1. به نام خدا

2. Emergencies in pediatric cardiology

3. Outlines Cardiogenic shock Approach to a cyanotic neonate Arrhythmias Brady arrhythmiasBrady arrhythmias TachyarrhythmiasTachyarrhythmias

4. Cardiogenic Shock

5. severe cardiac dysfunction before or after cardiac surgery septicemia severe burns anaphylaxiscardiomyopathy myocarditis myocarditis myocardial infarction or stunning myocardial infarction or stunning Central nervous system disorders

6. Cardiogenic Shock CardiomyopathyArrhythmias Mechanical abnormality Obstructive disorder

7. Treatment Treatment is aimed at reinstitution of adequate cardiac output and peripheral perfusion to prevent the -untoward effects of prolonged ischemia on vital organs, as well as management of the underlying cause.

8. Cardiac output in turn is dependent on two cardiac factors Cardiac output in turn is dependent on two cardiac factors 1) heart rate (HR) and 2) stroke volume (SV). As children are "heart rate dependent", the heart rate is the single most important vital sign when determining shock. As children are "heart rate dependent", the heart rate is the single most important vital sign when determining shock.

9. Stroke volume is the second determinant of cardiac output, and is dependent on three factors: 1) preload (intravascular volume/blood often called "venous return"), (the fuel), 2) myocardial contractility (heart muscle function), (the pump), and 3) afterload (systemic vascular resistance) (the pipes). Children are particularly dependent upon adequate intravascular volume, and when volume depleted, they peripherally vasoconstrict to maintain stroke volume. The myocardium in infants is "stiff" and plays little role in increasing cardiac output. Therefore, the heart rate must increase in order to maintain adequate circulatory function. Remember C.O.=H.R. x S.V C.O.=H.R. x S.V

10. Preload Optimal filling pressure is variable and depends on a number of extracardiac factors including ventilatory support with high positive end-expiratory pressure and intra-abdominal pressure. The increased pressure necessary to fill a relatively noncompliant ventricle should also be considered

12. Preload The mean difference between CVPs measured from the central and peripheral catheters was 8 ± 4 cm H2O. The linear regression equation showed : CVP = 0.32 PVP + 3.8 (r = 0.67; p<0.005). H. Amoozgar, N. Behniafard, M. Borzoee,G. H. Ajami. Correlation Between Peripheral and Central Venous Pressures in Children with Congenital Heart Disease. Pediatr Cardiol (2008) 29:281–284

13. Contractility Dopamine, epinephrine, and dobutamine improve cardiac contractility The use of cardiac glycosides to treat acute low cardiac output states should be avoided

14. Afterload Patients in cardiogenic shock may have a marked increase in systemic vascular resistance resulting in high afterload and poor peripheral perfusion Milrinone & nitroprusaid

15. Blood pressure measurement in neonates

19. the measured BP is 9 mm Hg higher than pulse method. In 86-92% of neonate the measured BP by pulse had only 10 mm Hg difference with BP by pulse oximetry. H. Amoozegar, M.Rastegar. Comparison of neonatal blood pressure measurement by pulse-oximetry and conventional method (Pulse) Iran J Pediatr, Vol 16, No 3, Sep 2006

20. Stages Disturbance of perfusion End organ damage Irreversible shock Death

22. Evaluation and initial management of cyanotic heart disease in the newborn

23. Cyanosis

26. HISTORY Family history Prenatal testing Perinatal history

27. PHYSICAL EXAMINATION Vital signs Second heart sound MurmurHepatomegaly

28. LABORATORY STUDIES Complete blood count Sepsis evaluation Chest radiograph Electrocardiogram Oxygen saturation Arterial blood gas Hyperoxia test Echocardiography

30. INITIAL MANAGEMENT General approach Antibiotics Prostaglandin E1 Cardiac catheterization

32. Hypercyanotic Episodes and Squatting severe and often prolonged decrease in arterial saturation The cyanosis is a result of an acute, substantial increase in right-to-left shunting owing to a change in the ratio between pulmonary and systemic vascular impedance. They tended to occur more commonly in patients with iron deficiency anemia changes in the degree of subpulmonic obstruction

