ĐĎॹá>ţ˙ ţ˙˙˙ýţ˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙ěĽÁ7 řż=bjbjUU Ř7|7|9˙˙˙˙˙˙lfffffffzœhœhœh8Ôh\0iząĹr@k\n(„n„n„nżqżqżqşÁźÁźÁźÁBţÁŹŞĂŹVĹ#Ç CɨVĹfżqCq|żqżqżqVĹYwff„n„nżkĹYwYwYwżqBf„nf„nşÁYwżqşÁYwYwg|⊹¤ ff~ž„n4k Ŕۍ]ă}Ŕz"dœhv..ź~ž<Ĺ0ąĹD˝:ëÉ/v*ëÉ~žYwzzffffŮCARDIOVASCULAR 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 (<1%), intra abdominal surgery has moderate risk (<5%). In patients who are able to exercise to at least 75% of predicted maximum heart rate for age without ischaemic changes, cardiac events are rare (0-7% quoted for patients with peripheral vascular disease). A study of 1081 patients awaiting vascular surgery has shown that routine thallium scanning adds little to clinical assessment for patients at either low or high risk, but it may be helpful in risk stratification in patients assessed to be at moderate risk. Little work has been done on the role of dobutamine stress echo in risk assessment for surgery. In one study, 15 of 35 patients with new regional motional abnormality went on to have cardiac events, while no patient with a normal scan had a cardiac event. Question 4 Septal: posterior wall ratio of > 1.3:1 Hypertrophic cardiomyopathy is characterised by left ventricular hypertrophy, typically of a nondilated chamber, without obvious cause such as hypertension or aortic stenosis. Two features of the disease have attracted the greatest attention: (1) heterogeneous left ventricular (LV) hypertrophy, often with preferential hypertrophy of the interventricular septum resulting in asymmetric septal hypertrophy (ASH); and (2) a dynamic left ventricular outflow tract pressure gradient, related to a narrowing of the subaortic area as a consequence of the midsystolic apposition of the anterior mitral valve leaflet against the hypertrophied septum, i.e., systolic anterior motion (SAM) of the mitral valve Initial studies of this disease emphasised the dynamic "obstructive" features, and it has been termed idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), and muscular subaortic stenosis. It has become clear, however, that only about one-quarter of patients with hypertrophic cardiomyopathy demonstrate an outflow tract gradient. The ubiquitous pathophysiological abnormality is not systolic but rather diastolic dysfunction, characterised by increased stiffness of the hypertrophied muscle that results primarily from an abnormality in calcium handling with attendant intracellular calcium overload. This results in elevated diastolic filling pressures and is present despite a hyperdynamic left ventricle. The pattern of hypertrophy is distinctive in hypertrophic cardiomyopathy and differs from that seen in secondary hypertrophy (as in hypertension). Most patients have striking regional variations in the extent of hypertrophy in different portions of the left ventricle, and the majority demonstrate a ventricular septum whose thickness is disproportionately increased when compared with the free wall. Other patients may demonstrate disproportionate involvement of the apex or left ventricular free wall; 10 percent or more of patients have concentric involvement of the ventricle. All, however, show a bizarre and disorganised arrangement of cardiac muscle cells in the septum, with disorganisation of the myofibrillar architecture, whether or not a systolic intraventricular pressure gradient is present, along with a variable degree of myocardial fibrosis and thickening of the small intramural coronary arteries. About half of all cases of hypertrophic cardiomyopathy have a positive family history compatible with autosomal-dominant transmission. About 40 percent of these are associated with mutations of the beta cardiac myosin heavy chain gene on chromosome 14, with certain mutations associated with prognoses that are more malignant. About 15 percent have a mutation of the cardiac troponin T gene, 10 percent a mutation of myosin binding protein L, and about 5 percent a mutation of the  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/alpha/black/med/base/glyph.gif" \* MERGEFORMATINET tropomyosin gene. The remainder of familial cases presumably are due to mutations of other genes. Echocardiography studies have confirmed that about one-third of the first-degree relatives (i.e., parents, siblings, and children) of patients with familial hypertrophic cardiomyopathy have evidence of the disease, although in many of these patients the extent of hypertrophy is mild, no outflow tract pressure gradient is present, and symptoms are not prominent. Since the hypertrophic characteristics may not be apparent in childhood and often appear first in adolescence, a single normal echocardiogram in a child does not entirely exclude the presence of the disease. In contrast to the obstruction produced by a fixed narrowed orifice, such as valvular aortic stenosis, the pressure gradient in hypertrophic cardiomyopathy, when present, is dynamic and may change between examinations and even from beat to beat. Obstruction appears to result from further narrowing of an already small left ventricular outflow tract by SAM of the mitral valve against the hypertrophied septum. While SAM may be found in a variety of other conditions besides hypertrophic cardiomyopathy, it is always found when obstruction is present in hypertrophic cardiomyopathy. Three basic mechanisms are involved in the production of the dynamic pressure gradient: (1) increased left ventricular contractility, (2) decreased ventricular volume (preload), and (3) decreased aortic impedance and pressure (afterload). Interventions that increase myocardial contractility, such as exercise, isoproterenol, and digitalis glycosides, and those that reduce ventricular volume, such as the Valsalva manoeuvre, sudden standing, nitroglycerin, amyl nitrite, or tachycardia, all may cause an increase in the gradient and the murmur. Conversely, elevation of arterial pressure by phenylephrine, squatting, sustained handgrip, augmentation of venous return by passive leg raising, and expansion of the blood volume all increase ventricular volume and ameliorate the gradient and murmur.   Question 5 False aneurysm Since cardiac catheterisation is an invasive technique, it is not surprising that potential complications include death, myocardial infarction, stroke, perforation of the heart or great vessels, and local vascular problems. Table 229-2 lists those characteristics associated with increased risk of death from cardiac catheterisation. PRIVATEINCLUDEPICTURE \d "/images/spacer.gif"Table 229-2 Patient Characteristics Associated With Increased Mortality From Cardiac CatheterisationINCLUDEPICTURE \d "/images/spacer.gif"Age: Infants (<1 month old) and the elderly (>80 years old) are at increased risk of death during cardiac catheterisation. Elderly women appear to be at higher risk than elderly men. Functional class: Mortality in class IV patients is more than 10 times greater than in class I–II patients. Severity of coronary obstruction: Mortality for patients with left main coronary artery disease is more than 10 times greater than in patients with one- or two-vessel disease. Valvular heart disease: Especially when severe and combined with coronary disease, is associated with a higher risk of death at cardiac catheterisation than coronary artery disease alone Left ventricular dysfunction: Mortality in patients with a left ventricular ejection fraction <30 percent is more than 10 times greater than in patients with an ejection fraction INCLUDEPICTURE \d \z "/__chars/greater/special/ge/black/med/base/glyph.gif"50 percent. Severe non cardiac disease: Patients with renal insufficiency, insulin-requiring diabetes, advanced cerebrovascular and/or peripheral vascular disease, or severe pulmonary insufficiency have an increased incidence of death and other major complications from cardiac catheterisation.INCLUDEPICTURE \d "/images/spacer.gif" Question 6 A Doppler cardiac echo is shown. It shows alternating positive and negative deflections from the midline and there are 2 cycles for each cardiac cycle timed by ECG – one cycle either side of the midline. This most likely represents? A) AI B) AS and MI C) AI and AS D) AS E) AS and MS Question 7 Pericarditis  INCLUDEPICTURE "http://www.harrisonsonline.com/images/Chapters/ch228fg18.gif" \* MERGEFORMATINET  FigurePRIVATE "TYPE=PICT;ALT=figure 228-18"INCLUDEPICTURE \d \z "/images/Chapters/ch228fg18.gif" Acute pericarditis often produces diffuse ST-segment elevations (in this case in leads I, II, aVF, and V2 to V6) due to a ventricular current of injury. Note also the characteristic PR-segment deviation (opposite in polarity to the ST segment) due to a concomitant atrial injury current. Question 8 Renovascular hypertension A simple explanation for renal vascular hypertension is that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system. Circulating angiotensin II elevates arterial pressure by directly causing vasoconstriction, by stimulating aldosterone secretion with resulting sodium retention, and/or by stimulating the adrenergic nervous