25. Applied Anatomy of the Heart

Question 1

What is the heart’s nervous supply and where is it found?

What 3 things does the heart’s nervous supply contain?

Where do the nervous fibres extend to?

Answer 1

The cardiac plexus, anterior to the bifurcation of the trachea and posterior to the aortic arch.

Parasympathetic (vagus) passing through, Sympathetic (from sympth. trunk), Visceral general afferants (VGAs)

From plexus to coronary vasculature and compoents of conducting system of heart (esp SAN)

Question 2

Describe what effect the parasympathetic and sympathetic innervation has on the heart.

What level do the sympathetic preganglionic fibres come out at?

Answer 2

Parasympathetic: slows HR, Path: reticular formation in medulla (cardioinhibitory centre) -> vagus nerve to SAN and AVN.

Sympathetic: increases HR and contraction force, medullary reticular formation (cardioacceleratory centre) -> preganglionic sympathetic neurons in thoracic SC -> post ganglionic sympathetic neurons to SAnN, AVN and coronary VSM

T1-T4

Question 3

What is cardiac pain?

Where is if usually felt?

Answer 3

Pain caused by ischemia, stimulates nociceptors in myocardium -> visceral afferents ascend to CNS via cardiac branches of sympathetic trunk. Pain not felt in heart - referred becuase nociceptors travel with sympathetic fibres back into SC at T1-T4 and SC and brain can’t differentiate between different innervations so get referred pain - feels as though it’s coming from the dermatome that the fibres enter.

Referred to skin supplied by T1-T4 on the L, medial upper arm and neck/jaw. Also for infarct on inferior wall, referred to epigastrum T5-9.

Question 4

Label A-G

Answer 4

A: RCA (emerges from aortic sinus)

B: Posterior (interventricular) descending

C: Right marginal

D: LCA (1-2 cm long, divides into E and G)

E: L circumflex

F: L marginal

G: LAD

Question 5

Label A-E

Answer 5

A: Circumflex

B: AVN (supplied by RCA)

C: LAD

D: Posterior (interventricular) descending

E: RCA

F: right marginal

Question 6

What are bundle branches?

What can cause bundle branch block?

Answer 6

Offshoots of the BoH, modified myocytes, carry AP to apex of heart, where it reached normal myocytes and contraction occurs.

LAD block

Question 7

What is left-sided dominance?

Answer 7

Coronary artery variation, in 15%, RCA doesn’t give off posterior (intrerventricular) descending - it’s given off by L. circumflex instead.

Pic: normal (red=RCA, orange =LCA) vs. LSD

Question 8

What ECG leads can the following parts of the heart be seen best by?

Lateral (top)

Lateral (bottom)

Anterior

Septal

Inferior

Answer 8

Lateral: I, aVL

Lateral (bottom): V5, V6

Anterior: V3, V4

Sepal: V1, V2

Inferior: II, III, aVF

Question 9

Label A-C. ECG leads vaguely correspond to areas of the myocardium supplied by the coronary arteries. Label which ones.

Answer 9

A: LCx or diagonal branch of LAD

B: RCA or LCx

C: LAD

Question 10

What happens in a bundle branch block?

What causes atrial enlargement?

What risk does atrial enlargement create? Describe the risk.

Answer 10

Ischemic BB stops conducting impulses appropriately -> uses altered pathways for depolarisaton -> impulse travels through myocytes (slows impulse speed - prolongs QRS) -> loss of ventricular synchrony

Any persistant change in atrial structure

Larger atrium = higher risk of AF (ectopic firing and reentry etc., absent P wave, reduced C.O., thrombi and syncope)

Question 11

What is cardiac remodelling, and what does it affect?

What 2 things happen in myocardial hypertrophy?

When can normal cardial remodelling happen physiologically?

Answer 11

Structural changes (increase in myocardial mass) with associated cardiac dysfunction, altered relationship between preload and SV.

Increased myocyte size, collagen synthesis (isn’t contractile so ventricles less efficient)

Pregnancy, athletes - hypertrophy induced by regular strenuous exercise, has no minimal effect

Question 12

Describe three pathologies that lead to cardiac remodelling.

Answer 12

1. Pressure overload (arterial hypertension/ aortic valve stenosis increases afterload)
2. Volume overload (valvular regurgiatation/hypervolaemia increases preload)
3. Cardiac injury (ischeamia/infarct) due to molecular factors, reduction in contractility (scar/thinning), compensatory hypertrophy (maladaptation - collagen laid down -> stoke vol and ejectile vol decreases -> HR increases, CYCLE)

Question 13

Describe the structural changes that happen in remodelling/ventricular hypertrophy.

Answer 13

New sarcomeres

Decreased capillary: myocyte ratio (norm= 1:1)

Increased fibrous tissue

Synthesis of abnormal proteins

Loss of myocytes - apoptosis

Question 14

Describe the 2 types of ventricular hypertrophy.

