Pediatric Cardiac Disorders

http://www.rnceus.com

http://www.childrensheartinstitute.org/

http://depts.washington.edu/physdx/heart/demo.html

http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm

http://www.med.ucla.edu/wilkes/inex.htm

http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm

http://www.youtube.com/watch?v=J2R8MOoQtd8&NR=1

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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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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.

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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 4th intercostal space in the child younger than 7 years old.

Apical impulse may be visible in children.

Assessment

History

Physical

Diagnostic

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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

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CHF in Children

Impaired myocardial function Tachycardia Diminished pulses Capillary refill > 2 seconds Pallor cool extremities; Hypotension Oliguria

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CHF in Children

Pulmonary congestion Tachypnea Dyspnea – even @ rest respiratory distress– like

what???? exercise intolerance cyanosis

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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 = CHFHow do you know when something is

wrong?

1. Tires easily during feeding2. Periorbital edema, weight gain3. Rales and rhonchi4. Dyspnea, orthopnea, tachypnea5. Diaphoretic / sweating6. Tachycardia7. Weight

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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 ArteriousAtrial 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 stenosisTetralogy 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:

1.

2.

3.4.

Signs and Symptoms1. 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

Coarctation of the Aorta1. Narrowing of Aorta

causing obstruction of left ventricular blood flow

2. Left ventricular hypertrophy

Signs and Symptoms

11 B/P in upper extremities

11 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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Promote adequate cardiac output and oxygenation

Position Neck slightly

hyperextented to keep airway open

Knee-chest or squatting to relieve “Tet” spells

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Promote adequate cardiac output and oxygenation

Pharmacologic agents

Digoxin

Vasodilators

ACE inhibitors

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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

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Energy is conserved which reduces workload of the heart

Vital signs within parameters for the child’s age, weight, height

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Promote adequate nutrition

Low sodium formulas

High calorie with low volume

I & O

Gavage feedings if needed

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Prevent infection

Standard precautions

Limit contacts with crowds

Report early signs & symptoms of infection

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Promote optimal growth & development

(Outcome)

Fluid and caloric requirements are met to enable physical growth to progress at consistent rate.

Development progresses.

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Meet teaching needs of patient, family

(Outcome) Family and child demonstrate

adequate coping mechanisms to deal with CHD.

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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.

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Preparing Children for Surgery

Infants Separation from parents Stranger Anxiety

Toddlers Need visuals

Preschool May view as punishment Misconceptions about

happenings in surgery

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School Age

Adolescent

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What materials would you use to teach

Preschool age

School age

Adolescent