Download 1. Coronary angioplasty

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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 (<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
2
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 autosomaldominant 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 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.
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Table 229-2
Patient Characteristics Associated With Increased Mortality From Cardiac Catheterisation
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 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.
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)
B)
C)
D)
E)
AI
AS and MI
AI and AS
AS
AS and MS
Question 7
Pericarditis
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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.
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Question 11
Decrease calorie intake, decrease cholesterol and organise an exercise program
Question 12
independent of cholesterol
FRACP 1999 (Paper 1)
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.
2.
Initial event in cardiac muscle contraction
a.
b.
c.
d.
e.
calmodulin
calcium mediated opening of T channels
 adrenoceptor mediated opening of calcium channels
decreased calcium influx
actin-myosin interaction
3. 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.
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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
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
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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 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 30 mm)
FRACP 1999 (Paper 2)
1.
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 betablockers. 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
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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.)
2.
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:
a.
b.
c.
d.
e.
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)
B)
C)
D)
Basal stimulation his aldosterone and renin
Baroreceptor ?insensitivity
Atrial naturetic factor
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 (V 1 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
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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 Twave 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)
B)
C)
D)
E)
Increased calmodulin activation
Myosin actin interaction
Formation of cross links
Fall in intracellular calcium
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)
B)
C)
D)
Postpone surgery until hypoxia is investigated
Treat hypertension as this increases risk of intraoperative complications
This man needs preoperative subcutaneous heparin to prevent DVT
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)
B)
C)
TTE
carotid doppler
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.
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The most effective treatment of atrial flutter is direct-current cardioversion, which can be accomplished at low
energy (25 to 50 W·s) under mild sedation. Higher energies (100 to 200 W·s) 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.
Table 341-8
Hypolipidemic Agents
Class
Mode of
Action
Lipoprotein
Class
Affected
Drug
Interactions
Combined
Use with
Dose
Side Effects
Contraindications
Cholestyramine
8–12 g bid or
tid
Cholestipol
10–15 g bid or
tid
Constipation,
gastric
discomfort,
nausea,
hemorrhoidal
bleeding
Biliary track
Absorption of
obstruction, gastric
phenylbutazone
outlet obstruction,
, phenobarbital,
hypertriglyceridemia thyroid
hormones,
digitalis,
warfarin,
thiazide
diuretics, some
antibiotics
Nicotinic
acid,
HMG-CoA
reductase
inhibitors,
gemfibrozil
Flushing,
tachycardia,
atrial
arrhythmias,
pruritus, dry
skin, nausea,
diarrhea,
hyperuricemia,
peptic ulcer
disease,
glucose
intolerance,
Peptic ulcer disease,
cardiac arrhythmias,
liver disease, gout,
diabetes mellitus
Bile acidbinding
resins,
HMG-CoA
reductase
inhibitors,
gemfibrozil
Bile acid–
binding
resins
Interrupts
enterohepati
c circulation
of bile acids;
Synthesis
of new bile
acids and
LDL
receptors
LDL
cholesterol
20–30%
HDL
cholesterol
and
triglycerides
Nicotinic
acid
Synthesis
of VLDL
and LDL
Niacin 50–100
Triglycerides mg tid initially
25–85%
then increase to
1.0–2.5 g tid
VLDL
cholesterol
25–35%
LDL
cholesterol
15–25%
HDL may
Gemfibrozil,
ketoconazole,
cyclosporine,
warfarin, niacin
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hepatic
dysfunction
CoA
reductase
inhibitors
Fibric acid
derivatives
Cholesterol
synthesis
LDL
receptors
LPL and
triglyceride
hydrolysis
VLDL
synthesis
LDL
catabolism
LDL
cholesterol
25–40%
VLDL
Lovastatin 10– Abnormal
80 mg/d
liver function,
Pravastatin 10– myositis
40 mg/d
Simvastatin 5–
40 mg/d
Fluvastatin20–
40 mg/d
Atorvastatin
10–80 mg/d
Gemfibrozil
Triglycerides 600 mg bid
25–40%
or LDL
cholesterol
HDL
Lithogenicity
of bile,
nausea,
abnormal liver
functions,
myositis
Myositis in
patients with renal
failure and in
patients on
gemfibrozil,
nicotinic acid, or
cyclosporine
Gemfibrozil,
ketoconazole,
cyclosporine,
warfarin, niacin
Bile acidbinding
resins
Hepatic or biliary
disease; dose in
renal insufficiency
Anticoagulant Bile acidbinding
activity of
resins
warfarin
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.
