PEM|BRS: Cardiology & Endocrinology

Pediatric ECG Evaluation:

Rate:

  • 300, 150, 100, 75, 60, 50
  • For Brady: cycles/6 sec strip (2 markers long) x 10 = Rate

Rhythm:

  • Is PR interval > one large square? (1st degree heart block)
  • Is there a P before every QRS and a QRS after every P? (2nd or 3rd degree heart block)
  • 2nd degree AV Block:
  • Mobitz Type I (Wenckebach) = PR gradually lengthens until last QRS dropped
  • Mobitz Type II =Ratio of P’s to QRS’s (2:1, 3:1, 4:1)
  • 3rd degree Block: AV Dissociation
  • Is QRS interval > 3 tiny squares? (BBB): Note: criteria then for VH are unreliable
  • RBBB: Find R,R’ in V1 or V2 (right chest leads)
  • LBBB: Find R,R’ in V5 or V6 (left chest leads)

Axis:

  • Is QRS + or – in leads I & AVF? (I+,AVF+=Nml; I+,AVF-=LAD; I-,AVF+=RAD)
  • Rotation: Find the isoelectric QRS in a chest lead (V1,V2=right; V3,V4=Nml; V5, V6=left)

Hypertrophy: Check V1!!!

  • RAH=Large diphasic P wave with tall initial component
  • LAH=Large diphasic P wave with wide terminal component
  • RVH:* R > S in V1 but R gets progressively smaller from V1-V6

* S wave persists in V5 and V6

* RAD with slightly widened QRS

* Rightward rotation in the chest leads

  • LVH:* S in V1 plus R in V5 = > 35mm

* LAD with slightly widened QRS

* Leftward rotation in the chest leads

* Inverted asymmetric T wave slants down gradually but up rapidly

Infarction:

  • Ischemia: inverted symmetrical T wave (normally, T is up when QRS is up, etc.)
  • Injury: ST segment elevation or depression
  • Infarction: Q waves (significant=1mm wide or 1/3 amplitude of entire QRS complex)
  • Location: I & AVL=Lateral; II, III, & AVF=Inferior; V1 & V2=Anterior

Syndrome Screen:

  • WPW Syndrome: Short PR interval, Delta wave
  • Long QT Syndrome: QTc > 0.46; QT/square root of R-R
  • HOCM: Deep Q, raised ST in II, III, aVF, & LVH; Lateral ST-T wave flattening & LAD
  • Arrhythmogenic RV Dysplasia: T inversion in V 1 - 3, epsilon wave
  • Brugada Syndrome: RBBB with ST elevation in V1-V3
  • Wellens Syndrome: T inversion in V2-V3 [Ant. Desc. Coronary Stenosis]
  • PE: SI, QIII, Inverted TIII, Right BBB/RAD; Inverted T V1-4, and ST depression II
  • Pericarditis: Flat or concave elevated ST segment, dec. voltages, entire T above baseline
  • Untx’d Kawasaki’s Dz: Inverted T, ST elevation, Q’s in Lateral leads (Lat wall MI)

Continued EKG Notes:

Potassium:

  • Increased K: (pick-up the T) Peaked T, wide QRS, wide, flat P, which progresses to no P
  • Decreased K: (push-down the T) Flat T and U wave appears

Calcium:

  • Increased Ca: Short QT
  • Decreased Ca: Long QT

Neonates:

  • During first week of life have RAD, large R waves and upright T’s in V3R, V4R, and V1, V2
  • Upright T’s that persist in the right precordial leads (V3R, V4R, V1, V2) beyond the first week of life are an abnormal finding indicative of RVH or RV strain even in the absence of QRS voltage criteria, until proven otherwise.

HOCM:

Syncope associated with exertion, and physical examination reveals a murmur whosedescription (midsystolic harsh ejection murmur at the lower left sternal border without any clicks or gallop) is typical for hypertrophic obstructive cardiomyopathy (HOCM). Echocardiography is diagnostic for HOCM.

Murmurs:

As many as 90% of children have an audible murmur at some point in time, particularly during a febrile illness. However, fewer than 5% of heart murmurs in children denote cardiac pathology. If the patient is asymptomatic, does not have extracardiac congenital malformation or evidence of cardiac abnormality, and has a murmur that demonstrates characteristic features of an innocent murmur, additional evaluation is not warranted.

Other serious or life-threatening causes of murmurs include valvulitis in association with rheumatic fever and myxoma. Valvulitis in association with acute rheumatic fever most commonly affects the mitral valve and produces a transient short mid-diastolic murmur (Carey Coombs). Untreated rheumatic fever can lead to destruction of the valve and result in mitral or aortic stenosis or insufficiency. A myxoma is the most common cardiac tumor that can occur at any age. The signs and symptoms usually stem from obstruction of the ventricular outflow tract or of the mitral valve as the tumor moves with blood flow.

