Cardiovascular Physiology

Question 1

-What do peripheral chemoreceptors sense?

Answer 1

Partial pressure of oxygen and carbon dioxide in your blood, along with the pH in your blood.

If there is less oxygen the receptors start firing off

Question 2

What are the peripherial chemoreceptors?

Answer 2

Carotid and aortic bodies

Question 3

Afferent information from the peripheral chemoreceptors.

Information from the carotid body is sent via the —— —– nerve to the ———- nerve to the ——- in the brain.

Information from the aortic body joins the —– nerve and goes to the —– in the brain.

Answer 3

Information from the carotid body is sent via the carotid sinus nerve to the glossopharyngeal nerve to the NTS in the brain.

Information from the aortic body joins the vagus nerve and goes to the NTS in the brain.

Question 4

What stimulates the carotid bodies in the respiratory and cardiovascular response?

Answer 4

Respiratory response
respiratory rate
tidal volume
airway resistance
airway secretions
respiratory muscles

Cardiovascular response
arterial pressure
heart rate
contractility
cardiac output
vascular resistance

Question 5

Stimulation of carotid bodies leads to an ——– in respiration (respiratory rate and tidal volume). Cardiovascular response = ——– arterial pressure, heart rate and contractility

Answer 5

Stimulation of carotid bodies leads to an increase in respiration (respiratory rate and tidal volume). Cardiovascular response = increased arterial pressure, heart rate and contractility

Question 6

Carotid body response

The carotid bodies sit at the base of the —— and monitor —- —— and the amount of ——– in the blood going to the ——-. When it senses the —– is receiving less ——– it gets activated as a reflex arc, you increase ———- to try and get more ——— in, if its not enough you also increase ———- drive to your kidney and peripheral ———-, so those arteries ———- to ——– total peripheral resistance (TPR), which ——– mean arterial pressure and redirects blood flow going to the ——–.

So the carotid bodies are trying to ——- the intake of ——- as well as insure there is —– flow going up to your —– that has a high —– content.

Answer 6

The carotid bodies sit at the base of the brain and monitor blood pressure and the amount of oxygen in the blood going to the brain. When it senses the brain is receiving less oxygen it gets activated as a reflex arc, you increase breathing to try and get more oxygen in, if its not enough you also increase sympathetic drive to your kidney and peripheral vasculature, so those arteries vasoconstrict to increase total peripheral resistance (TPR), which increases mean arterial pressure and redirects blood flow going to the brain.

So the carotid bodies are trying to increase the intake of oxygen as well as insure there is blood flow going up to your brain that has a high oxygen content.

Question 7

The aortic bodies

The aortic bodies sit at the origin at the ——- arch and the activation ———- the fusion of the heart (they are guarding the fusion of the heart)

Answer 7

The aortic bodies sit at the origin at the aortic arch and the activation increases the fusion of the heart (they are guarding the fusion of the heart)

Question 8

If your chemoreflex is blunted because the —— content is ——- you can’t increase ——– and —— — enough to get enough ——- to the carotid body and brain

Answer 8

If your chemoreflex is blunted because the oxygen content is low you can’t increase respiration and blood pressure enough to get enough oxygen to the carotid body and brain

Question 9

Do carotid bodies have a role in hypertension?

Answer 9

Yes - they might

Question 10

Respiratory arrest

There is an increased effort to ——- followed by loss of ——. If delivery of —— continues to be absent, death will follow.

Answer 10

There is an increased effort to breath followed by loss of consciousness. If delivery of oxygen continues to be absent, death will follow.

Question 11

As you hold your breath and no more ——- is coming in and all of your cells are utilising the ——–, the increased drive you feel to ——- a large part of that comes from the ——— bodies as well as ——- chemoreceptors, but the ——– is dropping which is sending more signals to the —– and ——— to contract and drag oxygen in.

Answer 11

As you hold your breath and no more oxygen is coming in and all of your cells are utilising the oxygen, the increased drive you feel to breathe a large part of that comes from the carotid bodies as well as central chemoreceptors, but the PaO2 is dropping which is sending more signals to the brain and diaphragm to contract and drag oxygen in.

