CARDIOVASCULAR DYSFUNCTION

By: Prof. Ryan D. Reyes Therapeutic Management

 Prostaglandin E (patency of ductus arteriosus)
 Proper Hydration
CONGENITAL HEART DISEASE  Serial Phlebotomy (for older children and adolescent)
- Exact cause unknown
 Aggressive pulmonary hygiene, chest physiotherapy, administration of
- Can be a result of multiple factors
antibiotics and use of oxygen
- 5 to 8 in 1000 live births
- One of the major cause of death in the first year of life Guidelines for Treating Hypercyanotic Spells
 Place infant in knee-chest position
2 PRINCIPAL CLINICAL CONSEQUENCES OF CHD:
 Employ calm, comforting approach
I – Congestive Heart Failure
II - Hypoxemia  Administer 100% oxygen by face mask
 Give Morphine subcutaneously or through IV
CHF  Begin IV fluid replacement and volume expansion
it is the inability of the heart to pump an adequate amount of blood to the systemic  Repeat morphine administration
circulation; cause by defects that result in left-to-right shunting of blood
Palliative Surgery
HYPOXEMIA Modified Blalock-Taussig Operation
refers to an arterial oxygen tension that is lower than normal and can be measured - a Gore-Tex or Impra tube graft is placed to create a communication between the
by O2sat and PaO2 ; cause by defects that result in decrease in pulmonary blood right or left subclavian artery and the pulmonary artery on the same side.
flow
Nursing Management
CAUSES  Fluid status monitoring and management
 Severe obstruction to pulmonary blood flow and blood shunting from the right  Fever, vomiting and diarrhea needs prompt treatment
side to the left side ( e.g Tetralogy of Fallot)  Preventive measures and accurate assessment of respiratory infection
 Mixing of arterial and venous blood within the chambers of the heart itself  Educate child and family about characteristic of hypoxemia and how to deal
 Transposition of Great Arteries with it like dealing with comments of other people and they need simple
explanation of hypoxemia and cyanosis and re-assurance that cyanosis does
2 Physiologic Changes in Response to Chronic Hypoxemia not imply lack of oxygen to the brain.
 Polycythemia  Educate child and family about care like managing “tet spell”.
 Clubbing of nails
CLASSIFICATION OF CONGENITAL HEART DISEASE
Signs and Symptoms ACYANOTIC CYANOTIC
 May be asymptomatic (mild hypoxemia) except for cyanosis ↑ Pulmonary blood flow Decreased Pulmonary Blood Flow
 Problems with growth and development Obstruction to Blood Flow from the Ventricles Mixed Blood Flow
 Flaccidity (sign of severe cardiovascular compromise)
ACYANOTIC
 Poor exercise tolerance
↑ Pulmonary blood flow
 Infant pale and dusky with increase cyanosis, cold to the touch with
 Atrial Septal Defect
diminished pulses, and lethargic with signs of respiratory distress (severe
form)  Ventricular Septal Defect
 Metabolic acidosis leading to hyperventilation ( 2º to tissue hypoxia)  Patent Ductus Arteriosus
 Hypercyanotic spell or blue spells or tet spells (Tetralogy of Fallot)  Atrioventricular Canal
 Neurologic Complications (2º to polycythemia, poor ventricular function and
Obstruction to Blood Flow from the Ventricles
atrial arrhythmias)
 Coarctation of the Aorta
 Bacterial endocarditis
  Aortic Stenosis • Surgical Treatment
 Pulmonic stenosis • Pulmonary artery Banding is occasionally done with infants severe symptoms
• Patch closure of the septal defect and reconstruction of the AV valve
Atrial Septal Defect
• Abnormal opening between the atria, allowing blood from the higher pressure left PATENT DUCTUS ARTERIOSUS
atrium to flow into the lower pressure right atrium • A failure of the fetal ductus arteriosus to close within the first week of life
• 3 types of ASD • The continued patency of this vessel allows blood to flow from the higher-pressure
• Ostium Primum aorta to the lower-pressure pulmonary artery which causes left –to right shunt
• Ostium Secundum • Medical Management
• Sinus Venosus defect • Administer Indomethacin (prostaglandin inhibitor)
• Surgical Management
• Patient may be asymptomatic • Surgical division or ligation of the patent vessel via left thoracotomy or
• May develop CHF thorascopic surgery
• Presence of murmurs • Coils to occlude the PDA via catheterization
• Risk for atrial dysrhythmias and pulmonary vascular obstructive disease and
emboli formation later in life COARCTATION OF THE AORTA
• Localized narrowing near the insertion of the ductus arteriosus, which results in
• Surgical Treatment increased pressure proximal to the defect (head and upper extremities) and
o Surgical patch closure decreased pressure distal to the obstruction (body and lower extremities)
o Cardiopulmonary bypass
o May require mitral valve repair • Surgical treatment ( surgical repair is the treatment of choice for infants younger than
• Non-surgical Treatment 6 months of age and for patient with long segment stenosis or complex anatomy
o ASD 2 closure with a device during cardiac catheterization • Repair is by resection of coarcted portion with an end-to-end anastomosis
• Enlargement of the constricted section with prosthetic material
• Non-Surgical treatment
VENTRICULAR SEPTAL DEFECT
• Balloon angioplasty is being performed as a primary intervention for COA in
• Abnormal opening between the right and left ventricles
older infants and children
• May be classified accdg. to location
• Membranous
AORTIC STENOSIS
• Muscular
• Narrowing or stricture of the aortic valve, causing resistance to blood flow in the left
• Frequently associated with other defects