Acute severe mitral regurgitation can occur in other clinical settings. These include infective endocarditis with destruction of the leaflet tissue; papillary muscle rupture as a delayed complication of acute myocardial infarction; blunt chest wall trauma (often seemingly trivial) leading to papillary muscle contusion or rupture or detachment of the chordae; and rupture of the chordaetendineae in the setting of a myxomatous mitral valve disease, usually as part of a generalized connective tissue disorder, as seen in Marfan syndrome.

MR is the common manifestation of valvular dysfunction in children with rheumatic heart disease.

MVP is the most common valvular problem seen in practice and is the most common cause of MR in the US. Mid-systolic click with a late-systolic murmur.

WPW Syndrome:

The ECG tracing for the patient below reveals a typical pattern for Wolf-Parkinson-White (WPW), characterized by a short PR interval, widened QRS intervals, and delta waves (particularly prominent in leads V1 and V6)

Patients who have WPW are at risk for supraventricular tachycardia, acute drop in blood pressure with resulting syncope, and in extreme cases, sudden death. Patients should be referred promptly to a cardiologist for possible ablation.

If unstable SVT (hypotensive and/or mental status changes), you need immediate synchronized cardioversion. Use amiodarone in these patients only if cardioversion fails to convert SVT to a normal rhythm.

Vagal maneuvers are the initial treatment of choice in stable SVT. Adenosine would be indicated if IV access was already established and immediately available.

PSVT is the most common symptomatic dysrhythmia

Syncope:

“Exertional syncope” or syncope with exercise and other physical activities, should raise suspicion for cardiac causes and prompt screening ECG in the ED. Another serious cause of exertional syncope is exercise-induced anaphylaxis.

The pathophysiology of syncope generally is believed to be transient loss of oxygen (due to hypoxia or loss of blood flow) or nutrient supply to the brain. Syncope can be difficult to distinguish from seizures, and both can occur together. One characteristic that distinguishes syncope from seizures is the lack of a postictal period for isolated episodes of syncope.

In infants, syncope usually is accompanied by other signs and symptoms. The most common cause is breath-holding spells, with the child crying and holding his or her breath until developing cyanosis or pallor. The transient hypoxia causes syncope. The episodes, although frightening to parents, are self-limited.

Situational syncope is another common entity in children and adolescents. The “situation” typically is activities that induce vagal tone, including micturition and hair combing.

The most common cause of syncope in children is “vasovagal syncope” (neurocardiogenic syncope), whose pathophysiology involves increased venous pooling that leads to hypotension. In susceptible individuals, the vagal tone increases paradoxically, leading to reflexive bradycardia, decrease of brain blood flow, and syncope.

Pregnancy causing syncope should be considered in any adolescent female. Fluid shifts and also bleeding from an ectopic pregnancy can cause syncope.

Under the age of 6 years, breath-holding, seizures, and arrhythmias are more likely to be the cause of syncope than in adolescents (where it’s caused mostly by neurocardiogenic syncope)

If a diaphoretic, weak, and tachycardic child has missed meals, hypoglycemia is a consideration. Dieting, diuretic use and exertion can lead to orthostatic hypotension

If, at the onset of the event, the child was crying, urinating, defecating, or coughing, a vagally-mediatedsyncopal event is probable; these are typically preceded by nausea, light-headedness, and a slow visual loss.

Changing positions from lying to standing just prior to syncope indicates orthostatic hypotension.

Syncope that occurs when a child is sitting is more likely to be a cardiac arrhythmia.

A slow recovery, mental confusion, abnormal eye movement, or urinary incontinence during the event suggest a seizure.

Severe pallor or cyanosis suggests a cardiac origin.

Orthostatic hypotension is when the systolic BP decreases by 20 or the diastolic BP decreases by 10 when going from supine to standing.

Intermittent AV block (“Stokes-Adam Attack”) can cause syncope that is accompanied by tonic clonic seizure activity 10-20 seconds after the onset of asystole with rapid return to normal mentation—this is why you always get an ECG with possible new-onset seizure disorder

Congenital Long QT Syndrome have a QTc >0.46sec; syncope may be triggered due to adrenergic arousal from intense emotion, exercise, awakening, swimming, diving, auditory stimuli, suddenly being startled)

Breath holding spells may respond to iron therapy for iron deficiency anemia; spell is heralded by emotional upset and escalating crying, followed by color change and LOC with a rapid return to baseline (may have jerking movements—brief)

Hypertrophic Cardiomyopathy:

In LVOT Obstruction (hypertrophic cardiomyopathy) patient may have a near syncopal event while active—feeling CP and SOB which resolve with rest. ECG reveals lateral ST-T wave flattening and LAD. Listen for a 4th heart sound as well as a murmur that classically increases in intensity during Valsalva or other activities that decrease venous return (standing). The murmur of HCM decreases with maneuvers that increase venous return (Squatting)

Pericarditis:

Diffuse ST segment elevations are found in patients with pericarditis, which would not resolve with rest and would present with a friction rub.