Question 12

What happens to your heart rate and blood pressure when you dive?

Answer 12

Heart rate decreases - bradycardia

Blood pressure - usually maintained or even elevated despite the increase in HR

Question 13

What is the bradycardia response during dive most driven by? How was this proved?

Answer 13

Driven by increased parasympathetic/vagal activity.

Atropine blocks vagal/parasympathetic (increase=decrease HR) drive to the heart. The HR doesn’t diminish as much when the subject has atropine.

Question 14

Holding your breath/ Voluntary apnea

There is ——— inhibition of respiratory muscles. There is a decrease in Pa— and an increase in Pa—– which is sensed by ———–. There is a small increase in ———- activity so —- —–decreases and an increase in ———- activity causing ——- in specific areas. This means the —— —– —– doesn’t change much.

Answer 14

There is increased inhibition of respiratory muscles. There is a decrease in PaO2 and an increase in PaCO2 which is sensed by chemoreceptors. There is a small increase in parasympathetic activity so heart rate decreases and an increase in sympathetic activity causing vasoconstriction in specific areas. This means the mean arterial pressure doesn’t change much.

Question 15

Facial immersion in cold water

There is ——— inhibition of respiratory muscles. There is a decrease in Pa— and an increase in Pa—– which is sensed by ———–. There is a small increase in ———- activity so —- —–decreases and an increase in ———- activity causing ——- in specific areas. This means the —— —– —– doesn’t change much.

You activate certain receptors near your —– and —- which causes a big increase in ——– and ——— activity. The large increase in parasympathetic activity decreases —– —– and —- —-. The large increase in sympathetic activity causes ———– which causes an increase ——– —– —- and therefore an ——— in mean arterial pressure.

Answer 15

There is increased inhibition of respiratory muscles. There is a decrease in PaO2 and an increase in PaCO2 which is sensed by chemoreceptors. There is a small increase in parasympathetic activity so heart rate decreases and an increase in sympathetic activity causing vasoconstriction in specific areas. This means the mean arterial pressure doesn’t change much.

You activate certain receptors near your nose and cheeks which causes a big increase in parasympathetic and sympathetic activity. The large increase in parasympathetic activity decreases heart rate and cardiac output. The large increase in sympathetic activity causes vasoconstriction which causes an increase total peripheral resistance and therefore an increase in mean arterial pressure.

Question 16

Breathing with a snorkel in cold water

In this case you don’t have ——– so there is —— inhibition of respiratory muscles and you don’t have the drive from the ———— because you are ——— through the snorkel.

You activate certain receptors near your —– and —- which causes a big increase in ——– and ——— activity. The large increase in parasympathetic activity decreases —– —– and —- —-. The large increase in sympathetic activity causes ———– which causes an increase ——– —– —- and therefore an ——— in mean arterial pressure.

Answer 16

In this case you don’t have apnea so there is no inhibition of respiratory muscles and you don’t have the drive from the chemoreceptors because you are breathing through the snorkel.

You activate certain receptors near your nose and cheeks which causes a big increase in parasympathetic and sympathetic activity. The large increase in parasympathetic activity decreases heart rate and cardiac output. The large increase in sympathetic activity causes vasoconstriction which causes an increase total peripheral resistance and therefore an increase in mean arterial pressure

Question 17

What is arrhythmia?

Answer 17

When the heart doesn’t work at 100% efficiency.

Question 18

What is trachycardia?

Answer 18

Heart is working faster than it should be so it gets less efficient because there isn’t enough time for the blood to fill up.

Question 19

The heart pumps blood by a continuing cycle of ——– and ———-(SYSTOLE & DIASTOLE). In order for muscle to contract, it must first be ——— activated.

Answer 19

The heart pumps blood by a continuing cycle of contraction and relaxation (SYSTOLE & DIASTOLE). In order for muscle to contract, it must first be electrically activated.

