Pre Clinical Medical Science SBAs
Pre Clin Cardiovascular: (63 questions)

Questions

• 1
  What is the effect of arteriolar constriction on downstream capillaries?
  Difficulty: Medium     Topic: Capillaries 1
  a

  Increased blood velocity

  b

  Increased capillary haematocrit

  c

  Increased capillary hydrostatic pressure

  d

  Reduced concentration gradients

  e

  Reduce surface area for exchange
  Explanation: Arteriolar constriction causes reduced pressure feeding capillaries - the effect is intermittent flow in some capillaries within a tissue bed. Fewer capillaries will contain red blood cells for exchange, thus there is a smaller surface area for diffusion. Blood velocity will be relatively unchanged as will capillary haematocrit. Hydrostatic pressure will markedly fall with arteriolar constriction. Concentration gradients will rise because as the rate of exchange falls metabolites accumulate in the tissues.
• 2
  What is responsible for the 1st heart sound?
  Difficulty: Easy     Topic: Heart sounds
  a

  Atrial contraction

  b

  Closure of the aortic and pulmonary valves

  c

  Closure of the atrio-ventricular valves

  d

  Opening of the aortic and pulmonary valves

  e

  Rapid early ventricular filling
  Explanation: The 1st heart sound is caused by closure of the atrio-ventricular valves, mitral and tricuspid. Atrial contraction may rarely cause the pathological 4th heart sound. Aortic and pulmonary valve closure causes the 2nd heart sound. Valve opening does not normally cause any sound. The 3rd heart sound, which is sometimes pathological, is caused by rapid ventricular filling in early diastole.
• 3
  When is end diastolic volume measured?
  Difficulty: Easy     Topic: End diastolic volume
  a

  Closure of the aortic valve

  b

  Closure of the atrio-ventricular valves

  c

  Opening of the aortic valve

  d

  Opening of the atrio-ventricular valves

  e

  -
  Explanation: End-diastolic volume (EDV) is measured at the end of diastole, which is when the aortic valve opens. At this point ventricular volume is at its highest and blood pressure is at it's lowest. End systolic volume (ESV) is measured at closure of aortic valve, when ventricular volume is at its lowest. EDV minus ESV is known as the stroke volume.
• 4
  What is the normal ventricular ejection volume? (approximately)
  Difficulty: Medium     Topic: Stroke volume
  a

  45-55ml

  b

  60-70ml

  c

  75-85ml

  d

  90-100ml

  e

  105-115ml
  Explanation: Ventricular volumes will vary with size and gender but stroke volume is usually around 60-70ml. End diastolic volume is 130-140ml and end-systolic volume is 65-70ml, giving an ejection fraction of just over 50%. Larger volumes will occur with high cardiac demand (e.g. exercise). Low stroke volumes with high end-diastolic volumes occur in low output cardiac failure.
• 5
  What is the relationship between total peripheral resistance (TPR) and arterial blood pressure (ABP)?
  Difficulty: Easy     Topic: Blood pressure
  a

  ABP = TPR x capillary pressure difference

  b

  ABP = TPR x flow

  c

  ABP = TPR x heart rate

  d

  ABP = TPR x heart rate x stroke volume

  e

  ABP = TPR x stroke volume
  Explanation: Arterial blood pressure is a function of cardiac output (= stroke volume x heart rate) and total peripheral resistance. Blood pressure is the force exerted by blood against the vessel wall. Increasing total peripheral resistance and heart rate predominantly increase diastolic blood pressure whilst increasing stroke volume mostly increases systolic.
• 6
  In what type of blood vessels is most pressure lost?
  Difficulty: Easy     Topic: Vessel types 1
  a

  Arterioles

  b

  Capillaries

  c

  Elastic arteries

  d

  Muscular arteries

  e

  Post-capillary venules
  Explanation: The most pressure is lost in the vessels where the greatest resistance is found. Arterioles are small vessels that have much smooth muscle in their wall. This creates high resistance that can be varied by vasoconstriction or dilatation. The more resistance, the greater the pressure loss across the vessel as energy is lost to overcome the resistance. Almost no pressure is lost through elastic and muscular arteries due to their elastic recoil. Blood pressure is low through capillaries to veins as most pressure has already been lost.
• 7
  In which type of blood vessel is the minimum velocity found?
  Difficulty: Easy     Topic: Vessel types 2
  a

  Arterioles

  b

  Capillaries

  c

  Muscular arteries

  d

  Veins

  e

  Venules
  Explanation: The speed of blood flow in vessels is inversely correlated to their total cross-sectional area. The entire capillary bed (very large cross-sectional area) must transmit the same blood flow (= speed x cross-sectional area) as the aorta. Therefore velocity must fall as cross-sectional area increases. Blood flow (volume/time) is the same in the vena cava and aorta, despite lower pressure in the vena cava.
• 8
  What causes the 1st Korotkoff sound?
  Difficulty: Medium     Topic: Korotkoff sounds
  a

  Aortic valve stenosis

  b

  Arterial collapse

  c

  Closure of the atrio-ventricular valve

  d

  Rapid ventricular filling

  e

  Turbulent arterial blood flow
  Explanation: The Korotkoff sounds are used to describe the sounds auscultated over the brachial artery during sphygmanonmetry. The 1st sound occurs when cuff pressure is reduced to below systolic pressure, this generates turbulent flow in the brachial artery, this indicates systolic blood pressure. The 5th sound occur when cuff pressure reaches diastolic pressure and sounds disappear as turbulent flow stops. Aortic valve stenosis causes an ejection systolic murmur. Arterial collapse causes no sound as there is no blood flow. AV-vale closure causes the 1st heart sound. The 3rd heart sound is due to rapid ventricular filling.
• 9
  What is the effect of increasing ventricular end-diastolic volume (EDV)?
  Difficulty: Hard     Topic: End-diastolic volume 2
  a

