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Cardiovascular Stressors and Adaptation

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Cardiovascular Stressors and Adaptation

Common Cardiovascular Disorders in Children

Congenital Heart Defects Congestive Heart Failure Acquired Heart Disease

Review of Normal Circulation

Fetal Shunts

ductus venosus: accessory (extra) vein, carries oxygenated blood to fetal liver from umbilical vein

foramen ovale: shunts oxygenated blood from right atrium to left atrium (hole in the atrial septum)

ductus arteriosus: accessory (extra) artery, shunts deoxygenated blood away from lungs to descending aorta to umbilical cord to placenta

Fetal Circulation of Oxygenated Blood

Oxygenated blood flows from placenta into the umbilical vein to fetal liver through ductus venosus

then inferior vena cava with the remaining unoxygenated blood from fetal legs & abdomen

Fetal Circulation of Oxygenated Blood

Inferior Vena cava empties into Right atrium

Little oxygenated blood flows into right ventricle to be pumped through the pulmonary artery to the lungs (because the lungs are not inflating)

Fetal Circulation of Oxygenated Blood

Most of the oxygenated blood in the right atrium is shunted through the foramen ovale into the left atrium

Then oxygenated blood travels from the left atrium, into the left ventricle, and pumped into the aorta to the body

Fetal circulation of Deoxygenated blood

Deoxygenated blood returns though the superior vena cava into the right atrium, right ventricle and into the pulmonary artery

Because resistance is high in the pulmonary artery, blood flows through the opening in the pulmonary artery- the ductus arteriosus, into the aorta, into the fetal arterial system and into the 2 umbilical arteries back to the placenta

How does the fetus receive sufficient oxygen from the

maternal blood supply?

Fetal hemoglobin carries 20-30% more oxygen than maternal hemoglobin

Fetal hemoglobin concentration is 50% greater than mother’s

Fetal heart rate 120-160bpm (increases cardiac output)

What happens to the shunts after birth?

Transition from intrauterine to extrauterine life

Cord is clamped, neonate initiated respirations

O2 levels rise = greater pressure in the left atrium, decreased pressure in the right atrium leading to an immediate closure of the foramen ovale

Transition from intrauterine to extrauterine life

After O2 circulates systemically, over 24 hours, the pressure in the left ventricle will become greater than the pulmonary artery and closes the ductus arterosis

The absent flow of blood through the umbilicus gradually closes the ductus venosus over 12 hr to 2 weeks

Cardiac Catheterization

Primary method to measure extent of cardiac disease in children

Shows type and severity of the CHD Insert tiny catheter through an artery in arm,

leg or neck into the heart Take blood samples and measure pressure,

measure o2 saturation, and as an intervention Sedation or anesthesia Outpatient vs Hospital

Cardiac Catheterization Pre-Op

NPO 4-6 hrs Check for known allergies, history

of recent fever, signs and symptoms of infection

Cardiac Catheterization-Post Op

Monitor closely (cardiac monitor, continuous pulse ox) VS q 15

Assess dressing at insertion site for infection, hematoma

Dressing must remain dry for 1st 48-72 hrs

No blood drawn from extremity used Palpate a pulse distal to the dressing to

assure blood flow to extremity is not obstructed: keep extremity straight for 48 hrs after procedure

Congestive Heart Failure

heart doesn’t pump blood well enough –can not provide adequate cardiac output due to impaired myocardial contractility

Causes in children:• Defects

• Acquired heart disease

• Infections

Congestive Heart Failure

Most common cause in children is congenital heart defects• Increased volume load or increased pressure

in heart Excess volume and pressure builds up in

lungs leading to labored breathing builds up in rest of body leading to edema (edema is a late sign in children)

Congestive Heart Failure Symptoms

1st sign: tachycardia tire easily rapid, labored breathing decreased urine output fluid and sodium are retained increased sweating, pallor edema

CHF Diagnosis and Treatment

CXR- shows enlargement Echocardiogram- dilated heart

vessels, hypertrophy, increase in heart size

Tx-aimed at reducing volume overload, improve contractility

May require surgery

Congestive Heart Failure Medical Management

1. Digoxin- Helps strengthen the heart muscle, enables it to pump more efficiently

1st line tx Dosing depends on wt and age Need HR, EKG, drug levels Parent teaching

2. ACE (Angiotension-converting-enzyme) inhibitors- dilates the blood vessels making it easier for the heart to pump blood forward into the body

Congestive Heart Failure Medical Management

Diuretics- Helps the kidneys remove excess fluid from the body• Potassium sparing• Potassium wasting

• Potassium supplements- given along with wasting diuretics

Lasix-1st agent for children-lose K esp. when taken with digoxin

Congenital Heart Disease

35 different types Common to have multiple defects Range from mild to life threatening and

fatal Genetic and environmental causes Caused by:

• Defect or

• Failure of shunt closure

Normal Blood FlowPressure in left is higher than

right side

Types of CHD

Acynotic defects• Septal defects

• VSD• ASD

• PDA Obstructive (Cyanotic) defects

• Pulmonic Stenosis• Coarctation of the aorta

Cyanotic defects• Transposition of the greater vessels• Tetrology of Fallot• Hypoplastic left heart

Septal Defects- increased pulmonary blood flow

Left to right shunting (acyanotic defect)• Increased cardiac

workload• Excessive pulmonary

blood flow• Right ventricular strain,

dilation, hypertrophy• CHF, pulmonary HTN,

bacterial endocarditis• Ventral Septal Defect• Atrial Septal Defect

Ventricular Septal Defect

Most common CHD High Pressure in LV

forces blood back to RV

Results in increased pulmonary blood flow (heart must pump extra blood), higher than normal artery pressure

Ventricular Septal Defect

S/S: vary with the size of the defect 4-8 weeks of age develop loud, harsh

systolic heart murmur Right ventricular hypertrophy 20-60% close spontaneously cardiac cath shows: O2 level of RV higher

than normal large defects: develop CHF, poor feeding,

failure to thrive

Ventricular Septal Defect

Treatment: Small defects: followed by cardiologist,

prophylactic ABX Large defect: open heart surgery with

cardiopulmonary bypass, will suture or patch hole closed• If child is not stable for open heart surgery:

pulmonary artery banding: narrowing of pulmonary artery to reduce blood flow to lungs

VSD Medical Management

For infants not medically stable for surgery or awaiting surgery-

Digoxin: to improve cardiac output; check apical pulse first, don’t give if HR < 100 bmp in infants and < 70 bpm in children

Digoxin toxicity: vomiting, bradycardia

Oxygen

Atrial Septal Defect

Pressure in LA is greater than RA (blood flows left to right)

Oxygen rich blood leaks back to RA to RV and is then pumped back to lungs, results in ventricular hypertrophy

Few if any symptoms, over time may experience fatigue and dyspnea on exertion

Atrial Septal Defect Clinical Presentation

Large defect may cause CHF Harsh systolic murmur Second heart sound is split: “fixed

splitting” ** diagnostic of ASD pulmonary valve closes later than

aortic valve Echocardiogram: shows enlarged

right side of heart, increased pulmonary circulation

ASD Management

Nonsurgical management: prosthetic umbrella patch

Surgical management: open-heart with CP bypass, edges are sutured or will use Silastic patch to cover hole

Diuretics to control symptoms until repair is performed

Patent Ductus Arteriosus

Failure of ductus arteriosus to close completely at birth

Blood from the aorta flows into the pulmonary arteries to be reoxygenated in the lungs, returns to LA and LV

Not enough oxygenated blood is getting out o nourish the body

More common in preemies

Patent Ductus Arteriosus

Preterm infants: present with CHF and respiratory distress

Fullterm infants: may be asymptomatic with a continuous “machinery” type murmur

Tire easily, growth retardation (shorter, weigh less, less muscle mass), prone to frequent respiratory tract infections

Patent Ductus Arteriosus

Chest radiographs (x-ray) show enlarged LA and LV

Medical management: Indomethacin (prostaglandin inhibitor that stimulates ductus to constrict)

Surgical management: ductus is divided and ligated (usually performed in first year of life to decrease risk of bacterial endocarditis

Obstructive Defects- decreased pulmonary blood

flow

Right to left shuntDefect present that obstructs LV

flow Pulmonic Stenosis Coarctation of the Aorta

Pulmonary Stenosis

Obstruction of the right ventricular outflow tract

Decreased pulmonary blood flow Right ventricular hypertrophy High ventricular pressure may cause

blood to back up into right atrium and force foramen ovale to open to allow blood to flow from right to left atrium

Pulmonary Stenosis

Usually asymptomatic Systolic ejection murmur with a palpable thrill Enlarged heart on x-ray Severe: right ventricular failure, CHF, if there is right to left

shunting through the foramen ovale, mild to moderate cyanosis

Pulmonary Stenosis

Medical Management: If asymptomatic: cardiac follow-up Prophylactic ABX

Surgical Management: Pulmonary balloon valvuloplasty via

cardiac cath if unsuccessful: valvotomy

Coarctation of Aorta

Localized constriction of the aorta at or near the insertion site of the ductus arteriosus

Reduces cardiac output (impedes blood flow from heart to body)

Aortic pressure is high proximal to the constriction and low distal to the constriction

Coarctation of Aorta

S/S: related to severity of the constriction and presence of associated cardiac defects

Mild: asymptomatic, sys. murmur, diminished pulses in lower ext

Severe: poor lower body perfusion, metabolic acidosis, CHF, systemic hypertension

