Regulation of stroke volume and heart rate Flashcards
What is heart rate set by?
the pacemaker of the heart- pacemaker cells of the sinoatrial node
What nervous system regulates heart rate?
autonomic nervous system
What branch increases heart rate?
sympathetic branch - responsible for fight or flight response
What decreases heart rate?
the parasympathetic nervous system (responsible for rest and digest) -decreases heart rate
What mechanisms lead to tachycardia? involves sympathetic nervous system
Sympathetic nerves release noradrenaline
plus circulating adrenaline from adrenal medulla
both act on adrenergic- beta one receptors on sinoatrial node
increases slope of pacemaker potential
increases heart rate= tachycardia
why does adrenaline binding to beta one receptors increase slope of pacemaker potential?
increases ion flow through sodium channels and calcium channels
causes pacemaker cells to depolarise to threshold sooner and evoke their action potentials.
Will decrease cardiac interval and therefore increase heart rate.
What mechanisms are involved in bradycardia? involves parasympathetic nervous system
vagus nerve releases acetylcholine
acts on cholinergic- muscarinic receptors on sinoatrial node
hyperpolarises cells and decreases slope of pacemaker potential
decreases heart rate= bradycardia
What does starling’s law state?
the energy of contraction is proportional to the initial length of the cardiac muscle fibre
Describe the relationship between tension and initial length of cardiac muscle fibre?
tension is proportional to preload
What is happening at peak tension?
optimal no. cross bridges forming between thin filaments (actin) and thick filaments (myosin).
Means we get a really strong muscle contraction.
Describe tension at smallest and largest lengths?
smallest- too much overlap. The actin and myosin filaments are interfering with each other. Not as many cross bridges forming and we don’ t get an efficient muscle contraction
largest- muscle at a larger length and fewer cross bridges can form, so therefore we get a slightly weaker contraction.
In physiology, what stretches cardiac muscle?
EDV (what volume of blood is filled into the ventricles before they contract)
What is preload?
how full the ventricle is before it starts contracting (i.e. the EDV)
affected by state of contraction of venules/ veins
What is afterload?
how difficult it is for the heart to pump blood out (i.e. TPR)
affected by state of contraction of arterioles
What is contractility?
How strong a contraction is for any given preload or afterload. After by sympathetic system
How is stroke volume affected by end diastolic volume?
ventricles not stretched- small EDV-weak contraction and low stroke volume
ventricles stretched-bigger EDV- stronger contraction and bigger stroke volume
At rest, what is hearts EDV?
not at optimal end diastolic vol
What happens if there is increased venous return to the heart?
increase EDV
stretch cardiac muscle more
get a stronger contraction
increase stroke volume
What is afterload?
load against which the muscle tries to contract
What is afterload determined by , in vivo?
afterload is determined by the arterial pressure which the blood is ejected- this in turn depends on the TPR.
If TPR increases, stroke volume will go down as (more energy is “wasted” building up enough pressure to open aortic valve)
What is stopping muscle from shortening in systole?
mitral valve
ventricle has to build up pressure to push the mitral valve closed
aortic valve being closed
Has to be enough pressure in left ventricle to exceed pressure in aorta and push aortic valve open.
What is aortic pressure affected by?
-how much blood you’re trying to pump out
-how easy it is to get blood up into the arterioles i.e. TPR
What is the major thing that influences total peripheral resistance?
how constricted or dilated the arterioles are
if constricted- going to increase the total peripheral resistance- that will increase the aortic pressure
What is the problem with increase in aortic pressure?
left ventricle will have to work much harder - longer in isometric contraction- to build up enough pressure so that the pressure in the left ventricle exceeds the pressure in the aorta and the aortic valve is pushed open.
This means the muscle is going to have less energy left do the useful bit of actually ejecting the blood. Stroke volume will decrease.
Where are other beta one receptors?
myocytes
-sympathetic nerves release noradrenaline
-plus circulating adrenaline from adrenal medulla
-both act on beta one receptors on the myocytes
What happens when beta one receptors in myocytes are activated?
increases contractility (ionotropic effect)
Why stronger contraction?
more release of calcium within cardiomyocytes and that causes more crossbridges to form between actin and myosin filaments- stronger contraction.
Shorter contraction as calcium being taken up quicker
How does the parasympathetic nervous affect contraction?
little effect
vagus innervates atria and sinoatrial node, doesn’t ventricular muscle
Cardic ouput equal to?
heart rate x stroke volume
What can happen to stroke volume if heart rate is increase?
stroke volume decreased
if increase heart rate much more- will start cutting into rapid filling phase. Will decrease EDV- decrease preload- decrease of cardiac muscle stretch- decrease strength of contraction. Stroke vol reduce
HR increases:
via decreased vagal tone
-at rest always have some acetylcholine being release and that slows down intrinsic heart rate of the pacemaker cells from 100bpm to 60-70bpm.
Increased sympathetic tone
Contractility of heart increases:
-via increased sympathetic tone
-alters ionotropic state and shortens systole- so more time for diastole
Venous return increases:
-via venoconstriction and skeletal/respiratory pumps - increase EDV
and
-maintains preload
total peripheral resistance falls:
-arterioles supplying regions of body that are most important during exercise
-will make it easier for heart to pump blood
-reduces afterload
