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PEM|BRS: Cardiology & EndocrinologyPediatric ECG Evaluation:Rate:300, 150, 100, 75, 60, 50For Brady: cycles/6 sec strip (2 markers long) x 10 = RateRhythm: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 droppedMobitz Type II =Ratio of P’s to QRS’s (2:1, 3:1, 4:1)3rd degree Block: AV DissociationIs QRS interval > 3 tiny squares? (BBB): Note: criteria then for VH are unreliableRBBB: 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 componentLAH=Large diphasic P wave with wide terminal componentRVH:* 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 leadsLVH:* 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 depressionInfarction: Q waves (significant=1mm wide or 1/3 amplitude of entire QRS complex)Location: I & AVL=Lateral; II, III, & AVF=Inferior; V1 & V2=AnteriorSyndrome Screen:WPW Syndrome: Short PR interval, Delta waveLong QT Syndrome: QTc > 0.46; QT/square root of R-RHOCM: Deep Q, raised ST in II, III, aVF, & LVH; Lateral ST-T wave flattening & LADArrhythmogenic RV Dysplasia: T inversion in V 1 - 3, epsilon waveBrugada Syndrome: RBBB with ST elevation in V1-V3Wellens 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 IIPericarditis: Flat or concave elevated ST segment, dec. voltages, entire T above baselineUntx’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 PDecreased K: (push-down the T) Flat T and U wave appearsCalcium:Increased Ca: Short QTDecreased Ca: Long QTNeonates:During first week of life have RAD, large R waves and upright T’s in V3R, V4R, and V1, V2Upright 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 whose description (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 chordae tendineae 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 dysrhythmiaSyncope:HYPERLINK "Javascript:Emblink('236/P31481')"“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 hypotensionIf, at the onset of the event, the child was crying, urinating, defecating, or coughing, a vagally-mediated syncopal 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 disorderCongenital 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. aureus bacteremia.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 simultaneouslyMost common dysrhythmia in pericarditis/myocarditis is sinus tachycardiaTx of myocarditis: diuretics, inotropes, and afterload reducing agents (nitroprusside), along with IVIG and PICU admissionAcute 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.HYPERLINK "Javascript:Emblink('236/P31602')"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 Corynebacterium diphtheriae 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. Rickettsia rickettsii, 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; Give Digoxin 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’s may be used in children over 1 year of ageMost 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 2gPericarditis: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 pulsus paradoxus.Typical ECG findings in pericarditis is PR segment depression and diffuse ST segment elevationCardiac Tamponade:Beck’s triad (hypotension, distended neck veins and muffled heart tones) is present in less than half of all patients with cardiac tamponadeIn 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 salicylatesHypertension:HTN in the first decade is most likely secondary HTN from a renal cause. Extrarenal causes of HTN emergencies include coarctation of the aorta, neuroblastoma, pheochromocytoma, and increased ICP. Drug ingestions such as steroids, sympathomimetics, cocaine, or theophylline may also cause this.A HTN emergency is defined by the presence of end-organ damage in addition to HTN; after stabilization, all these kids should be admitted to a PICUThe goal of tx for HTN emergencies is to reduce the MAP by 25% over the first 2-8 hours, then to gradually normalize the BP over the next 24-48 hours. Overly rapid reduction of the BP can lead to cerebral hypoperfusion and neurologic complications. ED workup of HTN emergency: Consider…ECG, CBC, Lytes, U/A, U Cx, Tox screen, plasma and urine catecholamines, plasma rennin, TFT’s, serum cortisol, CXR, Head CTSodium Nitroprusside: contraindicated in pregnancy and hepatic/renal disorder patients; A concern is that it is initially metabolized to cyanide which is then metabolized in the liver and finally cleared by the kidneys. Signs of cyanide toxicity include an odor of bitter almonds, tachypnea, mydriasis, dysrhythmias, hypotension, seizures, apnea, and coma. An elevated serum lactic acid level and an elevated anion gap metabolic acidosis would be present. S/S include tinnitus, blurred vision, nausea, altered mental status, seizures, and coma.Nicardipine: SE’s: tachycardia, palpitations, and flushing; not recommended in brain tumors due to the vasodilatory effects which can cause increased ICP; OK in post-op patients and