cardiac power point

Alterations in Cardiovascular Function

Ball & Bindler

Donna Hills APN EdD

Blood Flow

Transition from fetal to pulmonary circulation

• the umbilical cord is cut

• systemic vascular resistance is increased

• pressure in the L side of the heart increases

• foramen ovale closes

• breathing is initiated

• pulmonary vascular resistance falls

• blood that was shunted through the PDA now goes to the lungs.

FIGURE 26–1 Fetal circulation. Blood leaves the placenta and enters the fetus through the umbilical vein. The ductus venosus, the foramen ovale, and the ductus arteriosus allow the blood to bypass the fetal liver and lungs. After circulating through the fetus, the blood returns to the placenta through the umbilical arteries. From Ladewig, P. W., London, M. L., Moberly, S., & Olds, S. B. (2002). Contemporary Maternal-Child Nursing Care (8th ed,. p. 51 ). Upper Saddle River, NJ: Prentice Hall.

Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families

© 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458

All rights reserved.

FIGURE 26–2 A, Fetal (prenatal) circulation. B, Pulmonary (postnatal) circulation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.




Ductus Arteriosus

• an opening in fetal circ. between the pulmonary artery (PA) and aorta (Ao).

• in fetal circulation, most of the blood bypasses the lungs and returns to systemic circulation by way of the PDA (PA to Ao).

• In transition to pulmonary circulation, the PDA constricts over 10-15hrs; permanent closure should occur by 3wks of age, UNLESS SATURATION REMAINS LOW

FIGURE 26–3 Normal pressure gradients and oxygen saturation levels in the heart chambers and great vessels. The ventricle on the right side of the heart has a lower pressure during systole than the left ventricle because less pressure is needed to pump blood to the lungs than to the rest of the body.




Hypoxemia in the infant

• below 95% pulse oximetry.

• cyanosis results from hypoxemia

• perioral cyanosis indicates central hypoxemia

• acrocyanosis does not.

Response to Hypoxemia

• acute: HR increases

• chronic: bone marrow produces more RBC to increase the amount of Hgb available for oxygen transport.

• Hct>50 is called polycythemia.

• increased blood viscosity increases risk of thromboembolism.

Cardiac Functioning

• 02 requirements are high the first few weeks of life

• normally, HR increases to provide adequate oxygen transport

• infant has little cardiac output reserve capacity

• cardiac output depends almost completely on HR until the heart is fully developed (age 5 yr).

Compliance in the infant

• in infancy, muscle fibers are less developed and organized

• results in less functional capacity or less compliance

• less compliance means the infant is unable or less able to distend or expand the ventricles to achieve an increase stroke volume in order to compensate for increased demands.

Severe Hypoxemia

• children respond with bradycardia

• cardiac arrest generally results from prolonged hypoxemia related to respiratory failure or shock

• in adults, hypoxemia usually results from direct insult to the heart.

• therefore, in children, bradycardia is a significant warning sign of cardiac arrest.

• approp Rx for hypoxemia reverses brady.

Case Study

• Dylan is a 3 mo old with Down Syndrome and VSD, admitted for CHF. His birth weight was 7 lb 9 oz; a week ago he weighed 12 lb at the pediatrician’s office and now weighs 12.10 lb. He is breathing 72 bpm with a HR of 190 and a sat of 91%. He is diaphoretic and is not taking his usual 3 oz formula every 3-4 hours. He has had 4 moderately wet diapers in the past 24 hrs.

Study questions for case study

• Identify abnormal assessment data for Dylan

• What other data would you collect? (Hx and assessment)

• What is your priority nursing action?

• What other nursing interventions would you do for him? For his mother?

Down Syndrome

• A trisomy genetic abnormality; ;usually on chromo 21.

• Classic characteristics: – Some degree of mental retardation with variable

functional deficit– Microcephaly, flattened forehead, wide short neck.

Epicanthal eye folds, simian palmar crease, protruding tongue, low set ears, short broad hands, hearing loss, hypotonia.