“Tet Spell:”

Treatment for children having a “tet spell” focuses on promoting pulmonary blood flow by raising LV systolic pressure compared to that in the RV thereby reversing the right to left shunting. This is accomplished by either decreasing Pulmonary vascular resistance (PVR), increasing RV diastolic filling pressure, or by increasing systemic vascular resistance (SVR). Morphine and oxygen both decrease PVR, while IV fluids increases RV end diastolic filling pressure. If these interventions are not successful, phenylephrine, which would raise SVR, should be given.

Endocarditis:

Infective Endocarditis (IE), in the absence of congenital heart disease often is associated with CVL’s. In about 10% of pediatric cases, IE develops without structural heart disease or other identifiable risk factors and usually involves infection of the aortic or mitral valve secondary to S. aureusbacteremia.

Myocarditis:

Endomyocardial biopsy (EMB) remains the gold standard for unequivocally establishing the diagnosis of acute viral myocarditis. An earlier diarrheal episode likely represents an infection with one of the enterovirus species, which are the most common infectious agents associated with acute viral myocarditis.

Typical ECG findings in myocarditits are low-voltage QRS complexes < 5mm in all limb leads (which may also suggest tamponade)

Neonates and infants with myocarditis may present with lethargy, poor feeding, irritability, pallor, fever, or FTT; heart failure symptoms; pericarditis and myocarditis can occur simultaneously

Most common dysrhythmia in pericarditis/myocarditis is sinus tachycardia

Tx of myocarditis: diuretics, inotropes, and afterload reducing agents (nitroprusside), along with IVIG and PICU admission

Acute myocarditis is a heterogeneous condition caused by a variety of infectious agents, immunologic mechanisms, and structural lesions. Cases have a bimodal age distribution, with children younger than 4 years of age and older adolescents representing the two peaks. The signs and symptoms are subtle and nonspecific. Often a child who has myocarditis has a recent history of a mild febrile illness that may be followed by vomiting, dizziness, or respiratory symptoms. Because children usually present with predominantly respiratory symptoms, it is not surprising that affected children often are misdiagnosed initially with pneumonia or asthma. The diagnosis should be entertained for children who have resting tachycardia (or a tachycardia out of proportion to the height of fever) and normal hemoglobin values, as described for the boy in the vignette.

The two most common infectious organisms associated with acute myocarditis in North America are Coxsackievirus and adenovirus. In developing countries, organisms such as Trypanosome cruzi (Chagas disease) and Corynebacteriumdiphtheriae are more common pathogens.

Myocarditis is characterized microscopically by myocardial cellular inflammation and necrosis. The most common mechanism of injury is an autoimmune response following exposure to certain antigens in susceptible individuals. Such a response leads to signs and symptoms of congestive heart failure, such as tachycardia, exercise intolerance, respiratory distress, and diaphoresis.

Chest radiography often reveals cardiomegaly, although this finding is insensitive. Electrocardiography is relatively sensitive in detecting myocarditis, with the most important findings being sinus tachycardia, low-voltage QRS complexes, and flat or inverted T waves. Early evaluation with echocardiography may exclude other causes of congestive heart failure and document shortening ejection fraction. Supportive treatment, including management of arrhythmias and CHF, is the mainstay of therapy.

Atypical mycobacteria usually cause pulmonary infections in immunocompromised hosts. Rickettsiarickettsii, a species of bacteria spread by the Ixodid ticks, is the cause of Rocky Mountain spotted fever (RMSF). RMSF usually presents as an acute febrile illness with headache, muscle pain, and development of a petechial rash of the wrists and ankles. Staphylococcus aureus is a bacterial cause of pericarditis or complicated pneumonia. Streptococcus viridans is the most common cause of infectious endocarditis.

Acute Rheumatic Fever:

An 8 year old female presents with a persistent low-grade fever for 10 days and abrupt purposeless movements along with pain in her knees and elbows. Has a holosystolic heart murmur, best heard at the apex (mitral insufficiency). The test that establishes the diagnosis is an ASO titer in Acute Rheumatic Fever. (JONES criteria!) An ASO titer is elevated in 80% of patients with ARF. A positive throat culture for Group A Streptococcus is found in only 25% of patients at the time of presentation.

