CVS basics and concepts Flashcards
Describe the velocity equation in a pressure profile across circulation?
Velocity (cm/s) = Flow (cm3/s) / Area (cm2)
Where is the place that has the biggest pressure difference and why?
The biggest decrease in pressure is found in the arterioles because they can contract and relax which alters there diameter and radius. this alternation in radius has a dramatic effect on resistance.
smaller radius=higher resistance therefore higher pressure.
Changes in resistant vessels are the cause of clinical hypertension
What is the equation to find blood pressure?
blood pressure = cardiac output X total peripheral resistance
With clinical hypertension the cardiac output is the same, so the issue is the circadian resistance in those aterioles.
What is haemodynamics?
Hemodynamics is how your blood flows through your blood vessels.
How can you find the mean pressure of the aorta?
Systolic - diastolic
What is an incisura (dicrotic notch)
Downward notch in the curve recording aortic blood pressure that occurs between systole and diastole and is caused by backflow of blood for a short time before the aortic valve closes.
Where is blood pressure normally measured why?
brachial artery
The time in diastole is enhanced.
You have a rise caused by injection, then there is a long relaxation period and as a result the mean arterial pressure in this artery is much closer to the diastolic pressure.
How do you work out the mean arterial pressure in the brachial artery?
What is pulse pressure the same as?
systolic minus 1/3 of pulse pressure.
pulse pressure= systolic minus diastolic
What can cause an increase in blood pressure
feeling pain
exercise
Blood pressure can also vary due to vasoconstriction (radius smaller) and vasodilation(radius bigger).
Name the steps the heart goes through
what takes the longest and shortest amount of time?
*On the right side
1. Oxygen-poor blood from all over your body enters your right atrium through two large veins, your superior vena cava and inferior vena cava. These veins drain blood from your upper body and lower body, respectively, and directly empty it into your right atrium.
2 .Your tricuspid valve opens to let blood travel from your right atrium to your right ventricle.
3. When your right ventricle is full it squeezes, which closes your tricuspid valve and opens your pulmonary valve.
4. Blood flows through your main pulmonary artery and its branches to your lungs, where it gets oxygen and releases carbon dioxide.
*On the left side
1. Oxygen-rich blood travels from your lungs to your left atrium through large veins called pulmonary veins. These veins directly empty the blood into your left atrium.
2. Your mitral valve opens to send blood from your left atrium to your left ventricle.
3. When your left ventricle is full it squeezes, which closes your mitral valve and opens your aortic valve.
Your heart sends blood through your aortic valve to your aorta, where it flows to the rest of your body.
(shown only for left side normally)
diastole
1. ventricular filling (mitral open aortic v. closed)
atrial systole
ventricular systole
2. isovolumetric contraction (all valves are closed no change in volume but there is pressure as fibers shorten)
3.ejection (aortic v. opens)
ventricular diastole
4.isovolumetric relaxation
5.ventricular filling (mitral valve opens)
longest=ventricular filling
shortest=isovolumetric contraction because it is energetically expensive
Explain the volume changes in heart cycle
ventricular filling, atria contract gives final boost to ventricular volume giving an important volume = End-diastolic volume ( the maximum amount of fluid that will be in the ventricle.
isovolumetric contraction no change in volume.
Finally ejection, the first 3rd of the period of ejection is rapid then slower as blood trickles into periphery. Once ejected we then come to another important volume= end-systolic volume (minimum amount of blood left in the ventricle after contraction). this represents residual volume that never changes although exercise may decrease it slightly.
How do you find stroke volume?
Stroke volume is the amount of blood ejected from the ventricle with each cardiac cycle.
subtracting the end-systolic volume from the end-diastolic volume.
How can you work out the ejection fraction?
stroke volume / end-diastolic volume then X 100
this is important clinically as ejection fraction in normal hearts should be about 50-70%.
If it drops below 50% your heart is going into failure.
What is the maximal point of rise in the left ventricle?