Answer 14

1. concentric hypertrophy - increased afterload (from aortic stenosis or chronic HT) causes increase in wall thickness (new sarcomeres = reduced compliance and compromised ventricular filling). May lead to eccentric hypertrophy (reduced compliance leads to volume overload).

2. eccentric hypertrophy - caused by volume overload/ increased preload, or combination of preload and afterload from ischaemic heart diease) -> chamber dilation (due to valvular regurgitation, systolic dysfunction, volume overload or alcohol/cocaine) -> elevates O₂ demand -> lowers mechanical efficacy (Laplace’s law)

Question 15

Distinguish between the two types of ventricular hypertrophy:

Answer 15

A: ventricular hypertrophy

B: eccentric hypertrophy

Question 16

What makes the first heart sound?

What makes the second heart sound?

What vales are closed and opened in systole and diastole?

Answer 16

AV valves

Aortic and pulmonary valves

Systole: AV valves closed, aortic and pulmonary open

Diastole: Aortic and pulmonary closed, AV open

Question 17

What is valvular disease?

What can it be caused by?

What effects does rheumatic disease have on the valves?

Answer 17

Inflammation of the valve (infection, bacterial endocarditis, rheumatic disease)

Caused by ageing (bits of calcification), cardiomyopathy, ischemic heart disease, fibrosis and calcification, narrowing (stenosis), valvular incompetence (regurgitation)

Cusps fibrose, cordae tendinae soften

Question 18

Mitral regurgitation is the most common form of valvular heart disease. What is it?

What is it caused by?

What might long standing mitral regurgitation show?

Answer 18

Abnormal regurgitation of blood back into L atrium. Acute volume overload on L ventricle with an increase in end diastolic volume. Systolic murmur (b/c mitral valve closed through systole so sound of regurgitation heard throughout systole)

Mitral valve prolapse, rheumatic heart disease, complication of cardiac dilation

L atrial enlargement and L ventricular hypertrophy (dilation)

Question 19

Why can L sided heart failure cause pulmonary oedema?

What is congestive heart failure?

Answer 19

Failing backlog of blood at venous end = increase in pulmonary venous pressure so in the capillary bed the pressure is higher at the venous end so less fluid reenters capillary from interstitum = oedema.

L and R side both failing. When R side starts to fail = increase central venous pressure = ankle oedema and peripheral/systemic oedema

Question 20

What effect does aortic stenosis have on the ventricle?

Answer 20

L ventricle has to generate an increased pressure to overcome the increased afterload caused by stenotic aortic valve. May lead to LVH (concentric) in response to generate the increased force. But the hypertrophied myocardium has less compliance and decreased coronary blood flow reserve - systolic end diastolic failure

Hear it throughout systole because turbulence as blood pushed throuhg stenotic aortic valve (less severe - early systole)

Question 21

What is this image showing?

Answer 21

Aortic stenosis - calcifications on stenotic valve

Question 22

What is mitral valve stenosis, and what does it lead to?

Answer 22

L atrium has to generate higher pressure than normal to overcome increased gradient caused by mitral valve stenosis. Atrial ‘kick’ needs to be stronger - leads to atrial enlargement and increased atrial pressure -> pulmonary congestion (oedema). Ventricular filling reduced -> reduced C.O. L. atrial enlargement can lead to AF and loss of ‘kick’ and further decreased filling of L ventricle. Rarely produces diastolic murmur

Systemic embolic events see in about 1/3 pts with AF and mitral stenosis

Question 23

What is wrong in this Xray?

Answer 23

Mitral valve stenosis, enlarged L atrium and pulmonary oedema.

Question 24

What is aortic regurgitation, and what does it cause?

Answer 24

Chronic volume overload causes stretching and elongation of myocardial fibres (eccentric hypertrophy), L ventricule dilation and congestive heart failure, decreased C.O. due to regurgitation, increases preload (and afterload). Murmur heard during diastole.

Question 25

What does this CXR show and why?

What causes this condition? Give values.

What symptoms may this condition cause?

Answer 25

Pulmonary oedema - shows peri-hilar oedema (batwing) and kerley B-lines (fluid drained away by lymphatics so can see horizonal lines through lungs but hard to see)

Pulmonary venous hypertension (>25mmHg venous pulmonary pressure)

Respiratory distress and crackles, orthopnea (SoB when lying flat)

Question 26

What are the 2 main features of this CXR?

Answer 26

Batwing

Blunting of costophrenic angle. If fluid in pleural cavity, goes to this area due to gravity = indicitave of pleural effusion, can be caused by many things e.g. heart failure

Question 27

What can you see in this CXR?

Answer 27

2 pleural effusions

Question 28

List the two pathologies and how the kind of ventricular hypertrophy that is created for

a) diastolic murmur
b) systolic murmur

Answer 28

a) aortic regurgitation - eccentric

mitral valve stenosis - concentric

b) aortic stenosis - concentric

mitral regurgitation - eccentric