those with renal disease.Esmolol: Use cautiously in patients with RAD, high-degree heart block, bradycardia, and decreased LV function; SE’s: Nausea, vomiting, bronchospasm, and bradycardiaLabetalol: Also avoid in patients with RAD, high-degree heart block. SE’s: N/V, itching, rash, hepatotoxicity, hypoglycemiaPhentolamine: only indicated in the specific setting of acute HTN crises secondary to excess circulating catecholamines from a Pheo, or reactions involving a MAO-I.Generally, mean arterial pressure should be reduced by no more than 25% in the first 2 hours, with the ultimate goal of normalizing the blood pressure over a period of several days. The choice of drug to use in the emergency department treatment of a child who is experiencing a hypertensive crisis depends on the degree of hypertension present, current medication use, known underlying medical conditions, suspected cause of the hypertension, and organs involved. Titratable intravenous medications are recommended for symptomatic patients, beginning at the lowest recommended dosage and titrating up to effect. The Fourth Report on the Diagnosis, Evaluation, and Treatment of High blood Pressure in Children lists esmolol (a beta blocker), labetalol (alpha and beta blocker), nicardipine (calcium channel blocker), and sodium nitroprusside (vasodilator) as the most useful drugs for immediate reduction in blood pressure.Sublingual and oral short-acting nifedipine no longer are recommended routinely for acute reductions in blood pressure because their effects are variable and their use has been associated with an increase in adverse effects in both adults and children.CHF:The typical presenting symptoms of CHF in kids are dyspnea, tachypnea, tachycardia, sweating with feeding, and a palpable enlarged liver—note: peripheral edema and rales are usually absent. In children, BNP correlates with CHF.Cardiac Surgeries:For children with intrathoracic cardiac shunts (like a B-T) , dehydration can rapidly become life-threatening as the shunt may begin to clot and fail.Modified Blalock-Taussig (B-T) shunt: used in patients with TOF, TAT, Pulmonary atresia, and RV Hypoplasia as a way to get blood to the lungs from the systemic circulation—consists of a conduit between the subclavian artery and the pulmonary artery.A Fontan procedure is performed in patients who have a single functional ventricle such as those with TAT, hypoplastic left heart syndrome and pulmonary atresia with intact ventricular septum. Done so that the systemic venous return can reach the pulmonary circulation and by-pass the RV. Connect the SVC to the PA (Glen shunt) and the IVC to the PA.Pericardial effusions develop in 30-50% of patients who undergo a pericardiotomy.6 months after successful surgical correction of congenital heart defects, patients have negligible increased risk for endocarditis and do not need prophylactic antibiotics prior to invasive procedures.Acute cardiac transplant rejection occurs most frequently within the first year after heart transplantation. Presenting symptoms include poor feeding, irritability, low-grade fever, ileus, and dyspnea. Clinically, the patient may display tachycardia, tachypnea, hepatomegaly, gallop, or ventricular ectopy.Cardiac allograft vasculopathy (CAV) is the leading cause of death in patients greater than 3 years post-transplantation—it is a progressive form of atherosclerosis. Patients may present with syncope, CHF, chest pain, or dizziness—they need coronary angiography and motio Cordis:Commotio cordis, which occurs when the chest is struck at a critical point in the cardiac cycle, is known to induce ventricular fibrillation. If CPR is already in progress, the next step should be to attach an automated external defibrillator and defibrillate the patient if ventricular fibrillation (VF) is seen. Although establishment of vascular access to administer medications is a priority in pediatric advanced life support, it should not precede defibrillation in cases of VF or pulseless ventricular tachycardia (VT). If adequate bag-mask ventilation is being provided, placement of an advanced airway is not a priority. Endotracheal administration of medications is less preferred than intravenous or intraosseous administration and should be undertaken only when vascular access is not possible. Cardiopulmonary arrest is uncommon in pediatric patients. When it does occur, the most common cause is asphyxial arrest, in which a primary respiratory arrest or shock state with resulting cardiorespiratory failure leads to a secondary cardiac arrest. Sudden collapse during athletic competition, however, is very suspicious for a primary cardiac cause. For a young athlete struck in the chest by a projectile, commotio cordis is the most likely cause of the arrest. Commotio cordis occurs most commonly when a dense object, such as a baseball, hockey puck, butt end of the hockey stick, or