Dp/dt(max) pressure over time represents the ratio of pressure change in the ventricular cavity during the isovolumic contraction period helps find efficiency and useful clinically
Pressure does not fall uniformly across the vascular system. Where does the biggest change occur and why does this happen?
arterioles because they can contract and change their radius
Which valves are open during isovolumetric relaxation?
No valves are open, no change in volume
During what phase of the cardiac cycle does the greatest change in ventricular volume occur?
ventricular filling
During what phase of the cardiac cycle does the rapid rise in ventricular pressure occur?
isovolumetric contraction
What is the stroke work?
pressure X volume
Explain the sound we hear when our heart is pumping
The first thud is the atrioventricular valves closing (mitral and tricuspid valves). The second heart sound is the closure of the aortic and pulmonary valve
Name the valves and where they are found
tricuspid valve: located between the right atrium and the right ventricle.
pulmonary valve: located between the right ventricle and the pulmonary artery.
mitral valve: located between the left atrium and the left ventricle.
aortic valve: located between the left ventricle and the aorta
Why does the second thud sound split?
The pressure changes in the left ventricle means the aortic valve shuts sooner than the pulmonary valve
Why do the central veins oscillate and not the peripheral veins
There are no valves between the right atrium and central veins in particular the jugular vein
someone with heart failure has a raised jugular pressure
What is Starling’s law on the heart?
The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume.
‘The energy of contraction is proportional to the muscle fibre length at rest. The longer the muscle fibre the greater the contraction
How do you find stroke volume?
Cardiac output = heart rate x stroke volume of one ventricle
filling pressure and contractivity increases stroke volume.
arterial pressure (aorta) will oppose stroke volume
if aorta is constricted it’s more difficult for aorta to eject (afterload)
What can filling pressure also be known as?
filling pressure=central venous pressure
describe normal physiological condition
(starling curve)
we will always be on the ascending limb.
starling curve
What is Laplace’s law ?
what are the reasons that people with heart failure are given diuretics?
It relates wall tension to internal pressure;
pressure= 2X tension / radius
if R goes up you need more tension to produce the same pressure. so in a heart that is struggling R is going to be large and you can’t produce tension and therefore pressure is going to decrease.
If the RADIUS of the heart dilates excessively,
and if ACTIVE TENSION has reached the plateau,
then the systolic PRESSURE generated by
the contraction will FALL.
This reduces the STROKE VOLUME.
So, TREAT a dilated heart to reduce its distension
and thereby IMPROVE CARDIC OUTPUT
What governs central venous pressure (CVP)?
*VOLUME OF BLOOD in the circulation
-This can be reduced in haemorrhage.
*DISTRIBUTION OF BLOOD between central and
peripheral veins.
-Sympathetic nerve activity regulates peripheral venous tone
Gravity
Standing ‘pools’ venous blood in legs,
reducing CVP & stroke volume
Movement (walking etc) operates the calf muscle pump, so raises CVP and stroke volume.
What is venous return?
it IS the cardiac output
Why are RV and LV stroke volumes kept equal?
They are kept equal to prevent congestion e.g perhaps in the lungs.
high pressure gives more filling, give more stretch, gives bigger ejection.
right hand-side needs bigger ejections so it just keeps everything the same
The closure of which valves produces the second heart sound?
Pulmonary and aortic valves
What happens if a heart over distends?
It can’t pump as well so will led to heart failure
Name a determinant of central venous pressure
volume
Stroke volume and mean arterial pressure
The more you increase the mean arterial pressure the more the stroke volume will go DOWN this is due to resistance and contraction and smaller vessels increasing pressure.
Effect of sympathetic nerves on LV pressure
main effect of sympathetic nerves is greater contraction faster contraction.
1. Faster ejection, increased dP/dtmax
2. shorter ejection time
3.Smaller end-diastolic volume due to increased ejection fraction (>70%)
The sympathetic nervous system releases norepinephrine (NE) while the parasympathetic nervous system releases acetylcholine (ACh). Sympathetic stimulation increases heart rate and myocardial contractility.
