachycardia with aberrant conduction should be suspected rather than ventricular tachycardia. However, one should not forget that wide complexes are characteristic of ventricular tachycardia.

QUESTION N 35. At what tachyarrhythmias is a wide QRS complex recorded on the ECG?

1. Ventricular monomorphic tachycardia

2. Ventricular polymorphic tachycardia

3. Pirouette ventricular tachycardia

4. Supraventricular tachycardia with aberrant conduction

5. All answers are correct

Correct answer: 5

QUESTION N 36. What is the most common mechanism of supraventricular paroxysmal tachycardia?

1. re-entry mechanism involving additional pathways (atrioventricular,

intranodal).

2. with the appearance of active ectopic foci in the atria.

Correct answer: 1

The most common mechanism for the occurrence of supraventricular paroxysmal tachycardia is the re-entry mechanism involving additional pathways (atrioventricular, intranodal). Also, supraventricular tachycardia occurs when active ectopic foci appear in the atria.

QUESTION N 37. Transportation of a child with an attack of paroxysmal supraventricular tachycardia is performed:

2. reclining

3. on the stomach

4. upright

5. horizontally on the back with a raised foot end

Correct answer: 2

A child with an uncontrolled attack of supraventricular paroxysmal tachycardia is transported in a reclining position.

QUESTION N 38. Emergency treatment of sinus tachycardia at the prehospital stage:

1. required

2. not carried out

Correct answer: 2

Antiarrhythmic therapy is indicated only for poor subjective tolerance of rhythm disturbances and for hemodynamically significant (complicated by the development of syncope, collapse, heart failure) and prognostically significant arrhythmias; these situations are also an indication for hospitalization. We must not forget that therapy with antiarrhythmic drugs is not always safe. The probability of developing an arrhythmogenic effect (i.e., developing an arrhythmia due to the use of a drug) is on average 10% for each of the antiarrhythmics; especially often it develops with ventricular arrhythmias and with organic damage to the myocardium with dysfunction of the left ventricle. This is probably why in Germany, since 1993, the use of antiarrhythmic drugs for the treatment of non-life-threatening cardiac arrhythmias has been banned.

Emergency treatment of sinus tachycardia in the prehospital stage with antiarrhythmic drugs such as verapamil, propranolol (obzidan), procainamide (novocainamide), amiodarone (cordarone), moracizin

(ethmozin), not carried out. It is possible to use valocordin inside at the rate of 1 drop / year of life or 5 mg of diazepam (seduxen), providing emotional and physical rest, it is advisable to prescribe such herbal remedies as novopassitis or motherwort tincture, inside 1 drop / year of life 2-3 times a day.

QUESTION N 39. Massage of the carotid sinus area in order to stop an attack of paroxysmal tachycardia in children:

1. Apply

2. do not apply

Correct answer: 2

Of the reflex effects ("vagus" techniques) in childhood, it is possible to use the "Valsalva maneuver" - attempts to exhale strongly when the mouth and nose are clamped, the vocal cords are closed and the "diver's reflex" - a cold effect on the skin of the face, for example, applying an ice pack on the face for 10-15 seconds. Massage of the carotid sinus, pressure on the eyeballs (Ashner's reflex) is not recommended.

Massage of the carotid sinus area is accompanied by such stimulation phenomena n. vagus, as a decrease in respiration, heart rate and a decrease in blood pressure. Tachypnea, arterial hypertension and tachycardia develop with stimulation of the sympathetic nervous system.

QUESTION N 40. To control tachyarrhythmia atrial fibrillation that occurred in a patient with sick sinus syndrome, at the prehospital stage, it is advisable to use:

1. digoxin

2. verapamil

3. propranolol

4. procainamide (novocainamide)

5. All of the above

Correct answer: 1

To control tachyarrhythmia fibrillation in a patient with sick sinus syndrome at the prehospital stage, it is most advisable to use digoxin, the positive effect of which is associated with blocking the conduction of part of the impulses through the atrioventricular node and improving hemodynamics. The use of β-blockers (propranolol), calcium channel blockers (verapamil), amiodarone in sick sinus syndrome is dangerous, since there is an inadequate decrease in heart rate in relation to their administered doses, as well as severe bradycardia in the interictal period. Digoxin has fewer adverse side effects in terms of impact on cardiac automatism. However, with severe hemodynamic disorders, the relief of an attack of atrial fibrillation in patients with sick sinus syndrome is carried out in the same way as with supraventricular paroxysmal tachycardia. Calcium channel blockers are used, in particular, a 0.25% solution of verapamil (Isoptin), at a dose of 0.1 mg / kg IV slowly over 5-10 minutes in 5-10 ml of 0.9% sodium chloride solution.

QUESTION N 41. The heart rate is highest when:

1. supraventricular paroxysmal tachycardia

2. ventricular paroxysmal tachycardia

3. rhythm disturbances in sick sinus syndrome

Correct answer: 1

Heart rate in 1 min is higher with supraventricular paroxysmal tachycardia: more than 220 minutes in children under 1 year old, more than 180 minutes in children over 1 year old

QUESTION N 42. For the relief of supraventricular paroxysmal tachycardia in patients with Wolff-Parkinson-White syndrome, it is not recommended to use:

1. verapamil (isoptin)

2. phenylephrine (mesatone)

3. propranolol (obzidan)

4. digoxin

5. all of the above

Correct answer: 5

When stopping supraventricular paroxysmal tachycardia in patients with WPW syndrome, which is caused by a congenital anomaly of the conduction system of the heart with the presence of additional pathways, it is not recommended to use propranolol (obzidan), since when using β-blockers or calcium channel blockers that inhibit the conduction of an electrical impulse, it is possible development of the OSN.

QUESTION N 43. When identifying the Wolf-Parkinson-White phenomenon by ECG, it is necessary:

1. emergency treatment

2. consider its presence when stopping other cardiac problems

Correct answer: 2

When identifying the ECG phenomenon of WPW, it is necessary to take into account its presence in the relief of other cardiac problems, since as such it does not play a special role in changing the condition of children, however, attacks of supraventricular tachycardia may be associated with it.

QUESTION N 44. Absence of respiratory sinus arrhythmia in a child

1. indicator of "health"

2. indication for examination

3. indication for emergency treatment

Correct answer: 2

The absence of respiratory sinus arrhythmia in children is an indication for examination, since a rigid sinus rhythm may accompany an organic heart lesion, such as myocarditis.

QUESTION N 45. Atrial fibrillation in a child with a severe general condition indicates:

1. organic heart disease

2. response of the cardiovascular system

Correct answer: 1

Atrial fibrillation in a child with a severe general condition, in contrast to supraventricular paroxysmal tachycardia, which may be due to extracardiac causes, reflecting, in particular, diencephalic pathology, indicates an organic lesion of the heart.

QUESTION N 46. Specify the expected effect of the administration of lidocaine for the relief of supraventricular paroxysmal tachycardia:

1. fatal outcome

Correct answer: 1

With the introduction of lidocaine for the relief of supraventricular tachycardia, there is a high probability of cardiac arrest due to the ineffectiveness of the drug and the possibility of increasing the frequency of ventricular contractions by facilitating the conduction of excess impulses in the atrioventricular node, especially with atrial flutter.

