Factors Affecting Cardiac Output Flashcards
what is cardiac output
volume of blood ejected by one ventricle in one minute (l/min)
what is the cardiac index
cardiac output taking into consideration the size of animal (l/min/m2)
what are reference values of CO (conditioned greyhound, unconditioned dog, horse at rest, horse at exercise)
conditioned greyhound: 4.4
unconditioned dog: 2.7
horse at rest: 30
horse at exercise: 150-240
what factors affect cardiac output
sleep/standing reduces by ~10%
heavy meal/excitement/stress increases by ~20%
pregnancy increases by ~40%
heavy exercise increases 4-6 fold
what do changes in CO involve
both heart rate and stroke volume
what are the two opposing factors that influence stroke volume
- high energy of contraction: increases SV
- high atrial pressure: opposes ejection and hence SV (in absence of compensatory changes)
what is the energy of contraction
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
what is arterial pressure and how does it effect SV
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
what is preload
preload: a papillary muscle can be stretched to a known length by hanging a weight from it
what is isometric contraction
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
what is the isometric length tension relationship
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
what is the afterload
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
what is the isotonic contraction
since one end of muscle is free the muscle can contract and does so at a constant
what is after-load shortening relation
an increase in the afterload reduces both the rate and degree of shortening
what are the two mechanisms that affect the length-tension relation
- sliding filament theory: optimal length to form cross-bridges (bellshaped)
- 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
what are the contractile properties of the whole heartt
the greater the stretch of the ventricle in diastole, the greater the stroke work achieved in systole
what is central venous pressure (CVP) and what does it determine
pressure at the entrance to the right atrium
determines the right ventricular end-diastolic pressure and resting distention
what does central venous pressure depend on
- total volume of blood in the circulation (affected by blood transfusion and hemorrhage)
- 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)
what are starling’s law of the heart
- 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
- the greater the stretch of the ventricle in diastole, the greater the stroke work achieved in systole
what are factors that affect CVP and SV
- lower blood volume
- sympathetic nerves regulate peripheral venous tone
- venous muscle pump
- increased CO reduces filling pressure
- respiration’s effect on extramural cardiac pressure
- increased extramural pressure impairs filling
how does lower blood volume affect CVP and SV
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
how does sympathetic nerves regulating peripheral venous tone affect CVP and SV
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
how does venous muscle pump affect CVP and SV
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
how does increased CO reduce filling pressure and affect CVP and SV
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
what is respiration effect on extramural cardiac pressure effect CVP and SV
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
how does increase extramural pressure impair filling and how does this effect CVP and SV
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
how does arterial pressure affect the heart
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
what does chronic increase in arterial pressure results in
- LV undergoes concentric hypertrophyc (chamber wall thickness enlarges, no change in chamber size) induced by angiotensin II, endothelin
- hypertrophy increases the contractile force for a while helping the ventricle to cope with the hypertension
- long term the overloaded ventricle goes into faliure
draw a pressure volume loop with an increase in EDV
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
what occurs do pressure volume loop when the afterload is increased
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
what are extrinsic regulation of the heart
change in contracile energy by external chemical factors –> change in contractility or inotropism
sympathetic stimulation
what increases sympathetic activity in the heart
- exercise
- orthostasis (standing up)
- stress
- hemorrhage
what do left sympathetic fibres innervate
atrial and ventricular myocardium
what do right sympathetic fibres innervate
pace-maker-conduction system
what are the effects of sympathetic stimulation on the heart
shorter more forceful contraction of the myocyte
- 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
- ejection fraction is increased another clinical index of contracility
- 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)
- SV increases but the size of the increase is attenuated by the reduced EDV (hence frank starling effect) and increase arterial pressure (increased afterload)
how does sympathetic activity effect pressure-volume loop
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
what are positive inotropic influences
adrenaline and B-agonists
adrenal medulla secretes adrenaline (noradrenaline) –> activates cardiac B1-adrenoreceptors
what are negative inotropes (5)
- parasympathetic vagal activity and cholinergic agonists
- B-blockers such as propanolol, oxprenolol and atenolol
- Ca channel blockers such as verapamil
- hyperkalemia
- barbiturates and many anaesthetics
