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Flashcards in Cardiac physiology Deck (54):

What is meant by the term 'cardiac output'?

Volume of blood pumped per minute


What is a normal cardiac output at rest in humans?

Approx. 5ml (can be increased to >20ml in exercise)


What is meant by the term 'stroke volume'?

The volume of blood ejected per beat


What is a normal stroke volume at rest in humans?

Approx. 70ml


What is the pulse pressure?

The difference between systolic and diastolic pressure


What is the mean arterial pressure? How is it calculated?

The MAP is the average of systolic and diastolic pressure, taking into account the fact the the hart spends approx. 60% of the time in diastole

It is estimated as diastolic pressure + one third of pulse pressure e.g. 80+1/3(110-80)=90mmHg


What is meant by the term 'central venous pressure'

Pressure in the vena cava at the level of the heart. It is close to 0mmHg


At the end of diastole, which valves are open and which are closed?

AV valves are open
Semilunar valves are closed


What causes the first heart sound?

Closure of the AV valves


What is meant by the term isovolumetric contraction?

For a short period after the ventricular pressure exceeds atrial pressure but before it exceeds aortic pressure, both the AV and semilunar valves are shut. This is called isovolumetric contraction as the pressure in the ventricles increases but the volume does not change


What causes the rise in jugular venous pressure demonstrated by the a wave?

Atrial systole


What causes the atrial pressure wave known as the c wave?

Increasing pressure in the ventricles during isovolumetric contraction causes the AV valves to bulge into the atria


What causes the second heart sound?

Closure of the semi-lunar valves


What is the dicrotic notch?

A small dip on the aortic pressure line which coincides with aortic valve closure


What is meant by the term end systolic volume?

The mount of blood left in the ventricle at the end of systole, around 50ml. This is because the amount of blood in the ventricle after filling (the end diastolic volume- EDV) is around 120ml, and the amount ejected in one beat (the stroke volume) is around 70ml


What is meant by the term ejection fraction? What is a healthy ejection fraction in adults?

Ejection fraction is the proportion of the EDV that is ejected - stroke volume/EDV

This is normally around 0.6 but may be reduced to <0.5 in heart failure


What causes the v wave on the atrial pressure/jugular venous pressure plot?

Increased atrial pressure due to filling from veins


What is meant by the term isovolumetric relaxation?

Immediately after the closure of the semilunar valves, the ventricles relax. The AV valves remain closed however as the pressure in the ventricles is initially still greater than the pressure in the atria. This is isovolumetric relaxation as pressure in the ventricles is falling without a change in volume


What causes the x- and y-descent on the atrial pressure/jugular venous pressure plot?

x-descent= opening of the semi-lunar valves, reducing pressure in the ventricles and therefore stopping the AV valves 'bulging' into the atria
y-descent= opening of the AV valves


How is stroke work calculated?

MAP x stroke volume

Represented by the area of the ventricular pressure-volume loop


What is the resting potential of ventricular myocytes?

Approx. -90mV


What is the threshold potential of ventricular myocytes?

Approx. -65mV


What causes the initial depolarization or 'upstroke' of myocytes from the resting potential to +30mV?

Activation of fast, voltage gated Na+ channels leading to an inward current of Na+ ions


What causes the plateau phase?

Activation of L-type calcium channels (threshold potential approx -45mV) as a result of the initial depolarization of cardiac myocytes. Activation of L-type calcium channels is maintained for much longer than activation of Na+ channels, which rapidly inactivate


How long is the plateau phase?

Approx 250ms


How long is the cardiac AP?

300ms (as opposed to 2ms in skeletal muscle)


What causes repolarization of cardiac myocytes?

Activation of a voltage gated K+ outward current


What is the benefit of such a long AP in cardiac muscle?

The AP lasts almost as long as contraction itself, thus the refractory period prevents another AP being initiated until the muscle has fully relaxed, preventing tetanus


What is the resting potential in the SA node?



What causes the upstroke of the action potential in the SA node? What effect does this have?

The upstroke is caused by activation of slow L-type calcium channels. It is therefore much slower than the upstroke caused by fast Na+ channels in cardiac myocytes


What is meant by the rate of decay of the SA node resting potential?

This is the length of time between SA node action potentions. i.e. the length of time it takes for the resting potential to reach threshold and generate another AP. Thus the rate of decay determines heart rate and is called the pacemaker potential


What causes the pacemaker potential to decay?

A slowly reducing outward current of K+ ions set against inward currents


What is meant by the term "calcium-induced calcium release"?

Cardiac muscle contracts when intracellular calcium rises above 100nm. However, calcium entry during the AP is responsible for only 25% of the rise in intracellular calcium. The rest is produced from calcium stores in the sarcoplasmic reticulum. During the AP plateau phase, calcium enters the cell and actives calcium sensitive calcium release channels in the SR, allowing stored calcium to flood into the cytosol. This is calcium induced calcium release


What causes intracellular calcium to fall during relaxation?

1. Calcium is pumped back into the SR by ATP-dependent Ca2+ pumps

2. Calcium ions are exchanged for sodium ions via the Na+-Ca2+ exchanger in the myocyte membrane


What effect does acidosis have on force of contraction? Why?