QUESTION N 47. Determine the expediency of using vagotonic techniques and the introduction of adenosine to stop atrial tachycardia, if P waves of various types and an irregular RR interval are detected on the ECG:

1. use highly efficient

2. do not apply

Correct answer: 2

If, at a high heart rate, P waves of various types are detected on the ECG, and the PP interval is irregular, then this indicates polyfocal atrial tachycardia. Relief of tachycardia with adenosine or vagotonic techniques, such as vomiting, straining, massage of the carotid sinus area, pressure on the eyeballs, is ineffective, since they affect the atrioventricular node and additional pathways, but not the activity of heterotropic foci of excitation. Electropulse therapy is also not used. Therapeutic measures should be aimed at stopping acidosis and hypercapnia. It is possible to use a 0.25% solution of verapamil 0.1 mg / kg IV slowly, over several minutes, in 5-10 ml of a 5% glucose solution.

QUESTION N 48. The lack of effect from ongoing drug therapy for ventricular tachycardia with the presence of a pulse requires additionally:

1. conducting synchronized electropulse therapy

2. conducting unsynchronized electropulse therapy

Correct answer: 1

The lack of effect from drug therapy for ventricular tachycardia with the presence of a pulse requires synchronized electropulse therapy with a discharge force of 0.5-1.0 J / kg, against the background of intravenous, intramuscular injection of diazepam (seduxen) at a dose of 0.3-0.5 mg / kg and sufficient anesthesia with narcotic analgesics - 1-2% solution of promedol 0.1-0.2 mg / kg in children older than 6 months or 1% solution of morphine or omnopon 0.15 mg / kg in children older than 2 years.

QUESTION N 49. Specify what is uncharacteristic for ventricular

extrasystoles in children:

1. retrosternal pain

2. ST interval and T wave changes

3. dilated, deformed ventricular complexes

4. no compensatory pause

5. absence of a P wave before the QRS complex of extrasystole

Correct answer: 4

With ventricular extrasystoles in children, chest pain is possible, expanded deformed extrasystolic ventricular complexes, discordant T wave of the extrasystolic complex, post-extrasystolic compensatory pause, leveling of the P wave by the QRS complex are recorded on the ECG.

QUESTION N 50. Specify what is used when detecting life-threatening benign ventricular extrasystoles on the ECG in children:

1. procainamide (novocainamide)

2. cardiac glycosides

3. lidocaine

4. magnesium sulfate

5. none of the above

Correct answer: 5

Antiarrhythmic therapy in case of detection of non-life-threatening benign ventricular extrasystoles on the ECG in children is carried out in

in case of complaints of the child to interruptions in the heart, discomfort, as well as in case of syncope. It is recommended to use etmozin (tablets of 0.025 g) or aimalin (tablets of 0.05 g) orally at 2-3 mg / kg / day in 3-4 doses, first in a hospital, and then on an outpatient basis. Etmozin and Aymalin (giluritmal, tahmalin) reduce the permeability of cell membranes for sodium, potassium and partly for calcium, which is accompanied by inhibition of spontaneous cell depolarization, automatism of ectopic foci, conduction, as well as the return and circulation of excitation in the heart. These drugs belong to class IA antiarrhythmics.

A certain result is given by the appointment of amiodarone (cordarone), which has a blocking effect on α- and β-receptors in the heart and a membrane-stabilizing effect with inhibition of repolarization. As a result, the refractory period in the conducting pathways increases and the activity of heterotopic foci of excitation is inhibited. But cordarone has a large number of side effects and is currently used less often in childhood. The drug is prescribed orally (tablets of 0.2 g) at the rate of 5-10 mg / kg / day individually. In the absence of a change in the general condition, asymptomatic ventricular extrasystoles are usually not life-threatening and do not require antiarrhythmic therapy.

QUESTION N 51. Specify the expected effect of the introduction of calcium channel blockers for the relief of ventricular tachycardia:

1. relief of hemodynamic disorders

2. improvement of cerebral circulation

3. fatal outcome

Correct answer: 3

With the introduction of calcium channel blockers, such as verapamil or nifedipine, children with ventricular tachycardia are at a high risk of developing uncontrolled arterial hypotension with a fatal outcome. It is for this type of heart rhythm disturbance that severe hemodynamic changes are characteristic, expressed by a drop in blood pressure. The main action of calcium channel blockers is aimed at reducing the automatism of the sinus and atrioventricular nodes after a temporary period of their reflex activation due to a decrease in blood pressure due to the effect of these drugs on the smooth muscles of arterioles (especially when using nifedipine). Calcium channel blockers have no effect on reducing the automatism of the ventricular myocardium. Thus, their use in patients with ventricular tachycardia is accompanied by the development of only negative effects.

QUESTION N 52. If a child with loss of consciousness has bradycardia of 40 bpm, the PP interval is constant on the ECG, and the PR varies, then this is:

1. sinus bradycardia

2. atrioventricular block

3. sinoauricular block

4. sports heart syndrome

Correct answer: 2

If a child with loss of consciousness has bradycardia (40 beats / min), on the ECG the PP interval is constant, and the PR changes, then this reflects atrioventricular blockade, which caused the development of the Morgagni-Adams-Stokes syndrome clinic

QUESTION N 53. Emergency treatment when intraventricular blockade is detected on the ECG in children:

1. mandatory at the prehospital stage

2. not carried out

Correct answer: 2

Emergency treatment when intraventricular blockade is detected on the ECG at the prehospital stage is not carried out.

QUESTION N 54. With bradyarrhythmia and asystolic form of the Morgagni-Adams-Stokes syndrome, all are used, except:

1. external heart massage

2. atropine

3. adrenaline

4. Lidocaine

5. pacing

Correct answer: 4

In case of bradycardia with impaired peripheral circulation, cardiopulmonary resuscitation is performed before the administration of drugs. Against the background of CPR, a 0.1% solution of atropine 20 μg / kg is injected intravenously, or orciprenaline (alupent, asthmapent) 0.5-1 ml, or a 0.5% solution of isoprenaline (izadrin, isoproterenol) microstream 0.1- 1 mcg / kg / min, at an older age - from 2 to 10 mcg / min; with insufficient effectiveness of drug therapy, transesophageal, external percutaneous or intravenous

cardiac pacing under ECG control; 0.1% adrenaline solution 10 mcg/kg, used during CPR.

QUESTION N 55. The absence of an increase in the rhythm after the administration of atropine in a child with bradycardia may indicate:

1. autonomic dysfunction syndrome

2. functional heart block

3. sick sinus syndrome

Correct answer: 3

With autonomic (vagal) dysfunction of the sinus node, the rhythm in response to a change in body position (transition from a horizontal to a vertical position), the introduction of atropine leads to an increase in rit. With weakness of the sinus node of organic origin (dystrophic, ischemic changes in the myocardium in the area of ​​the sinus node), there is no increase in heart rate in the clino-orthostatic test and during the atropine test.

QUESTION N 56. Transportation of a child with bradyarrhythmia is carried out:

1. in a horizontal position on the back

2. reclining

3. on the stomach

4. upright

5. horizontally on the back with a raised foot end

Correct answer: 1

Transportation of a child with bradyarrhythmia is carried out in a horizontal position on the back.

QUESTION N 57. Sinus bradycardia can be caused by all of the following factors, except:

1. increased intracranial pressure

2. myxedema

3. digoxin

4. nifedipine

5. severe hyperbilirubinemia

Correct answer: 4

Taking nifedipine in children with intact sympathetic and parasympathetic nervous regulation will initially be accompanied by the development of reflex tachycardia due to a decrease in blood pressure and stimulation of the sinus node. At high doses of calcium channel blockers, bradycardia develops. On the contrary, an increase in intracranial pressure, hypothyroidism, the toxic effect of indirect bilirubin, as well as the intake of cardiac glycosides due to changes in general metabolism, increased tone n. vagus and a direct effect on the cells of the sinus node, with a decrease in its automatism, are accompanied by bradycardia.