Question 20

The heart is not activated all at one instant. Its activated by a wave of ——– that spreads throughout the ——-in a co-ordinated manner. Therefore ——— each area at the appropriate ——–,
so that ——- is effective in ——– the blood forward into the circulation.

If this pattern of spread of electrical activation is upset then the heart will not act as an effective pump with results ranging from relatively minor such as limiting exercise capacity (eg. atrial fibrillation) to fatal (eg. ventricular fibrillation).

Answer 20

The heart is not activated all at one instant. Its activated by a wave of excitation that spreads throughout the myocardium in a co-ordinated manner. Therefore stimulating each area at the appropriate time,
so that systole is effective in propelling the blood forward into the circulation.

Question 21

What are the myocyte electrical properties?

Answer 21

Excitability
Conductivity
Automaticity

Question 22

Excitability - Fast response AP

—— response cells are found throughout the ——-, are the most ———- action potential that is seen, are part of the contracting/working cardiac muscle in the —— and ——–, the fast part of specialized conduction system

These specialised cells are very important at coordinating this rapid spread of —— activity throughout the ——- and ensure the ——– is tightly coordinated

This is a fast response action potential because the ———– (phase —) is very fast (same speed as nerve).

Answer 22

Fast response cells are found throughout the heart, are the most common action potential that is seen, are part of the contracting/working cardiac muscle in the atria and ventricle, the fast part of specialized conduction system

These specialised cells are very important at coordinating this rapid spread of electrical activity throughout the ventricles and ensure the contraction is tightly coordinated

This is a fast response action potential because the depolarization (phase 0) is very fast (same speed as nerve).

Question 23

Fast response AP and ionic currents.

Phase 0: upstroke (rapid —— to —-mV from resting —-mV) very rapid increase in ——- permeability.

This occurs because the membrane potential is ——– externally which is usually due to a ——– passing through it by a neighboring —-.
The cell reaches a ——– potential and at this point it’s enough to trigger the opening of voltage gated —— channels which allows the rapid influx positively charged ——— ions
The ——– channels open and close very fast

Phase 1: early ———- (to near —- mV)
——– channels start closing (stopping influx of ——-) and chloride channels start opening (transcend outwards current - largely —-) brings the cell potential back a little bit
These channels close ——- as well

Phase 2: ——— i) slow inward ——- current (i—) ii) outward —— current (i—-)
Not much change in the membrane potential - the movement of ions is almost perfectly in ——– (doesn’t mean that the ions are not moving)

There is an inwards——— current (——— is needed to make the ——– contract not —-)
Outward ——- current opposes the inward current

Phase 3: ———–
——- and —— dependent channel is switched – by the initial ———- (phase –) but it takes time for the channel to actually —–

The ——– current is the ——- current which starts to —— the cell down towards the —— membrane potential

Phase 4: resting i— high ——- conductance defines ——- Potential

As the membrane potential —– more ——- channels (i—) will open and these are ——- sensitive and the i—- channels will begin to close.

At rest there is only one type of channel open the i— channels

Background activity
——— ——— - outward current

——— —— exchanger (3 — in for 1 —- out, net positive charge)

—— ——– ——— - (3 —out for 2 — in, maintains – gradient)

Answer 23

Fast response AP and ionic currents.

Phase 0: upstroke (rapid depolarization to +40mV from resting -70mV) very rapid increase in sodium permeability.

This occurs because the membrane potential is depolarized externally which is usually due to a depolarization passing through it by a neighboring cell.
The cell reaches a threshold potential and at this point it’s enough to trigger the opening of voltage gated sodium channels which allows the rapid influx positively charged sodium ions
The sodium channels open and close very fast

Phase 1: early repolarization (to near 0 mV)
Sodium channels start closing (stopping influx of sodium) and chloride channels start opening (transcend outwards current - largely chloride) brings the cell potential back a little bit
These channels close gradually as well

Phase 2: plateau i) slow inward calcium current (iCa) ii) outward potassium current (iK)
Not much change in the membrane potential - the movement of ions is almost perfectly in balance (doesn’t mean that the ions are not moving)

There is an inwards calcium current (calcium is needed to make the muscle contract not sodium)
Outward potassium current opposes the inward current

Phase 3: repolarization
Sodium and potassium dependent channel is switched – by the initial depolarization (phase 0) but it takes time for the channel to actually close.

