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Pediatric Cardiac Emergencies. Infant Cardiac Disease Leading to ER Presentation ä Congenital ä Acquired ä Cardiomyopathy ä Myocarditis (usually with.

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Presentation on theme: "Pediatric Cardiac Emergencies. Infant Cardiac Disease Leading to ER Presentation ä Congenital ä Acquired ä Cardiomyopathy ä Myocarditis (usually with."— Presentation transcript:

1 Pediatric Cardiac Emergencies

2 Infant Cardiac Disease Leading to ER Presentation ä Congenital ä Acquired ä Cardiomyopathy ä Myocarditis (usually with CHF) ä Dysrhythmias

3 Heart Failure- Definition: ä A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body ä It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent

4 CHF - Presentation ä infants: irritable, poor feeding (early fatigue), failure to thrive, respiratory symptoms ä always consider in patients with respiratory symptoms ä often misdiagnosed as respiratory illness / infection

5 CHF - Etiology ä Increased Preload ä L to R shunts (VSD, PDA, AV fistula) ä severe anemia ä Increased Afterload ä HTN ä Congenital (aortic stenosis, coarctation of aorta) ä Decreased Contractility ä myocarditis, pericarditis with tamponade ä cardiomyopathy (dilated or hypertrophic) ä Kawasaki syndrome (early phase) ä metabolic: electrolyte, hypothyroid ä myocardial contusion ä toxins: dig, calcium channel blockers, beta blockers ä Dysrhythmia

6 CHF - Etiology ä presents immediately at birth ä anemia, acidosis, hypoxia, hypoglycemia, hypocalcemia, sepsis ä presents at 1 day (congenital) ä PDA in premature infants ä presents in first month (congenital) ä HPLV, aortic stenosis, coarctation, VSD presents later ä presents later (acquired) ä myocarditis, cardiomyopathy (dilated or hypertrophic), SVT, severe anemia, rheumatic fever

7 Etiology ä It is a common end point for many diseases of cardiovascular system ä It can be caused by : -Inappropriate work load ( volume or pressure -Inappropriate work load ( volume or pressure overload) overload) -Restricted filling -Restricted filling -Myocyte loss -Myocyte loss by S. Soliman

8 Causes of left ventricular failure Volume over load: Regurgitate valve Volume over load: Regurgitate valve High output status High output status Pressure overload: Systemic hypertension Pressure overload: Systemic hypertension Outflow obstruction Outflow obstruction Loss of muscles: Post MI, Chronic ischemia Loss of muscles: Post MI, Chronic ischemia Connective tissue diseases Connective tissue diseases Infection, Poisons Infection, Poisons(alcohol,cobalt,Doxorubicin) Restricted Filling: Pericardial diseases, Restrictive Restricted Filling: Pericardial diseases, Restrictive cardiomyopathy, tachyarrhythmia cardiomyopathy, tachyarrhythmia by S. Soliman

9 Pathophysiology 1. Hemodynamic changes 2. Neurohormonal changes 3. Cellular changes by S. Soliman

10 Hemodynamic changes From hemodynamic stand point HF can be secondary to systolic dysfunction or diastolic dysfunction diastolic dysfunction by S. Soliman

11 Neurohormonal changes N/H changes Favorable effect Unfavor. effect  Sympathetic activity  Sympathetic activity  HR,  contractility, vasoconst.   V return, vasoconst.   V return,  filling  filling Arteriolar constriction  After load  workload  O 2 consumption  Renin-Angiotensin –  Renin-Angiotensin – Aldosterone Aldosterone Salt & water retention  VR Vasoconstriction   after load  Vasopressin  Vasopressin Same effect  interleukins &TNF   interleukins &TNF  May have roles in myocyte hypertrophy Apoptosis  Endothelin  Endothelin Vasoconstriction  VR  After load by S. Soliman

12 Cellular changes  Changes in Ca +2 handling.  Changes in adrenergic receptors: Slight  in α 1 receptors Slight  in α 1 receptors β 1 receptors desensitization  followed by down regulation β 1 receptors desensitization  followed by down regulation  Changes in contractile proteins  Changes in contractile proteins  Program cell death ( Apoptosis )  Program cell death ( Apoptosis )  Increase amount of fibrous tissue  Increase amount of fibrous tissue by S. Soliman

13 Symptoms Shortness of breath, Orthopnea, paroxysmal nocturnal dyspnea Shortness of breath, Orthopnea, paroxysmal nocturnal dyspnea Low cardiac output symptoms Low cardiac output symptoms Abdominal symptoms: Anorexia,nausea, Abdominal symptoms: Anorexia,nausea, abdominal fullness, abdominal fullness, pain pain by S. Soliman

14 Physical Signs 1. High diastolic BP & occasional decrease in systolic BP (decapitated BP) 2. JVD 3. Rales (Inspiratory) 4. Displaced and sustained apical impulses 5. Third heart sound – low pitched sound that is heard during rapid filling of ventricle by S. Soliman

15 Physical signs (cont.) ä Mechanism of S 3 sudden deceleration of blood as elastic limits of the ventricles are as elastic limits of the ventricles are reached reached ä Vibration of the ventricular wall by blood filling filling ä Common in children by S. Soliman