– Increased incidence of DM, CHD and Leukemia

What aspects of Down Syndrome have an affect on his ability to

maintain optimal health?• Protruding tongue

• Hypotonia

• Slower to reach milestones, compounded by hypotonia

Pulmonary Artery Hypertension

• irreversible condition that results from R sided heart circulation being overloaded and therefore shunting excessive blood to the lungs.

• overloads the R side of the heart, overloads the pulmonary system causing increased pulmonary vascular resistance (life threatening).

Obstructive Congenital Defects

• due to abnormally small pulmonary vessels• which restrict flow of blood, so the heart

hypertrophies to work harder to provide the blood flow to organs.

• however, CO increases initially but eventually hypertrophied muscle becomes ineffective.

• initially R sided failure, progressing to L sided and eventual bilateral failure

Congestive Heart Failure

• cardiac output is inadequate to meet the body’s needs

• may result from:– congenital heart defect that causes increased

pulmonary blood flow or obstruction of blood outflow tract

– problems with heart contractility– pathology that requires a high cardiac output

(severe anemia, acidosis, respiratory disease).

CHF in the infant

• can be subtle

• good assessment skills are a must

• tires easily, especially during feeding

• (initial) weight loss

• diaphoresis, irritability, frequent infection.

FIGURE 26–4 Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart failure.




CHF in older children

• exercise intolerance

• dyspnea

• abdominal pain or distention

• peripheral edema.

Symptoms of progressive disease

• tachycardia, tachypnea, pallor or cyanosis, F/G/R, cough, crackles.

• fluid volume overload: periorbital and facial edema, JVD, hepatomegaly, ascites.

• not mentioned in the book: increased weight gain, bounding pulses, edema of dependent body parts.

FIGURE 26–4 Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart failure.




FIGURE 26–5 Infants with cardiac conditions often require supplemental feedings to provide sufficient calories for growth and development. The parents of this infant girl have been taught how to give her nasogastric feedings at home.




Cardiomegaly

• occurs at the heart attempts to maintain CO

• if CHF is not adequately treated, precursors of Cardiogenic Shock arise: cyanosis, weak peripheral pulses, cool extremities, hypotension, heart murmurs

• clarification: not all heart murmurs are heralding cardiogenic shock.

Clinical diagnosis

• based upon clinical assessment: tachycardia, respiratory distress, crackles.

• cxray could show cardiac enlargement, venous congestion, PE, atelectasis.

• cardiac echo: defects or dysfunction

• EKG: tachycardia, bradycardia, ventricular hypertrophy

Goals of Management

• make the heart work efficiently

• remove excess fluid

• improve systemic circulation without overloading the pulmonary circulation

Medication therapy

• positive inotropic effect and afterload -reducing agents– Digitalis

• Digoxin

– ACE inhibitors (Angiotensin-converting enzyme inhibitors)

• Lisinopril

– Beta Blockers • Indural (Propranolol)

– Diuretics: Lasix, HCThiazide, aldactone.

Supportive treatment

• oxygen

• fluids, as indicated( in CHF, fluids may be restricted).

• increased calories or concentrated formula(prescribed)

• air way support/management

• rest and spacing of activity/rest periods

Surgical treatment

• cardiac catheterization, which may include procedural treatment in the cath lab

• valve replacement

• conduit placement

• cardiac transplant

FIGURE 26–6 Interventional catheterization, balloon valvuloplasty to open the pulmonary valve.




Developmental Assessment

• the child may be unable to reach developmental milestones until CHF is adequately controlled

• Taylor activity to child’s ability.• Energy must be adequate for motor milestones

to improve.• Dev. Assessment: DDST II: followed Q 2-

3mos in infancy/toddler.• limit contact with other children: risk of inf.