The calcium current is the repolarizing current which starts to bring the cell down towards the resting membrane potential

Phase 4: resting inward high potassium conductance defines resting Potential

As the membrane potential hyperpolarizes more potassium channels (iK) will open and these are voltage sensitive and the iNa channels will begin to close.

At rest there is only one type of channel open the iK channels

Background activity
Potassium efflux - outward current

Sodium-potassium exchanger (3 Na+ in for 1 K+ out, net positive charge)

Sodium-calcium exchanger - (3 Na+ out for 2 Ca2+ in, maintains electrochemical gradient)

Question 24

Slow response AP phases

Found in the ——- and ——- nodes.

The resting potential of the cells is —— than the fast response cells at about —-mV.

The upstroke (phase –) is —– because there is — current in these cells. It is produced by an influx of ———- via i—.

Phase 2 is a slight —–.

There are either no ——– channels, or there are inactive ——– channels. This is because the cells resting potential is ——, the —– channels become active by the rapid ———– so some of the channels that need to be turned on by the —— are not ———.

Answer 24

Slow response AP phases

Found in the SA and AV nodes.

The resting potential of the cells is higher than the fast response cells at about -60mV.

The upstroke (phase 0) is slow because there is no current in these cells. It is produced by an influx of calcium ions via iCa.

Phase 2 is a slight plateau.

There are either no sodium channels, or there are inactive sodium channels. This is because the cell’s resting potential is high, the sodium channels become active by the rapid depolarization so some of the channels that need to be turned on by the depolarization are not activated.

Question 25

Ischemia and AP Sometimes in ischemia (part of the heart that’s not getting any blood) you have cells that become sick and the —— potentials of the —– response cells can ——- resulting in a change in action potential with a —— upstroke and —— conduction. This can lead to ——

Answer 25

Sometimes in ischemia (part of the heart that’s not getting any blood) you have cells that become sick and the resting potentials of the slow response cells can depolarize resulting in a change in action potential with a slow upstroke and slow conduction. This can lead to arrhythmias.

Question 26

Cardiac AP - Excitability In the —– —— period all the cells in the heart within this time period after ——– with an action potential are not able to be ——– again. This is because the ——- channels responsible for the ——— have certain properties which mean that after they have —— they cant —— again after a certain —— delay has gone by, so they can’t be —— during this period. Therefore if you hit the heart with another —— stimulation in the —— ——- period you would get —- response. In the —- —– period you can ——— the cells but its ——- to do so you might need to inject more ——- to ——- the cells so that they are likely to be able to produce a ——-. This is because some of the —— channels have opened but others are still closed. You get a normal action potential after the —– —– time. Refractoriness over long periods prevents ——– of the heart

Answer 26

In the absolute refractory period all the cells in the heart within this time period after depolarization with an action potential are not able to be stimulated again. This is because the ion channels responsible for the depolarization have certain properties which mean that after they have opened they can't reopen again after a certain refractory delay has gone by, so they can’t be activated during this period. Therefore if you hit the heart with another electrical stimulation in the absolute refractory period you would get no response. In the relative refractory period you can stimulate the cells but its difficult to do so you might need to inject more current to depolarize the cells so that they are likely to be able to produce a response. This is because some of the ion channels have opened but others are still closed. You get a normal action potential after the refractory time. Refractoriness over long periods prevents fibrillation of the heart

Question 27

Conductivity Cardiac muscle cells do not contract in response to a ——- signal. They are ———. The signal begins within the heart itself in the —– node. ——– activation spreads throughout ——— from cell to cell. This occurs because each cell is electrically coupled to several other cells via ——- ——, so as one cell ———-, current spreads to ——— cells allowing coordinated ——-.