  Increased central venous pressure

  b

  Increased pre-contraction myofilament overlap

  c

  Increased stroke volume (SV) at all volumes

  d

  Increased stroke volume up to an optimum EDV

  e

  Increased ventricular contractility
  Explanation: The relationship between EDV and stroke volume is described by the Frank-Starling law of the heart. Increasing EDV increases the number of potential cross-bridges (by reducing myofilament overlap) that can form during contraction. The effect is an increased force of contraction, which increases stroke volume. This occurs up to an optimum EDV, above which stroke volume no longer increases despite further increases in EDV. Increased central venous pressure raises EDV, not the other way around. Ventricular contractility is controlled by sympathetic stimulation; force of contraction is controlled by EDV.
• 10
  What is the effect of increased beta-adrenergic stimulation on the heart?
  Difficulty: Medium     Topic: Sympathetics at heart 2
  a

  Increased end-diastolic volume for any given central venous pressure

  b

  Increased ejection fraction for any given stroke volume

  c

  Increased stroke volume for any given end-diastolic volume

  d

  Reduced end-diastolic volume for any given central venous pressure

  e

  Reduced ejection fraction for any given end-diastolic volume
  Explanation: Beta-adrenoreceptor stimulation increases ventricular contractility, which reduces end-systolic volume at any given end-diastolic volume. There is a vertical shift upwards for the Frank-Starling curve with increasing sympathetic stimulation. This increases the ejection fraction for any EDV. The relationship between central venous pressure and EDV is not affected. The change in stroke volume causes an increase in ejection fraction, so 'B' is not correct.
• 11
  How does the cardiovascular system change with ageing?
  Difficulty: Medium     Topic: Ageing and the CVS
  a

  Increased ejection fraction

  b

  Increased myogenic response from arterioles

  c

  Increased pulse pressure

  d

  Increased sympathetic response to standing

  e

  Increased ventricular compliance
  Explanation: With age, vessels become fibrosed and calcified with reduced elastic tissue. The effect is to increase systolic blood pressure as vessels are less compliant, but diastolic pressure decreases because of reduced elastic tissue - thus widening pulse pressure. Ejection fraction falls as ventricular contraction becomes less efficient. Myogenic tone fails so there is poorer autoregulation of blood flow. Autonomic nervous system degradation results in reduced sympathetic response. Ventricular compliance falls - there is increased resistance to filling.
• 12
  What endothelial ion change results in release of nitric oxide?
  Difficulty: Hard     Topic: Nitric oxide
  a

  Increased calcium

  b

  Increased potassium

  c

  Increased sodium

  d

  Reduced calcium

  e

  Reduced potassium
  Explanation: Vascular endothelial cells produce nitric oxide from (endothelial) nitric oxide synthetase (eNOS) in response to raised shear stress from blood flow. eNOS is activated by a rise in intracellular calcium. NO then diffuses into vascular smooth muscle cells and causes hyperpolarisation with a fall in intracellular calcium in myocytes. This reduces contraction and causes vasodilatation.
• 13
  What is the role of arteriolar myogenic tone?
  Difficulty: Easy     Topic: Myogenic tone
  a

  Increase downstream blood flow in high arterial blood pressure

  b

  Increase flow to superficial capillaries in hot weather

  c

  Regulate downstream blood flow over a pressure range

  d

  Regulation of capillary bed pressure

  e

  Reduce systemic arterial pressure given high peripheral resistance
  Explanation: Myogenic tone describes the response of arterioles to change in blood pressure, which regulates tissue flow. A rise in blood pressure causes an increase in arteriolar vasoconstriction, increasing resistance and maintaining downstream flow near constant. Myogenic tone operates only over a range of blood pressures e.g. mean arterial pressure 70-110mmHg.
• 14
  Increased concentration of which factor causes metabolic hyperaemia in cardiac arterioles?
  Difficulty: Medium     Topic: Cardiac metabolic hyperaemia
  a

  Adenosine

  b

  Carbon dioxide

  c

  Hydrogen ions

  d

  Oxygen

  e

  Potassium
  Explanation: Cardiac myocyte hypoxia causes an increase in the activity in 5'nucleotidase, which converts 5'AMP to adenosine. Adenosine diffuses into vascular smooth muscle in coronary arterioles and causes vasodilatation to correct the hypoxia. This is an example of metabolic hyperaemia - where raised tissue metabolism causes a rise in blood supply by vasodilatation.
• 15
  How does an angiotensin-converting enzyme-inhibitor reduce blood pressure?
  Difficulty: Easy     Topic: ACE-inhibitors 1
  a

  Increased anti-diuretic hormone levels

  b

  Increased sodium reabsorption

  c

  Reduced arteriolar vasoconstriction

  d

  Reduced arteriolar myogenic tone

  e

  Reduced levels of bradykinin
  Explanation: Angiotensin converting enzyme-inhibitors (ACEi) reduce conversion of angiotensin-I to angiotensin-II (Ang-II). Ang-II is a potent vasoconstrictor, promotes sodium reabsorption and increases aldosterone release. ACEi don't have any affect on ADH levels. ACEi will reduce sodium reabsorption by reducing Ang-II and aldosterone levels. Myogenic tone will be relatively unaffected by ACEi. There are raised levels of bradykinin, which is another vasodilator that is broken down by ACE. Raised bradykinin is responsible for ACEi-induced cough.
• 16
  What determines whether an arteriole vasodilates or vasoconstricts in response to circulating catecholamines?
  Difficulty: Easy     Topic: Circulating catecholamines
  a