lacrosse ball, strikes the chest at a critical point in the cardiac cycle, inducing VF. It is increasingly recognized as a cause of sudden death in athletes. Prompt recognition and initiation of CPR and defibrillation can be lifesaving. Commotio cordis also can be induced by a blow to the chest by a kick or strike from a hand. It occurs most commonly in teenagers and young adults playing competitive sports, possibly because their thin chest walls provide less protection for the heart in the event of a direct blow.VF or VT is the initial rhythm in only 5% to 15% of cases of cardiac arrest in childhood. Most cardiac arrests begin as respiratory arrest, and the most common rhythms are asystole and bradycardia with a wide QRS. However, VF or VT has been reported to occur in up to 27% of pediatric cardiac arrests at some point during the resuscitation. Pulseless electrical activity is characterized by a rhythm (not VF or VT) evident on cardiac monitoring but no associated pulse. VF is more common in older adolescents who have sudden witnessed collapse. Cardiac ion channel abnormalities increasingly are recognized as a cause of ventricular arrhythmias and sudden death in older children and young adults.Signs and symptoms of cardiopulmonary failure and arrest are unresponsiveness with weak or absent pulses and poor-to-no ventilatory effort. Agonal respirations are not considered adequate ventilation, and laypersons are prompted to provide CPR when an unresponsive victim is gasping. In the 2010 guidelines for CPR, the pulse check has been removed for laypersons in the presence of an unresponsive patient because it delays initiation of chest compressions. Health-care practitioners are directed to check for a pulse for no longer than 10 seconds in an unresponsive patient before beginning chest compressions and positive-pressure ventilations.Transcutaneous Pacing:Cardiac pacing can be lifesaving in cases of refractory bradycardia resulting from congenital or acquired heart disease in children. Emergency transcutaneous pacing may be lifesaving if the bradycardia is due to complete heart block or sinus node dysfunction unresponsive to ventilation, oxygenation, chest compressions, and medications. Another indication is overdrive pacing in cases of refractory tachyarrhythmia. Pacing is not useful for asystole or bradycardia due to hypoxic myocardial injury.Because transcutaneous pacing is painful, sedatives such as midazolam should be administered before initiating the procedure. Amiodarone and lidocaine may be indicated in cases of ventricular tachycardia. Antibiotics should be administered if Lyme carditis is suspected, although this is unlikely to result in immediate benefit.Three methods of temporary pacing are commonly available: transcutaneous, transesophageal, or transvenous. The primary difference between them is the location of the electrodes used in pacing. In transcutaneous pacing, electrode pads are placed anteriorly and posteriorly on the thorax. In transvenous pacing, electrodes are placed transvenously into the right heart. In transesophageal pacing, the electrodes are placed in the esophagus behind the heart.After positioning the appropriate electrodes, all pacing techniques involve obtaining capture, setting the rate, and setting a marginal output current. In step one, the electrodes are connected to the external pacemaker, and a current is induced and increased until capture is evident. For transcutaneous pacing, the current usually is approximately 50 mA for adult-sized patients. A QRS complex after each pacing spike indicates successful electrical capture. A palpable pulse corresponding to the QRS complex indicates mechanical capture. If the latter is not present, causes for pulseless electrical activity (eg, hypovolemia, hypoxia) should be sought.?Once capture is established, a rate is set. This is generally faster than the underlying intrinsic rate. For overdrive pacing, the rate is set higher than the underlying dysrhythmia to suppress the intrinsic pacemaker.?In step three, the output is reduced gradually until capture is lost. The final output is set at 1.5 to 2 times the threshold plications of pacing are related to the techniques used. Transvenous pacing may be associated with all the complications of central venous access, including vessel damage and pneumothorax. One additional possibility is perforation of cardiac chambers, leading to pericardial effusion or worse.Congenital Heart Disease:Patients who have cyanotic CHD may present in the first few hours or days after birth with respiratory distress and develop sudden cyanosis and shock upon closure of the ductus arteriosus. Management includes immediate administration of prostaglandin E1, hydration, and limited oxygen administration. Excessive oxygenation can lead to clinical deterioration by enhancing ductal closure and decreasing pulmonary vascular resistance