Answer 27

Cardiac muscle cells do not contract in response to a nervous signal. They are myogenic. The signal begins within the heart itself in the SA node. Electrical activation spreads throughout myocardium from cell to cell. This occurs because each cell is electrically coupled to several other cells via gap junctions, so as one cell depolarizes, current spreads to neighboring cells allowing coordinated contraction.

Question 28

Automaticity Ability of cells to initiate an —- impulse through their own ——- activity, or diastolic ——– (AP) These cells are found in the —— node in the ——. Some are found around the —– node and the __ ___-___ network

Answer 28

These cells are found in the SA node in the heart. Some are found around the AV node and the atrioventricular (AV) node network.

Question 29

Pacemaker AP phases (automaticity) The ——— membrane potential is never flat because there is a —– rate of —– in membrane potential which is responsible for the spontaneous firing. The ———- of these cells is either due to the influx of —– via i—- or ——–. The ——— current is slightly out doing the ——– current such that the balance of the net current movement is in favour of ——— resulting in the slow ——– membrane potential. The outward current is due to ———- via i—- and i—- channels which are on most of the time but it varies in strength throughout the action potential. The inward current is due to i— channels that switches on and then off and the i— current that is largely a —— current that is activated by hyperpolarization.

Answer 29

Pacemaker AP phases (automaticity) The resting membrane potential is never flat because there is a gradual rate of change in membrane potential which is responsible for the spontaneous firing. The depolarization of these cells is either due to the influx of sodium ions via iNa or calcium. The calcium current is slightly outdoing the potassium current such that the balance of the net current movement is in favor of depolarization resulting in the slow diastolic membrane potential. The outward current is due to potassium efflux via iK and iK1 channels which are on most of the time but vary in strength throughout the action potential. The inward current is due to iCa channels that switch on and then off and the iNa current that is largely a funny current that is activated by hyperpolarization.

Question 30

Mechanisms for altering the intrinsic rate of pacemaker discharge to increase HR; Alter rate of ——— by ——- inward current (open the i— more) or ——- outward current (close i—- channels) Alter ——— potential - —— to increase HR Alter maximum ——- potential resulting in a decreased ——- membrane potential (opening i— channels more)

Answer 30

Mechanisms for altering the intrinsic rate of pacemaker discharge to increase HR; Alter rate of depolarization by increasing inward current (open the iNa more) or decreasing outward current (close iK channels) Alter threshold potential - depolarize to increase HR Alter maximum diastolic potential resulting in a decreased resting membrane potential (opening iCa channels more)

Question 31

Regulation of heart rate HR is regulated primarily by the ——— ———- System. ——- —— —— slows heart rate, by the release of —— at ——– endings in the heart. At the ——- node ——— increases —— permeability of cells (increase i—-). This results in a hyperpolarized and ———- pacemaker slope. ——- stimulation also slows ——- through the —– node. Very strong ——– stimulation can stop the —— node or block the —— node. ——– speeds heart rate by the release of ———- at — node. This ——— the slope of the pacemaker ———–.

Answer 31

HR is regulated primarily by the Autonomic Nervous System. Parasympathetic Nervous System slows heart rate, by the release of acetylcholine at vagal endings in the heart. At the SA node acetylcholine increases potassium permeability of cells (increase iK). This results in a hyperpolarized and decreased pacemaker slope. Vagal stimulation also slows conduction through the AV node. Very strong vagal stimulation can stop the SA node or block the AV node. Sympathetic Nervous System speeds heart rate by the release of norepinephrine at SA node. This increases the slope of the pacemaker depolarization.

Question 32

What is the normal heart rate?

Answer 32

60-100 bpm

Question 33

What is the bradycardia heart rate?

Answer 33

less than 60 bpm

Question 34

What is the tachycardia heart rate?

