Pediatric Cardiology Dysfunction for Students--2011[1]

8/3/2019 Pediatric Cardiology Dysfunction for Students--2011[1]

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Cardiovascular

Dysfunction in the ChildN425

(ppt adapted from Norene Rouse, RN, MSN, CNS)Presented by:

Barbara Welton, RN, MSN CNS



Cardiac Disease in Children: Statistics

Thousands of infants born each yearhave congenital cardiovasculardefects.

Of those who have these defects:² 4²10% have atrioventricular septal

defect.² 8²11% have coarctation of the aorta.² 9²14% have Tetrology of Fallot.² 10²11% have transposition of the

great arteries.

² 14²16% have ventricular septaldefects.² 4²8% percent have hypoplastic left

heart syndrome

Source: © 2011 American Heart Association





Other Etiology«

Genetics Environment

Medications

Illegal drugs Alcohol

Chromosomal syndromes

Higher incidence if parent,(especially mother) had a defect.

Multi-factoral



The Heart«

Muscular, four-chamberedorgan

Primary purpose is to pump

blood to the body by:² electrical stimulation

² rhythmic contraction of heartmuscle

² blood flows from an area of highpressure to area of low pressure

² valves prevent back flow



Normal blood flow through the heart and lungs.



Flow of Blood« 1.Blood enters into RAfrom body.

2.Blood flows from RA toRV.

3.RV blood goes to thelungs through the PA.

4.Blood enters lungs foroxygenation and returnsvia the PV into the LA.

5.Blood flows from LA toLV.

6.Blood moves from LV tothe body via the aorta.



Assessment Priorities«

Abnormal heart sounds Color

Rales or crackles in lungs

Enlarged Liver (firm abdomen) Pulses and refill time

Edema

FTT



Stroke Volume the amount of blood ejected from the ventricles witheach contraction

Is influenced by: Preload, Contractility, Afterload and HR



Electrical Conduction of the Heart:

SA node (pacemaker), AV node, bundle of His (Leftand Right bundle branches), and the purkinje fibers.



Frank-Starling

Law

Cardiacoutput

Strokevolume

Heartrate

Preload

Myocardialcontractility

Afterload

In cardiac physiology, the rulestating that cardiac outputincreases in proportion to the

diastolic stretch of heart musclefibers.



Frank-Starling Law«

The preload in the intact heart isrelated to the resting length of themuscle fibers which in turn isdependent upon the amount of

filling of the chamber. Up to a point, an increase inpreload lengthens the myocyte andstimulates a more vigorouscontraction (Frank Starling Law) by

increasing the number of activatedmyosin-actin bridges and theamount of calcium released fromthe sarcoplamic reticulum.



Diagnostic Testing«

Blood work (Hct?)

Echocardiogram

EKG/Holter monitor

Chest X-ray

Heart Catheterization

Electrophysiology (

EP)

Stress/Exercise Testing

MRI or CT scan



Common Testing for CHD«

Echocardiography Can give information relating to

pressures, diameters,ventricular function

Hearth Catheterization Pros and Cons



Echocardiography:Transthoracic

-M-Mode

-2-D

-Doppler

T EEFetal

Blue = away; Red = towards



MRI

3D

4-D flowvectormapping



Cardiac Catheterization«

Study various functions of the heart. Observe vessels and flow when dye injected. Measure Oxygen concentration across the valves

and walls (septa) of the heart. Measure pressures within each chamber of the

heart and across the valves. Procedure can even be performed in

small, newborn infants. Perform procedures once done in

surgery.



The Child Going to Heart Cath

Answer questions

Keep things simple Validate anxiety Walk through the area

Prepare for procedure- Pre-op meds, monitoring- Insertion site prep- Equipment- Diversion activities- Time frame for procedure- Using pictures



Post Heart Catheterization

Focus on child after procedure- bedside report, check site

- control/prevent bleeding at site

- keeping flat

- monitoring of VS- check leg pulses, perfusion, color

- light diet initially

- comfort measures

Ask parents what they know Reinforce/provide appropriate

information after MD has discussed withfamily

Home care instructions



"Eisenmenger·s Syndrome"

When VSD defects go unrepaired into theteen or young adult years, increased pulmonaryblood flow can cause changes in the pulmonaryvasculature.

Eisenmenger Syndrome occurs when thenormal left to right shunting that occurs withseptal defects switches to a right to left shuntdue to the development of increased pulmonaryvascular damage leading to resistance.

