Cardiac Emergencies

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Chapter 31 Cardiac Emergencies

Sarah W. Alander, MD, James Edward Hulse, III, MD

1 What are the new pediatric advanced life support (PALS) recommendations regarding the use of endotracheal tube resuscitation medications?

The IV or intraosseous (IO) route of administration is preferred. The endotracheal tube (ETT) doses of resuscitation medications are not listed in the updated advanced cardiac life support algorithm for pulseless arrest. They may be used if IV or IO access is not obtained. The thinking is that drugs administered into the trachea result in a lower blood concentration than the same dose given via the IV route. Lower epinephrine concentrations may produce transient β-adrenergic effects, leading to hypotension and reduced coronary artery perfusion pressure.

American Heart Association: Currents in Emergency Cardiovascular Care. 16:2005–2006. Available at www.americanheart.org/downloadable/heart/1132621842912Winter2005.pdf.

2 If ETT resuscitation medications are used, how does the technique differ compared with the previous PALS recommendations?

The recommended dose should be diluted in water or normal saline and injected directly into the ETT. Previously, health care providers were urged to pass a catheter beyond the tip of the tracheal tube to inject the drugs.

American Heart Association: Currents in Emergency Cardiovascular Care. 16:2005–2006. Available at www.americanheart.org/presenter.jhtml?identifier=3012268.

3 Is high-dose epinephrine still recommended in pediatric cardiac arrest?

The 2005 American Heart Association recommendation is as follows: Use a standard dose of epinephrine (0.01 mg/kg body weight via IV/IO route) for the first and subsequent doses. There is no survival benefit from use of high-dose epinephrine, and it may be harmful, particularly in patients with asphyxia.

American Heart Association: Currents in Emergency Cardiovascular Care. 16:2005–2006. Available at www.americanheart.org/presenter.jhtml?identifier=3012268.

4 What is bradycardia? When is it a significant threat to the health and well-being of patients?

The definition of bradycardia is a heart rate less than 80 beats per minute in newborns and less than 60 beats per minute in infants and children. It is significant when it results in symptoms of shock such as hypotension, acidosis, lethargy, and coma.

5 What are indications for emergency or urgent intervention in a patient with bradycardia?

Intervention is necessary in the bradycardic patient with a history of syncope or with symptoms of poor perfusion (decreased capillary refill, hypotension, and altered consciousness).

6 What are the initial steps in treatment for a patient with hemodynamically compromising bradycardia?

Assess the airway. Remove any foreign body from the airway, if present, and reposition the patient (jaw-thrust maneuver). After securing a patent airway, assist respiration with 100% oxygen, and perform chest compressions for heart rate < 80 beats per minute in newborns, < 60 beats per minute in infants and children. Give atropine (0.002 mg/kg via IV route, with 0.1 mg as minimum dose and 0.5 mg as maximum dose) or epinephrine (1:10,000, 0.01 mg/kg via IV route). Recall that both atropine and epinephrine can be given via IV, IO, or endotracheal route. However, IV and IO routes are preferred.

7 What criteria are considered absolute indications for implantation of a permanent pacemaker for rate support?

Patients with a history of syncope or symptoms related to bradycardia should not be released from the emergency department (ED) until close cardiology follow-up has been arranged. Absolute indications for permanent pacemaker include the following:

Complete heart block with history of syncope or symptoms

Heart block after repaired congenital heart disease

Heart block in an infant with associated congenital heart disease

Heart block in an infant younger than 6 months of age with a sustained heart rate less than 55 beats per minute

KEY POINTS: CAUSES OF BRADYCARDIA IN CHILDREN

1 Noncardiac: Hypoxemia (most common), central nervous system insult, sepsis, hypothermia, poisoning, anorexia nervosa, hypothyroidism

2 Cardiac: Cardiomyopathy, complete heart block, sick sinus syndrome

8 Give the corrected QT criteria for determining prolongation of the QT interval for differences between children and adults and between males and females

Corrected QT is the calculation of QT measured/√RR interval.

In children and infants, the maximum normal corrected QT interval (QTc) is 440 msec.

In adolescent and adult males, it is 450 msec.

In adolescent and adult females, it is 460 msec.

Case CL: Diagnosis and treatment of pediatric arrhythmias. Pediatr Clin North Am 46:347–354, 1999.

9 List the associated electrocardiographic findings that may be useful clues to help establish the diagnosis of long QT syndrome

Torsades de pointes

Intermittent T-wave inversions (T-wave alternans)

Notched T waves

Low heart rate for age

10 What history in a patient presenting with sudden and unexpected syncope would make you consider familial long QT syndrome?