  Concentration of circulating adrenaline

  b

  Density of alpha- and beta-adrenoreceptors

  c

  Local metabolites

  d

  Systemic arterial blood pressure

  e

  Tissue metabolic demand
  Explanation: The response of a vessel is determined by the receptors it posses on its vascular endothelial cells. Most vessels have a higher density of alpha-adrenoreceptors than beta-, thus will vasoconstrict in response to circulating adrenaline and noradrenaline. Some vessels (e.g. coronary arterioles) have a higher density of beta-adrenoreceptors so they dilate in response to adrenaline. Adrenaline will act on either alpha- or beta-adrenoreceptors. Local factors and tissue demand are superimposed upon systemic factors.
• 17
  How do type 1 Vaughan-Williams anti-arrhythmics act?
  Difficulty: Medium     Topic: Anti-arrhythmics
  a

  Actives fast sodium channels

  b

  Actives potassium channels

  c

  Block beta-adrenoreceptors

  d

  Block voltage-gated calcium channels

  e

  Inhibit fast sodium channels
  Explanation: Vaughan-Williams described 4 classes of anti-arrhythmic drugs. Class 1 are fast voltage-gated sodium channel blockers (e.g. procainamide) - the same basic structure as local anaesthetics. Class 2 are beta-adrenoreceptor blockers (e.g. bisoprolol). Class 3 are potassium channel blockers (e.g. amiodarone) and class 4 are calcium channel blockers (e.g. verapamil).
• 18
  What factor influences movement of fluids but not diffusion of solutes?
  Difficulty: Easy     Topic: Capillaries 2
  a

  Blood viscosity

  b

  Concentration difference

  c

  Hydrostatic pressure

  d

  Oncotic pressure

  e

  Surface area
  Explanation: Oncotic pressure is the force generated by the presence of proteins in a fluid space. Proteins are negatively charged and attract water molecules towards them thereby promoting fluid movement towards high oncotic pressure. High oncotic pressure from plasma proteins causes fluid reabsorption at the venous end of capillaries. Whereas diffusion is a function of the concentration gradient, hydrostatic pressure and surface area.
• 19
  How is a rise in blood pressure signalled to the central nervous system?
  Difficulty: Easy     Topic: Baroreflex 1
  a

  Increased firing in IX afferent from aortic arch

  b

  Increased firing in CN IX afferents from carotid sinus

  c

  Increased firing in CN XI afferents from carotid sinus

  d

  Reduced firing in CN IX afferents from aortic arch

  e

  Reduced firing in CN X afferents from carotid body
  Explanation: A rise in blood pressure increases activation of baroreceptors in the aortic arch (innervated by the Vagus, X) and carotid sinus (innervated by glossopharyngeal nerve, IX). The increased activity causes a rise in the frequency of action potentials along the afferent nerves.
• 20
  What is the output from nucleus tractus solitarius following a fall in blood pressure?
  Difficulty: Easy     Topic: Baroreflex 2
  a

  Increased beta-adrenoreceptor vasodilatation in muscle

  b

  Increased muscarinic-acetylcholine stimulation at the heart

  c

  Increased venoconstriction

  d

  Reduced activation of the renin-angiotensin system

  e

  Reduced anti-diuretic secretion
  Explanation: The nucleus tractus solitarius (NTS) is the most important nucleus in the medulla responsible for the baroreflex. A fall in blood pressure results in increased sympathetic activation with peripheral vasoconstriction, a rise in heart rate and increased ventricular contractility. There is also an increase in ADH release and activation of the renin-angiotensin-aldosterone system.
• 21
  What is the Bainbridge reflex?
  Difficulty: Hard     Topic: Bainbridge reflex
  a

  A fall in end-systolic volume following increased right atrial stretch

  b

  A fall in heart rate following increased right atrial stretch

  c

  A fall in stroke volume following reduced right atrial stretch

  d

  A rise in ejection fraction following reduced right atrial stretch

  e

  A rise in heart rate following increased right atrial stretch
  Explanation: The Bainbridge reflex is a spurious cardiovascular reflex where there is an increase in heart rate in response to increased right atrial stretch. This is thought to be protective in hoping to prevent ventricular overfilling by increasing heart rate.
• 22
  What is the mechanism underlying ACE-inhibitor induced cough?
  Difficulty: Medium     Topic: ACE-inhibitors 2
  a

  Diaphragmatic irritation

  b

  Direct effect on medulla

  c

  Idiosyncratic

  d

  Increased kinins

  e

  Phrenic nerve activation
  Explanation: Angiotensin converting enzyme normally breaks down 'kinin' molecules (e.g. bradykinin). In the presence of an ACEi there is a rise in kinins, which stimulate irritant nerve endings and cause a dry cough. All the other mechanisms above may cause cough but are not related to ACE-inhibitors.
• 23
  How do dihydropyridine calcium channel blockers differ from verapamil and diltiazem?
  Difficulty: Medium     Topic: Calcium channel blockers
  a

  Act on central receptors

  b

  Act on only venous vessels

  c

  Do not cause bradycardia

  d

  Reduce blood pressure

  e

  They have no idiosyncratic side-effects
  Explanation: Dihydropyridine (DHP) calcium channel blockers (e.g. nifedipine, amlodipine) are much more selective of peripheral blood vessels than verapamil and diltiazem. The effect is that DHPs do not affect heart rate, whereas diltiazem/verapamil cause bradycardia by reducing the rate of depolarisation at the SAN and AVN. Nifedipine and amlodipine do not act on central receptors and they do also act on venous vessels. All forms of calcium channel blocker reduce blood pressure and all demonstrate idiosyncratic side effects (e.g. gum hyperplasia).
• 24
  Where is left coronary artery blood flow highest?
  Difficulty: Medium     Topic: Coronary blood flow
  a

