Alterations in Cardiovascular Function - Salem State University

Alterations in Cardiovascular Function - Salem State University

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 261 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. Bindler Child Health Nursing: Partnering with Children & Families

2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. FIGURE 262 A, Fetal (prenatal) circulation. B, Pulmonary (postnatal) circulation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families

2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. 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 263 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. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families

2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. 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 pediatricians 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 bodys 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 264 failure. Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458

All rights reserved. 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 264 failure. Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

FIGURE 265 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. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

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 266 Interventional catheterization, balloon valvuloplasty to open the pulmonary valve. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

Developmental Assessment the child may be unable to reach developmental milestones until CHF is adequately controlled Taylor activity to childs 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 Downs 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 267 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. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458

All rights reserved. FIGURE 268 A child with atrial septal defect repair. Surgery is performed with this type of defect to prevent pulmonary vascular obstructive disease as an adult. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

Atrioventricular Canal: Endocardial Cushing Defect accounts for 4-5% of CHD partial or complete ASD/VSD with some degree of involvement of mitral/tricuspid valves variable associated with Downs 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 Downs 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 accounts for 8-12% of 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 2613

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? Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. 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 269 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 malformationstetralogy of Fallot or transposition of the great vessels? Jane W. Ball and Ruth C. Bindler

Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. FIGURE 2610 A child with a cyanotic heart defect squats (assumes a kneechest position) to relieve cyanotic spells. Jane W. Ball and Ruth C. Bindler

Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. FIGURE 2612 Place the infant who has a hypercyanotic spell in the kneechest position. This position increases systemic vascular resistance in the lower extremities. Jane W. Ball and Ruth C. Bindler

Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved. 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 VSDs 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 2614 This child shows many of the signs of the acute stage of Kawasaki syndrome. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc.

Upper Saddle River, New Jersey 07458 All rights reserved. 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 2615 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. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458

All rights reserved. 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 childrens BP in >90th at incr risk for adult HTN HTN in adol correlates with obesity and elevated serum lipid level

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