Pediatric cardiovascular defects

1st up to the 8th week.

opening present between left and right sides of the heart-left to right shunt

• Does not present with cyanosis
• increased cardiac workload
• right ventricular strain-leads to hypertrophy and pulmonary HTN.- Will eventually lead to Cor pulmonale-RS HF.-pulmonary edema

• Permits unoxygenated blood to mix with oxygenated blood-Right to left shunt.
• Leads to cyanosis
• hypoxemia
• increased cardiac workload
• polycythemia-leads to high viscosity of the blood-leading to further decrease in perfusion
• CHF

Decreased Cardiac Output related to abnormal intracardiac pressures and blood flow patterns secondary to congenital heart defects and their surgical repair.

• Murmurs
• foramen ovale and ductus arteriosus should close after 1st day of life
• color-acrocyanosis
• temperature-cool extremities 
• Polycythemic children may have normal sats. but appear cyanotic. Monitor for liver enlargement

• digoxin is a positive inotropic and negative chronotropic. 
• Infants <90-100 in infants
• Children < 70-85 in children

tachypnea, dyspnea, feeding intolerance, SOB, poor perfusion-leading to shock

• Leads to anaerobic metabolism-cells use up stores of ATP and will lead to inability to operate sodium-potassium pump-sodium and chloride collect inside the cell and potassium on the outside.
• Sodium will draw water into cell leading to swelling

• VSD
• pulmonary artery stenosis
• RVH
• Over riding aorta

Dependent on the severity of the defects it will be classified as acyanotic or cyanotic.

Prostaglandin during birth keeps the DA open if premature they may give an inhibitor to help close the DA

• Hypercyanotic (Hypoxic spell)-decreased blood flow through pulmonary artery.
• Acute-onset-dyspnea, tachypnea-children often squat to relieve dyspnea.

• Prostaglandin E1 (PGE1) infusion started at birth to keep ductus open
• Prostaglandins to keep open

Will need surgical intervention

Right subclavian artery is anastomosed to the right pulmonary artery to provide sufficient blood flow to the lungs.

• Patent ductus arteriosus-PDA
• Ventricular septal defect-VSD
• Atrial Septal Defect-ASD
• Coarction of the aorta-narrowing of the aorta.

• Transposition of great arteries
• tetralogy of fallot/ pulmonary stenosis
• single ventricle defect-hypoplastic left  heart syndrome.

connects aorta to pulmonary artery allowing blood to bypass the lungs as a fetus. Most close within 15-72 hours after birth-some dont close up to 2 weeks.

• Fatigue
• sweating
• tachypnea
• dyspnea
• tiring while feeding
• poor weight gain
• frequent pulmonary infections

Similar to a murmur, machine like, harsh. Widening pulse pressures, wet lungs,leads to cor pulmonale.

• Indomethacin 0.2mg/kg IV q12 x 3
• inhibits prostaglandins, stimulates muscles in the heart to constrict causes closure of PDA 75-80% of the time.
• Surgical repair if it does not close-depending on how symptomatic they may wait until 6 months

• Crying, running, playing. all dependent on how severe the defects are.
• Becomes more worse around 6 months as pulmonary stenosis worsens.

• More deoxygenated blood flow that mixes with oxygenated blood (Right to Left shunt (More serious)) leading to hypoxia, cor pulmonale and TET spells
• Blood flow to the lungs is dependent on the PDA-they will give Prostaglandin E1 to keep it open.

• cyanosis
• pallor
• dyspnea
• tachypnea
• restlessness
• syncope
• decreased LOC

• Fatigue
• sweating
• tachypnea
• dyspnea
• tiring while feeding
• poor weight gain
• frequent pulmonary infections

decreases preload/right ventricular pressure and increases afterload and left ventricular pressure thus improving blood flow through the pulmonary circuit.

Boot shaped heart on xray

• usually done at 3-12months old
• VSD patched
• enlarge the pulmonary stenosis
• ligation of palliative shunts.