  Early diastole

  b

  Isovolumetric phase of contraction

  c

  Isovolumetric phase of relaxation

  d

  Late diastole

  e

  Mid-systole
  Explanation: Branches of the left coronary artery are subject to compression by the transmural pressure of the left ventricle. The transmural pressure is greatest during systole and despite blood pressure being highest in mid-systole the left coronary artery is almost entirely occluded with very little flow. Transmural pressures are lowest during diastole and at early diastole arterial pressure results in maximum blood flow. Flow is lowest during the isovolumetric phases of contraction & relaxation.
• 25
  Why is glyceryl trinitrate given sublingually in angina attacks?
  Difficulty: Medium     Topic: Glyceryl trinitrate
  a

  Acts on veins more than arteries

  b

  Extended half-life

  c

  High first-pass metabolism if given orally

  d

  Prevents toxic levels

  e

  Reduced drug interactions
  Explanation: 1st pass metabolism is the action of the liver on medications as they are absorbed from the gut via the portal vein. GTN is a medication that releases the vasodilator nitric oxide in blood vessels. GTN is subject to very large 1st pass metabolism if taken orally, this would mean that there is very would be little available for action. Sublingual administration also helps for a rapid onset of action. GTN does act more on veins than arteries but this is not the reason it is given sublingually. There is no effect on its half life, toxic levels or interactions.
• 26
  What examination finding suggests left ventricular failure?
  Difficulty: Easy     Topic: Cardiac failure 1
  a

  Central cyanosis

  b

  Enlarged liver

  c

  Peripheral oedema

  d

  Pulmonary oedema

  e

  Raised jugular venous pressure
  Explanation: In left ventricular failure there is reduced perfusion of the systemic arterial system with overload of the pulmonary venous system. This results in pulmonary oedema and symptoms of low cardiac output: fatigue & breathlessness. Right ventricular failure causes reduced pulmonary artery perfusion causing central cyanosis; and overload in the systemic venous system, causing peripheral oedema, a raised JVP, hepatomegaly & ascites. LVF and RVF are usually found together as congestive cardiac failure.
• 27
  How does the Frank-Starling curve of the heart change in cardiac failure?
  Difficulty: Medium     Topic: Cardiac failure 2
  a

  Fall in end-systolic volume

  b

  Increased ejection fraction

  c

  Increased stroke volume for any given end-diastolic volume

  d

  Reduced end-diastolic volume

  e

  Reduced stroke volume for any given end-diastolic volume
  Explanation: In early heart failure there is ventricular dilatation to increase EDV, attempting to increase stroke volume. As heart failure progresses the ventricular dilatation reaches a point where there is inefficient emptying - the peak of the Frank-Starling curve has been passed. Any further increase in EDV results in a lower stroke volume. The heart becomes inefficient and the curve falls vertically such that the stroke volume is lower at any given EDV.
• 28
  Which commonly administered treatment for cardiac failure is purely symptomatic?
  Difficulty: Hard     Topic: Cardiac failure 3
  a

  Aspirin

  b

  Bisoprolol

  c

  Furosemide

  d

  Ramipril

  e

  Simvastatin
  Explanation: There are many medications given in cardiac failure but diuretics (furosemide - a loop diuretic) are only symptomatic; they do not improve long-term prognosis. Whereas ACE-inhibitors (ramipril), angiotensin-II receptor blockers (irbesartan), aldosterone antagonists (eplenerone) and beta-blockers (bisoprolol) all improve prognosis. If ischaemic heart disease is the cause of heart failure then statins (simvastatin) and aspirin improve the prognosis.
• 29
  How is sinus arrhythmia generated?
  Difficulty: Medium     Topic: Sinus arrhythmia
  a

  Increased sympathetic stimulation during expiration

  b

  Increased sympathetic stimulation during inspiration

  c

  Reduced parasympathetic output during inspiration

  d

  Increased parasympathetic stimulation during expiration

  e

  Reduced sympathetic stimulation during inspiration
  Explanation: Sinus arrhythmia refers to the normal process where heart rate increases during inspiration. This occurs because the medullary inspiratory centre, which causes diaphragm contraction, inhibits the Vagus. This removes the tonic parasymapthetic action at the SAN and this results in an increase in heart rate.
• 30
  During exercise, what causes vasodilatation in muscle?
  Difficulty: Easy     Topic: Exercise reflex 1
  a

  Acetylcholine from parasympathetic nerves

  b

  Adrenaline from sympathetic neurones

  c

  Circulating catecholamines

  d

  Local metabolites

  e

  Noradrenaline from sympathetic neurones
  Explanation: The response to exercise is a combination of a co-ordinated neural reflex and local tissue effects. Sympathetic outflow causes vasoconstriction in muscle from noradrenaline released by sympathetic neurones. However potassium, phosphate and adenosine released during muscle contraction causes vasodilatation that overcomes the sympathetic mediated constriction. Acetylcholine does not cause vasodilatation in humans. Neurones do not release adrenaline. Circulating catecholamines play a very minor role in exercise.
• 31
  What changes occur in arterial blood when the anaerobic threshold is passed during dynamic exercise?
  Difficulty: Hard     Topic: Exercise reflex 2
  a

