Supraventricular Tachycardia

Synonym

Paroxysmal atrial tachycardia

Definition

                1. Supraventricular tachycardia (SVT) is defined as:

                a. Heart rate in infants and young children >220 bpm (range: 220 to 320 bpm; Fig. 5-10)

                b. Heart rate in older children >180 bpm (range: 180 to 250 bpm)

                2. SVT is the most common dysrhythmia seen in the pediatric age group.

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Figure 5-10. Supraventricular Tachycardia

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A ventricular rate of 250 bpm with a narrow QRS complex in a 12-day-old neonate who presented with poor feeding and irritability of several hours' duration. The patient had good capillary refill and peripheral perfusion with a BP of 104/73. The patient received one dose of IV adenosine followed by conversion to regular sinus rhythm.       

Etiology

                1. SVT is most commonly caused by a reentry mechanism involving atrioventricular [AV] nodal reentry, accessory pathways, or increased automaticity.

                2. SVT due to accessory pathway conduction (e.g., Wolff-Parkinson-White syndrome [WPW syndrome]) is the predominant mechanism in the fetus and young infant. AV nodal reentry typically appears in 5- to 10-year-old children, and is the predominant mechanism in adults.

                3. Primary atrial tachycardia (e.g., atrial flutter or fibrillation) accounts for 10 to 15% of SVT at all ages.

                4. Associated structural heart disease (e.g., Ebstein's anomaly, corrected transposition of the aorta) is present in about 20% of cases.

                5. Other etiologies include drugs (e.g., cold medications containing sympathomimetics), hyperthyroidism, myocarditis, cardiomyopathy, or infections.

Associated Clinical Features

                1. Usual presentation:

                a. Infants usually present with nonspecific symptoms of poor feeding, irritability, or restlessness.

                b. If SVT persists for many hours at rapid rates, signs of congestive heart failure (e.g., tachypnea, tachycardia, hepatomegaly) or cardiogenic shock/cardiovascular collapse (e.g., an acutely ill infant with prolonged capillary refill, thready pulses, poor tissue perfusion, ashen color, and metabolic acidosis) develop.

                c. About 20% of infants may be completely asymptomatic and SVT may be detected during a routine examination.

                d. Older children may present with pounding or racing heartbeat, dizziness, diaphoresis, or tiredness.

                e. Episodes of SVT are often paroxysmal; older children may give a history of episodes of a racing heartbeat that starts and stops suddenly.

                f. Chest pain is not a usual presenting symptom of SVT.

                2. Clinically the heart rate may be too rapid to count.

                3. Most common age at presentation:

                a. Most first episodes of childhood SVT occur in the first 2 months of life.

                b. About 60% of cases: infants <4 months of age

                c. About 80% of cases: infants <12 months of age

                4. Electrocardiography is required to confirm the diagnosis:

                a. P waves may not be visible (obscured by the ST segment).

                b. QRS complex

                1) Narrow QRS complex in 90% of cases

                2) Wide QRS complex in 10% of cases (aberrant SVT)

                c. With persistent tachycardia, ST- and T-wave changes consistent with myocardial ischemia may be seen.

                d. Features of WPW syndrome may be seen once the episode of SVT terminates, and may include a short PR interval, a delta wave (slow upstroke of QRS complex), and a wide QRS complex.

                5. A chest radiograph may show the presence of cardiomegaly, suggesting CHF or underlying structural heart disease.

Consultation

Cardiology consultation (once the patient is stabilized) for:

                1. Echocardiography in patents with a first episode of SVT (to rule out associated structural heart disease)

                2. Beginning chronic maintenance therapy (e.g., digoxin, propranolol, procainamide, or amiodarone) as indicated in patients with either a first episode or recurrent episodes of SVT

                3. Possible electrophysiology testing and radiofrequency catheter ablation for patients with refractory SVT, those requiring multiple medications, or those with undesirable side effects from medications

Emergency Department Treatment and Disposition

                1. Evaluation of the hemodynamic status and stabilization as indicated; high-flow oxygen, continuous cardiac, blood pressure, and pulse oximetry monitoring

                2. SVT without circulatory compromise (stable patient):

                a. Vagal maneuvers that heighten the vagal tone to the AV node

                1) Diving reflex: application of an ice bag to the face in infants or submersion of the face in ice cold water in older children (Caution:Application of ice to infants should be brief [10 to 20 seconds max], and a cloth or plastic barrier should be used to avoid the occurrence of fat necrosis. Avoid repeated applications of ice to the same location.)

