Cardiovascular Homeostasis Flashcards
Describe the pulmonary circulation:
blood pumped from heart to the lung
distance is short
pressure requirements are low (pulmonary artery pressure is low)
Describe the systemic circulation:
blood pumped from the heart to rest of the body
Long distance - large area to cover with extensive vascular network
Pressure requirements are high (aortic pressure is high)
function of the heart?
to pump blood at a pressure high enough that it is able to circulate throughout the entire body and reach all the target organs on time
how is the cardiac cycle accomplished?
through the regulation of pressure and volume within the chambers of the heart over a period of time
what is the cardiac cycle defined as?
defined as the events occurring from the state of one heart beat to the start of another heart beat - a full cycle
what is the cardiac cycle divided into?
into two major events
diastolic phase - relaxation of ventricles
systolic phase - contraction of ventricles
the description of the cardiac cycle is typically related to…?
to events that are occurring in the ventricle (specifically the left ventricles)
describe what happens during the diastolic phase of the cardiac cycle:
relaxation causes drop in ventricular pressure
when ventricular pressure drops lower than atrial pressure - AV valves open
blood fills ventricle
when the blood fills the ventricle in the diastolic phase - where is this blood coming from?
initially filled with blood that has been accumulating inside atria
then by blood from venous side flowing directly through atria into ventricles
and finally by the actual contraction of the atria, hence atrial contraction not entirely important for normal cardiac output
Significance in AF or during exercise
AF?
atrial fibrillation
describe what the aorta is doing during the diastolic phase:
aortic valve is closed because pressure in the aorta is higher than LV
over time, the aortic pressure falls as blood is sent to other parts of body + to the venous side
at the same time, LV pressure due to filling is beginning to rise
what happens during the systolic phase when ventricles contract?
as ventricles start contracting, ventricular pressure also starts rising quickly
this rise quickly exceeds atrial pressure
AV valve will close (prevents backflow)
for a brief period - all valves are closed - aortic valve also closed but pressure here is slowly reducing
cardiac muscle length is same but force exerted due to the stretch will further increase the pressure inside ventricle
When LV pressure exceeds aortic pressure aortic valve opens
Blood flows out
As blood leaves LV, the LV muscles start to shorten and this aids to keep expelling blood from LV
During systolic phase of cardiac cycle, what happens as soon as ventricles start contracting:
the ventricular pressure also starts rising quickly
During systolic phase of cardiac cycle, the rise in ventricular pressure does what quickly?
it will rise very quickly and exceeds atrial pressure and then AV valve will close (prevents backflow)
what happens for a brief period during systolic phase of cardiac cycle?
all valves are closed - aortic valve are closed by pressure here is slowly reducing
During systolic phase of cardiac cycle, what happens as the LV begins to relax?
the pressure drops significantly and blood from aorta will attempt to flow back in but this is when the aortic valve will close and this further propels blood forward into systemic circulation
after LV begins to relax during systolic phase of cardiac cycle, what happens?
LV pressure remains higher than atrial pressure so AV valves still remains closed and here the force exerted by the LV muscles on the blood falls
left atrial pressure indicators used for?
monitoring anaesthesia
During systolic phase of cardiac cycle, what happens when LV pressure falls below atrial pressure?
the AV valves open and filling begins
and this cycle is repeated for every beat
75% of blood entering the atrium flow directly into?
into ventricle
atrial contraction adds what percentage of blood?
adds 25% of volume (hence atrial contraction only essential in exercise)
3 ways when atrial pressure increases:
when atrium contracts
as ventricle contracts - bulging of AV valve into atria
increases slowly as atrium fills with blood from periphery
what can be used to measure LAP?
pulmonary capillary wedge pressure can be used to measure LAP - a surrogate marker
when does aortic pressure increase?
it increases during LV systole - blood ejected out
Increased when aortic valve closes - blood built up from backflow
Falls in ventricular diastole
P wave?
precedes the contraction of the atria (depolarisation of atria)
QRS complex - it is an electrical event?
precedes the mechanical event of contraction of the ventricle (depolarisation of ventricle and repolarisation of atria)
T wave?
precedes the relaxation of the ventricles (repolarisation of the ventricles)
1st heart sound?
closure of AV valves during ventricular contraction - dull/low pitch, long and loudest - LUBB
the valves vibrate as it shuts tight
2nd heart sound?
the fast shutting of the aortic/pulmonary valves - as ventricles relax - DUBB
higher pitched and shorter than 1st sound
what electrical events are there that result in mechanical events?