History of sudden unexplained death in an immediate family member under the age of 30

Definite family history of long QT syndrome or familial deafness

An episode of syncope precipitated by sudden stress or startle

11 What is the first treatment for patients with known familial long QT syndrome?

First-line treatment is a β-blocker, such as propanolol (2–4 mg/kg/day). In adolescents, a once-daily dose of long-acting propanolol can be used. Treatment should be instituted regardless of presence or absence of symptoms.

12 List several reasons for an abnormally long QTc interval that is not due to familial long QT syndrome

Electrolyte disturbances such as hypomagnesemia, hypocalcemia, hypokalemia

Central nervous system insult (increased intracranial pressure, hypoxia)

Anorexia nervosa or liquid protein diets

Many drug ingestions

13 What is the most common arrhythmia in childhood?

Supraventricular tachycardia.

14 What is the usual heart rate for infants and children with supraventricular tachycardia (SVT)?

Infants with SVT have heart rates of 220–230 beats per minute. Heart rates of older children are 150–250 beats per minute.

15 What is the most likely presentation for children with SVT?

Older children may report chest pain, palpitations, or dizziness. Infants may present with tachypnea, irritability or lethargy, poor perfusion, and other signs of congestive heart failure.

16 What are the preferred vagal maneuvers used to convert SVT to normal sinus rhythm in infants and children?

Consider vagal maneuvers if the patient is stable and without symptoms.

Application of a bag of ice with water to the face for 15–30 seconds is effective in 30–60% of patients.

In infants, rectal stimulation with a thermometer may be effective.

In children, the Valsalva maneuver via bearing down for 15–20 seconds provides vagal stimulation.

Orbital pressure and carotid massage are not recommended in children.

Kugler JD, Danford DA: Management of infants, children, and adolescents with paroxysmal supraventricular tachycardia. J Pediatr 129:324, 1996.

17 Which medication is the treatment of choice for SVT?

Adenosine (0.1 mg/kg) given as a rapid IV bolus, followed by an immediate bolus of saline, 5 mL. This prevents metabolism of adenosine by red blood cells before it reaches the heart. Double the dose of adenosine if conversion is unsuccessful. Adenosine has been reported to terminate atrioventricular reentrant tachycardia in 85–90% of cases. SVT recurs soon after termination in 25–30% of cases.

Losek JD, Endom E, Dietrich A, et al: Adenosine and pediatric supraventricular tachycardia in the emergency department: Multicenter study and review. Ann Emerg Med 33:185, 1999.

18 Which initial steps should be performed in the management of a pediatric patient presenting with an excessively fast heart rate?

As with all emergencies, establish ABCs first. Then perform synchronized cardioversion for the hemodynamically compromised patient. If the patient appears stable, obtain a brief history directed toward the underlying cause, such as dehydration or blood loss, febrile illness, and exposure to toxins or drug overdose. Obtain an electrocardiogram (ECG) and IV access. Assess the ECG for wide versus narrow tachycardia, rate for age, and rhythm. Remember that infants and children tolerate much more rapid rates than adolescents and adults.

19 Describe the appropriate treatment of a patient presenting with hemodynamic compromise (unconsciousness, shock, and disorientation) due to excessively fast rhythm (either wide or narrow complex tachycardia)

Maintain a patent airway, assist breathing with 100% oxygen, and treat with synchronized cardioversion with an initial energy dose of 0.5–1 J/kg. If this is not effective, increase the dose to 2 J/kg.

20 Give the initial rhythm differential diagnosis for patients presenting with sustained wide complex tachycardia

Unlike in adults, the definition of wide QRS is not always a duration longer than 100 msec. The normal QRS duration increases with age. The infant or small child may have a widened QRS complex (abnormal ventricular activation) without duration longer than 100 msec.

Regardless of the patient’s level of consciousness, consider ventricular tachycardia (VT) first in the patient with wide complex tachycardia. Other causes include SVT with bundle-branch block or SVT with aberrant conduction.

21 Describe the initial treatment/assessment plans for a patient presenting with sustained wide complex tachycardia not associated with hemodynamic compromise

Assess ABCs. Consider VT first, and give amiodarone, 5 mg/kg over 20–60 minutes, or procainamide, 15 mg/kg via IV route over 30–60 minutes, or lidocaine, 1 mg/kg via IV bolus.

American Heart Association: Handbook of Emergency Cardiovascular Care For Healthcare Providers. Dallas, TX, American Heart Association, 2006.