  Hypoxia with respiratory acidosis

  b

  Hypoxia with respiratory alkalosis

  c

  Metabolic alkalosis

  d

  Respiratory acidosis

  e

  Respiratory alkalosis with raised lactate
  Explanation: When the anaerobic threshold is passed energy consumption is greater than can be provided by oxidative metabolism therefore anaerobic metabolism of glycogen occurs to provide ATP. As a by-product lactate is produced, which stimulates peripheral chemoreceptors to raise the tidal ventilation (VT) in excess of CO2 production (VCO2). This causes a fall in PaCO2 and a rise in PaO2, with a raised lactate, resulting in a respiratory alkalosis with raised lactate.
• 32
  Which mechanoreceptors may activate a vasovagal syncope?
  Difficulty: Medium     Topic: Vasovagal syncope
  a

  Aortic arch

  b

  Carotid body

  c

  Carotid sinus

  d

  Renal artery

  e

  Ventricular
  Explanation: A vasovagal syncope can be activated by either high-threshold ventricular mechanoreceptors or from emotional stimuli via the defence response. The ventricular afferents are stimulated when the ventricle contracts with high contractility on a low volume e.g. after standing up after intensive exercise. The other mechanoreceptors listed are involved in the baroreflex. There are only chemoreceptors in the carotid body.
• 33
  Which vessel does the azygous vein drain into?
  Difficulty: Medium     Topic: Azygous vein
  a

  Hemi-azygous vein

  b

  Inferior vena cava

  c

  Left brachiocephalic

  d

  Right brachiocephalic

  e

  Superior vena cava
  Explanation: The azygous vein lies in the posterior mediastinum just to the right of the midline. It drains bloods from the chest wall as it ascends from T7-8 towards the superior mediastinum. At T3-4 the azygous vein arches anteriorly to join with the superior vena cava superior to the right atrium. The hemi-azygous and accessory azygous veins lie to the left of the midline on the posterior thoracic wall and drain into the azygous vein.
• 34
  Where is the apex beat palpated in individuals without cardiac pathology?
  Difficulty: Easy     Topic: Surface anatomy 2
  a

  4th intercostal space, anterior axillary line

  b

  4th intercostal space, mid-clavicular line

  c

  5th intercostal space, mid-axillary line

  d

  5th intercostal space, mid-clavicular line

  e

  6th intercostal space, mid-axillary line
  Explanation: The apex beat of the heart is the point where ventricular contraction is most easily palpated - this is normally in the 5th intercostal space mid-clavicular line. This is not necessarily the same are the anatomical apex, which is often angled posteriorly. Cardiac failure causes infero-lateral displacement of the apex.
• 35
  At what vertebral level is the superior border of the right atrium located?
  Difficulty: Hard     Topic: Surface anatomy 3
  a

  T1-2

  b

  T2-3

  c

  T3-4

  d

  T4-5

  e

  T5-6
  Explanation: The angle of Louis an important landmark located at the superior border of the right atrium, at T4-5. It divides the mediastinum into superior and inferior and is the level of the carina (tracheal division). With a patient lying at 45-degrees, the manubro-sternal junction is in the same horizontal plane as the angle of Louis.
• 36
  Which cardiac chamber forms the majority of the inferior border of the heart?
  Difficulty: Easy     Topic: Surface anatomy 4
  a

  Left atrium

  b

  Left atrial appendage

  c

  Left ventricle

  d

  Right atrium

  e

  Right ventricle
  Explanation: Inferior border, and most of the anterior face, of the heart is formed from the right ventricle. The right lateral border is formed from the right atrium. The left lateral border is almost entirely the left ventricle. The left ventricle also forms the posterior face, along with the left atrium.
• 37
  Which vein lies in the posterior mediastinum immediately right lateral to the descending thoracic aorta?
  Difficulty: Medium     Topic: Mediastinal anatomy
  a

  Accessory azygous vein

  b

  Azygous vein

  c

  Hemi-azygous vein

  d

  Inferior vena cava

  e

  Superior vena cava
  Explanation: The azygous vein lies in the posterior mediastinum, to the right of the aorta and ascends to join the SVC just before it enters the right atrium. The accessory (superiorly) and hemi-azygous (inferiorly) veins lie to the left of the aorta. The azygous system drains the posterior chest wall.
• 38
  Moving away from the heart, what is the third branches) of the aorta?
  Difficulty: Easy     Topic: Great vessels 1
  a

  Coronary arteries

  b

  Left brachiocephalic

  c

  Left common carotid

  d

  Left subclavian

  e

  Right brachiocephalic
  Explanation: The first branches of the aorta are the coronary arteries, immediately above the aortic valve. The second branch is the right brachiocephalic artery. This is followed by the left common carotid then left subclavian arteries - there is no left brachiocephalic artery. The right brachiocephalic artery later divides into right common carotid and right subclavian arteries.
• 39
  Which structures does the ligamentum arteriosum attach to?
  Difficulty: Easy     Topic: Ligamentum arteriosum
  a

  Pulmonary arteries and aorta

  b

  Pulmonary arteries and IVC

  c

  Pulmonary arteries and right atrium

  d

  Pulmonary veins and aorta

  e

  Pulmonary veins and right atrium
  Explanation: The ligamentum arteriosum is remnant of the foetal ductus arteriosus that allowed passage of blood from the high pressure pulmonary arteries to aorta. The ductus arteriosus closes on day 1-2 of life in response to hyperoxia and undergoes fibrosis to form the ligamentum arteriosum that inserts into the aortic arch opposite the left subclavian artery.
• 40
  What is the oblique sinus?
  Difficulty: Hard     Topic: Oblique sinus
  a