Congenital Heart Disease(CHD)

• refers to a defect in the heart, great vessels or persistence of a fetal structure

• occurs in 1% live births

• higher incidence in still births and aborted fetuses

• incidence has declined over past 25 yrs d/t techno advances in intrauterine assessment, surgical techniques and intensive care

Factors that increase risk for having a child with CHD

• family hx of CHD

• maternal age >35yr

• coexisting maternal disease: DM, collagen vascular disease, PKU

• exposure to teratogens or rubella infection

CHD

• most CHD develop during first 8 wks of gestation

• usually result of combined genetic and environmental interaction – fetal exposure to drugs:phenytoin & lithium– maternal viral infections:rubella– maternal metabolic disorders: DM, PKU– maternal complic of preg ie incr age, antepartal

bleeding

CHD etiologies cont.

– genetic factors: familial patterns– chromosomal abnormalities: most common is

Down’s syndrome with 40% occurrence rate of CHD.

• defects are divided into cyanotic and acyanotic (in pure form).

Acyanotic Heart Defects

• constitutes the majority of heart defects in children

• two types: obstructive and non-obstructive

• obstructive: PS, AoS, Coarc.

• non-obstructive:PDA, ASD, AV canal (endocardial cushing defect), VSD.

Cyanotic Heart Defects

• generally caused by a valvular or vascular formation

• ex: Tetralogy of Fallot, Transposition, hypoplastic LV, tricuspid atresia, pulmonary atresia, truncus arteriosus, and total anomalous venous return.

Acyanotic; non-obstructive lesions

• PDA

• ASD

• AV canal

• VSD

Pathophysiology of Acyanotic, non-obstructive CHD

• openings in the septal wall cause a L to R shunt

• oxygenated blood mixes with deoxygenated blood

• volume overload to the pulmonary system• can cause CHF• PHT occurs d/t chronic volume overload to

the lungs if uncorrected.

Patent Ductus Arteriosus

• common; 9-12% of all CHD • persistant fetal structure• when the PDA remains open, blood is shunted

from the Aorta to the Pulmonary artery, therefore increasing blood flow to the lungs: L to R.

• bounding pulses, dyspnea, tachypnea, FTT.• at risk for freq URI and endocarditis, CHF.• continuous systolic murmur and thrill palp.

Treatment of a PDA

• surgical ligation; transcatheter closure >18mos of age.

• Indomethacin may stimulate closure in premies

• Prostaglandin helps to keep the PDA open until surgical correction is optimal.

• left untreated, LVH, pulmonary hypertension (PHT) and vascular obstructive disease develop.

Atrial Septal Defect; ASD

• opening in the atrial shunting

• L to R shunting

• accounts for 6-10% of CHD

• small to moderate size may go undiagnosed until preschool years or later

• sx of large ASD: CHF, tiring easily, poor growth

• soft systolic murmur heard in pulmonic space; wide S2 split.

Treatment of ASD

• Echo shows RV overload and shunt size

• cxray and EKG may be normal unless a large shunt

• surgery to close or a patch via catheter during Cardiac Cath.

• atrial arrhythmias can be a late sx or associated with a large ASD involving conduction system in the septum

FIGURE 26–7 A, Septal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect (VSD). B, Coil used to close a patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when a thrombus forms in the mass of fabric and wire.




FIGURE 26–8 A child with atrial septal defect repair. Surgery is performed with this type of defect to prevent pulmonary vascular obstructive disease as an adult.




Atrioventricular Canal: Endocardial Cushing Defect


• partial or complete ASD/VSD with some degree of involvement of mitral/tricuspid valves variable

• associated with Down’s syndrome

• severity of sx depends on degree of mitral regurgitation.

• sx in infants: CHF, tachypnea, tachycardia, FTT, incr URI, systolic murmur (LLSB)

Treatment of AV Canal

• surgery during infancy to prevent PHT

• patches placed over septal defects; mitral valve replacement

• arrhythmias and mitral valve insufficiency occur post/op

• no difference between short term survival rates in infants with or without Down’s syndrome.

