Coarctation of the aorta may be defined as a constricted aortic segment that comprises localized medial thickening, with some infolding of the medial and superimposed neointimal tissue.The presence of associated defects and aortic arch anomalies, the extent of patency of the ductus arteriosus, the rapidity of the process of closure of the ductus arteriosus, and the level of pulmonary vascular resistance determine the timing of clinical presentation and the severity of symptoms. Young patients may present in the first few weeks of life with poor feeding, tachypnoea, and lethargy and progress to overt CHF and shock. These patients may have appeared well before hospital discharge, and deterioration coincides with closure of the patent ductus arteriosus. Presentation may be abrupt and acute with ductal closure.Neonates may be found to have tachypnoea, tachycardia, and increased work of breathing and may even be moribund with shock. Keys to the diagnosis include blood pressure (BP) discrepancies between the upper and lower extremities and reduced or absent lower extremity pulses to palpation. However, when the infant is in severe heart failure, all pulses are diminished.The murmur associated with coarctation of the aorta may be nonspecific yet is usually a systolic murmur in the left infraclavicular area and under the left scapula.

The best answer is Henoch-Schönlein Purpura (HSP). This patient has a characteristic rash and the labs are consistent with this diagnosis.

The most probable diagnosis for this child would be rheumatic fever due to a previous history of rheumatic fever, evidence of streptococcal disease from a throat swab, a raised ASO titre and a positive streptococcal antigen test or a leukocytosis.Acute Rheumatic Fever:ARF occurs because of an abnormal immune response to a streptococcal antigenic component. It has a latent period of 1–3 weeks and is more common in the lower socio-economic classes. It peaks at around 5–15 years of age and affects the blood vessels, joints, nervous system and subcutaneous tissues. It is characterised as an autoimmune disease, and there is a risk of rheumatic fever occurring after infection in 3% of the population. The recurrence is greater in younger children and increases with each attack. Duckett-Jones criteria:The diagnostic criteria for acute rheumatic fever.Major: – Pancarditis- Chorea (Sydenham’s) – Polyarthritis (flitting)- Erythema marginatum- Subcutaneous nodulesMinor criteria include the presence of arthralgia, fever, prolonged PR interval, raised ESR, raised CRP.Note that:To make the diagnosis of rheumatic fever: Two major and/or one major with two minor criteria are required. Evidence of a recent streptococcal infection with a raised ASO titre or an antiribonuclease B level is sufficient. Exceptions to this rule are mentioned below:- Chorea alone is diagnostic.- Insidious or late-onset carditis with no other explanation.- Rheumatic recurrence: The presence of one major and one minor criterion with a prior streptococcal disease that is recurring.Consequences of pericarditis include heart block, pericardial effusion, tachycardia, cardiomegaly, pericardial friction rub, congestive cardiac failure, valvular disease and a Carey–Coombes apical mid-diastolic rumbling murmur.New heart murmurs are often audible, including those of mitral regurgitation and aortic regurgitation. Skin nodules affect the perivascular tissues and are non-specific lesions resulting from fibroid degeneration.Management:Medication includes aspirin for the acute phase, non-steroidal anti-inflammatory drugs for arthritis, prednisolone for severe carditis, and high-dose penicillin for immediate management with antibiotic prophylaxis in the long term. Antibiotics may include penicillin V, erythromycin or benzylpenicillin. Diazepam and haloperidol may be required to control the chorea.

The most possible diagnosis is SVT. The boy is suffering from hemodynamic instability, as indicated by his cold extremities. DC cardioversion is the treatment of choice.

The murmur of tricuspid valve regurgitation is typically a high-pitched, blowing, holosystolic, plateau, nonradiating murmur best heard at the lower left sternal border. The intensity is variable, but tends to increase during inspiration (Carvallo’s sign), with passive leg raising, after a post-extrasystole pause, and following amyl nitrite inhalation. The intensity of the murmur tends to correlate positively with the severity of regurgitation. Right ventricular enlargement may displace the location of the murmur leftward. Right ventricular failure may abolish respiratory variation. When tricuspid regurgitation is caused by pulmonary hypertension, a pulmonic ejection click may be audible. Severe tricuspid regurgitation is commonly accompanied by a third heart sound emanating from the right ventricle and best heard at the lower left sternal border. Severe tricuspid regurgitation typically produces an accentuated jugular cv wave and may produce hepatic congestion with a pulsatile liver.The auscultatory findings associated with ventricular septal defect are variable, depending on a variety of morphologic and hemodynamic considerations. The systolic murmur associated with a Roger’s-type ventricular septal defect (regurgitant jet flows directly into the right ventricular outflow tract) in patients with low pulmonary vascular resistance is a low to medium pitched, holosystolic murmur with midsystolic accentuation. The intensity of the murmur is typically grade 3 or higher.Patent ductus arteriosus produces a continuous murmur in patients with normal pulmonary vascular resistance.

Torsade de pointes is an uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line.Conditions associated with torsade include the following:Electrolyte abnormalities – Hypokalaemia, hypomagnesemia, hypocalcaemiaEndocrine disorders – Hypothyroidism, hyperparathyroidism, pheochromocytoma, hyperaldosteronism, hypoglycaemiaCardiac conditions – Myocardial ischemia, myocardial infarction, myocarditis, bradyarrhythmia, complete atrioventricular (AV) block, takotsubo cardiomyopathyIntracranial disorders – Subarachnoid haemorrhage, thalamic hematoma, cerebrovascular accident, encephalitis, head injuryNutritional disorders – Anorexia nervosa, starvation, liquid protein diets, gastroplasty and ileojejunal bypass, celiac diseaseRisk factors for torsade include the following:Congenital long QT syndromeFemale genderAcquired long QT syndrome (causes of which include medications and electrolyte disorders such as hypokalaemia and hypomagnesemia)BradycardiaBaseline electrocardiographic abnormalitiesRenal or liver failure

Auscultatory findings of VSD vary with the size of the defect. Small VSDs typically produce murmurs ranging from a grade 1 to 2/6 high-pitched, short systolic murmur (due to tiny defects that actually close during late systole) to a grade 3 to 4/6 holosystolic murmur (with or without thrill) at the lower left sternal border| this murmur is usually audible within the first few days of life (see table Heart Murmur Intensity). The precordium is not hyperactive, and the 2nd heart sound (S2) is normally split and has normal intensity.Moderate to large VSDs produce a holosystolic murmur that is present by age 2 to 3 wk| S2 is usually narrowly split with an accentuated pulmonary component. An apical diastolic rumble (due to increased flow through the mitral valve) and findings of heart failure (e.g., tachypnoea, dyspnoea with feeding, failure to thrive, gallop, crackles, hepatomegaly) may be present. In moderate, high-flow VSDs, the murmur is often very loud and accompanied by a thrill (grade 4 or 5 murmur). With large defects allowing equalization of left ventricular and right ventricular pressures, the systolic murmur is often attenuated.

A ventricular septal defect (VSD) is a common form of congenital heart defects and is characterised by the presence of a hole in the wall that separates the right from the left ventricle. Medium or large defects can cause many complications. One of these complication is Eisenmenger syndrome, characterised by reversal of the shunt (from left-to-right shunt into a right-to-left) ,cyanosis and pulmonary hypertension.

ASD is an acyanotic congenital heart disease, characterized by the failure of the interatrial septum to form completely, which results in the mixing of left and right-sided blood. There are various types of ASD, some of them are ostium primum septal defect and patent foramen ovale. Clinical findings associated with ASD are a systolic ejection murmur, fixed splitting of second heart sound, prolonged PR interval, both left and right axis deviation (primum and secundum ASD, respectively). The most common finding is an incomplete right bundle branch block.

Blalock-Thomas-Taussig shunt is a surgical procedure done to increase pulmonary blood flow in cases like pulmonary atresia and results in a continuous murmur.The type of murmur which is heard during the systole and remains continuous till the second heart sound is known as a continuous murmur. This murmur is often intense and considered rough. It can also be accompanied by quivering. There are numerous causes of a continuous murmur that differ depending on the location and components of this murmur. It is caused by the shunting of blood from a high-pressure circulation to a low-pressure circulation. Pathological causes of a continuous murmur include patent ductus arteriosus, aortopulmonary window, AV malformation, coarctation of aorta, any acquired trauma, and iatrogenic cause like interventional or surgical procedures.