16 Physical signs (cont.) ä ä Fourth heart Sound (S 4 ) - Usually at the end of diastole - Exact mechanism is not known Could be due to contraction of atrium against stiff ventricle Pale, cold sweaty skin by S. Soliman

17 Framingham Criteria for Dx of Heart Failure ä Major Criteria: ä PND- paroxysmal nocturnal dyspnea ä JVD- jugular venous distention ä Rales ä Cardiomegaly ä Acute Pulmonary Edema ä S 3 Gallop ä Positive hepatic Jugular reflex ä ↑ venous pressure > 16 cm H 2 O by S. Soliman

18 Dx of Heart Failure (cont.) ä Minor Criteria LL edema, LL edema, Night cough Night cough Dyspnea on exertion Dyspnea on exertion Hepatomegaly Hepatomegaly Pleural effusion Pleural effusion ↓ vital capacity by 1/3 of normal ↓ vital capacity by 1/3 of normal Tachycardia 120 bpm Tachycardia 120 bpm Weight loss 4.5 kg over 5 days management Weight loss 4.5 kg over 5 days management by S. Soliman

19 Forms of Heart Failure ä Systolic & Diastolic ä High Output Failure ä Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, ä Low Output Failure ä Acute ä large MI, aortic valve dysfunction ä Chronic by S. Soliman

20 Forms of heart failure ( cont.) ä Right vs Left sided heart failure: Right sided heart failure : Right sided heart failure : Most common cause is left sided failure Most common cause is left sided failure Other causes included : Pulmonary embolisms Other causes included : Pulmonary embolisms Other causes of pulmonary htn. Other causes of pulmonary htn. RV infarction RV infarction MS MS Usually presents with: LL edema, ascites Usually presents with: LL edema, ascites hepatic congestion hepatic congestion cardiac cirrhosis (on the long run) cardiac cirrhosis (on the long run) by S. Soliman

21 Left ventricular failure - respiratory discomfort, vary with position,stress and activity, associated with physical signs of disturbances in the lungs - Dyspnea during modest exertion- usually the first symptoms of left heart failure, associated with increased rate of breathing - Ortopnea - Cough

22 Left ventricular failure On examination: -patient: pale and sweaty, cold hands because of periferal vasoconstriction - rapid heart rate - Gallop rhythm - Murmur of mitral insufficiency - Rales on auscultation of the lungs ( interstitial edema and fluid) ( interstitial edema and fluid)

23 Right Ventricular Failure -neck veins distention -hepatomegaly, splenomegaly -congestion and edema of the gastrointestinal tract, anorexia,nausea, vomiting - weight loss, failure to gain weight,malnutrition - Murmur or tricuspid insufficiency - Hydrothorax - Pericardial effusion - Irritability,restlessness - oliguria

24 Differential diagnosis ä Pericardial diseases ä Liver diseases ä Nephrotic syndrome ä Protein losing enteropathy by S. Soliman

25 Laboratory Findings ä Anemia ä Hyperthyroid ä Chronic renal insuffiency, electrolytes abnormality ä Pre-renal azotemia ä Hemochromatosis by S. Soliman

26 Electrocardiogram ä Old MI or recent MI ä Arrhythmia ä Some forms of Cardiomyopathy are tachycardia related ä LBBB→ may help in management by S. Soliman

27 Chest X-ray ä Size and shape of heart ä Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema) ä Pleural effusion by S. Soliman

28 Echocardiogram ä Function of both ventricles ä Wall motion abnormality that may signify CAD ä Valvular abnormality ä Intra-cardiac shunts by S. Soliman

29 Cardiac Catheterization ä When CAD or valvular is suspected ä If heart transplant is indicated by S. Soliman

30 TREATMENT ä Correction of reversible causes ä Ischemia ä Valvular heart disease ä Thyrotoxicosis and other high output status ä Shunts ä Arrhythmia ä A fib, flutter, permanent junctional reciprocating tachycardia ä Medications ä Ca channel blockers, some antiarrhythmics by S. Soliman

31 Diet and Activity ä Salt restriction ä Fluid restriction ä Daily weight (tailor therapy) ä Gradual exertion programs by S. Soliman

32 Diuretic Therapy ä The most effective symptomatic relief ä Mild symptoms ä HCTZ ä Chlorthalidone ä Metolazone ä Block Na reabsorbtion in loop of henle and distal convoluted tubules ä Thiazides are ineffective with GFR < 30 --/min by S. Soliman

33 Diuretics (cont.) ä Side Effects ä Pre-renal azotemia ä Skin rashes ä Neutropenia ä Thrombocytopenia ä Hyperglycemia ä ↑ Uric Acid ä Hepatic dysfunction by S. Soliman

34 Diuretics (cont.) ä More severe heart failure → loop diuretics ä Furosemide 1-3 mg/kg m.c. Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis and metabolic alkalosis Adverse reaction: pre-renal azotemia Hypokalemia Skin rash ototoxicity by S. Soliman

35 K + Sparing Agents ä Triamterene & amiloride – acts on distal tubules to ↓ K secretion ä Spironolactone (Aldosterone inhibitor) recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin- aldosterone system with subsequent effect on myocardial remodeling and fibrosis recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin- aldosterone system with subsequent effect on myocardial remodeling and fibrosis by S. Soliman