T his pressure in the lungs can equal or exceedsystemic vascular resistance which causes thereversal of blood flow.

T

his is a cyanotic condition.



Children born with Eisenmenger syndrome are born with a hole between the twochambers -- the left and right ventricles -- of the heart (ventricular septaldefect). T he hole allows blood that has already picked up oxygen from the lungs toflow back into the lungs, instead of going out to the rest of the body. T he

increased blood flow and high pressure damages the small blood vessels in thelungs.



Heart Disease in Children«

The two types of heart disease inchildren are "congenital" and"acquired."

Congenital heart disease ispresent at birth.

Acquired heart disease developssometime during childhood oradulthood.



Congenital Heart Disease«

These are structural problems About 40,000 children are born

with heart defects each year

At least 8 per 1000 are born

with a heart defect per year About 1 million Americans with

cardiovascular defects are alivetoday.

Many adults are being diagnosednow with heart defects



Congenital Heart Disease«

Acyanotic

Systemic arterial

saturation isnormal.

Pulmonary bloodflow is normal or

increased. Oxygenation is

taking place

Cyanotic

Systemic arterialsaturation is low.

Pulmonary bloodflow can beincreased ordecreased.

Mixing of bloodwith and withoutoxygen



Acyanotic Heart Defects

PDA ASD

VSD

AV canal Coarctation of the Aorta

Aortic Stenosis

Pulmonary Stenosis



Cyanotic Heart Defects«

Tetralogy of Fallot (TOF) (has VSD)

Pulmonary Atresia with IVS (no VSD)

Transposition of the Great Vessels

Total Anomalous Pulmonary VenousReturn (TAPVR)

Truncus Arteriosus

Tricuspid Atresia Hypoplastic Left Heart Syndrome



Atrial Septal Defect (ASD)

Abnormal holebetween the twoatria.

Excess blood movesfrom L to R throughhole causing increasedflow to RV and thento lungs.

This causes the heartto work harder



Signs & Symptoms of ASD«

Usually asymptomatic ininfancy and early childhood,may wait to see if close onown.

May show s/s of CHF

Shortness of Breath Difficulty feeding Poor weight gain

Enlarged right heart Pulmonary hypertension can

occur in time Atrial dysrhythmias



Treatment of ASD

Stitch repair

Amplatzer

Patch repairClosure recommendedbefore 5 years of age.



Placing the Amplatzer

during Heart Catheterization



Ventricular Septal Defect (VSD)

Most common cardiac lesion

Many close spontaneously

A hole or holes occurs between the

Left and Right ventricles Higher pressure on left causes

blood to leak back into the RV

Can cause enlargement of RV andthen weakening of the muscle

Repair to control CHF and maintainadequate growth



VentricularSeptalDefect(VSD)

Sites



Signs & Symptoms of a VSD«

Enlargement of the right heart fromincreased volume of blood. Possible lung congestion/CHF (moderate

sized defects)

Arrhythmias Inflammation

Treatment:

Stitches/Patches Closure device-not recommended-too

problematic



Patent Ductus Arteriosus

Increased pulmonaryblood flow.

Ductus arteriosus fails toclose after birth.

Normal lungs releasebradykinin causingconstruction of smoothmuscle in ductus

Hypoxia problems prevent

the release of bradykininso remains open Oxygenated blood flows

from aorta back into thelungs.

Connects aorta & pulmonary arteries



Signs & Symptoms of PDA«

May show no problems initially In time will show s/s of CHF Failure to thrive SOB on exertion

´Cold sweatµ Respiratory infections Bounding pulsesTreatment: Indomethacin or ibuprofen for

premature infants Surgery to tie off or divide if large Coil implantation



Patent Ductus Arteriosus (PDA)



Patent Ductus Arteriosus (PDA)

Size of thevesseldetermines

procedure used.



Coarctation of the Aorta (COA)

Pinching or narrowing of part ofthe aorta that sends oxygenatedblood from the heart to the restof the body. Could extend to asection of the aorta. Increased

risk of stroke.May have hypoplastic aortic arch



Signs & Symptoms of Coarc«

May not have anysymptoms until older orneed emergency surgery atbirth.

Higher BP to upper body sohigh risk of stroke. CheckBP in all 4 extremities.

Decreased or absent pulses

to lower body.