  A large cardiac vein

  b

  A reflection of pericardium

  c

  A vein draining into the left ventricle

  d

  An extension of the left atrium

  e

  An extension of the right atrium
  Explanation: The peritoneum has two layers, visceral and parietal, that are continuous with each other. This forms the pericardial sac, which attaches around the heart at the base of the great vessels. The oblique sinus and horizontal sinus are locations where the peritoneum reflects against itself and a potential space is created. The coronary sinus is a large cardiac vein. Thebsian veins drain the left ventricle myocardium. The auricles (or appendages) are extensions of the atria.
• 41
  Which cardiac valve normally has only 2 cusps?
  Difficulty: Easy     Topic: Cardiac valves
  a

  Left atrio-ventricular

  b

  Left semi-lunar valve

  c

  Right atrio-ventricular

  d

  Right semi-lunar valve

  e

  -
  Explanation: The left atrio-ventricular valve, or mitral valve, has only 2 cusps. These two cusps are attached to large papillary muscles via chordae tendinae. The right atrioventricular valve is called the tricuspid valve. Both semi-lunar valves have 3 semi-lunar shaped cusps; the aortic valve on left and pulmonary valve on the right.
• 42
  What is the function of the sinuses of Valsalva?
  Difficulty: Hard     Topic: Sinuses of Valsalva
  a

  Allow the heart to move resistance-free

  b

  Connect the pulmonary artery and aorta

  c

  Drain blood from the left ventricle

  d

  Maintain valvular competence

  e

  Promote coronary artery blood flow during diastole
  Explanation: The sinuses of Valsalva (also known as sinuses of Morgangi) are dilatations in the wall of the ascending aorta immediately above the aortic valve where the coronary arteries originate. At the beginning of diastole, the backflow of blood against the closed aortic valve and dilatation of the sinuses promotes flow of blood into the coronary vessels. Pericardial fluid facilitates resistance-free movement. The ligamentum arteriosum connects the pulmonary artery and aorta. The thebesian veins drain the left ventricle. The papillary muscles and chordae tendinae maintain mitral valve competence.
• 43
  In most humans, which vessel supplies the sino-atrial node?
  Difficulty: Medium     Topic: Coronary anatomy 1
  a

  Anterior interventricular artery

  b

  Left circumflex artery

  c

  Left coronary main stem

  d

  Posterior interventricular artery

  e

  Right coronary artery
  Explanation: In 60% of humans a branch of the right coronary artery, near its origin, supplies the sino-atrial node in the wall of the right atrium. The atrioventricular node is also supplied by the right coronary artery in 80% of humans, this branch originates from the posterior aspect of the heart near the posterior interventricular artery. The right coronary artery also supplies the right atrium and most of the right ventricle.
• 44
  Which vessels anastamose to form the posterior interventricular artery?
  Difficulty: Medium     Topic: Coronary anatomy 2
  a

  Right and left coronary

  b

  Right coronary and anterior interventricular

  c

  Right coronary and left circumflex

  d

  Right coronary and left marginal

  e

  Right marginal and left marginal
  Explanation: The posterior interventricular (PIV) artery is formed from the union of the left circumflex and the right coronary artery that run in the atrio-ventricular groove on the posterior aspect of the heart. The PIV artery supplies the posterior 1/3rd of the interventricular septum and most of the posterior wall of the left ventricle.
• 45
  Which vessels does the left main stem divide into?
  Difficulty: Easy     Topic: Coronary anatomy 3
  a

  Anterior interventricular and left circumflex

  b

  Anterior interventricular, left marginal and left circumflex

  c

  Left circumflex and left marginal

  d

  Posterior interventricular and left circumflex

  e

  Posterior interventricular and left marginal
  Explanation: The left main stem is the name of the vessel at the origin of the left coronary artery. This divides early into the anterior interventricular artery and left circumflex. The anterior interventricular passes down the interventricular groove anteriorly, supplying 2/3rd of the interventricular septum and much of the left ventricle, plus part of the anterior wall of the right ventricle. The left circumflex passes posteriorly in the atrio-ventricular groove to supply the left atrium, posterior aspect and form the posterior interventricular artery. The left marginal artery is an early branch of the left circumflex that supplies the lateral aspect of the left ventricular wall.
• 46
  Where does the coronary sinus lie?
  Difficulty: Easy     Topic: Coronary anatomy 4
  a

  Anterior atrio-ventricular groove

  b

  Anterior interventricular groove

  c

  Posterior atrio-ventricular groove

  d

  Posterior interventricular groove

  e

  Posterior and superior to pulmonary trunk
  Explanation: The coronary sinus is a wide venous channel that lies on the posterior aspect of the heart in the atrio-ventricular groove. It receives blood from the 3 main cardiac veins: great, middle and small. The coronary sinus drains directly into the posterior of the right atrium.
• 47
  The vertebral arteries are direct branches of which artery?
  Difficulty: Easy     Topic: Vertebral arteries
  a

  Aortic arch

  b

  Common carotid

  c

  External carotid

  d

  Internal carotid

  e

  Subclavian
  Explanation: The vertebral arteries are branches of the subclavian artery. The initial branch is known as the thyrocervical trunk, which also gives rise to the inferior thyroid artery and then goes on to form the vertebral artery that ascends in the lateral canal of the cervical vertebrae. The two vertebral arteries unite on the brainstem to form the basilar artery.
• 48
  Where does the subclavian vein lie in the thoracic outlet?
  Difficulty: Hard     Topic: Subclavian vessels
  a