that, in turn, decreases the systemic vascular perfusion that depends on patency of the ductus arteriosus (blood flows from the pulmonary artery into the descending aorta via the ductus arteriosus due to elevated right-sided pressure). This right-to-left shunt is essential for patient survival until surgical correction. Dopamine and other vasopressive agents are useful in the management of children who have cardiogenic shock. Interval illness can exacerbate cardiac failure, and administration of antibiotics is not harmful for critically ill patients in whom CHD is suspected.The incidence of CHD is estimated at 5 to 10 per 1,000 live births (1% of live births). It is much higher in stillbirths (3% to 4%) and in spontaneous abortuses (10% to 25%). The most common congenital heart lesion in live births is ventricular septal defect (28% to 35%). About 50% to 60% of infants who have CHD are diagnosed by 1 month of age. With the use of ultrasonography and fetal echocardiography in high-risk pregnancies, prenatal screening has decreased the number of undiagnosed cases after birth. About one third of neonates who have CHD have critical lesions that require management within the first postnatal year. Survival has increased in infancy, and death in adults is primarily due to rhythm disturbances.Although the cause of CHD has been suggested to be multifactorial, recent studies show point mutations as the most important factor. A small percentage of cases are due to chromosomal aberrations. Other cardiac conditions involving known genetic abnormalities are cardiomyopathies (hypertrophic and dilated cardiomyopathy) and arrhythmias (eg, prolonged QT syndrome).?Maternal medical conditions and teratogen exposure also have been associated with CHD (eg, maternal diabetes; systemic lupus erythematosus; viral infections such as rubella; and exposure to lithium, ethanol, warfarin, antiepileptics, and vitamin A).Fetal circulation is designed for blood to flow toward the placenta (Fig. 1). Blood from the placenta on the right side of the heart mixes with blood from the lungs on the left side of the heart at the level of foramen ovale, allowing perfusion of the head, neck, heart, and upper extremities. Mixing at the ductus arteriosus allows perfusion of the abdomen and lower extremities. This process is facilitated by elevated vascular resistance of the pulmonary system. Oxygen saturation of fetal blood is approximately26 to 38 mm Hg (returning toward and from placenta, respectively), and fetal hemoglobin aids in tissue oxygen delivery, despite the low oxygen gradient compared with that of the neonate and infant. Therefore, survival of patients who have CHD at low oxygen saturations is possible due to fetal acclimatization with low oxygen saturation in utero.At birth, pulmonary vascular resistance reduces due to opening of alveoli and dilation of pulmonary arterioles after exposure to higher ambient oxygen concentration. Systemic vascular resistance increases after removal of the placenta, aiding in diversion of right-sided blood flow toward the pulmonary system. Therefore, the returning volume of blood increases on the left side of the heart from the lungs, which helps in closure of the foramen ovale. The ductus arteriosus closes over the next few days due to the reduction in circulating prostaglandin E, increase in oxygen saturation, or other unknown mechanisms. Various forms of CHD depend on persistent fetal circulation for survival and present precipitously with the normal anatomic changes after birth, especially with ductal closure.CHD can be divided into acyanotic and cyanotic lesions (Fig. 2). The acyanotic lesions result in either volume or pressure overload on the heart, and cyanotic lesions are associated with decreased or increased pulmonary blood flow.Volume overload is due to a left-to-right shunt. Examples include ventricular septal defect, atrial septal defect, endocardial cushion defect, and patent ductus arteriosus. The age of presentation depends on the degree of pulmonary and systemic vascular resistance and size of the defect. With left-to-right shunts, patients develop symptoms of pulmonary edema, which include increased work of breathing, sweating, fatigue, irritability, and failure to thrive. Physical examination reveals hypoxia, wheezing, skin mottling, pallor, and poor capillary refill.Pressure overload lesions result from outflow tract obstruction and present earlier with severe obstructions. Dramatic symptoms of shock, circulatory collapse, and right-sided heart failure occur at closure of the ductus arteriosus. Examples include critical aortic stenosis, coarctation of the aorta, and pulmonic stenosis. Severe pulmonic stenosis in the presence of a patent foramen ovale can present with cyanosis due to a right-to-left shunt. In less severe forms, such as mild coarctation of aorta, the affected child can present later