Blood flow to lower bodyalso reduced including the

kidneys and gut.



Signs & Symptoms of Coarc cont«

Increased pressure above thenarrow area causing LV to workharder causing ventricle toenlarge then become weakened.

Blood then backs up into thelungs and CHF develops.

May present as a shelf-likeobstruction

May present as a tubularobstruction



SubclavianFlap Repair

Repair of Coarctation of the AortaRepair approach dependent on proximity of other

structures, severity of side effects, and age ofchild at diagnosis



Coarctation Repair

End to End

Anastomosis:

Uses lateral thoracotomy entryClosed heart procedure

End to end or end to side of

anastomosis preferred repairRe-coarctation after neonatalrepair not uncommon



Balloon Angioplasty for Coarctation Repair«

Effective for reducing discrete coarctation and/or add stent

to keep open.Can develop tearing or aneurysm formation in the aorta

Heart Cath procedure:



Coarctation of the Aorta«

Post op issues: Incision issues-picking child up

High blood pressure ² dam effect, willcome back from surgery with meds to

help and go home with meds. Body has adjusted to needing high

pressure to make blood flow.

Lower part of body may have adjustedto the lesser volume of blood and havesmaller vessels.

Development of collaterals



Cyanotic Heart Defects«

Increasedpulmonary bloodflow

T

ransposition ofthe greatarteries(mixed defect)

T runcus

arteriosus T APVR

Decreasedpulmonary bloodflow

Pulmonaryatresia T ricuspid atresia **Tetrology of

Fallot (TOF)**

**Know for exam



Tetrology of Fallot (TOF)1. PS - severity of

condition depends ondegree of obstruction.

2. VSD3. Overriding aorta

4. Hypertrophic RV



Signs & Symptoms of TOF..

Cyanosis at birth Pink vs. Blue T et

Murmur

Crying leads to cyanosis

Leads to irritability and

then can become

unresponsive (´T et spellµ)

Pulmonary artery may be hypoplastic,nonconfluent, and supplied by aortopulmonarycollaterals.

Size dictates surgical repair



Managing a ´Tet Spellµ«

A sudden change in blood flow from LR«to RL«

Prolonged spellsyncope, seizure, arrest

Knees to chest/squatting position to

decrease venous return from legs andraise systemic vascular resistance thusdecreasing R to L flow.

Oxygen

Morphine Inderal



Repair of TOF

Palliative repair withBlalock-TaussigShunt getting blood

to the lungs. Open and patch

Pulmonary Artery

VSD patch



Surgery for CHD (Pre-op)«

Knowledge deficit: child/family Promote nutrition (feeding tubes)

Altered cardiac output - fluid volumeexcess, pulmonary hypertension,

increased blood flow to lungs, CHF,frequent respiratory infections Activity intolerance ² fatigue,

weakness, disease process, circulatory

compromise Risk for infection ² debilitatedphysical status

Altered growth and development ²

decreased oxygenation



The Post-Op Heart« Decreased Cardiac Output - surgical

complications, bleeding, fluid shifting Altered Comfort ² incision site,

treatments and procedures

Risk for infection ² from surgery,

and IV lines

Compromised Family Coping ² from

child·s surgery, child·s hospitalization,

lack of support systems, financial

considerations

Activity Intolerance ² post op status Altered Growth and Development ²

from underlying disease process



Caring for the Child and Family...

Coping ² keeping family updatedat all times with the plan ofcare.

Educate regarding meds,therapies, and procedures

Allow family to help with care

when appropriate. ATC visiting. Encourage caringfor self.

Allow personal items at bedside.



The Discharge«

Discuss with DischargeCoordinator

Wound care Medications Monitoring progress Nutrition needs

Activities Equipment needs Educational needs



Congestive Heart Failure«CHF is a group of signs andsymptoms that reflect theheart·s inability to effectivelypump blood to meet the

metabolic requirements of thebody. The body wants equal amountsof blood going to the body

and the lungs to maintain afluid balance.

When one exceeds the other

heart failure occurs.



