Cardio Flashcards
(128 cards)
1
Q
What is the Bernheim effect and the reverse Bernheim effect?
A
● The Bernheim effect: under normal circumstances there is a slight
displacement of the inner ventricular septum into the right
ventricular cavity because of the higher pressures on the left side of
the heart.
● The reverse Bernheim effect: occurs when there is right ventricular
overload, when displacement of the intraventricular septum into the
left ventricular cavity occurs.
2
Q
Kindly explain why the left side of the heart is more prone to disease.
A
It is presumably related to thickness of the left ventricle and workload
compared to the right side. Diseases such as hypertension much more
frequently affect the left side.
3
Q
Is it always necessary to examine the cardiovascular system of a
patient in the 45° incline of the head end? Other than convenience for
examining the jugular venous pressure (JVP), does this position have
any other advantage?
A
No, it is mainly done for convenience; the JVP is normally just visible
at this angle. The top of the JVP must be seen and therefore the
position is irrelevant.
4
Q
If the JVP is not visible when the patient is in the upright position, can
one presume it is not raised?
A
Probably, unless it is very high and the top of the column is
behind the right ear. The JVP is acting like a U tube and does not
have to be measured at 45° because the measurement is a vertical one
(normal 3–4 cm above the manubrium sternum). 45° is convenient in
that the JVP should just be seen at this angle. Sitting the patient
up can allow a very high venous pressure to be seen whereas
lying the patient flat can allow a low venous pressure to become
visible.
5
Q
The mitral area (of auscultation) normally corresponds with the apex
beat. When the heart is dilated and the apex beat is shifted laterally, will
the mitral area follow the apex beat to its new location or remain at the
place where the apex beat is normally situated?
A
The mitral area follows the apex beat, often into the axilla.
6
Q
Please explain in detail how to measure the pulsus paradoxus using
a sphygmomanometer.
A
The pulse pressure (the difference between systolic and diastolic blood
pressure) falls during inspiration. If you blowup the sphygmoman ometer
cuff to roughly the mid-point between diastolic and systolic pressure, the
mercury column can be seen to be moving and falling on inspiration; an
exaggerated fall greater than 10 mmHg can be seen in pulsus paradoxus
7
Q
What is the difference between dicrotic pulse and pulsus bisferiens?
A
Pulsus bisferiens has two systolic peaks: the percussion and tidal waves.
In dicrotic pulse, the second peak is in diastole immediately after the
second heart sound
8
Q
Why does the radial pulse become more prominent when the hand is
lifted overhead?
A
Raising the arm does make the radial pulse easier to feel and this
is more obvious with a large-volume pulse, which occurs in aortic
regurgitation.
9
Q
Please explain the mechanism of a collapsing pulse. Which is the best
artery to elicit it: radial, brachial or carotid?
A
A collapsing pulse is due to an increased stroke volume, which gives
quick distension of the peripheral arteries followed by regurgitation of
blood back into the left ventricle, which gives a rapid fall, i.e. a quick
rise followed by collapse. The brachial is probably the best artery to
palpate.
10
Q
What is the mechanism of Durozier’s sign?
A
This is a femoral bruit (‘pistol shot’) due to a large volume pulse.
11
Q
What effects do aortic stenosis, aortic regurgitation and coarctation of the
aorta have on systolic and diastolic blood pressure, and why do they
produce these effects?
A
Aortic stenosis can produce a low systolic pressure with a normal
diastolic pressure because of outflow obstruction to the left ventricle
(systolic) but normal peripheral resistance (diastolic). Aortic
regurgitation produces normal or high systolic pressure because of
unimpeded left ventricular emptying with low diastolic pressure due to
a rapid fall in peripheral flow. Hypertension in coarctation is due to
reduced renal flow (the Goldblatt effect).
12
Q
In the section headed ‘Pulsus bisferiens’ (K&C 7e, p. 691) what do
‘percussion wave’ and ‘tidal wave’ mean? An illustration here would be
helpful.
A
The percussion wave is the first wave produced by the transmission of
the left ventricular pressure in early systole. With recoil of the vascular
bed a second weaker wave (tidal) occurs which can be felt in the radial
artery in the presence of slow ventricular emptying, e.g. in mixed aortic
valve disease. A double pulse is bisferiens
13
Q
When examining a patient’s carotid pulse, why should we not palpate
both carotids at once? Is it because it might block the blood supply to the
brain?
A
Yes, palpating each carotid separately is safer (one side may have a
stenosis/atheroma) and might provide more information, e.g. right
carotid sinus massage decreases the sinus node discharge. In addition,
carotid sinus syncope can occur, which can impair cerebral perfusion in
some elderly patients, causing loss of consciousness.
14
Q
How can I differentiate between jugular and arterial pulsation in the neck
practically?
A
● You can look for the double pulsation of the jugular venous pulse.
● You can feel the arterial pulse at the same time as you look at the
jugular venous pulsation.
● The point at which the venous column is seen varies with the position
of the patient.
● Pressure on the liver raises the jugular venous pressure, which can be
used to make sure that it is the venous wave (hepato-jugular reflux).
15
Q
Can you please help me with this: ‘Thrusting due to mitral or aortic
regurgitation. Heaving due to aortic stenosis and systemic hypertension.
There is often confusion about the terms thrusting and heaving’.
Another book I read considers aortic stenosis and hypertension for
thrusting and mitral/aortic regurgitation for heaving. Who should I go
with? Thank you.
A
There is indeed confusion regarding the terms ‘thrusting’ and ‘heaving’.
We ourselves have changed the terms used to describe the apex beat over
the seven editions! You are also correct in saying that different terms
are used by different authors. In the 7th edition we do not use the term
‘thrusting’. Sustained (heaving) apex beat occurs in pressure overload
situations, e.g. in aortic stenosis; forceful occurs with volume overload,
e.g. aortic regurgitation.