What are the different Starling curves?
- the normal
- The effect of increased contractility (positive inotropism) caused by sympathetic nerves,adrenoceptors, adrenaline, dopamine and isoprenaline mediators.
3.In heart failure this is going to be reduce. curve is flatter, an inotropic drug such as digoxin can help recover the curve.
How does contractility alter the P–V loop?
*Sympathetic stimulation;
bigger stroke volume,
higher arterial pressure,
bigger stroke work (PxSV),
bigger ejection fraction.
But smaller end-diastolic volume limits the size of the
SV increase (Starling L.O.H.) because we have ejected more, which means because we have less volume there is less stretch so a smaller contraction. This is not prefect in increasing cardiac output.
How does contractility & the Starling effect combine?
What does exercise do?
Optimal rise in Stroke Volume due to
combined effect of:
sympathetic drive, (reduced ESV)
Starling law of heart (increased EDV)
exercise:
rise in filling pressure due to peripheral veno-constriction & muscle pump
What does orthostasis do?
It creates a low cardiac filling pressure
low blood pressure (hypotension) that occurs upon standing.
Distribution of venous blood when supine (laying):
high central blood volume,
high cardiac filling pressure,
large stroke volume (Starling’s law)
What are the Immediate consequence of a fall in CVP?
What makes it worse?
CVP has gone down
less filling
less stretch
ventricular stroke volume goes down
left ventricular pressure has gone down and a decrease in arterial pressure
decrease in central cerebral blood flow which causes
cerebral underperfusion
-dizziness
-visual fade
Exacerbated by:
warmth (venodilatation)
bed rest
alpha-adrenoceptor blocker
zero gravity
fortunately we have the baroreceptor reflex
What does the baroreflex do?
buffers acute fluctuations in blood pressure that occur during posture, stress, or other maneuvers.
It increases your heart rate.
Describe summary of all cardiovascular reflexes both excitatory and depressor.
Sensory receptors, central pathways and effects (via sympathetics/vagus-regulation)
*Sensory receptors
Arterial baroreceptors – depressor (to BP)
Cardiac stretch receptors – some depressor (mixed)
Arterial chemoreceptors – excitatory
Muscle work receptors – excitatory
*Central pathways
-Medulla relay station (nucleus tractus solitarius) to:
Vagal motor neurons (nucleus ambiguus)
Presympathetic neurons (rostroventrolateral medulla, RVLM)
*Effects (via sympathetics/vagus-regulation)
Heart – rate, stroke volume (contractility)
Resistance vessels – TPR (total peripheral resistance)
Veins – CVP (central venous pressure)
What is the location of arterial baroreceptors & chemoreceptors?
What are the names of nerve number 9 and 10?
Baroreceptors are found in the aortic arch where they protect the systemic circulation and they are also found in the carotid sinus where they protect the cerebral circulation.
Afference from carotid sinus travel in nerve number 9 which is the Glossopharyngeal Nerve in contrast afference from the aortic baroreceptors travel through nerve 10 the vagus nerve they are mixed both carry sympathetic and parasympathetic
What are the different bodies?
you have carotid bodies and aortic bodies they are different. bodies are chemoreceptors.
Regulation of the baroreceptor response
This is a typical negative feedback loop let’s say blood pressure increases due to pain response as a result you have vasoconstriction which is detected by baroreceptors which will make receptor fire more to medulla, more firing will lead to turning off of the sympathetic nervous system and turn up the parasympathetic to decrease heart rate and less vasocontraction and total peripheral resistance to return blood pressure to normal.
Reflex effects of baroreceptor unloading (low BP, reduced firing) e. g. after haemorrhage
high sympathetic activity, low vagal parasymp. activity
high Heart rate & contractility, aiding the CO
Arteriolar vasoconstriction, so increase in TPR
Venoconstriction, supporting CVP and SV
These 3 effects can restore mean blood pressure,
or at least minimise how far it falls, since:
BP = CO x TPR
What are other thing we can see in response to low BP over a longer period of time?
