The QT interval is the time from the start of the Q wave to the end of the T wave. It represents the time taken for ventricular depolarisation and repolarisation. The QT interval should be measured in either lead II or V5-6.

The classic history in this high risk patient is suggestive of a dissecting aortic aneurysm. His transoesophageal echocardiogram confirms the diagnosis. ST elevation in ECG is probably due to the extension of the dissection of the aorta which results in compromised coronary blood supply.

The cardiac conduction system is a collection of nodes and specialised cells including the:
Sinoatrial node
Atrioventricular node
Atrioventricular bundle (bundle of His)
Purkinje fibres

Causes for right axis deviation:
-Right ventricular hypertrophy and Left posterior fascicular block
-Lateral myocardial infarction.
-Acute or chronic lung diseases: Pulmonary embolism, pulmonary hypertension, chronic obstructive pulmonary disease (COPD), cor pulmonale.
-Congenital heart disease (e.g., dextrocardia, secundum atrial septal defect).
-Wolff-Parkinson-White syndrome.
-Ventricular ectopic rhythms (e.g., ventricular tachycardia).

Ebstein’s anomaly is characterised by apical displacement and adherence of the septal and posterior leaflets of the tricuspid valve to the underlying myocardium, thereby displacing the functional tricuspid orifice apically and dividing the right ventricle into two portions. The main haemodynamic abnormality leading to symptoms is tricuspid valve incompetence. The clinical spectrum is broad; patients may be asymptomatic or experience right-sided heart failure, cyanosis, arrhythmias and sudden cardiac death (SCD). Many Ebstein’s anomaly patients have an interatrial communication (secundum atrial septal defect (ASD II) or patent foramen ovale). Other structural anomalies may also be present, including a bicuspid aortic valve (BAV), ventricular septal defect (VSD), and pulmonary stenosis. The morphology of the tricuspid valve in Ebstein anomaly, and consequently the clinical presentation, is highly variable. The tricuspid valve leaflets demonstrate variable degrees of failed delamination (separation of the valve tissue from the myocardium) with fibrous attachments to the right ventricular endocardium.
The displacement of annular attachments of septal and posterior (inferior) leaflets into the right ventricle toward the apex and right ventricular outflow tract is the hallmark finding of Ebstein anomaly.

Varicose veins (venous insufficiency syndrome) are dilated, tortuous veins due to reverse venous flow. All the given veins can be affected from this condition. As the patient has varicose veins over lateral aspect of ankle, the short saphenous vein is affected. The great or long saphenous vein travels along the medial aspect of the ankle

Absolute contraindications for fibrinolytic use in STEMI

Prior intracranial haemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed head trauma or facial trauma within 3 months
Intracranial or intraspinal surgery within 2 months
Severe uncontrolled hypertension (unresponsive to emergency therapy)
For streptokinase, prior treatment within the previous 6 months

Class I indications (i.e., the benefit greatly outweighs the risk, and the treatment should be administered): -Structural heart disease, sustained VT
-Syncope of undetermined origin, inducible VT or VF at electrophysiologic study (EPS)
-Left ventricular ejection fraction (LVEF) ≤35% due to prior MI, at least 40 days post-MI, NYHA class II or III
-LVEF ≤35%, NYHA class II or III
-LVEF ≤30% due to prior MI, at least 40 days post-MI
-LVEF ≤40% due to prior MI, inducible VT or VF at EPS

Class IIa indications (i.e., the benefit outweighs the risk and it is reasonable to administer the treatment):
-Unexplained syncope, significant LV dysfunction, nonischaemic cardiomyopathy
-Sustained VT, normal or near-normal ventricular function
-Hypertrophic cardiomyopathy with 1 or more major risk factors
-Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) with 1 or more risk factors for sudden cardiac death (SCD)
-Long QT syndrome, syncope or VT while receiving beta-blockers
-Nonhospitalized patients awaiting heart transplant
-Brugada syndrome, syncope or VT
-Catecholaminergic polymorphic VT, syncope or VT while receiving beta-blockers
-Cardiac sarcoidosis, giant cell myocarditis, or Chagas disease

Infective endocarditis (IE) is an infectious inflammation of the endocardium that affects the heart valves. The condition is a result of bacteraemia, which is most commonly caused by dental procedures, surgery, distant primary infections, and nonsterile injections. IE clinically presents with either an acute or subacute course. Acute disease is usually caused by Staphylococcus aureus and causes rapid endocardium destruction. Subacute progression is most commonly caused by viridans streptococci species and generally affects individuals with pre-existing damage to the heart valves, structural heart defects, or the presence of prosthetic valves. Clinical features include constitutional symptoms (fatigue, fever/chills, malaise) in combination with signs of pathological cardiac changes (e.g., new or changed heart murmur, heart failure signs) and possibly manifestations of subsequent damage to other organs (e.g., glomerulonephritis, septic embolic stroke). Diagnosis is made based on the Duke criteria, whose main features include positive blood cultures and evidence of endocardial involvement in echocardiography. Initial treatment of IE consists of empiric IV antibiotic therapy, which is then adapted to blood culture results and continued for four to six weeks. Prophylaxis is only administered in specific circumstances, e.g., in patients with pre-existing heart conditions undergoing dental or surgical procedures. If left untreated, infective endocarditis can be fatal within a few weeks.

Atrial septal defect (ASD) is one of the more commonly recognized congenital cardiac anomalies presenting in adulthood. ASD is characterized by a defect in the interatrial septum allowing pulmonary venous return from the left atrium to pass directly to the right atrium. Depending on the size of the defect, size of the shunt, and associated anomalies, this can result in a spectrum of disease ranging from no significant cardiac sequelae to right-sided volume overload, pulmonary arterial hypertension, and even atrial arrhythmias.

With the routine use of echocardiography, the detection and, therefore, the incidence of ASD is increased compared to earlier incidence studies using catheterization, surgery, or autopsy for diagnosis. The subtle physical examination findings and often minimal symptoms during the first 2-3 decades of life contribute to a delay in diagnosis until adulthood, the majority (more than 70%) of which is detected by the fifth decade of life.

J waves in an ECG is associated with hypothermia, hypercalcemia, the Brugada syndrome, and idiopathic ventricular fibrillation. The other responses are all associated with atrial myxoma

The overall diagnosis is Fallot’s tetralogy. Ventricular septal defect with left to right shunt is indicated by drop of oxygen saturation from left atrium to left ventricle. Pulmonary stenosis is indicated by the pressure difference between the pulmonary artery and the right atrium. There is oxygen saturation drop from the left ventricle to the aorta which can be due to the overriding aorta.

The patient is diabetic and at major risk for an MI. The duration and location of the pain, the cold sweats and the difficulty in speaking suggest an MI. Pericarditis pain worsens upon inspiration or in a supine position. Patients usually lean forward to relieve the pain. (antalgic position). Pneumothorax pain is pleuritic in regards to location. Pulmonary embolism is accompanied by dyspnoea and pleuritic pain. Costochondritis pain is localized at the costochondral junction and it worsens with movements of the chest such as coughing or sneezing.

Patients with a long QT wave syndrome are prone to recurrent syncope if they have Torsade’s de pointes since it degenerates into fibrillation of the ventricles.

The diagnosis is acute inferior ST elevation myocardial infarction so the most appropriate management is primary angioplasty.

Pacemaker spikes on the ECG indicate that pacemaker is functioning. The most probable cause for this presentation is the change of the position of the tip of the pacing wire. Increasing the voltage will solve the problem. If it works, repositioning of the pacing wire should be done.

Becks triad (hypotension, elevated systemic venous pressure, often with jugular venous distention and muffled heart sounds) is a characteristic collection of clinical findings found in cardiac tamponade. Pulsus paradoxus is also associated with it. The history and clinical findings in this scenario are compatible with the diagnosis of cardica tamponade. The normal respiratory examination excludes tension pneumothorax.

According to the history the patient has cardiogenic shock and pulmonary oedema. On-going ischaemia is indicated by persisting symptoms. So the most appropriate management is coronary angiography and rescue PCI. There are no indications for blood transfusion at this moment and it will aggravate the pulmonary oedema. Haemodialysis, beta blockers and furosemide cannot be given due to low blood pressure.

The chief symptoms of pericarditis comprise of sudden onset of sharp chest pain, that is relieved by bending forward and is exacerbated by deep inspiration. Symptoms can vary among the individuals but these are the chief symptoms.

The cardinal symptom of the cardiac tamponade is a shocked patient with tachycardia and congested neck veins.