P wave
QRS complex
T wave
how easy are the 1st/2nd sound to hear using a stethoscope?
they are easily heard - heard in all normal animals
3rd/4th sound - heard using stethoscope?
typically not heard, pathological if clearly audible. in dogs both are not heard. S3 - DCM, chronic volume overload. S4 - HCM, chronic hyperT, pressure overload
3rd heart sound?
heard immediately after 2nd heart soun - changes in filling speed
4th heart sound?
heard immediately before 1st heart sound - contraction of atria causes vibration of ventricles
how does the body have the ability to increase and decrease HR when necessary?
this is done by controlling the impulse generated by the SA node
information is sent to SA node to either decrease or increase rate of firing
what controls the regulation of the heart?
it is controlled by the nervous system
specifically the autonomic nervous system (ANS) via neurotransmitter of the heart
how does the sympathetic nervous system help control the heart?
stimulates heart by acting on beta-1 adrenoreceptors
innervates - SA node, AV node, atria and ventricles
Stimulation of sympathetic fibres increase adrenalin/epinephrine release into the blood and pacemaker depolarisation rate increases - increased HR
How does the parasympathetic nervous system control heart rate?
vagus nerve stimulation - inhibit heart rate by acting on M2 muscarinic receptors
innervates - SA node, AV node and atria
stimulation of parasympathetic increase release of Acetylcholine and this causes a reduction in HR
When there is an increased HR - what happens to sympathetic and parasympathetic activity?
Sym activity is increased
whereas Psym activity is reduced
What is cardiac output defined as?
defined as the amount of blood pumped by each of the ventricles in a minute
how is cardiac output calculated?
calculated by multiplying the volume of blood ejected per beat with the number of beats per minute
stroke volume =
volume of blood ejected per minute
what is the equation for cardiac output?
cardiac output = stroke volume X heart rate
THEREFORE changes in SV and HR will influence CO
what is cardiac output typically given as/units?
given as mL/min or L/min
EDV?
the volume of blood that is present at the very end of the diastolic phase just immediately prior to contraction
ESV?
the volume of blood that is present inside the ventricle immediately after contraction is completed
the volume of blood that is ejected at every beat is determined by?
EDV and ESV
EDV?
end diastolic volume
ESV?
end systolic volume
afterload?
the load or tension that the ventricular walls have to work against to eject blood from the heart (this load is developed during the ejection of blood)
It’s the amount of work required by the walls to expel the blood into aorta
Typically related to aortic pressure (if aortic pressure is high e.g. aortic stenosis of systemic vascular resistance then afterload will be high)
Preload?
The load or tension exerted on the muscles at the end of diastole (load or tension just on ventricular walls just prior to contraction)
related to the initial stretching of the cardiac myocyte - sarcomere length
typically related to the end diastolic pressure/volume
anything that regulates SV and HR, will indirectly regulate?
Cardiac output
three major controls of CO?
nervous control
intrinsic control
atrial reflex
Effect of sympathetic stimulation on ventricular contraction/relaxation?
increase force of contraction
increase stroke volume (increasing venous return)
contraction of vascular smooth muscle cells in the veins to increase amount of blood returning back to heart
Effect of parasympathetic stimulation on ventricular contraction/relaxation?
no effect on ventricles (this is no longer true)
Decrease atrial contractility (less blood pumped into ventricles thus drop in stroke volume)
the heart has an intrinsic ability to regulate what?
the stroke volume
how does the heart regulate stroke volume?
done via the cardiac muscle fibre and the properties of these fibres (allowing them to stretch unless it gets too large and loses its recoil ability)
what are the atrial reflexes associated with?
with the regulation of blood volume
what system plays an important role in the regulation of blood volume?
the renal system - hence regulates blood pressure
atria has low pressure receptors in them - these detect changes in blood volume so?
when blood volume is increased, stretch receptors detect these change and the cv inhibitory centres is activated (medulla)
this is not the only compensatory - several others - renal, receptors in the aorta etc
ANP?
atrial natriuretic peptide (ANP)
effects of tissue demand on CO - during sleep?
sleep - decreased demand for oxygen - cardiac output drops in this sitch - blood only to vital organs e.g. brain, heart, digestive system (muscle minimal demands)
effects of tissue demand on CO - during exercise?
increased O2 consumption - more blood required by muscles - increased supply
vasodilation (initially drop in cardiac output cause decreased peripheral resistance thus decreased BP - then drop in BP detected and CO is increased to keep BP within normal range
Increased heart rate
pathological effect on Cardiac output? (high)
High CO - chronic vasodilation e.g. hyperthyroidism - increased basal metabolic rate - more O2 consumption - vasodilation
pathological effect on Cardiac output? (low)
drop in cardiac function (CHF, blood loss) - not enough blood is being pumped out
CHF - abnormal contractility and stiffening of ventricular walls
blood loss - decreased venous return
