Cardiac structure and function

Question 1

What are the four layers of the heart and their functions?

Answer 1

• Epicardium (outside layer): connective tissue (areolar)
• Myocardium (middle): cardiomyocytes and connective tissue
• Endocardium (inner layer): thin layer of connective tissue and endothelium
• Pericardium (parietal and visceral (epicardium)) - cavity contains pericardial fluid for lubrication

Question 2

Pericarditis

Answer 2

Multiple causes (infections, trauma, cancer, autoimmune), overall effect is the accumulation of fluid (effusion) which restricts ventricular filling

Question 3

Excitation-contraction coupling

Answer 3

• Autorhythmic cells stimulate cardiomyocytes
• AP down sarcolemma
• AP generated by autorhyhmic cells, arrived at cardiomyocytes, is propagated along the sarcolemma into t-tubules
• On membrane are calcium channels (L-type calcium channels)
• As voltage changes, it opens channels and opens extracellular fluid and space
• Ca2+ into cell and increases concentration inside cytosol
• L-type calcium channel closely associated with SR
• SR has 10,000x greater amount of calcium than cytosol
• RyR receptors on membrane of SR - calcium binds to RyR and causes calcium within SR to enter cytosol - this is calcium induced calcium release
• Increase in calcium in intracellular space needed to bind to troponin to cause muscle contraction

Question 4

Excitation propagation

Answer 4

Somatic neurone terminates at muscle fibres = NMJ

AP travels towards NMJ = vesicles and ACh travel across membrane

Question 5

Gap junctions

Answer 5

• Occur between cardiomyocytes
• Sharing of cytosol - environment in one cardiomyocyte influences another = transfer of excitation between gap junctions
• Apoptosis can be transmitted across gap junctions - causes wave of cell death
• Autorhythmic cells = excitability, cause AP on first cardiomyocyte
• Propagation of AP along sarcolemma
• Influx of sodium ions causes transfer into adjacent cell
• Voltage gated channels along membrane, causes them to open, causes AP wave = peristaltic process
• Directional flow of blood out of heart

Question 6

Preload

Answer 6

• Cardiac output = HR x SV
• Stroke volume = (end diastolic volume) - (end systolic volume)
• EDV is the volume of blood just before contraction
• ESV is volume of blood after contraction
• No change in volume of ventricle

Question 7

Stroke volume

Answer 7

• Physical factors - more optimum myofilament overlapping
• Decrease lattice spacing - decreased distance between myofilaments - increased probability of interaction between contractile components
• Activating factors - increase in calcium sensitivity (multiple mechanisms - increased calcium release and sensitivity)

Question 8

Length-force relationship

Answer 8

• Shortening = loss of energy, stretch is gained energy

- Increase starting length of muscle means increased net power until optimum

Question 9

Pressure-volume loop (increase in EDV)

Answer 9

• Increases the overall shortening length - generates more total force/power
• Preload/EDV increases with venous return
• Increase in EDV = increased contractility
• Increases SV and therefore CO

Question 10

Pressure-volume loop (increased ESV)

Answer 10

• Increase in afterload means increase in EDV because reduction in stroke volume = higher ESV (more left in ventricle after contraction)
• Length of muscle increased so ability of muscle fibres to shorten decreases which means stroke volume decreases
• Increase in afterload alters slops (correlation) between pressure and volume - less opportunity for muscle to shorten - decreased SV if no compensatory response
• Increase in afterload means overall stroke volume decreases for variety of factors

Question 11

What happens when contractility falls?

Answer 11

• Caused by weak ventricle - it can’t generate force in systole
• Stroke volume will then fall

Question 12

What happens when compliance falls?

Answer 12

• Stiff fibrotic ventricle
• Reduced compliance
• Reduced SV

Question 13

Contractility

Answer 13

• Increase in calcium release leads to increase in contractility
• Sympathetic drive due to ventricular muscle fibres (NA at B1 R in cardiac muscle cells)
• Hormonal control (circulating A and NA)

Question 14

Ejection fraction

Answer 14

• Quantification of contractility: ejection fraction, ratio of stroke volume to EDV
• EF = SV/EDV
• Expressed as a percentage - normally between 55 and 75 percent
• Measures ability of ventricle to contract - >75% indicates hypertrophic cardiomyopathy
• <40% = heart failure

Question 15

Heart rate

Answer 15

• Neuronal and endocrine regulation
• Increase HP - positive chronotropic factors (including A and NA)
• Decrease HP - negative chronotropic response (including ACh)
• Symapthetic increases membrane permeability to Na+ = spontaneous depolarisation = reduces time to depolarise = increases HR
• Parasympathetic decreases permeability to Na+ but increases to K+ = decreased spontaneous depolarisation = increased time to initiate depolarisation