QUESTION N 58. In the emergency treatment of bradyarrhythmias, all methods are used, except:

1. emergency cardioversion

2. temporary pacing

3. in / in the introduction of atropine

* Recommended by experts from the American Heart Association (AHA).
** Recommended by AAS experts for absolute (heart rate less than 60 bpm) or relative (heart rate slower than expected) bradycardia
Electrical activity without pulse is diagnosed in cases of absence of pulsation in large arteries on palpation in combination with the presence of electrical activity of the heart, other than ventricular tachycardia and ventricular fibrillation. Its appearance indicates a pronounced dysfunction of the contractile myocardium or the conduction system of the heart.

Types of electrical activity of the heart

With narrow ventricular complexes:
. electromechanical dissociation (organized electrical activity in the absence of mechanical contraction of the myocardium);
. pseudoelectromechanical dissociation (organized electrical activity with very weak mechanical activity of the myocardium, detected only by special methods).
With wide ventricular complexes:
. idioventricular rhythms;
. ventricular escape rhythms;
. bradiasystolic rhythms;
. idioventricular rhythms after electrical defibrillation.

The basis of the treatment of electrical activity of the heart without a pulse is the earliest possible identification and elimination of specific causes.
Non-specific treatment of pulseless electrical activity:

Carry out artificial ventilation of the lungs in hyperventilation mode;
. periodically inject epinephrine (in the absence of pulsation in large arteries after a dose of 1 mg, discuss the advisability of using a higher dose);
. use atropine for bradycardia;
. if hypovolemia is suspected, start intravenous fluid infusion (eg, 250–500 mL of normal saline over 20 minutes);
. the use of calcium salts and alkalization of the blood in all patients is not recommended, except for specific cases (hyperkalemia, decreased blood calcium levels, an overdose of calcium antagonists, acidosis, prolonged cardiopulmonary resuscitation).
Interventions in the presence of blood flow detected by Doppler ultrasound of the vessels (pseudo-electromechanical dissociation): . increase the volume of circulating blood, infuse norepinephrine, dopamine, or combine these three methods (treatment tactics, as in severe hypotension, when systolic blood pressure is below 70 mm Hg. Art.);
. possible benefit from early initiation of transcutaneous pacing.
The value of detecting electrical activity without a pulse for the prognosis of the disease:

Indicates a poor prognosis of the disease, unless it is due to potentially reversible causes or is a transient phenomenon during cardiac arrest;
. wide-complex electrical activity is usually the result of severe damage to the heart muscle and represents the last electrical activity of a dying myocardium, unless it occurs due to hyperkalemia, hypothermia, hypoxia, acidosis, drug overdose, and other non-cardiac causes.

Introduction
In children, cardiac arrest develops as:

• Hypoxic/Asphyxic Cardiac Arrest
• Sudden cardiac arrest

Hypoxic/Asphyxic Cardiac Arrest
Although the term asphyxia is erroneously confused with suffocation, it refers to a condition resulting in a lack of oxygen in the tissues. This variant of cardiac arrest may be called hypoxic arrest, but the term asphyxial arrest has been widely used for many years. Asphyxia is the most common pathophysiological mechanism of cardiac arrest in infants and children up to adolescence. This is an extreme degree of tissue hypoxia and acidosis that develops with shock, respiratory, or heart failure. Regardless of the nature of the initial disease, the progression of the pathological process leads to the development of cardiopulmonary insufficiency, preceding asphyxial cardiac arrest (Figure 1).
PALS courses emphasize the importance of recognizing and treating respiratory distress, respiratory failure, and shock before the development of cardiopulmonary failure and cardiac arrest. Early diagnosis and treatment are critical to saving the life of a child with a severe illness or injury.
Sudden cardiac arrest
Sudden cardiac arrest is rare in children. It is most often associated with arrhythmias, especially VF or pulseless VT. Predisposing factors for sudden cardiac arrest include:

• Hypertrophic cardiomyopathy
• Abnormal origin of the coronary artery (from the pulmonary artery)
• Long QT syndrome
• Myocarditis
• Drug or drug poisoning (eg, digoxin, ephedrine, cocaine)
• Concussion of the heart (Commotio cordis) with a sharp blow to the chest

Primary prevention of selected episodes of sudden cardiac arrest is possible with cardiac screening (eg, for long QT syndrome) and treatment of predisposing conditions (eg, myocarditis, abnormal origin of a coronary artery). With the development of sudden cardiac arrest, the main event aimed at preventing death is timely and effective resuscitation. Timely assistance to children with sudden cardiac arrest will be possible only by informing coaches, parents and the general public about the possibility of developing sudden cardiac arrest in childhood. Only if the cardiac arrest occurs in the presence of trained bystanders can prompt assistance be provided with activation of the Emergency Response System (ERS), high quality CPR, and use of an automated external defibrillator (AED) as soon as available.
Ways of development of cardiac arrest

Figure 1. Ways of development of cardiac arrest.

Causes of cardiac arrest
The causes of cardiac arrest in children are different depending on age, state of health, as well as the place of development of events, namely:

• outside the hospital
• In the hospital

In infants and children, most out-of-hospital cardiac arrests occur at or near the home. Trauma is the leading cause of death in children over 6 months of age and adolescents. Causes of cardiac arrest in trauma include airway obstruction, tension pneumothorax, hemorrhagic shock, and severe traumatic brain injury. In infants under 6 months of age, the leading cause of death is sudden infant death syndrome (SIDS). In recent years, the incidence of SIDS has decreased due to the "sleep on back" campaign, which instructs parents to put their babies to sleep in the supine position.
The most common immediate causes of cardiac arrest in children are respiratory failure and hypotension. Arrhythmia is a less common cause.
Figure 2 shows common causes of in-hospital and out-of-hospital cardiac arrest, categorized by underlying respiratory, shock-related, or sudden cardiac events.


Figure 2 Causes of cardiac arrest in children.

Diagnosis of cardiopulmonary insufficiency
Regardless of the nature of the initial event or disease, cardiac arrest in children with respiratory distress, respiratory failure, or shock is preceded by the development of cardiopulmonary failure. Cardiopulmonary failure is defined as a combination of respiratory failure and shock (usually hypotensive). It is characterized by inadequate oxygenation, ventilation, and tissue perfusion. Clinical manifestations of cardiopulmonary failure are cyanosis, agonal sighs, or irregular breathing, and bradycardia. Cardiac arrest in a child with cardiopulmonary failure can develop within minutes. With the development of cardiopulmonary insufficiency in a child, it is no longer easy to reverse the pathological process.
You must promptly recognize and treat cardiopulmonary failure before it leads to cardiac arrest. Using the initial assessment algorithm, look for signs of cardiopulmonary failure, which may present with some or all of the following symptoms:

	Symptoms
A - airway patency	Due to depression of consciousness, obstruction of the upper respiratory tract is possible
B - breath	Bradypnea (i.e. low breathing rate) Irregular, inefficient breathing (weakening of breath sounds or agonal sighs)
C - circulation	Bradycardia Delayed capillary refill (usually >5 seconds) Central pulse weak No peripheral pulse Hypotension (usually) cold extremities Marbling or cyanosis of the skin
D - neurological examination	Decreased level of consciousness
E - complete examination of the patient	Postponed until the life-threatening condition is resolved

Diagnosis of Cardiac Arrest Introduction
Cardiac arrest is diagnosed when:

• Absence of signs of breathing and circulation (immobility, lack of breathing and response to artificial breaths during resuscitation, lack of pulse)
• The appearance on the monitor of the heart rate associated with cardiac arrest (Important: the connection of the monitor is not necessary for the diagnosis of cardiac arrest)

Clinical signs
When using the algorithm for the initial assessment of the state, cardiac arrest is determined by the following signs:

There is no pulse in children with cardiac arrest. According to studies, medical professionals are wrong about 35% of the time when they try to determine the presence or absence of a pulse. When a reliable measurement of the pulse is difficult, the absence of other clinical signs, including:

• Breathing (agonal sighs are not adequate breathing)
• Movement in response to stimulation (eg, in response to rescue breaths)

Rhythm in cardiac arrest
Cardiac arrest is associated with one of the following heart rhythms, also known as cardiac arrest rhythms:

• Asystole
• Electrical activity without pulse; the rhythm is most often slow, but may be accelerated or at a normal rate
• Ventricular fibrillation (VF)
• Ventricular tachycardia (VT) without pulse (including torsades de pointes)

Asystole and pulseless electrical activity are the most frequently reported rhythms at baseline in children with both in-hospital and out-of-hospital cardiac arrest, especially those under 12 years of age. The development of asystole may be preceded by bradycardia with narrow QRS complexes, worsening with decreasing rate, widening of the QRS, and disappearance of the pulse (pulseless electrical activity). VF and pulseless VT are more common with sudden collapse in a child.
Asystole
Asystole is the arrest of cardiac activity with the disappearance of bioelectrical activity, which is manifested by a straight (flat) line on the ECG (Figure 3). The causes of asystole and pulseless electrical activity are conditions that lead to the development of hypoxia and acidosis, such as drowning, hypothermia, sepsis, or poisoning (sedative, hypnotic, narcotic drugs).
Asystole on the monitor must be confirmed clinically by determining the child's unconsciousness, breathing and pulse, as the appearance of a "straight line" on the ECG can also be caused by the disconnection of the ECG electrode.

Figure 3. An agonal rhythm turning into asystole.

Electrical activity without pulse
Pulseless electrical activity is any organized electrical activity observed on an ECG tape or monitor screen in the absence of a pulse in a patient. VF, VT, and asystole are excluded from this definition. Although aortic pulsation can be detected on Doppler examination, the central pulse is not detected in a patient with pulseless electrical activity.
Pulseless electrical activity may be caused by reversible conditions such as severe hypovolemia or cardiac tamponade. Treatment of pulseless electrical activity can be successful if the underlying condition is quickly resolved. If it is not possible to quickly establish and eliminate the cause of electrical activity without a pulse, the rhythm will worsen to asystole. Potentially reversible causes of cardiac arrest (including pulseless electrical activity) are listed later in this chapter.
The ECG may show normal or wide QRS complexes or other abnormalities:

• Low amplitude or high amplitude T waves
• Prolonged PR and QT intervals
• AV dissociation or complete AV block

When monitoring heart rate, note the dynamics of heart rate and the width of the QRS complexes.
The pattern of the ECG may indicate the etiology of cardiac arrest. In recent onset disorders such as severe hypovolemia (bleeding), massive pulmonary embolism, tension pneumothorax, or cardiac tamponade, QRS complexes may initially be normal. Wide QRS complexes, slow rhythm with EMD are more often observed with prolonged existence of disorders, especially those characterized by severe tissue hypoxia and acidosis.
ventricular fibrillation
VF is one of the rhythms that cause circulatory arrest. During VF, an unorganized rhythm is recorded, reflecting the chaotic contraction of individual groups of muscle fibers of the ventricles (Figure 4). Electrical activity is chaotic. The heart "trembles" and does not pump blood.
VF often develops after a short period of VT. Primary VF is rare in children. Studies of cardiac arrest in children have shown that VF was the initially recorded rhythm in

1. 15% of out-of-hospital and 10% of cases of in-hospital cardiac arrest. However, the overall prevalence may be higher because the VF that caused the cardiac arrest may worsen to asystole before rhythm recording begins. During resuscitation during cardiac arrest in children in the hospital, VF develops in approximately 25% of cases.

Out-of-hospital causes of VF in children include diseases of the cardiovascular system, poisoning, exposure to electric current or lightning, drowning, and trauma.
Patients with VF or pulseless VT as baseline have a better survival rate in circulatory arrest than patients with asystole or EMD. Rapid identification and treatment of VF (i.e., CPR and defibrillation) improves outcome.

A

IN
Figure 4. Ventricular fibrillation. A - Large-wave VF. High-amplitude non-rhythmic waves of various sizes and shapes reflect the chaotic electrical activity of the ventricles. P, T waves and ORS complexes are not defined. C - Small-wave VF. The electrical activity is reduced compared to the previous (A) ECG tape.

Ventricular tachycardia without pulse
Pulseless VT is one of the circulatory arrest-inducing rhythms that, unlike VF, is characterized by organized, wide QRS complexes (Figure 5A). Almost any cause of VT can lead to the disappearance of the pulse. See chapter 6 for more information.
Pulseless VT is treated differently than pulsed VT. Treatment of pulseless VT is the same as for VF and is given in the Treatment Algorithm for Circulatory Arrest in Children.
Torsades de Pointes
Pulseless VT can be monomorphic (the QRS complexes are the same shape) or polymorphic (the shape of the QRS complexes varies). Torsades de pointes (pirouette tachycardia) is a peculiar form of polymorphic VT, which is characterized by a change in the polarity and amplitude of the QRS complexes, which seem to wrap around the isoelectric line (Figure 5B). Torsades de pointes may occur in conditions associated with QT prolongation, including congenital disorders and drug toxicity. See chapter 6 for more information.

A

IN
Figure 5. Ventricular tachycardia. A - VT in a child with muscular dystrophy and established cardiomyopathy. The ventricular rate is fast and regular at a rate of 158/min (greater than the VT minimum heart rate of 120/min). The QRS complexes are wide (more than 0.08 sec), there are no signs of atrial depolarization. B - Torsades de pointes in a child with hypomagnesemia.

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1 80 O.L. BOQERIA, T.N. KANAMETOV, 2015 ANNALS OF ARHYTHMOLOGY, 2015 UDC DOI: /annaritmol ELECTRICAL ACTIVITY WITHOUT PULSE Article type: lecture by O.L. Bokeria, T.N. Kanametov FGBNU "Scientific Center for Cardiovascular Surgery named after A.I. A.N. Bakuleva” (Director, Academician of the Russian Academy of Sciences and Russian Academy of Medical Sciences L.A. Bokeria); Rublevskoe shosse, 135, Moscow, Russian Federation Bokeriya Olga Leonidovna, Dr. med. Sciences, Professor, Ch. scientific collaborator, deputy department head; Kanametov Teimuraz Nartshaovich, post-graduate student, cardiologist; Pulseless electrical activity (PEAP) is a fairly common mechanism for cardiac arrest. The causes of EALD are extremely diverse, respectively, the treatment of a particular condition provides for extremely accurate diagnosis, since a misunderstanding of the situation can lead to a loss of time and the adequacy of the approach to treatment. In case of suspicion of EALD, it is necessary to strictly follow the protocol for the provision of cardiopulmonary resuscitation and examination (determination of the heart rhythm, pH-metry, pulse oximetry, echocardiography at the patient's bedside, etc.). In the future, etiotropic treatment is required (pericardiocentesis, inotropic, anticholinergic and oxygen therapy, correction of the acid-base state, etc.). After the patient exits the state of electrical activity without a pulse, strict monitoring of all vital signs of the body is necessary. In the case of inpatient observation of patients with a high risk of EALD, preventive measures should be taken (balance control, prevention of deep vein thrombosis, appropriate drug therapy). Key words: pulseless electrical activity, diagnosis, treatment. PULSELESS ELECTRICAL ACTIVITY O.L. Bockeria, T.N. Kanametov A.N. Bakulev Scientific Center for Cardiovascular Surgery; Rublevskoe shosse, 135, Moscow, Russian Federation Bockeria Ol "ga Leonidovna, MD, PhD, DSc, Professor, Chief Research Associate, Deputy Chief of Department; Kanametov Teymuraz Nartshaovich, MD, Postgraduate, Cardiologist; The pulseless electrical activity is one of the frequent mechanisms of cardiac arrest. patients in whom the pulseless electrical activity is suspected the protocol for cardiopulmonary resuscitation and examination should be strictly followed (determination of the heart rhythm, ph-metry, pulseoximetry, bedside EchoCG, etc. ). Further ethiotropic treatment should be initiated (pericardiocentesis, inotropic, anticholinergic therapy and oxygenation, correction of acid-base status, etc.). The patients require strict monitoring of all vital signs of an organism after recovery from the pulseless electrical activity. For patients with a high risk of the pulseless electrical activity development appropriate preventive measures should be taken (balance control, prevention of deep vein thrombosis, appropriate drug therapy). Key words: pulseless electrical activity, diagnosis, treatment.

