Linn Lee 1206279 Case 2: David Marsden

Case 2: David Marsden

Case Summary
Lucinda did an excellent job of the EF Case Summary so this is will just give some supporting information as well
as cover any new topics:

Describe the structure and function of the cardiovascular system in more detail
Fibrous skeleton of the heart

 Framework of dense connective tissue – mainly collagen

 Consists of four rings surrounding the ostia (openings) of the four heart valves, the right and left fibrous
trigones (located between the rings of the semilunar ostia and those of the atrioventricular ostia) and
membranous portions of the interatrial, interventricular and atrioventricular septa.
 Functions:
o Anchors valve cusps and leaflets
o Reinforce valve ostia
o Point of insertion for myocardium
o Insulator that prevents direct electrical conductivity between atria and ventricles (so action
potentials can spread only through the conducting fibres)

A little bit more detail on cardiac valves

 Lined with endothelium

 Made up of the fibrosa, spongiosa and ventricularis layers
o Beneath the endothelium is the fibrosa (dense collagenous core)
o Beneath the fibrosa is the spongiosa (loose connective tissue)
o The final layer below the spongiosa is the ventricularis (elastin-rich layer)

Details of the cardiac cycle

Some useful definitions (not officially part of the case objectives)

 Preload is the stretch of the myocyte sarcomeres caused by EDV just before ventricular contraction.
Preload is increased by increased central venous pressure and rate of venous return. It affects stroke
volume through the Frank-Starling law.
 The Frank-Starling law of the heart states that an increase in EDV will result in greater contractility of
the myocytes and therefore a greater stroke volume.
 Afterload is actually the tension produced by the heart muscle in a particular chamber in order to
contract. It is often described as the pressure the LV needs to generate to eject blood from the
chamber. It is a direct consequence of aortic pressure (for example, increased pressure gradient across
aortic valve would mean increased afterload).
 End-systolic volume (ESV) is the volume of blood in the LV at the end of a full contraction. This is the
lowest volume of blood found in the LV in the whole cardiac cycle. ESV is affected by afterload and
contractility of the heart.
 End-diastolic volume (EDV) is the volume of blood in the LV at the end of ventricular filling. This is the
highest volume of blood found in the LV in the whole cardiac cycle. EDV affects the preload of the heart
and, together with ESV, the stroke volume.
 Stroke volume is the difference between the EDV and ESV. The typical stroke volume is about 70mL.
Linn Lee 1206279 Case 2: David Marsden

Diastole

 During diastole, ventricular relaxation and filling occurs.

 The semilunar valves close just as ventricular pressures are starting to fall, as at this point, ventricular
pressures have fallen enough to be lower than pressures in the aorta and pulmonary trunk.
 In systole, blood had accumulated in the atria due to the AV valves being closed.
 The very short time between the closure of the semilunar valves and the opening of the AV valves is
known as isovolumetric (or isovolumic) relaxation.
 As diastole is about to begin, ventricular pressures fall significantly and the period of rapid filling of the
ventricles begins as atrial pressures now exceed ventricular pressures. (Diastole begins just as atrial
pressures exceed ventricular pressures).
 This pressure gradient causes blood to push open the AV valves and rush into the ventricles (passive
flow). Most of the atrial blood flows to the ventricles in this way.
 Towards the end of diastole, the SA node fires.
 The action potential spreads throughout the atria, causing them to contract and push about 20% of atrial
blood into the ventricles.

Systole

 In systole, the action potential from the SA node has spread to the AV node, causing it to fire.
 The action potential spreads to the Bundle of His and then to the Purkinje fibres which distributes the
action potential to the myocytes, causing the myocardium of the ventricles to contract.
 Ventricular contraction is a wringing motion that begins at the apex and finishes at the base. This
ensures that blood is effectively “squeezed” out of the ventricles.
Linn Lee 1206279 Case 2: David Marsden

 Ventricular pressure rise above atrial pressures, causing blood to push against the cusps of the AV
valves and this causes the AV valves to close. (Papillary muscles are also involved: they contract just
before ventricular contraction to pull on the valve cusps via chordae tendineae and this prevents
prolapsing of the cusps when pressure is exerted against them)
 The very short period of time between the closure of the AV valves and the opening of the semilunar
valves is known as isovolumetric contraction.
 Ventricular pressures then rise above arterial pressures, specifically that of the aorta and the pulmonary
trunk.
 The pressure gradient causes blood to push open the semilunar valves and rush out of the ventricles
into the aorta/pulmonary trunk.

Anatomy of the coronary circulation

So I thought I’d just put what Lucie had written into a table to make it look pretty.

