Differential diagnosis of cardiac arrhythmia
in сhildren.
Emergency aid in acute heart failure. Emergency assistance for paroxysmal disorders of rhythm and Morgagni-Adams-Stokes syndrome.
Cardiac arrhythmias (Greek arrhythmia is the lack rhythm) are
various functional disorders of automatism, excitability and conductivity of the myocardium, often resulting in failure of normal sequence, or heart rate.
Etiology
Cardiac arrhythmias may be caused by:
– functional disorders (psychogenic, reflex)
– organic disorders (heart disease, cardiomyopathy,
myocardiodystrophy, carditis, etc.)
– toxic disorders (eg, an overdose of drugs digitalis)
-hormonal disorders (eg, imbalance of hormones thyroid)
– electrolyte disturbances (eg, changes in the level of potassium in the blood)
– mechanical disorders (surgery, trauma)
– congenital disorders (eg, WPW syndrome).
Types of Arrhythmia in Children
There are many different kinds of abnormal heart rhythms. If an abnormal rhythm occurs, it’s important to find out what kind it is. Treatment recommendations depend on its type. Arrhythmias can cause the heart rate to be irregular, fast or slow. Fast rhythms are called tachycardia. Slow ones are called bradycardia.
Causes:
Causes of fast heart rate (Tachycardia):
• Supraventricular Tachycardia
– Atrioventricular nodal reentrant tachycardia
– Atrioventricular reentrant tachycardia including WPW syndrome
– Others
• Ectopic atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• Ventricular tachycardia
• Ventricular fibrillation
Causes of slow heart rate (Bradycardia):
• Sick sinus syndrome
• Various degree of heart block
Premature atrial contraction (PAC) and premature ventricular
contraction (PVC)
· Tachycardia
· Supraventricular tachycardia (SVT)
· Wolff-Parkinson-White syndrome
· Ventricular tachycardia (VT)
· Bradycardia
· Sick sinus syndrome
· Complete heart block
ECG diagnostics
Premature beats or extra beats most often cause irregular heart rhythms. Those that start in the upper chambers (atria) are called premature atrial contractions or PACs. Premature ventricular contractions or PVCs start in the ventricles. If you’ve ever had the feeling that your heart “skipped a beat,” it was probably from this type of arrhythmia. The heart really doesn’t skip a beat. Instead, an extra beat comes sooner than normal. Then there’s usually a pause that causes the next beat to be more forceful. You felt this more-forceful beat.
Often the cause of VPBs is not known. They can happen even though you may have a normal, healthy heart.
Sometimes, something happens to make a part of the heart’s ventricle muscle electrically unstable, causing the extra heartbeat. The electrical instability can be caused by:
Ø a scar in the heart muscle
Ø too little oxygen getting to the muscle because of heart disease
Ø medicines such as pseudoephedrine
Ø a blow to the chest
Ø imbalance of electrolytes (body minerals) in the body.
An electrocardiogram (ECG) is the only test that can confirm a diagnosis of VPBs. The ECG records the electrical activity of your heart. A 24-hour tape recording of the ECG shows when you have VPBs. It also shows how many occurred. These recordings can help your healthcare provider decide on treatment.
Tachycardia
A fast heart rate is called tachycardia. The definition of “too fast” usually depends on the person’s age and physical activity. A newborn has tachycardia if the resting rate is more than 160 beats per minute. A teenager is considered to have tachycardia if the resting heart rate is more than 90 beats per minute. An exercising teenager may have a normal heart rate of up to 200 beats per minute.
Paroxismal tachycardia
Paroxismal tachycardia is the attacks of acute tachycardia (more than 150-180 per 1 minute), which arises up suddenly and lasts from a few seconds to a few hours. The reasons of paroxismal tachycardia are various: congenital pathology of the explorer system of heart (the WPW syndrome), organic heart diseases, neurovegetative disturbances of organism, acute infectious diseases etc. There is the ektopic nidus of excitation in some area of myocardium or explorer system, which sends the impulse of high- frequency and becomes the driver of cardiac rhythm. Acute increasing of cardiac contractions diminishes efficiency of separate paroxismal tachycardia, causes diminishment of percussion volume of heart and violation of blood circulation . Blood supply of organs, tissues and heart are diminished. It predetermines violation of exchange processes in myocardium. As a result of attack of paroxismal tachycardia there is coronal insufficiency and insufficiency of circulation of blood. Depending on localization of pathological nidus the supraventricular and abdominal forms of paroxismal tachycardia are distinguished.
Clinic. The attack of tachycardia begins suddenly. Children complain on the unpleasant feelings in the region of heart, squeezing pain in a breast, pain in a epigastrial area. Quite often the attack is accompanied by dizziness, vomit. Children often feel fear. Skin is pale, cyanosys appears sometimes, swelling and pulsation of neck veins are present. The signs of cardiac insufficiency occur with the long duration attack: cyanosys increases, the shortness of breath appears, enlargement of liver, oliguria, the edema. Pulse of the weak filling, frequency cardiac contractions arrives at 150-300 per 1 minute. Cardiac tones are increased, embriocardia. Arterial pressure is reduced.
Diagnostics of paroxismal tachycardia at the children of breast-feeding age is difficulte. The common state of child is severe, that is related to the signs of cardiac insufficiency. Quite often the attack is accompanied by pneumonia, myocarditis, fibroelastosis of heart and other pathology. The diagnosis and determination of form of paroxismal tachycardia is conducted by electrocardiography. The general electrocardiography criteria of paroxismal tachycardia are: outbreak and sudden end, absence of compensating pause, frequency of cardiac contractions more than 150 per 1 minute, presence of 3 and anymore group of extrasystols. In addition, for supraventricular paroxismal tachycardia characteristically are: presence of the unusual indent Р (at atria form) and its absence at a аrtrioventricular form, well-kept form of the QRS complex, duration of the QRS complex not more than 0,12 seconds. At abdominal paroxismal tachycardia always indent Р is absent, the QRS complex is deformed and extended (more than 0,12seconds),it is marked presence of аrtrioventricular dissociation.
This exercise electrocardiogram shows wide QRS tachycardia during exercise. The recovery ECG arly shows atrial flutter with variable conduction. The rest ECG probably represents atrial flutter with 2:1 conduction rather than sinus rhythm. Exercise testing helped establish this atrial arrhythmia.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 210.)
Severe sinus arrhythmia in a 15-year-old boy was detected by a Holter monitor during sleeping and waking (this tracing) hours. The patient also had severe sinus bradycardia with dizziness and syncope.
A permanent pacemaker was implanted, and the patient had no further symptoms.
Paper speed was 25 mm/s, and calibration was 1 mV/10 mm.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 255.)
An example of complete AV block. Note the lack of conduction to the ventricle of P waves occurring after the T wave.(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias.
Standard 12-lead electrocardiogram showing atrial flutter with classic “sawtooth” flutter waves in leads II, III, aVF, V<SB:0.039>1</SS>, V<SB:0.039>2</SS>, and V<SB:0.039>3</SS>.
There is 4:1 atrioventricular conduction. (From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 334.)
Standard 12-lead electrocardiogram showing atrial flutter with undulating P waves in all leads.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 335.)
Atrial flutter with 1:1 atrioventricular conduction. <IT+>Top panel:<IT-> Surface electrocardiogram (ECG).
<IT+>Bottom panel:<IT-> Atrial electrogram (AEG). Small arrows show the atrial activity at approximately 300 bpm; the atrial polarity changes midway through the tracing; initially the atrial deflections are positive, and later they are negative. Large arrows point to ventricular activation.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 346.)
IT+>A,<IT-> Sinus tachycardia, rate 200–230/min. P waves are clearly visible, with normal P wave axis. <IT+>B,<IT-> Supraventricular tachyarrhythmia, rate 230/min. P waves are clearly visible with an abnormal P wave axis. (From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p393.)
Atrial flutter with varying second-degree AV block.
Ventricular tachycardia alternating with sinus rhythm.