16
Q
Where is the best place on the precordium to auscultate a split-second
heart sound?
A
In the so-called pulmonary area: left substernal edge, second intercostal
space.
17
Q
What is the mechanism by which murmurs of mitral valve prolapse
(MVP) and hypertrophic cardiomyopathy (HC) are accentuated by
standing or the Valsalva manoeuvre?
A
Standing or the ‘strain phase’ of the Valsalva manoeuvre decreases the
left ventricular volume which increases the intensity and the duration
of the murmur. ‘Squatting’ increases left ventricular volume and the
murmur becomes shorter and softer.
18
Q
What is the correct procedure for a fluoroscopy and why is this essential
for the insertion of cardiac catheter, pacemaker and prosthetic valve?
A
Fluoroscopy is dynamic radiography. X-rays are being taken continually
so that the image is moving, not static as in a chest X-ray. Radiation hazards limit the time used but it is invaluable in placing catheters etc. in
the correct position.
19
Q
What is the role of amiodarone in the acute management of asystole or
pulseless electrical activity (PEA)?
A
There is no role for amiodarone in asystole. Vasopressin does seem to be
helpful.
20
Q
Is there any contraindication to the use of microwaves or mobile
phones in patients with pacemakers?
A
None with microwaves. Mobile phones should not be held right next
to a pacemaker.
21
Q
What, if any, appliances should be avoided in a patient with
a pacemaker?
A
With modern pacemakers, no household appliances need to be
avoided.
22
Q
- What is tachy-brady arrhythmia in the sick sinus syndrome?
- How can it be managed?
A
- In the sick sinus syndrome, patients develop episodes of sinus
bradycardia or sinus arrest and commonly, owing to diffuse atrial
disease, experience paroxysmal tachyarrhythmias. These together are
called the tachy-brady syndrome. - A permanent pacemaker (paces the two (Dual) chambers, senses
both D and reacts to both (DDD)) is required with antiarrhythmics to
control the tachycardia element.
23
Q
Practically, how can we differentiate between a second-degree
atrioventricular (AV) block Mobitz I and Mobitz II? What is the meaning
of first-degree block? What is the difference between heart asystole, heart
arrest and third-degree AV block?
A
First-degree AV block (Fig. 13.2a)
This is prolongation of the PR interval to more than 0.22 s.
Second-degree AV block
● Type I, also called Mobitz type I or Wenckebach phenomenon (Fig.
13.2b): there is a progressive increase in the PR interval until a P wave
fails to conduct.
● Type II or Mobitz type II (Fig. 13.2c): some P waves do not conduct
to the ventricles and there is no progressive increase in the preceding
complexes of the PR interval as in Mobitz type I.
Third-degree AV block
Complete heart block occurs when there is complete failure of
conduction to the ventricles.
24
Q
How can a complete atrioventricular (AV) block be diagnosed on an
electrocardiogram (ECG)?
A
The ECG shows complete dissociation between the P wave and QRS
complex
25
Usually, we look for an RSR pattern for bundle branch block in the chest
leads. What does it mean if there is an RSR pattern in the limb leads?
This usually indicates a right bundle branch block with either right
or left axis deviation, sometimes called a Wilson-type right bundle
branch block.
26
What is Wolff–Parkinson–White syndrome?
This describes patients with a history of palpitations in whom there
is conduction down an accessory pathway producing a ‘pre-excited’
electrocardiogram. There is a short PR interval followed by a slurred
initial part of the QRS complex known as the δ wave.
In one form the electrical impulse is conducted quickly over the
accessory pathway, thereby depolarizing the ventricle early, i.e. preexcitation,
with atrial activation via retrograde conduction through the
AV node.
27
In management of atrial fibrillation (AF), is the priority to control
ventricular rate or to restore cardiac rhythm?
There is greater emphasis at the present time in trying to control the
rhythm, if this can be achieved, because anticoagulation can be stopped
28
Can digoxin be given in paroxysmal atrial fibrillation?
Digoxin should not be used to prevent episodes of paroxysmal atrial
fibrillation. Digoxin can be used to slow the heart rate in a patient who is
in atrial fibrillation. The treatment of choice to prevent further attacks is
by catheter ablation of the arrhythmic focus.
29
In a patient with atrial fibrillation and bronchial asthma, what is
the recommended treatment and do beta-blockers make the condition
worse?
The treatment is either cardioversion (rhythm control) or AV nodal
slowing agents (rate control) but you need to carefully study the
management of this common condition. Beta-blockers should not be used
in patients with asthma; it makes the asthma worse
30
What is the difference between atrial flutter and atrial tachycardia?
Atrial flutter is an organized atrial rhythm at 250–350 beats per minute.
The most frequent is counterclockwise flutter, but re-entry flutter also
occurs. Atrial tachycardia is slower and is either a re-entry or automatic
tachycardia.
31
What are the possible causes of atrial extrasystoles, in a patient with
a normal echo, which last for several days and then disappear
spontaneously? Is treatment with anxiolytics recommended?
Atrial ectopic beats are usually of no significance. Treatment is not usually
required but a beta-blocker can be used, particularly with anxiety
32
In the treatment of ventricular tachycardia, could lidocaine be used in the
absence of any other drug? How effective is lidocaine?
Yes, lidocaine given as a bolus followed by intravenous infusion
(2–4 mg/min) is very effective. DC cardioversion is the other option.
33
Why is an extremely low level of potassium in the blood sometimes
a cause of ventricular fibrillation?
Hypokalaemia affects repolarization with progressively smaller T waves.
Usually, this has no immediate consequence but, particularly in the
presence of digoxin, ventricular fibrillation can occur
34
How often does verapamil cause impotence and inhibit ejaculation?
