Question-mark assessment Q's and A's

Question 1

Concerning the electrical activity of the heart: Sympathetic stimulation hyperpolarises and slows down the rate of depolarisation of the pacemaker cells.

Answer 1

False

This describes the effect of vagal (parasympathetic) stimulation

Question 2

Regarding control of the peripheral circulation: Constriction of the arterioles in a tissue results in an increase in pressure in the capillaries of that tissue.

Answer 2

False

Constriction of arterioles will decrease the pressure in the vessels downstream

Question 3

Concerning the electrical activity of the heart: The sinoatrial node is the only region of the heart capable of showing pacemaker activity.

Answer 3

False

Other regions also have some pacemaker activity, but normally they depolarise slower, and therefore reach threshold later, than cells of the SA node.

Due to the presence of gap junctions, the heart will always beat at the rate of the fastest pacemaker, and therefore slower pacemakers are not normally evident.

Question 4

Concerning the electrical activity of the heart: Hyperkalemia (a high concentration of K+ in the plasma is liable to cause fibrillation of the myocardium.

Answer 4

True

This is a direct consequence of the effect of raising extracellular K+ concentration on the resting membrane potential. Reducing the concentration gradient for K+ will reduce the equilibrium potential that it can sustain (ask Mr Nernst), and therefore myocardial cells will depolarise towards threshold. Instead of waiting to be told to fire an action potential by the sinoatrial node, they will start spontaneously firing action potentials and contracting in an uncoordinated manner. This is the definition of fibrillation.

Question 5

Concerning the cardiac cycle: Most of the stroke volume leaves the ventricle during the first third of systole.

Answer 5

True

This corresponds to the rapid ejection phase.

Question 6

Concerning the arterial baroreflex: If the mean arterial pressure rises, cardiac output must also have risen.

Answer 6

False

Mean arterial pressure (MAP) = cardiac output (CO) x total peripheral resistance (TPR). Therefore a rise in mean arterial pressure may be due to a rise in cardiac output, or total peripheral resistance.

Question 7

Concerning the vascular system: Increased capillary permeability may cause oedema.

Answer 7

True

Increased capillary permeability allows plasma and proteins to flow out; hence the osmotic gradient drawing water back into the capillaries is not developed.

Question 8

Concerning the cardiovascular system: Cardiac output is approximately 75ml/beat.

Answer 8

False

Correct. This is the stroke volume. Cardiac output is a flow and would be measured in litres/min. In normal adult at rest, cardiac ouptut is likely to be about 5 litres/min.

Question 9

Concerning the cardiac cycle: The first heart sound is caused by opening of the mitral and tricuspid valves.

Answer 9

False

The first sound is caused by closure of the mitral and tricuspid valves. Opening of the valves does not cause any sound.

Question 10

Concerning the arterial baroreflex: A fall in blood pressure triggers a reflex increase in sympathetic outflow.

Answer 10

True

Hence, evoking a pressor response to restore mean arterial pressure back to normal

Question 11

Regarding control of the peripheral circulation: Arterioles in most organs constrict in response to local hypoxia.

Answer 11

False

Most arterioles in the systemic circulation dilate in response to hypoxia, hence increasing blood flow to that tissue and helping to match O2 delivery to O2 demand. The exceptions are the pulmonary arterioles, which constrict in response to hypoxia. This has the effect of redirecting blood to the better-ventilated parts of the lung where it can pick up more O2.

Question 12

Concerning the vascular system: Most vascular beds are arranged in parallel.

Answer 12

True

This allows all tissues to receive oxygenated blood, and enables regional redirection of cardiac output when required.

Question 13

Regarding control of the peripheral circulation: Angiotensin II is a powerful vasodilator.

Answer 13

False

Angiotensin II is a vasoconstrictor

Question 14

Concerning the cardiac cycle: At resting heart rate, systole takes approximately twice as long as diastole.

Answer 14

False

At resting heart rate, systole occupies about 1/3rd of the cardiac cycle. Therefore diastole is twice as long as systole.

Question 15

Concerning the electrical activity of the heart: Cardiac contraction is initiated by sympathetic nerves.

Answer 15

False

Cardiac contraction is initiated by the spontaneous depolarisation of pacemaker cells in (usually) the sino atrial node. This inherent firing rate can be increased by activity in sympathetic nerves, releasing norepinephrine and acting on beta-receptors, but they do not initiate it.

Question 16

Concerning the pumping ability of the heart: Increased afterload causes an increased stroke volume.

Answer 16

False

Increased afterload will mean the ventricle spends a longer time in the isometric contraction phase before it is able to open the aortic (or pulmonary) valve and will therefore eject a reduced stroke volume.

Question 17

Regarding control of the peripheral circulation: The injury response depends on intact nociceptive nerve function.

Answer 17

True

It requires release of peptides from peripheral axon collaterals of nocicieptive fibers

Question 18

Concerning the pumping ability of the heart: Increased venous return causes an increased stroke volume.

Answer 18

True

Increased venous return increases end diastolic volume, hence increasing the preload on the cardiac muscle fibers and, by Starlings law, increasing the strength of contraction.

Question 19

Concerning the vascular system: The smooth muscle surrounding the arterioles of the coronary circulation expresses beta 2 receptors..

Answer 19

True

The coronary circulation is one of the regions in which the arterioles express a high density of beta 2 receptors. As in other regions, stimulation of sympathetic nerves releases norepinephrine, which activates alpha 1 receptors and stimulates arteriolar constriction. However, circulating epinephrine is also able to activate beta 2 receptors, which trigger arteriolar dilation. This, combined with the strong metabolic autoregulation of blood flow, swamps the alpha 1 receptor mediated effect and ensures that the myocardium receives sufficient blood flow during the fight-or-flight response.