Answer 34

Above 100 bpm

Question 35

Pathway of depolerisation Sinoatrial node Specialised tissue in the —- —- near the —- —- —-. Cells are continuous with the ——- myocardial cells Spontaneous ———— at —-bpm at rest Atria Activation spreads through the muscle cells via —— junctions. Atrioventricular node —— conduction velocity —— contraction between the —— and ——— allowing the —– to top up the ——- with blood before they contract. Bundle of His (AV bundle) —- node and AV bundle is the only path between the —– and ——– due to the ——- —– blocking the depolerisation wave. Bundle branches —– bundle splits into right and left branches Purkinje fibres Bundle branches split into the purkinje fibre network which spreads across the ——— surface. The conduction speed is ——-. Ventricular myocardium Activation spreads through the muscle cells via —- junctions

Answer 35

Pathway of depolarization Sinoatrial node Specialized tissue in the right atrium near the superior vena cava. Cells are continuous with the surrounding myocardial cells Spontaneous depolarization at 60-100 bpm at rest Atria Activation spreads through the muscle cells via gap junctions. Atrioventricular node Slows conduction velocity delaying contraction between the atria and ventricles allowing the ventricles to top up the atria with blood before they contract. Bundle of His (AV bundle) AV node and AV bundle is the only path between the atria and ventricles due to the fibrous skeleton blocking the depolarization wave. Bundle branches AV bundle splits into right and left branches Purkinje fibers Bundle branches split into the Purkinje fiber network which spreads across the ventricular surface. The conduction speed is rapid. Ventricular myocardium Activation spreads through the muscle cells via gap junctions

Question 36

Wolff-Parkinson-White Syndrome (or Pre-excitation) People with this condition have extra conductive tissue linking the — and the ——. When the —- node fires the activation comes down the normal pathway through the —— node and also the pathway with the extra atria-ventricle pathway resulting in part of the ——– contracting earlier.

Answer 36

Wolff-Parkinson-White Syndrome (or Pre-excitation) People with this condition have extra conductive tissue linking the atria and the ventricles. When the SA node fires the activation comes down the normal pathway through the AV node and also the pathway with the extra atrioventricular pathway resulting in part of the ventricles contracting earlier.

Question 37

The electrocardiogram (ECG) visualizes the ——– activity spreading through the ——. It’s the sum of the ——— activity of the heart = VOLTAGE / TIME recording. It is recorded by ——— at different sites on the body that are connected to the —–, and are able to measure a ——– difference between different sites on the body caused by the electrical activity of the heart. This electrical activity can be recorded at a site distant from the heart because the body tissues act as ———. The heart is not the only source of electrical activity in the body, e.g. skeletal muscle

Answer 37

The electrocardiogram (ECG) visualizes the electrical activity spreading through the heart.. It’s the sum of the electrical activity of the heart = VOLTAGE / TIME recording. It is recorded by electrodes at different sites on the body that are connected to the skin, and are able to measure a potential difference between different sites on the body caused by the electrical activity of the heart. This electrical activity can be recorded at a site distant from the heart because the body tissues act as conductors. The heart is not the only source of electrical activity in the body, e.g. skeletal muscle

Question 38

Because of the ——– conducting network the different groups of cells along the ——– are ———– very close together and the depolarization stacks up to give the ——- complex

Answer 38

Because of the purkinje/fast conducting network the different groups of cells along the ventricle are depolarizing very close together and the depolarization stacks up to give the QRS complex

Question 39

What is a dipole?

Answer 39

A pair of equal but opposite charges separated by a small distance

Question 40

If there is a bigger potential difference between the 2 electrodes, there will be more —– and change in ——- measured.

Answer 40

If there is a bigger potential difference between the 2 electrodes, there will be more current and change in voltage measured.

Question 41

When electrodes are placed at ——- distances the fields become ———, changing the size of the —- and measured ——–.

Answer 41

When electrodes are placed at greater distances the fields become weaker, changing the size of the dipole and measured voltage.

Question 42

What factors does the measured potential depend on?

Answer 42

Magnitude of charges (dipole) Orientation of dipole & electrodes Distance between dipole and electrodes

Question 43

What factors does the measured potential depend on?