Ventricular Septal Defect; VSD

• opening in the ventricular septum

• shunts L to R; increases pulmonary bld flow

• most common: accounts for 20% CHD

• only 15% large enough to generate symptoms: tachypnea, dyspnea,, FTT, reduced fluid intake, CHF, PHT.

• systolic murmur ; LLSB

• most small VSD close spontaneously

Treatment of VSD

• if no sx CHF or PHT, treatment is conservative

• surgical patching during infancy if FTT

• closure by transcatheter device during CC for some defects: Rashkind procedure.

• prophylaxis for infective endocarditis is required

• high risk for surgical repair in first few months of life

Acyanotic; obstructive lesions

• PS

• AoS

• Coarctation of the Aorta

Pathophysiology of Acyanotic, obstructive CHD

• narrowing across the valves causes pressure overload and hypertrophy of the closest ventricle

• child will have a murmur• some experience fatigue and exercise intol d/t

inability to increase CO• many are asympto and grow normally• older children: exercise induced dizziness and

syncope: requires immediate attention

Pulmonary Stenosis: PS

• narrowing of the pulmonary valve or valvular area

• obstructs flow to the PA

• increases pre-load; results in RVH

• second most common CHD


• systolic murmur with fixed split S2 in Pulmonic area.

Treatment of PS

• dx usually made at birth with murmur ascultated

• cxray may show heart enlargement

• EKG may demonstrate RVH

• echo provides info re pressure gradient across the valve

• may dilate during CC using balloon valvuloplasty or valvular replacement

• lifelong endocarditis prophylaxis is required

Aortic Stenosis: AoS

• narrowing of the aortic valve; obstructs blood flow to systemic circulation

• accounts for 3-6% of CHD; progressive during childhood

• often associated with bicuspid rather than normal tricuspid aortic valve.

• asymptomatic, grow normally; BP wnl but may have a narrow pulse pressure

• systolic m; thrill in Ao; c.p. after exer.

Treatment of AoS

• cxray and EKG are usually normal if mild• echo can reveal number of valve leaflets, pressure

gradient across the valve, and size of the aorta.• surgical valvuloplasty or dilated with balloon

during card. cath.• valvular replacement • requires lifelong SBE prophylaxis• c/p, syncope or sudden death poss. s/p ex.

Coarctation of the Aorta

• narrowing or obstruction of descending Ao.• obstructs systemic blood flow• accounts for 5-8% CHD• grow normally but constriction is progressive• lower BP in LE and higher in UE, neck, head.• pulse weak or absent in LE; full/bounding in UE

Treatment of Coarc

• EKG shows LVH

• cxray reveals enlargement and pulm venous congestion and constricted aorta

• balloon dilation in card cath or surgical resection/anastomosis/patch.

• risks of reoccurrance, persistent HTN in adulthood, 20% develop post-coarctectomy syndrome (abdominal pain and distention).

• SBE prophylaxis needed.

Cyanotic Heart Defects

• Tetralogy of Fallot

• Transposition of the Great Vessels

• caused by malformation or a combination of defects that prevent adequate level of oxygenation

• R to L shunt occurs resulting in chronic hypoxemia and cyanosis.

Pathophysiology of Cyanotic Heart Disease

• P02 is lower than normal; PC02 rises• hypoxemia becomes progressively worse as

respiratory center overreacts and incr respiratory effort

• incr resp effort attempts to incr CO; contributes to a downward spiral without intervention

• at risk for thromboembolism d/t hypoxemia causing polycythemia

Clinical Manifestations of Cyanotic Heart Disease

• chronic hypoxemia causes fatigue, clubbing, exertional dyspnea, delayed milestones, tire easily with feeding, reduced growth, CHF

• hypercyanotic (hypoxic) spells: incr rate and depth of respir, incr cyanosis, incr HR, pallor and poor perfusion, agitation and irritability.

FIGURE 26–13 Clubbing of the fingers is one manifestation of a cyanotic defect in an older child. What neurologic signs may be associated with such a defect?




