the subject does not need to be in ‘steady state’.

a six-fold increase in oxygen uptake mean six-fold increase in cardiac output.

cardiac catheterization is not necessary.

cardiac output (CO) is calculated as pulmonary oxygen uptake (U) multiplied by the difference in oxygen content between arterial

blood (A) and mixed venous blood (V); CO = U(A-V).

pulmonary blood flow is equated with cardiac output.

Causes vasoconstriction.

Stimulates tachycardia.

Increases arterial blood pressure.

Increases cardiac output.

Constricts

capillaries.

has capillaries which connect arteries and veins.

reabsorbs protein and foreign particles from the interstitial fluid.

forms a filtrate which eventually becomes urine.

removes damaged erythrocytes from the circulation.

has a role in controlling blood pressure.

The relationship does not apply to capillaries, as they are so narrow.

The relationship applies equally to laminar and turbulent flow.

Flow is increased by increasing the length of the

vessel.

Resistance to flow is independent of the diameter of the conducting vessel.

If outflow pressure is doubled with no change in inflow pressure, flow will be reduced.

causes an

increase in heart rate on moving from lying down to standing.

is important for long-term control of blood

pressure.

increases systemic arterial blood pressure.

is mediated by special pressure receptors in the abdominal

aorta.

is an example of a positive feedback control system.

Decrease, vasodilation

Increase, vasodilation

Increase, vasoconstriction

Decrease, vasoconstriction

Stay the same, vasoconstriction

increases cardiac output.

increases the ‘firing rate’ of the pacemaker cells.

causes bradycardia.

increases the force of ventricular contraction.

has the same effect as adrenaline.

48%

10%

34%

19%

59%

decrease pre-load and stroke volume.

decrease pre-load and increase arterial blood

pressure.

increase pre-load but not alter stroke volume or

arterial blood pressure.

increase pre-load and decrease arterial blood

pressure.

increase

pre-load and stroke volume.

Smooth muscle myosin is inactivated when myosin-light-chain phosphatase

removes the phosphate residue attached by myosin-light-chain kinase

Intracellular calcium binds to calmodulin (CaM) and the Ca-CaM complex activates a kinase.

An increase in cytosolic calcium induces calmodulin binding to myosin-light chain kinase.

The regulation of the actin-myosin interaction occurs by calcium binding to troponin.

Phosphorylation of the myosin light chain converts the myosin into its active form which can then bind to F-actin.