  Anterior to the tendon of scalenus anterior

  b

  Inferior to the first rib

  c

  Posterior to the cords of the brachial plexus

  d

  Posterior to the tendon of scalenus anterior

  e

  Posterior to the subclavian artery
  Explanation: The subclavian artery and vein run infero-posterior to the clavicle and superior to the first rib. As with many other parts of the body, the vein lies anterior to the artery and both are anterior to the brachial plexus. Scalenus anterior inserts into the first rib between the artery and the vein such that the vein lies anterior to the tendon.
• 49
  What defines the surface anatomy of the superior border of the heart?
  Difficulty: Medium     Topic: Surface anatomy 1
  a

  2cm each side of the manubrium in 4th intercostal space

  b

  4cm each side of the manubrium in the 2nd intercostal space

  c

  6cm horizontally along the angle of Louis

  d

  6cm in the left 3rd intercostal space

  e

  From right 2nd costo-chondral joint to left 3rd cost-chondral joint
  Explanation: The superior border runs 4cm either side of the sternum in the horizontal plane in the 2nd intercostal space. The right border runs from here down to the 6th costal cartilage. The inferior border runs from here to the apex in the mid-clavicular line in the 5th intercostal space. The left heart border connects the apex and the left edge of the superior border as described above.
• 50
  At what vertebral level do the renal arteries branch from the aorta?
  Difficulty: Medium     Topic: Abdominal aorta
  a

  T11-T12

  b

  T12-L1

  c

  L1-L2

  d

  L3-L4

  e

  L4-L5
  Explanation: There are 5 pairs of arteries that branch from the abdominal aorta. From superior to inferior: Inferior phrenic, middle suprarenal, renal arteries (at T12-L1), gonadal arteries and common iliac arteries. The unpaired branches (superior to inferior) are: coeliac trunk, superior mesenteric, inferior mesenteric and median sacral artery.
• 51
  Where may the dorsalis pedis pulse be palpated?
  Difficulty: Easy     Topic: Foot pulses
  a

  Inferior to the medial malleolus

  b

  Lateral to the tendon of flexor hallux longus

  c

  Medial to the head of the 3rd metatarsal

  d

  Over the lateral cuneiform bone

  e

  Posterior to the lateral malleolus
  Explanation: The two arteries supplying the foot are that dorsalis pedis (a branch of the anterior tibial artery) and posterior tibial. The dorsalis pedis is palpated over the 1st cuneiform bone immediately lateral to the tendon of flexor hallux longus. Posterior tibial pulse is felt postero-inferior to the medial malleolus.
• 52
  What is the role of the vasa vasorum?
  Difficulty: Easy     Topic: Vasa vasorum
  a

  Maintain concentration in the renal medulla

  b

  Supply blood to the myocardium

  c

  Supply blood to large nerves

  d

  Supply blood to large vessel walls

  e

  Wide capillaries in the spleen
  Explanation: The vasa vasorum are capillaries that lie in the wall of large blood vessels to perfuse large the large muscular layer. The vasa recta are capillaries that supply the loop of Henle and help prevent wash-out of the hypertonic medulla. There is no specific name for vessels supplying the myocardium. Vasa nervosum perform a similar role for large neurones, these lie within the epineurium but outside the endoneurium. Sinusoids are large capillaries with fenestrations found in the spleen and liver.
• 53
  How does the ultrastructure of a vessel change in atherosclerosis?
  Difficulty: Medium     Topic: Atherosclerosis
  a

  Adventitia thickening

  b

  Intimal thickening

  c

  Media thinning

  d

  Reduced elastin deposition

  e

  Reduced internal elastic lamina
  Explanation: The main change in atherosclerosis is intimal thickening, which occurs due to a number of factors: lipid deposition, inflammatory cell infiltration, fibrin deposition and myofibroblast migration. There is relatively little change to the adventitia. The media also thickens, with increased elastin and muscle - this adds to the raised resistance.
• 54
  What forms the fenestrations in sinusoidal capillaries?
  Difficulty: Medium     Topic: Fenestrations
  a

  Amino acid chains

  b

  Glycoproteins

  c

  Hyaluronic acid

  d

  Plasma membrane

  e

  Thin cytoplasm
  Explanation: Fenestrations are pores in the walls of capillaries that reduce the diffusion distance to increase substance transport. Fenestrations are areas where there is no endothelial cytoplasm, only double-layered plasma membrane. Amino acid chains have a wide variety of roles but are not structural molecules. Glycoprotiens and hyaluronic acid are components of the extracellular matrix. All endothelial cells have thin cytoplasm, but it is not present at the site of fenestrations.
• 55
  Where is the cisterna chyli located?
  Difficulty: Easy     Topic: Cisterna chyli
  a

  At the bifurcation of the aorta

  b

  At the union of the brachiocephalic veins

  c

  Immediately inferior to the diaphragm

  d

  Immediately superior to the diaphragm

  e

  In the posterior mediastinum
  Explanation: The cisterna chyli is a large lymphatic vessel located on the posterior wall of the abdomen immediately inferior to the diaphragm. All lymph from the lower half of the body passes through the cisterna chyli. The thoracic duct drains the cisterna chyli, it ascends the thorax in the posterior mediastinum and joins the right brachiocephalic vein.
• 56
  What feature does myocardium have that is not present in skeletal muscle?
  Difficulty: Medium     Topic: Cardiac muscle
  a

  Branching fibres

  b

  Dense bodies

  c

  Multinucleate myocytes

  d

  T-tubules

  e

  Z-lines
  Explanation: Only cardiac muscle has fibres that branch. Dense bodies are areas for insertion of myofilaments in smooth muscle. Both cardiac and skeletal muscle are multinucleate striated muscles because they have sarcomeres composed of thin and thick fibres arranged in a regular pattern. This includes Z-lines, where thin filaments attach. T-tubules are invaginations of sarcolemma that lie close to sarcoplasmic reticulum, this facilitates electrical-contraction coupling.
• 57
  What is the role of the atrioventricular node?
  Difficulty: Easy     Topic: Atrioventricular node
  a