Arrows mark fusion complexes.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 393.)
Sinus tachycardia is a normal increase in the heart rate. It occurs with fever, excitement and exercise. No treatment is needed. Rarely, disease, such as anemia (low blood counts) or increased thyroid activity can cause this fast heart rate. In these cases, when the disease is treated, the tachycardia goes away.
Supraventricular tachycardia (SVT)
The most common abnormal tachycardia in children is supraventricular tachycardia (SVT). It’s also called paroxysmal atrial tachycardia (PAT) or paroxysmal supraventricular tachycardia (PSVT). The fast heart rate involves both the heart’s upper and lower chambers. This isn’t a life-threatening problem for most children and adolescents. Treatment is only considered if episodes are prolonged or frequent. For many infants, SVT is a time-limited problem. Treatment with medications often stops after six to 12 months.
SVT may occur in very young infants with otherwise-normal hearts. The heart rate is usually more than 220 beats a minute. Infants with an SVT episode may breathe faster thaormal and seem fussy or sleepier than usual. This situation must be diagnosed and treated to return the heart rate to normal. Once the rhythm is normal, medication usually can prevent future episodes.
Sometimes SVT can be detected while a baby is still in the womb. Then the mother may take medications to slow her baby’s heart rate. If an older infant or child has SVT, the child may be aware of the rapid heart rate. This may be associated with palpitations, dizziness, lightheadedness, chest discomfort, upset stomach or weakness. Some children can learn ways to slow down their heart rate. Straining — such as closing the nose and mouth and trying to breathe out — may be successful. This is called a Valsalva maneuver.
Older children are more likely to have more episodes of tachycardia. They’re more likely to need prolonged treatment. They also may need more diagnostic tests. It’s unusual for episodes of SVT to keep a child from enjoying normal activities. Most children who have episodes of tachycardia stay well even though they may need to keep taking medicine.
Treatment
Treating SVT usually has two parts. The first is stopping a current episode; the second is preventing recurrences. The approach to preventing recurrences depends on the child’s age. In some cases — especially those of infants — the child may need to enter the hospital for treatment and special studies.
Vagal Maneuvers
ü Gagging
ü Quickly drinking ice-cold water
ü Straining by sealing the nose and closing your mouth while trying to breath out hard
ü Using tension by pushing hard against a wall and holding your breath
ü Headstand
ü Diving reflex (immersion of face into ice cold water)
ü Placing an ice cold cloth on the face
Sometimes simple procedures can stop a fast heart rhythm. Gagging or putting ice on the face are examples. Child’s doctor can explain this in more detail. At other times intravenous medications may be needed to control or stop the tachycardia. Another way to stop SVT is to place a small catheter (a thin, flexible tube) through the nostril into the esophagus. A small amount of electricity is sent through this catheter to stop the SVT. On rare occasions doctors stop SVT by giving a small electrical shock to the chest wall. This is called electrical counter shock or cardioversion. A sedative or anesthetic is given before this procedure.
Wolff-Parkinson-White syndrome
Wolff-Parkinson-White (WPW) syndrome is a condition where the heart ventricles become pre-excited. In the normal heart beat, first the sinoatrial (SA) node signals the atria of the the heart to contract, This is then followed by the atrioventricular (AV) node signalling the heart ventricles to contract. The electrical signal for this contraction travels from the SA node to the AV node via the electrical pathway of the bundle of its.
In Wolff-Parkinson-White (WPW) syndrome another additional electrical pathway called the bundle of
If an abnormal conduction pathway runs between the atria and ventricles, the electrical signal may arrive at the ventricles sooner thaormal. This condition is called Wolff-Parkinson-White syndrome (WPW syndrome). It’s named after the three people who first described it. WPW syndrome is recognized by certain changes on the ECG. Many people with WPW syndrome don’t have symptoms but are at risk of sudden cardiac arrest.
Recognition of WPW on the ECG
Not all patients with WPW will present with ECG changes, but the ones that do are at the highest risk for sudden cardiac arrest.
ECG characteristics:
· Very fast rate, SVT, or A-fib/flutter patients may have much faster rates thaormal (well normal for an accelerated rhythm)
· Delta wave
· Shortened PR-Interval
· Fast broad and irregular rhythm that isn’t torsades
Wolff-Parkinson-White syndrome, type A, with the most positive delta wave being at surface lead V<SB:0.039>1</SS>. Abnormal depolarization can also be seen well on leads II and aVF.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 363.)
Classic changes of ECG at WPW syndrome
Often medication can improve this condition. Sometimes, though, such treatment doesn’t work. Then a child will need more tests. Eliminating the abnormal pathway by passing energy through a catheter may be needed. Surgery is another option. The most common treatment options for Wolff-Parkinson-White syndrome are medications and catheter radiofrequency ablation, a minimally-invasive procedure to remove the abnormal, extra electrical heart pathway. Rarely, open-heart surgery may be performed if patients have other heart conditions in addition to WPW syndrome.
The tip of the catheter burns tissue with radio waves. By burning tissue around the openings of the four pulmonary veins that empty into the left atrium, the procedure isolates cells that start the erratic electrical activity that leads to atrial fibrillation.
Catheter Ablation: (a) Radiofrequency Ablation: The catheter tip delivers the bursts of high-energy waves that destroys the abnormal areas – Source: (Biosense), (b) Cryoablation using catheter based approach – Source: (CryoCath); It is required the tip to apply consistent contact pressure to the tissue to make the width and depth of the lesion predictable in both cases.
Cryo-ablation Catheter (CryoCath)
Ventricular tachycardia (VT)
Ventricular tachycardia (VT) is a fast heart rate that starts in the lower chambers (ventricles). This uncommon but potentially serious condition can threaten a child’s life. VT may result from serious heart disease; it usually requires prompt treatment. VT occasionally occurs in children with otherwise normal hearts. Often specialized tests, including an intracardiac electrophysiologic procedure, may be needed to evaluate the tachycardia and the effect of drug treatment. Some forms of VT may not need treatment.
Ventricular tachycardias arise from the major pumping chambers at the bottom of the heart. VT is a more serious rhythm problem because it often occurs in a setting of previous heart damage (e.g. a heart attack) and may be best managed with an implanted defibrillator.
Sometimes with VT, the heart is otherwise healthy and the abnormal rhythm arises from an abnormal trigger point. This trigger can often be localised and successfully ablated.
Normal Electrocardiogram (ECG).
ECG of a patient suffering ventricular tachycardia (VT).
Ventricular tachycardia can originate from the left or right ventricle, with left ventricular tachycardia more common in those patients with heart failure and coronary artery disease. Ventricular tachycardia encompasses all fast heart rhythms, typically >100 beats per minute, originating from the ventricles. It can be fast and regular, with one repetitive form or morphology, known as monomorphic VT. If it is fast and irregular, with beat-to-beat variations, it is known as polymorphic VT. Ventricular tachycardia in patients with structural heart disease is typically due to a “reentry” mechanism, where the electrical current travels in a loop of tissue that is scarred with slowed electrical conduction. This allows the rhythm to continually perpetuate itself, as the head of the myocardial electrical current chases its tail.
Clinic
The attack develops suddenly, cardiac activity moves to another rhythm. Children complained of discomfort in the area of the heart, constricting pain in the chest, pain in the epigastric area. This is often accompanied by dizziness, vomiting. Children often feel fear. Skin is pale, sometimes there is cyanosis, there is swelling and throbbing neck veins. In the long process align signs of heart failure: increased cyanosis, appears short of breath, increased liver, decreases urine flow, align edema. Pulse is weak filling, heart rate reaches 150-300 for 1 minute. Heart tones reinforced embryocardia. Blood pressure is decreased.
The number of heart contractions in ventricular shape is usually within 180-200 pulses per minute. At supraventricular forms – 200-300 pulses. Often during the attack thereis pulsing neck vessels. Auscultation: characteristic oscillating rhythm (embryocardia), there is no difference between I and II tone. The duration of attack is from several minutes to several days. Nodal and atrial paroxysmal tachycardias has no significant effect on central hemodynamics. However, in children with cardiovascular failure, it could get worse, increase swelling. Supraventricular paroxysmal tachycardia increases myocardial oxygen demand and may provoke attacks of acute coronary insufficiency. Characteristically, the sinus form does not begin suddenly and also gradually ends.