in childhood with diminished pulses in the lower extremities and upper extremity hypertension. Studies that can aid in diagnosing acyanotic CHD are chest radiography showing cardiomegaly and pulmonary edema, electrocardiography documenting ventricular hypertrophy and right or left axis deviation, and echocardiography.Reduced pulmonary blood flow in cyanotic CHD is due to obstruction at the right outflow tract, such as in tetralogy of Fallot, tricuspid and pulmonic valve atresia, and Epstein anomaly of the tricuspid valve. Systemic blood flow is maintained by a right-to-left shunt at the level of the atrial or ventricular septum, and pulmonary blood flow is maintained by the ductus arteriosus. Circulatory collapse, cyanosis, and hypoxemia ensue with closure of the ductus. The degree of cyanosis correlates with the degree of pulmonic outflow tract obstruction. Transposition of the great vessels and totally mixing lesions such as truncus arteriosus, single ventricles, and total anomalous pulmonary venous return are examples of cyanotic CHD with increased pulmonary blood flow. In these cases, pulmonary blood flow is dependent on intracardiac defects, and systemic blood flow is dependent on ductus arteriosus, facilitated by elevated pulmonary vascular resistance and reduced systemic resistance. After ductal closure, patients present with significant cyanosis and signs of shock and cardiac failure. Clinically apparent differential cyanosis (upper body blue and lower body pink) is always due to CHD.Helpful investigations in cyanotic CHD include arterial blood gases, chest radiography, electrocardiography, and echocardiography. Arterial blood gas is helpful to differentiate between cardiac and pulmonary causes of cyanosis. The hyperoxia test assesses for improvement in cyanosis after administration of 100% oxygen for 10 minutes. With cyanotic CHD lesions, arterial partial pressure of oxygen does not increase greater than 150 mm Hg, in contrast to cyanosis due to congestive cardiac failure or pulmonary pathology. Chest radiography shows evidence of decreased or increased pulmonary blood flow with diminished pulmonary vascular flow, severe acidosis, and hypoxia in patients who have persistent pulmonary hypertension. Electrocardiography exhibits the specific ventricular hypertrophy, depending on the lesion. For example, right ventricular hypertrophy is seen with tetralogy of Fallot and hypoplastic left heart syndrome and right axis deviation is seen with right atrial hypertrophy.Chest Pain:Although cardiac causes represent a minority of all diagnoses for children presenting with chest pain, chest pain with exertion should always alert the physician to the possibility of a cardiac cause. A thorough history and physical examination should be undertaken to evaluate for this possibility. Left ventricular outflow obstruction from hypertrophic cardiomyopathy is the most likely explanation for the pain experienced by the child in the vignette, based on the character of his murmur, his lack of breathing difficulty, and the absence of symptoms when he is not exerting himself. Children who have hypertrophic cardiomyopathy are at risk for ischemia with exercise as well as arrhythmias, which are the most common cause of sudden death in young athletes.Exercise-induced bronchospasm or asthma is a common cause of chest discomfort during exercise, but this child reports no breathing difficulty or wheezing and has no prior history of asthma. A previous history of asthma or wheezing in the emergency department is not necessary to diagnose exercise-induced bronchospasm. Coughing or chest tightness associated with exercise is sufficient. A trial of beta-agonist inhaler before exercise often alleviates the symptoms and confirms the diagnosis.An anomalous coronary blood vessel causing ischemia with exercise would not be expected to cause a murmur unless the boy was experiencing congestive heart failure. Gastroesophageal reflux disease, although not an uncommon cause of substernal burning chest pain, would not cause a pathologic murmur. Precordial catch or “Texidor twinge” causes sudden, sharp chest pain that lasts a few seconds and can occur at rest or with mild activity and can be exacerbated with inspiration. Its cause is unknown.?The proportion of children who have chest pain attributable to different causes varies widely, depending on the source population and case series. In studies focused on pediatric emergency department populations, cardiac causes were responsible for fewer than 5% of cases. The largest category reported in most series is idiopathic and extensive testing generally is not performed. If the history and physical examination findings are compatible with musculoskeletal chest pain, reassurance, rest, and analgesia with a nonsteroidal anti-inflammatory drug are sufficient treatment. A thorough history and physical examination can uncover