Essentials of Human Evolution

Lecture 4 – Cardiac Output

Ventricular contraction

Excitation (ventricular AP) essential for ventricular contraction[pic 1]

Heart

Muscular pump

Left ventricular wall – inner lining called endocardium which is made up of endothelial cells

• outer layer called epicardium – made up of connective tissue and fats
• everything between inner endocardium and outer epicardium – myocardium – made up of ventricular muscle cells

Cardiac contraction

• Involves shortening of contractile units (sarcomeres)
• Cardiac muscle – striated due to arrangement of thin (actin) filaments and thick (myosin) filaments called sarcomeres
• smooth muscle – no arrangement of contractile filaments – smooth appearance

Contraction involves cross-bridge cycling (sliding filaments)

Myosin heads (de)attach from thin actin filaments – cross bridges  → cause filaments to slide over each other → shortening contractile units → shortening cardiac muscle cells – involves hydrolysis of ATP → energy for contraction

• Requires excitation = extracellular calcium entry into cardiac muscle cells
• Increase [Ca2+] → increase force of contraction
• In relaxed state – tropomyosin covers up binding site → myosin head cannot attach to binding site on actin filament
• Ca2+ binds to a component of the troponin complex (TnC) → alters position of adjacent tropomyosin → exposing myosin-binding site on actin filament
• Excitation → Ca2+ influx → contraction

Ventricular muscle cells connected via intercalated discs

• within intercalated disks are desmosomes → glue cells together

• gap junctions allow passage of current/ions from one cell to next

• Plasma membrane – sarcolemma
• Transverse (T)-tubules
• Plasma membrane goes into the cytoplasm of the cardiac muscle cell
• Along t-tubules is the SR – contains internal stores of Ca2+ [pic 2]

AP → depolarisation → Ca2+ entry → enters ventricular muscle cells through long lasting L-type calcium channels (open and close slowly) located on both sarcolemma and T-tubules → binds to Ryanodine receptors on the SR → open to release Ca2+ from internal stores of the SR into cytoplasm→ Ca2+ binds to TnC → myosin heads revealed → cross-bridge formation → contraction

Ca2+-induced Ca2+ release

SRCaATPase – Hydrolyse ATP to pump Ca2+ back into SR        [pic 3]

Summary – expiation-contraction coupling

• AP (excitation/depolarisation) → increase in intracellular [Ca2+]
• Both SR and extracellular Ca2+ pools are involved
• Ca2+ influx from extracellular space essential for contraction
• If no extracellular Ca2+ or Ca2+ influx is blocked – no contraction
• Ca2+ influx → triggers release of Ca2+ from SR

• Ca2+ induced Ca2+ released

Cardiac output

Effectiveness of pump (heart) alters the pump output (cardiac output – most of time left ventricular cardiac output)

Cardiac output

• Stroke volume – volume of blood ejected
• Heart rate – contractions per min[pic 4]

Cardiac output increases with exercise

Distribution of LV CO with exercise

• During exercise increase CO and distribution of blood flow to organs changes
• Blood ejected into aorta from Left ventricle → into system
• Right cardiac output goes into lungs → pulmonary circuit[pic 5]

Cardiac output capacity reduced with heart disease

Damage/blocking of coronary arteries → decrease of supply of blood to muscle

Cardiac output can be changed by changing Heart rate and/or stroke volume[pic 6]

During exercise → Heart rate increased

• Reduced parasympathetic input to SA node (vagal withdrawal)
• Increased sympathetic input to SA node pacemaker cells

Stroke volume

Stroke volume altered by two mechanisms

• Changes in muscle cell length (end diastolic volume; EDV – volume of blood in ventricles at end of relaxation)
• Changes in calcium release (contractility)

Changes in muscle length

Stroke volume = end-diastolic – end-systolic volume → how much blood left in ventricles after contraction and ejection

• diastole – resting potential of ventricular AP – no excitation – ventricles are resting and passively filling with blood
• EDV – volume of blood in left ventricle at end of ventricular filling
• Systole – period of excitation and contraction – ejection of blood from left ventricle into aorta
• Ventricles do not eject all their blood after contraction

Frank-Starling mechanism

Relationship between EDV and SV

• Increase EDV → pressure in ventricles
• Increase pressure → stretches heart muscle fibres[pic 7]
• Increase length of muscle fibres → increase force of contraction

EDV

Control of stroke volume by EDV is intrinsic property of heart

Main determinants of EDV

• Filling time (excitation/heart rate)
• Venous pressure (venous return) – pressure in veins returning blood back into heart
• Increase venous return → increase ventricular EDV → increase stroke volume
• Increase venous return automatically increases stroke volume
• means of matching output to input (ventricles tend to eject as much blood as they receive)
• Important in matching the output of the right and left sides of the heart

Matching right and left cardiac outputs

Increase in RVCO → increase pulmonary blood volume → increase in pressure in pulmonary veins → increase pressure in left atrium → increase LV EDV → increase length of muscle cells → increase contractile force → increase SV → increase CO in LV