Which physiologic consequences are used to classify cyanotic congenital heart defects? quizlet

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Which structural defects constitute tetralogy of Fallot?
a. Pulmonic stenosis, ventricular septal defect, overriding aorta, right ventricular hypertrophy
b. Aortic stenosis, ventricular septal defect, overriding aorta, right ventricular hypertrophy
c. Aortic stenosis, atrial septal defect, overriding aorta, left ventricular hypertrophy
d. Pulmonic stenosis, ventricular septal defect, aortic hypertrophy, left ventricular hypertrophy

Sets with similar terms

Pathophysiology and Etiology

Failure of fetal ductus arteriosus to close
5%-10% congenital heart lesions; Incidence inversely correlates to gestational age
Altered Hemodynamics

Increased systemic pressure moves saturated blood from aorta into pulmonary arteries. Increased left-sided cardiac workload and pulmonary blood flow
Manifestations

Presentation depends on age and size of defect
Signs of heart failure
Machinery-like murmur, best heard in 2nd and 3rd intercostal spaces
Widened pulse pressure and bounding pulses
Cardiac enlargement
PDA

Interventions address heart failure (HF)
Medications such as Indomethacin and Ibuprofen to close

PDA
If medication unsuccessful, surgery is necessary
Interventional cardiac catheterization can be used to place coil and occlude ductus
Surgical ligation of ductus via left thoracotomy may be necessary to obliterate remaining vessel

Dilated cardiomyopathy (DCM), is characterized by thinning of the left ventricular myocardium, dilation of the ventricular cavity, and systolic functional impairment
The broad number of etiologies range from genetic or familial forms to those caused by infections, metabolic derangements, toxic exposures, and degenerative disorders.
S/S: Tachypnea, tachycardia, gallop rhythm, diminished pulses, hepatosplenomegaly
CXR: Cardiomegaly, pulmonary vascular congestion
EKG Rhythm disorders (most likely cause of this D/O), dilated left ventricle with decreased systolic function
Treatment
Medical: aim is to stabilize the patient using afterload reduction, inotropic support, and gentle diuresis.(know!)
◦The infusion of large fluid boluses is poorly tolerated and can result in hemodynamic decompensation and cardiovascular collapse.
◦Surgery: some children's disease state remains stable or improves others eventually require cardiac transplantation

CHD has become the primary risk factor for IE in children in developed countries.
Risk is largely based on the nature of the cardiac condition. The infection results from deposition of bacteria or other pathogens on tissues in areas of abnormal or turbulent blood flow
DX: Made with differing numbers of combinations of major & minor criteria. Major criteria: positive blood cultures & pathologic lesions on echo.
Minor criteria include:
-splinter hemorrhages, Janeway lesions (small painful nodule on the finger)s
-Roth spots (retinal hemorrhages with clear centers)
The presentation of the disease can be acute or subacute.
S/S: new or changing murmurs and signs of systemic embolization
◦Acute: high fever, myalgias, fatigue lethargy and shock
◦Subacute: low grade fever, malaise, anemia, fatigue or weakness
TEE: Routinely done to assess for vegetations or other abnormalities
Treatment
Parenteral antibiotics are initiated after blood cultures are collected.
In some cases, children with IE require surgical intervention. Failure of medical therapy (i.e., inability to clear the bacteremia), abscess formation, refractory heart failure, large vegetation, and serious embolic phenomenon are indications for surgical intervention.

Kawasaki disease is a fairly common and potentially fatal form of systemic vasculitis of unknown origin.9
It's a condition seen predominantly in infants and young children. The disease can affect the coronary arteries resulting in dilation and aneurysmal formation
The diagnosis relies on clinical features. To meet criteria, a child must have persistent fevers and at least four of the following findings:
◦Polymorphous exanthem
◦Peripheral extremity changes (e.g., erythema, desquamation, edema of the hands or feet)
◦Bilateral, nonexudative conjunctivitis
◦Cervical lymphadenopathy (often unilateral)
◦Oral changes (i.e., strawberry tongue; red, dry, or cracked lips)
Intravenous gamma globulin (IVIG) and high-dose aspirin are recommended during the acute phase of the disease.
In children with coronary artery aneurysms, low-dose aspirin therapy is administered, in some cases in combination with anticoagulants or antiplatelet drugs.
Myocardial ischemia and infarction, although uncommon, are important potential complications.
Anesthetic care in these children requires careful consideration regarding myocardial oxygen demand and supply; on rare occasions, coronary revascularization may be necessary.

Pediatric heart failure results from markedly different etiologies from those reported in adults.
The causes of heart failure in children vary with age.
In the perinatal period,
◦cardiac dysfunction can be related to birth asphyxia, sepsis or constitute an early presentation of CHD.
◦The neonate with heart failure frequently presents with clinical signs of a low cardiac output state.
First year of life
◦predominantly caused by structural heart disease (problem with heart tissue or valves. Many are congenital). Other causes include metabolic cardiomyopathies or acute events such as myocarditis.
◦In infants with heart failure, tachypnea, dyspnea, tachycardia, feeding difficulties, and failure to thrive are prominent features.
◦The physical examination can display grunting respirations, rales, intercostal retractions, a gallop rhythm, and hepatosplenomegaly. Frequently, a mitral regurgitant murmur is present.
Beyond the first year of life
◦Consequence of previous surgical interventions, unrepaired CV disease, cardiomyopathies, myocarditis or chemotherapy
◦Older children with heart failure exhibit exercise intolerance, fatigue, and growth failure

These children require a thorough preoperative evaluation and an assessment of several perioperative challenges including
◦cyanosis
◦intracardiac shunting
◦impaired hemostasis
Medical Assessment
◦Type of CHD and coexisting diseases
◦Review history from the medical record. Particular attention should be paid to the imaging (cardiac cath/echo, CXR), EKG and lab data (Hgb polycythemic?, K, Bun/Cr)
◦Need to know the Age (may manage the same lesion differently in newborn vs. Infant vs. child), lesion type, effects of CHD on other organs, associated anomalies, preoperative condition and procedure (lap chole vs spine procedure)
◦Must know the presence and degree of cardiac failure, cyanosis, or risk of pulmonary HTN.
◦Nutritional state of the child should be evaluated as poor growth and development may be a sign of sever CHD
◦Prior surgical interventions? (redo sternotomy)
◦Will the planned procedure impact where I can place my arterial live or IVs?
◦ROS: Cyanosis, respiratory, sweating, poor feeding, syncope, liver or renal dysfunction
◦Medications: Prostaglandin E1, Digoxin, ACE inhibitors, diuretics

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