                2) Valsalva maneuver: Ask the patient to strain as if attempting straining at stool.

                3) Unilateral carotid massage: Massage at the junction of the carotid artery and the mandible.

                4) Ocular pressure should not be used (due to the risk of retinal detachment).

                b. Adenosine (Box 5-22; Figs. 5-11 and 5-12)

                c. Verapamil

                1) Do not use in infants < 1 year of age (life-threatening side effects include profound bradycardia, hypotension, and cardiac arrest).

                2) Do not use in children with CHF, myocardial depression, or those receiving beta-blockers.

                3. SVT with circulatory compromise or severe CHF (unstable patient with shock, acidosis):

                a. Adenosine (Box 5-22) if immediate vascular access is available

                b. Synchronized cardioversion (synchronization of the delivered energy with the ECG reduces the possibility of inducing VF, which can occur if the energy is delivered during the relative refractory period of the ventricle)

                1) Consider sedation in older children (if the patient is conscious and time and clinical condition allow; however, sedation must not delay cardioversion).

                2) Initial dose: 0.5 to 1 joule/kg

                3) Double the dose if SVT persists.

                4) Reconsider the diagnosis of SVT if conversion to sinus rhythm does not occur; patient may actually have sinus tachycardia.

                4. Admit to the ICU to monitor for recurrences of SVT and for further management.

                a. Any patient presenting with hemodynamic instability

                b. Any patient with a first episode of SVT (e.g., for parental and patient education, and to begin maintenance therapy, especially in neonates and infants with possible recurrences of SVT)

                5. Patients known to have SVT can be discharged home once converted to sinus rhythm; make a follow-up appointment with the cardiologist or primary care physician.

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Figure 5-11. Supraventricular Tachycardia

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Following one dose of IV adenosine, an abrupt change from SVT to one premature ventricular contraction followed by sinus rhythm is seen.    

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Figure 5-12. Two-Hand/Two-Syringe Technique for Administration of Adenosine

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Because of its extremely short half-life, adenosine must be given as a rapid IV bolus (inject in 1 to 3 seconds to maximize the concentration that reaches the heart). While maintaining pressure on the plunger of the syringe containing the adenosine, simultaneously inject a rapid bolus of 3 to 5 mL of normal saline to accelerate delivery to the heart. Injection should be made close to the hub of the catheter, so that it is done closest to the patient. Intravenous tubing above the injection port should be clamped before the adenosine/normal saline push, and it should be unclamped after the injection.               

Clinical Pearls: Supraventricular Tachycardia

                1. SVT is the most common dysrhythmia seen in the pediatric age group.

                2. Aberrant SVT presents with a wide QRS complex and may resemble VT. If uncertain, all wide-complex tachycardias are assumed to be VT.

                3. A diagnosis of sepsis may be mistakenly made in an infant with SVT presenting with poor feeding, irritability, rapid breathing, or shock.

                4. Heart rates >220 bpm are highly unusual for ST and probably suggest SVT.

                5. Do not delay cardioversion in severely compromised patients while trying to establish vascular access.

                6. Do not prescribe sympathomimetics (common in over-the-counter decongestants) for the treatment of upper respiratory infections in children with SVT, and advise patients also to avoid caffeine.