36 Inhibitors of renin-angiotensin- aldosterone system ä Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an important role in the progression of the syndrome ä Angiotensin converting enzyme inhibitors ä Angiotensin receptors blockers ä Spironolactone by S. Soliman

37 Angiotensin Converting Enzyme Inhibitors ä They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II → vasodilation and ↓ Na retention ä ↓ Bradykinin degradation ↑ its level → ↑ PG secretion & nitric oxide ä Ace Inhibitors were found to improve survival in CHF patients ä Delay onset & progression of HF in pts with asymptomatic LV dysfunction ä ↓ cardiac remodeling by S. Soliman

38 Side effects of ACE inhibitors ä Angioedema ä Hypotension ä Renal insuffiency ä Rash ä cough by S. Soliman

39 Angiotensin II receptor blockers ä Has comparable effect to ACE I ä Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough) by S. Soliman

40 Digitalis Glycosides (Digoxin, Digitoxin) ä The role of digitalis has declined somewhat because of safety concern ä Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant ä Reduction in hospitalization ä Reduction in symptoms of HF by S. Soliman

41 Digitalis (cont.) Mechanism of Action ä +ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase → inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange ä Vagotonic effect ä Arrhythmogenic effect by S. Soliman

42 Digitalis Toxicity ä Narrow therapeutic to toxic ratio ä Non cardiac manifestations Anorexia, Anorexia, Nausea, vomiting, Nausea, vomiting, Headache, Headache, Xanthopsia sotoma, Xanthopsia sotoma, Disorientation Disorientation by S. Soliman

43 Digitalis Toxicity ä Cardiac manifestations ä Sinus bradycardia and arrest ä A/V block (usually 2 nd degree) ä Atrial tachycardia with A/V Block ä Development of junctional rhythm in patients with a fib ä PVC’s, VT/ V fib (bi-directional VT) by S. Soliman

44 Digitalis Toxicity Treatment ä Hold the medications ä Observation ä In case of A/V block or severe bradycardia → atropine followed by temporary PM if needed ä In life threatening arrhythmia → digoxin-specific fab antibodies ä Lidocaine and phenytoin could be used – try to avoid D/C cardioversion in non life threatening arrhythmia by S. Soliman

45 β Blockers ä ä Has been traditionally contraindicated in pts with CHF ä ä Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV function ä ä In addition to improved LV function multiple studies show improved survival ä ä The only contraindication is severe decompensated CHF by S. Soliman

46 Vasodilators ä ä Reduction of afterload by arteriolar vasodilatation (hydralazin)  reduce LVEDP, O 2 consumption,improve myocardial perfusion,  stroke volume and COP ä ä Reduction of preload By venous dilation ( Nitrate)  ↓ the venous return  ↓ the load on both ventricles. ä ä Usually the maximum benefit is achieved by using agents with both action. by S. Soliman

47 Positive inotropic agents ä These are the drugs that improve myocardial contractility ( β adrenergic agonists, dopaminergic agents, phosphodiesterase inhibitors), dopamine, dobutamine, milrinone, amrinone dopamine, dobutamine, milrinone, amrinone ä Several studies showed ↑ mortality with oral inotropic agents ä So the only use for them now is in acute sittings as cardiogenic shock by S. Soliman

48 Anticoagulation (coumadine) ä Atrial fibrillation ä H/o embolic episodes ä Left ventricular apical thrombus by S. Soliman

49 Antiarrhythmics ä Most common cause of SCD in these patients is ventricular tachyarrhythmia ä Patients with h/o sustained VT or SCD → ICD implant by S. Soliman

50 Antiarrhythmics (cont.) ä Patients with non sustained ventricular tachycardia ä Correction of electrolytes and acid base imbalance ä In patients with ischemic cardiomyopathy → ICD implant is the option after r/o acute ischemia as the cause ä In patients wit non ischemic cardiomyopathy management is not clear ä Amiodarone may have a role in this group of patients by S. Soliman

51 New Methods ä Implantable ventricular assist devices ä Biventricular pacing (only in patient with LBBB & CHF) ä Artificial Heart by S. Soliman

52 Nursing Interventions - CHF   Decrease energy expenditure ä ä Frequent rest periods ä ä Small, frequent feedings ä ä Minimize crying ä ä Prevent cold stress   Provide nutrition ä ä Use soft nipple ä ä Gavage feeding if needed

53 Nursing Interventions - CHF   Monitor fluid status   I & O, specific gravity   Daily weight   Provide adequate rest, position for comfort   Prevent infections   Promote growth & development   Reduce respiratory distress

54 Digoxin ä ä Check dosage with another RN ä ä Give 1 hour before feeding or 2 hours after feeding ä ä Give at 12 hour intervals ä ä Take apical pulse for 1 minute ä ä Hold if HR <90 in infants or<70 in children ä ä Monitor serum potassium levels ä ä Monitor for toxicity: vomiting, nausea, bradycardia, lethargy

55 Myocarditis ä leading cause of dilated cardiomyopathy and one of the most common causes of CHF in children ä etiology: idiopathic, viral, bacterial, parasitic ä hallmark is CHF ä failure to respond to bronchodilators in wheezing child ä treatment includes inotropes, afterload reduction, diuretics, antibiotics, antivirals