Artery/Branch Branches off from Route Supplies

Left coronary artery
Left anterior descending/
anterior interventricular
artery
Circumflex branch
Right coronary artery
Right marginal branch
Posterior descending/
Posterior interventricular
artery
Aorta Along coronary sulcus
Left C.A. Along anterior interventricular
groove/sulcus towards apex
Left C.A. Along the coronary sulcus then
down towards the apex
Aorta Along coronary sulcus
Right C.A. Branches off at inferior border
and runs along the side of the
right ventricle towards the apex
Right C.A. Along coronary sulcus and then
posterior interventricular
groove/sulcus towards apex
LA
Anterior two thirds of the
interventricular septum,
anterior walls of both
ventricles
LA and LV
RA
(Overall, the RCA plus
branches supply the RA
and most of RV)
RA and RV
Posterior third of the
interventricular septum,
posterior walls of both
ventricles

Some other stuff you may find helpful:

 The septum is supplied by the septal branches of the anterior and posterior interventricular arteries,
which branch out further into capillaries lying adjacent to the myocytes that allow perfusion of the
myocardium.
 Coronary artery dominance can be determined by which coronary artery supplies the posterior
interventricular branch.
 More accurately, coronary artery dominance is determined by which coronary artery supplies the AV
artery (and therefore the AV node).
 In most people (70%), right dominance is observed.
 Coronary arteries (like all other arteries) maintain a certain level of tone. Vascular tone is the degree of
constriction or tension in a blood vessel and therefore its ability to dilate when necessary, i.e. when the
tissue it supplies requires greater perfusion.
 Coronary arteries have an especially high level of tone due to the importance of adequate myocardial
perfusion.
Linn Lee 1206279 Case 2: David Marsden

Table showing the different areas of the heart muscle and the coronary arteries/branches that supply them:
(This is useful for determining which coronary artery was involved in a particular MI)

Area of heart Coronary artery involved

Inferior and/or Posterior Right coronary artery
Anteroseptal Left anterior descending
Anteroapical (nearer to apex) Distal left anterior descending
Anterolateral Circumflex

 In the anatomy of the heart, inferior refers to the “back” of the heart because the heart actually sits in the
thoracic cavity and is attached to the diaphragm on its “back”; hence, it is the inferior part. (In most
diagrams we’re used to seeing hearts sort of just hanging in the air. In such diagrams, the “back” of the
heart would be the inferior aspect. Hope this doesn’t just confuse everything.)
 The “front” of the heart is called the anterior aspect; it is the visible aspect of the heart in an opened
thoracic cavity.
 Most of the anterior aspect consists of the right atrium and ventricle; part of the left ventricle can be
seen at the side.

A few veins to know:

(some orientations and positions were figured out using Moore’s anatomy and Netter’s atlas)

Vein/Tributary Location/Route Area of drainage

Coronary sinus Posterior coronary sulcus Empties into right atrium
Great cardiac vein Begins at cardiac apex and runs along anterior LA, LV, RV (these areas are
interventricular groove with the LAD, curves around supplied by the left CA)
coronary sulcus to join coronary sinus
Middle cardiac vein Begins near apex and ascends along the posterior RA, RV, some of LV
IV groove with the posterior descending artery to
join the coronary sinus
Small cardiac vein Ascends along inferior border of the heart (near Posterior aspects of RA and
marginal branch of RCA) and then along the RV
posterior coronary sulcus to join the coronary sinus
Oblique vein Descends obliquely on back of left atrium to join LA
coronary sinus as it is about to reach the RA
Anterior cardiac veins Arise on anterior surface of RV, cross the coronary Anterior RV
sulcus and enter anterior wall of RA
Posterior vein of LV Begins near apex and runs with circumflex branch, LA and LV
ascends to meet coronary sinus

General outline of the systemic circulatory system, particularly the arterial supply to the
lower limbs
 Oxygenated blood leaves the left ventricle via the aorta.
 The arch of the aorta has three branches coming off it
o Brachiocephalic trunk (innominate artery) – branches off into the right common carotid and
right subclavian arteries.
o Left common carotid artery
o Left subclavian artery
Linn Lee 1206279 Case 2: David Marsden