This is unclear. Most people think all hypotensive agents can produce
erectile dysfunction, but, in one study comparing a number of drugs only
thiazides caused more dysfunction than placebo
35
Why does a patient with congestive cardiac failure have excessive
sweating?
Excessive sweating is related to increased circulating sympathomimetics
such as epinephrine (adrenaline).
36
What is cardiac asthma?
Wheezing due to bronchial endothelial oedema occurs in cardiac failure
and is sometimes called ‘cardiac asthma’ to compare and contrast it with
bronchial asthma.
37
I wanted to ask whether a third heart sound is present, or should be
present, in all cases of heart failure, whatever the underlying cause.
Yes, it is present in left ventricular failure of whatever cause. The precise
mechanism of the cause of the third heart sound is not entirely clear. It is
associated with rapid ventricular filling.
38
Why can left heart failure lead to right heart failure but not vice versa?
What is the physiology involved in this transition?
Left heart failure is much more common than right heart failure and in
the backward pressure theory of heart failure right ventricular failure
develops as a consequence of left ventricular failure
39
Could you explain the fetal gene program, activated in heart failure?
Changes in the myocardial gene expression occur when the ventricle is
overloaded, i.e. heart failure and there is a return to the fetal pattern, as shown in animal models. There is a shift from αα (usually predominates
in the atrium) to ββ (usually mainly in the ventricles) myosin heavy
chains in the atria.
40
How safe is it to stop administration of carvedilol to a patient with
heart failure? Can the drug be tapered off? What are the effects/dangers of stopping carvedilol suddenly? What, if any, are the reasons for
discontinuing carvedilol in patients with heart failure?
There appear to be no dangers in stopping carvedilol suddenly or indeed
tapering off the drug. However, most patients should not have the drug
withdrawn, because of the good results reported with beta-blocker
usage. In one small study in patients who were taken off a beta-blocker,
deterioration or death occurred in 50% of a small group of patients.
Finally, bradycardia and poor cardiac output are the usual reasons for
discontinuing carvedilol and it is not appropriate to use it if a drug such
as milrinone is being considered
41
What are the advantages and disadvantages of furosemide in the
treatment of cardiac failure?
Furosemide promotes renal excretion of water and sodium, so relieving
fluid overload, i.e. oedema. It also has a venodilatory action, which is
why pulmonary oedema responds rapidly to IV furosemide. Its main
side-effect is hypokalaemia.
42
In heart failure, can furosemide be given once daily?
Yes; usually 40 mg in the morning is given, to avoid nocturnal urinary
frequency.
43
What are the clinical features of a ruptured sinus of Valsalva?
This usually occurs in a previously fit young man who suddenly has
shortness of breath and ischaemic chest pain. Heart failure is present
with a loud continuous murmur on auscultation. Echocardiography is
diagnostic. Treatment is urgent surgery.
44
```
Does dobutamine (dose range 2.5–10 μg/kg/min) cause significant
tachycardia?
```
At this dosage there is an increase in myocardial contractility with little
effect on rate.
45
Are beta-blockers indicated in heart failure; if yes, in all cases or in
selected cases?
All patients with heart failure should receive a beta-blocker if there is no
contraindication, e.g. asthma, and if the drug is tolerated (in clinical trials
85% of patients tolerated beta-blockers). The initial dose should be low
to avoid initial side-effects, e.g. hypotension. In randomized controlled
trials, beta-blockers have been shown to improve symptoms as well as
reduce the risk of death and retard the progression of heart failure.
46
Why does long-term treatment by digitalis cause gynaecomastia?
Elevated plasma oestradiol levels (digoxin has intrinsic oestrogenic
properties) and decreased plasma testosterone levels occur
47
Why do toxic doses of digoxin (which cause a decrease in excitability of
cardiac tissue) cause arrhythmias, whereas therapeutic levels of digoxin
(which cause increase in excitability) cause no arrhythmias?
Toxic levels of digoxin cause an increase in intracellular calcium, which
leads to depolarization of the cells, initiating arrhythmia
48
Hypokalaemia is one of the complications of digitalis. In treatment
we give K
. How does the hyperkalaemia enhance the digitalis
toxicity?
Hypokalaemia is not a direct complication of digitalis therapy. Vomiting,
anorexia and diarrhoea are side-effects of digoxin therapy and can
contribute to hypokalaemia. Hyperkalaemia does not enhance digitalis
toxicity but too rapid a correction of hypokalaemia can lead to heart
block
49
Why should we measure serum potassium before we start digoxin?
Digoxin acts by inhibiting the Na
K
-ATPase pump. Hypokalaemia
increases the binding of digoxin to cardiac myocytes, potentiating its
action and decreasing its clearance as well as further inhibiting the
Na
K
-ATPase pump. Hypokalaemia should be corrected (it should
of course not be allowed to occur) in patients on digoxin. Paradoxically,
hyperkalaemia can occur in severe digoxin overdose, and might need
treatment with glucose and insulin.
50
The intravenous administration of loop diuretics such as furosemide
relieves pulmonary oedema rapidly. Is this due to arteriolar
vasodilatation reducing afterload which is an action that is independent
of its diuretic effect? I ask this because I have been told that this drug has
no effect on arterioles (except on efferent arterioles of the kidney), but
rather a venodilatatory effect. What could be the cause of such different
opinions?
Loop diuretics do primarily act on venules producing an acute increase
in systemic venous capacitance and thereby decreasing left ventricular
filling pressure. This effect is probably mediated by prostaglandins
released from the kidney. Some workers think that furosemide has an
effect on arterioles similar to morphine in pulmonary oedema
51
There have been a number of recent publications concerning aspirin
versus warfarin trials. Would you recommend prescribing warfarin for
secondary prevention of coronary heart disease in patients suffering from
their first myocardial infarction (MI)?