Box 5-21. Differential Diagnosis: Sinus Tachycardia versus Supraventricular Tachycardia

Sinus Tachycardia             Supraventricular Tachycardia

History of volume loss (vomiting, diarrhea, blood loss), fever, hypoxia    History nonspecific (e.g., irritability, poor feeding, excessive crying)

Signs of dehydration or hypovolemic shock or sepsis (depending on underlying etiology)              Signs of cardiogenic shock (tachypnea, sweating, pallor, or hypothermia)

Rate greater than normal for age (usually <220 bpm)      Rate > 220 bpm in infants; rate >180 bpm in older children

Regular rhythm Usually regular rhythm (associated AV block extremely rare)

Beat-to-beat variation (e.g., HR decreases with sleep or when quiet)      No beat-to-beat variation; monotonous/fixed rate

Normal P-wave axis        P-wave axis usually abnormal

P wave may not be identifiable (with very high ventricular rate)                P wave may not be identifiable (with very high ventricular rate)

Some variation in RR interval may be present     Monotonous/fixed RR interval

Normal QRS duration     Normal QRS duration in >90% of cases

Heart rate slows gradually with treatment (e.g., O2 therapy for hypoxia or fluids for dehydration)

                Abrupt termination to sinus rhythm (either spontaneously or with treatment)

Normal P-QRS-T–wave sequence            

Box 5-22. Adenosine and Supraventricular Tachycardia

 Drug of choice in stable patients or acutely ill patients with readily available vascular access

 Relatively safe drug that can be given to infants and children of all ages, including full-term and preterm newborn infants

 May also be used in children with WPW syndrome or other AV bypass tracts

 After its administration:

   (1) It transiently depresses sinus and AV nodes, leading to slowed conduction and interruption of the reentry pathway

   (2) Be prepared to expect brief periods of sinus arrest (asystole).

   (3) Also be prepared to treat other hemodynamically compromising cardiac effects such as bradycardia, AV block, atrial fibrillation, atrial flutter, ventricular tachycardia, or ventricular fibrillation.

 Untoward effects are brief (ultra-short half-life [ < 10 seconds]):

   (1) Dyspnea, flushing, chest pain/discomfort, headache, episodes of apnea

   (2) Bronchospasm (asthma is not a contraindication to adenosine use; however, be prepared to treat immediate or delayed bronchospasm)

 Dose and route of administration:

   (1) Initial dose 0.1 to 0.3 mg/kg (maximum first dose: 6 mg)

   (2) If initial dose is unsuccessful, may double and repeat dose once (maximum second dose: 12 mg)

   (3) Maximum single dose: 12 mg

   (4) Use rapid IV bolus followed by normal saline flush (see two-hand technique, Fig. 5-12).

   (5) May be given intraosseously

   (6) Adolescents  50 kg: 6 mg rapid IV push; if no response after 1–2 min, give 12 mg rapid IV push. May repeat a second 12 mg dose after 1–2 min, if required.

The Case of antenatally diagnosed sacral mass

The Case:
A female neonate who had an antenatally diagnosed sacral mass is admitted to the neonatal intensive care unit immediately after birth.

Figure 1

Prenatal History:
The 26-year-old mother had two previous normal pregnancies. In the current pregnancy, a mass was discovered at 20 weeks’ gestation. The woman underwent serial ultrasonographic imaging to monitor the mass. Fetal magnetic resonance imaging obtained at 24 weeks’ gestation revealed a mixed solid-cystic mass in the sacrococcygeal region, extending inferiorly (Figure 2). Elective cesarean section is performed at 37 weeks’ gestation
Birth History and Presentation:

• Apgar scores of 8 at 1 minute and 9 at 5 minutes
• Term female infant has a 14×15–cm mass attached caudally to the sacrum (Figure 1)
• Mass does not transilluminate, has vessels coursing over the surface, and is palpably solid in some places and cystic in others

Figure 2

 Case Progression:
Abdominal radiographs reveal a 13×15-cm broad-based pedunculated soft-tissue mass projecting from the lower sacrococcygeal area (Figure 3).