 The common carotid arteries branch off into internal and external carotid arteries. They supply the head
(including the brain) and the neck.
 The vertebral arteries branch off both the subclavian arteries and supply parts of the brain.
 The subclavian arteries become the axillary arteries, then the brachial arteries.
 Just after the elbow joints, the brachial arteries branch off into the radial and ulnar arteries.
 The radial and ulnar arteries branch off into the palmar branches, which then branch off into the palmar
digital arteries.
 The descending aorta runs through the thoracic cavity and abdominal cavity.
 Several main arteries branch off the descending aorta:
o Celiac artery/trunk – supplies blood to the liver, stomach, abdominal oesophagus, spleen, and
part of the duodenum and pancreas.
 Gastric arteries – carry blood to the stomach
 Hepatic artery – carries blood to the liver
 Splenic artery – carries blood to the spleen
o Mesenteric arteries – carries blood to the small intestines
o Renal arteries – carry blood to the kidneys
 The descending aorta then branches off into the right and left iliac arteries.
 The iliac arteries become the femoral arteries, then the popliteal arteries, which branch off into anterior
and posterior tibial arteries.
 The anterior tibial arteries become the dorsalis pedis arteries, which then form the plantar arch and
branch off into the dorsal digital arteries.

Demonstrate a more detailed understanding of the pathology and pathogenesis of

atherosclerosis in the coronary and peripheral arteries and the consequences in different
regions
Atherosclerosis is the presence of lesions in the arteries called atheromas (atherosclerotic plaque) and can lead
to ischaemia of the tissues being supplied by those arteries as these lesions protrude into the vascular lumen
and narrow it. Atherosclerosis also causes weakening of the arterial walls.

 Endothelial tissue damage

 LDL accumulation in arterial intima
 LDLs get oxidised by free radicals
 Recruitment of monocytes, which turn into macrophages
 Release of cytokines attracts more WBCs to the lesion (inflammatory response)
 WBCs phagocytose oxidised LDLs and become foam cells (fatty streaks)
 Inflammatory response stimulates migration of smooth muscle cells
 Layers of SMC form on top of foam cells
 Proliferation of SMCs
 Degeneration of intima
 Damaged areas invaded by fibroblasts which produce dense connective tissue
 Fibrous cap (consisting of SMCs and dense connective tissue – mostly collagen) has now formed over
the foam cells
 Atheroma/atherosclerotic plaque has formed

Possible consequences of atherosclerotic plaque in the arteries:

Linn Lee 1206279 Case 2: David Marsden

 Calcification of the atheromas

 Rupture of the fibrous cap  blood exposed to damaged endothelium and collagen fibres  platelets
clot together and blood coagulates  thrombus (blood clot) formation  acute thrombosis
 The thrombus formed by acute thrombosis may partially occlude the artery (unstable angina) or fully
occlude it (acute MI)
 If thrombosis occurs, thrombus may partially occlude the artery, or over time it will gradually become a
bigger thrombus and completely occlude the artery.
 Thrombi may heal become part of the intimal plaque, further occluding the artery.
 If the thrombus embolises, it may cause an acute condition such as a stroke (if a thrombus from the
carotid artery embolises in a small artery of the brain) or a myocardial infarction (if a thrombus
embolises in the coronary arteries). Thromboemboli can sometimes lyse (e.g. during a transient
ischaemic attack).
 Atherosclerosis also causes significant weakening and stiffening of the artery walls, causing them to
lose their elasticity. Submitted to high blood pressures, the artery walls will weaken further and stretch
(aneurysmal dilatation) and a rupture may occur (aneurysm). This most commonly occurs in the
abdominal aorta.

Describe the compensatory changes in the heart (hypertrophy [concentric hypertrophy]

and/or dilatation [eccentric hypertrophy]) to haemodynamic challenges (pressure and/or
volume) arising from pathology in the myocardium and/or valves.
Concentric hypertrophy is when the wall of the myocardium uniformly increases in thickness

 Due to increased pressures in the heart chambers over a period of time

 Involves new sarcomeres being arranged in parallel (thus increasing muscle thickness)

Eccentric hypertrophy (or dilatation) is when the actual chamber within the myocardium gets bigger

 Due to an increase in the volume of blood within the chamber e.g. due to regurgitant flow from an
incompetent valve
 Involves new sarcomeres being arranged in series.

In aortic regurgitation, the aortic valve is incompetent and during diastole, some aortic blood flows back into the
left ventricle. This causes an increase in end-diastolic volume of the left ventricle and therefore an increase in
preload. Afterload also increases since there is an increased volume of blood in the LV and therefore an
increased LV pressure. Over time, the heart chamber will enlarge (left ventricular dilatation or eccentric
hypertrophy, as well as concentric hypertrophy) to accommodate for the increased volume and pressure.

In aortic stenosis, the aortic valve is narrowed and the pressure gradient across the valve increases. This means
that during systole blood needs to be pumped out of the left ventricle at a higher pressure and with a stronger
contraction to maintain cardiac output even with the increased afterload. Over time, the increased pressure within
the left ventricle causes the heart to compensate by increasing the thickness of the myocardium (left ventricular
concentric hypertrophy). The thicker myocardium is able to withstand higher pressures and to pump more
forcefully.

