Factors Affecting Cardiac Output

Question 1

what is cardiac output

Answer 1

volume of blood ejected by one ventricle in one minute (l/min)

Question 2

what is the cardiac index

Answer 2

cardiac output taking into consideration the size of animal (l/min/m²)

Question 3

what are reference values of CO (conditioned greyhound, unconditioned dog, horse at rest, horse at exercise)

Answer 3

conditioned greyhound: 4.4

unconditioned dog: 2.7

horse at rest: 30

horse at exercise: 150-240

Question 4

what factors affect cardiac output

Answer 4

sleep/standing reduces by ~10%

heavy meal/excitement/stress increases by ~20%

pregnancy increases by ~40%

heavy exercise increases 4-6 fold

Question 5

what do changes in CO involve

Answer 5

both heart rate and stroke volume

Question 6

what are the two opposing factors that influence stroke volume

Answer 6

1. high energy of contraction: increases SV
2. high atrial pressure: opposes ejection and hence SV (in absence of compensatory changes)

Question 7

what is the energy of contraction

Answer 7

energy of contraction is increased by stretching the myocardium in diastole, through a rise in end-diastolic pressure (starling’s law of heart)

depends on venous filling pressure

Question 8

what is arterial pressure and how does it effect SV

Answer 8

depresses SV since ejection cannot begin until ventricular pressure > aortic pressure

if arterial pressure is high much of contractile energy is consumed in raising ventricular blood pressure during the isovolumetric contraction phase, leaving less energy for ejection phase

Question 9

what is preload

Answer 9

preload: a papillary muscle can be stretched to a known length by hanging a weight from it

Question 10

what is isometric contraction

Answer 10

if ends of muscle are anchored at the preload length to rigid points and the muscle electrically stimulated the active tension (force) develops without shortening

Question 11

what is the isometric length tension relationship

Answer 11

the active tension increases with stretch

positive correlation –> up to a certain point at which it will decrease

the more stretch (preload) the more the force of contraction –> intrinsic ability of the heart

Question 12

what is the afterload

Answer 12

the preparation can also be set up such that one end of the muscle is left free and when it begins to shorten it lifts a weight

Question 13

what is the isotonic contraction

Answer 13

since one end of muscle is free the muscle can contract and does so at a constant

Question 14

what is after-load shortening relation

Answer 14

an increase in the afterload reduces both the rate and degree of shortening

Question 15

what are the two mechanisms that affect the length-tension relation

Answer 15

1. sliding filament theory: optimal length to form cross-bridges (bellshaped)
2. increased sensitivity to Ca^2+: stretch increases the fraction of cross bridges activated by a given [Ca2+]. this may be due to the lattice spacing hypothesis. since cell volume is fixed any increase in length reduces the cell diameter and this reduces the side-to-side separation of the actin and myosin filaments that may allow cross bridges to form more readily

Question 16

what are the contractile properties of the whole heartt

Answer 16

the greater the stretch of the ventricle in diastole, the greater the stroke work achieved in systole

Question 17

what is central venous pressure (CVP) and what does it determine

Answer 17

pressure at the entrance to the right atrium

determines the right ventricular end-diastolic pressure and resting distention

Question 18

what does central venous pressure depend on

Answer 18

1. total volume of blood in the circulation (affected by blood transfusion and hemorrhage)
2. how the volume is distributed between the peripheral and central veins (affected by gravity, peripheral venous tone, skeletal muscle pump, breathing, pumping action of heart)

Question 19

what are starling’s law of the heart

Answer 19

1. the energy of contraction of a cardiac muscle fibre, like that of a skeletal muscle fibre, is proportional to the initial fibre length at rest
2. the greater the stretch of the ventricle in diastole, the greater the stroke work achieved in systole

Question 20

what are factors that affect CVP and SV

Answer 20

1. lower blood volume
2. sympathetic nerves regulate peripheral venous tone
3. venous muscle pump
4. increased CO reduces filling pressure
5. respiration’s effect on extramural cardiac pressure
6. increased extramural pressure impairs filling

Question 21

how does lower blood volume affect CVP and SV

Answer 21

two thirds of entire blood volume is in the venous system, therefore hemorrhage or dehydration will reduce CVP and consequently SV

ex. upright posture in humans –> gravity redistributes approx 500ml of blood from the thorax into the veins of lower limbs (venous pooling). SV therefore decreased in the upright position

Question 22

how does sympathetic nerves regulating peripheral venous tone affect CVP and SV

Answer 22

sympathetic venoconstrictor fibres innervate the skin, kidneys and splanchnic system

blood can be shifted into the central veins from these organ and increases cardiac filling pressure

this may occur during exercise, stress, deep respiration, hemorrhage, shock and cardiac failure

converse is true for skin temp regulation in hot enviornments where venodilation results in a fall in CVP and SV