Etiology of CHF in Children«

Heart rate- Arrhythmias: SVT , VT ,

Bradycardia

Preload- Shunt lesions: VSD, AV canal,Single Ventricle; Anemia and Volume overload

Afterload- Left heart obstructive

lesions: Coarctation, Aortic Stenosis, HT N

Contractility- Myocardial disease:

Myocarditis, Cardiomyopathy

l l f



Clinical Signs of CHF«

Tachycardia

Pale color

Feeding difficulties

Diaphoresis especially with feeding

Tachypnea with increased WOB Retracting and Grunting and wet lungs

Decreased distal pulses and coolextremities

Facial edema

Distended abdomen, enlarged spleenand liver with weight gain, but FTT



Treatment of CHF«

Diuretics:- Furosemide (Lasix) 0.5 to 2 mg/kg/dose IV- Hydrochlorothiazide (HydroDiuril) 2-4

mg/kg/day- Chlorothiazide (Diuril) 20-40mg/kg/day- Ethacrynic acid (Edecrin) 1mg/kg/dose- Spironolactone (Aldactone) 1-3 mg/kg/day

Potassium sparing?

Electrolyte changes?



Treatment of CHF

Digitalis ² Digoxin- T otal Digitalizing Dose 0.04 mg/kg

- Give ½ dose, then ¼ dose in 4-8 hoursand the last ¼ dose in 4-8 hours

- T oxicity: vomiting & arrhythmias- Rarely causes bradycardia (HR < 90)- More concern regarding heart block- T each parents to take HR?

- What should you teach?- Maintenance dose: 10 mcg/kg/daydivided



Treatment of CHF«

Reducing Afterload (ACE Inhibitors)

- Enalapril: 0.1 mg/kg (may increase to 0.2-0.3mg/kg/day)

- Captopril: Neonates: 0.1-0.4 mg/kg/dose every6-24 hrInfants: 0.5-0.6 mg/kg/day dividedevery 6-24 hrChildren: 25 mg/day divided every 12

hrsAdolescents: begin 25 mg T ID, Max450 mg

Works by causing vasodilation of peripheral vessels.



Nursing Care Plan for Child with CHF

Increased caloric requirements Infection control issues-handwashing

Energy conservation (frequent naps)

Balance fluids and electrolytes (labs) Do they have IV fluids running on

top of their feedings? Look at totalvolume intake.

Medication administration

Monitor results of above



Acquired Heart Disease«

Rheumatic Fever

Bacterial Endocarditis

Kawasaki·s Disease



Rheumatic Fever«

Autoimmune reaction to Group ABeta-hemolytic streptococcal(GABHS) pharyngitis.

It involves joints, skin, brain, heart

valves, blood vessels Major cardiac findings of RF is

inflammation of the heart in:endocardium, pericardium, and

myocardium Less frequent in US due to quickdiagnosis and antibiotic treatmentof strep throat or scarlet fever.

S/S Rh ti F



S/S Rheumatic Fever«

Joint inflammation - swelling, tenderness,and redness over multiple joints. Usuallythe larger joints in the knees or ankles.T he inflammation "moves" from one joint toanother over several days.

Small nodules or hard, round bumps underthe skin Change in the child's neuromuscular

movements: chorea Rash - a pink rash with odd edges that is

usually seen on the trunk of the body orarms and legs. Fever, weight loss, fatigue, stomach pains

Jones Criteria



Major Manifestations* Minor ManifestationsCarditis Clinical features:

Polyarthritis Arthralgia and Fever

Chorea Laboratory features:Erythema marginatum 1. Previous infection (ASO)

Subcutaneous nodules 2. Elevated Sed Rate (ESR)

Aschoff bodies 3. Positive C-reactive protein4. Prolonged PR interval

Supporting Evidence of Previous Group A Strep Infection:1. Positive throat culture or rapid streptococcal antigen test

2. Elevated or increasing streptococcal antibody titer

*The presence of two major or of one major and two minor manifestationsindicates a high probability of acute rheumatic fever if supported by

evidence of previous group A streptococcal infection.

Jones Criteria



Jones Criteria Terminology«

C-Reactive Protein ² marker for acuteinflammation

Antistreptolysin-O titer (ASO) -streptococcal antibody tests for

previous infection Erythrocyte sedimentation rate

(ESR) ² used to monitor inflammatoryor malignant disease

Subcutaneous nodules (Aschoffbodies)

Histological findings



Management of RF«

Administration of Penicillin Prevent permanent heartdamage

Treat other symptoms Prevent recurrences of RFthrough prophylactic use of

antibiotics



Nursing management of RF«

Encourage compliance with medsespecially for long-term therapy.