Diagnosis
The diagnosis of VT is typically based on capture of the rhythm disturbance on a 12-lead EKG or outpatient monitoring system, such as a Holter or Event monitor. Your physician can make this determination with clues from the careful inspection of the initiation, continuation, and perpetuation of your tachyarrhythmia. In general, VT tends to be a wide-complex rhythm as opposed to narrow-complex typically seen with supraventricular tachycardias (SVT). However, this is not necessarily true 100% of the time, with some SVT appearing wide at faster rates, making the concrete discrimination between the two difficult at times.
Electrocardiogram illustrates repetitive monomorphic right ventricular outflow tract ventricular tachycardia, left bundle branch block morphology, and an inferior axis.
Electrocardiogram illustrates sustained right ventricular outflow tract ventricular tachycardia, left bundle branch block morphology, and an inferior axis.
Electrocardiogram shows an epsilon wave (arrow) in a patient with arrhythmogenic right ventricular dysplasia.
Ventricular bigeminy. Uniform premature ventricular contractions
alternate with sinus beats. Premature ventricular contractions tend to occur following long cycles.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias.
Ventricular trigeminy. Uniform premature ventricular contractions occur after every two sinus beats.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias.
IT+>A,<IT-> Ventricular tachycardia with complete right bundle branch block pattern in a 10-year-old. The QRS duration is 0.15 s and the QRS rate is 140/min.
<IT+>B,<IT-> Ventricular tachycardia with complete left bundle branch block pattern in a 10-day-old infant.
Ventricular tachycardia is shown beginning in lead V<SB:0.039>6</SS>.
Note the fusion complex (F). The QRS duration is 0.09 s, which is longer than the sinus QRS duration of 0.06 s.
The ventricular tachycardia rate is 200/min.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias.
Different morphologies of ventricular tachycardia as recorded by 24-hour electrocardiographic tape monitoring. All tracings are a modified lead II.
Sinus beats are shown for comparison. <IT+>A,<IT-> 8-year-old child; QRS duration 0.13 s, QRS rate 140/min. <IT+>B,<IT-> 12-year-old child; QRS duration 0.11 s, QRS rate 200/min.
IT+>C,<IT-> 4-year-old child; QRS duration 0.11 s, QRS rate 140/min. <IT+>D,<IT-> 15-year-old child; QRS duration 0.17 s, QRS rate 130/min.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias.
Treatment
If treatment is required, it includes medicines and addressing the cause, if possible. The type and length of treatment depends on what’s causing the problem. In some people radiofrequency ablation or surgery may be needed to control the tachycardia.
Therapy for VT is based on many different factors. First and foremost, patients will need to be on optimal medical therapy for their cardiac condition. Those patients with heart failure will need to be on maximal medications and avoid episodes of decompensated heart failure leading to hospitalizations. As well, patients with coronary artery disease will need to be on optimal chronic medical management to limit the progression of disease and recurrent myocardial infarctions. In situations with recurrent episodes of ventricular tachycardia, the physician will likely recommend tiered therapy with antiarrhythmic medication and implantation of an implantable cardioverter defibrillator (ICD).
The goal of antiarrhythmic medication is to reduce the episodes of symptomatic life-threatening VT. Ventricular tachycardia is indeed the most dangerous of the cardiac arrhythmias, with a real risk of sudden cardiac death. Antiarrhythmic medications can act to slow ventricular muscle conduction and therefore disturb the formation and perpetuation of these reentry loops; or they can reduce the ability of the ventricular muscle tissue to be electrically excited and conduct the rhythm disturbance. Most antiarrhythmic drugs carry a small risk of “pro-arrhythmia”, that is of causing secondary heart rhythm disturbances, therefore careful consultation with the physician is important. Finally, antiarrhythmic medications will not protect completely from recurrent episodes of VT and sudden cardiac death.
Help on prehospital stage
1. To give the promoted, halfsitting position to the child.
2. To release a patient from squeezing clothes.
3. To provide access of fresh air.
4. Reflex irritation of vagus nerve: vomit reflex, tension (the Valsalvi method), delay of breathing, squat, drink of cold water, cold rub of skin, sharp transition from sitting position in horizontal one, the Ashner reflex (pressure on the upper inside of eyeballs), caroic reflex (massage and stamping in the area of carotic sinus), bending of feet to the abdomen and their unbending. These meatures are effective at supraventricular paroxismal tachycardia and do not influence on the abdominal form of tachycardia.
5. Sedative therapy: infuse of valleriani 10-20 drops, Corvaloli – 1 drop per theyear of life.
6. Potassium orotatis 10-20 mg/kg of mass per day or other medicines of potassium orally.
7. Hospitalization.
Help on hospital stage
At the supraventricular form of tachycardia:
1. Oxygentherapy by the 40 % moistened oxygen.
2. 0,25 % Isoptini solution 0,1-0,15 mg/kg of mass of intravenously streamly slowly on 20 ml 10 % of glucose solution (except for the syndrome of preterm excitation of ventricles).
3. In default of effect – 10 % Novocainamidi solution 3-6 mg/kg of mass on a 10-15 мл isotonic solution of chloride sodium together with 1 % Mesatoni (0,1-0,3 ml) intravenously streamly slowly.
4. In 1,5-2 hours – 0,05 % Strophantini solution 0,01-0,015 mg/kg of mass (0,1-0,3 ml depending on age) with 10 ml 10 % of glucose solution intravenously streamly slowly (it is not used for the syndrome of preterm excitation of ventricles).
5. At presence of syndrome of preterm excitation of ventricles – Cordaroni (Amiodaron) 0,5 % solution per 5 mg/kg of mass on 20 ml of 10 % glucose solution intravenously streamly, then intravenously in drops in the same dose on 100,0 ml of 10 % glucose solution.
6. 0,5 % Seduxeni solution 0,3-0,5 mg/kg of the masses intravenously streamly slowly.
7. In default of effect electro-impulsive therapy is used.
At the ventricular form of tachycardia:
1. Oxygentherapy through the mask by 40 % the moistened oxygen
2. Lidocaini 1 or 2 % solution in dose 1-3 mg/kg of the masses on a 10-15 ml or 5 % glucose solution intravenously streamly, farther slow infusion in supporting dose 1-2 mg/kg/hr on a 50-100 ml of іsotonic solution of sodium chloride or 5 % glucose solution.
3. In default of effect in 20-30 minutes – 10 % solution of Novocainamidi 3-6 mg/kg of mass on a 10-15 ml of іsotonic solution of sodium chloride together with 1 % Mesatoni solution (0,1-0,3 ml) intravenously streamly slowly.
4. After 2-4 hours – 2,5 % Aymalini solution 1 mg/kg of mass on a 10 ml of іsotonic solution of sodium chloride of intravenously streamly slowly (during 7-10 minutes).
5. Cordaroni (Amyodran) 0,5 % solution in the dose of a 5 mg/kg of mass on 20 ml of 10 % glucose solution , then intravenously in drops in that dose on 100 ml of 10 % glucose solution.
6. In default of effect electro-impulsive therapy is used.
ICD therapy is recommended not only for those patients with structural heart disease and recurrent life-threatening VT, but also empirically (prophylactically) for patients with diminished left ventricular (LV) heart function, with scientific studies pointing to LV function less than 35% as a high-risk group. A normal ejection fraction is 55%. This assessment of
This image shows how the ablation catheter is placed.
Image of an ICD generator with the electrical circuitry housed inside the “can”. The top of the device, also known as the “header” is where the intracardiac leads are screwed into position.
Bradycardia
A heart rate that’s too slow is called bradycardia. What’s “too slow” depends on a person’s age and activity. A newborn usually won’t have a heart rate of less than 80 beats a minute. An athletically trained teenager may have a normal resting heart rate of 50 beats a minute.