important clues to the presence of cardiac causes of chest pain. The quality of chest pain should be described, along with precipitating and alleviating factors. A specific detailed past medical history regarding asthma, sickle cell disease, Kawasaki disease, cardiac disease, and hypercholesterolemia and a family history focused on sudden cardiac death, arrhythmia, cardiomyopathy, or hypercholesterolemia should be elicited. Genetic disorders such as Marfan, Turner, and Ehlers-Danlos syndromes should be considered. Finally, a history of trauma, drug use (cocaine, methamphetamines, sympathomimetics), and psychological stressors should be sought.Some physical findings that may suggest cardiac causes include tachycardia, abnormal murmurs, friction rub, displaced point of maximal impulse, increased intensity of the murmur with a Valsalva maneuver or at the end of expiration, hepatomegaly, and edema.If a cardiac cause is suspected, electrocardiography and chest radiography are appropriate initial diagnostic interventions. Echocardiography and urgent cardiac consultation are useful in selected circumstances in which there is a high index of suspicion for pericarditis, myocarditis, cardiomyopathy, anomalous coronary artery, or left ventricular outflow obstruction. If myocardial ischemia is suspected (cocaine ingestion, pain relief with nitrates, previous history of Kawasaki disease or heart transplant), assessment of serum troponin may be helpful. If aortic dissection or rupture is a consideration (severe persistent substernal pain with hemodynamic changes, especially in a child who has Marfan or Ehlers-Danlos syndromes), computed tomography scan should be ordered and surgeons consulted emergently.?Pulmonary causes of chest pain can also be life-threatening. Pneumothorax and pulmonary embolism must be recognized and addressed promptly. Both blunt and penetrating trauma can cause severe injuries such as pulmonary contusion, hemothorax, and rarely, cardiac contusion.Endocrinology Notes:DKA:Cerebral edema is the leading cause of mortality in patients with DKA (which is the leading cause of death in IDDM)—Mannitol should be given immediately at a starting dose of 0.25 to 0.5g/kg. Cerebral edema occurs in approximately 1% of pediatric DKA episodes. Children at greatest risk for cerebral edema are those with high BUN and severe hypocapnia.DKA results in metabolic acidosis with an elevated anion gap.DKA diagnosis is confirmed when the labs demonstrate: 1) serum glucose over 200, 2) venous pH below 7.30 (or serum bicarbonate below 15), and 3) ketonuria.Rarely, you can have euglycemic DKA—usually occurs in pregnant females; but can also occur in kids with known IDDM because home insulin given in response to hyperglycemia may correct the glucose prior to arrival but the ketones and acidosis remain.Predicted Na = Serum Na + 1.6 * (per 100 glucose over 100)Predicted K = Serum K – 0.6 * (per 0.1 unit pH < 7.4)After first hour of IVFP in DKA (typically 10-20 cc/kg of NS) depending on the circulatory status (i.e. if hypotensive, you’d need to give more); then start insulin drip at 0.1 Units/kg/hr and continue at that rate until pH > 7.3, HCO3 > 15, and normalization of anion gap. Add glucose to IVF when glucose <350. Use 2 bag technique to titrate the amount of glucose you are giving—run at 2xmaintenance rate…? NS + 20mEq/L KCl + 10 mEq/L KPhos + 10 mEq/L KAcetateD10 ? NS + 20mEq/L KCl + 10 mEq/L KPhos + 10 mEq/L KAcetateDon’t give K in maintenance fluids until it is < 6Hypoglycemia:Babies with galactosemia (child cannot metabolize galactose) present with jaundice, vomiting, diarrhea, FTT, hypoglycemia, and hepatomegaly, and are at risk for Gram negative sepsis. The most critical issue to address in the patient with CAH is the hypoglycemia. After glucose administration, hydrocortisone should follow and will correct the hyponatremia.In a hypoglycemic seizure, the standard dose for glucose administration is 0.5g-1g/kg IV push (correlates with 5-10cc/kg of D10W) or 50cc of D50W in adults.Hypoglycemia should be considered in any child who presents with unexplained lethargy, shock, seizures, or an altered mental status.Toxic ingestions may cause hypoglycemia: sulfonylureas, B-Blockers, ethanol, and salicylates.Ketotic hypoglycemia is also a common cause of hypoglycemic episodes in children over 6 months of age and under 5 years of age. These children present with symptomatic hypoglycemia during the morning hours after a fast of 10-16 hours. Many have a concurrent illness (AGE) that contributes to the hypoglycemia. Children outgrow this by 8 years of age when their muscle mass increases—it is a diagnosis of exclusion.Thyrotoxicosis:For patients in thyroid storm, treat hypertension and tachycardia with a beta blocker.The 3 most common causes of pediatric thyrotoxicosis (tachycardia, sweating, hypertension, possible seizures, etc.) are: (Remember to