Cardiology Flashcards
Congenital disorders that can result in CHF
- Increased pulmonary blood flow
- Obstructive lesions
- AV malformations
- Mitral or tricuspid regurgitation
Acquired heart disorders that can result in CHF
- Viral myocarditis
- Endocarditis
- Pericarditis
- Metabolic disease (eg hypothyroidism)
- Medications (eg doxorubicin)
- Cardiomyopathies
- Ischemic diseases
- Dysrhythmias (tachycardia and bradycardia)
Miscellaneous causes of CHF
- Severe anemia (high-output CHF)
- Rapid infusion of IV fluids, esp in premature infants
- Obstructive processes of the airways (enlarged tonsils or adenoids, laryngomalacia, CF - may cause CHF as a result of chronic hypoxemia that results in right sided heart failure)
Clinical features of CHF
- Tachypnea
- Cough
- Wheezing
- Rales
- Pulmonary edema on CXR
- Tachycardia
- Sweating
- Pale or ashen skin color
- Diminished urine output
- Enlarged cardiac silhouette
- Hepatomegaly
- Peripheral edema
- Failure to thrive
- POOR FEEDING (common in newborns)
- Exercise intolerance
- Cyanosis and shock (late manifestations)
Innocent cardiac murmurs
- Result from turbulent blood flow and are NOT caused by structural heart disease and have no hemodynamic significance
- Up to 50% of children
- INCLUDE: Still’s murmur, pulmonic systolic murmur/ systolic ejection murmur, venous hum
Still’s murmur
- Ages 2-7
- Mid-left sternal border
- Grade 1-3
- Systolic
- Vibratory, twanging, or buzzing
- Loudest supine
- Louder with exercise
Pulmonic systolic murmur/ systolic ejection murmur
- Any age
- Upper left sternal border
- Grade 1-2
- Peaks early in systole
- Blowing, high-pitched
- Loudest supine
- Louder with exercise
Venous hum
- Any age
- Neck and below clavicles
- Continuous murmur
- Heard only sitting or standing
- Disappears if supine; changes with compression of the jugular vein or with neck flexion or extension
Classifications of ASDs
- Ostium primum
- Ostium secundum
- Sinus venosus
Ostium primum
- Defect in the lower portion of the atrial septum
- A cleft, or divison, in the anterior mitral valve leaflet may also be present and may cause mitral regurgitation
- Common in Trisomy 21
Ostium secundum
- Defect in middle portion of the atrial septum
- Most common type of ASD
Sinus venosus
- Defect high in the septum near the junction of the right atrium and SVC
- Right pulmonary veins usually drain anomalously into the right atrium or SVC instead of into the left atrium
Physical exam findings of ASD
- Increased right ventricular impulse as a result of right ventricular overload
- Systolic ejection murmur (from excessive pulmonary blood flow) best heard at mid and upper left sternal borders (a mid-diastolic filling rumble representing excessive blood flow through the tricuspid valve may also be heard)
- Fixed split second heart sound because of the excessive pulmonary blood flow, the normal physiologic variation in timing of the aortic and pulmonic valve closure with respiration is absent
VSD classification
By location - inlet, trabecular (muscular), membranous, and outlet (supercristal)
Clinical features and course of small VSDs
- Little to no shunt across the VSD
- May close spontaneously
- Thrill at the lower left sternal border and a grade 4 high pitched holosystolic murmur
Clinical features and course of moderate VSDs
- May have a large shunt across the VSD that may result in signs and symptoms of CHF
- Holosystolic murmur
- If 2:1 pulmonary to systemic flow, then a diastolic murmur of mitral turbulence (mitral filling rumble representing the excess blood from the lungs now passing through the mitral valve) may be heard at apex
Clinical features and course of large VSDs
- Often cause signs and symptoms of CHF
- Less turbulence across the VSD so systolic murmur is shorter and lower in pitch
- Mitral filling rumble may be heard at the apex
Large VSDs are associated with a high incidence of
Pulmonary infections from excessive blood flow
Indications for surgical closure of VSDs
- Heart failure refractory to medical management
- Large VSDs with pulmonary hypertension are usually surgically closed at 3-6 mo of age
- Small to moderate VSDs are usually surgically closed between 2 and 6 years of age
Symptoms of small PDAs
Usually produce no symptoms
Symptoms of moderate and large PDAs
Generally result in signs and symptoms of VHF due to increased pulmonary blood flow
Clinical features of neonates or infants with severe coarctation
- Depend on a right to left shunt through the PDA for perfusion of the lower thoracic and descending aorta
- May be minimally symptomatic initially, but symptoms of CHF develop and progress as PDA closes
- BP may be elevated in the upper extremities and low in the lower extremities before the onset of CHF
- Once CHF develops, pulses in all 4 extremities are poor, any murmur is absent and hypotension may develop
Clinical features of older children or adolescents with coarctation
- May have no symptoms and may have only hypertension or a heart murmur
- HTN is typically noted in the right arm and BP is reduced in the lower extremities
- Femoral pulse, which normally precedes the radial pulse is dampened and delayed until after the radial pulse (radio-femoral delay)
- BP and pulse findings may be less prominent if collateral vessels (intercostal arteries) develop that allow the ascending aortic pressure and flow to circumvent the coarctation
- Bicuspid aortic valve or aortic stenosis is present in 50% of patients
- Bruit of turbulence through the coarctation may be audible at the left upper back near the scapula
Initial management of coarctation
- Directed at improving circulation to the lower body
- IV prostaglandin E (PGE) is given urgently to open the ductus arterioles
- Inotropic medications are given to overcome myocardial depression and low dose dopamine is used to maximize renal perfusion and function