Correction of offending cause:
If the bradycardia is due to a systemic disease like hypothyroidism or due to any drugs like beta blocker, calcium channel blocker which is administered for another aliment, then correction of these can lead to recovery from bradycardia.
Pacemaker therapy:
If excessive bradycardia leads to symptoms in a patient, then a pacemaker may be necessary. Pacemaker is a device consisting of a long lasting battery; an electronic circuit encased in a can and is placed below the collarbone underneath the subcutaneous tissue. Lead/Leads are inserted to the cardiac chambers and the proximal end is connected to the pacemaker. Pacemaker does beat to beat monitoring and delivers pacing therapy wheeeded.
Dual chamber pacemaker: Leads placed at right upper chamber and right lower chamber. It senses the electrical activity in both the chambers and if required delivers pacing therapy
Sick sinus syndrome
Sometimes the sinus node doesn’t work properly. Some children after open-heart surgery have this problem. When the sinus node’s work is seriously disturbed, it’s called sick sinus syndrome. A child with this syndrome may not have any symptoms or may be tired, dizzy or faint. Children with sick sinus syndrome have episodes of tachycardia and bradycardia. Fortunately, sick sinus syndrome is unusual in children. If it does occur, an artificial pacemaker, medications or both may be needed.
Clinic
Here are some signs and symptoms of sick sinus syndrome.
Ø Fainting (called syncope)
Ø Dizziness or lightheadedness
Ø Confusion that comes and goes
Ø Heart palpitations (the feeling that the heart has skipped a beat)
Ø Chest pain
Ø Angina
Ø Shortness of breath
Ø Fatigue
Ø Muscle aches
Sick sinus syndrome can be hard to diagnose because you may not have many of the symptoms. The doctor will take a medical history, ask about symptoms, and listen to heart with a stethoscope. With the stethoscope, the doctor may be able to hear an irregular heartbeat, which can be a sign of sick sinus syndrome. Here is a list of other tests that the doctor may order.
· A standard electrocardiogram (ECG or EKG), which is the best test for diagnosing arrhythmia. This test helps doctors analyze the electrical currents of the heart and determine the type of arrhythmia.
· Holter monitoring gets a non-stop reading of the heart rate and rhythm over a 24-hour period (or longer). With certain types of monitors, patient can push a “record” button to capture a rhythm when he feels symptoms. Doctors can then look at a printout of the recording to find out what causes arrhythmia.
· Event monitors, which are devices that record problems that may not be found within a 24-hour period. The devices used for this type of test are smaller than a Holter monitor. One such device is the size of a beeper, and another is worn like a wristwatch. These devices also work during episodes of fainting.
· Electrophysiology studies (EPS), which are usually done in a cardiac catheterization laboratory. A long, thin tube called a catheter is inserted in an artery in your leg and guided to your heart. Electrical impulses from your heart are sent through the catheter and mapped out. This map helps doctors find out what kind of arrhythmia you have and whether it is caused by sick sinus syndrome.
The PSD 410 Pacemaker Transmitter allows for the easiest and most accurate transtelephonic follow-up of pacemaker patients. The PSD 410 digitizes the incoming signal and translates it to a frequency synthesized output that will result in a clear tracing with identically consistent pacer enhancements.
The PSD 410 improves testing throughput with touch-tone controls or a reversible telephone cradle.
Figure A shows how a Holter or event monitor attaches to a patient. In this example, the monitor is clipped to the patient’s belt and electrodes are attached to his chest. Figure B shows an electrocardiogram strip, which maps the data from the Holter or event monitor.
Electrophysiology studies (EPS)
Complete heart block
Heart block means that the heart’s electrical signal can’t pass normally from the upper to the lower chambers. The electrical signal within the heart is blocked, not the blood flow. When this occurs, another “natural” pacemaker in the lower chambers takes over, but at a slower rate.
Heart block may be present at — or even before — birth. (This is congenital heart block.) Disease or an injury to the electrical conduction system during heart surgery can also cause it. When the natural pacemaker in the lower chambers isn’t fast enough or reliable enough, an artificial pacemaker is put in.
Symptoms of heart block
§ dizziness
§ fainting or nearly fainting
§ chest pain
§ breathlessness following exercise/activity
§ seizures, caused by not enough oxygen getting to the brain
Atrial fibrillations
In atrial fibrillation, the electrical signals from the upper chambers of the heart (the atria) are fast and irregular, causing the atria to quiver instead of beating effectively. To fix it, surgeons seek to isolate the electrical signals causing the problem. This is typically done by creating a lesion or burn around the atrium through microwave energy.
In AF, multiple circuits in the atria occur simultaneously, stimulating the heart in an unco-ordinated fashion. As a result the atria quiver quickly and ineffectively.
Atrial Flutter
In Atrial Flutter, there is a single short circuit that conducts electrical impulses rapidly around the inlet valve of the right ventricle.
Usually every second beat is conducted from this abnormal circuit to the ventricles resulting in a heart rate of around 150 beats per minute. This rhythm can often be difficult to treat with medication. Similarly to Atrial Fibrillation, there can be risk of blood clots forming in the atria. If the heart rate cannot be controlled, there can be risk of weakened heart muscle pumping function.
Symptoms
Episodes of atrial flutter can lead to rapid heartbeats with symptoms of palpitations and chest fluttering or tremoring. Similar to other SVTs, patient may feel short of breath, fatigue, dizziness, or rarely, even fainting. However, some people with atrial flutter may not have any symptoms at all. Episodes of atrial flutter can last anywhere from minutes to days or months. Patients with sustained rapid heartbeats should seek medical attention.
Diagnosis
Atrial flutter can be diagnosed by physician via an electrocardiogram or an Ambulatory monitoring device, i.e. Holter or Event monitor, specifically during an arrhythmia episode. Some episodes of atrial flutter are intermittent (also referred to as paroxysmal) and not reliably present on a daily basis. In these situations, the physician may recommend a special ambulatory monitoring device that is patient-triggered, i.e. an Event monitor.
EKG strip of atrial flutter with the “flutter waves” denoted by the red arrows. The ventricular response, or heart rate, is determined by the ratio of atrial beats that are conducted to the ventricles via the normal AV node. It appears to be 3:1, with every 3 atrial flutter waves associated with one ventricular beat.
Therapy
Therapy for patients suffering from atrial flutter has three components:
§ Control of the ventricular rate (heart rate)
§ Conversion and maintenance of sinus rhythm
§ Reduction of subsequent stroke risk (as discussed earlier, with anticoagulation)
Medications used to control the ventricular rate during atrial flutter include b-blockers, calcium channel blockers, and less commonly digoxin. These medications can be administered orally on a routine outpatient basis, or via intravenous route if necessary in the emergency room. Some patients may need a combination of medications from different classes. Patients may experience alleviation of symptoms due to slowing of the ventricular response (heart rate) with the use of b-blockers or calcium-channel blockers that delay electrical conduction through the AV node.
Attempts to convert and maintain sinus rhythm can be approached in one of three ways:
ü In-hospital electrical or chemical cardioversion
ü Outpatient antiarrhythmic medication therapy
ü Catheter ablation procedure.
Implantable cardioverter and defibrillator (ICD):
Very fast rhythm like ventricular tachycardia carries a high risk of sudden cardiac death. This kind of tachycardia needs immediate detection and deployment of appropriate therapy. Very often ICD device is used in such patients. ICD looks like a pacemaker device and consists of a long lasting battery, a capacitor and an electronic circuit encased in a can. This device is implanted below the left collar bone under the subcutaneous tissue. A high voltage lead is inserted to the cardiac chamber and the ICD is connected to it at its proximal end. Via the lead, the ICD detects if there is any tachycardia and immediately determines the nature of the tachycardia and delivers appropriate therapy. Different kinds of therapy are programmed by the implanting physician depending on the nature of the underlying tachycardia which varies from antitachycardia pacing to shock therapy. ICD is often lifesaving.
