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Week 5b – Cardiovascular Physiology 1:

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Week 5b – Cardiovascular Physiology 1:

Role of the cardiovascular system:

• Supply of nutrients & hormones

• Removal of metabolic waste products

• Exchange of nutrients & waste products (at capillaries) Ø 5% of blood is found in capillaries

• Helps to produce heat/warm the body up

Design of the cardiovascular system:

Ø Pulmonary circulation:

o Right ventricle to lung to left atria

o Role is to oxygenate blood and remove CO2

Ø Systemic circulation:

o Left ventricle to tissues to right atria o Supplies oxygen to the bodies’ tissues

Arteries carry blood away from the heart. (Note – not all arterial blood is oxygenated).

Veins carry blood back towards the heart. (Note – not all venous blood is de- oxygenated).

Ø Arterioles are resistance vessels – the smooth muscle surrounding them can constrict or relax depending on what blood pressure is required.

Ø Veins are known as capacitance vessels (they can hold up to 60% of blood volume)

Pressure, flow & resistance:

• Blood flow (F) is always from a region of high hydrostatic pressure to a region of low hydrostatic pressure

Hydrostatic pressure is the pressure exerted by a liquid in response to an applied force (e.g. heart beat)

Blood pressure is the hydrostatic pressure pushing blood through the circulatory system

• Blood flow = pressure difference (ΔP)/resistance (friction force impeding flow) Determinants of resistance:

o Blood viscosity (the thickness of blood) – viscosity increases with haematocrit, however is normally kept constant.

o Length of blood vessels – kept constant throughout adulthood.

o Blood vessel radius (the most important determinant).

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Heart valves:

• Function is to ensure unidirectional blood flow

• The opening & closing of valves is determined by the pressure difference across the valves

• The papillary muscle & chordae tendinae prevent valve eversion

Structure of cardiac muscle cells:

• Striated due to the arrangement of thick & thin filaments into sarcomeres

• Shorter than skeletal muscle, and branched

• Mononucleated (have 1 nucleus), rich in mitochondria but poor in sarcoplasmic reticulum

• Cells are connected via intercalated disks and gap junctions

Heart beat coordination:

• The atria contract first, then the ventricles.

• Depolarization begins at the sinoatrial (SA) node located in the posterior wall of the right atrium.

Cardiomyocte action potentials:

• Cardiomyocte AP’s are different from neurons & skeletal muscle cells.

• Contain a plateau phase, which is ~200 times longer than the excitation phase in other cells.

• The plateau phase is due to the influx of Ca2+ via slow voltage-activated Ca2+

channels, matched by the efflux of K+ via K+ channels. Na+ influx becomes reduced markedly because Na+ channels close.

Repolarization occurs when K+ and Ca2+ permeability return to the resting state (i.e.

when enough K+ leaves the cell).

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Pacemaker potential:

• Where resting potential is not steady but gradually depolarizes

• Pacemaker potential results from the influx of Na+ via special Na+ channels activated by the repolarizing phase of the previous action potential

• Other cells of the conducting system also display depolarization during the resting phase, but their rate of depolarization is normally slower than SA node cells

Week 6a – Cardiovascular Physiology 2:

The electrocardiogram (ECG):

P wave – atrial depolarization.

QRS complex – ventricular depolarization (and atrial repolarization).

T wave – ventricular repolarization.

ST segment – ventricular systole (ventricular contraction & emptying).

TP interval – ventricular diastole (ventricular relaxation & filling).

Þ With a partial block of the AV node (the node between the atria and the ventricles), there is less ventricular contraction occurring (but still the same amount of atrial contraction).

Þ With a complete block of the AV node, there is no association between the P wave &

the QRS complex.

Excitation-contraction coupling:

• The process by which an action potential in the muscle cell membrane induces muscle contraction.

• In cardiac muscle, excitation-contraction coupling is dependent upon extracellular Ca2+ entering cells

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Ca2+ channel antagonists can block calcium channels from opening. This reduces Ca2+ release from the sarcoplasmic reticulum, which reduces the strength of contraction. This is useful for conditions such as high BP.

Cardiac muscle refractory period:

• Unlike skeletal muscle, cardiac muscle cannot summate contractions (this allows for filling of the heart). This prevents uncoordinated contractions. This occurs due to a long absolute refractory period (~250msecs).

• During the absolute refractory period, contraction cannot occur no matter how strong the stimulus is.

• Cells can only be excited again when the cardiac muscle twitch is almost complete.

This ensures that max HR is around 200bpm.

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