system. In practice, only about one-half of patients with renovascular hypertension have an absolute elevation in renin activity in peripheral plasma, although when renin measurements are referenced against an index of sodium balance, a much higher fraction have inappropriately high values. Activation of the renin-angiotensin system also has been offered as an explanation for the hypertension in both acute and chronic renal parenchymal disease. In this formulation, the only difference between renovascular and renal parenchymal hypertension is that the decreased perfusion of renal tissue in the latter case results from inflammatory and fibrotic changes involving multiple small intrarenal vessels. There are enough differences between the two conditions, however, to suggest that other mechanisms are active in renal parenchymal disease. Question 9 Terfenadine Recognised interaction of erythromycin & Terfenadine – Erythromycin inhibits cytochrome P450 3A4 in liver & gut wall. Terfenadine is normally metabolised by CYP 3A4, so inhibition of the enzyme by erythromycin increases serum level of unchanged terfenadine, which causes prolonged QT & potentially Torsades de Pointes. Similar reactions can occur when Ketaconazole & grapefruit juice (enzyme inhibiters) are given concomitantly with terfenadine, cisapride or astemizole. Question 10 Cessation of smoking Non drug therapeutic intervention is probably indicated in all patients with sustained hypertension and probably in most with labile hypertension. The general measures employed include (1) relief of stress, (2) dietary management, (3) regular aerobic exercise, (4) weight reduction (if needed), and (5) control of other risk factors contributing to the development of arteriosclerosis Cigarette smoking is not a risk factor for the development of hypertension; however, hypertensives who smoke are at a greater risk of developing malignant hypertension and of dying from hypertension. Question 11 Decrease calorie intake, decrease cholesterol and organise an exercise program Question 12 independent of cholesterol FRACP 1999 (Paper 1) increase in hypertension In the Framingham study, 392 persons developed congestive heart failure. Hypertension preceded heart failure in 91% of the patients, and by multivariate analysis, hypertension was the most important risk factor for the development of heart failure (Levy et al, 1996). Among hypertensive subjects, myocardial infarction, diabetes, left ventricular hypertrophy, and valvular heart disease were predictive of increased risk for CHF in both sexes. Therefore, in order to reduce the incidence of heart failure, aggressive strategies must be taken to identify and treat hypertension. Initial event in cardiac muscle contraction calmodulin calcium mediated opening of T channels ( adrenoceptor mediated opening of calcium channels decreased calcium influx actin-myosin interaction 5 days Steady state concentration is independent of loading dose Question 4 ?Syncope – is listed as risk factor for HOCM, does this also apply for dilated cardiomyopathy? Identification of Patients at Risk for Sudden Cardiac Death Primary prevention of cardiac arrest depends on the ability to identify individual patients at high risk. One must view the problem in the context of the total number of events and the population pools from which they are derived. In Fig 39-2A, the inverted triangle demonstrates that the annual incidence of SCD among an unselected adult population is 1 to 2 per 1000 population, largely reflecting the prevalence of those coronary heart disease patients among whom SCD is the first clinically recognised manifestation (20 to 25 percent of first coronary events are SCD). The incidence (percent per year) increases progressively with addition of identified coronary risk factors to populations free of prior coronary events. The most powerful factors are age, elevated blood pressure, LV hypertrophy, cigarette smoking, elevated serum cholesterol level, obesity, and non-specific electrocardiographic abnormalities. These coronary risk factors are not specific for SCD but rather represent increasing risk for all coronary deaths. The proportion of coronary deaths that are sudden remains at approximately 50 percent in all risk categories. Despite the marked relative increased risk of SCD with addition of multiple risk factors (from 1 to 2 per 1000 population per year in an unselected population to as much as 50 to 60 per 1000 in subgroups having multiple risk factors for coronary artery disease), the absolute incidence remains relatively low when viewed as the relationship between the number of individuals who have a preventive intervention and the number of events that can be prevented. Specifically, a 50 percent reduction in annual SCD risk would be a huge relative decrease but would require an intervention in up to 200 unselected individuals to prevent one sudden death. These figures highlight the importance of primary prevention of coronary heart disease. Control of coronary risk factors may be the only practical method to prevent SCD in major segments of the population, because of the paradox that the majority of events occur in the large unselected subgroups rather than in the specific high-risk subgroups (compare "Events/Year" with "Percent/Year" in Fig 39-2A). Under most conditions of higher level of risk, particularly those indexed to a recent major cardiovascular event (e.g., MI, recent onset of heart failure, survival after out-of-hospital cardiac arrest), the highest risk of sudden death occurs within the initial 6 to 18 months and then decreases toward baseline risk of the underlying disease (Fig 39-2B). Accordingly, preventive interventions are most likely to be effective when initiated early.  INCLUDEPICTURE "http://www.harrisonsonline.com/images/Chapters/ch39fg2.gif" \* MERGEFORMATINET  PRIVATE "TYPE=PICT;ALT=figure 39-2"INCLUDEPICTURE \d \z "/images/Chapters/ch39fg2.gif" FIGURE 39-2: A. Incidence of sudden and nonsudden cardiac deaths in population subgroups, and the relation of total number of events per year to incidence figures. Approximations of subgroup incidence figures, and the related population pool from which they are derived, are presented. Approximately 50 percent of all cardiac deaths are sudden and unexpected. The incidence triangle on the left ("Percent/Year") indicates the approximate percentage of sudden and nonsudden deaths in each of the population subgroups indicated, ranging from the lowest percentage in unselected adult populations (0.1 to 2 percent per year) to the highest percentage in patients with VT or VF during convalescence after an MI (approximately 50 percent per year). The triangle on the right indicates the total number of events per year in each of these groups, to reflect incidence in context with the size of the population subgroups. The highest risk categories identify the smallest number of total annual events, and the lowest incidence category accounts for the largest number of events per year. (EF, ejection fraction; VT, ventricular tachycardia; VF, ventricular fibrillation; MI, myocardial infarction.) B. Time dependence of risk among survivors of out-of-hospital cardiac arrest. Recurrence risk is highest in the first 6 months of the index event. Survival is expressed as a percentage. High risk is best predicted initially by an ejection fraction INCLUDEPICTURE \d \z "/__chars/less/special/le/black/med/base/glyph.gif"35 percent during the first 6 months, and subsequently persistent inducibility of VT during electrophysiological testing becomes an added major risk. n = 101 at t = 0. [After T Furukawa et al, in RJ Myerberg et al, Circulation 85(Suppl 1):2, 1992. Reproduced with permission of the American Heart Association.]  