56 Pericarditis ä sharp stabbing precordial pain ä worse with supine and better leaning forward ä no sensory innervation of the pericardium ä pain referred from diaphragmatic and pleural irritation

57 Etiology ä infectious ä viral ä bacterial ä TB ä fungal ä parasitic ä Connective tissue ä RA ä Rheumatic fever ä SLE ä Metabolic / Endocrine ä uremia ä hypothyroid ä Hematology / Oncology ä bleeding diathesis ä malignancy ä Trauma ä Iatrogenic

58 Pericarditis ä usually a benign course ä virulent bacteria (H. flu, E. coli) can cause constrictive pericarditis and subsequent tamponade – may need urgent pericardiocentesis ä uncomplicated pericarditis usually responds to rest and anti-inflammatories

59 Chest Pain ä 4% of children will have a cardiac origin ä remainder: MSK, pulmonic (asthma, bronchitis, pneumonia), GI ä Cardiac causes: myocarditis, pericarditis, structural abnormalities such as congenital heart disease or hypertrophic cardiomyopathy

60 Syncope ä 20-50% of adolescents experience at least one episode of syncope ä most cases benign ä Pathophysiology ä vascular ä orthostatic, hypovolemia ä neurally mediated ä hypoxia: PE, CNS depression from OD, CO ä cardiac

61 Cardiac Syncope ä Dysrhythmias ä tachy ä brady ä Outflow obstruction ä Myocardial Dysfunction ä cardiac syncope often precedes future sudden cardiac death

62 Sudden Cardiac Death ä Etiology ä myocarditis ä cardiomyopathy (hypertrophic) ä cyanotic and noncyanotic congenital heart disease ä valvular heart disease ä congenital complete heart block ä WPW ä long QT syndrome ä Marfan syndrome ä coronary artery disease ä anomalous coronary arteries

63 Risk Factors for Serious Cause of Syncope ä history of cardiac disease in patient ä FH of sudden death, cardiac disease, or deafness ä recurrent episodes ä recumbent episode ä exertional ä prolonged loss of consciousness ä associated chest pain or palpitations ä medications that can alter cardiac conduction

64 What to look for in the Department: EKG ä Long QT syndrome ä congenital or acquired ä get paroxysmal v tach with torsades de pointes ä congenital long QT associated with hypertrophic cardiomyopathy ä long QT defined as corrected QT longer than 0.44 s ä T wave alternans sometimes present ä can have normal ECG in the department ä two clinical syndromes not associated with structural heart disease: Romano-Ward and Jervell-Lange-Nielsen

65 Other dysrhythmias ä WPW and other SVT’s ä AV block ä usually acquired, rarely congenital ä Sick sinus syndrome

66 Other structural cardiac diseases ä dilated cardiomyopathy ä usually secondary to myocarditis ä syncope and death secondary to ventricular dysrhythmias or severe myocardial dysfunction ä arrhythmogenic RV dysplasia ä congenital cyanotic and non-cyanotic heart disease ä valvular diseases ä aortic stenosis ä coronary artery anomalies ä exertional syncope or sudden death ä aberrant artery passes between aorta and pulmonary artery

67 Definition- cardiomyopathy “A primary disorder of the heart muscle that causes abnormal myocardial performance and is not the result of disease or dysfunction of other cardiac structures … myocardial infarction, systemic hypertension, valvular stenosis or regurgitation”

68 Cardiomyopathy-definition  According to World Health Organisation and International Society and Cardiology Federation (WHO/ISFC) from 1996, cardiomyopathy is definied as any disease of heartmuscle which is connected with its disfunction

69 WHO Classification ä Unknown cause (primary) ä Dilated ä Hypertrophic ä Restrictive ä unclassified ä Specific heart muscle disease (secondary) ä Infective ä Metabolic ä Systemic disease ä Heredofamilial ä Sensitivity ä Toxic Br Heart J 1980; 44:

70 Functional Classification ä Dilatated (DCM) ä ventricular enlargement and syst dysfunction ä Hypertrophic ( HCM) ä inappropriate myocardial hypertrophy in the absence of HTN or aortic stenosis ä Restrictive (infiltrative) ä abnormal filling and diastolic function

71 Idiopathic Dilated Cardiomyopathy

72 IDC - Definition ä a disease of unknown etiology that principally affects the myocardium ä LV dilatation and systolic dysfunction ä pathology ä increased heart size and weight ä ventricular dilatation, normal wall thickness ä heart dysfunction out of portion to fibrosis

73 Incidence and Prognosis ä 3-10 cases per 100,000 ä 20,000 new cases per year in the U.S.A. ä death from progressive pump failure 1-year25% 2-year35-40% 5-year40-80% ä stabilization observed in 20-50% of patient ä complete recovery is rare

74 Clinical Manifestations ä Highest incidence in middle age ä blacks 2x more frequent than whites ä men 3x more frequent than women ä symptoms may be gradual in onset ä acute presentation ä misdiagnosed as viral URI in young adults ä uncommon to find specific myocardial disease on endomyocardial biopsy

