Clinical specialties
Andrew Schofield, Paul Schofield in The Complete SAQ Study Guide, 2019
A newborn is seen by the paediatric SHO for a routine baby check. On examination, a heart murmur is noted. Further investigation is undertaken, and the baby is found to have a congenital heart disease. What prenatal investigation can be used to detect congenital heart diseases? (1)In which direction is blood flowing in the heart in acyanotic congenital heart disease? (1)Give two causes of acyanotic congenital heart disease. (2)In which direction is blood flowing in the heart in cyanotic congenital heart disease? (1)Give two causes of cyanotic congenital heart disease. (2)In decompensated congenital heart disease, give two clinical features which may be seen. (2)What is Eisenmenger’s syndrome? (1)
Cardiovascular System:
Michel R. Labrosse in Cardiovascular Mechanics, 2018
Heart murmurs are usually a result of a valve abnormality. A valve stenosis refers to a faulty opening of the valve and can be a result of stiff valve flaps or a narrowing of the valve annulus. This may be a congenital defect, caused by an illness such as rheumatic fever. With aging, calcification of the valve flaps also results in stenosis. A valve insufficiency (or regurgitation) refers to a faulty closure of the valve that allows for the backflow of blood. This “leak” can also be a result of a congenital condition, disease, or aging. Both conditions result in less forward blood flow and a drop in stroke volume and cardiac output, which can lead to heart failure. Defective valves may either be replaced with a valve prosthesis—a mechanical valve or a pig or cow valve—or be repaired. These aspects, along with the structure and function of the aortic and mitral valves, will be discussed in more detail in Chapters 9 and 10. Tissue engineering may soon allow for the development of valves from a patient’s own cells.
Electrocoagulation Of Vascular Abnormalities Of The Large Bowel
John P. Papp in Endoscopie Control of Gastrointestinal Hemorrhage, 2019
Case 3: This 70-year-old woman was referred because of intermittent tarry stools of 2-year’s duration, which caused anemia and progressive worsening of her angina. During the 2 years prior to referral, the patient had had 6 gastrointestinal work-ups using conventional techniques without elucidation of the source of bleeding. The patient had a known heart murmur for many years. On examination, it was a soft, blowing, systolic murmur at the apex which radiated to the axilla. Ischemic changes in the anterior wall of the electrocardiogram became less prominent after transfusions. Echocardiography was consistent with idiopathic hypertrophic subaortic stenosis. Cardiac catheterization confirmed the diagnosis and also showed minimal mitral insufficiency. Coronary arteriography revealed severe disease. At colonoscopy, three mucosal vascular abnormalities were noted in the cecum. The largest was 1 cm in diameter. Each was electrocoagulated with the dome-tip electrode. She was discharged home on the following day. She did well with minimal angina while taking Inderal® until 3 years later, when massive rectal bleeding occurred. After transfusions, colonoscopy revealed a 5 ≈ 8-mm lesion close to the opening of the appendix. Close by was a smaller lesion. The larger lesion was biopsied and in the process it was noted that the center appeared to contain some fibrous tissue which caused it to assume a plate-like configuration when elevated. The lesions were then destroyed with electrocoagulation. The biopsy showed angiectasis. The patient has done well for 3V2 years.
Management of congenitally corrected transposition from fetal diagnosis to adulthood
Published in Expert Review of Cardiovascular Therapy, 2023
Ewa Kowalik
Patients diagnosed early in the adulthood usually have isolated ccTGA or well-balanced complex anomaly (ccTGA with VSD and PS with mild cyanosis). They might be identified with abnormal findings on the physical examination, such as heart murmur (in the presence of tricuspid regurgitation or other concomitant lesions), loud second heart sound (due to location of the aortic valve close to the chest wall) or cardiac arrhythmia. Abnormalities found on cardiovascular testing (electrocardiogram, chest radiograph, echocardiography, or advanced cardiac imaging tests) performed for other indications (Figure 1) can also lead to the recognition of ccTGA. In some cases, the correct diagnosis is not established despite a prior cardiology consultation with cardiac imaging [17]. Occasionally, ccTGA is diagnosed in athletes [18] or adults with very advanced age [19].
Transcatheter Aortic Valve Replacement Associated Infective Endocarditis: A Clinical Update
Published in Structural Heart, 2020
Simrat Kaur, Rabel Misbah Rameez, Wael Jaber, Brian P. Griffin, Bo Xu
Fever accompanied by other signs of systemic inflammatory response syndrome is common, immediately post TAVR and is typically transient.16 Unrelenting fever, congestive cardiac failure, persistently elevated biomarkers and positive blood cultures should raise the suspicion and prompt a thorough evaluation for IE. A suggested diagnostic pathway for suspected TAVR – IE is shown in Figure 2. Presence of heart murmurs may not be as valuable in the diagnosis of TAVR-IE contrary to native valve endocarditis (NVE), due to the frequent occurrence of mitral regurgitation in these patients.17 Since advanced age, multiple comorbidities and frailty are common in TAVR recipients, infections in these patients usually present in an atypical manner.
Oral indomethacin versus oral ibuprofen for treatment of patent ductus arteriosus: a randomised controlled study in very low-birthweight infants
Published in Paediatrics and International Child Health, 2018
Varangthip Khuwuthyakorn, Chuleeporn Jatuwattana, Suchaya Silvilairat, Watcharee Tantiprapha
After obtaining informed consent from parents, infants were enrolled who satisfied the inclusion criteria: (i) birthweight 500–1500 g, (ii) gestational age 24–32 weeks, (iii) postnatal age 1–30 days, and (iv) hsPDA confirmed by echocardiography. Echocardiography was undertaken in patients clinically suspected to have PDA which included two or more of the following: (i) heart murmur, (ii) active precordium, (iii) persistent tachycardia (>160 bpm), (iv) bounding pulse, (v) wide pulse pressure (systolic–diastolic BP ≥ 25 mm Hg) or (vi) inability to be weaned from mechanical ventilation or respiratory deterioration (conventional ventilation: peak inspiratory pressure [PIP]≥18 mm Hg and FiO2 ≥ 50%; high-frequency oscillation ventilation: mean arterial pressure [MAP]≥12 mm Hg and FiO2 ≥ 0.5 to maintain pH 7.25–7.35, PaCO2 45–55 mm Hg, SpO2 90–95%). If PDA was identified and its diameter was > 1.5 mm (or > 1.4 mm/kg) and/or left atrium to aorta (LA/AO) ratio was > 1.4, with left-to-right shunting [2,20], PDA closure with either IDC or IB was randomly initiated. Exclusion criteria were major congenital anomalies, life-threatening infection, hydrops fetalis, severe IVH, severe bleeding, urine output < 1.0 ml/kg/hr in the previous 8 h, impaired renal function with serum creatinine ≥ 159 μmol/L, BUN > 40 mg/dL, platelet count < 80,000/mm3 or a previous course of treatment with IDC or IB for PDA. Criteria for discontinuation of the treatment included GI perforation, severe GI bleeding and urine output < 0.5 ml/kg/hr over a 24-h period and serum creatinine > 159 μmol/L after receiving medication for 24 h.
Related Knowledge Centers
- Auscultation
- Palpation
- Physiology
- Stethoscope
- Heart Sounds
- Hemodynamics
- Heart Valve
- Signs & Symptoms
- Cardiac Examination
- Functional Murmur