DVT’s:

Anticoagulation is the mainstay of treatment for DVT’s. Heparin prevents thrombus extension and reduces the risk of PE’s. Note: warfarin is contraindicated in pregnancy—not heparin.

3rd Degree Heart Block:

The patient with 3rd degree heart block and mental status changes with poor profusion requires transcutaneous pacing.

Acute Chest Syndrome:

Acute Chest Syndrome in a child with Sickle Cell Disease is characterized by a pulmonary infiltrate in a child with difficulty breathing, pain, cough, and frequently fever—have a low threshold for admitting these kids, even if no infiltrate is seen but they have chest pain and tachypnea.

Arrhythmias:

Arrhythmia treatment depends on whether the patient has a pulse, hemodynamic stability, and the presenting rhythm.

Most infants with dysrhythmias present with vague and nonspecific symptoms such as “fussiness” or “difficulty feeding.”

Amiodarone is contraindicated in neonates because it may cause a gasping syndrome (respiratory distress, metabolic acidosis, followed by cardiac arrest.)

Immediate synchronized cardioversion is indicated in a child with unstable SVT. Adenosine may be given prior to cardioversion only if IV access is already available—in unstable patients,cardioversion should not be delayed for attempts at IV access.

Contraindications to adenosine include a denervated heart (transplant) and 2nd or 3rd degree heart block unless a pacemaker is present.

Atrial flutter and atrial fibrillation in children are due to congenital heart disease (repaired or unrepaired); may also see atrial flutter in Duchenne’s muscular dystrophy and CNS injury.

An unstable patient with atrial flutter or atrial fibrillation needs cardioversion but first add heparin to prevent embolization. Avoid cardioversion in patients on digoxin as it may cause a malignant ventricular arrhythmia; GiveDigoxin to patients who are stable; may also add propranolol.

PAC’s are usually benign but are also seen with hypoxia, use of sympathomimetic drugs, hyperthyroidism, and digoxin toxicity. With the exception of treating the above, no treatment is necessary with PAC’s.

3 or more consecutive PVC’s = VT; PVC’s are considered malignant if they are associated with underlying heart disease, if there is a history of syncope or family history of sudden death, if they are precipitated or increased with activity, if they have multiform morphology, or if there are symptomatic runs of PVC’s. Treatment is with IV lidocaine 1mg/kg followed by a lidocaine drip.

AED’smay be used in children over 1 year of age

Most common cause of bradycardia is hypoxia; if patient is unstable and not hypoxic, atropine or pacing may be indicated.

Children with first degree heart block are usually asymptomatic; Management is to treat the cause if possible (myocarditis, rheumatic fever, lyme disease, cardiomyopathies, congenital heart disease)

Children with second-degree heart block type I (Wenchkeback) rarely progress to complete heart block; however, those with Mobitz II frequently progress to 3rd degree heart block—in Mobitz II (or in 3rd degree heart block) a pacemaker is warranted.

Long QT Syndrome:

A QTc from 0.42-0.46 is borderline and warrants further assessment.

Jervell and Lange-Nielsen syndrome is an AR form of LQTS associated with congenital deafness. Romano-Ward syndrome is an AD form of LQTS not assoc. with deafness.

LQTS may be congenital or acquired (usually caused by medications or electrolyte abnormalities like hypokalemia, hypocalcemia, and hypomagnesemia).

Patients with LQTS present between the age of 9 and 15 years with recurrent episodes of syncope; syncope with exertion is almost always an ominous sign; the hallmark dysrhythmia of LQTS is torsades de pointes; tx=IV magnesium at 25-50mg/kg to a maximum of 2g

Pericarditis:

Pleuritic chest pain that is relieved by sitting upright and increased with the supine position suggests pericarditis; may have respiratory difficulty, fever, substernal chest pain that radiates to the left shoulder, scapula, or trapezius; may have recent history of URI; may hear friction rub, have tachypnea and tachycardia, lungs are usually clear to auscultation; Signs of cardiac tamponade include distended neck veins, clear lungs, weak peripheral pulses, tachycardia, distant heart tones, and a pulsusparadoxus.

Typical ECG findings in pericarditis is PR segment depression and diffuse ST segment elevation

Cardiac Tamponade:

Beck’s triad (hypotension, distended neck veins and muffled heart tones) is present in less than half of all patients with cardiac tamponade

In an unstable patient with cardiac tamponade, a pericardiocentesis should be performed expeditiously; IV Nafcillin and Cefotaxime and PICU admission; stable patients can be admitted for IV ABX and salicylates

Hypertension: