1. Coronary angioplasty



CARDIOVASCULAR ANSWERS

FRACP 2000 questions

Question 1

Diastolic dysfunction

Diastolic heart failure may be caused by increased resistance to ventricular inflow and reduced ventricular diastolic capacity (constrictive pericarditis and restrictive, hypertensive, and hypertrophic cardiomyopathy), impaired ventricular relaxation (acute myocardial ischaemia, hypertrophic cardiomyopathy), and myocardial fibrosis and infiltration (dilated, chronic ischaemic, and restrictive cardiomyopathy).

Question 2

Hypotension

Acute aortic dissection presents with the sudden onset of pain, which is often described as very severe and tearing and is associated with diaphoresis. The pain may be localised to the front or back of the chest, often the interscapular region, and typically migrates with propagation of the dissection. Other symptoms include syncope, dyspnoea, and weakness. Physical findings may include hypertension or hypotension, loss of pulses, aortic regurgitation, pulmonary oedema, and neurological findings due to carotid artery obstruction (hemiplegia, hemianaesthesia) or spinal cord ischaemia (paraplegia). Hypotension is more common in dissections of the ascending aorta (20-25%) & may be due to blood loss acute aortic incompetence or tamponade. Bowel ischaemia, haematuria, and myocardial ischaemia have all been observed. MKSAP says dissection involves coronary artery causing MI in only 1% of cases. These clinical manifestations reflect complications resulting from the dissection occluding the major arteries. Furthermore, clinical manifestations may result from the compression of adjacent structures (e.g., superior cervical ganglia, superior vena cava, bronchus, oesophagus) by the expanding dissection aneurysm and include Horner's syndrome, superior vena caval syndrome, hoarseness, dysphagia, and airway compromise. Haemopericardium and cardiac tamponade may complicate a type A lesion with retrograde dissection. Acute aortic regurgitation is an important and common (over 50 percent) complication of proximal dissection. This is the outcome of either a circumferential tear that widens the aortic root or a disruption of the annulus by dissecting haematoma that tears a leaflet(s) or displaces it below the line of closure. Signs of aortic regurgitation include bounding pulses, a wide pulse pressure, a diastolic murmur often radiating to the right sternal border, and evidence of congestive heart failure. The clinical manifestation depends on the severity of the regurgitation.

Question 3

Proceed to surgery

Bundle branch block may occur in a variety of conditions. In subjects without structural heart disease, right bundle branch block is seen more commonly than left bundle branch block. Right bundle branch block also occurs with heart disease, both congenital (e.g., atrial septal defect) and acquired (e.g., valvular, ischaemic). Left bundle branch block is often a marker of one of four underlying conditions: ischaemic heart disease, long-standing hypertension, severe aortic valve disease, and cardiomyopathy. Bundle branch blocks may be chronic or intermittent. A bundle branch block may be rate-related; for example, often it occurs when the heart rate exceeds some critical value.

ST segment elevation in the Brugada syndrome is often associated with RBBB; the role of this conduction defect is a matter of some controversy. Many investigators have challenged the dominant opinion that the conduction delay in the right ventricle is an integral part of the syndrome. There is no correlation between RBBB and sudden cardiac death, whereas a definite link exists between the magnitude of ST segment elevation and the incidence of life-threatening arrhythmic events in patients with Brugada syndrome.

From Fiona Stewart’s article “Cardiac Risk Assessment for Non Cardiac Surgery”, Cardiac risk is determined by patient characteristics, surgical factors & anaesthetic factors. Superficial surgery has low risk ( ................
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