CVS session 6: control of cardiac output and response of the whole system Flashcards
Effect of TPR on arterial and venous pressures
Rise in TPR increases arterial pressure and decreases venous pressure
Fall in TPR decreases arterial pressure and increases venous pressure
Effect of cardiac output on arterial and venous pressures, when TPR is constant
CO rises: arterial pressure will rise and venous pressure will fall, because a larger pressure is needed to move more blood and less is being stored in veins
CO falls: arterial pressure will fall and venous pressure rise, as a smaller volume of blood is being moved but more is stored in veins
Demand
TPR proportional to 1/demand
If body needs more blood the heart needs to pump more to meet demand, AP and VP brought back to normal once demand is met
Calculation of cardiac output
CO= stroke volume x heart rate
Arterial and venous pressures affect both SV and HR
What is stroke volume and how does venous and arterial pressure affect it?
The amount of blood remaining after contraction, therefore the difference between end diastolic volume and end systolic volume:
SV=EDV - ESV
VP increase causes increased SV and heart rate
AP fall causes increased SV (less resistance) and heart rate
Ventricular filling
In diastole the ventricle is isolated from arteries and connected to veins. The ventricles will therefore fill until their walls stretch enough to produce an intraventricular pressure which is equal to venous pressure
Higher venous pressure=more heart fills in diastole
- more blood enters atria increasing atrial pressure
- therefore more ventricle will fill
- relationship between venous pressure and ventricular volume shown on VENTRICULAR COMPLIANCE CURVE (draw)
Describe Starling’s law in relation to contractility
If muscle is stretched before contracting, it contracts harder due to increased binding of actin and myosin as the sarcomere stretches. Therefore, the more the heart fills, the harder it contracts (up to a point: fibrous pericardium). The harder it contracts, the bigger the stroke volume. So rises in venous pressure lead to rises in stroke volume. This is an intrinsic cardiac property
Increase in EDV (=venous pressure) causes SV to increase, because preload is increased
On graph shows LVEDP (left ventricular end diastolic pressure) against stroke volume: as LVEDP=filling pressure
Frank-Starling mechanism
The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.
Increased venous return increases the ventricular filling (end-diastolic volume) and therefore preload, which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere length, which causes an increase in force generation and enables the heart to eject the additional venous return, thereby increasing stroke volume.
What is ESV and what does it depend on?
End systolic volume: how much the ventricle empties. Depends on:
1. Force of contraction: determined by EDV (Starling’s law) and contractility (increased by sympathetic activity). Can be affected by neurotransmitters, hormones or drugs
- Difficulty of ejecting blood: “aortic impedance”. Depends mainly on TPR. Harder to eject=increased arterial pressure; if AP falls from lower TPR then ESV will fall and SV will increase
What is preload?
The initial stretching of cardiac myocytes prior to contraction. Related to sarcomere length but this can’t be determined in situ, so measure by ventricular EDV or EDP. Can be applied to atria or ventricles
When venous return increased, EDV and ventricular volume increased, so sarcomere stretched, so preload increased
Increased preload increases stroke volume; decreased preload decreases it by decreasing force of contraction
What increases ventricular preload?
Increased central venous pressure due to decreased compliance or hypervolaemia
Increased atrial force of contraction from sympathetic stimulation or increased filling
Bradycardia (more filling time)
Increased aortic pressure: first increases afterload then reduces SV so increases preload secondarily
Heart failure e.g. aortic stenosis
What decreases ventricular preload?
Haemorrhage: decreased CVP
Atrial arrhythmias e.g. AF
Atrial tachycardia: increases ventricle filling time
Decreased ventricular afterload as enhances ejection so reduces ESV and EDV
Mitral and tricuspid valve stenosis
What is afterload?
The resistance the left ventricle must overcome in order to circulate blood. Higher afterload = higher cardiac workload. Closely related to aortic pressure
How is afterload increased?
When aortic pressure and systemic vascular resistance is increased, causing increased ESV and decreased SV:
- hypertension
- vasoconstriction
- aortic valve stenosis
Affect of increased afterload on Starling curve?
Shifts it down and to the right: decreased SV, increased LVEDP
Describe the autonomic control of heart rate
Decreased arterial pressure:
- Arterial pressure sensed by BARORECEPTORS in the CAROTID SINUS and AORTIC ARCH
- Sends signals to MEDULLA OBLONGATA
- Increases heart rate by reducing parasympathetic and increasing sympathetic activity (so increases contractility) [vv. for decreasing HR]
Rises in venous pressure:
- sensed in RIGHT ATRIUM
- lead to decreased parasympathetic activity so increases HR
- Bainbridge reflex: not very important, little clinical relevance
What determines stroke volume?
- venous return: CVP-RAP drives ventricular filling
- aortic pressure: drives baroreceptor sensor output
- ANS and hormones
- cardiac fitness: ventricular distensibility/contractility
Where are baroreceptors found and what do they do?