Cardio-vascular failure.
Cardio-vascular failure (insufficiency) – is a syndrome in which the heart cannot maintain adequate circulation of blood to tissues, or in accomplishes perfusion through compensatory mechanisms that themselves produce organ dysfunction due to metabolic disorders results in the decreased haemodynamic, neurological and humeral adaptation reactions directed to support circulation of blood in accordance with the necessities of human.
The СF Classification.
Acute: Left-heart
Right-heart
Arythmogenes
Total
Chronic: I – А, B
ІІ- A, B
ІІІ
Systolic
Diastolic
Mixed
Acute Left-Heart insufficiency
The decline of conductive ability of myocardium of left ventricle causes the diminishment of percussive and minute volume of blood. A heart is not able to pump necessary volume of blood to peripheral tissues. The worsen moment of the situation is so that a left atrium works well and pumps the blood to ventricle. But it caot send this plenty vein blood in the adequate cardiac output. Increased diastolic volume occurs in left ventricle that leads to increasing of pressure in a left ventricle, then in a left atrium. Haemostasia in the vein part of small circle of circulation (passive, venous, retrograde hypotention in a small circle) of blood occurs.
Hydrostatical pressure is increasing in veins and capillaries.
The peculiarity of the left heard insufficiency is unfavorable, because the circulation in the coronal vessels of left ventricle is carried out only in the phase of diastole and is irregular. As the result of this any decline of the cardiac output lands to decreasing of coronal circulation and increases diminishment of contraction ability of myocardium.
The developed syndrome of the small output of left ventricle leads to the decline of the system circulation and circular hypoxia, which comes forward the starting mechanism of activating of the sympathoadrenal system. That has the protective adoption reaction on stress. Activating of this system is the reason of output of catecholamines and generalization of vascular constriction. Contraction ability of myocardium is increased, tahycardia develops.
It is the protective reaction of organism on a certain stage, but reserves are small.
Hypoxia is the start mechanism not only for sympathoadrenal system. It activates freeing of bioactive substances (hystamini, serotonini, kinins, prostoglandins) with action of which the spasm of vessels of small circle of circulation of blood occurs. Next phase is increasing of hydrostatical pressure and increasing of penetration of capillaries.
The last phase of pathogenesis is development of cardiac asthma and edema of lungs.
In the conditions of acute cardio-vascular insufficiency, the role of increasing of contraction of myocardium as compensatory mechanism is also important in according to the Franck-Starling law, which consists in: the force of cardiac contraction depends on initial length of myofibrils .The force of contraction of muscle is determined by the degree of its tension before the beginning of contraction. This mechanism is very important at the increase of overload (promoted vein returning to the vessels).
Clinic.
The considerable pallor of skin as a result of vasoconstriction, tachycardia, weak pulse
or undetermined.The shortness of breathing, dyspnea without the change of its depth and rhythm. It is mostly an inciter or mixed.
Cyanosis of nose labial triangle
Percussion: increasing of left areas of heart.
Auscultation: considerably low tones, on an apex may be absent, as valvular and
muscular component is eliminated as a result of decline of contractive ability of myocardium, of considerable increasing of cavity of left ventricle and distension of fibrin cycle of AV-aperture.
Appearance of systolic murmur with an epicenter above an apex occurs due to development
of relative insufficiency to the AV-valve.
The accent of ІІ tone above a pulmonary artery is determined. There is often rhythm of gallop (protodiastolic -ventricular) connective with the appearance of the ІІІ tone at the beginning of diastole. The pathological rhythm of gallop develops in that moment when blood quickly enters enlarged left ventricle, contractive ability of which is acutely reduced.
There is centralization of blood circulation with the BCV increase:
1. Decresing of hydrostatical pressure and moving of blood from intersticia in a blood circulation;
2. Output of additional blood from depot;
3. Increase of readsorbtion of sodium and water in proximal kidney ducts.
The BCV increasing is a protective compensating mechanism that arises up to reply the insufficient output of blood from a left ventricle. At the same time more of loading are on the staggered heart.
ЕEG: voltage is reduced or high, leftgramm, Т-negative in pectoral left branches,
ІІ and AVL.This features are the marker of success in treatment.
As a result of increase of hydrostatical pressure and penetration of capillaries in the small circle of blood circulation intersticia edema–cardiac asthma arises up.
In a prodromal period weakness, head ache, compression under sternum,dyspnea, dry cough are observed.The wheezes in lungs are yet absent.
The attacks of inciter shortness of breathing appear farther, during which exitement, sufferning face, attacts of the dry cough occur.
Farther attacts of dyspnoe, arterial hypertension, tachycardia, dyspnoe,additional muscular help in the forced breathing appear due to increasing of circulation in a small circle.
A pathological circle is closed. Activity of work of heart goes down, central cyanosis grows, arterial pressure decreases, a pulse is threadlike. Hypoxia, cyanosis progress, that violate work of heart and reduce the effect of therapy.
An attack can last minutes-hours, mainly at night, because:
1:CNS and vegetative NS sensitiveness is decreased during sleep, that worsens the interchange of gases in lungs, strengthens bronchospasm and transsudation;
2. Tonus of vagus nerve is increased;
3. Hypovolemia in horizontal position, which is accompanied by the increasing of BCV.
Later penetration of liquid part of blood, albumins , cellular elements in the alveolarsoccur. Together with the bubbles of air they ventilate the alveolars membranes, they damage the alveolar-capillary interchange of gases. Changes of activity of surfactant with development of atelectasis occur. Acute respiratory insufficiency due to cardiac asthma give the development of edema of lungs.
The state of patient is acutely worse. The shortness of breathing grows, breathing is raging, feeling of fear, cold sweat, circulation hypoxia passes in hypoxic . Central cyanosys with the protracted moist cough, with foamy excretions from a mouth, whis moist wheezes in lungs.
X-ray changes: pulmonary picture, roots lose the structure, the road clearance of main bronchial tubes is not differentiated.
PhonoCG at hypertrophic left ventricular
EchoCG at hypertrophic left ventricular
URGENT THERAPY OF ACUTE LEFT-HEART FAILURE.
Help on prehospital stage
1. To give half sitting position to the child.
2. To free a patient from squeezing clothes.
3. To provide access of fresh air.
4. To put mustard plasters on shin muscles.
5. By a rubber bulb or gauze clearing the cavity of mouth and nose from mucus and foamy excretions.
6. Oxygen therapy through a mask from an oxygen pillow.
7. 3 % solution of Prednisoloni 2 mg/kg of the masses intramuscular or intravenously streamly.
8. 1 % solution of Lasix for one dose 1-2 mg/kg of the masses of intravenously streamly.
9. 0,5 % solution of Seduxeni (Sibasoni, Relanium, Diasepami) for one dose 0,3-0,5 mg/kg of the masses of intravenously streamly slowly on 20 ml 10 % glucose solution . At the third stage Seduxeni is not indicated, Cocarboxylazae a 10 mg/kg of mass and 5 % solution of sodium ascorbinati 0,2 ml/kg on 5 ml of 20 % glucose solution intravenously streamly.
10. 2 % solution of No-spani 0,5-2,0 ml intramuscular or nitroglycerine ½-1 tablets under a toungh.
11. Hospitalization.
Help on a hospital stage
1. To give half sitting position to the child.
2. Oxygentherapy whith the promoted pressure on expiration by the 40 % moistened oxygen skipped through 90 % ethyl spyritus. At newborn and preterm children firstly take 30 %, then 50 % ethyl spyritus, gradually multiplying concentration to 90 % of solution. It is possible to use 10 % solution of Antiphomsilani or 10 % Silicani solution for inhalation (2-3 ml per one inhalation).
3. 1 % solution of Lazix in one dose 1-2 mg/kg of the masses intravenously streamly.
4. 3 % solution of Prednisoloni in the dose of 3-6 mg/kg of mass of intravenously streamly.