75 History and Physical Examination ä Symptoms of heart failure ä pulmonary congestion (left HF) dyspnea (rest, exertional, nocturnal), orthpnea ä systemic congestion (right HF) edema, nausea, abdominal pain, nocturia ä low cardiac output fatigue and weakness ä hypotension, tachycardia, tachypnea, JVD

76 Cardiac Imaging ä Chest radiogram ä Electrocardiogram ä 24-hour ambulatory ECG (Holter) ä lightheadedness, palpitation, syncope ä Two-dimensional echocardiogram ä Radionuclide ventriculography ä Cardiac catheterization ä age >40, ischemic history, high risk profile, abnormal ECG

77 Clinical Indications for Endomyocardial Biopsy ä Definite ä monitoring of cardiac allograft rejection ä monitoring of anthracycline cardiotoxicity ä Possible ä detection and monitoring of myocarditis ä diagnosis of secondary cardiomyopathies ä differentiation between restrictive and constrictive heart disease

78 Management of DCM ä Limit activity based on functional status ä salt restriction of a 2-g Na + (5g NaCl) diet ä fluid restriction for significant low Na+ ä initiate medical therapy ä ACE inhibitors, diuretics ä digoxin, carvedilol ä hydralazine / nitrate combination

79 Management of DCM ä consider adding ß-blocking agents if symptoms persists ä anticoagulation for EF <30%, history of thromboemoli, presence of mural thrombi ä intravenous dopamine, dobutamine and/or phosphodiesterase inhibitors ä cardiac transplantation

80 Hypertrophic Cardiomyopathy

81 ä First described by the French and Germans around 1900 ä uncommon with occurrence of 0.02 to 0.2% ä a hypertrophied and non-dilated left ventricle in the absence of another disease ä small LV cavity, asymmetrical septal hypertrophy (ASH), systolic anterior motion of the mitral valve leaflet (SAM)

82 65% 35% 10%


84 Clinical Manifestation ä Asymptomatic, echocardiographic finding ä Symptomatic ä dyspnea in 90% ä angina pectoris in 75% ä fatigue, pre-syncope, syncope  risk of SCD in children and adolescents ä palpitation, PND, CHF, dizziness less frequent

85 Natural History ä annual mortality 3% in referral centers probably closer to 1% for all patients ä risk of SCD higher in children may be as high as 6% per year majority have progressive hypertrophy ä clinical deterioration usually is slow ä progression to DCM occurs in 10-15%

86 Risk Factors for SCD ä Young age (<30 years) ä “Malignant” family history of sudden death ä Gene mutations prone to SCD (ex. Arg403Gln) ä Aborted sudden cardiac death ä Sustained VT or SVT ä Recurrent syncope in the young ä Nonsustained VT (Holter Monitoring) ä Brady arrhythmias (occult conduction disease) Br Heart J 1994; 72:S13

87 Management ä beta-adrenergic blockers ä calcium antagonist ä disopyramide ä amiodarone, sotolol ä DDD pacing ä myotomy-myectomy ä plication of the anterior mitral leaflet

88 Restrictive Cardiomyopathy

89 Restrictive Cardiomyopathies ä Hallmark: abnormal diastolic function ä rigid ventricular wall with impaired ventricular filling ä bear some functional resemblance to constrictive pericarditis ä importance lies in its differentiation from operable constrictive pericarditis

90 Exclusion “Guidelines” ä LV end-diastolic dimensions  7 cm ä Myocardial wall thickness  1.7 cm ä LV end-diastolic volume  150 mL/m2 ä LV ejection fraction < 20%

91 Classification ä Idiopathic ä Myocardial 1. Noninfiltrative ä Idiopathic ä Scleroderma 2. Infiltrative ä Amyloid ä Sarcoid ä Gaucher disease ä Hurler disease 3. Storage Disease ä Hemochromatosis ä Fabry disease ä Glycogen storage ä Endomyocardial ä endomyocardial fibrosis ä Hyperesinophilic synd ä Carcinoid ä metastatic malignancies ä radiation, anthracycline

92 Clinical Manifestations ä Symptoms of right and left heart failure ä Jugular Venous Pulse ä prominent x and y descents ä Echo-Doppler ä abnormal mitral inflow pattern ä prominent E wave (rapid diastolic filling) ä reduced deceleration time (  LA pressure)

93 Basic Life Support

94 Cardiopulmonary Arrest Cardiac arrest is the sudden loss of cardiac output, which is potentially reversible with prompt restoration of circulation and oxygen delivery. Sudden cardiac death and cardiac arrest are not synonymous. Sudden cardiac death is unexpected death within 1 hour of symptom onset because of a primarily cardiac cause in a victim with or without previously diagnosed heart disease.

