Pediatric Cardiac Disorders

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Fetal Circulation Main Blood Flow Placenta  Umbilical Vein  Liver  Ductus Venosus  Inferior Vena Cava Vena Cava  Right Atrium  Foramen Ovale  Left Atrium  Left Ventricle  Aorta  Body

Fetal Circulation Secondary Route: Right Atrium  Right Ventricle  Pulmonary Artery  Ductus Arteriosus  (so does not go to lungs) Aorta  Body

Fetal Circulation Third route of blood flow Right Atrium  Right Ventricle  Pulmonary Artery  Lungs (needs to perfuse the lungs and upper body with oxygen)  Left Atrium  Left Ventricle  Aorta  Body

Transition from Fetal Circulation to Pulmonary circulation The umbilical arteries and vein and the ductus venosus become non-functional Decreased pulmonary vascular resistance and increased pulmonary blood flow Increase in pressure of the left atrium, decrease pressure in right atrium, causing closure of foramen ovale. Pulmonary resistance is less than systematic resistance so there is left-to-right shunting resulting in closure of the ductus arteriosus.

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15 Infants increase cardiac output by increasing rate. In young children, heart rate is usually higher and stroke volume is lower than in adults. Sinus arrhythmias are normal findings in infants.

16 Chest wall is thinner in children than in adults, with little musculature. Tip of xiphoid process may protrude slightly. Point of maximal impulse is located at the 4 th intercostal space in the child younger than 7 years old. Apical impulse may be visible in children.

Assessment History Physical Diagnostic

18 Diagnostic Data CBC Chest x-ray Pulse oximetry ECG Echocardiography Cardiac Cath MRI Angiography

Congestive Heart Failure

Congestive heart failure The inability of the myocardium to circulate enough oxygenated blood to meet the demands of the body. When the heart fails, cardiac output is diminished. Heart rate, preload, contractitility, and afterload are affected. Peripheral tissue is not adequately perfused. Congestion in lungs and periphery develops.

Etiology and Pathophysiology Congenital defects – allow blood to flow from the left side of the heart to the right so that extra blood is pumped to the pulmonary system rather than through the aorta when the ventricle contracts. Obstructive congenital defects – restricts the flow of blood so the heart hypertrophies to work harder to force blood through the narrowed structures. The hypertrophied muscle becomes ineffective. Other defects which weaken the heart muscle.

Compensatory Mechanisms Stimulation of the sympathetic nervous system which releases norepinephrine from the adrenals. This stimulates blood vessels to constrict and an increase in the heart rate. Tachycardia increases venous return to the heart which stretches the myocardial fibers and increases preload. Only successful for short period of time. Increased renin and ADH secretion caused by decrease renal perfusion. Resultant increase in Na and H2O retention to increase fluid to the heart and leading to edema

Slide 23 CHF in Children Impaired myocardial function Tachycardia Diminished pulses Capillary refill > 2 seconds Pallor cool extremities; Hypotension Oliguria

Slide 24 CHF in Children Pulmonary congestion Tachypnea Dyspnea – rest respiratory distress– like what???? exercise intolerance cyanosis

Slide 25 CHF in Children Systemic venous congestion periorbital edema Peripheral edema weight gain ascites hepatomegaly

CHF in Children High Metabolic Rate Failure to Thrive Slow weight gain

Clinical Manifestations Pump Fails – cannot meet the demands of the body = CHF How do you know when something is wrong? 1.Tires easily during feeding 2.Periorbital edema, weight gain 3.Rales and rhonchi 4.Dyspnea, orthopnea, tachypnea 5.Diaphoretic / sweating 6.Tachycardia 7.Weight

Slide 28 Pathophysiology of CHF

Treatment of Congestive Heart Failure Medication Therapy Digoxin– increases contractility and decreases heart rate. Heart Rate Parameters?????? ACE-inhibitors - arterial vasodilator / afterload reducing agent Diuretics - enhance renal secretion of sodium and water by reducing circulating blood volume and decreasing preload. Beta Blocker - increases contractility

Treatment of Congestive Heart Failure Diet – ????? sodium, small frequent feedings (be sure you can pick the right foods for a low NA diet. Nursing care: Measure intake and output – weighing diapers Observe for changes in peripheral edema and circulation If ascites present – take serial abdominal measurements to monitor changes. Skin care Turning schedule

Congenital Cardiac Anomalies

Defects that increase pulmonary blood flow Patent Ductus Arterious Atrial septal defects Ventricular septal defects

Atrial Septal Defect 1.Oxygenated blood is shunted from left to right side of the heart via defect 2.A larger volume of blood than normal must be handled by the right side of the heart  hypertrophy 3.Extra blood then passes through the pulmonary artery into the lungs, causing higher pressure than normal in the blood vessels in the lungs  congestive heart failure

Treatment Medical Management Medications – digoxin Cardiac Catheterizaton - Amplatzer septal occluder Open-heart Surgery

Cardiac Catheterization Pre-care: History and Physical Lab work – EKG, ECHO cardiogram, CBC NPO Preprocedural teaching Post Care: Monitor vital signs Monitor extremity distal to the catheter instertion, Keep leg immobilized Vital signs Check for bleeding at insertion site Measure I&O

Treatment Device Closure – Amplatzer septal occluder During cardiac catheterization the occluder is placed in the Defect

Ventricular Septal Defect 1.Oxygenated blood is shunted from left to right side of the heart via defect 2.A larger volume of blood than normal must be handled by the right side of the heart  hypertrophy 3.Extra blood then passes through the pulmonary artery into the lungs, causing higher pressure than normal in the blood vessels in the lungs  congestive heart failure