Figure 3

Postnatal ultrasonography demonstrates a large mass posterior to the coccyx. The mass has a heterogeneous echotexture with solid, cystic, and vascular components. The lower spinal canal appears normal. Serum α-fetoprotein (AFP) concentration is 335,700 ng/mL (35,700 µg/L). The infant undergoes surgery on the third day after birth. Histopathologic examination of the surgical specimen reveals the presence of mature neuroglial tissue, choroid plexus, adipose tissue, smooth muscle cells, squamous epithelium, cartilage, and bone (Figures 4 and 5).

Figure 4 and 5

Differential Diagnosis:
Newborn who has a sacral mass

• Lipoma
• Lymphangioma
• Meningocele
• Rhabdomyosarcoma
• Sacrococcygeal teratoma
• Other malignant pediatric neoplasms

Actual Diagnosis: 
Sacrococcygeal teratoma (SCT)

The Experts:
SCTs are the most common tumors in newborns, occurring in 1 per 20,000 to 40,000 births. Females are four times more likely to be affected than males, but malignant change is seen more frequently in males. Sizes range from 1 to 30 cm, and a large teratoma may account for half of a newborn’s weight. SCTs are believed to arise from embryologically multipotent cells of Hensen’s node, which lies within the coccyx.
The outcome for SCTs diagnosed in utero is much worse than those diagnosed in the neonatal period; the survival rate was 53% in fetuses compared with 85% in neonates in one large series. Potential complications in utero include polyhydramnios, tumor hemorrhage, anemia, congestive heart failure, and nonimmune hydrops fetalis. Development of hydrops is an ominous sign. The presence of hydrops before 30 weeks’ gestation has an abysmal prognosis, with a 93% mortality rate. Because of the poor prognosis associated with development of hydrops prior to 28 to 30 weeks’ gestation, affected fetuses may benefit from in utero resection of the tumor that resolves the hydrops. Development of hydrops after 30 weeks’ gestation is associated with a mortality rate of 25%. If recognized, delivery is recommended as soon as lung maturity is documented. For fetuses that have tumors larger than 5 cm, cesarean delivery should be considered to prevent dystocia or tumor rupture.
SCTs can be diagnosed prenatally as early as 13 weeks of gestation. Ultrasonography reveals a nonhomogenous sacral mass, with calcification in one third of cases. It also defines the extension of the tumor into the pelvis or abdomen as well as mass displacement of the bladder and rectum, with compression of the ureters resulting in hydroureter or hydronephrosis. Prenatally diagnosed tumors should be monitored closely for development of fetal hydrops.
Fetal magnetic resonance imaging is superior to ultrasonography in distinguishing solid tumor from hemorrhage. In addition, absence of acoustic shadowing by the pelvic bones permits accurate definition of cephalic extent and total dimension of the tumor, colon displacement, urinary tract dilatation, and intraspinal extent of a SCT. Such findings are important for surgical planning. 
Ninety percent of infants who have SCTs have a visible mass with a characteristic physical appearance over the sacrum at the time of delivery. The Altman Classification of the Surgical Section of the American Academy of Pediatrics classifies the tumors morphologically, according to their relative extent outside and inside the body, into four types (frequencies are indicated in parentheses):

1. Type I (45%): Predominantly external, projecting from the sacrococcygeal region and presenting with distortion of the buttocks
2. Type II (35%): Predominantly external, but have a large intrapelvic component
3. Type III (10%): Predominantly intrapelvic, with a small external buttock mass
4. Type IV (10%): Entirely internal, with no external or buttock component