  Co-ordinate atrial depolarisation

  b

  Delay atrio-ventricular depolarisation

  c

  Initiation of cardiac rhythm

  d

  Initiate ventricular contraction

  e

  Prevent atrio-ventricular tachycardias
  Explanation: The atrioventricular node is the only part of the heart that allows transmission of action potential from atria to ventricles. It causes a delay to allow the atria to completely empty of blood before the ventricles contract. This delay occurs due to the 'pre-potential' of the AVN pacemakers cells. There is no specific system to co-ordinate artial contraction, the action potential spreads via gap junctions. Normally rhythm is initiated by the sino-atrial node. Contraction is a physical process, unlike depolarisation which is an electrical process. Atrio-ventricular tachycardias may even involve the AVN - it does not prevent them.
• 58
  What ventricular ion movements are responsible for the Q-T segment seen on ECG?
  Difficulty: Medium     Topic: ECG principles 1
  a

  Calcium influx only

  b

  Potassium efflux only

  c

  Sodium influx only

  d

  Sodium and calcium influx with potassium efflux

  e

  Sodium influx with potassium efflux
  Explanation: The Q-T segment on ECG takes place during the plateau phase of ventricular myocyte depolarisation. The plateau occurs when there is sodium influx (through slow voltage-gated channels) and calcium influx that is balanced by potassium efflux through voltage gated channels. Repolarisation occurs at the end of the plateau phase, when sodium and calcium channels shut but potassium efflux continues
• 59
  Where is atrial repolarisation seen on ECG
  Difficulty: Easy     Topic: ECG principles 2
  a

  Not normally visible

  b

  P-R interval

  c

  Q-T segment

  d

  T-wave

  e

  U-wave
  Explanation: Atrial repolarisation is not usually seen on ECG because it is of a small voltage and occurs during ventricular depolarisation so is almost always hidden by the QRS complex. The P-R interval represents the delay at the AVN. The Q-T segment represents ventricular myocyte plateau phase. The T-wave is ventricular repolarisation. A U-wave is a pathological wave that occurs in hypokalaemia.
• 60
  What ion movement is responsible for the pre-potential of SAN and AVN?
  Difficulty: Easy     Topic: Pacemaker cells
  a

  Calcium influx through leak channels

  b

  Calcium influx through voltage-gated channels

  c

  Sodium influx through fast voltage-gated channels

  d

  Sodium influx through leak channels

  e

  Potassium efflux through voltage-gated channels
  Explanation: The pre-potential of pacemaker cells in the AVN and SAN is a slow depolarisation that eventually reaches threshold to allow activation of voltage-gated channels. There are 'leak' channels that are continuously open to allow sodium influx that causes gradual depolarisation. There is minimal calcium movement through leak channels. Voltage-gated calcium channels cause the action potential spike in pacemaker cells. There are no fast sodium channels in pacemaker cells. Potassium efflux causes repolarisation.
• 61
  What is the cause of the absolute refractory period of ventricular myocytes?
  Difficulty: Medium     Topic: Refractory period
  a

  Almost all fast Na+ channels are inactive

  b

  Lack of a large depolarising stimulus

  c

  Lack of calcium in sarcoplasmic reticulum

  d

  Membrane potential below -80mV

  e

  Too many K+ channels are open
  Explanation: The absolute refractory period is a state where no action potential can be generated no matter the magnitude of the depolarising stimulus. This occurs because too many fast sodium channels are in the 'inactive' phase - they cannot be activated no matter the membrane potential. In contrast, the relative refractory period is when a larger than normal stimulus is needed to pass threshold because the myocyte is hyperpolarised and some sodium channels are inactive but there is sufficient to cause an action potential.
• 62
  What is the effect of sympathetic stimulation on the heart?
  Difficulty: Easy     Topic: Sympathetics at heart 1
  a

  Increased heart rate & increased AVN delay

  b

  Increased heart rate & reduced AVN delay

  c

  Increased heart rate, increased AVN delayed and increased ventricular contractility

  d

  Increased heart rate, reduced AVN delay and increased ventricular contractility

  e

  Increased heart rate, reduced AVN delay and reduced ventricular contractility
  Explanation: Noradrenaline from sympathetic neurones and circulating adrenaline binds beta-1-adrenoreceptors in the heart. This causes an increase in the rate of depolarisation of pacemakers cells at the SAN and AVN, to increase heart rate and reduce delay at the AVN. Stimulation also increases ventricular contractility by raising intracellular calcium levels in ventricular myocytes. The effect to raise cardiac output by increasing heart rate and stroke volume.
• 63
  How does parasympathetic stimulation alter ion movements in cardiac pacemaker cells?
  Difficulty: Hard     Topic: Parasympathetics at heart
  a

  Increased potassium efflux

  b

  Increased potassium influx

  c

  Increased sodium and calcium influx

  d

  Reduced potassium efflux

  e

  Reduced sodium influx
  Explanation: Acetylcholine from the Vagus acts on muscarinic acetylcholine receptors. Receptor ligation causes a downstream pathway to increase the opening of potassium leak channels. The effect is to hyperpolarise pacemaker cells and reduce the gradient of their pre-potential, which reduces heart rate. There is no effect on calcium so no effect on ventricular contractility. This is in contrast to sympathetic stimulation that increases sodium and calcium permeability via beta-1-adrenoreceptor activation.