KEY POINTS: WIDE COMPLEX TACHYCARDIA

1 Causes may be VT, SVT with bundle-branch block, or SVT with aberrant conduction.

2 Assume VT, regardless of clinical status of patient, and give lidocaine.

22 Define congestive heart failure. List signs and symptoms in infants or small children

Congestive heart failure is the pathophysiologic state in which the heart is unable to pump enough blood to meet metabolic demands. The primary symptoms in infants are tachycardia (heart rate > 160 beats per minute) and respiratory distress, indicated by tachypnea and grunting. The infant may have hepatomegaly and decreased capillary refill as well. Older children have tachycardia with heart rate > 100 beats per minute, extra heart sounds (S₃ and S₄), and decreased capillary refill. They may also have peripheral edema and ascites.

23 What are the most likely causes of heart failure in neonates presenting to the ED?

Structural congenital heart disease is the most likely cause of heart failure in the neonate. In the first week of life, transposition of the great vessels or total anomalous pulmonary venous return are the most likely causes. Between weeks 1 and 4, critical aortic stenosis or pulmonary stenosis or preductal coarctation of the aorta is the most likely cause.

Lee C, Mason LJ: Pediatric cardiac emergencies. Anesth Clin North Am 19:287–308, 2001.

24 What is the clinical presentation of the neonate with congestive heart failure?

Congestive heart failure in the very young infant is easily confused with sepsis, meningitis, pneumonia, or bronchiolitis. Affected infants have a history of poor feeding, grunting, tachypnea, tachycardia, pulmonary rales, or rhonchi. Presence of hepatomegaly, weak or absent peripheral pulses, and cardiomegaly on chest radiograph help to distinguish heart failure from other illnesses. Echocardiography confirms the diagnosis.

25 What is the initial ED management of the neonate with congestive heart failure?

Secure the airway and ventilate. Administer oxygen to maintain SaO₂ at 75–80%. Obtain IV access and administer prostaglandin E₁ (0.05 μg/kg/min) to reopen the ductus arteriosus.

26 Describe the difference between “digoxin effect” and “digoxin toxicity”—both clinically and in terms of ECG findings

The patient who is therapeutic while receiving digoxin may show ST segments that are depressed and concave upward. The QT interval is shortened, and the PR interval is increased. Heart rate decreases. The patient with significant digoxin toxicity may present with nausea and vomiting. The ECG may show profound sinus bradycardia, atrioventricular block, or tachyarrhythmia (junctional tachycardia).

27 List the expected ECG findings or clinical manifestations of patients who have received overdoses of the following medications:

β-blockers: Bradycardia, increased PR interval

Calcium-channel blockers: Bradycardia, prolonged atrioventricular node conduction or block

Tricyclic antidepressants: Tachycardia, prolonged QRS, decreased atrioventricular conduction time, VT, ventricular fibrillation, torsades de pointes

Phenothiazines: QTc prolongation, torsades de pointes

Type 1A antiarrhythmic medications (quinidine, procainamide, disopyramide): Prolongation of QT interval, torsades de pointes, and ventricular tachycardia

Amiodarone: Atrioventricular block, sinus node dysfunction (marked bradycardia), torsades de pointes

Clancy C: Electrocardiographic evaluation of the poisoned or overdosed patient. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Goldfrank’s Toxicologic Emergencies, 6th ed. Stamford, CT, Appleton and Lange, 2002, pp 105–128.

28 What potential long-term cardiac toxicity is likely in a patient who has a history of previously treated cancer?

Cardiomyopathy has been described in patients who have been treated with anthracyclines such as doxorubicin and daunomycin. Pericarditis may be seen in patients who have had mediastinal radiation.

29 List some of the late complications after the Fontan operation that may be encountered in the ED

Supraventricular arrhythmias: Atrial flutter, atrioventricular reentry tachycardia, atrial ectopic tachycardia, pleural effusions

Thromboembolic complications: Cerebrovascular accident, inferior or superior vena cava syndrome, pulmonary embolus

Protein-losing enteropathy

Pulmonary arteriovenous fistulas

Tsai W, Klein B: The postoperative cardiac patient. Clin Pediatr Emerg Med 6:216–221, 2005.

30 Describe the ECG changes seen at varying levels of hyperkalemia

K⁺ 5–6 mEq/L: Peaked T waves

K⁺ > 6 mEq/L: ORS widening

K⁺ > 7 mEq/L: Increased P-R interval

K⁺ 8–9 mEq/L: Disappearance of P waves and irregular ventricular rate

K⁺ 12–14 mEq/L: Ventricular fibrillation or asystole

Gewitz M, Woolf P: Cardiac emergencies. In Fleisher G, Ludwig S, Henretig F (eds): The Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, p. 744.

31 What is the most common cause of chest pain in children?

Parents often fear chest pain as a sign of cardiac disease. Fortunately, most chest pain in children is noncardiac in origin. The most common causes are idiopathic chest pain, musculoskeletal, costochondritis, asthma, gastroesophageal reflux and esophagitis, pneumonia, and pneumothorax.