2 81 Introduction Pulseless electrical activity (PAPA) is a clinical condition characterized by the absence of consciousness and a palpable pulse while maintaining regular cardiac electrical activity. The term "electromechanical dissociation" was previously used to refer to electrical activity without a pulse. While the absence of ventricular electrical activity always implies the absence of ventricular contractile activity (asystole), the converse is not true. In other words, electrical activity is a necessary but not sufficient condition for mechanical work. In cardiac arrest, the presence of organized ventricular electrical activity is not necessarily accompanied by significant ventricular contractility. The concept of "significant" is used to describe the degree of contractile activity of the ventricle, sufficient to create a palpable pulse. The presence of EABP does not mean a state of rest of the muscle tissue. Patients may have weak ventricular contractions and a fixed pressure in the aorta (pseudoelectric activity without a pulse). True pulseless electrical activity is a condition in which there is no heartbeat in the presence of coordinated electrical activity. EABP includes a group of coordinated heart rhythms, including supraventricular (sinus versus non-sinus) and ventricular (accelerated idioventricular or escape) rhythms. The absence of a peripheral pulse should not be equated with EALD, as it may be a sign of severe peripheral vascular disease. Etiology Pulseless electrical activity occurs when significant cardiovascular, respiratory, or metabolic disturbances result in the inability of the heart muscle to contract with sufficient force in response to electrical depolarization. EALD is always caused by profound cardiovascular injury (eg, due to severe prolonged hypoxia, acidosis, extreme hypovolemia, or pulmonary embolism that restricts blood flow). The above conditions initially lead to a significant decrease in the force of contractions of the heart, which is usually aggravated by increased acidosis, hypoxia, and an increase in vagal tone. Violation of the inotropic properties of the heart muscle leads to insufficient mechanical activity in the presence of adequate electrical activity. This event leads to the closing of a vicious circle, which is the reason for the conversion of the rhythm and the subsequent death of the patient. Transient occlusions of the coronary arteries usually do not cause pulseless electrical activity, provided that severe hypotension and severe arrhythmias do not occur. Hypoxia secondary to respiratory failure is probably the most common cause of EALD, as respiratory failure occurs in 40% to 50% of cases. Situations that cause abrupt changes in preload, afterload, or contractility also often result in pulseless electrical activity. Antipsychotic drug use has been found to be a significant and independent predictor of pulseless electrical activity. Reduced preload Efficient contraction requires optimal length (ie, pretension) of the cardiac sarcomere. If this distension cannot be achieved due to volume loss or pulmonary embolism (resulting in decreased venous return to the left atrium), the left ventricle is unable to produce enough pressure to overcome its own afterload. Volume loss leading to EALD most often occurs in cases of severe traumatic injury. In such situations, rapid blood loss and subsequent hypovolemia can deplete cardiovascular compensatory mechanisms, resulting in pulseless electrical activity. Cardiac tamponade can also lead to decreased ventricular filling.

3 82 Increased afterload Afterload is inversely proportional to cardiac output. A significant increase in afterload causes a decrease in cardiac output. However, this mechanism is rarely responsible for the development of pulseless electrical activity. Reduced contractility Optimal myocardial contractility depends on optimal preload pressure, afterload pressure, and the presence and availability of inotropic substances (eg, epinephrine, norepinephrine, or calcium). The entry of calcium into the cell and its binding to troponin C is essential for the implementation of cardiac contraction. If calcium intake is not possible (for example, with an overdose of calcium channel blockers) or if the affinity of calcium for troponin C decreases (as in conditions of hypoxia), contractility suffers. Depletion of intracellular stores of adenosine triphosphate (ATP) causes an increase in adenosine diphosphate (ADP), which can bind calcium, further reducing energy reserves. Excess intracellular calcium can lead to reperfusion injury, causing severe damage to intracellular structures, predominantly mitochondria. Additional etiological factors Pulseless electrical activity can be classified according to a number of criteria. While most classifications contain all possible causes leading to EALD, this tool is not suitable for practical use in the treatment of patients. The American Heart Association (AHA) and the European Resuscitation Council (ERC) recommend the use of mnemonics "Hs" (in the Russian version "G") and "Ts" (in the Russian version "T"): hypovolemia; hypoxia; hydrogen ions (hydrogen ions) (acidosis); hypokalemia / hyperkalemia; hypoglycemia; hypothermia; toxins; cardiac tamponade; tension pneumothorax; thrombosis (coronary or pulmonary); injury. The above list of causes does not provide any clues as to the frequency or reversibility of each etiological factor. However, it can be useful when it comes to the need for a quick decision. N.A. Desbiens proposed a more practical "3 and 3" rule that makes it easy to reproduce the most common correctable causes of pulseless electrical activity. The author distributes the causes into three main groups: 1) severe hypovolemia; 2) violation of the pumping function; 3) circulatory disorders. And the main causes of circulatory disorders, N.A. Desbiens names the following three conditions: 1) tense pneumothorax; 2) cardiac tamponade; 3) massive pulmonary embolism. Pumping dysfunction is the result of a massive myocardial infarction with rupture of the heart muscle and severe heart failure or without them. Massive traumatic lesions can cause hypovolemia, tension pneumothorax, or cardiac tamponade. Metabolic disorders (acidosis, hyperkalemia, hypokalemia), although not initiating pulseless electrical activity, are often contributing factors. An overdose of drugs (tricyclic antidepressants, cardiac glycosides, calcium channel blockers, and beta-blockers) or toxins is also sometimes the cause of EALD. Hypothermia should be considered in the appropriate clinical setting of community-acquired pulseless electrical activity. Pulseless postdefibrillation electrical activity is characterized by the presence of organized electrical activity that occurs immediately after electrical cardioversion in the absence of a perceptible impulse. Pulseless postdefibrillation electrical activity may have a better prognosis than ongoing ventricular fibrillation. The probability of spontaneous appearance of a pulse is