At the present time, aspirin is used routinely in all patients following
an MI unless there are contraindications. Warfarin is used if there is
evidence of a deep vein thrombosis (DVT), pulmonary embolism, mural
thrombosis on an echocardiogram, the presence of atrial fibrillation or a
previous embolic cardiovascular event.
52
Is it true that in future the ApoA : ApoB ratio will be used to predict
the risk of coronary artery disease more efficiently than low-density
lipoprotein (LDL)?
Apo A : Apo B ratio is not more effective for predicting coronary artery
disease than LDL.
53
What is the exact link between C-reactive protein (CRP) and coronary
artery disease?
There is much debate as to whether CRP is an independent risk factor
for coronary artery disease. Atherosclerosis is an inflammatory condition
and CRP elevation (using a high sensitivity assay) may therefore occur.
Recent data have also suggested that hs-CRP may be of prognostic value
after excluding other prognostic factors
54
In angina pectoris, why does the chest pain get radiated to the left side,
i.e. left arm and back?
Pain from the heart is transmitted by visceral afferent fibres
accompanying sympathetic fibres and is typically referred to the upper
chest and left arm, which have afferent fibres with cell bodies in the same
spinal ganglion and central processes that enter the spinal cord through
the same dorsal roots. The pain is typically felt in the area supplied
by the medial cutaneous nerve of the arm (T1 spinal segment).
Communicating fibres in the spinal cord to the right side explain the
occurrence
55
Please explain why thrombolytic therapy is not indicated in cases of
unstable angina and non-ST-segment elevation myocardial infarctions
(nSTE-MI) despite the fact that both nSTE-MI and ST-elevated MI
(STEMI) are caused by a thrombus for which thrombolytic therapy is
highly indicated? Could it be true that, in the case of unstable angina and
nSTE-MI has a higher incidence of intracranial haemorrhage than in the
case of ST-segment elevation MI?
The terminology has changed slightly. STEMI still refers to ST segment
elevation myocardial infarction but both non-ST elevation myocardial
infarction and unstable angina are now referred to as nSTE-ACS (ACS
being acute coronary syndrome).
Fibrinolytic agents are not used in nSTE-ACS because they do not
reduce the mortality. Coronary intervention is now used for high-risk
cases in many institutions
56
Doesn’t the term ‘acute coronary syndrome’ include unstable angina, non-
ST-segment elevation myocardial infarctions and ST-elevated MI (STEMI)?
The term ‘acute coronary syndrome’ (ACS) was introduced to refer
to unstable angina but now includes nSTE-ACS and STEMI as well as
unstable angina (see above and McClelland et al. 2004). It is necessary,
for optimal treatment, to stratify patients with acute coronary syndrome
into high and low risk.
57
Kindly mention the indications for clopidogrel in acute coronary
syndrome (ACS). Should it be used along with aspirin or alone if the
latter is contraindicated? Are there any studies that combine both
with either low-molecular-weight heparin (LMWH) or unfractionated
heparin? How long should clopidogrel be continued?
The CURE trial, which involved over 12 000 patients, compared
treatment with aspirin and aspirin plus clopidogrel. There was some
suggestion of a better outcome with the two drugs but there was an
increase in haemorrhagic complications. It was therefore recommended that clopidogrel be used for those people in whom aspirin is
contraindicated. However, current guidelines recommend that aspirin
and clopidogrel should be given to all patients with acute coronary
syndromes unless cardiac bypass surgery is planned. There have been no
published studies on unfractionated heparin or low-molecular-weight
heparin with clopidogrel. Finally, the clopidogrel should be continued for
at least 9–12 months.
58
What role do IV fluids play in the management of acute inferior wall
myocardial infarction?
Acute inferior wall infarction can be accompanied by right ventricular
dysfunction, when hypotension might be present, with a low cardiac
output and low venous pressure. A fluid challenge with 0.9% saline can
be helpful, as volume expansion might be needed
59
Is there any benefit in combining aspirin with clopidogrel in post-MI
angina and ischaemic stroke? A MATCH trial showed this combination not to be of benefit – would you therefore recommend we stop using this
combination in our hospital unit?
Initial studies showed that long-term use of clopidogrel with aspirin
increases the risk of bleeding without having much effect on outcome.
However, the Scottish Medicine Consortium advised (in February 2004)
that clopidogrel be accepted for restricted use with low-dose aspirin
for non-ST elevation acute coronary syndrome (nSTE-ACS) and many
authorities now use clopidogrel and aspirin in all patients with acute
coronary syndrome. Not useful in ischaemic stroke.
60
In a patient with the typical chest pain of myocardial infarction (MI) and
no other criteria for thrombolysis would highly elevated cardiac enzymes
indicate thrombolysis?
With chest pain and high troponins only non-ST elevation acute coronary
syndrome (nSTE-ACS) is not usually considered an indication for
thrombolysis. Risk stratification is necessary to decide upon timing of
coronary intervention
61
I cannot figure out the role of an acetylcholinesterase inhibitor in postmyocardial
infarction
Acetylcholinesterase inhibitors (i.e. antimuscarinics, which is a better
term) such as atropine are used for sinus bradycardia following
myocardial infarction.
62
Can thrombolytic therapy for myocardial infarction (MI) be started
in patients who have cardiac pain and raised cardiac markers? Can
streptokinase be given irrespective of electrocardiogram (ECG) changes
(according to some books, ST elevation has to be present)?
The use of thrombolytic therapy continually changes. The diagnosis of
MI was also changed to include a classic history and raised troponins.
More recently, however, streptokinase therapy or other thrombolytics
have been recommended only for patients with ECG changes of ST
elevation (STEMI) (Fig. 13.4). Non-STEMI (no ST elevation) patients are
not given thrombolytic therapy, even though troponins are raised,
but are referred for coronary intervention
63
Can carvedilol be used in an elderly patient who developed left
ventricular failure after a very recent myocardial infarction, or should it
wait until the condition becomes stable?