May need monthly IM injections if

non-compliant Assist with recovery from s/s--chorea movements are particularly

frustrating Emotional support

Prevent recurrence




Bacteria in the bloodstream lodge onabnormal heart valves or otherdamaged heart tissue.

Certain normal bacteria that live onparts of your body can enter thesystem through surgical and dentalprocedures which cause a briefbacteremia.

Although bacteremia is common aftermany invasive procedures, only certainbacteria commonly cause endocarditis.



Risks of Bacterial Endocarditis«

Microorganisms grow on theendocardium that is subjected toturbulence within the heart.

An artificial (prosthetic) heart valve

Heart valves damaged (scarred) byconditions such as rheumatic fever

Congenital heart or heart valve

defects (narrowing) Mitral valve prolapse with a murmur



Risks of Bacterial Endocarditis«.

Hypertrophic cardiomyopathy Patients who already have somekind of heart problem have a

greater risk² Children with congenital, rheumatic,or degenerative heart diseases havea 60-80% risk

Drug abusers have a much higherrisk of getting endocarditis.



S/S of BE«

Low-grade intermittent fever New heart murmur Anorexia, myalgias, HA

Enlarged spleen Petechiae oral mucosa Osler nodes: painful nodules--sign of vasculitis

Janeway spots/nodules: painlesshemorrhagic areas on palms and soles

Roth·s spots: retinal hemorrhages



A ² C are Osler Nodes and were painful

D is a Janeway Lesion and was non-tender




Treatment: Penicillin IVfor 4-6 weeks

70% streptococcal species

20% staph species 10% other: H flu, fungal,

gram negative bacteria

May need prophylaxis for

procedures but this ischanging

May need surgicalintervention



Kawasaki·s Disease«

A.K.A. ´mucocutaneous lymphnode syndromeµ

This condition was described byDr Kawasaki in Japan in the

1960s and is an inflammation ofthe arteries of the body -probably triggered by a virusinfection. The danger in the

disease is that the inflammationcan cause damage to thecoronary arteries and affect theheart muscle.

k ·




80% are under 5 years of age Peak incidence in toddlers

Boys > Girls

Without treatment, 20-25% candevelop damage to blood vesselsthat supply the heart³esp.

Coronary dilation Greatest risk in <1 yr of age

Will form aneurysms

k · D




Specific cause is unknown(possibly a virus)

Progressive inflammation of small andmedium sized vessels (vasculitis).

Walls can become damaged to the pointof developing coronary artery

aneurysms in some which can lead toblood clot formation.

Ph f K k ·



Phases of Kawasaki·s«

Acute phase: abrupt onset of highfever that doesn·t respond toantibiotics or antipyretics. Symptomsthen progress

Subacute phase: resolution of fever,high risk of developing coronary arteryaneurysms. Peeling begins

Convalescent phase: all clinical signshave resolved. Lab values altered.Resolved at the end of 6-8 weeksafter onset.

S/S f K ki· Di



S/S of Kawasaki·s Disease«

Requires 5 of 6 principle criteria Fever ranging between 38-41° C Discrete conjunctival injection

without exudate

Changes in the mouth consistingof:--Erythema of lips--Strawberry tongue--Diffuse oropharyngeal

erythema



S/S of Kawasaki·s Disease



Polymorphous erythematous rash

Changes in the hands and feet consistingof:

--Firm indurative peripheral edema--Diffuse erythema of palms and soles--Convalescent desquamation of digits,

palms, and soles Unilateral cervical lymphadenopathy

S/S of Kawasaki s Disease

T t t f K ki·



Treatment for Kawasaki·s«

Reduce fever, rash, joint inflammation,pain and to help prevent blood clots fromforming.

--Aspirin 80-100 mg/kg/day, every 6 hours(once fever resolved reduce aspirin to 3-5mg/kg/day, give daily)

Decrease the risk of developing coronaryartery abnormalities (when given early)

--IV Immune Globulin (2g/kg) give over10-12 hours (special blood product)

Treatment for Kawasaki·s



Treatment for Kawasaki s

For patients with coronary arteryaneurysms, blood clots or high risk:

Warfarin (Coumadin),

Lovenox (injection)

High dose aspirin Once the fever has resolved aspirin

dose is reduced.

Once stable child can go home. Aspirinis usually continued for weeks orindefinitely.

F/U monitoring

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Pediatric Cardiology Dysfunction for Students--2011[1]