4 83 juice, and cardiopulmonary resuscitation should be continued for 1 min to facilitate spontaneous recovery of parameters. Epidemiology In Russia, the contribution of cardiovascular diseases to mortality from all causes is 57%, of which the share of coronary heart disease is 50.1%. According to official statistics, 40% of people die at working age. In 85% of cases, the mechanism of circulatory cessation is ventricular fibrillation. In other cases, it may be electrical activity without a pulse or asystole. The frequency of EALD varies according to different patient groups. This condition occurs in approximately 20% of cardiac arrests that occur outside the hospital. G. Raizes et al. found that pulseless electrical activity was reported in 68% of in-hospital deaths in patients with continuous monitoring and in 10% of total in-hospital mortality. As a result of the escalation of disease seen in patients admitted to the emergency department, pulseless electrical activity may be more likely in hospitalized patients. In addition, pulmonary embolism and conditions such as ventilator-induced lung injury (auto-PEEP positive end-expiratory pressure) are more common in these patients. Pulseless electrical activity is the first rhythm recorded in 32-37% of adults with in-hospital cardiac arrest. The use of beta-blockers and calcium channel blockers may increase the frequency of pulseless electromechanical activity due to the effect of these drugs on the contractility of the heart muscle. Demographics Women are more likely to develop pulseless electrical activity than men. The reasons for this trend remain unclear, but may relate to a different etiology of cardiac arrest. The average age of patients is 70 years. Elderly patients are more likely to develop EALD as a cause of cardiac arrest. The association of age with disease outcome has not been clearly established. However, in old age, a worse outcome is more expected. Prognosis The overall prognosis for patients with pulseless electrical activity is poor unless rapidly reversible causes are diagnosed and corrected. Experience shows that electrocardiographic (ECG) characteristics are associated with patient prognosis. The more abnormal the ECG pattern, the less likely the patient is to recover from pulseless electrical activity; patients with a wide QRS complex (greater than 0.2 s) have a very poor prognosis. It should be noted that patients with out-of-hospital EALD are more likely to recover from this pathological condition than those patients in whom pulseless electrical activity develops in a hospital. In one study, 98 out of 503 (19.5%) patients experienced community-acquired EALD. This difference is likely due to the different etiology and severity of the disease. Patients with out-of-hospital pulseless electrical activity most often have a reversible etiology (eg, hypothermia). Overall, pulseless electrical activity remains a poorly understood disease with a poor prognosis. The Oregon Sudden Cardiac Death Study, which included more than 1,000 patients with advanced EALD (versus those with ventricular fibrillation), indicates a significantly higher prevalence of syncope other than ventricular fibrillation. Potential links between syncope and manifestation of pulseless electrical activity in the future should be investigated. Mortality Overall mortality is high in those patients in whom pulseless electrical activity was the initial rhythm during cardiac arrest. In a study conducted by V.M. Nadkarni et al., only 11.2% of patients who were diagnosed

5 84 were diagnosed with EABP as an initially documented rhythm, survived until discharge from the hospital. In another study conducted by R.A. Meaney et al., patients with EALD as the initially documented rhythm had a lower survival rate at discharge than patients with ventricular fibrillation or ventricular tachycardia as the initially recorded rhythm. Given this bleak outlook, prompt initiation of extended cardiac support and identification of reversible causes are absolutely essential. Initiation of advanced cardiac support may improve outcomes if reversible causes of pulseless electrical activity are identified and corrected promptly. Anamnesis and physical examination Knowledge of the previous medical history allows you to quickly identify and correct reversible causes of the disease. For example, a malnourished patient who develops acute respiratory failure and then manifests pulseless electrical activity may be suffering from pulmonary embolism (PE). If an elderly woman develops EALD 2 to 5 days after myocardial infarction, cardiovascular pathology should be considered as an etiological factor (ie, heart rupture, recurrent myocardial infarction). Knowledge of the patient's medications is critical, as it allows prompt treatment to be started with suspected drug overdose. In the presence of pulseless electrical activity in the setting of a traumatic injury, bleeding (hypovolaemia), tension pneumothorax, and cardiac tamponade are the most likely causes. Patients with EALD, by definition, have no palpable pulse while maintaining organized electrical activity. Physical examination should focus on identifying reversible causes, e.g., bronchial breathing or unilateral absence of breathing indicate a tension pneumothorax, while normal findings on auscultation of the lungs and distended jugular veins indicate the presence of cardiac tamponade. Diagnosis Echocardiography Ultrasonography, particularly bedside echocardiography, can quickly identify reversible heart problems (eg, cardiac tamponade, tension pneumothorax, massive myocardial infarction, severe hypovolemia). The protocol proposed by A. Testa et al. uses the acronym PEA (pulseless electrical activity), which also corresponds to the initial letters of the main scanning locations of the lungs (Pulmonary), epigastrium (Epigastrium) and abdominal cavity (Abdominal), used to assess the causes of electrical activity without pulse. Echocardiography also identifies patients with weak heartbeats, who may be diagnosed with pseudo-PAEA. This group of patients benefits most from aggressive resuscitation tactics. Patients with pseudo-EAP may also have rapidly reversible causes (hypovolemia). Echocardiography is also invaluable in establishing right ventricular dilatation (with possible visualization of a thrombus) of pulmonary hypertension suggestive of pulmonary embolism, cardiorrhexis, and ventricular septal rupture. Differential diagnosis Differential diagnoses can be: accelerated idioventricular rhythm; acidosis; cardiac tamponade; drug overdose; hypokalemia; hypothermia; hypovolemia; hypoxia; myocardial ischemia; pulmonary embolism; fainting; tension pneumothorax; ventricular fibrillation. Features of treatment The development of the clinical picture usually contains useful information. For example, in previously intubated patients, tense

6 85 Pneumothorax and automatic positive end-expiratory pressure are more likely, while patients with prior myocardial infarction or congestive heart failure are more likely to have myocardial dysfunction. In patients on dialysis, hyperkalemia is considered as the etiological cause of EALD. Thermometry results should always be obtained if the patient is suspected of hypothermia. In such cases, resuscitation should be continued at least until the patient is completely rewarmed, since patient survival is possible even after prolonged resuscitation. It is necessary to measure the duration of the QRS complex due to its prognostic value. Patients with a QRS duration of less than 0.2 s have a better prognosis for survival, so they can be prescribed high doses of epinephrine. A sharp turn of the electrical axis of the heart to the right suggests a possible pulmonary embolism. Due to the urgent nature of the problem, the use of laboratory tests does not seem appropriate in the direct management of a patient with EALD. If data on arterial blood gases and serum electrolytes are readily available, information on pH, oxygenation, and serum potassium should be used. Evaluation of glucose levels may also be helpful. Invasive monitoring (eg, arterial line) may be established if this does not delay the provision of extended cardiac support. Setting up an arterial line facilitates the identification of patients with recorded (but very low) blood pressure. In such patients, the best result is observed with relatively aggressive resuscitation. A 12-lead ECG during resuscitation is difficult to record, but can be used to diagnose hyperkalemia (eg, spiked T-waves, transverse heart block, ventricular rate jogging) or acute myocardial infarction. Hypothermia, if not diagnosed by the time the ECG is taken, may be suspected in the presence of Osborne waves. With an overdose of certain drugs (for example, tricyclic antidepressants), the duration of the QT interval increases (see figure). Therapeutic Approach For patients with suspected pulseless electrical activity, the AHA Advanced Cardiovascular Life Support ACLS protocol, revised 2010. , recommends the following: start cardiopulmonary resuscitation; provide intravenous access; intubate the patient; correct hypoxia with 100% oxygen. 50 mm/s Electrocardiogram with electrical activity without pulse