Answer 43

Magnitude of charges (dipole) Orientation of dipole & electrodes Distance between dipole ad electrodes

Question 44

Wave front dipole - propagating wave The resting potential of non active tissue inside is ——-, in cardiac tissue about —– and outside is ——–. As the wave of activation spreads, the cells ——- and you get ——– rushing into the cells making the membrane potential ——–, therefore the extracellular space becomes relatively more ———-. ECG is measuring from the —– of the body, so what we see is measured from the —– fluid ECG recording is designed so that we get a +ve deflection when +ve pole faces the +ve electrode.

Answer 44

The resting potential of non active tissue inside is negative, in cardiac tissue about -80 and outside is positive. As the wave of activation spreads, the cells depolerize and you get sodium rushing into the cells making the membrane potential positive, therefore the extracellular space becomes relatively more negative. ECG is measuring from the outside of the body, so what we see is measured from the extracellular fluid ECG recording is designed so that we get a +ve deflection when +ve pole faces the +ve electrode.

Question 45

A bipolar system measures the difference in potential between —- electrodes. Potentials are recorded between combinations of –,– and –

Answer 45

A bipolar system measures the difference in potential between 2 electrodes. Potentials are recorded between combinations of RA, LA and LL.

Question 46

What are the 3 standard bipolar limb leads?

Answer 46

Lead l = LA-RA Lead ll = LL-RA Lead lll = LL-LA

Question 47

At any instant during the cardiac cycle: Lead – + Lead—– = Lead —-

Answer 47

Lead l + Lead lll = Lead ll

Question 48

A unipolar system measures potential of —– electrode relative to some constant reference. To use unipolar leads we need to form a —— lead. All —– electrodes are connected together into one end of the ——– called the wilson’s central terminal. This can be the ——- lead. The combination of the —- electrodes during the cardiac cycle gives a constant voltage of —V as the volts —– each other out. We have another electrode which is the ——– electrode. If the ——- is facing the —— electrode a ——– deflection is recorded. One end of the electrode (negative) is in the centre of the chest and can be paired up with VR, VL or VF

Answer 48

A unipolar system measures potential of 1 electrode relative to some constant reference. To use unipolar leads we need to form a reference lead. All 3 electrodes are connected together into one end of the voltmeter called the wilson’s central terminal. This can be the reference lead. The combination of the 3 electrodes during the cardiac cycle gives a constant voltage of 0V as the volts cancel each other out. We have another electrode which is the exploring electrode. If the dipole is facing the exploring electrode a positive deflection is recorded. One end of the electrode (negative) is in the centre of the chest and can be paired up with VR, VL or VF

Question 49

What set of leads are used to measure the electrical activity in the horizontal plane?

Answer 49

Unipolar chest leads V1-V6

Question 50

How is the cardiac vector seen by leads l, ll and lll.

Answer 50

Lead 1&3 - see a smaller projection than the actual dipole Lead 2 - closer to the orientation of the dipole so bigger projection

Question 51

Sarcomere length tension relationship The —— force that can be generated by skeletal muscle is proportional to the ——– length. The normal operating zone is between 1.8-2.2μm. This is when the maximum — heads are binding to the —- fibres. It’s seen on the graph as a ——- phase. ——- tension only increases when the sarcomeres are at long lengths. The ——– myocytes operate over a much ——– zone of the sarcomere length than —— muscle, which is due to their ——— - there is much stronger ——– tissue that’s much more restrictive The ——– stiffness of cardiac muscle limits ———. The —— myocytes have length dependent activation. This means that the force generated by the cardiac myocyte at different lengths is not just driven by the __-___ interaction. Its also driven by ——-. The cardiac myocyte changes how it deals with the release of ——— at different lengths. This means a smaller change in ——– can give a greater force in cardiac vs skeletal muscle As length increases there is an ———- sensitivity to ———, so as the myocyte gets ————you get a ———- contractile response for the same input of ———-. Increased Ca2+ sensitivity of Troponin - C at greater sarcomere lengths Increased Ca2+entry through stretch activated channels at greater SL