Sense arterial blood pressure by responding to change in stretch of the arterial wall:
- in aortic arch (innervated by aortic nerve, combines with vagus nerve) increase firing of AP when pressure >100 mmHg
- in carotid sinus (innervated by sinus nerve of Hering; branch of glossopharyngeal nerve) increase firing when pressure >50 mmHg most important as threshold close to normal level so keeps at set point
- set point can change with exercise, hypertension, heart failure: explains how arterial pressure remains elevated during chronic hypertension
and decreased stretch decreases AP firing (most importantly during loss of blood or when stand up)
Modulates activity of S and P neurones in medulla, either increasing or decreasing activity to affect heart rate and force of contraction: this alters cardiac output. Also affects TPR. So after blood loss, baroreceptors cause increase in cardiac output and TPR to try to restore arterial blood pressure
Role of arterioles
Control TPR
Vascular smooth muscle cells in tunica media/pre-capillary sphincters precisely regulate flow under SNS or metabolite autacoid control
Interaction causes vasodilatation
Role of veins and great veins
Control stroke volume
Act as a reservoir for blood
Large volume, low pressure: CVP usually between 2 and 10 mmHg
Mean arterial blood pressure
At rest is ~ 95 mmHg: this provides adequate pressure to perfuse and drive blood through whole vasculature, ensuring a positive CVP
Significant functional reserve available: many capillary beds are not perfused
If hypotensive, MABP is
Describe the effects of rapid orthostasis
Gravity redistributes blood: mainly moves from intrathoracic vessels into the legs (legs take up an extra 500ml i.e. 10%)
CVP falls directly, so RA filling drops, so SV decreases by 10-25% and MABP falls by 20-25 mmHg. Arterial and venous pressures fall acutely
Describe the baroreceptor response to rapid orthostasis
- Drop in MABP increases heart rate by 10-25 bpm
- TPR briefly drops, then increases to offset MABP drop, but then decreases venous return so affects stroke volume. The increased TPR increases vasoconstriction and venoconstriction
- Veins limit gravitational pooling (leg vein distensibility lower than great veins), so muscular contraction when standing up forces venous blood upwards to increase CVP
A complex response involving at least 15 factors; usually stabilises after about 30 seconds
Syncope?
Conflict between differing flow demands (e.g. temperature/food) and delay in response time can cause dizziness and syncope:
- acute decrease in cerebral flow leads to loss of conscioussness
- need to maintain CVP by balancing response
Describe the responses involved in supplying the GI tract to digest a large meal
Flow to abdomen increases at the sight of food, as GI demand after a large meal becomes 25-30% of cardiac output. There is a phased response along the duodenum/jejunum as digestion takes place
Effect on CVS:
- ANS increases parasympathetic activity
- local autacoids and vasodilators
- local GI vasodilatation decreases TPR
Effect on venous supply:
- TPR decreases so arterial pressure initially decreases arterial pressure
- flow out via liver increases so CVP increases
- CVP and RA filling increase, so CO increases
Response of CVS:
- baroreceptors detect fall in MABP, modest increase in CO via HR and SV
- increased CVP then decreases by extra pumping of the heart
- arterial pressure returned to normal
- GI demand met: CVS goes back to normal MABP operating range by adjusting CO
- perfusion pressure maintained for other tissues
Why should strenuous exercise not take place immediately after eating?
After eating there is a high GI demand however is used for exercise instead, so high SNS activity on the GI renders digestion unpleasant: can cause vomiting
Effects of exercise on the heart (in terms of HR etc)
At rest: total muscle demand is ~ 15-20% of cardiac output (so 0.75-1 litre per minute)
During exercise demand is ~70% of CO (12-17.5 L per min)
-HR increases to >180 bpm
-SV increases to 150-200 ml [max SV higher when fitter]
Acute effects of exercise on the CVS
Increased peak flow demand so:
- increase substrate demand: need higher CO
- decrease in TPR: vasodilators in metabolising tissue (K+, H+, adenosine, lactate), plus endothelial autacoids which reduce the local SNS effect
- exercise-induced hyperaemia
- decreased TPR will initially increase CVP (so increase SV) and initially decrease MABP
Response of the CVS to exercise
Central voluntary control: brain increases HR with expectation of exercise, avoids CVP overfilling
Baroreceptors: signal acute exercise-induced increase in BP so increase HR and SV
Skeletal muscle: contractile activity actively aids the whole circulation. Not as pulsatile as in the heart
Other effects:
- increased SNS to gut
- initially skin decreases supply then increases for heat loss
- brain and heart spared
- kidney perfusion drops by nearly 1/2
What happens if residual blood volume drops below 3.5-4L?
Hypovolaemic shock
- cannot perfuse tissues
- MABP
Effect of hypovolaemic shock on the CVS
- rapid drop in CVP
- SV, CO and MABP all decrease
- tissues react badly: build up of metabolites so would decrease TPR
- conflict as need to preserve systemic systemic MABP
Response of the CVS to hypovolaemic
- baroreceptors signal drop in blood pressure, so very large SNS output to increase HR and SV, and increase in TPR of arterioles to keep MABP up and to veins to keep CVP and SV up
- tachycardia
- all systems decrease supply except to the heart and brain, can cause kidney failure
- conserving heart and blood perfusion: need adequate CVP and MABP. If can;t maintain=organ failure and death