*Adrenaline secretion
( high sympathetic drive to adrenal medulla)
*Vasopressin (makes you pee less) secretion from posterior pituitary
*Angiotensin II formation (due to sympathetic stimulation of renin secretion by kidneys). (vasal constrictor)
*Plasma volume expansion
-capillary absorption, due to low Pc following vasoconstriction of resistance vessels
-antidiuresis, due to renal action of vasopressin (ADH) (pee less)
Arterial chemoreceptors: key facts
where are they found?
What are they stimulated by?
What happens when they are stimulated?
Located in carotid BODIES (to do with chemoreceptors) (not sinus) & aortic bodies
Stimulated by CO2, H+ and hypoxia
therefore stimulated by asphyxia & by haemorrhage (unlike baroreceptors)
Reflex effects: (what happens when chemoreceptors are stimulated)
vasoconstriction (via high sympathetic activity)
raise blood pressure (important in severe haemorrhage)
preservation of cerebral blood flow
Where are the mechanoreceptors and what do they do and where are other receptors found?
they are in the aortic arch and are sensitive to pressure. Other mechanic receptors sense overfilling of the heart
Others are found near the opening of the superior and inferior vena cava, these help to signal filling of the heart.
nociceptors signal pain during angina and when having a heart attack
Where are the baroreceptors located?
Aortic arch and carotid sinus
What happens if there is increased firing of the baroreceptors?
It will lower the blood pressure.
The secretion of which of the following is not increased following baroreceptor unloading?
Adrenaline
Vasopressin
Acetylcholine
Angiotensin II
adrenaline
Central pathways which cause regulation from the baroreceptors (sympathetic outflow)
Baroreceptors send afferent fire either from nerve 9 (Glossopharyngeal Nerve) and 10 (vagus nerve) up to the nucleus tractus solitarius in medulla. signal walls are also sent to higher centres such as cerebellum, hypothalamus limbic system and cortex, but the main thing is the nucleus tractus solitarius fires to the caudal ventrolateral medulla. This then sends up an inhibitory signal to the rostro-ventro-lateral medulla which then fires down to the spinal cord, this means if u have an increase in pressure, increase firing up to NTS on to CVM inhibit the RVLM and so the firing down sympathetic pathways is reduced.
Increase firing from baroreceptor decrease sympathetic and decrease firing increases sympathetic
What is the difference between afferent and efferent
Afferent is used to describe things like nerves, blood vessels, and arteries that lead toward or bring things (like blood, in the case of arteries) to an organ, such as the heart or brain. Efferent means the opposite—it’s used to describe parts that carry or lead things away from organs or other parts.
Central pathways regulating vagal parasympathetic
outflow to pacemaker
Firing (reduction firing) going up nerve 9 and 10 to Nucleus tractus solitarius fires to the nucleus ambiguus which is either positive or negative depending on if increased or unloaded baroreceptors.
Interesting effect called sinus arrhythmia, there is an inhibitory input from inspiration centre to nucleus ambiguus which has an effect to turn down parasympathetic. As a result when you breath in heart rate increases, breath out heart decreases so you get sinus arrhythmia.
Excitation-Contraction coupling in cardiac myocytes
The arrival of an action potential, which penetrates deep into the myocyte through transverse tubules, triggers a sharp increase in the influx on calcium across the cell membrane through voltage gated calcium channels. Calcium binds to calcium release channels called ryanodine receptors which are located on the membrane of the sarcoplasmic reticulum. When calcium binds to the ryanodine receptors it stimulates release of calcium from the SR into the cytosol. This stimulates contraction, by binding to Troponin C, causing a conformational change, and exposing the myosin binding site, initiating cross-bridge formation.