 Type IV sacrococcygeal teratomas may occur as a familial form inherited in an autosomal dominant pattern. All of the four types may have an intraspinal component.
Most SCTs, even those that have an intrapelvic component, produce few or no functional symptoms. Large pelvic masses may create rectal or urinary tract compression. Neurologic deficits rarely are present in neonates. The physical examination always should include a rectal examination to evaluate any intrapelvic component. The most helpful imaging studies are plain anteroposterior and lateral radiographs of the pelvis and spine, looking for calcifications in the tumor and for spinal defects, and ultrasonography of the abdomen, pelvis, and spine. 
The recommended treatment is resection of the tumor en bloc with the coccyx in the first week after birth because long delays may be associated with a higher rate of malignancy. Histopathologic examination of SCTs shows the presence of a variety of parenchymal cell types representative of more than a single germ layer, usually all three (ectoderm, mesoderm, and endoderm), as described for the infant in the vignette. Neuroglial tissue, skin, respiratory and enteric epithelium, cartilage, smooth muscle, and striated muscle are the most common elements found. Bone, pancreatic tissue, choroid plexus, and adrenal tissues are identified less commonly. The degree of histologic immaturity is not of prognostic significance because immature tissue is considered normal in neonatal teratomas. The most common malignant component within a teratoma is a yolk sac tumor, also known as endodermal sinus tumor. 
The primary differential diagnosis of neonatal SCTs is meningocele. Typically, meningoceles occur cephalad to the sacrum and are covered by dura, but sometimes they are covered by skin. Physical examination reveals bulging of the fontanelle with gentle pressure on a sacral meningocele, which helps to establish the diagnosis before plain radiography, ultrasonography, and magnetic resonance imaging confirm it. The coexistence of meningocele with teratoma is recognized in the familial form of SCT, but these tumors usually are located presacrally. On histologic examination, meningoceles are characterized by the presence of fragments of spinal cord, glial cells, meningeal tissue, and nerves; glandular tissue is absent.
Other lesions in the differential diagnosis of neonatal sacrococcygeal masses include lymphangiomas, lipomas, rhabdomyosarcomas, and other malignant pediatric neoplasms. The presence of disorganized tissue originating from more than one germ cell layer is a hallmark of SCTs. Lipomas are comprised of mature adipose tissue, lymphangiomas of proliferating lymphatic channels, and rhabdomyosarcomas of rhabdomyoblasts in the absence of mature parenchymal cells from other germ layers.
Postpartum morbidity associated with SCTs is attributable to associated congenital anomalies, mass effects of the tumor, recurrence, and intraoperative and postoperative complications. Approximately 10% of SCTs are associated with other congenital anomalies, primarily defects of the hindgut and cloacal region. The recurrence rate varies between 7.5% and 22%.
Malignancy at birth is uncommon but increases with age and with incomplete resection.  Only 7% to 10% of tumors diagnosed before age 2 months are malignant. However, after 2 months, the incidence of malignancy rises to 66% in boys and 50% in girls. Malignancy generally is not believed to be a function of tumor size but is associated with the invasion of normal structures. Thus, type I lesions almost always are benign, and presacral (type IV) teratomas tend to be diagnosed at an older age and have an increased rate of malignancy. Most yolk sac tumors, the malignant component in SCTs, secrete AFP, which can be measured in the serum and demonstrated in the cells by immunohistochemistry. This marker is particularly useful for assessing the presence of residual or recurrent disease. AFP concentrations normally are very high in neonates and decrease with time. Therefore, high AFP values in the neonatal period have no prognostic significance but are important to assess completeness of tumor resection. The postoperative half-life is approximately 6 days.  Persistently high values after total resection of primary SCT together with the coccyx have been found to be a reliable marker of recurrence of poorly differentiated yolk sac tumors and may be an indication of the need for further surgical procedures or chemotherapy. 
All patients who have SCTs should be re-evaluated every 3 to 6 months for 3 years because there is a small but definite risk of malignant recurrence. The outpatient visit should include a thorough physical examination, including a rectal examination, and measurement of AFP. 

Third-Degree Atrioventricular Block

Third-Degree Atrioventricular Block

Synonym

Complete heart block (CHB)

Definition

                1. PR interval and QRS duration are age-dependent measures of atrioventricular (AV) conduction. Impaired conduction is described as first-degree, second-degree, or third-degree heart block (see Box 5-7).