Beta-blockers such as carvedilol have shown a significant improvement
in the survival in patients with chronic stable heart failure. Therefore wait
until the patient is stabilized with angiotensin-converting enzyme (ACE)
inhibitor diuretics.
64
I have seen some patients with chronic rheumatic heart disease with no
obvious evidence of rheumatic fever (i.e. they could not recall if there
was an episode of severe infection with subsequent fever and joint pain).
So, actually, how is chronic rheumatic heart disease diagnosed?
Only 50% of patients with chronic rheumatic heart disease give a history
of rheumatic fever or chorea. There is no absolute way one can be sure
that the valvular disease is rheumatic – it is by exclusion of other causes,
e.g. syphilis in aortic regurgitation. Mitral stenosis is almost always due
to rheumatic fever.
65
If a young patient presents with hemiparesis and rheumatic atrial
fibrillation and is already on oral anticoagulant, with an international
normalized ratio (INR) 3 and a normal computed tomography (CT)
scan done 2 hours after onset, should he receive heparin for prophylaxis
against further embolism? Should aspirin be combined with oral
anticoagulant later, or should target INR be increased?
This is difficult, but there is no evidence that using another agent, e.g.
heparin, helps. Aspirin has been used but efficacy is not very good.
Consideration should be given to treatment of the valvular lesion,
which will include removal of clot from the left atrium and then DC
cardioversion or drug therapy to control the rhythm.
66
When treating mitral stenosis using a balloon valvotomy, how come no
thrombus develops at the site of the atrial septum or at the separated
commissure of the valve leaflets?
It is unclear why this does not happen but it does not seem to!
Percutaneous treatment using a balloon compares very favourably
with open and closed valvotomy with no evidence of early or late
thromboembolism in any group
67
Why does a mitral stenosis produce a loud S1?
The valve leaflets are widely open when ventricular systole begins and
therefore they close with a loud noise
68
Why is the mitral valve more affected than any other valve in the heart in
most valvular diseases?
There is no good reason for this.
69
What is William’s syndrome (supravalvular obstruction)? Why does
hypercalcaemia occur with this syndrome?
Williams syndrome is a rare genetic syndrome that includes
supravalvular alveolar aortic stenosis, narrowing of the pulmonary
arteries and many other features.
It is unclear why hypercalcaemia occurs. There is no abnormality of
parathyroid hormone (PTH) secretion and vitamin D levels are normal.
An abnormality in the gene regulating calcitonin and calcitonin-gene-related
peptide has been suggested
70
Kindly tell me all the causes postulated for the collapsing pulse seen in
aortic regurgitation.
Rapid ejection of left ventricular volume into a low-resistance arterial
system followed by regurgitation back into the left ventricle leads to a
rapid fall in pressure with collapse of the arterial pressure.
71
Does pulmonary stenosis cause pulmonary hypertension?
No, there is no significant rise in pulmonary pressure in most cases of
pulmonary stenosis.
72
Under what conditions would a pulsatile liver be found and what is its
clinical significance?
A palpable liver that pulsates in systole is seen in a tricuspid
regurgitation. It is associated with right heart failure
73
Can we use warfarin during pregnancy or during menstruation in
a patient with a prosthetic valve? Is anticoagulation necessary in a
patient with a corrected ventricular septal defect (VSD) or corrected
coarctation of aorta?
Warfarin is teratogenic and should not be given in the first trimester,
and women at risk of pregnancy should be warned to stop the drug very early. The use of anticoagulation in pregnancy is a very complicated
problem and should only be done under careful supervision by people
expert in the field. Anticoagulation is not necessary for a corrected VSD
or coarctation of the aorta
74
Duke criteria in diagnosing infective endocarditis
two major criteria are a positive blood culture and evidence of
valvular disease, either clinical or echocardiographic. Minor criteria
include fever, evidence of emboli, etc. Two major or one major and three
minor are required for the diagnosis of infective endocarditis.
75
Is Staphylococcus aureus the most frequent causative agent of acute
bacterial endocarditis? And is this typical of acute bacterial endocarditis?
Staph. aureus is the most common cause of acute bacterial endocarditis.
The clinical picture is very typical.
76
Please explain the mechanism of the mycotic aneurysm in infective
endocarditis.
Small septic emboli block vasa vasorum or a small distal cerebral artery
itself, leading to damage to the muscular layer with dilatation and
aneurysm formation.
77
Why are the right valves more commonly affected in infective
endocarditis when the microbes enter through the IV route, for example
with IV drug users?
Because a large number of organisms go directly to the valves on the
right side. However, even in intravenous drug users, left-sided valve
involvement is more common.
78
You have said that in IV drug users the microbes go directly to the right
ventricle, thus causing endocarditis in the right heart. But in dental procedures the microbes also go through the veins to the right heart first,
so why are the left heart valves more commonly affected?
It is a question of the amount of bacteria, which is large in IV drug users
and small in dental sepsis. The reason for the left heart valves being
affected more in, for example, dental procedures is probably because the
incidence of damage to the left heart valves, e.g. from rheumatic fever, is
greater than the right.
79
What causes splenomegaly in infective endocarditis?
This is probably due to chronic infection with stimulation of both
humoral and cellular immunity
80
We know that Janeway lesions appear with infective endocarditis, but is
there any other disease that can cause it?
not really
81
Patent ductus arteriosus (PDA) is also called duct-dependent circulation.
What is the meaning of this phrase and do any other conditions present
with a similar condition? What is the implication of this condition to the
human body?
Duct-dependent circulation occurs in fetal life when there is no
pulmonary circulation. The blood is diverted through the duct (that is,
duct dependent) into the systemic circulation and is then re-oxygenated as it passes through the placenta. There is no comparable situation.
