Q1 An infarct is an area of dead tissue caused by interruption of blood flow.

In a myocardial
infarction (heart attack) caused by interruption of coronary blood flow, an area of cardiac muscle
cells dies because of ischaemia. The patient may recover but the affected area of muscle may not
survive: it may be without blood flow for a prolonged period or the coronary blood vessel may be
permanently blocked. The affected cardiac muscle is eventually replaced by fibrous scar tissue.

Q2 A defibrillator administers a large direct current (DC) shock (starting at ∼200 J) across the chest
wall in order to depolarize the whole heart and stop the activity of the dysrhythmic areas, which
are producing ectopic (abnormal) beats. It is hoped that this will allow the normal pacemaker, the
SA node, to start again and generate the cardiac impulse in a normal rhythm: this is known as
sinus rhythm.

Q3 Epinephrine is a non-selective adrenoceptor agonist, capable of stimulating both alpha- and

beta-adrenoceptors (α- and β-adrenoceptors). When the heart is failing, epinephrine can stimulate
contraction of cardiac muscle via β1-receptors and so raise the cardiac output, without causing
bronchoconstriction, as it simultaneously relaxes airways via its action on β2-receptors.
Epinephrine is used in emergency situations because, when given intravenously, it acts rapidly, in
approximately 1 min. Sometimes the damaged heart develops an unsuitably slow beat,
bradycardia, which needs to be increased to maintain an adequate circulation. The drug of choice
for this action is atropine, which counteracts the effects of vagal slowing. Atropine is a cholinergic
antagonist acting on cardiac muscarinic cholinoceptors.

Q4 Cardiac enzymes are released into the blood following heart muscle damage during a heart
attack. Creatine kinase, particularly its MB isoenzyme, is one of the most specific of these
enzymes, which reaches a peak 24 hours after infarction. It rises and then falls within the first 72
hours of the heart attack. Aspartate transaminase is also released, but levels of this enzyme can be
raised in several other conditions, so it is less specific than creatine kinase MB. Troponin T is also
specific for myocardial damage and is raised for approximately two weeks following infarction.
Finding a high concentration of these enzymes in a patient’s blood therefore supports the
evidence obtained from the ECG and confirms that the patient has suffered a myocardial
infarction.

Q5 The heart may be regarded as lying in the centre of an equilateral triangle: the apices of the
triangle are marked by the two shoulders and the mid-line of the hips. The limbs act as linear
conductors. Depolarization and repolarization of the cardiac cells causes small currents to flow
through body fluids and tissues; this produces voltage changes at the body surface which can be
measured from electrodes placed at specific points on the skin. The ECG amplifies and records
these small voltage changes which occur at the body surface during each cardiac cycle.
Six of the 12 leads of the ECG are placed directly on the chest wall. By international convention,
these electrodes are placed in predetermined locations and record activity from sites directly over
specific parts of the heart. The other six leads are associated with recordings from the limbs. The
conventional limb leads record potentials between two apices of the triangle. Lead 1 records
potentials between the right arm and left arm, lead 2 records potentials between the right arm
and left leg and lead 3 records potentials between the left arm and left leg. These are known as
bipolar leads. In addition there are three unipolar leads attached to the limbs, which record
potentials between the limb and a reference zero. The normal ECG has a recognizable pattern
which varies only a little from person to person. When electrical or rhythmic changes in the heart
occur, specific changes can be seen in the ECG which can be used to aid diagnosis

Part 2

Q7 The purpose of using aspirin after a heart attack is to minimize the risk of blood clotting in the
circulation. It is recommended (in the United Kingdom) for use in the long-term management of
patients following myocardial infarction, unless there are contraindications to its usage in a
particular patient. Aspirin is a non-steroidal anti-inflammatory drug which inhibits the COX enzyme
responsible for the production of a range of prostaglandins. The latter agents are involved in
inflammation, control of body temperature, pain, platelet aggregation and many other body
processes. Aspirin reduces fever and pain and stops platelets from aggregating (clumping), so
preventing blood coagulation.