95 Pathophysiology of CPA ä CPA causes hypoxia, respiratory and metabolic acidosis ä cell death appears to be mediated by substances released from anoxic cell membranes ä agents associated with brain and heart injury are free iron, hydroxyl radicals, calcium ä CPA for as little as 5 minutes may cause permanent brain injury or death

96 The Most Common Causes of Pediatric CPA ä infants ä SIDS (40%) ä respiratory diseases ä airway obstruction ä sepsis ä neurological diseases ä metabolic abnormalities ä chidren ä injury

97 Pediatric CPA ä the epidemiology of pediatric CPA is different from that of adults ä sudden, primary cardiac arrest is rare ä ventricular fibrillation has been reported in less than 10% (more likely in children with complex congenital heart disease) ä respiratory insufficiency is the more common cause ä 50% of all children who require CPR are infants

98 Out-of-Hospital CPA Out-of-hospital primary cardiac failure with cardiopulmonary arrest (CPA) is unusual in children. It may occur in children with chronic diseases ä cardiomyopathy ä myocarditis ä congenital heart diseases. It occur around the home, where children are under the supervision of parents. Parents of children at high risk should be educated in BLS.

99 In-Hospital CPA Primary cardiopulmonary arrest is often in hospitalised children ä after cardiac surgery ä with rare arrhythmia caused by ä cardiac catheterization or angiography ä general anesthesia ä antiarrhythmic drug administration

100 Respiratory Causes of Pediatric Cardiopulmonary Arrest Upper airway obstruction Lower airway obstruction - croup- asthma - foreign body- bronchiolitis - strangulation- foreign body - inhalation injury- inhalation injury Intrinsic lung conditions - pneumonia - drowning - chest trauma

101 Cardiovascular Causes of Pediatric Cardiopulmonary Arrest Hypovolemia Dysrrhythmias - trauma- open heart surgery - burns- cardiac catheterization - gastroenteritis- coronary angiography Sepsis- general anesthesia Cardiogenic shock - prolonged QT syndrom - congenital heart diseases Intoxication - cardiomyopathy - myocarditis - post-open heart surgery

102 Basic Life Support Strictly defined, basic life support (BLS) is the initial phase of emergency cardiac care, encompassing recognition of cardiac arrest and delivery of rescue breathing (ventilation) and chest compressions (circulation).

103 Advanced Life Support Advanced life support (ACLS) includes BLS, ECG monitoring, rhythm identification, and restoration of hemodynamic stability through intubation, defibrillation, and pharmacologic therapy. Cardiopulmonary resuscitation effectively restores hemodynamic stability, return of spontaneous circulation (ROSC), in 40% to 60% of arrests.

104 Modern CRP Modern CPR began in 1960 with the landmark study by Kouwenhoven which reported combining closed chest compression, mouth-to-mouth breathing, and external defibrillation. As they explained it, their algorithm was remarkably easy to perform: "Anyone, anywhere, can now initiate cardiac resuscitative procedures. All that is needed are two hands."

105 Modern CPR Cardiac arrest outcomes will be most improved with public education and earlier initiation of CPR, both Basic Life Support and Advanced Life Support, notably defibrillation. After unresponsiveness, lack of pulse, and apnea are confirmed in unmonitored cardiac arrests, the initial management consists of ä BLS ä closed-chest compressions ä artificial ventilation.

106 The Cardiac Pump Theory Circulation: The Cardiac Pump Theory The mechanism by which closed-chest compressions increase forward cardiac output remains controversial. The traditional cardiac pump theory states the heart is massaged and blood forced out by direct compression between the sternum and spine.

107 The Thoracic Pump Theory Circulation: The Thoracic Pump Theory The thoracic pump theory suggests that forward blood flow increases through a passive cardiac conduit by a general increase in intrathoracic pressure transmitted to the cardiac chambers and the intrathoracic portion of the great vessels. Because of intact venous valves, the pressure generated during compression is not transmitted to the periphery, forcing blood to flow from the arteries to the veins.

108 The ABCs of Cardiopulmonary Resuscitation ä Airway ä Breathing ä Circulation

109 The ABCs of CPR - Responsiveness ä Quickly assess the presence or extent of injury and determine whether the child is conscious. The level of responsiveness is determined by tapping the child and speaking loudly to elicit a response. ä Carefully look, listen, and feel the pulse to determine that a cardiopulmonary arrest has occurred. ä Call for help once CPA is diagnosed.

110 The ABCs of CPR - Airway ä Open the airway. Use the head-tilt/chin-lift maneuver, avoiding hyperextension of the neck. Too vigorous head-tilt may occlude the trachea or injure the cervical spine. In infants, large head may flex the neck and compromise air exchange. ä If spinal injury is suspected, use a jaw-thrust instead of head-tilt. ä Suction may be needed to clear secretions, blood, or foreign bodies from the airway.

111 Foreign-Body Airway Obstruction ä the infant: ä back blows ä chest thrusts ä the child: the Heimlich maneuver ä abdominal thrusts with victim standing or sitting (conscious) ä abdominal thrusts with victim laying or sitting (conscious or unconscious)

112 Foreign-Body Airway Obstruction If the airway remains obstructed attempt to evacuate a possible aspirated foreign body. ä For infants give 5 sharp blows to the back with the heel of the hand between securely held shoulder blades. Then, deliver 5 chest thrusts to the mid-sternum. ä For children deliver 5 rapid subdiaphragmatic abdominal thrusts using the heel of the hand (modifed Heimlich maneuver) with the patient supine. If airway patency isn’t established, repeat the sequence. If 2 rapid series of maneuvers fail, perform immediate direct laryngoscopy to inspect the obstructed area.