Cyanotic Spell

• most signif prob to develop in infants and toddlers with cyanotic heart disease

• brought on by crying, feeding, exercise, warm bath, or straining to defecate

• during a hypoxic spell, child will often squat knee to chest to decrease venous return (by incr systemic vascular resistance) from LE which decr CO and relieves the cyanotic spell.

Tetralogy of Fallot

• combination of four defects– pulmonary stenosis: degree determines severity

– VSD

– over-riding of the aorta

– RVH

• accounts for 10% of CHD

• elevated R sided pressures: R to L shunt

• xray: boot shaped heart d/t RVH

• risk for metabolic acidosis and syncope.

Treatment of TOF

• total repair is done by 6 mo if cyanotic spells

• surgery is not necessarily currative, but most have improved quality of life and improved longevity

• residual problems: arrhythmias and RV dysfunction

• lifelong SBE required

Transposition of the Great Arteries: TGA

• position of the PA and Ao are switched

• life threatening at birth;cyanosis, hypoxia, acidosis

• cyanosis does not improve with 02 admin

• survival depends upon a patent DA and foramen ovale

• accounts for 5% of CHD

• may be assoc with an ASD or VSD

Treatment of TGA

• xray show egg on a string

• prostaglandin E1 used to keep PDA open until palliative procedure

• corrective surgery (artery switch) usually performed by 1 wk of age

• balloon atrial septostomy during card cath may be used to open foramen ovale

• survival depends upon surgery; risk for arrhy, SBE, RV failure, sudden death LT.

FIGURE 26–9 This infant has a congenital heart defect with decreased blood flow. What is the prognosis for an infant who has either of the most common malformations—tetralogy of Fallot or transposition of the great vessels?




FIGURE 26–10 A child with a cyanotic heart defect squats (assumes a knee–chest position) to relieve cyanotic spells.




FIGURE 26–12 Place the infant who has a hypercyanotic spell in the knee–chest position. This position increases systemic vascular resistance in the lower extremities.




Murmurs in children

• are not necessarily indicative of pathology but require a careful assessment and possibly a cardiac workup

• innocent murmurs are more prevalent than pathologic murmurs

• caused by increased turbulence of blood flow • heard especially well in a child with a thin

chest wall

Patent Ductus Arteriosus Murmur

Pearls

• some VSD’s close spontaneously with time• weight gain or growth of the child may increase

the probability of success of cardiac surgery• defects that cause PHT are corrected in infancy

to prevent irreversible pulmonary vascular disease.

• major complication of acyanotic heart defects: PHT

Cardiac Catheterization

• used to be used for diagnosis, now more commonly used for treatment

• potential complications: perf of PA, allergic reaction to contrast media, arrhythmias, hypotension, stroke, vascular compromise in the leg, and bleeding

• post cath: activity is limited and pressure dressing is applied

• risks: thrombosis, hemorrhage, dehydration

Nursing care of the child undergoing heart surgery

• parents may need genetic counseling; fetal echo can id structural heart defects as early as 18-20 weeks; some intrauterine procedures available.

• ICU care post-op with intubation and sedation

• will have an arterial line; may have chest tubes

Heart Transplantation

• improved statistical survival to 5 yrs (65%) d/t improved immunosuppressive protocols and surgical techniques

• infection and rejection are the major causes of M&M

• immunosuppressive drugs: cyclosporine A, azathioprine, and corticosteroids– drugs can cause physical side effects– prevents immunization with live viruses

Pulmonary Artery Hypertension: PHT

• incr load to the lungs causes pulmonary vascular changes in an attempt to decrease the blood flow

• inflammation, hypertrophy of the pulm vessels and fibrosis develop

• pulmonary venous hypertension develops and leads to R to L shunting, with R sided heart function impaired.