Failure of ductal closure at birth results in persistent ductus arteriosus,
which can lead to cardiac problems if not treated.
82
What is the recommended treatment for a child with both congenital and
valvular heart disease?
Careful evaluation in a designated centre with echocardiography
(including Doppler) and MRI is carried out initially. Corrective surgery is
performed if necessary in a stepwise fashion
83
Is a single ventricle disease associated with any syndrome? If so, what is
its name and what are its characteristics?
Single ventricle disease is where the blood flowing through the mitral
and tricuspid valves enters one common ventricle, morphologically in
90% of cases it is the left ventricle. The effects are complex and most
require surgery as a baby, with the formation of anastomoses between
the systemic venous and pulmonary circulations
84
What is the cause of splitting of the second sound in breathing and why
is it wide and fixed in atrial septal defect (ASD)?
In inspiration left ventricular systole shortens causing A2 to occur earlier.
In inspiration there is increased venous return to the right heart which
further delays P2. Therefore the split in the second sound is wider. In an
uncomplicated ASD, shunting of blood from the left to the right heart
occurs, which counterbalances the normal respiratory variation in
systemic venous return; therefore the split is fixed.
85
Why are deep-sea divers considered a ‘high-risk’ group if they have an
atrial septal defect (ASD)?
Because paradoxical emboli occur with production of a stroke.
86
Is it prognostically beneficial to start treatment of impending cor
pulmonale in a case of chronic obstructive pulmonary disease (COPD)
with no symptoms of failing heart but with investigational evidence
(electrocardiogram and chest X-rays)?
Oxygen therapy given continuously has been shown to reduce
pulmonary artery pressure, and to decrease mortality in COPD. Other
agents to reduce pulmonary pressure, such as vasodilators, are probably
of no benefit and may be harmful.
87
What would be the ideal investigation for a suspected pulmonary
embolism according to the protocol in a UK hospital?
Ventilation–perfusion scan. A normal scan virtually excludes a
pulmonary embolism. A ‘high probability’ scan indicates a 95% chance of
a pulmonary embolism. A negative D-dimer assay excludes a pulmonary
embolism. All of these investigations must be evaluated with the clinical features. If obtainable, a multi-slice CT has a high sensitivity of 83% and
a specificity of 92% even with a small embolus
88
Can the apical pulsation in right ventricular enlargement be
| hyperdynamic?
Not usually.
89
Please explain concentric and eccentric left ventricular hypertrophy.
When the hypertrophied ventricle dilates and the wall thins out, is it still
called a hypertrophied ventricle?
Concentric hypertrophy occurs with hypertension; the left ventricular
wall becomes uniformly thickened but the intraventricular end-diastolic
volume remains unchanged. Eccentric hypertrophy occurs with mitral
regurgitation; the end-diastolic volume is increased but wall thickness is
not. In both, histologically and ultrastructurally, there is hypertrophy.
90
What is viral pericarditis?
```
Acute pericarditis (inflammation of the pericardium) is often due to a
virus. Coxsackie and echovirus are the most common causes in the UK.
```
91
I want to know why thrombolytic therapy is contraindicated in acute
pericarditis.
Thrombolytic therapy is not required in acute pericarditis; there is no
problem with the coronary arteries. Pericarditis complicating myocardial
infarction is not a contraindication to thrombolytic therapy, although
of course thrombolytic therapy should have been given long before
pericarditis developed
92
Why would sitting bring pain relief to, and lying aggravate, a patient
with acute pericarditis?
Sitting forward in some way separates the chest wall fractionally from
the parietal pericardium. There must be other local factors
93
How do you determine whether a patient is in a ‘hypertensive
| condition’? And what is wide pulse pressure?
Hypertension is defined as a systolic pressure above 130–139 and/or a
diastolic blood pressure of 85–89 mmHg. Wide pulse pressure means
an increase in the pressure between systolic and diastolic values. For
example, normal pulse pressure in a patient with BP 120/70 50; wide
pulse pressure in a patient with BP 160/60 100. This is common in the
elderly with stiff, non-compliant arteries.
94
What is the clinical importance of a diastolic
pressure? And what problems might arise if a patient has a too high/low
diastolic blood pressure?
The diastolic pressure is of critical value and until fairly recently was
the main target of treatment. This was because the diastolic pressure does not vary as much as the systolic and therefore clear guidance could
be given that patients with a diastolic pressure 100 mmHg should be
treated; this value is now more usually 90 mmHg. Recently, it has been
realized that the systolic pressure is as important in the production of
complications – both cerebrovascular and cardiac events.
Isolated systolic hypertension occurs frequently in the elderly
160 mmHg and needs treatment (
95
What causes hypertension in children?
Look for:
● renal disease
● endocrine disease
● coarctation of the aorta.
96
Is haemochromatosis a cause of hypertension?
No; haemochromatosis is not a cause of hypertension
97
What are the most recent advancements in management of hypertensive
crisis? Is there any new approach or method under trial?
The most recent advance in management reflects CT and MRI imaging,
which show the effect of accelerated hypertension on the brain. In terms
of treatment, the most important thing is not to reduce the pressure too quickly except in very urgent situations, e.g. a dissecting aneurysm. Here
parenteral therapy is necessary. In other situations, oral hypotensive
therapy only should be used. This can be with atenolol, labetalol or a
calcium-channel blocker, e.g. amlodipine. Try to reduce pressure over
24 hours to between 100 and 110 mmHg diastolic.
98
Why does hypertension not cause headache, and why does only the
accelerated hypertension cause headaches. You say in ‘coarctation of
aorta’ that there is headache and epistaxis from hypertension
Hypertension does not normally cause headache. Accelerated
hypertension does cause headaches because there is some degree of
cerebral oedema. In a number of descriptions of coarctation of the aorta it
does say that headache and epistaxis is a clinical feature; there is no good
explanation for this headache.