For patients with acute or prior clinical manifestations of coronary heart disease, high-risk subgroups having a much higher ratio of SCD risk to population base can be identified. The acute, convalescent, and chronic phases of MI provide large population subsets with more highly focused risk. The potential risk of cardiac arrest from the onset through the first 72 h after acute MI (the acute phase) may be as high as 15 to 20 percent. The highest risk of SCD in relation to MI is found in the subgroup that has experienced sustained VT or VF during the convalescent phase (3 days to 8 weeks) after MI. A greater than 50 percent mortality in 6 to 12 months has been observed among these patients, when managed with conservative medical therapy, and at least 50 percent of the deaths are sudden. Since the development of aggressive intervention techniques, the incidence appears to have fallen dramatically. After the acute phase of MI, long-term risk for total mortality and SCD are predicted by a number of factors. The most important for both SCD and non-SCD is the extent of myocardial damage sustained during the acute event. This is measured by the degree of reduction in the ejection fraction (EF), functional capacity, and/or the occurrence of heart failure. Increasing frequency of post infarction PVCs, with a plateau above the range of 10 to 30 PVCs per hour on 24-h ambulatory monitor recordings, also indicates increased risk, but advanced forms (salvos, nonsustained VT) are probably the more powerful predictor. PVCs interact strongly with decreased left ventricular EF. The combination of frequent PVCs, salvos or nonsustained VT, and an EF INCLUDEPICTURE \d \z "/__chars/less/special/le/black/med/base/glyph.gif"30 percent identifies patients who have an annual risk of 20 percent. The risk falls off sharply with decreasing PVC frequency and the absence of advanced forms, as well as with higher EF. Despite the risk implications of post infarction PVCs, improved outcome as a result of PVC suppression has not been demonstrated. The extent of underlying disease due to any cause and/or prior clinical expression of risk of SCD (i.e., survival after out-of-hospital cardiac arrest not associated with acute MI) identify patients at very high risk for subsequent (recurrent) cardiac arrest. Survival after out-of-hospital cardiac arrest predicts up to a 30 percent 1-year recurrent cardiac arrest rate in the absence of specific interventions (see below). A general rule is that the risk of SCD is approximately one-half the total cardiovascular mortality rate. Thus, the SCD risk is approximately 20 percent per year for patients with advanced coronary heart disease or dilated cardiomyopathy severe enough to result in a 40 percent 1-year total mortality rate. As shown in Fig 39-2A, the very high risk subgroups provide more focused population fractions ("Percent/Year") for predicting cardiac arrest or SCD; but the impact on the overall population, indicated by the absolute number of preventable events ("Events/Year"), is considerably smaller. The requirements for achieving a major population impact are effective prevention of the underlying diseases and/or new epidemiological probes that will allow better resolution of subgroups within large general populations. It is possible to regard the high-risk profile for Hypertrophic Cardiomyopathy as characterised by one or more of the following clinically identifiable risk factors: family history of HCM-related sudden death; exertional syncope (particularly if repetitive and in the young); multiple-repetitive or prolonged, nonsustained, ventricular tachycardia on ambulatory (Holter) ECG; or extreme left-ventricular hypertrophy (wall thickness INCLUDEPICTURE \d \z "/__chars/greater/special/ge/black/med/base/glyph.gif"30 mm) FRACP 1999 (Paper 2) reassure Wenckebach/ Mobitz type 1 2o heart block is characterised by progressive PR interval prolongation prior to block of an atrial impulse. The resultant pause is less than compensatory & the PR interval of the first conducted impulse is shorter than the last conducted impulse prior to the blocked P wave. This type of block is almost always localised within the AV node & associated with a normal QRS duration. It most commonly occurs as a transient abnormality with inferior wall infarction or with drug intoxication – digitalis, calcium channel blockers, and beta-blockers. It is also seen occasionally in normal individuals with heightened vagal tone. Mobitz Type 1 rarely progresses to CHB other than in the setting of acute inferior wall infarction. Even then the heart block is usually well tolerated because the escape pacemaker usually arises in the proximal bundle of His & provides a stable rhythm. The presence of Mobitz type 1 rarely requires aggressive therapy; observation is usually sufficient. In contrast Mobitz type 2 has a high incidence of progression to CHB with an unstable escape rhythm & usually requires pacemaker insertion  INCLUDEPICTURE "http://www.harrisonsonline.com/images/Chapters/ch230fg7.gif" \* MERGEFORMATINET  FIGURE 230-7: A. Mobitz type I second-degree AV block. Intracardiac recordings demonstrate that the PR prolongation (320, 615 ms) is localized to the AV node (AH 240, 535 ms, respectively). HBE, His bundle electrogram; A, atrium; H, His; V, ventricle. Time lines (T) = 100 ms. B. Mobitz type II second-degree AV block. Intracardiac recordings document block below the His bundle. (From ME Josephson, SF Seides, Clinical Cardiac Electrophysiology: Techniques and Interpretations. Philadelphia, Lea & Febiger, 1979.) A sixty year old female who is asymptomatic presents for pre operative assessment for an inguinal hernia repair. No chest pain on exertion. Physical examination is normal. ECG: sinus rhythm, right axis deviation, right bundle branch block with some ST ( (if any). Next best action: dobutamine stress echo ETT Dipyridamole thallium scan Coronary angiography Proceed with surgery Question 3 An 87 year old man presents with light headedness on a hot day. He has no other significant medical history. Which of the following in this otherwise well elderly gentleman is going to be the cause of his symptoms. A) Basal stimulation his aldosterone and renin B) Baroreceptor ?insensitivity C) Atrial naturetic factor D) Thirst Question 4 Posterior MI The ECG leads are more helpful in localizing regions of Q wave than non-Q-wave ischaemia. For example, acute anterior wall ischaemia leading to Q-wave infarction is reflected by ST elevations or increased T-wave positivity in one or more of the praecordial leads (V1 to V6) and leads I and aVL. Anteroseptal ischaemia produces these changes in leads V1 to V3, apical or lateral ischaemia in leads V4 to V6. Inferior wall ischaemia produces changes in leads II, III, and aVF. Posterior wall ischaemia may be indirectly recognized by reciprocal ST depressions in leads V1 to V3. Prominent reciprocal ST depressions in these leads also occur with certain inferior wall infarcts, particularly those with posterior or lateral wall extension. Right ventricular ischaemia usually produces ST elevations in right-sided chest leads. When ischaemic ST elevations occur as the earliest sign of acute infarction, they are typically followed within a period ranging from hours to days by evolving T-wave inversions and often by Q waves occurring in the same lead distribution. (T-wave inversions due to evolving or chronic ischaemia correlate with prolongation of repolarisation and are often associated with QT lengthening.) Reversible transmural ischaemia, for example, due to coronary vasospasm (Prinzmetal's variant angina), may cause transient ST-segment elevations without development of Q waves. Depending on the severity and duration of such ischaemia, the ST elevations may either resolve completely in minutes or be followed by T-wave inversions that persist for hours or even days. Patients with ischaemic chest pain who present with deep T-wave inversions in multiple praecordial leads (e.g., V1 to V4) with or without cardiac enzyme elevations typically have severe obstruction in the left anterior descending coronary artery system. In contrast, patients whose baseline ECG already shows abnormal T-wave inversions may develop T-wave normalization (pseudonormalisation) during episodes of acute transmural ischaemia. Question 5 Which of the following is least likely to be involved in vascular smooth muscle contraction? A) Increased calmodulin activation B) Myosin actin interaction C) Formation of cross links D) Fall in intracellular calcium E) Phosphorylation of myosin Question 6 A 90 year old man with a history of hypertension, acute myocardial infarction ten years ago and total knee replacement 4 years ago presents for an elective inguinal herniorraphy. He has not had a history of recent angina pectoris. On examination you note a 2/4 ejection systolic murmur at the base of the heart that radiates to the carotids. His BP is 170/103. The surgical resident enquires whether this man is fit for surgery. An ABG shows a pH of 7.4, PO2 70 and PCO2 40. Your advice would be: A) Postpone surgery until hypoxia is investigated B) Treat hypertension as this increases risk of intraoperative complications C) This man needs preoperative subcutaneous heparin to prevent DVT D) Postpone operation and perform an exercise stress test and arrange a cardiology consult Question 7 A man is awaiting an elective cholecystectomy. He is said to have been in previously good health. Physical examination reveals a 2/6 ejection systolic murmur in the aortic area and radiates to the carotids. An ECG is shown and said to demonstrate sinus rhythm and left ventricular hypertrophy and right bundle branch block. Which of the following investigations is likely to be most helpful. A) TTE B) carotid doppler C) Coronary angiogram Question 8 Cardioversion within 24 hours Atrial flutter occurs most often in patients with organic heart disease. Flutter may be paroxysmal, in which case there is usually a precipitating factor, such as pericarditis or acute respiratory failure, or it may be persistent. Atrial flutter (as well as AF) is very common during the first week following open-heart surgery. Atrial flutter is usually less long-lived than is AF, although on occasion it may persist for months to years. Most commonly, if it lasts for more than a week, atrial