32 What are cardiac causes of chest pain in children?

Obstructive hypertrophic cardiomyopathy, aortic stenosis, pericarditis, arrhythmias, coronary insufficiency, and mitral valve prolapse can all cause chest pain.

33 What are the cutaneous criteria of rheumatic fever?

Erythema marginatum and subcutaneous nodules. Erythema marginatum appears on the trunk and proximal extremities and is evanescent. It is described as a lacy rash and is not pruritic. Subcutaneous nodules are found over extensor aspects of joints, such as the elbows. They are firm and mobile.

34 How does a child with myocarditis present?

The manifestations of myocarditis are very nonspecific; the affected child often presents with symptoms of congestive heart failure. Also consider the diagnosis of myocarditis in a child with unexplained tachypnea and tachycardia or a new onset of sustained arrhythmia. A low-grade fever is often present. Some children report chest pain, or possibly back pain.

35 What are the ECG findings of myocarditis?

The ECG findings are nonspecific, adding to the diagnostic dilemma. Delayed atrioventricular conduction (AV block), prolongation of QTc, decreased amplitude of the T wave, low QRS amplitude (5 mm or less in all six limb leads), arrhythmias, or ectopic beats may all be seen in the patient with myocarditis.

36 Describe the two murmurs that may be heard in a patient with tetralogy of Fallot

Classically, tetralogy of Fallot consists of pulmonic stenosis, ventricular septal defect (VSD), dextroposition of the aorta, and right ventricular hypertrophy. The two murmurs are of pulmonic stenosis and VSD. The VSD murmur is generally early to holosystolic, harsh, and heard best at the lower left sternal border. The pulmonic stenosis murmur is a high-pitched, systolic ejection murmur that is best heard at the upper left sternal border and radiates to the left infraclavicular area. It is a crescendo-decrescendo type.

37 What is a hypercyanotic, or “tet,” spell?

A “tet” spell is an episode of cyanosis that occurs in the infant or small child with uncorrected tetralogy of Fallot. Such spells can occur in both acyanotic patients (“pink tets”) and in patients who are consistently cyanotic. The underlying problem is a decrease in pulmonary blood flow, probably due to a spasm of the infundibular muscle, thus obstructing the right ventricular outflow tract. The spells occur most often in the morning after awakening, may be precipitated by activity and are heralded by the infant becoming fussy. As the hypoxemia worsens, the infant may become lethargic or unconscious.

38 How should a tet spell be managed initially?

Place the infant in knee-chest position, either prone with the knees brought up under the abdomen or held against an adult’s chest with the knees drawn up. Administer oxygen and give morphine sulfate (0.1–0.2 mg/kg via intramuscular or subcutaneous route).

39 What is the mechanism of action of morphine in alleviating a tet spell?

Morphine may help either because of its negative inotropic effect on the infundibular myocardium or by breaking the cycle of agitation that leads to an increased oxygen requirement.

40 When should echocardiography be performed in a patient with suspected Kawasaki disease?

An echocardiogram should be obtained as soon as Kawasaki disease is suspected. It may help to confirm the disease; if the disease is certain, it allows a baseline evaluation of cardiac function.

Newburger JW, Takahashi M, Gerber MA, et al: Diagnosis, treatment, and long-term management of Kawasaki disease: A statement for health professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation 110:2747, 2004.

41 What are the cardiac complications of Kawasaki disease?

Coronary artery aneurysm (major complication)

Decreased myocardial contractility

Pericardial effusion

Mild valvular disease

Coronary arteritis

Sundel R: Clinical manifestations and diagnosis of Kawasaki’s disease, 2006. Available at www.uptodate.com.

42 What are the cardiac conditions causing sudden death in young athletes?

Hypertrophic cardiomyopathy

Coronary artery anomalies

Aortic rupture (Marfan syndrome)

Commotio cordis

Arrhythmogenic right ventricular hypertrophy

Maron BJ, Shirani J, Poliac LC, et al: Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA 276:199–204, 1996.

43 What is the most common cause of sudden cardiac death in the pediatric population?

Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in children and adolescents, accounting for about half of the 500 annual deaths. There currently are no guidelines for screening of athletes, although the ECG will be abnormal in 75–95% of cases.

Berger S, Kugler J, Thomas J, et al: Sudden cardiac death in children and adolescents: Introduction and overview. Pediatr Clin North Am 51:1201–1210, 2004.

44 What are the common ECG findings in children with hypertrophic cardiomyopathy?

The ECG shows left ventricular hypertrophy in most patients with hypertrophic cardiomyopathy. Echocardiography provides definitive diagnosis.

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