7 86 Once the underlying parameters are stabilized, reversible causes of EALD should be sought and corrected, such as: hypovolemia; hypoxia; acidosis; hypokalemia / hyperkalemia; hypoglycemia; hypothermia; toxic injury (eg, tricyclic antidepressants, digoxin, calcium channel blockers, beta-blockers); cardiac tamponade; tension pneumothorax; massive pulmonary embolism; acute myocardial infarction. After identifying reversible causes, their immediate correction is necessary. This process includes needle decompression for tension pneumothorax, pericardiocentesis for cardiac tamponade, volumetric infusions, temperature correction, administration of thrombolytics, or surgical embolectomy for pulmonary embolism. Consultations Once the cause of EALD has been determined and the patient's condition has been stabilized, the patient can be consulted by the appropriate medical specialists. A consultation with a cardiac surgeon may be necessary for patients with massive pulmonary embolism to decide on an embolectomy. Patients with drug overdose after recovery of hemodynamic stability should be consulted at the toxicology department or local poison control center. Translation Some facilities may not be able to provide specialized care (eg, heart surgery, pulmonary embolectomy). After stabilization in these medical institutions, patients can be transferred to the third level centers for final treatment. Prevention The following measures may prevent some cases of nosocomial pulseless electrical activity: in patients on prolonged bed rest, prevention of deep vein thrombosis of the lower extremities; in patients on mechanical ventilation, careful monitoring to prevent the development of auto-peep; in patients with hypovolemia, aggressive treatment tactics, especially in patients with active bleeding. Drug Therapy Drug therapy used in cardiac recovery includes epinephrine, vasopressin, and atropine. Adrenaline should be administered at 1 mg intravenously every 3-5 minutes during the entire time the patient is in the state of EABP. The use of higher doses of epinephrine has been studied: this tactic does not increase survival or improve neurological outcomes in most patients. In special groups of patients, namely those with an overdose of beta-blockers and calcium channel blockers, it is possible to obtain good results when using high doses of epinephrine. IV/IO vasopressin can replace the first or second dose of epinephrine in patients with EALD. If the main rhythm is bradycardia (i.e. heart rate does not exceed 60 beats / min), accompanied by hypotension, then atropine should be administered (1 mg intravenously every 3 5 minutes to 3 mg). This will lead to the achievement of a total vagolytic dose, with an increase in which additional positive effects are not observed. It should be noted that atropine can cause pupillary dilation, so this reflex can no longer be used to assess neurological status. The introduction of sodium bicarbonate is possible only in patients with severe systemic acidosis, hyperkalemia or an overdose of tricyclic antidepressants. Routine administration of sodium bicarbonate is not recommended due to worsening of intracellular and intracerebral acidosis and lack of proven efficacy in reducing mortality. Thus, inotropic, anticholinergic, and alkalizing drugs are used to treat pulseless electrical activity.

8 87 Inotropic drugs Inotropic drugs increase central aortic pressure and counteract myocardial depression. Their main therapeutic effects are cardiac stimulation, bronchial wall smooth muscle relaxation, and skeletal muscle vasodilatation. Epinephrine (adrenaline) is an alpha agonist that results in increased peripheral vascular resistance and reversed peripheral vasodilation, systemic hypotension, and increased vascular permeability. The effects of epinephrine as a beta agonist include bronchodilation, a positive chronotropic effect on cardiac activity, and a positive inotropic effect. Anticholinergics Anticholinergics improve conduction through the atrioventricular node by reducing vagal tone by blocking muscarinic receptors. Atropine is used to treat bradyarrhythmias. Its action leads to an increase in heart rate due to the vagolytic effect, indirectly causing an increase in cardiac output. The total vagolytic dose is 2-3 mg; doses less than 0.5 mg may exacerbate bradycardia. Alkaline preparations Useful for alkalizing urine. Sodium bicarbonate is used only in cases where the patient is diagnosed with bicarbonate-sensitive acidosis, hyperkalemia, tricyclic antidepressant overdose, or phenobarbital. Routine use is not recommended. Surgical treatment Pericardiocentesis and emergency cardiac surgery can be life-saving procedures when properly identified. In severe cases, if the patient has suffered a chest injury, a thoracotomy may be performed, subject to appropriate experience. Immediate initiation of cardiopulmonary resuscitation may play a role in carefully selected patients. This maneuver requires experience and support materials. Determining the indication is of paramount importance because cardiopulmonary resuscitation should only be used in patients who have an easily reversible etiology of cardiac dysfunction. In an animal model, timely CPR was more likely to result in circulatory success than administration of high or standard doses of epinephrine. Pacing may result in the delivery of an electrical stimulus, which does not necessarily increase the rate of mechanical contractions. Thus, this procedure is not recommended as there is sufficient electrical activity. In the presence of pulseless electrical activity or low cardiac output syndrome, various types of temporary cardiovascular support (eg, intra-aortic balloon pumping, extracorporeal membrane oxygenation, ventricular assist device) may be used. Conclusion Pulseless electrical activity is a fairly common mechanism for cardiac arrest. The causes of EALD are extremely diverse, respectively, the approach to the treatment of a particular condition provides for extremely accurate diagnosis, since a misunderstanding of the situation can lead to a loss of time and the adequacy of the approach to treatment. In case of suspicion of EALD, it is necessary to strictly follow the protocol for the provision of cardiopulmonary resuscitation and examination (determination of the heart rhythm, pH-metry, pulse oximetry, EcoCG at the patient's bedside, etc.). In the future, etiotropic treatment is required (pericardiocentesis, inotropic, anticholinergic and oxygen therapy, correction of the acid-base state, etc.). After the patient exits the state of EABP, strict monitoring of all vital signs of the body is necessary. In the case of inpatient observation of patients who have a high risk of developing this condition, preventive measures should be taken (balance control, prevention of deep vein thrombosis, appropriate drug therapy). Since in most cases the cause of EALD is clear and identified