Bile acid-binding resins. The bile acid-binding resins cholestyramine and colestipol have been in use as lipidlowering 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
12
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.
b.
c.
d.
e.
Verapamil
Decreased potassium
Increased calcium
Flecainide
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
13
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: The Stentless Aortic Prosthesis for Aortic
Stenosis)
Percutaneous Balloon Aortic Valvuloplasty
This procedure, described in 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:
a.
b.
c.
d.
e.
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.
b.
c.
d.
Serum IgE
Serum Tryptase
Serum Histamine
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.
b.
c.
d.
e.
Cardiac paracentesis
Nitroprusside and Beta blocker
Pulmonary embolectomy
Thrombolysis
Observe
9. 22 year old with flu, soft systolic murmur noticed. BP 120/70. ECG shows LV
hypertrophy. The best explanation:
a.
b.
c.
d.
e.
Normal variant
Coarctation of aorta
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.
14
Angiogram - most likely result lesion
a.
b.
c.
d.
e.
Occluded LAD and poor LV function
Occluded circumflex
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.
b.
c.
d.
e.
Angiography
Pacemaker
Thallium stress test
Exercise test
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
55%
85%
85%
85%
95%
RA
RV
PA
PACWP
LV
Pressure
8
40/8
42/10
12
80/40
What is the diagnosis?
a.
b.
c.
d.
e.
VSD
Aortic incompetence with a VSD
Ruptured sinus of Valsalva
Intra-atrial shunt
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)
B)
C)
D)
E)
Ruptured sinus valsalva
Tetralogy of Fallot
VSD
ASD
Patent ductus arteriosus
FRACP 1997 (Paper A)
1.
Heart failure with normal LV systolic function in a 70 year old. Common cause
A. Increased atrial contraction
B. Decreased heart rate
C. Myocardial ischaemia
D. Decreased LV compliance
E. AV degeneration
15
2.
Pregnant lady 20 weeks, with mitral stenosis. Best indicator of severity is
A. Pre pregnancy exercise tolerance
B. Duration of murmur
C. Cardiac echo
D. Displaced apex
E. Symptoms prior to pregnancy
3.
All the following are actions of  blockers except:
A.  AV conduction
B.  insulin secretion
C.  glycogenolysis
D. venodilation
E. Hypnogogic hallucinations
4.
Nitric oxide induced vasodilatation. Least likely reason:
A. Platelet aggregation
B. Serotonin
C. Acetyl choline
D. Blood flow
E. Haemoglobin
5.
Question on prolonged QT - most likely cause:
A. Inherited defect of Na+ channels
B. Inherited defect of K+ channels
C. Hypocalcaemia
D. Myocardial infarction
E. ACE inhibitors
FRACP 1997 (Paper B)
1.
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:
A. anterior ischaemia with exercise
B. false positive thallium scan
C. post MI
D. 3 vessel disease
E. –
2.
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?
A. CT adrenals
B. Renal angiogram
C. Renal IVP
D. Renal scintiscan
E.
3.
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
SVC
RA
RV
PA
77% - O2 sat.
74% - O2 sat.
76% - O2 sat.
79% - O2 sat.
79% - O2 sat.
A.
B.
C.
D.
Lose weight
Close ASD
Close VSD
Penicillin prophylaxis
16
E.
Diuretics
4.
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:
A. therapeutic abortion
B. bed rest and medical management until after delivery
C. open mitral valve commissurotomy
D. mitral valve replacement
E. mitral valve balloon valvuloplasty
5.
Chest x-ray with pericardial calcification:
A. CV wave in JVP
B. RA and PCW pressures equal
C. Increased PCW pressures with inspiration
D. RV pressure more in systole
E. RV & LV pressures equal in systole
6.
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?
A. continue current therapy
B. ACE inhibitor
C. aortic balloon valvuloplasty
D. aortic valve replacement
E. cardiac transplant.
7.
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?
A. HOCM
B. MVP
C. congenital pulmonary stenosis
D. ASD
E. VSD
8.
18 year old IV drug user shown a Roth spot on picture of fundus. Presents with fever. Most likely
organism:
A. Klebsiella
B. Staph. aureus
C. Acinetobacter
D. Strep. bovis
E. Pseudomonas
9.
75 year old man with ventricular demand pacemaker, experiences palpitations, no dizziness. ECG tachycardia, 150/min, p waves present. Cause of palpitations:
A. AF
B. Atrial flutter
C. VT
D. Pacemaker induced tachycardia
E. AVN RT
10.