flutter will convert to AF. Systemic embolisation is less common in atrial flutter than in AF. Atrial flutter is characterized by an atrial rate between 250 and 350 beats per minute. Typically, the ventricular rate is half the atrial rate, i.e., approximately 150 beats per minute. If the atrial rate is slowed to <220 beats per minute by antiarrhythmic agents such as quinidine, which also possess vagolytic properties, the ventricular rate may rise suddenly because of the development of 1:1 AV conduction. Classically, flutter waves are seen as regular sawtooth-like atrial activity, most prominent in the inferior leads. When the ventricular response is regular and not a simple fraction of the atrial rate, complete AV block is present, which may be a manifestation of digitalis toxicity. Activation mapping suggests that atrial flutter is a form of atrial re-entry localized to the right atrium. The most effective treatment of atrial flutter is direct-current cardioversion, which can be accomplished at low energy (25 to 50 Wˇs) under mild sedation. Higher energies (100 to 200 Wˇs) are often used because they are less likely to cause atrial fibrillation, which not infrequently occurs following lower energy delivery. In patients who develop atrial flutter following open-heart surgery or recurrent flutter in the setting of acute myocardial infarction, particularly if they are being treated with digitalis, atrial pacing (using temporary pacing wires implanted at the time of operation or a pacing lead inserted into the atrium pervenously) at rates of 115 to 130 percent of the atrial flutter rate can usually convert the atrial flutter to sinus rhythm. Atrial pacing also may result in the conversion of atrial flutter to AF, which allows for easier control of the ventricular response. If immediate conversion of atrial flutter is not mandated by the patient's clinical status, the ventricular response should first be slowed by blocking the AV node with a beta blocker, calcium antagonist, or digitalis. Digitalis is the least effective and occasionally converts atrial flutter into AF. Once AV nodal conduction is slowed with any of these drugs, an attempt to convert flutter to sinus rhythm using a class I (A or C) agent or amiodarone should be made. Increasing doses of the drug selected are administered until the rhythm converts or side effects occur. Quinidine, quinidine-like drugs, flecainide, propafenone, and amiodarone may be useful in preventing recurrences of both atrial flutter and atrial fibrillation.   FRACP 1998 1. Nicotinic acid Three classes of lipid-lowering agents are recommended as first-line therapy against hypercholesterolemia: the bile acid sequestrants or -binding resins; niacin; and the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors. Fibric acid derivatives such as gemfibrozil are second-line agents for hypercholesterolemia and are most effective for lowering of triglycerides.  INCLUDEPICTURE "http://www.harrisonsonline.com/images/spacer.gif" \* MERGEFORMATINET    Table 341-8 Hypolipidemic Agents    INCLUDEPICTURE "http://www.harrisonsonline.com/images/spacer.gif" \* MERGEFORMATINET    Class Mode of Action Lipoprotein Class Affected Dose Side Effects Contraindications Drug Interactions Combined Use with Bile acid–binding resins Interrupts enterohepatic circulation of bile acids;  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET Synthesis of new bile acids and LDL receptors  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET LDL cholesterol 20–30%  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET HDL cholesterol and triglycerides Cholestyramine 8–12 g bid or tid Cholestipol 10–15 g bid or tid Constipation, gastric discomfort, nausea, hemorrhoidal bleeding Biliary track obstruction, gastric outlet obstruction, hypertriglyceridemia  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET Absorption of phenylbutazone, phenobarbital, thyroid hormones, digitalis, warfarin, thiazide diuretics, some antibiotics Nicotinic acid, HMG-CoA reductase inhibitors, gemfibrozil Nicotinic acid  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET Synthesis of VLDL and LDL  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET Triglycerides 25–85%  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET VLDL cholesterol 25–35%  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET LDL cholesterol 15–25% HDL may  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET  Niacin 50–100 mg tid initially then increase to 1.0–2.5 g tid Flushing, tachycardia, atrial arrhythmias, pruritus, dry skin, nausea, diarrhea, hyperuricemia, peptic ulcer disease, glucose intolerance, hepatic dysfunction Peptic ulcer disease, cardiac arrhythmias, liver disease, gout, diabetes mellitus Gemfibrozil, ketoconazole, cyclosporine, warfarin, niacin Bile acid-binding resins, HMG-CoA reductase inhibitors, gemfibrozil CoA reductase inhibitors  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET Cholesterol synthesis  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET LDL receptors  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET LDL cholesterol 25–40%  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET VLDL Lovastatin 10–80 mg/d Pravastatin 10–40 mg/d Simvastatin 5–40 mg/d Fluvastatin20–40 mg/d Atorvastatin 10–80 mg/d Abnormal liver function, myositis  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET Myositis in patients with renal failure and in patients on gemfibrozil, nicotinic acid, or cyclosporine Gemfibrozil, ketoconazole, cyclosporine, warfarin, niacin Bile acid-binding resins Fibric acid derivatives  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET LPL and  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET triglyceride hydrolysis  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET VLDL synthesis  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET LDL catabolism  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET Triglycerides 25–40%  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET or  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET LDL cholesterol  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET HDL Gemfibrozil 600 mg bid  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET Lithogenicity of bile, nausea, abnormal liver functions, myositis Hepatic or biliary disease;  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/down/black/med/base/glyph.gif" \* MERGEFORMATINET dose in renal insufficiency  INCLUDEPICTURE "http://www.harrisonsonline.com/__chars/arrow/special/up/black/med/base/glyph.gif" \* MERGEFORMATINET Anticoagulant activity of warfarin Bile acid-binding resins     INCLUDEPICTURE "http://www.harrisonsonline.com/images/spacer.gif" \* MERGEFORMATINET    NOTE: LDL, low-density lipoprotein; HMG-CoA, 3-hydroxy-3-methylglutaryl-coenzyme A; HDL, high-density lipoprotein; VLDL, very low density lipoprotein; , LPL lipoprotein lipase.    INCLUDEPICTURE "http://www.harrisonsonline.com/images/spacer.gif" \* MERGEFORMATINET Bile acid-binding resins. The bile acid-binding resins cholestyramine and colestipol have been in use as lipid-lowering agents for almost three decades. These drugs interfere with reabsorption of bile acids in the intestine, resulting in a compensatory increase in bile acid synthesis and upregulation of LDL receptors in hepatocytes. The bile acid sequestrants are primary agents in the treatment of patients with elevated levels of LDL cholesterol and normal triglycerides. Sequestrants produce dose-dependent decreases on the order of 15 to 25 percent in total cholesterol and of 20 to 35 percent in LDL cholesterol. The agents cause modest increases in HDL cholesterol. A limitation of the sequestrants is their tendency to raise triglyceride levels through compensatory increases in hepatic synthesis of VLDL, and they should not be given to hypertriglyceridemic individuals. Bile acid-binding resins are efficacious and safe and are recommended for young adult men and premenopausal women with moderate cholesterol elevations. Patient compliance is low, in part because of the need to dissolve these powdered agents in fluid; the availability of colestipol as a tablet may alleviate this problem. Gastrointestinal side effects include constipation, bloating, and gas. Niacin. The mechanism of action of niacin is not fully understood, but it appears to inhibit the secretion of lipoproteins containing apo B100 from the liver. Niacin decreases both total and LDL cholesterol approximately 15 to 25 percent, reduces VLDL levels by 25 to 35 percent, and raises HDL cholesterol levels by as much as 15 to 25 percent. Thus, on the basis of its effects on three major lipoproteins, VLDL, LDL, and HDL, niacin would appear to be an optimal agent. Efficacy of monotherapy was confirmed in a long-term secondary prevention trial in which niacin significantly reduced the incidence of myocardial infarction. An even longer-term follow-up of that study (15 years total) showed an 11 percent decrease in all-cause mortality among patients randomized to niacin. Like