In both: BP is 20mmHg higher in arms than in lower extremities

Coarctation of Aorta

Diagnosis-clinical exam, echo

Treatment is based on severity

Treatment of Coarctation of Aorta

Symptomatic newborn treated with: Digoxin diuretics to manage CHF may also receive PGE1

(prostaglandin) infusions to maintain ductal patency and improves perfusion to lower extremities

surgical repair within first 2 years

Cynaotic Defects

Decreased pulmonary blood flow• Transposition of the greater vessels• Tetrology of Fallot• Hypoplastic left heart

Tetralogy of Fallot Consists of 4 Parts:

VSD RV hypertrophy Overriding aorta Pulmonic Stenosis:

impedes blood flow to the lungs, forces unoxygenated blood through the VSD & into aorta

S/STetralogy of Fallot

The degree of pulmonic stenosis governs the onset and severity of symptoms.

Mild: little to no right to left shunting infant has “tet spells” hypercyanotic episodes

Mod-severe: some cyanotic at birth when PDA closes, other infants become increasingly cyanotic over the first few months of life

Tetralogy of Fallot

Tire easily especially with exertion, difficulty feeding and gaining weight,

Other signs: chronic hypoxemia

Management Tetralogy of Fallot

Over time may have hypercyanotic episodes (tet spells)

often preceded by crying, feeding or stooling, worsening cyanosis, increased respiratory rate, may lose consciousness

Treatment of tet spells: calm infant, knee-chest position, O2 Do not leave alone- cyanosis can cause LOC, death

Tetralogy of Fallot

Medical management: Symptomatic newborn: PGE1 infusion to

maintain ductal patency Older infants: close monitoring for

worsening of hypoxia Surgical management: done at 3-12 months

of age, in stages primary open-heart repair: close VSD, open

pulmonary valve, remove obstructing muscle

Hypoplastic Left Heart Syndrome

pulmonary venous blood is shunted through foramen ovale into right atrium

mixed blood travels through the right ventricle to the pulmonary artery, patent ductus arteriosus

as ductus begins to close in first few days of life infant becomes symptomatic

Hypoplastic Left Heart Syndrome

symptoms: CHF hypoperfusion,

shock grayish-blue

color dyspnea hypotension

DiagnosisClinical presentation and echo (increased size in right side)

Hypoplastic Left Heart Syndrome

Medical Management: PGE1 to keep ductus arteriosus open Correct acid-base and electrolyte

imbalances

Surgical management: Heart transplant Three-stage repair

Transposition of Great Arteries

Aorta is connected to RV (unoxygenated blood goes to body)

Pulmonary artery is attached to LV (oxygen rich blood is recirculated to lungs)

Survival depends on mixing these two circulations through the fetal structures (foramen ovale and ductus arteriosus)

Transposition of Great Arteries

Cyanosis apparent at birth or shortly after, no response to oxygen

Prompt diagnosis and treatment needed for survival

Arterial switch procedure: redirects blood flow, may be done in stages within 1st year

Caring for the Child with a Congenital Heart Defect

Nursing Care: taking infant home before corrective surgery

Provide parents with information about care

Review steps for follow-up care, emergency management (s/s respiratory distress, CPR)

Key: promote normalcy within the limits of the child’s condition

Caring for the Child with a Congenital Heart Defect

Preoperative:undergoing corrective surgery

Explain procedures to parents and child, assure understanding

Encourage child and parents to express fears

Prepare child for surgery and post-op, show models of equipment (chest tube)

Caring for the Child with a Congenital Heart Defect

Postoperative: Monitor cardiac output Support respiratory function Maintain fluid and electrolyte balance Promote comfort (IV morphine,

sedatives) Promote healing and recovery

Acquired Heart Diseae

HTN Endocarditis Rheumatic Fever Kawasaki Disease

Hypertension

Primary HTN• Caused by increased body mass• Genetics

Secondary HTN• Cause is from an underlying condition

such as kidney disease or heart defects

Hypertension

No set systolic and diastolic number for diagnosis

Need to compare to child’s age, gender and height

If 3 different readings are above the 95th percentile for that child then diagnosis is confirmed

Hypertension

Managed by eliminating the primary cause if possible• Exercise, life style modification

ACE inhibitors ARBs Beta-Blockers Ca Channel Blockers

Infective Endocarditis

Inflammation of the lining of the valves and arteries

Caused by bacterial and fungal infections in the blood stream that infects an already existing injured endocardium

Children at risk: cardiac defects, severe valve disorders

Infective Endocarditis

Symptoms:• Fever, fatigue, headache, N/V, new or

changed murmur, CHF, dyspnea Treatment:

• Antibiotics IV for 2-8 weeks, surgery to replace valves, treatment of CHF

Rheumatic Fever

Acute RF is leading cause of acquired heart disease (but has decreased in US b/c abx)

Inflammatory autoimmune condition Seen in children age 5-15 Usually follows untreated strep A

infection (pharyngitis) Causes scarring of the mitral valves

Rheumatic Fever

S/S: Polyarthritis Carditis Chorea Erythema marginatum Subcutaneous nodules

Rheumatic Fever

Diagnosis- clinical symptoms and +ASO titer

Rheumatic Fever

Management: Treat infection Treat other symptoms Streptococcal prophylaxis

• PCN IM every monthor

• PCN PO BID (if allergic Sulfadiazine PO QD)

Kawasaki Disease

Acquired heart disease in children under age 5

Boys>girls Asian decent Multisystem vasculitis (inflammation of

blood vessels) 3 stages of illness Affects the coronary arteries Occurs due to antibody vascular injury

post infection

Kawasaki Disease first stage day 1-14

Prolonged fever Bilateral, nonpurulent conjunctivitis Changes in mouth (erythema, fissures,

crusting of lips, strawberry tongue) Induration of hands and feet Erythema of palms and soles Erythemous rash Enlarged cervical lymph nodes

Kawasaki Diseasesecond stage day 15-25

Fever and most of the previous symptoms resolve

Extreme irritability develops Anorexia Lip cracking and fissuring Desquamation of fingers and toes Arthritis Vascular changes in myocardium and

coronary arteries

Kawasaki DiseaseThird phase- day 26-40

Lasts until erythrocyte sed rate returns to normal and all symptoms disappear

Beau’s lines may appear

Management

Prevent or reduce coronary artery damage

Gamma-globulin IV in a dosage of 2gm/kg over a 12h infusion

High dose aspirin therapy at same time (80-100mg/kg/day once daily), continued through weeks 6-8 of disease

Kawasaki Disease

Nursing care: Administer meds Comfort measures Hydration Parental support

A parent of a toddler with Kawaski’s disease tells the nurse “I just don’t know what to do with my child. He’s never acted like this before.” The nurses best reply is:

1. Don’t worry. This type of behavior is typical for a toddler

2. Irritability is part of Kawasaki’s disease. Please don’t be embarrassed

3. Perhaps your child would benefit from stricter limits4. You seem to be in need of a referral to our Child

Guidance Center

When assessing a child for signs and symptoms of rheumatic fever, which symptoms should the nurse anticipate?

1. Tachycardia and joint pain2. Bradycardia and swollen joints3. Loss of coordination and pruritic rash4. Bradycardia and fever

Which nursing intervention is most effective in preventing rheumatic fever in children?

1. Refer children with sore throats for a throat culture

2. Include an ECG in the child’s yearly physical examination

3. Assess the child for a change in the quality of the pulse

4. Assess the child’s blood pressure

Which is most beneficial in achieving the goal of preventing infection in a child with cardiac disease?

1. Give the child extra immunizations2. Keep the child on daily prophylactic

antibiotics3. Keep the child away from others who are ill4. Place the child in protective isolation

A newborn with patent ductus arteriousus is scheduled to receive indomethacin. The nurse administers this medication to:

1. Open the ductus arteriosus2. Close the ductus arteriosus3. Enlarge the ductus arteriosus4. Maintain the size of the ductus

arteriosus

Which congenital heart defect necessitates that the nurse take upper and lower extremity blood pressure readings?

1. Coarctation of the aorta2. Tetralogy of Fallot3. Ventricular septal defect4. Patent ductus arteriosus

An infant with ventricular septal defect develops congestive heart failure and is placed on digoxin therapy twice a day. The infant vomits the morning dose of digoxin. The most appropriate nursing intervention is to:

1. Notify the pediatrician as soon as possible2. Take the infant’s pulse for 1 minute and repeat the

dose of digoxin3. Skip the dose and give twice the amount at the next

dose4. Repeat the dose and chart that the infant vomited the

first dose

The parents of a newborn with ventricular septal defect ask why their baby is being sent home instead of undergoing immediate open heart surgery. The nurse’s best response is:

1. Your baby’s condition is too serious for immediate open heart surgery

2. Ventricular septal defects are not repaired until the infant is older

3. Your baby has a small defect, and we hope that is closes spontaneously

4. Your baby must be fully immunized before surgery

When reviewing the chart of an infant with tetralogy of Fallot, the nurse should anticipate which laboratory findings?

1. Anemia2. Polycythemia3. Increased white blood cell count4. Decreased hematocrit

An infant with tetralogy of Fallot becomes hypoxic following a prolonged bout of crying. The nurse’s first action should be to:

1. Administer oxygen2. Administer morphine3. Place the infant in the knee-chest

position4. Comfort the infant