5. Cocarboxylazae 5-10 mg/kg of mass on 5,0 ml of 10 % glucose of intravenously streamly.
6. 5 % solution of sodium ascorbinatis 0,2 ml/kg of the masses on 5,0 ml of 10 % glucose intravenously streamly.
7. A polarizing mixture : glucose -insulin-potassium solution- 10 % glucose solution 100 мл, insulin 2 units, 7,5 % potassium chloride solution 4 mlмл intravenously in drops slowly, or Panangini 0,75-1 ml/hr of life on 20,0 ml of 10 % glucose solution intravenously streamly slowly.
8. Vasodilatations: Nitroprussidi sodium 0,5 mkg/kg of mass per the minute (contents of ampoule –
9. Dopamini 5 mkg/kg of the masses per 1 minute (5 ml of 0,5 % Dopamini solution dissolve in 125ml 5 % glucose solution , 1 ml of solution contains 200 mkg of dissolve) intravenously in drops to stabilization of hemodynamic indexes (starting introduction at the ІІІ stage of cardiac insufficiency).
10. Solution of Strophantini 0,05 % or Corglyconi 0,06 % in dose 0,01-0,015 ml/kg of the masses on 10 ml of 10 % glucose solution intravenously streamly slowly (carefully at the ІІІ stage of cardiac insufficiency).
At the edema of lungs additionally to enter 3 % Prednisolone in one dose 1-2 mg/kg of the masses intravenously streamly and 2,4 % solution of Euphyllini in the one dose 3-5 mgг/kg (0,1-0,2 ml/kg) of mass on a 10-20 ml of isotonic solution of sodium chloride intravenously streamly slowly.
Volume of liquid for intravenous introduction must be not more than a 40-50 ml/kg of mass per day at the first stage, 30-40 ml/kg of the masses at the second stage and 20-30 ml/kg of the masses at the third stage of insufficiency (polarizing mixture, colloid solutions).
Acute Right-Heart insufficiency.
Arises up at the states which are accompanied by sudden limitation of circulation in a small circle:
– severe attack of bronchial asthma
– hydrothorax
– atelectasis
– trachea obturation
– thromboembolia of pulmonary artery
– RDS iew-born
– congenital heart abnormalities with increased pulmonary circulation
– at the rapid introduction of Calcium, cytric blood, hypertensive solutions.
All these factors are the reason of the spasm of vessels of pulmonary artery and increase their resistance.
Clinic. There is the pallor of skin with acrocyanosis, shortness of breathing, tachycardia, decreased tones of heart, accent of ІІ tone on a pulmonary artery, slight pulse. Swelling of veins, edema, increase of liver, edematatous feet, sometimes ascit, hydrothorax. At acute right-heart insufficiency three stages are also distinguished. At the first stage characteristic is increasing of cardiac contractions, breathing, the increasing of liver on 2-3 sm, the edema is absent. The second stage is characterized by the increase of frequency of cardiac contractions, dyspnea , increasing of liver on 3-5 sm, by edema of tissues, swelling of neck veins, appearance of oliguria. The third stage includes the considerable increase of cardiac contractions (more than 50-60 %), breathing (more than 70-100 %), hepatosplenomegaly, considerable edema, anasarca.
X-ray: increase of right ventricle and conus of pulmonary artery.
ЕEG: rightgramm.
PhonoCG
EchoCG
Doppler Echo
A prognosis is very serious. Sudden death may occur.
Help on prehospital stage
1. To give half sitting position to the child.
2. To free a patient from squeezing clothes.
3. To provide access of fresh air.
4. 1 % solution of Lasix in one dose 1-2 mg/kg of the masses of intravenously streamly.
5. 3 % Prednisoloni solution 2-6 mg/kg of mass intramuscular or intravenously streamly.
6. 0,25 % Droperidoli solution 0,3 mg/kg of mass intramuscular or intravenously streamly.
7. 2 % No-spani solution 0,5-2,0 ml intramuscular or nitroglycerine half or 1 tablets under tongue.
8. Hospitalization.
Help on a hospital stage
1. To give halfsitting position to the child.
2. Oxygentherapy by 40 % the moistened oxygen through a nasal catheter.
3. 1 % Lasix solution for one dose 1-2 mg/kg of the masses of intravenously streamly.
4. 3 % solution of Prednisoloni 2-6 mg/kg of mass intramuscular or
intravenous streamly.
5. Cocarboxylazae 5-10 mg/kg of mass on 5,0 ml of 10 % glucose intravenously streamly.
6. 5 % solution of sodium ascorbinati 0,2 ml/kg of the masses on 5,0 ml of 10 % glucose intravenously streamly.
7. Panangini 0,2 ml/kg of the masses on 10-20 ml of 10 % glucose solution intravenously streamly slowly.
8. 0,5 % solution of Seduxeni (Sibasoni, Relanium, Diasepami) in one dose 0,3-0,5 mg/kg of the masses intravenously streamly slowly on 20 ml of 10 % glucose solution, or 0,25 % solution of Droperidoli in one dose 0,25-0,5 mg/kg of the masses intravenously streamly slowly on 20 ml of 10 % glucose solution (carefully at the third stage of cardiac insufficiency).
9. 2 % solution of No-spani 0,5-2,0 ml intramuscular.
10. At congenital heart-diseases with increasing of pulmonary blood stream 0,1 % solution of Anapryllini 1 mg/kg of very slowly intravenously streamly on a 10 ml of isotonic solution of sodium chloride.
11. 2,4 % solution of Euphyllini 3-5 mg/kg of mass on 10-20 ml of isotonic solution of sodium chloride intravenously streamly slowly.
12. Dopamini 5 mkg/kg of the masses per 1 minute (5 ml of 0,5 % Dopamini solution dissolve in 125ml 5 % glucose solution , 1 ml of solution contains 200 mkg of dissolve) intravenously in drops to stabilization of hemodynamic indexes (start drug at the ІІІ stage of cardiac insufficiency).
13. At thromboembolia of pulmonary artery branches Heparini 100-150 U/kg of mass intravenously streamly (or Fraxyparini 225 U/kg of mass smbcutaneously), Streptolyazae 10-15 thousand of units in 20 ml of 0,9 % sodium chloride solution intravenously in drops.
Volume of liquid for intravenous introduction must be not more than a 40-50 ml/kg of mass dayly at the first stage, 30-40 ml/kg of the masses at the second stage and 20-30 ml/kg of the masses at the third stage of insufficiency (polarizing mixture, colloid solutions).
Total cardiac insufficiency develops at the decline of conductive ability of both ventricles myocardium. Usually at first there are the signs of left-heart insufficiency, then right-heart failure.
Clinic
Symptoms of total acute cardiac insufficiency are characterized by combination of right-heart and left-heart failure.
Symptoms of heart failure: a cough, severe shortness of breath, pulmonary edema, pleurisy, ascites, edema of the extremities.
ACUTE VASCULAR INSUFFICIENCY
Acute vascular insufficiency is the damage of extacardiac blood circulation , that develops acutely and is characterized by disparity of vascular volume to circulatory blood volume. The reasons of acute vascular insufficiency are various: from psychical and reflex influence on regulation of blood circulation to the severe infectious diseases.
Two forms of acute vascular insufficiency are distinguished: syncope and collapse.
Syncope
A syncope is the sudden, more frequent brief loss of consciousness, conditioned by acute low hemorrhagic circulation of cerebrum, that occur as a result of psychogenes or reflex influence on regulation of blood circulation. It is the most frequent, mild form of acute vascular insufficiency. It occurs at children with the liability of the vascular system. The reason very often may be: a fright, strong emotions, tension, promoted sensitiveness to the pain irritants or unpleasant procedures (injections, blood analysis, blood view). The overstrain, insufficiency of oxygen in the apartment, long durations of orthostatic loadings, infectious diseases, anaemias, vegeto-vascular distonias of pubertal age can lead to the loss of consciousness.
Clinic.