99
Why is a headache one of the signs and symptoms of hypertension?
Headache only occurs with severe hypertension where there are
associated changes in the small cerebral arteries and cerebral oedema
100
In a hypertensive hypercholesterolaemic patient, is it contraindicated to
use a bisoprolol–hydrochlorothiazide combination to control the patient’s
hypertension if it is not controlled on bisoprolol alone?
No, the combination is not contraindicated as it is an effective treatment
of hypertension. Beta-blockers are however being less used because
of their side effects. Thiazide and beta-blocker therapy does affect the
cholesterol but the change is usually small and if necessary a statin can
be co-prescribed.
101
Should a hypertensive patient with recurrent ischaemic strokes, a total
cholesterol of 200mg/dL (5.2mmol/L), low-density lipoprotein (LDL)
cholesterol of 120mg/dL (3.12 mmol/L) and high-density lipoprotein
(HDL) cholesterol of 35mg/dL (1mmol/L), have a statin therapy?
Total cholesterol 200 mg/dL (5.2 mmol/L) is desirable with an LDL
cholesterol 100 mg/dL. The HDL cholesterol should be greater than
60 mg/dL (1.5 mmol/L). So, yes, statin therapy is required, with
lifestyle changes.
102
Has Tenormin any advantage over other beta-blockers in the control of
hypertension?
Tenormin (atenolol) is the most commonly prescribed beta-blocker for
hypertension. It is water soluble, and therefore has no effect on the brain.
It has no other advantage, except that it is cheap. Recent data suggest that
atenolol only reduces the brachial and not aortic pressure and therefore
has no effect on outcome. Other antihypertensives appear to be more
effective at reducing the incidence of stroke and are now preferred
103
Is the use of sublingual captopril 25 mg/h, in combination with IV
furosemide 40 mg/h to a maximum of 120 mg, safe to lower greatly
elevated blood pressure?
We have not used this combination. Captopril is almost always used
orally not sublingually. ‘Do not reduce the blood pressure too rapidly’ is
the rule, even when the initial readings are very high.
104
Is ACEI superior to calcium channel blockers in the treatment of
hypertension, in terms of prognosis and of the prevention of
complications?
ACE inhibitors are thought to be the drug of choice for hypertension in
the diabetic as they are renoprotective. Both reduce the risk of stroke.
Often both drugs are needed for good control of hypertension. In nondiabetics,
both are useful.
105
Are angiotensin-converting enzyme (ACE) inhibitors more effective
than beta-blockers in reducing the risk of stroke in hypertensive
patients?
No. Beta-blockers are still as effective as the newer agents such as ACE
inhibitors, although the new drugs are being more and more used
because side-effects are less. ACE inhibitors or ACE antagonists are
recommended in diabetics.
106
Do non-steroidal anti-inflammatory drugs (NSAIDs) affect the
antihypertensive effect of angiotensin-converting enzyme (ACE)
inhibitors? If so, how?
Yes. They promote Na retention and have an effect on prostaglandin
synthesis in the kidney.
107
What antihypertensive is recommended for a patient with aortic stenosis
(AS) and hypertension, as a mono- and combination therapy?
If the patient is asymptomatic no treatment is required for aortic stenosis
(AS). Hypertension could be treated with beta-blockers. Surgery is usually
indicated in patients with symptoms from AS. Hypertension could be
treated with a diuretic plus beta-blockers with careful evaluation
108
Impotence is a common side-effect of antihypertensive drugs. How can
I solve this problem in young hypertensive patients?
Impotence (a better term is erectile dysfunction) is common with
antihypertensive therapy. Try to avoid drugs such as bendroflumethiazide,
which is well recognized as causing erectile dysfunction. Fortunately,
most patients respond to phosphodiesterase type 5 inhibitors (PDE5),
e.g. sildenafil, even on hypotensive therapy.
109
In the treatment of hypertension, is it recommended to commence
treatment with two drugs containing a thiazide (if elderly) or a betablocker
(if young)?
It is usual to start with a single agent, although this is often not adequate
and a second agent is required. Conventional treatment is to start with
a thiazide diuretic, then adding a beta-blocker as you suggest. Many
doctors now, however, go straight to an angiotensin-converting enzyme
inhibitor or ACE blocker, which tend to have a better side-effect profile.
Also, calcium-channel blocking drugs are often used.
110
1. Following a stroke, both haemorrhagic and ischaemic, in previously
hypertensive and normotensive patients, can you explain precise
blood pressure control and the desired blood pressure levels?
2. In the case of a hypertensive emergency, with a blood pressure of
220/130 with acute myocardial infarction, what immediate measures
should be taken?
1. Control of blood pressure is of vital importance but should not be
achieved rapidly. Oral therapy, e.g. amlodipine, is used to bring the diastolic pressure to below 100 mmHg initially. Longer-term
combination therapy is usually required to get blood pressure to
120 systolic, 80 diastolic, ideally.
2. In the patient with a myocardial infarction the same principles apply:
use oral medication to get the diastolic pressure down to
100–110 mmHg over 24 hours.
111
On lowering blood pressure, to what extent can heart failure secondary
to chronic hypertensive heart disease be reversible?
Controlling hypertension in the elderly can reduce the incidence of heart
failure by 30%. Heart failure is reversible but still carries a high mortality.
112
Is the use of amlodipine or furosemide recommended to normalize blood
pressure in a case of hypertensive heart failure? If so, which is most
effective?
Both can be used and dual or triple therapy is often required in
hypertension.
113
How can diabetes cause endothelial dysfunction? What are the roles of
ACE inhibitors in the kinin–kallikrein system? What are the mechanisms
by which a decrease in the level of nitric oxide causes endothelial
dysfunction?