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:
A. stop everything and recheck Dig. level
B. stop NSAID
C. stop Captopril, NSAID and recheck Dig. level
11.
Patient on Atenolol for angina. HR 64, BP 170/100, still has some exertional angina. Which drug to add
next:
A. Nitrate
B. Nifedipine
C. Enalapril
D. Diltiazem.
17
Other FRACP Questions
1.
e.
2.
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
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
3.
Concerning the chronic haemodynamic and pathological consequences of compensated MR:
a.
b.
c.
d.
e.
4.
Concerning CAD risk factors:
a.
b.
c.
d.
e.
5.
IV heparin
SKA
SKA followed by PTCA on day 3
emergency PTCA
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.
b.
c.
d.
e.
8.
dobutamine infusion
high dose Lasix
PEEP
colloid infusion
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.
b.
c.
d.
e.
7.
inc. risk of CAD with an inc. chol. with the range
reduced HDL is an independent risk factor in men
inc. risk with inc. # of cigarettes smoked
use of clofibrate is assoc. with inc. incidence of gallstones
low fat diet is assoc. with inc. incidence of colonic cancer.
The next best treatment following failure of percardiocentesis for acute cardiac tamponade:
a.
b.
c.
d.
e.
6.
reduced pulmonary blood flow
reduced pulmonary vascular resistance
increased LV mass
increased LV sarcomere length
increased LV EDD
change all lines and send for culture
culture secretions from ETT
blood cultures
broad spectrum antibiotics
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
18
b.
c.
d.
e.
9.
IV heparin and atenolol
IV GTN
atenolol
await CK
Young female with MS in 1st trimester of pregnancy. Which is the best predictor of response to pregnancy:
a.
b.
c.
d.
pre-pregnancy symptoms
apex beat displacement
valve area on echocardiogram
length of the murmur
10. 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
11. Pathogenic mechanisms of myocardial reperfusion injury — following ischaemia in animal experiments
include:
A.
B.
C.
D.
E.
excessive cytosolic calcium.
precipitation of intracellular adenosine.
upset of the osmotic - hydrostatic pressure balance across the capillary wall.
formation of oxygen free radicals.
adherence of neutrophils preventing flow through capillaries.
12. Which of the following statements concerning coronary artery disease risk factors and their management
is/are correct?
A.
B.
C.
D.
E.
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.
13. With regard to beta 1 receptor agonist inotropic agents:
A.
B.
C.
D.
E.
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.
14. Concerning supraventricular tachycardia (SVT):
A. SVT is due to re-entry in about 30% of patients
B. Approximately 30% of accessory atrio-ventricular connections responsible for SVT do not produce delta
waves during sinus rhythm.
C. Frequently recurrent SVT results in reduced left ventricular function.
D. Greater than 80% of patients with disabling SVT have a surgically curable lesion
E. SVT may produce angina and ST segment depression in the absence of atheromatous coronary artery
disease.
15. Regarding cardiology formulae:
A.
B.
C.
D.
E.
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
19
16. 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
17. 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
18. With respect to automatic implantable defibrillators:
A.
B.
C.
D.
E.
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.
19. Which of the following statements is/are true of percutaneous transluminal coronary angioplasty?
A.
B.
C.
D.
E.
The primary success rate of the procedure is more than 70%.
Re-stenosis, if it occurs, is within 6 months of the procedure.
Long-term anticoagulant therapy reduces the frequency of re-stenosis.
The mortality rate as an elective procedure is about 2%.
Long-term antiplatelet therapy reduces the frequency of re- stenosis.
20. Concerning the prognosis of myocardial infarction:
A.
B.
C.
D.
E.
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.
21. 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
A.
B.
C.
D.
E.
change all lines and send for culture
culture endotracheal secretions
bronchoscopy +/- TBB
echo
broad spectrum antibiotics
22. Haemodynamic response to SVT can be predicted by
A.
B.
C.
D.
E.
ventricular rate
QT interval
relationship between P waves and QRS complexes
QRS width
variability in the P wave morphology
20
23. Concerning drug metabolism in congestive cardiac failure
A.
B.
C.
D.
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
24. Which of the following are consistent with Constrictive Pericarditis
A.
B.
C.
D.
mitral regurgitation
atrial fibrillation
RVEDP=LVEDP
unimpeded early diastolic ventricular filling
25. Vascular endothelium is affected by
A.
B.
C.
D.
E.
thrombomodulin
TXA2
Pc
NO
endothelin
26. Which of the following lead to increased progression of CAD
A.