There are: weakness, dizziness, nausea, appeals on vomit. It is accompanied by darkening in eyes, by noise in ears with a next brief loss of consciousness. Consciousness is gradually lost, a patient falls or slowly goes down on the floor. Skin covers pale, pupils are extended, react on light. Extremities are cold by touch. Breathing is superficial, rare, bradycardia, pulse of the weak filling and tension, threadlike. Tones of heart are muffled. Arterial pressure is reduced.
Help on prehospital stage
1. To put a patient on the back with high position of feet.
2. To free a child from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To splash or to wipe a person by cold water.
5. To slap a patient on cheeks.
6. To give to breathe the exhalations of liquid ammonia, vinegar or other irritating substants.
7. To put a warm hot-water bottle to the feet and pound a body and extremities of patient.
Help on hospital stage
1. Oxygentherapy by the 40 % moistened oxygen through a mask.
2. Subcutaneously to enter Cordiamini in dose 0,015 mlл/kg of the masses.
3. it is possible to do subcutaneous or intramuscular introduction of 10 % Coffeine sodium bensoatis 0,1 ml/yr of life.
4. Prednisoloni 3 % solution intravenously streamly in one dose 1-2 mg/kg of the masses of body.
Collapse
A collapse is the acute falling of vascular tone, as a result of defeat of vascular-regulative center, which is characterized by the increase of circulatory volume blood due to its depositing in tissues. Decreasing of volume of circulatory blood results in the insufficient returning of blood to the heart, decreases the minute volume and development of hypoxia of brain, all organs and tissues. The reason of collapse is severe forms of acute infectious, purulent-septic diseases, different genesis toxemia, expressed pain syndrome, supraadrenal insufficiency.
Three forms of collapse are distinguished: symphatotonic, paralytic, vagotonic.
Symphatotonic collapse is the initial start of some severe toxemia and hypercatecholamines. As a result of irritation of alpha-receptors the spasm of arteriolles and commulation of blood in the vein system through arteriovenousis anasthomosis occur. The less of blood comes back to the heart, microcirculation is violated, hypoxia of organs and tissues is the result of the process.
Clinic: A pallor skin, cold extremities, the increase of body temperature and systolic arterial pressure. Tones of heart are loud, tense, diuresis are diminished. The patient is excited, reflexes are promoted, convultions may occur.
Help on prehospital stage
1. To lay a child on the back with high position of feet.
2. To release a patient from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To give plenty of warm drink.
5. To put a warm hot-water bottle to the feet, rub a body and extremities by 40 % ethyl alcohol solution.
6. Hospitalization.
Help on hospital stage
1. Oxygentherapy through the mask by 40 % of the moistened oxygen 5liter per minute.
2. Reopolyglucini (Polyglucini or plasma) 10 ml/kg of the masses intravenously in drops.
3. 5 % solution of ascorbinati sodium 0,2 ml/kg of mass for one dose on 5,0 ml of 10 % glucose solution intravenously streamly.
4. Cocarboxylazaea 5 mg/kg of mass for one dose on 5,0 ml of 10 % glucose solution intravenously streamly.
5. To renew the vascular tone:
– 0,25 % solution of Droperidoli in dose 0,2-0,3 mg/kg of the masses intravenously streamly slowly;
– 2,4 % solution of Euphyllini in dose of 3-6 mg/kg of mass on a 50-100 ml of isotonic solution of sodium chloride intravenously in drops;
– when the effect is low – 2,5 % solution of Aminasini in a dose 3 mg/kg or 0,1 ml/kg of the masses on 50 ml of 5 % glucose solution intravenously in drops .
Paralytic collapse – is the second more severe phase of the same pathological state. As a result of damage of microcirculation and hypoxia histamins, kinings, prostoglandins etc. are accumulated. Action of these products on alpha-receptors results in the loss of their sensitiveness. Paresis of vessels, increase of penetration of their walls occurs. The blood yet in a greater amount is deposited in tissues. Considerably flow of the blood to the heart goes down, arterial pressure falls.
Clinic. The child is undynamic, consciousness is darkened, the lines of face are sharp. The marble skin is covered with cold, sticky sweat, veins are empty. The first tone is slamming, a pulse is threadlike, arterial pressure is reduced, diuresis is considerably diminished.
Help on prehospital stage
1. To lay a child on the back with high position of feet.
2. To release a patient from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To give plenty of warm drink.
5. To put a warm hot-water bottle to the feet, rub a body and extremities by 40 % solution of ethyl spiritus.
6. Cordiamini in dose 0,015-0,02 ml/kg of the masses subcutaneously.
7. 3 % solution of Prednisoloni in a dose 1-2 mg/kg of the masses intramuscular.
8. Hospitalization.
Help on a hospital stage
1. To lay a child on the back with high position of feet.
2. Oxygentherapy through the mask by 40 % of the moistened oxygen 5liter per a minute.
3. Cordiamini in a dose 0,015-0,02 ml/kg of the masses subcutaneously.
4.3 % solution of Prednisoloni in a dose 1-2 mg/kg of the masses of intravenously streamly.
5. Reopolyglucini (Polyglucini or plasma) 10 ml/kg of the masses intravenously in drops.
6. 5 % solution of ascorbinati sodium 0,2 ml/kg of the masses on 5,0 ml of 10 % glucose solution intravenously streamly.
7. Cocarboxylazaea 5 mg/kg of mass on 5,0 ml 10 % of glucose solution intravenously streamly.
8. To renew the vascular tone:
– 1 % solution of Mesatoni in dose 0,01-0,03 ml/kg of the masses (or
0,2 % solution of Noradrenalini in dose 0,05-0,1 ml/hr of life) intravenously in drops in 200 ml of 5 % glucose solution (40-60 drops per 1 minute till achievement of the subnormal sizes of arterial pressure, then the speed of infusion is regulated so that arterial pressure must be supported at attained level).
Vagotonic collapse is conditioned by the increase of tone of vagus nerve, that results in expansion of аrteriovenousis anasthomosisthe. This type of collapse is marked at traumas and operations on the organs of abdominal region. A blood is deposited in the vein system, microcirculation is violated, returning of blood to the heart diminishes, hypoxia of organs and tissues develops.
Clinic. A hiccup, vomit, proof red dermographism are present, salivation, bradycardia, multiplied difference between maximal and minimum arterial pressure.
Help on prehospital stage
1. To lay a child on the back with high position of feet.
2. To release a patient from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To give plenty of warm drink.
5. To put a warm hot-water bottle to the feet, rub a body and extremities by 40 % solution of ethyl alcohol.
6. Cordiamini in a dose of 0,015-0,020 ml/kg of the masses subcutaneously.
7. 3 % solution of Prednisoloni in dose 1-2 mg/kg of the masses intramuscular.
8. Hospitalization.
Help on a hospital stage
1. To lay a child on the back with high position of feet.
2. Oxygentherapy through the mask by 40 % of the moistened oxygen
3. Cordiamini in dose 0,015-0,020 ml/kg of the masses subcutaneouly.
4. 3 % solution of Prednisolony in dose 1-2 mg/kg of the masses of intravevously streamly.
5. Reopolyglucini (Polyglucini or plasma) 10 ml/kg of the masses intravevously in drops.
6. 5 % solution of sodium ascorbinati 0,2 ml/kg of the masses on 5,0 ml of 10 % glucose solution intravevously streamly.
7. Cocarboxylazae 5 mg/kg of mass on 5,0 ml of 10 % glucose solution intravevously streamly.
8. To renew of vascular tone:
– 1 % solution of Mesatoni in a dose 0,01-0,03 ml/kg of the masses (or 0,2 % solution of Noradrenalini in a dose 0,05-0,1 ml/hr of life) of intravevously in drops in 200 ml of 5 % glucose solution (40-60 drops per 1 minute till the subnormal sizes of arterial pressure, then speed of infusion is regulated so that arterial pressure must be supported at attained level).