                2. No impulses from the atria reach the ventricles in third-degree heart block.

Associated Clinical Features

                1. Third-degree heart block is rare in the pediatric age group.

                2. Signs and symptoms in patients with an otherwise normal heart include:

                a. Usually asymptomatic

                b. Older children may present with syncope (syncope from a high-degree AV block not related to positional changes or exertion is called a Stokes-Adams attack).

                c. Older infants may present with night terrors, irritability, or tiredness with frequent naps.

                d. Acquired heart block is frequently symptomatic, with syncope, congestive heart failure (CHF), shock, or sudden death.

                3. Prominent peripheral pulses (secondary to large compensatory stroke volume)

                4. Cardiomegaly (secondary to increased diastolic ventricular filling)

Consultation

Cardiology

Emergency Department Treatment and Disposition

                1. Patients presenting with symptoms (e.g., syncope, CHF) or newly diagnosed patients require hospitalization.

                2. Symptomatic newborns (e.g., heart failure, evidence of hydrops) with CHB with ventricular rates  50 bpm require cardiac pacing. Adrenergic agents (epinephrine or isoproterenol) or a vagolytic agent (atropine) may be tried to increase the heart rate while awaiting placement of the pacemaker.

                3. Cardiac pacing (transthoracic [epicardial], transcutaneous, or transvenous) is also required in symptomatic patients with CHB and congenital heart disease (CHD).

                4. Temporary pacing may be required in postoperative CHB following surgery for CHD.

Clinical Pearls: Third-Degree Heart Block

                1. Autoimmune disease accounts for 60 to 70% of all cases of congenital CHB.

                2. About 25 to 33% of cases of CHB occur in patients with associated structural heart disease.

                3. Complete heart block may not present at birth in infants born to mothers with SLE, and may develop within the first 3 to 6 months after birth (Fig. 5-6). Unlike other manifestations of neonatal lupus that resolve, CHB is permanent and patients often require cardiac pacing.

                4. An implantable pacemaker is used to prevent sudden death in symptomatic patents with CHB.

Box 5-13. Third-Degree Atrioventricular Heart Block

Characteristic features:

 Failure of conduction of atrial impulses to the ventricles

 AV dissociation (the atria and ventricles beat completely independently and P waves and QRS complexes have no constant relationship)

 The ventricles are paced by an escape pacemaker at a rate slower than the atrial rate.

 The QRS duration may be prolonged or may be normal if the heartbeat is initiated high in the bundle of His (generally, the lower the location of the pacemaker within the ventricular conduction system, the slower the heart rate and the wider the QRS complexes).

Box 5-14. Etiology of Third-Degree Atrioventricular Block

Some examples of congenital or acquired diseases leading to complete heart block include:

 Infants born to mothers with systemic lupus erythematosus (SLE), rheumatoid arthritis, dermatomyositis, or Sjögren's syndrome (autoimmune destruction of AV tracts by maternally-derived IgG antibodies)

 Complex congenital heart anomaly (e.g., common AV canal)

 Abnormal embryonic development of the conduction system

 Postsurgical repair of congenital heart disease involving the ventricular septum

 Myocarditis

 Long QT syndrome

 Lyme disease (87% incidence of AV block in patients with carditis with Lyme disease)