Treatment Surgical repair with a patch inserted

Patent Ductus Arteriosus 1.Blood shunts from aorta (left) to the pulmonary artery (right) 2.Returns to the lungs causing increase pressure in the lung 3.Congestive heart failure

Treatment for PDA Medical Mangement Medication Indomethacin - inhibits prostaglandin‘s Promotes closure of the ductus arteriosus Surgery Ligate the ductus arteriosus

Treatment for PDA Cardiac Catheterization Insert coil – tiny fibers occlude the ductus arteriosus when a thrombus forms in the mass of fabric and wire

Pulmonic stenosis Tetralogy of fallot Transposition of the great arteries Truncus arteriosus Defects with decrease pulmonary blood flow and mixed defects

Pulmonic Stenosis Narrowing of entrance that decreases blood flow Treatment: Medications – Prostaglandin E 1 to keep the PDA open Cardiac Catheterization Baloon Valvuloplasty Surgery Valvotomy

Tetralogy of Fallot Four defects are:

Signs and Symptoms 1. Failure to thrive 2. Squatting 3. Lack of energy 4. Infections 5. Polycythemia 6. Clubbing of fingers 7. Cerebral absess 8. Cardiomegaly

Treatment Surgical interventions Blalock – Taussig or Potts procedure – increases blood flow to the lungs. Open heart surgery

Transposition of Great Vessels Aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle - which is not compatible with survival unless there is a large defect present in ventricular or atrial septum. artery aorta

Truncus arteriosus A single arterial trunk arises from both ventricles that supplies the systemic, pulmonary, and coronary circulations. A vsd and a single, defective, valve also exist. Entire systemic circulation supplied from common trunk.

Defects obstructing Systemic blood flow Aortic stenosis Coarctation of the Aorta

1.Narrowing of Aorta causing obstruction of left ventricular blood flow 2.Left ventricular hypertrophy Signs and Symptoms 1.  B/P in upper extremities 2.  B/P in lower extremities 3.Radial pulses full/bounding and femoral or popliteal pulses weak or absent 4.Leg pains, fatigue 5.Nose bleeds

Treatment Goals of management are to improve ventricular function and restore blood flow to the lower body. Medical management with Medication A continuous intravenous medication, prostaglandin (PGE-1), is used to open the ductus arteriosus (and maintain it in an open state) allowing blood flow to areas beyond the coarctation. Baloon Valvoplasty

Surgery for Coarctation of Aorta 1. Resect narrow area 2. Anastomosis

Ask Yourself ? Laboratory analysis on a child with Tetralogy of Fallot indicates a high RBC count. The polycythemia is a compensatory mechanism for: a. Tissue oxygen need b. Low iron level C. Low blood pressure d. Cardiomegaly

Acquired Cardiac Diseases

RHEUMATIC FEVER A systemic inflammatory (collagen) disease of connective tissue that usually follows a group A beta-hemolytic streptococcus infection. This disorder causes changes in the entire heart (especially the valves), joints, brain, and skin tissues.

Rheumatic Fever Assessment Jones Criteria Major Minor Treatment Antibiotic Therapy Aspirin

MAJOR Manifestations Carditis Polyarthritis Chorea Erythema Marginatum Subcutaneous nodules

MINOR Arthralgia Fever ESR C-reactive protein Prolonged PR Interval

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Subacute Bacterial Endocarditis / Ineffective Endocarditis: Microorganisms grow on the endocardium, forming vegetations, deposits of fibrin, and platelet thrombi. The lesion may invade adjacent tissues such as aortic and mitral valves.

Subacute Bacterial Endocarditis / Ineffective Endocarditis: Assessment Diagnosis – blood cultures Treatment Antibiotics Patient teaching – take antibiotics prior to surgery, dental work, etc.

Kawasaki Disease Multisystem vasculitis – inflammation of blood vessels in the body especially the coronary arteries with antigen-antibody complexes.

Kawasaki Disease Signs and Symptoms / Treatment Three Phases of clinical manifestations: Acute Subacute Convalesant Treatment Aspirin Gamma Globulin Nursing Care

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Kawasaki Disease Which phase of Kawasaki is this child exhibiting? Inflamed, Cracked, Peeling Lips Strawberry tongue

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77 Promote adequate cardiac output and oxygenation Position Neck slightly hyperextented to keep airway open Knee-chest or squatting to relieve “Tet” spells

78 Promote adequate cardiac output and oxygenation Pharmacologic agents Digoxin Vasodilators ACE inhibitors

79 Reduce workload of heart to conserve energy Avoid extremes of temperature Organize care Semi-folwer’s position Feed no longer than 30 minutes Diuretics if ordered

80 Energy is conserved which reduces workload of the heart Vital signs within parameters for the child’s age, weight, height

81 Promote adequate nutrition Low sodium formulas High calorie with low volume I & O Gavage feedings if needed

82 Prevent infection Standard precautions Limit contacts with crowds Report early signs & symptoms of infection

83 Promote optimal growth & development (Outcome) Fluid and caloric requirements are met to enable physical growth to progress at consistent rate. Development progresses.

84 Meet teaching needs of patient, family (Outcome) Family and child demonstrate adequate coping mechanisms to deal with CHD.

85 Fluid and caloric requirements are met to enable physical growth to progress at a consistent rate. The child/family verbalize understanding of the type of CHD, its treatment and prognosis.

86 Preparing Children for Surgery Infants Separation from parents Stranger Anxiety Toddlers Need visuals Preschool May view as punishment Misconceptions about happenings in surgery

87 School Age Adolescent

88 What materials would you use to teach Preschool age School age Adolescent