Question 23

how does venous muscle pump affect CVP and SV

Answer 23

rhythmic exercise repeatedly compresses the deep veins of the limbs and displaces their blood centrally due to venous valve

this raises CVP and SV

converse true for standing for prolonged periods of time in hot weather

Question 24

how does increased CO reduce filling pressure and affect CVP and SV

Answer 24

heart pumpts out of the venous system into the arterial system

pumping not only increases the volume and pressure of blood in the arterial system but also reduces the volume and pressure of blood in central veins

this is simply because speeding up the transfer of blood out of the central veins and into the arteries reduces the filling pressure (reduced preload)

the rise in arterial pressure (increased afterload) also limits the SV unless compensatory changes take place

true of cardiac failure where sudden cardiac failure results in a rise in filling pressure

Question 25

what is respiration effect on extramural cardiac pressure effect CVP and SV

Answer 25

filling pressure is the difference between the internal and external pressures or transmural pressure

the external pressure is normally the intrathoracic pressure which oscillate between (5cmH2 at end expiration and 10cmH2) at end inspiration

inspiration makes the intrathoracic pressure more negative and the intra-abdominal pressure more positive due to the decent of the diaphragm

this promotes the filling of the thoracic vena cava and enhances right ventricular filling and SV

however at the same time lung expansion increases the pulmonary blood pool that temporarily reduces the return of blood to the left ventricle

consequently the left ventricle SV falls transiently during each inspiration

converse true expiration

therefore respiration results in synchronous oscillation in arterial pressure called Traube-hering waves

Question 26

how does increase extramural pressure impair filling and how does this effect CVP and SV

Answer 26

forced expiration such as bout of coughing or valsalva maneuver raises intrathoracic pressure to positive values

this reduces the ventricular transmural pressure, ventricular filling and CO

this can occur in certain diseases where the pericardium exerts increased extramural pressure around heart

old vs. young heart (young expands easily, in older animals and diseased states ventricles are less compliant at normal preload so there is less filling and smaller CO)

higher preload is required

Question 27

how does arterial pressure affect the heart

Answer 27

an increase in afterload is an increase in arterial pressure and the equivalent of reduced shortening is a fall in stroke volume

heart has to work harder over longer periods of time –> cells of heart can’t divide so they increase in size (hypertrophy) eventually muscle wall thickness will become too thick and won’t allow heart to relax –> leads to heart failure

Question 28

what does chronic increase in arterial pressure results in

Answer 28

1. LV undergoes concentric hypertrophyc (chamber wall thickness enlarges, no change in chamber size) induced by angiotensin II, endothelin
2. hypertrophy increases the contractile force for a while helping the ventricle to cope with the hypertension
3. long term the overloaded ventricle goes into faliure

Question 29

draw a pressure volume loop with an increase in EDV

Answer 29

EDV and pressure raised (ex. lying down) so it is shifted up the lower boundary

the increase in stretch raises the preload and hence the contractile energy through the Frank-Starling mechanism

SV and loop area (SW) increase

the operation of Frank-starling mechanism means that the ventricle is getting bigger at the end-diastolic side

Question 30

what occurs do pressure volume loop when the afterload is increased

Answer 30

deleterious effect if increasing afterload

it starts from the same end-diastolic stretch as loop2

raising the arterial pressure (using a vasoconstrictor drug) raises afterload

more energy is consumed in raising the ventricular pressure to a higher level so less energy remains for ejection

SV therefore falls

Question 31

what are extrinsic regulation of the heart

Answer 31

change in contracile energy by external chemical factors –> change in contractility or inotropism

sympathetic stimulation

Question 32

what increases sympathetic activity in the heart

Answer 32

1. exercise
2. orthostasis (standing up)
3. stress
4. hemorrhage

Question 33

what do left sympathetic fibres innervate

Answer 33

atrial and ventricular myocardium

Question 34

what do right sympathetic fibres innervate

Answer 34

pace-maker-conduction system

Question 35

what are the effects of sympathetic stimulation on the heart

Answer 35

shorter more forceful contraction of the myocyte

1. ventricular pressure rises more rapidly and reaches a higher systolic pressure. systolic pressure increases because the elastic arteries are expanded by an increase SV over shorter time
2. ejection fraction is increased another clinical index of contracility
3. diastolic volume falls because systolic ejection is more complete. thus increased contractility makes the ventricle smaller in diastole and systole (in contrast to the frank starling mechanisms where diastolic and systolic volume increase)
4. SV increases but the size of the increase is attenuated by the reduced EDV (hence frank starling effect) and increase arterial pressure (increased afterload)

Question 36

how does sympathetic activity effect pressure-volume loop

Answer 36

peak pressure, SV and ejection fraction and SW (loop area) are all increased –> loop becomes more wide

curve therefore shifts to the left however because end-diastolic volume reduces and limits the frank starling mechanism

Question 37

what are positive inotropic influences

Answer 37

adrenaline and B-agonists

adrenal medulla secretes adrenaline (noradrenaline) –> activates cardiac B1-adrenoreceptors

Question 38

what are negative inotropes (5)

Answer 38

1. parasympathetic vagal activity and cholinergic agonists
2. B-blockers such as propanolol, oxprenolol and atenolol
3. Ca channel blockers such as verapamil
4. hyperkalemia
5. barbiturates and many anaesthetics