B.
C.
D.
increased tar content of smokes
cigar smoking
increased nicotine content of smokes
number of cigarettes smoked
27. Concerning snake bites, which of the following is/are true
A. detection kits are used to define specific type of antivenom to be used
B. presence of bite marks necessitates use of antivenom
C. first aid involves use of a pressure-immobilisation bandage
D. previous use of antivenom in a patient requires that subsequent use involves a smaller dose
28. 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?
A.
B.
C.
D.
E.
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
29. Which of the following drugs are linked to their possible effects in overdose
A. digoxin: hyperkalaemia
B. theophylline: seizures
C. colchicine: ascending polyneuropathy
21
30. 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.
B.
C.
D.
E.
non-narcotic paracetamol based analgesia
Lithium
ketorolac
heroin-narcotics
antidepressant/antipsychotic medications
31. Elderly female with treatment for HT, arthritis and angina experiences postural symptoms. Which of the
following drugs is the most likely cause:
A.
B.
C.
D.
E.
B-blockers
GTN patch
NSAIDS
enalapril
diuretics
32. TCA overdose associated with:
A.
B.
C.
D.
constricted pupils
hypotension and tachycardia
convulsions
hypokalaemia
33. 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:
A.
B.
C.
D.
E.
MV replacement
enalapril
frusemide
aspirin
digoxin
34. Coronary angioplasty
A.
B.
C.
D.
E.
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
35. In which of the following patients would you expect to find evidence of recent coronary thrombosis?
A. a 60 year old man who dies of cardiogenic shock 2 days after a large anterior infarct
B. a previously fit 70 year old woman successfully resuscitated from cardiac arrest
C. 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
D. a man with stable angina and a positive exercise test
E. a 40 year old man with recurrent hospital admissions for unstable angina who has further pain with ST
depression on his ECG
36. Massive digoxin overdose classically produces
A.
B.
C.
D.
E.
nephrotoxic ATN
grand mal seizures
second degree HB
VT
hyperkalaemia
37. SVT is commonly caused by
22
A.
B.
C.
D.
E.
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
38. Regarding ECG
A.
B.
C.
D.
E.
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
39. Digoxin toxicity characteristically is assoc. with:
a/
b/
c/
d/
e/
AF with slow rate
SVT with P waves ST seg. (?retrograde P)
Torsades
ventricular arrhythmia with odd numbers QRS complexes
tachyarrhythmia with varying rate
40. Concerning cardiac transplantation:
a/
b/
c/
d/
1yr survival >80%
endomyocardial biopsy best to dx acute rejection
constrictive pericarditis reflects chronic rejection
pulmonary venous HT is a contraindication
41. Which of the following congenital conditions is associated with a reduced life-expectancy:
a/
b/
c/
d/
e/
coronary AV fistula
LAD arising from pulmonary artery
single coronary artery
anomalous
tract between aorta and RV outflow tract
LAD arising from R sinus of valsalva
42. Concerning elective coronary angiography:
a/
b/
c/
d/
e/
has 1/1000 mortality
arterial damage 5/1000
nonfatal MI 7/1000
CVA 1/100
serious arrhythmia 6/1000
43. Atrial fibrillation in non-rheumatic heart disease:
a/
b/
c/
d/
e/
the risk of embolism is inc 2-5times
10-20% early (<2wks) recurrence rate
commonly embolises to the lenticulostriate a.
prevented by anticoagulation
haemorrhagic transformation relates to infarct size
44. Regarding thrombolysis:
a/
b/
c/
d/
TPA decreases mortality >SK
SK readministered within <3/12 - allergic Rx
PTCA to total occlusion post-lysis inc mortality
PTCA post successful lysis prevents re-occlusion
45. Surgery is indicated for symptomatic pt with:
a/ AAA>7cm in 68yo
23
b/
c/
d/
e/
PDA in adolescent with 3:2 shunt
ASD secundum in adolescent with 2.3:1 shunt
MS in valve 1.2cm sq in nulliparous woman
2VCADx with normal LV function
46. ECG - SR with widespread deep TWI. This would be consistent with:
a/
b/
c/
d/
e/
acute MI
hypokalaemia
proximal LAD lesion
SAH
Amiodarone Tx
47. ECG - torsades : Conditions predisposing to this include:
a/ digoxin
b/ hypomagnesaemia
c/ flecainide
d/ quinidine
e/ CAD
f/ MVP
48. Coronary angiogram in 42 year old man with AP , RCA injection, told LCA is normal
a/
b/
c/
d/
e/
this is an LAO view
demonstrates coronary atresia
R posterior descending is not demonstrated
a high se cholesterol would be expected
surgery is indicated
49. 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
50. 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
51. 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
52. 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
53. 45yo man presents with 2hrs of chest pain highly suggestive of AMI. ECG shows LBBB. Best Rx:
24
a/ IV SKA and ASA
b/ IV heparin and atenolol
c/ IV GTN
d/ atenolol
e/ await CK
54. 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:
A.