  Digoxin toxicity

 Myocardial tumors

 Myocardial abscess due to endocarditis

Ventricular Tachycardia

Ventricular Tachycardia

Definition Ventricular tachycardia (VT) is defined as three or more consecutive premature ventricular contractions (PVCs). Associated Clinical Features 1. Ventricular tachycardia is uncommon in the pediatric age group. 2. Heart rate in VT varies from near normal to more than 200 bpm. 3. Stroke volume and cardiac output may become compromised with rapid ventricular rates, and VT may deteriorate into pulseless VT or VF. 4. Presenting signs and symptoms of VT include: a. Sudden onset of rapid heartbeat and palpitations b. Chest pain c. With slower tachycardia: fatigue, lethargy, or symptoms of CHF d. Syncope e. Occasionally asymptomatic f. Cardiac arrest g. Signs of circulatory impairment (poor end-organ perfusion) 1) Skin perfusion: color pale, cyanotic, or mottled, cool extremities, prolonged capillary refill 2) Peripheral pulses: rapid, thready, weak, or absent 3) Discrepancy in volume between peripheral and central pulses 4) CNS: irritable, lethargic, confused, or decrease in level of consciousness 5) Diminished response to pain 6) Respiratory difficulty 7) Pulse pressure decrease of >20 mmHg 8) Hypotension (decompensated shock) 9) Decreased or no urine output 5. Electrocardiographic findings of VT include: a. P waves usually not identifiable b. If P waves are present, they are not related to the QRS complex (AV dissociation; P wave slower than the QRS rate) c. Ventricular rate at least 120 bpm (usually 120 to 200 bpm) d. Ventricular rate regular e. Wide QRS complex (>0.08 second [QRS width is age dependent in children]; Fig. 5-15) f. T waves usually opposite in polarity to QRS complex 6. Radiographic findings seen in VT are related to the presence of underlying heart disease. View Large Figure 5-15. Ventricular Tachycardia Add to 'My Saved Images' Ventricular rhythm is rapid and regular. Note QRS widening of >0.08 second and absence of atrial depolarization. Consultation Cardiology (usually after initial stabilization) Emergency Department Treatment and Disposition 1. Assess and support ABCs as needed (provide 100% oxygen, ventilation as needed, continuous cardiac and pulse oximetry monitoring) 2. During evaluation identify and treat possible contributory causes (see Box 5-1 for "H"s and "T"s of CPR). 3. VT with palpable pulses and adequate perfusion: a. Consult a pediatric cardiologist. b. Synchronized cardioversion: 0.5 to 1 joule/kg (consider sedation; may double dose if initial dose ineffective) or c. Consider alternative medications (any of the following; do not give amiodarone and procainamide together): 1) Amiodarone given intravenously at a loading dose of 5 mg/kg over 20 to 60 minutes followed by a continuous infusion at rates of 5 to 10 g/kg per minute (5 to 10 mg/kg per day) or 2) Procainamide given IV at a loading dose of 15 mg/kg over 30 to 60 minutes followed by a continuous infusion of 30 to 50 g/kg per minute (rate of infusion directed by measurement of serum levels) or 3) Lidocaine (easiest and safest drug) given as an IV bolus at a dose of 1 mg/kg followed by a continuous infusion of 30 to 50 g/kg per minute (rate of infusion directed by measurement of serum levels [2 to 5 g/mL]) 4. VT with palpable pulses and poor systemic perfusion: a. Immediate synchronized cardioversion (same as above; do not delay cardioversion for sedation) or b. Consider alternative medications (amiodarone, procainamide, or lidocaine; same as above) 5. VT without palpable pulses and poor systemic perfusion (pulseless VT): a. Begin CPR and attempt defibrillation. b. Treatment same as for ventricular fibrillation/pulseless arrest (see Box 5-29) 6. Following stabilization, all patients require hospitalization in the PICU for continuous monitoring and subsequent management. Clinical Pearls: Ventricular Tachycardia 1. Ventricular tachycardia may degenerate into ventricular fibrillation. 2. Aberrant SVT presents with a wide QRS complex and may resemble VT. If uncertain, all wide-complex tachycardias are assumed to be VT unless proved otherwise. 3. Both amiodarone and procainamide prolong the QT interval, and when given rapidly together can cause vasodilatation, hypotension, and increase the risk of heart block and polymorphic VT. Box 5-25. Etiology of Ventricular Tachycardia Structural congenital heart disease or post–cardiac surgery (most common etiologies)    (1) Tetralogy of Fallot    (2) Eisenmenger's syndrome    (3) Aortic stenosis    (4) Transposition of the great arteries    (5) Anomalies of coronary arteries Cardiac catheterization (mechanical irritation) Prolonged QT syndrome (see Fig. 5-7) Myocarditis (e.g., viral) Cardiomyopathy (e.g., dilated, hypertrophic) Pulmonary hypertension Arrhythmogenic RV dysplasia Cardiac tumors Drugs or poisons (see Box 5-26) Possible contributory causes: "H"s and "T"s of CPR (see Box 5-1) Box 5-26. Drugs That Cause Ventricular Tachycardia and Supraventricular Tachycardia    (1) Anticholinergics    (2) Antihistamines    (3) Catecholamine infusion    (4) Digitalis toxicity    (5) Tricyclic antidepressants    (6) Phenothiazines    (7) Sympathomimetics (e.g., beta-agonists, alpha-agonists, cocaine, amphetamines, phencyclidine)    (8) Sedative hypnotics (e.g., chloral hydrate, ethanol)    (9) Antidysrhythmics (classes I through IV)    (10) Thyroid hormone    (11) Carbamazepine Box 5-27. Differential Diagnosis of Ventricular Tachycardia Supraventricular tachycardia (SVT) with aberrant conduction (due to bundle-branch block or WPW syndrome)    (1) Seen in 10% of children with SVT    (2) Presents with wide QRS complex and may resemble VT    (3) The ability to terminate tachycardia with vagal maneuvers does not distinguish SVT from VT.    (4) Hemodynamic stability also does not predict SVT versus VT (e.g., a patient without signs of circulatory impairment with a wide-complex tachycardia is more likely to have VT, and should not be assumed to have SVT).    (5) Erroneously treating VT as SVT can be devastating (VT deteriorates into pulseless VT/VF).