In mitral regurgitation, the mitral valve is incompetent and during systole, some blood from the left ventricle flows
back into the left atrium. This causes the volume of blood in the left atrium to increase. Over time, the left atrium
will enlarge (left atrial dilatation or eccentric hypertrophy of the left atrium) to accommodate for the increased
volume. In the long run, even compensation may eventually be insufficient and the reduced contractility of the
Linn Lee 1206279 Case 2: David Marsden

heart will lead to increased end-systolic volume, worsening the existing condition.
Note: In mitral regurgitation, afterload actually decreases because blood from the LV can eject blood through the
aortic valve as well as the incompetent mitral valve, so the LV does not have to contract as much.

In mitral stenosis, the narrowed mitral valve means that there is an increased pressure gradient across the mitral
valve and it takes a greater force for blood to flow from the left atrium into the left ventricle. Over time, the left
atrium compensates by thickening its muscular wall (left atrial concentric hypertrophy).

Mechanism of production of normal first and second heart sounds

 The two heart sounds are known as S1 and S2.
 S1 is produced by the closure of the two AV valves (mitral and tricuspid). It occurs during systole.
 S2 is produced by the closure of the two semilunar valves (aortic and pulmonary). It occurs during
diastole.
o Physiological splitting of S2 occurs upon deep inspiration.
o This is due to a decreased pressure in the thoracic cavity.
o Temporary delay in the closure of the pulmonary valve

Major valvular causes of systolic and diastolic murmurs

Valve pathology Timing Location Radiation Phonogram
Aortic stenosis Systolic ejection 2RICS SB Carotids
murmur

Aortic regurgitation Early diastolic 2LICS SB -

Best heard upon (murmur is heard
expiration with patient as soon as aortic
leaning forward valve closes)
Mitral stenosis Mid/late diastolic 5LICS MCL -
Best heard with patient’s (murmur is heard
body turned slightly to when left atrium
the left; bell of steth contracts)
Mitral regurgitation Pansystolic 5LICS MCL Left axilla
 Linn Lee 1206279 Case 2: David Marsden

Demonstrate understanding of the mechanisms by which a valve lesion causes other

symptoms and signs (including chest pain on exertion, dyspnoea, changes in pulse)

Crepitations upon auscultation

Pulmonary oedema

Imbalance of Starling forces in capillaries Reduced lung compliance

Stimulation of J- receptors
Dyspnoea
Pulmonary hypertension

Peripheral oedema
Ectopic beats (palpitations)
Increased pressure in pulmonary circulation

Displaced apex beat Increased peripheral venous pressures

Stronger contraction needed

Increased pressure in LA

Dilatation of LV Peripheral vasoconstriction

Increased preload
Stimulation of renin-angiotensin-aldosterone system
Increased volume in LV

Aortic regurgitation
Decreased CO

Reduced cardiac perfusion

Increased afterload Increased thickness of myocardium

Concentric hypertrophy

Ischaemia upon exertion

urmur heard best at 2LICS SB with diaphragm, patient leaning

Forceful
forward
apexand
beat/heave
in full expiration.

Anaerobic respiration of myocytes

Lactic acid accumulation

Stimulation of nociceptors

Chest pain
 Linn Lee 1206279 Case 2: David Marsden

Forceful apex beat

Greater perfusion required due to thicker myocardium

Concentric hypertrophy Exertion

Myocardial ischaemia

Increased pressure in LV
Increased pressure in LA

Decreased CO Lactate accumulation

Increased afterload
Increased pressure in pulmonary capillaries
Pulmonary oedema Stimulation of nociceptors
Decreased cerebral perfusion

Aortic stenosis
J-receptors
Reduced lung compliance Chest pain

Syncope/dizziness
Dyspnoea

Decreased perfusion of tissue in peripheries (with sufficiently oxygenated

Systolic crescendo-decrescendo ejection murmur that may radiate to carotids; best heard in 2RICS SB

Peripheral cyanosis
Linn Lee 1206279 Case 2: David Marsden

Chest pain

Stimulation of
nociceptors

Pansystolic murmur
heard best with Lactate accumulation
diaphragm at 5LICS MCL

Myocardial Exertion
Irregularly irregular ischaemia
heartbeat
Mitral
Palpitations regurgitation Decreased cardiac
perfusion