B.
C.
D.
E.
march haemoglobinuria
cold agglutinin disease
valve haemolysis
blood loss
paroxysmal cold haemoglobulinaemia
55. Increased cardiac comorbidity for abdominal surgery if
A.
B.
C.
D.
DBP > 105 mmHg
anterior subendocardial infarction in the last 2 months
asymptomatic bifascicular block on ECG
frequent ectopic beats
56. Radio frequency ablation is >90% successful in
A. SVT with AV nodal re-entry
B. recurrent AF
C. VT with a bypass tract
D. VF originating in the Right ventricle
E. VT due to a prolonged QT interval
57. What potentiates re-entrant tachycardia
A.
B.
C.
D.
E.
increases conduction velocity in the bypass tract
decreased refractory period in the bypass tract
increased catecholamines
decreased coronary blood flow
decreased left ventricular filling
58. What are the pathological and haemodynamic consequences of chronic compensated mitral regurgitation
A.
B.
C.
D.
E.
decreased pulmonary blood flow
decreased pulmonary vascular resistance
increased LVEDV
increased sarcomere length
increased LV mass
59. Concerning cyanotic congenital heart disease
A.
B.
C.
D.
E.
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
60. Which of the following increases coronary thrombosis in a previously atherosclerotic coronary tree
A.
B.
C.
D.
E.
von Willebrand factor deficiency
anti thrombin III deficiency
homocysteinuria
decreased apolipoprotein (a)
decreased HDL in men
25
61. 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)
A.
B.
C.
D.
E.
IV digoxin
IV verapamil
more IV lignocaine
wait another 15 min
elective cardioversion with sedation
62. 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)
A.
B.
C.
D.
E.
IV streptokinase
IV heparin
await cardiac enzyme results
transthoracic echo
CT thorax
63. Echo shown ?MVP ?HOCM Young female with dyspnoea on exertion. Which of the following is/are true?
A.
B.
C.
D.
E.
increased risk of sudden death
SBE prophylaxis is required
calcium channel blockers improve survival
beta-blockers are contraindicated
vasodilators improve symptoms
64. 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)
A.
B.
C.
D.
E.
aspirin
IV streptokinase
IV atenolol
IV heparin
IV nitroprusside
65. The haemodynamic significance of SVT is affected by
A.
B.
C.
D.
E.
QT interval
P wave morphology
P-QRS dissociation (relationship of P to QRS)
QRS width
ventricular rate (RR interval)
66. Concerning CAD risk factors
A. there is an increased risk of CAD with an increased cholesterol, within the normal serum range of
B.
C.
D.
E.
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
67. Regarding cardiovascular formulae
A.
B.
C.
D.
E.
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
26
68. Concerning mitral regurgitation
A.
B.
C.
D.
E.
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
69. HOCM
A. X-linked autosomal recessive inheritance occurs
B. involves an abnormality in myosin
C. LV chamber is dilated
D. has abnormal diastolic filling
E. is associated with pulmonary congestion
70. 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
A.
B.
C.
D.
E.
Streptokinase and aspirin
atenolol and heparin
atenolol and aspirin
IV GTN
observe until first cardiac enzymes
71. A 150kg lady presents with exertional dyspnoea and a systolic murmur at the left sternal edge catheter study
shows
SVC
IVC
RA
RV
PA
71%
76%
75%
79%
78%
39/15
34/15
The most appropriate management would be
A. advise to lose weight
B. close sinus venosus defect
C. close VSD
72. 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/-
A.
B.
C.
D.
E.
RV infarct
LV infarct
asthma
acute PE
primary pulmonary hypertension
73. 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
A.
B.
C.
D.
reassure the patient
recommend PPM insertion
repeat holter
angiography.
27
74. 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
A.
B.
C.
D.
PAWP increases on inspiration
cV waves in venous pressure tracing (? in PAWP)
RAP = PAWP
RVEDP > LVEDP
75. 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. Best management
A.
B.
C.
D.
E.
PTCA
Streptokinase
GTN
heparin
IV atenolol