RCCS cheat sheet

Fetal circulation: placental oxygenated blood enters via umbilical vein, largely bypasses the liver through the ductus venosus, reaches the right atrium, crosses the foramen ovale to the left atrium, and supplies the brain; the right ventricle ejecting to the descending aorta through the ductus arteriosus supplies the lower body and placenta.

Fetal oxygen saturation is highest in the umbilical vein (about 80%), lower in the ascending aorta (about 65%), and lowest in the descending aorta (about 55%); fetal PO2 is low, but oxygen delivery is supported by high hemoglobin and high cardiac output.

At birth, rising left atrial pressure functionally closes the foramen ovale; anatomic closure may take months to years. The ductus arteriosus closes functionally within 24–72 hours and anatomically in about 2–3 weeks; the ductus venosus closes functionally within days and anatomically in about 2–3 weeks.

The newborn right ventricle is relatively dominant, with right ventricular mass exceeding left ventricular mass at birth; left ventricular mass exceeds right ventricular mass by about 6 months of age.

Normal fetal heart rate is approximately 110–160 beats per minute; persistent rates below 100 or above 180 warrant further evaluation.

In the normal fetal great vessel crossing, the pulmonary artery is anterior and leftward and the aorta is posterior and rightward; the ductal arch appears as a hockey stick and the aortic arch as a candy cane.

Cardiac output = heart rate × stroke volume. The Fick principle gives cardiac output = oxygen consumption ÷ arteriovenous oxygen content difference; cardiac index = cardiac output ÷ body surface area.

The four-chamber view is generally obtainable by 12–14 weeks, outflow tracts by about 16 weeks, and routine fetal cardiac screening is performed at 18–22 weeks.

Cyanotic lesions with decreased pulmonary blood flow include tetralogy of Fallot, pulmonary atresia, tricuspid atresia, and severe right ventricular outflow tract obstruction; these may be ductal dependent for pulmonary blood flow.

Cyanotic lesions with increased pulmonary blood flow include D-transposition of the great arteries, total anomalous pulmonary venous return, truncus arteriosus, and single ventricle without pulmonary stenosis.

Ductal-dependent systemic lesions include hypoplastic left heart syndrome, critical aortic stenosis, interrupted aortic arch, and severe coarctation; prostaglandin E1 maintains ductal patency until intervention.

Ductal-dependent pulmonary lesions include pulmonary atresia, critical pulmonary stenosis, and severe tetralogy of Fallot; prostaglandin E1 preserves pulmonary blood flow through the ductus arteriosus.

Tetralogy of Fallot consists of a ventricular septal defect, overriding aorta, right ventricular outflow tract obstruction, and right ventricular hypertrophy; the degree of outflow obstruction determines the severity of cyanosis.

D-transposition of the great arteries has the aorta arising from the right ventricle and the pulmonary artery from the left ventricle, creating parallel circulations; mixing occurs through an atrial septal defect, ventricular septal defect, or ductus arteriosus.

Hypoplastic left heart syndrome includes underdevelopment of mitral and aortic valves and the left ventricle; systemic output depends on the ductus arteriosus, and atrial-level mixing is obligatory.

Qp/Qs = (systemic arterial saturation − mixed venous saturation) ÷ (pulmonary venous saturation − pulmonary arterial saturation). A Qp/Qs above 1.5 suggests a significant left-to-right shunt; Eisenmenger physiology is pulmonary vascular disease with shunt reversal and cyanosis.

Higher transducer frequency improves spatial resolution but reduces penetration; select the highest frequency that adequately penetrates the required depth, such as 5–8 MHz in infants and lower frequencies in older children or fetal imaging.

The Nyquist limit equals half the pulse repetition frequency; velocities above this limit alias. Adjust scale, baseline, color map, or transducer frequency to reduce aliasing.

Continuous-wave Doppler measures high velocities without depth discrimination; pulsed-wave Doppler provides depth-specific sampling but is limited by the Nyquist limit.

Frame rate = pulse repetition frequency ÷ number of scan lines per frame; reducing depth, sector width, and line density increases frame rate.

Doppler velocity accuracy depends on beam alignment; an intercept angle of 20 degrees or less keeps cosine error below about 6%.

M-mode provides high temporal resolution along a single line and is useful for timing valve motion and measuring chamber dimensions.

Tissue harmonics improve endocardial border definition; mechanical index and thermal index should be monitored, especially during prolonged fetal or pediatric studies.

Fetal Doppler exposures should follow ALARA principles: use the lowest output for the shortest time, avoid prolonged Doppler, and limit exposure when unnecessary.

Qp/Qs = (systemic arterial saturation − mixed venous saturation) ÷ (pulmonary venous saturation − pulmonary arterial saturation); values above 1.5 indicate a significant left-to-right shunt and above 2.0 indicate a large shunt.

Ventricular septal defect peak velocity gives the systolic pressure difference by ΔP = 4v². When no left ventricular outflow obstruction is present, RVSP = systolic blood pressure − VSD gradient.

Aortic stenosis severity uses peak gradient = 4v², mean gradient, and continuity-equation valve area: AVA = LVOT area × TVI_LVOT ÷ TVI_AV.

Tricuspid regurgitation peak velocity estimates RVSP = 4(TR Vmax)² + right atrial pressure; the PDA gradient can be used similarly when a ductal jet is measurable.

Regurgitant severity is assessed with vena contracta width, jet area, PISA, and reversal of pulmonary or hepatic vein flow; pediatric thresholds may differ from adult thresholds.

Coarctation shows increased systolic velocity, persistent diastolic forward flow, and a sawtooth pattern; the peak gradient is estimated by the Bernoulli equation, and a diastolic runoff pattern supports severity.

Fractional shortening = (LVIDd − LVIDs) ÷ LVIDd; ejection fraction, TAPSE, MAPSE, and speckle-tracking strain provide additional assessment of ventricular systolic function.

Great vessel assessment includes aortic arch sidedness and branching, pulmonary artery confluence and branch size, ductus arteriosus patency, and relationship of the great vessels to one another.

Norwood stage I palliation for hypoplastic left heart syndrome reconstructs the aorta from the pulmonary artery, performs an atrial septectomy, and provides pulmonary blood flow by a modified Blalock-Taussig shunt or right ventricle-to-pulmonary artery conduit.

The bidirectional Glenn anastomoses the superior vena cava to the pulmonary arteries, usually at 3–6 months of age, reducing ventricular volume load and requiring acceptable pulmonary artery pressures.

The Fontan operation directs inferior vena cava blood to the pulmonary arteries without a ventricular pump; fenestration may preserve cardiac output at the cost of mild cyanosis, and complications include protein-losing enteropathy, plastic bronchitis, arrhythmia, and hepatic dysfunction.

A modified Blalock-Taussig shunt connects a systemic artery, usually the innominate or subclavian artery, to the pulmonary artery; shunt flow is continuous, and target oxygen saturation is often about 75–85% in cyanotic lesions.

Prostaglandin E1 can cause apnea, hypotension, fever, and irritability; airway monitoring and readiness for ventilatory support are required during infusion.

In cyanotic congenital heart disease with right-to-left shunting, falling systemic vascular resistance increases the shunt and worsens hypoxemia; dehydration and prolonged fasting should be minimized.

Endocarditis prophylaxis before dental procedures is generally recommended for prosthetic heart valves, previous endocarditis, and certain unrepaired or palliated congenital heart lesions.

Safety practices include ALARA radiation and ultrasound exposure, appropriate transducer disinfection, infection control, patient identification, and monitoring during sedation or contrast administration.