It is negatively ionotopic as H+ ions compete with calcium ion binding sites


How does noradrenaline increase force of contraction?

Increases force by binding to B1 receptors on the membrane which causes increased calcium entry via L-type calcium channels during the AP, and thus increased release of calcium from the SR


How does digoxin increase force of contraction?

It inhibits the Na+ pump which removes Na+ from the cell. Intracellular Na+ then increases and the Na+ gradient across the cell membrane is reduced. This depresses Na+-Ca2+ exchange so calcium is pumped out of the cell less rapidly


What is cardiac output?

heart rate x stroke volume


What factors influence cardiac output?

1. Preload (filling pressure)
2. Cardiac muscle force
3. Afterload (the pressure against which the heart has to pump)


What is Starling's law?

As EDP (and therefore EDV) increases, the force of systolic contraction increases and thus stroke volume increases. As EDV increases, the cardiac muscle is stretched, thus force of contraction is related to degree of stretch. Thus Starling's law states "the energy released during contraction depends on the initial fibre length"


Why does force of contraction increase with stretch?

1. As muscle is stretched, more myosin cross-bridges can form, increasing force (sliding-filament theory)

2. In cardiac muscle, stretch also increases the calcium sensitivity of troponin so more force is generated for the same intracellular calcium


What is implied by a steep ventricular function curve?

Small increases in EDP lead to large increases in SV (i.e. increased cardiac contractility)


What is the most important consequence of Starling's law?

SV in the left and right ventricles is matched


What happens to LV stroke volume if RV stroke volume increases? Why?

LV stroke volume will also increase. This is because if RV stroke volume increases, the amount of blood in the lungs and thus pulmonary vascular pressure will also increase. As the latter determines LV EDP, left ventricular stroke volume will now increase according to Starling's Law until it matches that of the RV


Why does an increase in afterload, as seen in hypertension, have little effect on cardiac output?

Increased afterload initially reduces stroke volume. This means that there is then more blood left in the LV at the end of systole, and that the outputs of the two ventricles no longer match. As a result, blood accumulates on the venous side and filling pressure rises. Cardiac force therefore increases according to Starling's law until it overcomes the increased afterload and after a few beats CO is restored at the expense of an increased EDP


What causes postural hypotension

When a person stands up rapidly after lying down, gravity causes blood to pool in the legs so CVP falls. This then causes a fall in CO due to Starling's law and thus a fall in blood pressure. Even in healthy people, this can lead to reduced cerebral perfusion leading to temporary dizziness or fainting.


What determines MAP?

Total peripheral resistance and cardiac output (MAP=TPR x CO)


Where are baroreceptors located?

Carotid sinus and aortic arch


Explain what happens if MAP decreases

A decrease in MAP reduces arterial wall stretch so reduces baroreceptor activity. This results in reduced firing in afferent nerves travelling via the glossopharyngeal and vagus to the medulla of the brain stem, where the activity of the autonomic nervous system is coordinated. Sympathetic nervous activity consequently increases, causing an increased heart rate and cardiac contractility. Parasympathetic activity decreases, contributing to the rise in heart rate. MAP therefore returns to normal


Between what pressures are baroreceptors most sensitive? What increases their sensitivity?

Large pulse pressure


Why is the baro-receptor reflex not useful for buffering long term changes to MAP?

Because it shows adaptation- if a new pressure is maintained for more than a few hours, activity slowly returns towards normal. Thus the baro-receptor reflex is most useful for buffering short-term changes in MAP such as increases in exercise


How does the baro-receptor reflex help to prevent dizziness when rising from a sitting or lying position?

When rising from supine, blood pools in the legs causing a reduction in CVP. CO and MAP then fall. The baro-receptor reflex is then activated. Increased sympathetic firing causes veno-constriction which helps to restore CVP and, coupled with increases in heart rate and contractility, helps to return CO to normal


How is blood volume controlled?

Blood volume is dependent on total body Na+ and water, regulated by the kidneys. An increase in blood volume will increase MAP and vice versa.

Activation of the baro-receptor reflex by a reduction in MAP will increase sympathetic innervation to the kidneys, causing constriction of renal arterioles. This, and the fall in MAP itself, causes a reduction in renal perfusion pressure which reduces glomerular filtrate rate, inhibiting excretion of Na+ and water in the urine.

Sympathetic stimulation and reduced arteriolar pressure also activate the renin-angiotensin system and thus the production of angiotensin II, a potent vasoconstrictor than increases TPR. Angiotensin II also stimulates aldosterone production which further promotes renal Na+ resorbtion.

The net effect is Na+ and water retention and an increase in blood volume and MAP.


How are changes in blood volume sensed?

Cardiopulmonary receptors- veno-atrial and atrial receptors.

These respond to changes in CVP and blood volume

Stimulation supresses the renin-angiotensin system, sympathetic activity and secretion of ADH, but increases release of ANP from the atria

Together these changes promote renal sdoum and water excretion and reduce blood volume