the bile acid-binding resins, niacin is safe, having been in use for almost 30 years. Niacin, however, has unpleasant side effects that limit patient acceptability, including uncomfortable and potentially dose-limiting cutaneous flushing with or without pruritus. However, the cutaneous symptoms tend to subside after several weeks and may be minimized by initiating therapy at low doses. Less common adverse effects include elevations of liver enzymes, gastrointestinal distress, impaired glucose tolerance, and elevated serum uric acid levels with or without gouty arthritis. Liver enzymes may be elevated in 3 to 5 percent of patients on full doses of niacin (>2 g/d). HMG-CoA reductase inhibitors. HMG-CoA reductase inhibitors, which include lovastatin, simvastatin, pravastatin, fluvastatin, and atorvastatin inhibit the rate-limiting step in hepatic cholesterol biosynthesis (the conversion of HMG-CoA to mevalonate), which causes a rise in LDL receptor levels in hepatocytes and enhanced receptor-mediated clearance of LDL cholesterol from the circulation. At usual doses, the HMG-CoA reductase inhibitors decrease total cholesterol by 20 to 30 percent and LDL cholesterol by 25 to 40 percent. Larger reductions may be achieved with higher doses. Treatment with reductase inhibitors often produces reductions in triglycerides of 10 to 20 percent, possibly due to reduced secretion of VLDL by the liver. HDL cholesterol levels rise about 5 to 10 percent. In comparison with other lipid-lowering agents, HMG-CoA reductase inhibitors are relatively free of side effects, which have been reported by fewer than 5 percent of patients. Mild, transient elevations in liver enzymes occur with all of the agents at the highest doses, but elevations in serum aminotransferases to more than three times the upper limits of normal occur in fewer than 2 percent of patients. Therapy should be discontinued when elevations of this magnitude occur. A rare but potentially serious adverse effect of HMG-CoA reductase inhibitors is myopathy, with elevations of serum creatine phosphokinase (CPK) more than 10 times the upper limit of normal; this occurs in fewer than 1 percent of patients treated with reductase inhibitors alone but is more common (about 5 percent) when used in combination with gemfibrozil, niacin, or cyclosporine. Combination therapy. Combinations of bile acid-binding resins and reductase inhibitors are effective for the treatment of severe, isolated elevations of LDL cholesterol. Combinations of either resins and niacin or reductase inhibitors and niacin are useful for the treatment of high LDL and low HDL cholesterol levels, although the latter combination carries an increased risk of myositis (2 to 3 percent). If triglyceride and LDL levels are both elevated (HDL is usually reduced as well), resins and niacin are an excellent combination, with resins and gemfibrozil as an alternative. The combination of a reductase inhibitor and gemfibrozil can be useful when LDL cholesterol is very high in the face of concomitant hypertriglyceridemia, but the risk of myositis (about 5 percent) must be considered. Combinations of reductase inhibitors with either niacin or gemfibrozil might best be reserved for patients with CHD and combined hyperlipidemia. LDL apheresis. In patients with homozygous FH and in ordinary FH patients who respond poorly to diet and drug therapy or who cannot tolerate drugs, apheresis at 7- to 14-day intervals can cause profound lowering of LDL cholesterol levels. Diet and drug regimens are continued during treatment. The long-term efficacy/safety of such therapy is not established, but the therapy should be considered for patients with few therapeutic options. 2. Most likely cause of prolonged QT: a. Verapamil b. Decreased potassium c. Increased calcium d. Flecainide e. Propanolol 3. Intellectual impairment Intellectual impairment is listed as a feature of most forms of hyperhomocysteinaemia (Harrison’s Table 349-1), while it is noted listed as a classic feature of Marfan’s syndrome. Marfan’s syndrome has autosomal dominant inheritance, while hyperhomocysteinaemia appears to have autosomal recessive inheritance. 4. Abdominal pain 5. Valve replacement All patients with moderate or severe AS require careful periodic follow-up. In patients with severe AS, strenuous physical activity should be avoided even in the asymptomatic stage. Digitalis glycosides, sodium restriction, and the cautious administration of diuretics are indicated in the treatment of congestive heart failure, but care must be taken to avoid volume depletion. While nitroglycerin is helpful in relieving angina pectoris, vasodilator therapy for heart failure is usually of little value and may, in fact, be harmful. Surgical Treatment   The most critical decision in the management of AS concerns the advisability of surgical treatment which, in the majority of adults with calcific AS and critical obstruction (aortic orifice <0.5 cm2/m2 body surface area), consists of valve replacement. In most instances, it is prudent to postpone operation in patients with severe calcific AS who are asymptomatic, since their future course is difficult to predict and they may continue to do well for many years. However, they should be followed carefully by clinical examination for the development of symptoms and by serial echocardiograms for evidence of deteriorating left ventricular function; operation is generally indicated in patients with severe AS and progressive left ventricular dysfunction, even if they are asymptomatic. In patients without heart failure, the operative risk of aortic valve replacement is approximately 4 percent. When angina pectoris, syncope, or left ventricular decompensation develops in adults with severe valvular AS, the outlook, despite medical treatment, is very poor and can be improved significantly by replacement of the aortic valve. The operative risk in this group of patients (approximately 7 to 10 percent) is considerably lower than the risk incurred by nonoperative treatment; moreover, the symptomatic improvement in some survivors of operation has been remarkable. There is evidence that regression of left ventricular hypertrophy may occur following relief of obstruction. Operation should, if possible, be carried out before frank left ventricular failure develops; at this late stage, the operative risk is high (15 to 20 percent), and evidence of myocardial disease may persist even when the operation is technically successful. Furthermore, long-term postoperative survival also correlates inversely with preoperative left ventricular dysfunction. Nonetheless, in view of the very poor prognosis of such patients when they are treated medically, there is usually little choice but to advise immediate surgical treatment. In patients in whom severe AS and coronary artery disease coexist, relief of the AS and revascularisation of the myocardium by means of aortocoronary bypass grafting may result in striking clinical and haemodynamic improvement. Since many patients with calcific AS are elderly, particular attention must be directed to the adequacy of hepatic, renal, and pulmonary function before valve replacement is recommended. The mortality rate depends to a substantial extent on the patient's preoperative clinical and haemodynamic state. The 10-year survival rate of patients with aortic valve replacement is approximately 60 percent. Approximately 15 percent of bioprosthetic valves evidence primary valve failure in 10 years, requiring re-replacement, and an approximately equal percentage of patients with mechanical prostheses develop significant hemorrhagic complications as a consequence of treatment with anticoagulants. (See Concise Review:  HYPERLINK "http://www.harrisonsonline.com/server-java/Arknoid/harrisons/1096-7133/Updates/Editorials/?Up=edl2144" \t "_top" The Stentless Aortic Prosthesis for Aortic Stenosis) Percutaneous Balloon Aortic Valvuloplasty   This procedure, described in  HYPERLINK "http://www.harrisonsonline.com/server-java/Arknoid/harrisons/1096-7133/Chapters/ch-245?Page=1" \t "_top" Chap. 245, is an alternative to surgery in children and young adults with congenital AS. It is not commonly employed in elderly patients with severe calcific AS because of a high restenosis rate. Nonetheless, this procedure has been employed in patients who are too ill or frail to undergo operation, in patients with life-threatening AS and advanced extra cardiac disease, and as a "bridge to surgery" in patients with severe left ventricular dysfunction. 6. 69 year old male, 2 days post CABG, loss of vision in 1 eye, fundoscopy - pale optic disk with peri-retinal haemorrhage. What is the cause: Central retinal artery embolus Central retinal vein occlusion Optic nerve sheath meningioma Posterior cerebral artery occlusion Ischaemic optic neuropathy 7. Young female with mitral valve disease. Penicillin prophylaxis for dental procedure for which she received GA. During procedure hypotension and ventilatory compromise. Best test to say anaphylaxis a. Serum IgE b. Serum Tryptase c. Serum Histamine d. Penicillin RAST 8. 