ventricle, decrease cardiac output, left ventricular hypertrophy and pulmonary
• Spontaneous closure is most likely to occur during the first year of life in children
vascular congestion
having small or moderate defects
PULMONARY STENOSIS
• Surgical Treatment
• Narrowing at the entrance to the pulmonary artery that causes resistance to blood
• Pulmonary artery Banding
flow leading to right ventricular hypertrophy and decrease pulmonary blood flow
• Suturing for small defects
• Pulmonary atresia is the extreme form of pulmonic stenosis
• Dacron patch for large defects
• Cardiopulmonary bypass
CYANOTIC
• Non-surgical
↓ Pulmonary Blood Flow
• Device closure during cardiac catheterization
 Tetralogy of Fallot
ATRIOVENTRICULAR CANAL DEFECT  Tricuspid Atresia
• Incomplete fusion of the endocardial cushions Mixed Blood Flow
• Consists of a low ASD that is continuous with a high VSD and clefts of the mitral and  Transposition of Great Arteries
tricuspid valves, which creates a central AV valve that allows blood to flow between 4  Total Anomalous Pulmonary venous return
chambers of the heart.  Truncus arteriosus
  Hypoplastic left heart syndrome • Rare defect characterized by failure of the pulmonary veins to join the left atrium,
instead it is abnormally connected to the systemic venous circuit via right atrium or
TETRALOGY OF FALLOT vena cavae
• CLASSIC 4 DEFECTS
• Ventricular septal defect •Classification
• Pulmonic stenosis • Supracardiac
• Right ventricular hypertrophy • Cardiac
• Overriding of aorta • Infracardiac
• Surgical Treatment
• The alteration in hemodynamic varies widely • Corrective repair in early infancy via anastomosis back to the left atrium,
close ASD and ligate the TAPVC
• Surgical treatment •
• Palliative: Modified Blalock – Taussig shunt operation TRUNCUS ARTERIOSUS
• Complete repair (indicated if there is increasing cyanosis and the • Failure of normal septation and division of the embryonic bulbar trunk into the
development of hypercyanotic spells pulmonary artery and the aorta, which results in development of a single vessel that
overrides both ventricles
TRICUSPID ATRESIA • For surgical treatment of VSD and excising the pulmo artery and attaching them to
• The tricuspid valve fails to develop; consequently there is no communication from the the right ventricles via homograft
right atrium & right ventricle
• Often associated with pulmonic stenosis and transposition of the great arteries HYPOPLASTIC LEFT HEART SYNDROME
• Blood flows through the left side is via ASD or a foramen ovale • Underdevelopment of the left side of the heart resulting in a hypoplastic left ventricle
and aortic atresia
• Medical management • Most blood from the left atrium flows across the foramen ovale to the RA to the RV to
• Continuous infusion of prostaglangin E1 the pulmo artery, then the descending aorta receives blood from the PDA to the
• Surgical Treatment systemic circuit
• Palliative: placement of a shunt ( pulmonary-to-systemic artery anastomosis) •
& Atrial septostomy ACQUIRED CARDIOVASCULAR DISORDERS
• Modified Fontan procedure NOTE:
Acquired Cardiac Disorders are disease processes or abnormalities that occur after
TRANSPOSITION OF GREAT VESSELS birth and can be seen in the otherwise normal heart or in the presence of congenital
• The pulmonary artery leaves the left ventricle, and the aorta exits from the right heart disease
ventricle They occur for a variety of reasons, including infection, autoimmune response,
• Associated defects such as septal defects or patent ductus arteriosus must be environmental factors and familial tendencies.
present to permit blood to enter the systemic circulation or the pulmonary circulation
for mixing of saturated and desaturated blood. BACTERIAL (INFECTIVE) ENDOCARDITIS
 It is an infection of the valves and inner lining of the heart, which can potentially
• Manifestation depends on the type and size of the associated defects damage or destroy the heart valves
• Cardiomegaly is usually evident a few weeks after birth
 Most often a sequelae of bacteremia
• Therapeutic management
 It also occurs among children who undergone surgery to repair congenital heart
• IV prostaglandin E1
defect
• Balloon atrial septostomy
• Surgical Treatment  Most common causative agent is Sreptococcus viridans; other agents are
• Arterial switch procedure Staphylococcus aureus, gram-negative bacteria and fungi such as Candida Albicans
• Reimplantation of the coronary arteries
PATHOPHYSIOLOGY
TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION  Unexplained low-grade, intermittent fever
  Non-specific symptoms are malaise, myalgias, arthralgias, headache,  Prevention of permanent cardiac damage
diaphoresis and weight loss  Palliation of other symptoms
 Presence of “new murmur”  Prevention of recurrences (secondary prevention) Penicillin IM monthly for indefinite
 Splenomegaly (prolonged illness) time
 Signs of embolus formation elsewhere in the body  Use of Salicylates or Prednisone (after diagnosis)
 Neonates may have feeding difficulties, respiratory distress, tachycardia, Surgery: Valve repair if needed
CHF or symptoms of septicemia
Nursing Management
Diagnostic Evaluation  Encourage compliance with drug regimens
 ECG changes  Facilitate recovery from the illness
 Decrease Hgb  Provide emotional support
 Elevated ESR, WBC  Prevent recurrence of disease
 X-ray showing cardiomegaly  “Nurses also have role in prevention , primarily in screening school-age children for
 Several blood culture (definitive) sore throats”
 Echocardiography