Atrial fibrillation
Retrograde flow
through incompetent Decreased CO
valve into LA
Disrupted conduction
pathways of LA
Increased
preload
Eccentric Increased
Stagnant volume in LA
hypertrophy of LA
blood in LA
Eccentric
hypertrophy of LV
Thrombosis Increased
pressure in LA
Displaced
Thrombus apex beat
embolises in Stroke/TIA
cerebral artery Increased pressure
in pulmonary
capillaries

Stimulation of Pulmonary
Dyspnoea
J-receptors hypertension

Pulmonary
Reduced lung
oedema
compliance
 Linn Lee 1206279 Case 2: David Marsden

Disrupted conduction pathways of action potentials

Concentric hypertrophy ofIncreased
LA pressure in pulmonary capillaries
Pulmonary hypertension

Increased pressure in LA Pulmonary oedema

Atrial fibrillation
Stimulation of J receptors

Palpitations Increased resistance to LV filling Reduced lung compliance

Irregularly irregular heartbeat Dyspnoea

Mitral stenosis

Decreased CO

Decreased perfusion of myocardium

Exertion Myocardial ischaemia

Chest pain
Linn Lee 1206279 Case 2: David Marsden

Here’s a random mech I decided to make. Hope it helps:

(Reference: Kumar & Clark)

Valve lesion

Blood redirected Decreased Activation

Decreased CO
to vital organs renal perfusion of RAAS

Myocardial Compensates for Increased

ischaemia venous pressure

Reduced Increased systemic

Past MI
contractility venous pressure

Hepatomegaly Dependent
Increased
oedema
ESV

Extra ESV combines

with normal EDV of
next filling cycle

Increased EDV

Eventual decompensation of
Frank-Starling law

Heart failure
Linn Lee 1206279 Case 2: David Marsden

Demonstrate knowledge of the major potential causes and mechanisms of:

Shortness of breath caused by a cardiac condition, including orthopnoea

Lungs stiffened, bronchioles and alveoli compressed

Heart failure Reduced contractility

Pulmonary oedema
Increased afterload
Reduced lung compliance

Build up of pressure in LA
Hydrostatic forces push fluid out of capillaries
Increased work of breathing

Build up of pressure in pulmonary capillaries

Capillaries stretched by pressure

Stimulation of J-receptors Sensation of dyspnoea

Lying in the supine position

Heart failure

Redistribution of blood from lower limbs

Reduced contractility

Increased venous return Exacerbates poor contractility of heart

Increased hydrostatic pressures in pulmonary capillaries

Exacerbated pulmonary congestion

J-receptors stimulated

Orthopnoea
 Linn Lee 1206279 Case 2: David Marsden

Chest discomfort during myocardial ischaemia

Atherosclerosis of coronary arteries

Lactate builds up as byproduct

Myocytes respire anaerobically pH change sensed by nociceptors
pH drops
Myocardial ischaemia

Decreased cardiac perfusion

Nociceptors stimulated

Decreased CO due to heart failure Chest pain/discomfort Impulse carried by C-fibres

Calf pain during walking (claudication)

Atherosclerosis in arteries of lower Stenosed

limbs arteries

Decreased tissue perfusion

Calf pain
Exertion

Myocytes of calf muscles respire anaerobically

Increased demand for blood in tissues Build up of lactate Stimulation of nociceptors
Ischaemia

Differentiating chest pain and dyspnoea

Condition/Cause Differentiating factors

Angina due to myocardial
ischaemia
Myocardial infarction
Pulmonary embolism
Pericarditis
GORD (spasm/reflux)
Pneumothorax
Aortic dissection
Musculoskeletal
Note: Pleuritic = exacerbated by coughing or breathing
Dull and retrosternal, feels like a heavy pressure, sometimes radiates to upper
arm, neck or jaw, onset upon exertion, lasts for about 5-10 minutes and is
alleviated by rest/nitroglycerin if stable. If onset at rest, angina is unstable.
Accompanied by dyspnoea.
Similar to angina, except lasting for >20 minutes. May be accompanied by
nausea, sweating and anxiety.
Sharp and pleuritic, accompanied by dyspnoea and sometimes haemoptysis.
Sharp, stabbing and pleuritic, also exacerbated by movement of the torso. May
radiate to the back/scapulae. Sometimes relieved by sitting up and leaning
forward.
Burning sensation in the chest, often mistaken for an MI. May taste acid/fluid at
the back of the throat. Onset by eating and alleviated by antacids.
Sharp pleuritic pain accompanied by dyspnoea and sometimes cyanosis.
Tearing, ripping pain; prolonged
Brief, sharp, localised, stabbing, pleuritic pain
Linn Lee 1206279 Case 2: David Marsden