27 Male sudden onset mid scapula pain, BP left arm 240/120, BP right arm 80/60, quiet heart sounds. Best initial therapy a. Cardiac paracentesis b. Nitroprusside and Beta blocker c. Pulmonary embolectomy d. Thrombolysis e. Observe 9. 22 year old with flu, soft systolic murmur noticed. BP 120/70. ECG shows LV hypertrophy. The best explanation: a. Normal variant b. Coarctation of aorta c. HOCM Bicuspid aortic valve Flow murmur 10. 60 year old male. No past history but recent dyspepsia. Acute chest pain. CK 800, CKMB increased, anterior ST elevation treated with tPA. Associated idiosyncratic ventricular rhythm. 3 days later inverted T waves and Q waves anteriorly. Angiogram - most likely result lesion a. Occluded LAD and poor LV function b. Occluded circumflex c. 70% lesion right coronary 70% lesion LAD, 50% lesion in circumflex, 50% lesion right coronary No abnormality 11. 40 year old competitive athlete - notices intermittent irregular pulse - no other symptoms. On examination - normal HR/BP etc. ECG and echo normal. Strip from Holter (while sleep) - shows Wenckebach 2° heart block. Next course of action: a. Angiography b. Pacemaker c. Thallium stress test d. Exercise test e. Reassure 12. A young man falls unconscious while lifting a beam. On examination his blood pressure is 80/40 with a pulse of 120 per minute. Cardiac catheterisation reveals the following results. 0xygen sats Pressure RA 55% 8 RV 85% 40/8 PA 85% 42/10 PACWP 85% 12 LV 95% 80/40 What is the diagnosis? a. VSD b. Aortic incompetence with a VSD c. Ruptured sinus of Valsalva d. Intra-atrial shunt e. ASD Question 13 A 38 year old male presents with sudden onset of dyspnoea and hypotension. Examination reveals a continuous murmur over the left sternal edge. The following oxygen saturations are obtained by cardiac catheter: IVC 75% LA 98% SVC 73% LV 97% RA 85% AO 97% PA 84% These findings are consistent with: A) Ruptured sinus valsalva B) Tetralogy of Fallot C) VSD D) ASD E) Patent ductus arteriosus FRACP 1997 (Paper A) Heart failure with normal LV systolic function in a 70 year old. Common cause Increased atrial contraction Decreased heart rate Myocardial ischaemia Decreased LV compliance AV degeneration 2. Pregnant lady 20 weeks, with mitral stenosis. Best indicator of severity is Pre pregnancy exercise tolerance Duration of murmur Cardiac echo Displaced apex Symptoms prior to pregnancy 3. All the following are actions of ( blockers except: ( AV conduction ( insulin secretion ( glycogenolysis venodilation Hypnogogic hallucinations 4. Nitric oxide induced vasodilatation. Least likely reason: Platelet aggregation Serotonin Acetyl choline Blood flow Haemoglobin 5. Question on prolonged QT - most likely cause: Inherited defect of Na+ channels Inherited defect of K+ channels Hypocalcaemia Myocardial infarction ACE inhibitors FRACP 1997 (Paper B) 46 year old pilot with a history of chest pains on exertion. ECG shows sloping ST changes. Stopped due to chest pain. No echo changes. Thallium scan done with exercise showed anterior ischaemic changes. Most probable: anterior ischaemia with exercise false positive thallium scan post MI 3 vessel disease – 65 year old female, history of claudication, angina and hypertension for 2 years that has been very difficult to control. Already on thiazide and ( blocker, now needs a Ca2+ channel blocker. BP 150/90. Renal U/S – R/kidney 10 cm, L/kidney 10.3cm. Urine – Alb +1, trace blood. Na+ 140, K+ 3.0, Urea 9, Creatinine 0.12, urinary catecholamines – NA 700 (normal <600), A 80 (normal). What would be the best test? CT adrenals Renal angiogram Renal IVP Renal scintiscan A 23 year old obese male (weight 150% normal). ?Cleft palate repair and rheumatic fever at age of 8. Now a 2 year history of exertional dyspnoea. Right heart catheterisation given: IVC 77% - O2 sat. SVC 74% - O2 sat. RA 76% - O2 sat. RV 79% - O2 sat. PA 79% - O2 sat. Lose weight Close ASD Close VSD Penicillin prophylaxis Diuretics 25 year old female pregnant 4 months. Presents with dyspnoea, AF, CHF. Echo shows mitral valve area of 0.6 cm2. Increased pulmonary pressures, calcification minor, mild MR only, mobile anterior mitral valve leaflet. Next best step after management of AF: therapeutic abortion bed rest and medical management until after delivery open mitral valve commissurotomy mitral valve replacement mitral valve balloon valvuloplasty Chest x-ray with pericardial calcification: CV wave in JVP RA and PCW pressures equal Increased PCW pressures with inspiration RV pressure more in systole RV & LV pressures equal in systole 50 year old female, increased SOB. Exam - CHF, AF, L systolic murmur, BP 150/100. Echo enlarged LV, concentric hypertrophy, decreased LV function, narrowing of aortic valve with peak gradient 45mmHg. Given digoxin and diuretics and stabilised. After echo findings what do you do next? continue current therapy ACE inhibitor aortic balloon valvuloplasty aortic valve replacement cardiac transplant. 16 year old school boy, murmur since age 2, asymptomatic. Brought for a check up. O/E: systolic murmur lower LSE, L thrill, BP, pulse, splitting normal. Murmur ?change in Valsalva? HOCM MVP congenital pulmonary stenosis ASD VSD 18 year old IV drug user shown a Roth spot on picture of fundus. Presents with fever. Most likely organism: Klebsiella Staph. aureus Acinetobacter Strep. bovis Pseudomonas 75 year old man with ventricular demand pacemaker, experiences palpitations, no dizziness. ECG - tachycardia, 150/min, p waves present. Cause of palpitations: AF Atrial flutter VT Pacemaker induced tachycardia AVN RT Elderly woman on Digoxin and Frusemide. 2 weeks ago added Captopril & NSAID. Now nauseated. Digoxin level 2.8, Creatinine 0.14 - 0.3. Next step: stop everything and recheck Dig. level stop NSAID stop Captopril, NSAID and recheck Dig. level Patient on Atenolol for angina. HR 64, BP 170/100, still has some exertional angina. Which drug to add next: Nitrate Nifedipine Enalapril Diltiazem. Other FRACP Questions Young female with a history of personality disorder, drug abuse being treated for chronic pain develops pulmonary oedema, generalised oedema and nephrotic range proteinuria. Which of the following is most likely: a. non-narcotic paracetamol based analgesia b. Lithium c. ketorolac d. heroin-narcotics e. antidepressant/ antipsychotic medications. A 21 year old man presents to hospital 30 minutes after ingesting 10g of chloroquine: A. this is a life -threatening overdose. B. toxicity is likely to be delayed at least 4 hours. C. diazepam should be given at once. D. gastric lavage with instillation of charcoal is not indicated. E. the most likely ECG abnormality is bradycardia with Q-T prolongation Concerning the chronic haemodynamic and pathological consequences of compensated MR: a. reduced pulmonary blood flow b. reduced pulmonary vascular resistance c. increased LV mass d. increased LV sarcomere length e. increased LV EDD Concerning CAD risk factors: a. inc. risk of CAD with an inc. chol. with the range b. reduced HDL is an independent risk factor in men c. inc. risk with inc. # of cigarettes smoked d. use of clofibrate is assoc. with inc. incidence of gallstones e. low fat diet is assoc. with inc. incidence of colonic cancer. The next best treatment following failure of percardiocentesis for acute cardiac tamponade: a. dobutamine infusion b. high dose Lasix c. PEEP d. colloid infusion e. digoxin An extensive anterior AMI occurs in a young man who is five days post-operative following major abdominal surgery. This occurs in a hospital with access to cardiac catheterisation and surgery. The best treatment is: a. IV heparin b. SKA c. SKA followed by PTCA on day 3 d. emergency PTCA e. angiogram and CABG. Young male, post trauma develops ARDS. Ventilated, CVL for TPN, SG catheter for 10 days. CXR shows bilateral infiltrates consistent with ARDS. He becomes very unwell, septic, fever (40c), haemodynamically unstable. After initial resuscitation you would: a. change all lines and send for culture b. culture secretions from ETT c. blood cultures d. broad spectrum antibiotics e. echocardiogram. A 45 year old man presents with 2 hr of chest pain highly suggestive of AMI. ECG shows LBBB. Best Rx: a. IV SKA and ASA b. IV heparin and atenolol c. IV GTN atenolol await CK Young female with MS in 1st trimester of pregnancy. Which is the best predictor of response to pregnancy: a. pre-pregnancy symptoms b. apex beat displacement c. valve area on echocardiogram d. length of the murmur 24 year old female presents with three episodes of collapse in the last four months during which she is totally unconscious. Her mother died suddenly in swimming pool, her grandfather in MVA. Examination unremarkable. ECG is shown - inc QT. Which of the following is most likely to stop further attacks: a. phenytoin b. inderal c. amiodarone d. sotalol Pathogenic mechanisms of myocardial reperfusion injury — following ischaemia in animal experiments include: A. excessive cytosolic calcium. B. precipitation of intracellular adenosine. C. upset