113 The ABCs of CPR - Breathing 1 Assessment of breathing ä look for a rise and fall of the chest and abdomen, listen for exhaled air, and feel for exhaled air flow at the mouth or the palm Rescue breathing ä if no spontaneous breathing is detected, begin mouth- to-mouth or mouth-to-nose-and-mouth or bag-valve- mask ventilation ä provide 2 slow breaths, pausing after the first one to take a breath to maximize oxygen content and minimize CO 2 concentration in the delivered breaths

114 The ABCs of CPR - Breathing 2 ä rescue breaths are the most important support for a nonbreathing infant or child ä the pressure and volume of ventilation should be sufficient to cause the chest to rise ä rapidly performed rescue breathing may cause gastric distention, which elevating the diaphragm and decreasing lung volume

115 The ABCs of CPR - Circulation 1 Assessment of circulation ä ineffective cardiac contraction will result in the absence of a palpable pulse in a large central artery ä in children older than 1 yr, the carotid artery, on the side of the neck, is the most accessible central artery to palpate ä in infants palpation of the brachial artery is recommended, due to the short, chubby neck ä the femoral artery is often used by health care professionals

116 The ABCs of CPR - Circulation 2 Chest compressions ä serial rhythmic compressions of the chest circulate blood to the vital organs to keep them viable until advanced life support (ALS) care can be provided ä chest compressions must always be accompanied by ventilation ä the child should be supine on a hard, flat surface ä for an infant the hard surface can be rescuer’s hand or forearm

117 The ABCs of CPR - Coordination of Compressions and Rescue Breathing ä external chest compression must always be accompanied by rescue breathing ä at the end of every fifth compression, a pause of 1 to 1.5 sec should be allowed for a ventilation ä in infant and child the 5:1 compression-ventilation ratio is maintained for both one and two rescuers ä the infant and child should be reassessed after 20 cycles of compression and ventilation (apr. 1 min) and every few minutes thereafter

118 Normal Pacemaker Rates at Various Ages ä month bpm ä 1 year bpm ä 5 years bpm ä 10 years bpm ä adult bpm

119 Advanced Life Support

120 Medication Administration 1 ä venous administration (IV) is the preferred route for drug delivery during advanced life support ä in neonatal resuscitation the umbilical vein is more easily cannulated than scalp or peripheral veins ä in older infants and children, peripheral access is usually more easily established than central access ä all doses should be followed by a 5 ml normal saline flush to help move the drug more rapidly into the central circulation

121 Medication Administration 2 ä in patients less than 6 yrs of age, an intraosseous (IO) needle may be used ä all resuscitation medications, including catecholamines, may be administered into the bone marrow ä intramuscular (IM) and sublingual (SL) routes are not recommended due to delayed drug delivery ä intracardiac injection is not recommended due to the risks of hemopericardium and vessel injury; questionable drug absorption

122 Medication Administration 3 ä some medications may be given endotracheally (ET) during advanced life support if IV or IO access is unavailable ä the dose should be diluted in 3 to 5 ml of normal saline (1 to 2 ml for neonatal resuscitation) ä catheter inserted below the end of the endotracheal tube ä each dose should be followed by several positive-pressure ventilations using a hand resuscitation bag to ensure drug deposition into the lungs

123 Epinephrine 1 ä epinephrine is the most frequently used resuscitation medication in infants and children ä alpha-adrenergic effects cause an intense vasoconstriction, increases systemic vascular resistance, improves coronary blood flow ä reduction in blood flow to renal, mucosal, and dermal vascular beds, preserving blood flow to more critical organs ä beta-adrenergic effects cause an increase in cardiac contractility and heart rate, while relaxing smooth muscle

124 Epinephrine 2 ä epinephrine is used for cardiac arrest, asystole, symptomatic bradycardia, and hypotension unrelated to volume depletion ä it can be administered every 3 to 5 minutes as needed ä in neonatal resuscitation to 0.03 mg/kg (0.1 to 0.3 ml/kg of the 1:10,000 solution) IV or ET ä in the newborn higher doses are not recommended due to risk of intracranial hemorrhage and hypertension ä in pediatric resuscitation, the recommended initial dose of epinephrine is 0.01 mg/kg (0.1 ml/kg of the 1:10,000 solution) IV for bradycardia and cardiac arrest

125 Epinephrine 3 ä if pulseless arrest persists, the dose may be increased to 0.1 mg/kg (0.1 ml/kg of the 1:1000 solution ä this is the same dose used for endotracheal administration (ET) ä patients with continued hypotension, epinephrine may be given as a continuous infusion (drip) ä starting dose is 2 mcg/kg/min, with the infusion rate then reduced to maintain the desired response, usually to 0.1 to 1 mcg/kg/min. ä infusion of doses greater than 5 mcg/kg/min may produce profound vasoconstriction at the site of administration

126 Acidosis ä mixed metabolic and respiratory acidosis is common during cardiopulmonary arrest as a result of anaerobic metabolism and carbon dioxide retention ä acidosis may cause a decrease in myocardial contractility, lowering of blood pressure, and a blunting of the response to catecholamines ä optimal method to reverse this situation is to provide adequate ventilation (excretion of CO 2 ) and systemic perfusion ä sodium bicarbonate is reserved for severe metabolic acidosis and only when ventilatory support can be assured