Diabetes is associated with atherosclerosis, which causes endothelial
dysfunction (Gaenzer et al. 2002). ACE inhibitors inhibit the inactivation
of bradykinin and substance P. Nitric oxide causes vasodilatation so
that any decrease in nitric oxide promotes constriction and therefore
endothelial damage
114
Can sublingual nifedipine be given to a patient with malignant
hypertension/accelerated hypertension? It seems to be a controversial
issue with some favouring it and some against it.
Sublingual nifedipine is recommended by some authorities for malignant
hypertension and therefore you can give it. The main aim is not to lower
the blood pressure too rapidly. You are best to use the agent that you are
familiar with. Other agents include atenolol or amlodipine but sublingual
modified-release nifedipine is quite acceptable
115
Is the diagnosis of malignant hypertension based only on the basis of the
retinopathy (even in the presence of a normotensive state)? Labetalol,
parenterally, is suggested as a treatment for malignant hypertension.
What other more readily available preparations (besides sodium
nitroprusside) are recommended in addition to this drug? Parental
labetalol is not available in Pakistan!
To diagnose hypertension you must have a raised blood pressure.
Malignant hypertension is associated with grade 3–4 retinopathy.
Malignant hypertension should always be treated with oral
medication if possible. Parenteral therapy might be required if there
are complications; parenteral nitroprusside is the preferred agent but
requires careful monitoring. Intravenous diazoxide, oral clonidine and
oral nifedipine are used when labetalol is not available.
116
Patients at medium risk of DVT and pulmonary embolism are usually
given specific prophylaxis with low-dose heparin at a dose of 5000 units
subcutaneously every 8–12 hours until the patient is ambulatory. Is the first dose given immediately after, say, extensive varicose vein surgery of
small and great saphenous veins?
Many experts now advocate preoperative treatment (e.g. 2 hours before
surgery) in medium- and high-risk patients. Many clinicians now
use low-molecular-weight heparin, e.g. enoxaparin 40 mg, rather than low-dose unfractionated heparin. Note: other prophylactic techniques,
e.g. compression stockings, should also be used
117
‘Anticoagulants are not necessary, as embolism does not occur from
superficial thrombophlebitis why?
There is inflammation of the vein wall so that the thrombus adheres to it
and pulmonary embolism occurs only rarely
118
Can we use enoxaparin for deep vein thrombosis (DVT) prophylaxis
in the immediate postoperative period and in a case of cerebral
haemorrhage? Wouldn’t it increase the risk of haemorrhage in
either case?
No, it should not be used in a case of cerebral haemorrhage. Enoxaparin,
a low-molecular-weight heparin, is used quite safely without monitoring
in DVT prophylaxis postoperatively.
119
For how long does a patient have to stay in bed to be labelled as
bedridden and to merit low-molecular-weight heparin (LMWH) as
prophylaxis for deep vein thrombosis?
This depends partly on risk factors such as age, obesity, degree of
immobilization and how long the period in bed is likely to be. Medical
patients are sometimes not treated with LMWH as early as they should
be; guidelines suggest that 3 days or longer in bed should be treated.
Treat early, if possible, with LMWH.
120
Is an inferior vena cava filter an alternative treatment for a patient with
a history of recurrent deep vein thrombosis on lifelong anticoagulation
with warfarin?
Filters in the inferior vena cava are useful for preventing recurrent
pulmonary emboli rather than using long-term warfarin. Anticoagulation
can be stopped with a filter in place.
121
```
Can you explain why a decrease in serum lipid levels follows an acute
myocardial infarction (MI)? For how long does this decrease last and
how is it known whether the patient has hyperlipidaemia in such a case?
```
The decrease in lipid levels is related to increased adrenalin which affects
lipid levels for up to 3 months. It doesn’t occur for 24–36 hours so there
is usually time for samples to be taken. Otherwise, you will have to wait
3 months to confirm hyperlipidaemia, unless of course the serum lipids
are high after the M
122
In patients with myocardial infarction, why is aspirin to be taken
chewed, and not by any other method?
Aspirin chewed goes directly into the systemic circulation; if you
swallow it, it has to be absorbed in the gut and then be transported by
the portal system
123
Must beta-blockers prescribed for hypertension be stopped if the heart
rate falls below 60 beats per minute?
No; not if the patient is stable and not having syncopal attacks.
Beta-blockers are becoming less commonly used for hypertension
124
How can aspirin resistance in patients with recurrent ischaemic stroke
be assessed; is the clotting time a factor? Does the substitution of aspirin
with clopidogrel solve this problem?
‘Aspirin resistance’ implies that aspirin does not inhibit tests of
platelet function in vitro. This is unusual. The term is wrongly used to
cover patients whose cardiovascular events are not helped by aspirin
(treatment failure). Clopidogrel is used in these circumstances
125
In a patient with heart failure and atrial fibrillation on warfarin who
experiences frequent transient ischaemic attacks, will the patient benefit
from having aspirin prescribed?
Aspirin will increase the risk of bleeding, but aspirin may well benefit
such a patient. Warfarin therapy will need constant monitoring.
126
Is there a role for anticoagulation in inoperable carotid stenosis 70%?
No; there are no good data to support the use of anticoagulants in carotid
stenosis. Aspirin therapy should be used.
127
What is the upper limit of serum creatinine reflecting renal damage from
hypertension above which thiazides should not be prescribed?
The upper limit is a creatinine clearance (estimated GFR) of <30 mL per
minute per 1.73m2, which is approximately >300 mmol/L.
128
Where should both cuff and stethoscope be placed in cases where the
patient is suspected of having coarctation of the aorta?
In coarctation of the aorta, the blood pressure in the legs is often
normal. This can be measured with a thigh cuff placed around the
thigh with the stethoscope over the popliteal artery.