33. Treatment Knee chest position O2 2L/Min Hydration 20 cc/Kg Morphine 0.2 mg/Kg Bicarbonate 1 meg /KG Propranolol 0.01-0.1 mg/KG Phenylephrine

34. Arrhythmias

35. Brady arrhythmia

36. Abnormalities of impulse propagation and/or inhibitory neural influence in the AV conduction system may result in abnormalities including intra-atrial block, block within the AV node, block within the His, or aberrant ventricular conduction owing to block within one of the specialized intraventricular fascicles.

37. Management Treatment for sinus node dysfunction depends on symptoms, which may include syncope, exercise intolerance, and/or cardiac dysfunction aggravated by loss of AV synchrony, all of which are treated with pacing.

38. Isoperoteranol (B1,B2 agonist) 0.05-2 mac/Kg/Min Pacing

39. Supraventricular tachycardias (SVTs) categories: re-entrant tachycardias usingre-entrant tachycardias using an accessory pathway an accessory pathway Re-entrant tachycardias without an accessoryRe-entrant tachycardias without an accessory pathway, and ectopic or automatic tachycardiaspathway, and ectopic or automatic tachycardias

41. CLINICAL MANIFESTATI0N The heart rate usually exceeds 180 beats/min and may occasionally be as rapid as 300 beats/min The only complaint may be awareness of the rapid heart rare.

42. ECG

43. SVT may occur in the presence of unoperated congenital heart disease (Ebstein anomaly). In children, SVT may be precipitated by exposure to the sympathomimetic amines contained in over-the-counrer decongestants associated with abnormal hearts (cardiomyopathy) or with posroperative congenital heart disease

44. Differentiation from sinus tachycardia Differentiation from sinus tachycardia may be difficult; if the rate is >230 beats/min with an abnormal P-wave axis (a normal P wave is positive in leads I and aVF)

45. TREATMENT Vagal stimulation by submersion of the face in iced saline (in older children) or by placing an ice bag over the face (in infants) may abort the attack To abolish the paroxysm, older children may be taught vagotonic maneuvers such as the Valsalva maneuver, straining, breath holding, drinking ice water, or adopting a particular posture.

46. Pharmacologic In stable patients, adenosine by rapid intravenous push is the treatment of choice because of its rapid onset of action and minimal effects on cardiac contractility. Adenosine 0.1-0.2 mg/Kg over 1-2 sec(Max 0.25 Mg/Kg up to 12 Mg)

47. DC cardio version when symptoms of severe heart failure have already occurred, synchronized DC cardio version (0.5-2 W-sec/kg) is recommended as the initial management

48. maintenance therapy In patients without an antegrade accessory pathway, digoxin or propranolol is the mainstay of therapy. In children with evidence of preexcitation (WPW syndrome) digoxin or calcium channel blockers may increase the rate of anterograde conduction of impulses through the bypass tract and should be avoided. In children with evidence of preexcitation (WPW syndrome) digoxin or calcium channel blockers may increase the rate of anterograde conduction of impulses through the bypass tract and should be avoided. Radiofrequency ablation

49. Ventricular tachycardia

50. Ventricular tachycardia (VT) is less common than SVT in pediatric patients. VT is defined as at least three PVCs at >120 beats/min

52. Treatment For patients who are hemodynamically stable, intravenous amiodarone, lidocaine, or procainamide are the initial drugs of choice. Lidocaine 1 mg/Kg slowly IV *2 times 15 min and then 20-50 mcg /Kg/Min ETT Dose 2-2.5* IV Amiodarone 5-10 mg/Kg over 30 min

53. DC shock when symptoms of severe heart failure have already occurred, synchronized DC cardioversion (4 J/kg) is recommended as the initial management

54. Unless a clearly reversible cause is identified, electrophysiologic study is usually indicated for patients in whom VT has developed