Q8 When a blood clot causes blockage to a coronary blood vessel, the cardiac muscle beyond the
blockage starts to die. There is a short period following a heart attack when the muscle can be
saved by dissolving the clot, so reinstating blood flow to the damaged region. Intravenous
thrombolytic drugs, such as streptokinase, need to be given within 12 hours of the infarction,
preferably in the first hour. They lyse clots by activating circulating plasminogen to plasmin.
Plasmin degrades fibrin and so breaks up blood clots, allowing blood to flow through the coronary
vessel once more. Streptokinase and tissue plasminogen activators have been shown to reduce
mortality following acute myocardial infarction.

Q9 A patient who has recently received a head injury, or had surgery, or who has haemorrhaged
recently may bleed excessively; in this situation, thrombolytics are contraindicated. These drugs
are also unsuitable for patients who have previously experienced an adverse reaction to one of the
drugs, such as an allergic reaction to streptokinase.

Q10 The word angina means pain; angina pectoris refers to pain in the chest. The usual cause of
pain arising from the heart is a deficiency of blood flow to cardiac muscle, which is usually caused
by atheroma in coronary vessels, which restricts blood flow. Diminished blood flow to the heart
muscle causes ischaemia and pain. A patient may have no problems at rest and show a normal
ECG trace when sitting or lying down, but he or she may complain that walking fast or climbing a
hill, both of which require an increased delivery of oxygen to the cardiac muscle, brings on the
angina. Ischemic hearts show characteristic changes in the ECG, involving mainly the ST segment
and T wave. These changes can be particularly prominent when the heart is stressed by exercise.
Graded exercise, often using a treadmill, is used diagnostically to investigate possible myocardial
ischaemia. Mild ischaemia is usually shown by a depression in the ST segment of the ECG.

Part 3

Q11 The failing heart cannot efficiently pump out the volume of blood which returns in the veins.
Venous pressure therefore rises and tissues become oedematous. If the left heart fails, pulmonary
venous pressure rises and oedema occurs in the lung. When the patient stands up, there is a fluid
shift towards the lower parts of the body and oedema is often first observed in the lower legs,
particularly in the ankles. On lying down at night, there is a tendency for fluid to move from the
lower body into the thorax, increasing pulmonary oedema. The decreased efficiency of gas
exchange in the oedematous lung plus stimulation of sensory receptors in the lung causes
dyspnoea. Characteristically, the patient wakes soon after retiring, feeling breathless or unable to
breathe. Propping up the upper body with pillows, or raising the head of the bed, helps to keep
any excess fluid in lower parts of the body, away from the lung. The patient is therefore more
comfortable and is usually able to sleep.

Q12 Furosemide is a loop diuretic. The site of action of this drug in the nephron is the ascending
limb of the loop of Henle. This tubule pumps sodium, potassium and chloride out of the filtered
fluid into the medullary interstitial fluid, without accompanying water, producing a large osmotic
gradient in the medulla. Since furosemide inhibits the activity of ion pumps in the ascending loop
of Henle, the medullary osmotic gradient is diminished, less water can be reabsorbed in the
collecting duct and a large amount of salt and water is excreted by the kidney. Loop diuretics are
the most powerful of the diuretic drugs and can mobilize oedema fluidfrom the lungfor excretion
by the kidney. Reducing pulmonary oedema improves the gas exchange in the patient’s lung and
reduces dyspnoea.

Q13 The diuretic treatment should make Charlie more comfortable and improve his breathing. In
addition he should be advised to reduce salt intake, try to keep his weight at a suitable level (BMI
20–25) and take gentle exercise, such as walking each day. He now needs someone else to do the
heavy work, like digging, in the garden. Chronic heart failure is difficult to manage, as most
patients’ cardiac function gradually continues to decline. If systemic venous congestion has
reduced his appetite, several small meals each day will be more suitable for him than one or two
large ones.