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Description		We are committed to your success in more than 10 medical PG entrance exams (PGI, AIIMS, JIPMER, CMC etc) conducted every year all over India. We provide self learning modules to learn practice and improve speed for acing tough entrance exams. Our content is developed by Dr. N.S. Mani, Professor of Pediatrics at Government Medical College, Thrissur. Dr Mani was university gold medalist in all 16 subjects of MBBS curriculum. He has aced medical PG entrance exams securing 1st rank in Kerala state PG entrance, 3rd rank in PGI, 4th rank in CMC Vellore in 1984.
Mission		To provide Medical PG aspirants the BEST content for acing entrance examinations
Products		1. PG Entrance Test Practice Session (PGET) : Carefully selected questions collected over last 27 years. These sessions are arranged in topic/subject wise. Learn to ace 20 high impact questions in each 10 minute session. 2. Concept Bridge (CB) : A unique presentation of theoretical concepts using advanced learning techniques (logical sequential problem solving) perfected by Dr Mani in his rich 30 years of teaching experience. CBs are aimed at preparing you to meet the unknown challenges faced in entrance tests (and real life). These are presented in 5-10 minutes of power packed Youtube videos. 3. Clinical Pathological Correlation (CPC) : Youtube videos providing simple explanation of esoteric cases. Fortify concepts learnt in CB and during your classes by seeing how real life cases are successfully solved to the expectation of patients (and your professors!).

Email	acepgmed@gmail.com
Phone	+91 9400314583

 What to do?

First visit the  Channel - http://www.youtube.com/acepgmed

By subscribing once in the channel by clicking on the “subscribe” button you will get updates as and when a new video is streamed.

The viewer can use the “pause” button in the browser to freeze a frame to complete the reading of one frame while the video is being streamed.

Then use the “play button” in the browser to resume the video.

 

Use the full screen option to enlarge the view

Topics are arranged on the basis of subjects. Table of Contents (TOC) will be mailed to you regularly.

If you have face book account then link your FB home page to http://www.facebook.com/acepgmed to get updated.

 

Almost all new generation mobile phones which came to market after 2010 can support the YouTube video streaming.

Have a nice experience with

Dr N S Mani MD

Additional professor

Govt Medical College Thrissur,680004