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THE BEST CARDIOLOGISTS NEAR HSR LAYOUT Coronary angiography (cardiac catheterisation) This procedure enables the cardiologist to visualise the coronary arteries . It is the standard against which other less-invasive investigations are assessed. Selective catheterisation of the right and left coronary ostia is performed. Contrast is then injected into the vessels and digital tape or disc storage of the images obtained. In most hospitals the patient is admitted on the morning of the test and allowed to go home that afternoon. The procedure is most often performed through the femoral artery (Judkins technique) . This artery can be punctured through the skin under local anaesthetic. A fine softtipped guide wire is then advanced into the artery and the needle withdrawn (Seldinger method). A short guiding sheath can then be placed over the wire and long cardiac catheters advanced through this sheath along a long guide wire into the femoral artery and up via the aorta to the aortic arch. The catheter and wire are advanced under X-ray control. Usually one catheter with a curved tip (pig-tail catheter; is advanced across the aortic valve into the left ventricle where left ventricular pressures are measured via a pressure transducer connected to the other end of the catheter. Measurement of the left ventricular end-diastolic pressure gives an indication of left ventricular function. Raised end-diastolic pressure (over 15 mmHg) suggests left ventricular dysfunction . The catheter is then connected to a pressure injector. This enables injection of a large volume of contrast over a few seconds; for example, 35 mL at 15 mL/second. X-ray recording during injection produces a left ventriculogram , Here left ventricular contraction can be assessed and the ejection fraction (percentage of end-diastolic volume ejected with each systole) estimated. The normal is 60% or more. The figure obtained by this method tends to be higher than that produced by the nuclear imaging method—gated blood pool scanning. The guide wire is reintroduced and the catheter withdrawn to be replaced by one shaped to fit into the right or left coronary orifice...
THE BEST CARDIOLOGISTS IN YELAHANKA Aortic regurgitation The incompetent aortic valve allows regurgitation of blood from the aorta to the left ventricle during diastole for as long as the aortic diastolic pressure exceeds the left ventricular diastolic pressure. Symptoms: Occur in the late stages of disease and include exertional dyspnoea, fatigue, palpitations (hyperdynamic circulation) and exertional angina. General signs: Marfan’s syndrome may be obvious. The pulse and blood pressure: The pulse is characteristically collapsing; there may be a wide pulse pressure. The neck: Prominent carotid pulsations (Corrigan’s sign). Palpation: The apex beat is characteristically displaced and hyperkinetic. A diastolic thrill may be felt at the left sternal edge when the patient sits up and breathes out. Auscultation): A2 (the aortic component of the second heart sound) may be soft; a decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and extending for a variable time into diastole—it is loudest at the third and fourth left intercostal spaces; a systolic ejection murmur is usually present (due to associated aortic stenosis or to torrential flow across a normal diameter aortic valve). Signs indicating severe chronic aortic regurgitation: Collapsing pulse; wide pulse pressure; long decrescendo diastolic murmur; left ventricular S3 (third heart sound); soft A2; signs of left ventricular failure. Causes of chronic aortic regurgitation: (i) Rheumatic (rarely the only murmur in this case), congenital; (ii) aortic root dilatation—Marfan’s syndrome, dissecting aneurysm. 8• THE PATIENT WITH A MURMUR 305 a b Valve cusps often thickened and calcified Left ventricle may be hypertrophied Ascending aorta may be dilated Systole Diastole S1 A2 P2 S1 Ejection click (Suggests congenital AS) Normal Mild S1 S1 Moderate S1 P2 A2 S1 Severe Reversed S2 Single (S2)
CARDIOLOGIST IN YELAHANKA SECOND DEGREE AV BLICK There are two basic types of second-degree AV block: AV nodal Möbitz type I (Wenckebach) heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (Fig 3.10) (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB (Fig 3.11), since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block (Fig 3.12). There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as
THE BEST CARDIOLOGISTS IN YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
THE BEST CARDIOLOGISTS IN YELAHANKA Indications for coronary angiography 1 Angina not responding to medical treatment in a patient without contraindications (e.g. extreme old age—usually older than about 85 these days—or severe co-morbidities) to cardiac surgery or angioplasty. 2 Continuing chest pain whose cause is not clear despite non-invasive investigations. The procedure may well be worthwhile if it reveals normal coronary arteries and prevents a patient being treated unnecessarily with more and more anti-anginal drugs. Non-invasive investigations are more often equivocal in women, and more women than men are found to have normal coronaries at angiography. 3 Preparation of a patient older than 35 or so for some other cardiac surgery (e.g. valve replacement). The surgeon needs to know whether significant coronary disease is present so that coronary grafting can be performed at the time of valve surgery. Otherwise, patients are at risk of ischaemic problems in the post-operative period. 4 Diagnosis of cardiomyopathy (p. 267) by excluding coronary artery disease and infarction as the cause of angina or cardiac failure. These patients may benefit from revascularisation if significant coronary disease is also present (‘ischaemic cardiomyopathy’). 5 Investigation of patients following myocardial infarction. Routine transfer to a centre with angiographic facilities after successful thrombolytic treatment is a grade D recommendation. There is no proof that a patient without continuing ischaemia has an improved prognosis when angiography and revascularisation are carried out routinely after infarction. The Open Artery Trial results suggest there is no benefit compared with optimal medical treatment for patients without ischaemic symptoms in having an occluded vessel opened five days or more after an infarction. However, spontaneous or induced ischaemia (by modified stress testing or perfusion imaging) leads to a grade B recommendation for angiography and intervention. The management of post-infarct patients is definitely easier if the coronary anatomy is known, and many units adopt the policy of early (within a week) angiography of infarct patients without contraindications to revascularisation. 6 Non-ST elevation acute coronary syndromes (p. 156). 7 Acute myocardial infarction in a unit where primary angioplasty can be performed
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