of the osmotic - hydrostatic pressure balance across the capillary wall. D. formation of oxygen free radicals. E. adherence of neutrophils preventing flow through capillaries. Which of the following statements concerning coronary artery disease risk factors and their management is/are correct? In the normal range of serum cholesterol (4.0 - 5.5 mmol/l)the likelihood of developing clinical manifestations of coronary heart disease increases with the serum cholesterol level. Decreased HDL is an independent risk factor for coronary artery disease in men. Lowering serum cholesterol by clofibrate results in an increased risk of cholelithiasis. Lowering serum cholesterol by reducing dietary fat results in an increased risk of colonic cancer. The level of risk of coronary heart disease in smokers is related to the number of cigarettes smoked. With regard to beta 1 receptor agonist inotropic agents: Their effects are mediated through cyclic AMP. The relationship between developed tension in the myocardium and cytosolic calcium concentration remains unaltered. They have a negative inotropic action in the presence of severe limitation of coronary blood flow. Their inotropic effects are additive with Digoxin. Their myocardial receptor number is normal in heart failure. Concerning supraventricular tachycardia (SVT): SVT is due to re-entry in about 30% of patients Approximately 30% of accessory atrio-ventricular connections responsible for SVT do not produce delta waves during sinus rhythm. Frequently recurrent SVT results in reduced left ventricular function. Greater than 80% of patients with disabling SVT have a surgically curable lesion SVT may produce angina and ST segment depression in the absence of atheromatous coronary artery disease. Regarding cardiology formulae: vascular resistance is inversely related to the cardiac output. ejection fraction is calculated by dividing end diastolic volume into stroke volume. area of a stenotic valve is inversely related to the square root of the pressure gradient. blood flow is inversely related to the difference in arterial and venous oxygen content. Cardiac index is calculated by dividing cardiac output by body surface area A reduced effect of a standard dose of oral digoxin may be encountered in which of the following clinical settings? A. Renal failure. B. Hyperthyroidism. C. Concomitant cholestyramine administration. D. Concomitant quinidine administration. E. Hypercalcaemia Bioprostheses of the aortic valve A. eventually develop the same disease as the native valve. B. last longer in younger than older patients. C. do not require prophylaxis against endocarditis. D. do not require long-term anticoagulation. E. . are haemodynamically superior to mechanical prostheses With respect to automatic implantable defibrillators: implanting a defibrillator with epicardial patches carries a mortality rate of about 2%. pace-termination functions are available in these devices. the incidence of sudden arrhythmia death after successful defibrillator implantation is about 1% per annum defibrillator shocks are dangerous for those in contact with the patient at the time. implantation is not indicated in severe cardiac failure. Which of the following statements is/are true of percutaneous transluminal coronary angioplasty? A. The primary success rate of the procedure is more than 70%. B. Re-stenosis, if it occurs, is within 6 months of the procedure. C. Long-term anticoagulant therapy reduces the frequency of re-stenosis. D. The mortality rate as an elective procedure is about 2%. E. Long-term antiplatelet therapy reduces the frequency of re- stenosis. Concerning the prognosis of myocardial infarction: hospital mortality is unrelated to age. late sudden death in survivors of ventricular fibrillation is more likely if acute myocardial infarction evolves than if no evidence for acute infarction is found survival up to one year after infarction is mainly dependent on the number of diseased coronary arteries. D. poor left ventricular function is associated with an increased likelihood of later ventricular tachycardia. E. electrophysiological study identifies patients prone to die suddenly in the next year. A young male following trauma develops ARDS. He is intubated and ventilated but now breathing spontaneously. He has a central line with TPN and a Swan Ganz catheter in situ - both for 10 days. He is on Ceftriaxone for persisting bilateral pulmonary infiltrates and blood cultures to date have been negative. He becomes very unwell and septic, T 40, BP 70/50. His blood and urine are sent for culture and his CXR is unchanged. After the initial resuscitation you should change all lines and send for culture culture endotracheal secretions bronchoscopy +/- TBB echo broad spectrum antibiotics Haemodynamic response to SVT can be predicted by ventricular rate QT interval relationship between P waves and QRS complexes QRS width variability in the P wave morphology Concerning drug metabolism in congestive cardiac failure decreased gastric absorption decreased oral bioavailability of drugs with “low” hepatic extraction decreased clearance of drugs with “high” hepatic extraction decreased distribution of intravenously administered drugs Which of the following are consistent with Constrictive Pericarditis mitral regurgitation atrial fibrillation RVEDP=LVEDP unimpeded early diastolic ventricular filling Vascular endothelium is affected by thrombomodulin TXA2 Pc NO endothelin Which of the following lead to increased progression of CAD increased tar content of smokes cigar smoking increased nicotine content of smokes number of cigarettes smoked Concerning snake bites, which of the following is/are true detection kits are used to define specific type of antivenom to be used presence of bite marks necessitates use of antivenom first aid involves use of a pressure-immobilisation bandage previous use of antivenom in a patient requires that subsequent use involves a smaller dose 19yr old male presents with dyspnoea. Examination reveals systolic thrill. Cardiac catheter studies reveal SaO2 Pressure SVC 72 IVC 78 RA 85 mean 12 mmHg RV 85 36 LPA 84 36 RPA 85 femoral 92 Which of the following is/are true? should have endocarditis prophylaxis anomalous pulmonary venous drainage can be excluded there is a significant right to left shunt a split S1 will be audible clinically >80% are associated with a RBBB Which of the following drugs are linked to their possible effects in overdose digoxin: hyperkalaemia theophylline: seizures colchicine: ascending polyneuropathy Young female with a history of personality disorder, drug abuse being treated for chronic pain develops pulmonary oedema, generalised oedema and nephrotic range proteinuria. Which of the following is most likely: non-narcotic paracetamol based analgesia Lithium ketorolac heroin-narcotics antidepressant/antipsychotic medications Elderly female with treatment for HT, arthritis and angina experiences postural symptoms. Which of the following drugs is the most likely cause: B-blockers GTN patch NSAIDS enalapril diuretics TCA overdose associated with: constricted pupils hypotension and tachycardia convulsions hypokalaemia A 43 year old female with increasing SOB has findings of inc. JVP, bilateral LL oedema. Echo shows dilated LV/N MV. Which of the following is most likely to inc. survival: MV replacement enalapril frusemide aspirin digoxin Coronary angioplasty is contraindicated in left main disease reduces mortality in acute infarction more than thrombolytic therapy relieves symptoms in chronic stable angina is associated with a reduction in infarct rate at 5 years most restenosis occurs within the first 6 months In which of the following patients would you expect to find evidence of recent coronary thrombosis? a 60 year old man who dies of cardiogenic shock 2 days after a large anterior infarct a previously fit 70 year old woman successfully resuscitated from cardiac arrest a 55yr old man with 15 min of chest pain associated with 3 mm anterior ST elevation. The pain and ECG changes are relieved by anginine and the CK is normal a man with stable angina and a positive exercise test a 40 year old man with recurrent hospital admissions for unstable angina who has further pain with ST depression on his ECG Massive digoxin overdose classically produces nephrotoxic ATN grand mal seizures second degree HB VT hyperkalaemia SVT is commonly caused by increased sinus node automaticity re-entry between the sinus node and the atrium increased AV node automaticity re-entry between the AV node and the atrium re-entry from the ventricle to the atrium via an accessory pathway Regarding ECG ST elevation in V4R is found in RV infarction a LAH is associated with a frontal axis of 0( - -30( posterior infarcts have a large R wave in V1 pericarditis produces ST elevation typically followed by TWI a 10mm S wave in V1 and a 12 mm R wave in V5 represents LVH Digoxin toxicity characteristically is assoc. with: a/ AF with slow rate b/ SVT with P waves ST seg. (?retrograde P) c/ Torsades d/ ventricular arrhythmia with odd numbers QRS complexes e/ tachyarrhythmia with varying rate Concerning cardiac transplantation: a/ 1yr survival >80% b/ endomyocardial biopsy best to dx acute rejection c/ constrictive pericarditis reflects chronic rejection d/ pulmonary venous HT is a contraindication Which of the following congenital conditions is associated with a reduced life-expectancy: a/ coronary AV fistula b/ LAD arising from pulmonary artery c/ single coronary artery d/ anomalous tract between aorta and RV outflow tract e/ LAD arising from R sinus of valsalva Concerning elective coronary angiography: a/ has 1/1000 mortality b/ arterial damage 5/1000 c/ nonfatal MI 7/1000 d/ CVA 1/100 e/ serious arrhythmia 6/1000 Atrial fibrillation in non-rheumatic heart disease: a/ the risk of embolism is inc 2-5times b/ 10-20% early (<2wks) recurrence rate c/ commonly embolises to the lenticulostriate a. d/ prevented by anticoagulation e/ haemorrhagic transformation relates to infarct size Regarding thrombolysis: a/ TPA decreases mortality >SK b/ SK readministered within <3/12 - allergic Rx c/ PTCA to total occlusion post-lysis inc mortality d/ PTCA post successful lysis prevents re-occlusion Surgery is indicated for symptomatic pt with: a/ AAA>7cm in 68yo b/ PDA in adolescent with 3:2 shunt c/ ASD secundum in adolescent with 2.3:1 shunt d/ MS in valve 1.2cm sq in nulliparous woman e/ 2VCADx with normal LV function ECG - SR with widespread deep TWI. This would be consistent with: a/ acute MI b/ hypokalaemia c/ proximal LAD lesion d/ SAH e/ Amiodarone Tx ECG - torsades : Conditions predisposing to this include: a/ digoxin b/ hypomagnesaemia c/ flecainide d/ quinidine e/ CAD f/ MVP Coronary angiogram in 42 year old man with AP , RCA injection, told LCA is normal a/ this is an LAO view b/ demonstrates coronary atresia c/ R posterior descending is not demonstrated d/ a high se cholesterol would be expected e/ surgery is indicated Concerning the chronic haemodynamic and pathological consequences of compensated MR: a/ reduced pulmonary blood flow b/ reduced pulmonary vascular resistance c/ increased LV mass d/ increased LV sarcomere length e/ increased LV EDD Concerning CAD risk factors: a/ inc. risk of CAD with an inc. chol with the range b/ reduced HDL is an independent risk factor in men c/ inc. risk with inc. # of cigarettes smoked d/ use of clofibrate is assoc. with inc. incidence of gallstones e/ low fat diet is assoc. with inc. incidence of colonic cancer The next best treatment following failure of pericardiocentesis for acute cardiac tamponade: a/ dobutamine infusion b/ high dose Lasix c/ PEEP d/ colloid infusion e/ digoxin An extensive anterior AMI occurs in a young man who is 5 days post-operative following major abdominal surgery. This occurs in a hospital with access to cardiac catheterisation and surgery. The best treatment is: a/ IV heparin b/ SKA c/ SKA followed by PTCA on day 3 d/ emergency PTCA e/ angiogram and CABG 45yo man presents with 2hrs of chest pain highly suggestive of AMI. ECG shows LBBB. Best Rx: a/ IV SKA and ASA b/ IV heparin and atenolol c/ IV GTN d/ atenolol e/ await CK 22yo female who has AVR runs 10km four times weekly at night time and presently it is Winter. She also suffers from menorrhagia and gives a history of lethargy and notices passage of dark urine after running a distance. Hb 8.8, haptoglobin reduced, blood film shows fragmented cells. The most likely Diagnosis: march haemoglobinuria cold agglutinin disease valve haemolysis blood loss paroxysmal cold haemoglobulinaemia Increased cardiac comorbidity for abdominal surgery if DBP > 105 mmHg anterior subendocardial infarction in the last 2 months asymptomatic bifascicular block on ECG frequent ectopic beats Radio frequency ablation is >90% successful in SVT with AV nodal re-entry recurrent AF VT with a bypass tract VF originating in the Right ventricle VT due to a prolonged QT interval What potentiates re-entrant tachycardia increases conduction velocity in the bypass tract decreased refractory period in the bypass tract increased catecholamines decreased coronary blood flow decreased left ventricular filling What are the pathological and haemodynamic consequences of chronic compensated mitral regurgitation decreased pulmonary blood flow decreased pulmonary vascular resistance increased LVEDV increased sarcomere length increased LV mass Concerning cyanotic congenital heart disease almost always presents shortly after birth associated with tachypnoea at rest associated with gout in children associated with increased risk of embolic stroke improves with intermittent positive pressure ventilation Which of the following increases coronary thrombosis in a previously atherosclerotic coronary tree von Willebrand factor deficiency anti thrombin III deficiency homocysteinuria decreased apolipoprotein (a) decreased HDL in men 60yr old male with broad regular tachycardia in RBBB pattern and no evident p waves, rate 200/min and BP 90/70, dyspnoeic and dizzy. No response to CSM. Given IV lignocaine bolus and 30 mins of lignocaine infusion 4mg/min with no effect. The next best management would be (one answer) IV digoxin IV verapamil more IV lignocaine wait another 15 min elective cardioversion with sedation 20 year old thin tall male with sudden onset of severe chest pain. JVP 4cm, HS dual with diastolic murmur at LSE. Carotids normal, BP 120/70, ECG shows 2mm ST elevation in leads II and III with no Q waves. Best management would be (one answer) IV streptokinase IV heparin await cardiac enzyme results transthoracic echo CT thorax Echo shown ?MVP ?HOCM Young female with dyspnoea on exertion. Which of the following is/are true? increased risk of sudden death SBE prophylaxis is required calcium channel blockers improve survival beta-blockers are contraindicated vasodilators improve symptoms ECG shown with ST elevation ( 2 saddle shaped) in I, aVL, II, III and aVF, V3-6. Rate 100/min BP 170/110. 46 year old male with crushing chest pain for 2 hours. No other clinical abnormalities - no murmurs or rubs. The best initial treatment would be (one answer) aspirin IV streptokinase IV atenolol IV heparin IV nitroprusside The haemodynamic significance of SVT is affected by QT interval P wave morphology P-QRS dissociation (relationship of P to QRS) QRS width ventricular rate (RR interval) Concerning CAD risk factors there is an increased risk of CAD with an increased cholesterol, within the normal serum range of cholesterol a reduced HDL is an independent risk factor in men increased risk with the number of cigarettes smoked use of clofibrate is associated with an increased incidence of gall stones a low fat diet is associated with increased incidence of colonic cancer Regarding cardiovascular formulae vascular resistance is inversely related to the cardiac output ejection fraction is calculated by dividing end diastolic volume into stroke volume area of a stenotic valve is inversely related to the square root of the pressure gradient blood flow is inversely related to the difference in arterial and venous oxygen content cardiac index is calculated by dividing cardiac output by body surface area Concerning mitral regurgitation afterload is decreased can be a feature of Marfan’s syndrome there is increased myocardial oxygen demand systolic anterior motion of the mitral valve occurs in MVP concentric myocardial shortening is reduced HOCM X-linked autosomal recessive inheritance occurs involves an abnormality in myosin LV chamber is dilated has abnormal diastolic filling is associated with pulmonary congestion A 50 year old man presents with 2 hours of chest pain. Clinically you think he has a >50% chance of a myocardial infarct. ECG shows LBBB. The best treatment would be Streptokinase and aspirin atenolol and heparin atenolol and aspirin IV GTN observe until first cardiac enzymes A 150kg lady presents with exertional dyspnoea and a systolic murmur at the left sternal edge catheter study shows SVC 71% IVC 76% RA 75% RV 79% 39/15 PA 78% 34/15 The most appropriate management would be advise to lose weight close sinus venosus defect close VSD A 60 year old presents acutely short of breath, hypotensive 60/-. A Swan Ganz is performed and shows CVP 20 PAP 45/- RVP 46/- PCWP 9 systolic BP 60/- RV infarct LV infarct asthma acute PE primary pulmonary hypertension A marathon runner notices an irregular pulse. He has had no presyncope or syncope. A Holter monitor is performed and a strip is shown (Wenckebach). You proceed to reassure the patient recommend PPM insertion repeat holter angiography. An elderly male presents with exertional dyspnoea and ankle swelling. His CXR is shown. (Pericardial calcification++) The most likely finding on right heart catheter is PAWP increases on inspiration cV waves in venous pressure tracing (? in PAWP) RAP = PAWP RVEDP > LVEDP A young male presents with chest pain 5 days post hernia repair. His ECG shows evidence of acute myocardial infarction and he is in a hospital with access to a catheter lab. 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