127 Sodium Bicarbonate 1 - Paradoxical Acidosis ä bicarbonate infusion has the potential to induce paradoxical intracellular and central nervous system acidosis ä it combines with protons (H + ) to produce CO 2 and water ä CO 2 is freely diffusable into myocytes and the subarachnoid space where it combines with water to produce free hydrogen ions (CO 2 + H 2 O = H + + HCO 3 - )

128 Sodium Bicarbonate 2 ä standard dose is 1 to 2 mEq/kg IV or IO ä additional doses (0.5 mEq/kg) should be guided by assessment of laboratory values ä standard solutions of 8.4% (1 mEq/ml) sodium bicarbonate are very hyperosmolar (2,000 mOsm/L) and should be used with caution ä in neonates, only the 4.2% (0.5 mEq/ml) solution should be used to avoid increasing the risk of intraventricular hemorrhage ä rate of administration should be no greater than 1 mEq/kg/min

129 Sodium Bicarbonate 3 ä sodium bicarbonate should not be given endotracheally - it can cause substantial tissue injury - it can cause substantial tissue injury ä it should not be mixed with other medications -precipitation of calcium and inactivation of catecholamines may occur if they are mixed with sodium bicarbonate

130 Atropine - indications ä treatment of symptomatic bradycardia, as a second-line therapy after epinephrine ä bradycardia as the result of increased vagal tone (such as during intubation) ä bradycardia as the result of documented atrioventricular block

131 Atropine ä in children, the dose of atropine is 0.02 mg/kg IV,ET or IO, with a minimum dose of 0.1 mg to avoid paradoxical bradycardia ä the recommended maximum single dose is 0.5 mg for a child and 1 mg for an adolescent or adult ä this dose may be repeated once, if no response is seen within 5 minutes

132 Naloxone - indications ä pure antagonist which reverses the effects of opioids such as morphine and fentanyl ä in resuscitations, it is used to reverse the respiratory and central nervous system depression and hypertension caused by administration of opioids ä naloxone is also indicated for severe respiratory depression in neonates whose mothers received opioids within four hours of delivery

133 Naloxone ä naloxone acts within 2 to 3 minutes and has a duration of 30 to 60 minutes ä dose for total reversal is 0.1 mg/kg for infants and children up to 5 years of age or 20 kg body weight ä children over 5 years or 20 kg should receive a standard 2 mg dose ä smaller doses may be used if only partial opioid reversal is desired ä naloxone may be administered by rapid IV push, IO, or ET ä intramuscular or subcutaneous administration may result in erratic absorption and reduced efficacy

134 Calcium chloride ä calcium enhance cardiac contractility and increase systemic vascular resistance ä calcium administration is recommended only in cases of hypocalcemia, hyperkalemia, hypermagnesemia, and calcium channel blocker overdose ä dose of calcium chloride is 0.2 to 0.25 ml/kg of a 10% solution, to provide 5 to 7 mg/kg elemental calcium (20 to 25 mg/kg calcium salt) ä this dose should be infused at a rate no faster than 100 mg/min and may be repeated one time - rapid infusion may result in bradycardia or asystole

135 Dopamine - indications ä patients who remain hypotensive or poorly perfused after initial resuscitation ä dopamine acts at a variety of receptors dopaminergic2 to 5 mcg/kg/min beta-adrenergicabove 5 mcg/kg/min alpha-adrenergic10 to 20 mcg/kg/min

136 Dopamine ä low doses, 2 to 5 mcg/kg/min, dopamine causing increased renal, coronary, splanchnic, and cerebral blood flow ä above 5 mcg/kg/min, dopamine stimulates beta- adrenergic receptors and increases release of norepinephrine, producing an increase in cardiac contractility ä in the range of 10 to 20 mcg/kg/min, dopamine begins to act at alpha-adrenergic receptors, producing vasoconstriction and significant tachycardia ä because of its rapid elimination, dopamine can only be administered as a continuous infusion

137 Dobutamine ä dobutamine stimulates beta-adrenergic receptors and produces a positive inotropic response ä it does not act on dopaminergic or alpha-adrenergic receptors ä dobutamine produces a mild vasodilatation ä it is recommended in cases of cardiogenic or septic shock when the patient is not already hypotensive ä dobutamine is typically started at a dose of 5 mcg/kg/min and titrated to achieve the desired blood pressure response

138 Adenosine ä adenosine is a pharmacologic alternative to defibrillation in patients with supraventricular tachycardia ä produces a transient block of the atrioventricular node ä its short elimination half-life (approximately 9 seconds) makes it a safe medication, but also makes it difficult to get adequate drug concentrations at the site of action ä dose for infants and children is 0.1 to 0.2 mg/kg administered by rapid IV push, followed immediately by a 2 to 3 ml normal saline flush (maximum dose is 12 mg)

139 Lidocaine ä lidocaine is used to control ventricular tachycardia or fibrillation ä recommended method of administration is a 1 mg/kg bolus loading dose, followed by a continuous infusion of 20 to 50 mcg/kg/min ä the dosage should be reduced in children with low cardiac output or reduced hepatic blood flow or function to avoid lidocaine accumulation ä signs of toxicity include drowsiness, confusion, tremors, and seizures.

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