Ionic gradients govern cardiac excitability
A variety of ion channels control inward and outward ionic fluxes, which determine action potential shape, height, duration
Cardiac conduction, action potentials and gap junctions
Conduction velocity is governed by inward currents and gap junctions (connexins)
Excitation is transmitted through the conduction system and myocardium by local currents acting ahead of the action potential. Internal current flows through the sarcoplasm and gap junctions which are made up of protein called connexin of the intercalated disc. External current flows through the extracellular fluid. The currents discharge the membrane ahead, triggering its action potential
Signal transduction pathways in a pacemaker cell and heart rate
sympathetic and parasympathetic
(SYMPATHETIC)
Noradrenaline is a sympathetic neurotransmitter so there is an increase in contraction, stroke volume and heart rate. It binds to beta one adrenergic protector this stimulates a gene stimulatory proteins whose effect is to turn up Adenylyl cyclase which will catalyse ATP to cAMP then has various effects. It has an effect on sodium channel, stimulates protein kinase A so more calcium coming into cell, more calcium means more calcium release so bigger contractory. It makes the calcium pump which restores calcium back to sarcoplasmic reticulum after contraction more efficient so more calcium can be released therefore more binding to troponin so bigger contraction.
To summarise sympathetic stimulation noradrenaline input makes everything quicker and more forceful contraction.
(PARASYMPATHETIC)
Acetylcholine binds to muscarinic receptors and it binds to a gene inhibitory protein this then opens a potassium channel in the membrane (more potassium in cell than outside) so potassium moves out, this then increases positive charge outside, so cell becomes more negative which means it makes it more difficult to reach threshold potential to then fire an action potential this then slows things down.
Altering the ionic environment can cause dangerous cardiac events
Describe what could happen
The ionic balance is not only important in setting off action potentials, things can go wrong which has bad effects such as;
*Hypocalcaemia reduces myocardial contractility
*Extreme hypercalcaemia can arrest the heart in systole
*Hyperkalaemia (too much potassium) can induce heart block and ventricular tachyarrhythmia (too fast a heart rate) /fibrillation
*Hypokalaemia (too little potassium) induces arrhythmia in patients with existing cardiac dysfunction
*Ischaemia raises external [K+], and increases [H+]= compete with Ca2+ for TroPC binding site
*Hypoxia and ischaemia activate KATP channels, which reduces action potential duration – transmural electrical instability
Where is the cardiorespiratory control centre located in the brain?
In the medulla
Describe the sequence of cardiac excitation
The SA node starts the sequence by causing the atrial muscles to contract. Next, the signal travels to the AV node, through the bundle of HIS, down the bundle branches, and through the Purkinje fibers, causing the ventricles to contract
Describe the steps involved in excitation contraction coupling
excitation from cell next door triggers excitation in existing cell, calcium permeates down transverse tubules enters cell via calcium channel, triggers sarcoplasmic reticulum to release more calcium this then allows calcium to bind to troponin c induces conformational changes which allows for contraction. Then calcium is returned back over the membrane.
What ion channel is responsible for the upstroke of the action potential?
voltage gated sodium channel
What is an ECG
There are excited myocytes and resting myocytes there will be a potential difference between these two myocytes and currents can flow from one to the other this results in a change of about 100mV but conducting fluids in the body allow us to measure the change in voltage up to 1mV in the skin surface which is the basis of an ECG
What is the diagnostic use of ECG’s?
Arrhythmias due to -
delayed afterdepolarizations = ectopic beats
Conduction defects = heart block
Circus movement (re-entry) = tachycardias, flutter
Pathology of myocardium
Myocardial infarcts & angina
Hypertrophy
Plasma K+ abnormalities
Reading
An introduction to cardiovascular physiology (2011) J.R.Levick
The cardiovascular system at a glance (2010) P.I. Aaronson & J.T. Ward
Cardiovascular Physiology Berne and Levy, 7th Ed.
http://www.CVphysiology.com