KAWASAKI DISEASE
THERAPEUTIC MANAGEMENT  Aka Mucucutaneous Lymph Node Syndrome
 It is an acute systemic vasculitis of unknown cause
High dose of antibioticsv (IV for 2 to 8 weeks)  The child may develop cardiac sequelae like ectasia (dilation) or aneurysm formation
If CHF or valvular obstruction develops, surgical intervention is warranted  Common among boys below 5 years old
Prevention is important in susceptible children (e.g prophylactic antibiotic)
• 3 PHASES OF KD
RHEUMATIC FEVER • Acute phase
 Is a poorly understood inflammatory disease that occurs after pharyngitis caused by • Fever (abrupt onset that is unresponsive to antibiobiotics and
group A-beta hemolytic streptococci. antipyretics)
 It is self-limited illness that involves the joints, skin, brain, serous surfaces, and heart • Eye redness
 Rheumatic Heart Disease is the most significant complication • Inflamed pharynx and oral mucosa
 Mostly common in third world country • “Strawberry tongue”
PATHOPHYSIOLOGY & MANIFESTATION • Skin rash ( common in perineum)
 JONES CRITERIA ( major and minor manifestation) • Hands and feet becomes edematous
- • Cervical lymphadenopathy
- • Temporary arthritis
- • Cardiac manifeastation like myocarditis with ECG changes
-
- • Subacute phase
• Resolution of fever
Diagnostic Evaluation • Outward clinical signs disappears
 No single symptom or laboratory test can provide a definitive diagnosis of RF • Enlargement of coronary arteries and affected vessels
 Use of Jones criteria • Periungual desquamation of the hands and feet
 ASLO titer • Arthritis affecting large weight bearing joints
• Irritability
Therapeutic Management
 Eradication of GABHS (primary prevention) via antibiotics like Penicillin (choice) , • Convalescent phase
macrolides and cephalosporin • All clinical signs of KD have resolved
 • Lab. Values have not yet returned to normal
• Thrombocytosis may still be present
• Arthritis may still be present
• Coronary complication is still a concern

• The most serious complication of KD is the potential for “myocardial infarction” in

children with aneurysm formation
• Ischemia generally results from thrombotic occlusion or stenotic occlusion of a
coronary aneurysm

• Diagnostic Evaluation
• Currently no specific diagnostic test exists for KD. Diagnosis is established
on the basis of clinical findings and associated laboratory results
• Therapeutic Management
• High Dose IV IG along with salicylate therapy ( most effective when given
within the first 10 days of illness)
• Low dose aspirin
• Anticoagulant therapy

• Nursing Management
• Monitor cardiac status carefully
• Administer fluid with caution (patency of line should be check regularly)
• Inpatient care focuses on symptomatic relief
• Emotional support
• Medication administration
• Education of child and family