do a parental history of thyroid disease!!!); Treatment: beta blockers and steroids!Graves’ Disease—antibodies stimulating TSH receptors Neonatal thyrotoxicosis—maternal Graves’ Disease—mom’s antibodies cross placenta; symptoms may be present at birth or may be delayed up to 6 weeks; may develop high-output cardiac failure; may have goiter and exophthalmos; tachycardia, normal or supranormal feeding yet poor weight gain, CHF, jaundice, may look septic.Thyroid hormone ingestionHyponatremia:A patient with SIADH and a hyponatremic seizure requires hypertonic saline first.Hypercalcemia:Hyperparathyroidism may lead to hypercalcemia causing renal calculi and muscle fasciculations. Management includes bisphosphonates, which inhibit osteoclast activity, fluid boluses to dilute the acute hypercalcemic state, and furosemide to increase calcium excretion. Surgery may be indicated. Avoid thiazide diuretics because they increase the reabsorption of calcium in the kidney.Pheochromocytomas:In patients with pheochromocytomas, use alpha-blockers first to control hypertension. Beta blockers are avoided because they may cause unopposed alpha adrenergic stimulation and further increases in BP.Adrenal Insufficiency:If adrenal insufficiency is known or strongly suspected, IV Hydrocortisone should be given at a dose of 50 mg for children under 4 years and 100 mg for children over 4 years.Steroid dependent children are susceptible to acute renal insufficiency and require the administration of “stress-dose-steroids” when ill or injured.A child who has been on 2 consecutive weeks of systemic corticosteroids may be adrenal suppressed.Management of the known steroid dependent child in the ED focuses on 4 principles:Administration of Stress-dose steroids as above to ill or injured childrenThese children are immunocompromised and are at increased risk for serious infectionThese children have muted signs and symptoms of inflammation—think of this if they have possible OM, cellulitis, appendicitis, etc. so you don’t downplay symptoms that are muted in these children!Poor wound healing—therefore use non-absorbable sutures and leave them in place longer and use antibiotics for all wounds, and do frequent re-checks.The characteristic features of addisonian crisis are altered mental status, hypotension, and hypoglycemia. The critical, specific intervention in cases of suspected addisonian crisis is the administration of parenteral steroids.Congenital adrenal hyperplasia: autosomal recessive defect; addisonian crisis occurs in early infancy; presents in females with ambiguous genitalia in the newborn nursery; in males, presents at 1-2 weeks of age with darkly pigmented scrotum, hypotension, altered mental status, lethargy, hypoglycemia, hyponatremia, hyperkalemia, mild metabolic acidosis.Waterhouse-Friderichsen Syndrome: the syndrome of meningitis (or MRSA), fever, coma, cyanosis, petechial hemorrhages, and adrenal hemorrhages accompanied by adrenal insufficiency. Rickets: Overt signs of hypocalcemia include laryngospasm, carpopedal spasm, and Trousseau's sign. Classically, Trousseau's sign is carpal spasm with occlusion of arterial blood flow; the patient in the vignette experiences pedal spasm as the blood pressure cuff is applied to lower extremity.HYPERLINK "Javascript:Emblink('236/P31674')"Although the prevalence of rickets has markedly decreased with vitamin D supplementation of foods, certain populations, including preterm infants, exclusively breastfed infants who do not have enough exposure to sunlight, and individuals from ethnic or religious groups who eat fewer meat products and whose skin is almost completely covered with clothes when outdoors remain at risk. Patients who have inherited problems with vitamin D and calcium metabolism or other renal, endocrine, or metabolic diseases also may experience hypocalcemia and become symptomatic. Recognition of the signs and symptoms of hypocalcemia allows for appropriate investigation, prompt treatment, and reversal of its complications.Hypocalcemia should be treated with intravenous 10% calcium gluconate at a dose of 0.5 to 1.0 mL/kg administered over 3 to 5 minutes. The rate should not exceed 50 mg/min. Patients must be kept on cardiac monitors and the infusion stopped or slowed if bradycardia develops. Once acute symptoms are relieved, calcium gluconate may be added to maintenance intravenous fluids to achieve a dose of 100 mg/kg per 24 hours of elemental calcium. If hypomagnesemia is believed to be the cause of the hypocalcemia, the magnesium imbalance should be corrected before the calcium imbalance. All patients who have symptomatic hypocalcemia or serum calcium concentrations less than 7 mg/dL (1.75 mmol/L) at presentation should be admitted to the hospital. Anticonvulsants are not indicated for patients who have tetany due to hypocalcemia.The laryngospasm associated with hypocalcemia may be mistaken