• life threatening: irreversible

Acquired Heart Diseases

• Rheumatic Fever

• Infective Endocarditis

• Cardiac Arrhythmias

• Kawasaki Disease

• Hyperlipidemia

• Hypertension

Rheumatic Fever

• inflammatory connective tissue disorder that follows initial infection by group A beta-hemolytic streptococci

• may lead to permanent mitral or aortic valve damage

• sx: migratory polyarthritis, subcutaneous nodules, erythema marginatum, fevers, St. Vitus dance (chorea movements)

• dx: Jones criteria and an elevated ASO

Treatment for Rheumatic Fever

• antibiotics to treat the strept infection: pcn, erythromycin

• asa for joint pain and fever• monitored by cardiac echo (serial)• steroids for severe carditis with CHF• SBE prophylaxis• long term antibiotics until adulthood

– daily oral or 1x/mo IM (Pen G)

Infective Endocarditis

• inflammation of the lining, valves, and arterial vessels of the heart

• caused by bacterial, enterococci and fungal infections

• significant M&M for children with CHD, prosthetic valves and shunts, and in immunocompromised children with long term central venous catheters.

SBE Prophylaxis

• Prophylaxis for infective bacterial endocarditis

• aka SBE prophylaxis ;systemic bacterial endocarditis prophylaxis

• see Table 14-4 p 489 in B&B

• commonly given before dental procedures to prevent oral bacteria from entering the blood stream and seeding in the area of defect, causing a bacterial endocarditis

• one large dose given 1 hr before a procedure requiring prophylaxis

Cardiac Arrhythmias

• not uncommon in children

• sinus tachycardias;sinus bradycardias, SVT.– May occur with an acute condition and then

resolve

• sinus arrhythmia:variation of normal– increased HR with inspir/decr with expir.

Supraventricular Tachycardia: SVT

• pathologic tachycardia

• abrupt onset of a rapid heart rate >200

• recurrent or prolonged SVT can cause symptoms, CHF or shock

• rx with vagal stimulation (ice to the face), or valsalva maneuver (hold breath or straining)

• meds used: Adenosine or Amiodarone

• cardioversion or ablation if needed

Long QT Syndrome

• inherited genetic disorder that puts the child at risk for ventricular fibrillation and sudden death

• may also result from electrolyte imbalance, malnutrition (anorexia and bulimia), myocarditis and CNS trauma

• speculation that it may be associated with SIDS (unproven)

• no warning; results in death

Kawasaki Syndrome

• acute systemic inflammatory disease• aka mucocutaneous lymph node syndrome• most common cause of acquired heart disease• etiology unknown• 3 stages:

– acute, subacute and convalescent

• dx based upon clinical signs

Diagnostic Criteria for Kawasaki Syndrome

• fever > 102.2 x 5 days plus 4 of the following:• bilateral conjunctivitis• strawberry tongue; cracks/fissures of lips• palmar/plantar erythema, induration,then

desquamation• maculopapular rash on trunk• acute cervical lymphadenitis

FIGURE 26–14 This child shows many of the signs of the acute stage of Kawasaki syndrome.




Treatment of Kawasaki Syndrome

• high dose ASA and IgG given early significantly decreases the risk of cardiac involvement

• greatest risks are coronary artery lesions and cardiac aneurysms

• monitor for cardiac involvement for months: aneurysms, early atherosclerosis, arrhythmias, CHF, coronary stenosis, MI and potential death.

FIGURE 26–15 This child has returned for one of her frequent follow-up visits to assess her cardiac status after treatment for Kawasaki syndrome. Notice the lips that show the inflammation and cracking.




Dyslipidemia

• fam hx incr risk of CAD d/t high levels of LDL and cholesterol

• total lipid panel, nutritional history and life style needs to be considered.

• children need fats to grow, metabolize vitamins and produce hormones

• high fat/sat fat diet is not recommended.

• long term studies of effect of childhood lipid levels on life span inconclusive

Hypertension

• 1-3% of the pedi population• unknown cause = essential or primary HTN• underlying kidney or cardiac

disease=secondary HTN• children’s BP in >90th at incr risk for adult

HTN• HTN in adol correlates with obesity and

elevated serum lipid level

cardiac power point

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