SUDDEN HEART STOP
The stop of heart is the most severe display of cardio-vascular insufficiency. The principal reasons of heart stop are hypoxiaя, violation of electrolyte balans, hypercapnia and acidosis. All transferred reasons cause the exchange processes in myocardium, excitability changes. Conductivity is reduced and contractive ability of myocardium diminishes. Stroke volume diminishes at first, and later minute volume of heart, as a result circulation of blood gets worse in coronal vessels. 3 types of stopping of blood circulation are distinguished: stop of heart in a systole or diastole (more frequent all at children); fibrillation of ventricles; “uneffective heart” (circulation of blood is kept only in large vessels).
Clinic. Independently of etiology and type of heart stop there are general clinical symptoms. All symptoms of heart stop are unspecific, each of them separately does not allow to put a diagnosis at once. Only the combination of symptoms determines doctor tactics. Four basic symptoms are selected: stop of breathing; change of skin colour (appearance of cyanosis or waxlike pallor); absence of pulse on carotid and femoral arteries; expansion of pupils.
Help on prehospital stage
It is necessary to remember that maximum possible term of hypoxia of cerebrum is 4 minutes. Therefore the first stage of emergency help (renewal of circulation of oxygenic blood) must be completed not later than 4th minutes from the beginning of stop of blood circulation.
1. To lay a child on a hard surface with updown head, underlay bolster under the neck.
2. To provide passage of respiratory tracts (to clean a mouth cavity by the finger, wrapped up by a handkerchief, bandage, a succer is used, the position of little child is downward by a head).
3. To conduct the indirect massage of heart: the place of compression is lower third of sternum; depth of compression for babies – 1-2 sm, to the children of preschool age – 2-3 sm, to the schoolboys – 3-
4. At the same time to conduct artificial ventilation of lungs: to take aside a lower jaw, position of head in a for “smelling” (neutral) pose, ventilation “mouth in a mouth”( “mouth in a mouth- iose”) with frequency from 16 to 40 breathings per 1 minute depending on age. Oxygentherapy by the 100 % moistened oxygen.
5. 0,1 % solution of Adrenalin hydrochloridi 0,01 mg/kg (0,01 ml/kg) intravenously streamly on a 1-2 ml of isotonic solution of sodium chloride (intracardiac introduction must be used as extreme mean).
6. 4 % solution of sodium hydrocarbonati 1-2 ml/kg of the masses on one dose of intravenously streamly.
7. Hospitalization.
Automatic indirect heart massage device Autopulse from Zoll
Help on hospital stage
1. To continue the closed massage of heart and artificial ventilation of lungs with transferring of child on the artificial breathing.
2. Permanent oxygentherapy by 100 % moistened oxygen.
3. Craniocerebral hypothermia.
4. 0,1 % Adrenalin solution in the first dose 0,01 mg/kg of the masses (0,01 ml/kg) intravenously streamly on 1-2 ml of isotonic solution of sodium chloride or 0,1 mg/kg of the masses endotrachealy.
5. In default of effect during 5 minutes to repeat introduction of 0,1 % Adrenalin solution 0,01 mkg of mass of intravenously streamly or endotrachealy. At saving of asystolia to repeat introduction of this dose of adrenalin every 3-5 minutes.
6. 4 % solution of sodium hydrocarbonati 1-2 ml/kg of the masses on dose intravenously streamly , in default of effect to repeat introduction every 10 minutes.
7. At symptomatic and vagoreflex bradycardia 0,1 % Atropine sulfate solution 0,02 mg/kg of the masses on one dose intravenously streamly on 1-2 ml of isotonic solution of sodium chloride.
8. At fibrillation of ventricles – defibrillation 500-1000 V during 0,1-0,25 seconds.
Double phase defibrillator – monitor surveillance Corpuls 3
Defibrillator Defigard 5000 from Schiller.
It combines the advantages of pulsed double phase defibrillators and accurate monitor with the largest color screen
9. Infusion therapy during the reanimation and in a postreanimation period with the purpose of the VBC correction, Acid-alkaloid balance and electrolyte balance.
Adams-Stokes syndrome (Robert Adams)
The term Stokes-Adams Attack refers to a sudden, transient episode of syncope, occasionally featuring seizures. It is named after two Irish physicians, Robert Adams (1791–1875)and William Stokes (1804–1877).Roberts
Also known as:
Adams-Stokes disease
Adams-Stokes syncope (Robert Adams)
Morgagni’s syndrome
Morgagni-Adams-Stokes attack (Robert Adams)
Morgagni-Adams-Stokes syndrome (Robert Adams)
Spens’ syndrome
Stokes’ syndrome
Stokes-Adams attacks (Robert Adams)
Stokes-Adams syncope (Robert Adams)
Stokes-Adams syndrome (Robert Adams)
Gerbezius-Morgagni-Adams-Stokes syndrome
Gerbec-Morgagni-Adams-Stokes syndrome
A syncope triggered by heart arrythmia. The condition is characterized by sudden transient attacks of lightheadedness or unconsciousness, with or without convulsions, due to a temporary cessation of blood supply to the brain. It is caused by complete or incomplete heart block due to disturbances of the conductive path of the heart. Deep and fast respiration changes to weak and slow pulse and respiration, convulsions and respiratory pauses that may last for 60 seconds. Other symptoms may be fixed pupils, incontinence, bilateral Babinski’s sign with resumption of heart beats, and flushing of the face. Onset is usually after 40 years of age. Occurs in diseases of the brain and the heart and is usually a serious symptom.
Causes
The attacks are caused by loss of cardiac output due to cardiac asystole, heart block, Lev’s disease or ventricular fibrillation. The resulting lack of blood flow to the brain is responsible for the faint.
Etiology
In this condition, the normal heartbeat passing from the upper chambers of the heart to the lower chambers is interrupted. This results in a condition called a “heart block.” When a heart block occurs, the heart rate usually slows considerably. This can cause inadequate blood flow to the brain and result in fainting.
Signs and symptoms
Prior to an attack, a patient may become pale, their heart rhythm experiences a temporary pause, and collapse may follow. Normal periods of unconsciousness last approximately thirty seconds; if seizures are present, they will consist of twitching after 15–20 seconds. Breathing continues normally throughout the attack, and so on recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.
As with any syncopal episode that results from a cardiac dysrhythmia, the faints do not depend on the patient’s position. If they occur during sleep, the presenting symptom may simply be feeling hot and flushed on waking.
Diagnosis
Stokes-Adams attacks may be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic. The ECG will show asystole or ventricular fibrillation during the attacks.
Treatment
The patient should immediately be placed in a recumbent position with the legs elevated. Long-term treatment consists of implanting a cardiac pacemaker.
Initial treatment can be medical, involving the use of drugs like isoproterenol (Isuprel) and epinephrine (adrenaline). Definitive treatment is surgical, involving the insertion of a pacemaker – most likely one with sequential pacing such as a DDI mode as opposed to the older VVI mechanisms, and the doctor may arrange the patient to undergo Electrocardiography to confirm this type of treatment.
The most little girl in the world with cardiac pacemaker
Cardiac pacemakers
Prognosis
If undiagnosed (or untreated), Stokes-Adams attacks have a 50% mortality within a year of the first episode. The prognosis following treatment is very good.
Referens:
A – Basic:
1. Pediatrics. Textbook. / O. V. Tiazhka, T. V. Pochinok, A. N. Antoshkina et al. / edited by O. Tiazhka – Vinnytsia : Nova Knyha Publishers, 2011 – 584 pp. : il.ISBN 978-966-382-355-3
2. Nelson Textbook of Pediatrics, 19th Edition Kliegman, Behrman. Published by Jenson & Stanton, 2011, 2608. ISBN: 978-080-892-420-3.
3. Illustrated Textbook of Paediatrics, 4th Edition. Published by Lissauer & Clayden, 2012, 552 p. ISBN: 978-072-343-566-2.
4. Denial Bernstein. Pediatrics for medical Students. – Second edition, 2012. – 650 p.
2. http://www.merckmanuals.com/professional/index.html
3. http://www.nemours.org/content/dam/nemours/www/filebox/service/medical/cardiology.swf