9 88 predisposing factors, it is possible to implement preventive measures in patients with a high risk of developing this condition. In addition, such patients should be under the dynamic supervision of cardiologists. References 1. Zilber A.P. Etudes of critical medicine. Book. 1. Critical care medicine: general problems. Petrozavodsk: Petrozavodsk University Press; Kuznetsova O.Yu., Danilevich E.Ya., Shalnev V.I., Gupo S.L. Sudden cardiac arrest. St. Petersburg: SPbMAPO Publishing House; Teodorescu C., Reinier K., Dervan C. et al. Factors associated with pulseless electric activity versus ventricular fibrillation: the Oregon sudden unexpected death study. circulation. 2010; 122 (21): Hutchings A.C., Darcy K.J., Cumberbatch G.L. Tension pneumothorax secondary to automatic mechanical compression decompression device. Emerg. Med. J. 2009; 26 (2): Steiger H.V., Rimbach K., Müller E., Breitkreutz R. Focused emergency echocardiography: lifesaving tool for a 14-year-old girl suffering out-ofhospital pulseless electrical activity arrest because of cardiac tamponade. Eur. J. Emerg. Med. 2009; 16 (2): Fuzaylov G., Woods B., Driscoll W. Documentation of resuscitation of an infant with pulseless electrical activity because of venous air embolism. paediatr. Anaesth. 2008; 18 (11): Youngquist S.T., Kaji A.H., Niemann J.T. Beta-blocker use and the changing epidemiology of out-of-hospital cardiac arrest rhythms. resuscitation. 2008; 76 (3): Hernandez C., Shuler K., Hannan H. et al. C.A.U.S.E.: Cardiac arrest ultra-sound exam a better approach to managing patients in primary non-arrhythmogenic cardiac arrest. resuscitation. 2008; 76(2): Hazinski M.F., Nolan J.P., Billi J.E. et al. Part 1: executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. circulation. 2010; 122 (16 Suppl. 2): S Hazinski M.F., Nadkarni V.M., Hickey R.W. et al. Major changes in the 2005 AHA Guidelines for CPR and ECC: reaching the tipping point for change. circulation. 2005; 112 (24 Suppl.): IV Desbiens N.A. Simplifying the diagnosis and management of pulseless electrical activity in adults: a qualitative review. Crit. Care Med. 2008; 36(2): Nichols R., Zawada E. A case study in therapeutic hypothermia treatment post-cardiac arrest in a 56-year-old male. S. D. Med. 2008; 61 (10): Golukhova E.Z., Gromova O.I., Merzlyakov V.Yu., Shumkov K.V., Bockeria L. A. Heart rate turbulence and brain natriuretic peptide as predictors of life-threatening arrhythmias in patients with coronary heart disease. Creative cardiology. 2013; 2: Raizes G., Wagner G.S., Hackel D.B. Instantaneous nonarrhythmic cardiac death in acute myocardial infarction. Am. J. Cardiol. 1977; 39 (1): Kotak D. Comment on Grmec et al.: A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with an increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. Int. J. Emerg. Med. 2009; 2 (1): Morrison L.J., Deakin C.D., Morley P.T., Callaway C.W., Kerber R.E., Kronick S.L. et al. Part 8: advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. circulation. 2010; 122 (16 Suppl. 2): S Nadkarni V.M., Larkin G.L., Peberdy M.A. et al. First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults. JAMA. 2006; 295(1): Meaney P.A., Nadkarni V.M., Kern K.B. et al. Rhythms and outcomes of adult in-hospital cardiac arrest. Crit. Care Med. 2010; 38(1): Wagner B.J., Yunker N.S. A pharmacological review of cardiac arrest. Plast. Surg. Nurs. 2014; 34(3): Testa A., Cibinel G.A., Portale G. et al. The proposal of an integrated ultrasonographic approach into the ALS algorithm for cardiac arrest: the PEA protocol. Eur. Rev. Med. Pharmacol. sci. 2010; 14 (2): Grmec S., Strnad M., Cander D., Mally S. A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. Int. J. Emerg. Med. 2008; 1 (4): References 1. Zil "ber A.P. Critical studies of medicine. Book 1. Critical care medicine: General issues. Petrozavodsk: Izdatel "stvo Petrozavodskogo universiteta; 1995 (in Russian). 2. Kuznetsova O.Yu., Danilevich E.Ya., Shal "nev V.I., Gupo S.L. A sudden cardiac arrest. Saint-Petersburg: Izdatel" stvo SPbMAPO; 1993 (in Russian). 3. Teodorescu C., Reinier K., Dervan C. et al. Factors associated with pulseless electric activity versus ventricular fibrillation: the Oregon sudden unexpected death study. circulation. 2010; 122 (21): Hutchings A.C., Darcy K.J., Cumberbatch G.L. Tension pneumothorax secondary to automatic mechanical compression decompression device. Emerg. Med. J. 2009; 26(2): Steiger H. V., Rimbach K., Müller E., Breitkreutz R. Focused emergency echocardiography: lifesaving tool for a 14-year-old girl suffering out-of-hospital pulseless electrical activity arrest because of cardiac tamponade. Eur. J. Emerg. Med. 2009; 16 (2): Fuzaylov G., Woods B., Driscoll W. Documentation of resuscitation of an infant with pulseless electrical activity because of venous air embolism. paediatr. Anaesth. 2008; 18 (11): Youngquist S.T., Kaji A.H., Niemann J.T. Beta-blocker use and the changing epidemiology of out-of-hospital cardiac arrest rhythms. resuscitation. 2008; 76 (3): Hernandez C., Shuler K., Hannan H. et al. C.A.U.S.E.: Cardiac arrest ultra-sound exam a better approach to managing patients in primary non-arrhythmogenic cardiac arrest. resuscitation. 2008; 76(2): Hazinski M.F., Nolan J.P., Billi J.E. et al. Part 1: executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. circulation. 2010; 122 (16 Suppl. 2): S Hazinski M.F., Nadkarni V.M., Hickey R.W. et al. Major changes in the 2005 AHA Guidelines for CPR and ECC: reaching the tipping point for change. circulation. 2005; 112 (24 Suppl.): IV Desbiens N.A. Simplifying the diagnosis and management of pulseless electrical activity in adults: a qualitative review. Crit. Care Med. 2008; 36(2): Nichols R., Zawada E. A case study in therapeutic hypothermia treatment post-cardiac arrest in a 56-year-old male. S. D. Med. 2008; 61 (10): Golukhova E.Z., Gromova O.I., Merzlyakov V.Yu., Shumkov K.V., Bockeria L.A. Heart rate turbulence and brain natriuretic peptide level as predictors for life-threatening arrhythmias in patients with coronary artery disease. Kreativnaya cardiologiya. 2013; 2: (in Russian). 14. Raizes G., Wagner G.S., Hackel D.B. Instantaneous nonarrhythmic cardiac death in acute myocardial infarction. Am. J. Cardiol. 1977; 39 (1): Kotak D. Comment on Grmec et al.: A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with an increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. Int. J. Emerg. Med. 2009; 2 (1): Morrison L.J., Deakin C.D., Morley P.T., Callaway C.W., Kerber R.E., Kronick S.L. et al. Part 8: advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. circulation. 2010; 122 (16 Suppl. 2): S Nadkarni V.M., Larkin G.L., Peberdy M.A. et al. First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults. JAMA. 2006; 295(1): Meaney P.A., Nadkarni V.M., Kern K.B. et al. Rhythms and outcomes of adult in-hospital cardiac arrest. Crit. Care Med. 2010; 38(1): Wagner B.J., Yunker N.S. A pharmacological review of cardiac arrest. Plast. Surg. Nurs. 2014; 34(3): Testa A., Cibinel G.A., Portale G. et al. The proposal of an integrated ultrasonographic approach into the ALS algorithm for cardiac arrest: the PEA protocol. Eur. Rev. Med. Pharmacol. sci. 2010; 14 (2): Grmec S., Strnad M., Cander D., Mally S. A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. Int. J. Emerg. Med. 2008; 1 (4): Received d. Signed for publication d.

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In this section, you will learn how to diagnose and treat cardiac arrest in children.

Introduction

Cardiac arrest occurs in the absence of effective cardiac arrest. Before starting specific therapy, it is necessary to carry out the main complex of resuscitation measures.

In this section, four types of arrhythmias accompanied by cardiac arrest will be presented:

2. Pulseless electrical activity (including electromechanical dissociation).
3. Ventricular fibrillation.
4. Pulseless form of ventricular tachycardia.

These four types of cardiac disorders can be grouped into two groups: those that do not require (non-shock) and those that require (shock) defibrillation (electrical shock). The algorithm for cardiac arrest therapy is shown in Figure 6.1.

Rhythm disturbances not requiring defibrillation

This group of disorders combines asystole and pulseless electrical activity.

Rice. 6.1. Resuscitation algorithm for cardiac arrest

Asystole is the most common arrhythmia accompanied by cardiac arrest in children, since the response of the child's heart to severe prolonged hypoxia and acidosis is progressive bradycardia leading to asystole.

ECG distinguishes asystole from ventricular fibrillation, ventricular tachycardia, and pulseless electrical activity. The electrocardiographic manifestation of ventricular asystole is a straight line; sometimes P-waves can be detected on the ECG. Check if this is an artifact, for example due to detachment of the monitor electrode or wire. Increase the ECG amplitude on the monitor.

Rice. 6.2. Asystole

Pulseless Electrical Activity (BEA)

BEA is characterized by the absence of a palpable pulse in the presence of recognizable complexes on the ECG. Treatment of BEA is the same as for asystole, and BEA is usually the pre-asystolic stage.

Sometimes BEA occurs due to identifiable and reversible causes. In children, it is most often associated with trauma. In this case, severe hypovolemia, tension pneumothorax, and pericardial tamponade may be the cause of BEA. BEA can also be observed with hypothermia and in patients with electrolyte imbalance, including hypocalcemia due to an overdose of calcium channel blockers. Less commonly in children, the cause of BEA is massive pulmonary embolism.

Rice. 6.3. Pulseless electrical activity