for croup. Based on the time of year and absence or presence of other upper respiratory tract symptoms, other possible explanations should be sought. Physical examination of the child who has rickets may reveal a rachitic rosary due to enlarged costochondral junctions of the ribs. Radiographs may show metaphyseal widening of long bones (Figs. 1 and 2).?Fig 1 above, Fig 2 below?The increasing irritability in this child may be due to bone pain from rickets and poor bone mineralization. During episodes of crying, mild hyperventilation may produce a decrease in the ionized calcium in her serum, precipitating laryngospasm and carpopedal spasm.Rickets occurs when intake of vitamin D is inadequate or its active metabolite cannot be formed through hydroxylation in the kidney or liver. Vitamin D also may be synthesized in the body from cholesterol through the action of sunlight on its precursor compound. Inadequate vitamin D leads to poor bone mineralization, decreased calcium absorption from the gut, and to a lesser degree, renal calcium wasting. Hypocalcemia is a late manifestation of rickets but accounts for most of its life–threatening complications.Treatment of rickets involves the administration of vitamin D unless there are indications of an underlying illness that would make this therapy ineffective. However, administering vitamin D to patients who have low calcium concentrations without first providing calcium can worsen the acute neuromuscular symptoms of hypocalcemia because calcium is driven into the bone and serum calcium concentrations decrease.?Transient hypoparathyroidism may occur in preterm infants of diabetic mothers and may lead to hypocalcemia causing increased muscle tone and seizure activity along with a prolonged QTc. Give Calcium Gluconate 10mg/kg IV over 30 minutes.Hypopituitarism:The hypoglycemia and hypovolemia require rapid correction, which can be facilitated through the administration of a combination of isotonic saline and dextrose. Intravenous hydrocortisone should be used in an unstable patient who has hypopituitarism for rapid correction of the cortisol deficiency and to support vascular tone. A common dosing regimen is hydrocortisone 2 mg/kg or 40 mg/m2. Because this boy’s primary deficit is pituitary, mineralocorticoid concentrations should be maintained, making fludrocortisone acetate replacement unnecessary.?In addition, hydrocortisone has both glucocorticoid and mineralocorticoid activity. Thyroid hormone replacement should not be undertaken in a patient who has hypopituitarism until cortisol concentrations have been corrected. Early correction of thyroxine concentrations may result in more rapid clearance of circulating cortisol, worsening cortisol deficiency. Hypotonic fluids, such as dextrose 10% in water, are inappropriate for volume expansion and may be particularly dangerous for a patient who has hypovolemic shock and cortisol deficiency. Oral rehydration or maintenance intravenous fluid administration is inadequate for a patient in hypovolemic shock.Hypopituitarism can result from a variety of insults, including tumors in or around the pituitary gland, therapy for such tumors such as surgery and radiation, infiltrative processes, infection, trauma, and hypothalamic dysfunction. Tumors and their treatment are the most common causes.The clinical manifestations of hypopituitarism are associated with the rate of onset, severity, and extent of pituitary injury. If the pituitary dysfunction is caused by a tumor, symptoms related to the mass may predominate, including headaches, visual disturbances, or vomiting. Deficiency of one, several, or all pituitary hormones may ensue, depending upon the location, nature, and severity of the insult.?The specific hormone(s) involved determine(s) which target glands are affected and what constellation of signs and symptoms occur. Acute onset of hormone deficiency is more likely to produce significant symptoms, while gradual loss of function may produce mild or no noticeable symptoms. Treatment of hypopituitarism is based on the specific hormone deficiencies. Acute cortisol deficiency, particularly during times of physiologic stress, as with the boy in the vignette, may result in cardiovascular collapse and requires immediate replacement of cortisol as well as intravascular volume expansion. Maintenance therapy involves the use of glucocorticoid in an amount and timing designed to mimic the normal cortisol secretion pattern as closely as possible while maximizing compliance. Families should be instructed to increase dosing (“stress dose”) during times of acute illness. Management of other pituitary hormone deficiencies should be guided by clinical symptoms and hormone values and generally is the same as the treatment of hormone deficiencies associated with the involved target glands. ................
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