cardiac output Flashcards
what is cardiac output
the volume of blood pumped by each ventricle per minute
the product of heart rate (bpm) and stroke volume
CO = HR x SV
what is stroke volume
the volume of blood in ml ejected per contraction
SV = end diastolic volume - end systolic volume
how is CO controlled
according to physiological requirements
via control of HR and SV
what is the CO of a young adult at rest
5
what is the CO of a young adult during exercise
23
what is the CO of a marathoner
30 - 40
what factors affect SV and CO
the strength of cardiac muscle contraction and SV can be graded by
1. intrinsic control
2. extrinsic control
3 end diastolic volume
what is intrinsic control of CO
varying the initial length of the cardiac muscle fibres, which in turn depends upon end-diastolic-volume
what is extrinsic control of CO
varying the extent of sympathetic stimulation
what is the effect of end diastolic volume on CO
an increase in EDV increases SV
intrinsic control of SV depends on the direct correlation between EDV and SV
as more blood returns to the heart, the heart pumps out more > the heart does not eject all the blood it contains
intrinsic control depends on the length-tension relationship of cardiac muscle
what is the frank-starling curve
⬆️ in tension = ⬆️ in length
cardiac muscle does not normally operate within the descending limb of the length-tension curve
what is the frank-starling law of the heart
degree of diastolic filling (preload) causes muscle fibres to vary in length before contraction
increased EDV, the more the heart is stretched
the more the heart is stretched, the longer the initial cardiac fibre length before contraction
the increased length results in a greater force on the subsequent cardiac contraction and thus a greater SV
what is the intrinsic relationship of the frank-starling law
the heart normally pumps out during systole, the volume of blood returned to it during diastole; increased venous return results in increased stroke volume
what are the advantages of the cardiac length-tension relationship
- equalising output between the left and right sides of the heart
- when a larger CO is required, venous return is increased through action of the sympathetic nervous system, the resulting increase in EDV automatically increases SV
what is the cellular basis of the frank-starling mechanism
- greater initial length increases sensitivity of contractile proteins in the myofibrils to Ca2+
- increased initial fibre length may also increase Ca2+ release from the sarcoplasmic reticulum
what is sympathetic stimulation in the heart
increases the contractility of the heart
extrinsic control of SV
sympathetic stimulation and adrenaline both increase the hearts contractility (strength of contraction at any given EDV)
how does sympathetic stimulation increase contractility of the heart
due to increased Ca2+ entry triggered by noradrenaline/adrenaline
increase in inward Ca2+ flux during the plateau phase of the action potential enhances intracellular calcium store
Ca2+ is required for excitation-contraction coupling in cardiac muscle cells
increase the rate of relaxation of cardiac muscle cells by stimulating Ca2+ pumps > take up Ca2+ from cytoplasm more rapidly > shortens systole
inotropic actions
what is the effect of high blood pressure
increases the workload of the heart
when the ventricles contract they must generate sufficient pressure to exceed the blood pressure in the major arteries
this will open the semilunar valves and allow ejection of blood;
> afterload -> arterial blood pressure
what is afterload
the workload imposed on the heart after the contraction has begun
what is hypertrophy
caused by enlargement of the heart to compensate for a sustained increase in afterload
a disease or weakened heart may not be able to compensate completely which can lead to heart failure
what is dP/dt
a useful index of contractility
important for determining the severity or progress of valve dysfunction
the simplest measurements of myocardial contractility use analyses of the pressure waveform during the isometric contraction phase, the advantage being that this is independent of afterload, the aortic valve is shut (as is the atrioventricular valve).
provide a global assessment of myocardial contractility, not of the cellular and molecular status of the myocardium
what is max dP/dt
the maximum rate of rise of pressure