Answer 51

The active force that can be generated by skeletal muscle is proportional to the sarcomere length. The normal operating zone is between 1.8-2.2μm. This is when the maximum myosin heads are binding to the actin fibres. It’s seen on the graph as a plateau phase. Passive tension only increases when the sarcomeres are at long lengths. The cardiac myocytes operate over a much shorter zone of the sarcomere length than skeletal muscle, which is due to their structure - there is much stronger connective tissue that’s much more restrictive The passive stiffness of cardiac muscle limits stretch. The cardiac myocytes have length dependent activation. This means that the force generated by the cardiac myocyte at different lengths is not just driven by the myosin-actin interaction. Its also driven by calcium. The cardiac myocyte changes how it deals with the release of calcium at different lengths. This means a smaller change in calcium can give a greater force in cardiac vs skeletal muscle As length increases there is an increased sensitivity to calcium, so as the myocyte gets longer you get a greater contractile response for the same input of calcium. Increased Ca2+ sensitivity of Troponin - C at greater sarcomere lengths Increased Ca2+entry through stretch activated channels at greater SL

Question 52

What causes the release of calcium from the sarcoplasmic reticulum in skeletal muscle?

Answer 52

Depolarization - Sodium influx

Question 53

What causes the release of calcium from the sarcoplasmic reticulum in cardiac muscle?

Answer 53

Calcium

Question 54

Myocardial contraction Action potential (triggered by ——-) Inward ——— current through ——- channels ——- induces rapid —— release from ——— ——-. ——- binds to ____-__ and starts cycle of ——— interactions for contraction.

Answer 54

Action potential (triggered by -sodium) Inward calcium current through calcium channels calcium induces rapid calcium release from sarcoplasmic reticulum. Calcium binds to Troponin-C and starts cycle of filament interactions for contraction.

Question 55

Myocardial relaxation Removal of ——- from cytoplasm via; ——– ——- calcium ATPase (reuptake of calcium) —— ——- exchange out of cell (Na+ gradient) ———- Ca2+ ATPase As the calcium concentration drops the calcium will unbind form ___-__ and the contractile proteins will relax.

Answer 55

Removal of calcium from cytoplasm via; sarcoplasmic reticulum calcium ATPase (reuptake of calcium) sodium calcium exchange out of cell (Na+ gradient) sarcolemma Ca2+ ATPase As the calcium concentration drops the calcium will unbind from Troponin-C and the contractile proteins will relax

Question 56

Factors influencing the inotropic state of cardiac muscle: Action Potential duration ↑ AP ——– length –> ↑ —— influx so increased —– release –> ↑ ——- state External Ion Concentrations ↑ external —— –> ↑ —— because increased ——- –> ↑inotropic state Lower external —— —> slows ——- —— exchange —> —– accumulates inside –> ↑ inotropic state Heart rate ———- heart rate—> more —- entry due to more —– —> —– time for calcium —— —-> Ca2+ accumulation –> ↑ inotropic state Calcium removal is depended on the time that the ——– have to get it out of the cells. The amount of calcium that comes in changes with rate because the number of openings of the channels changes as well with rate. Neurotransmitters ——- and ———- - SNA, act through beta receptors Mainly through activation of _-____ pathways adrenergic agonist Cause phosphorylation of —— channels making them be open for longer Phosphorylation of phospholamban - increased rate of pump to remove calcium, so that relaxation can occur faster Cholinergic muscarinic agonist (PNS) Reduction of [Ca2+]i decreased inotropic state Hormones and Drugs Xanthines (eg. caffeine) Prevents cAMP breakdown —> increased inotropic state Cardiac Glycosides (eg. digoxin - short term, the underlying damage continues to accumulate) Inhibit Na+/K+ pump so there is an accumulation of Na inside the cell. Diminished Na+ gradient. Slow Na+/Ca2+ exchange . Ca2+ accumulation inside cell. Increased inotropic state Calcium channel blockers (eg. verapamil) reduce Ca2+ entry across sarcolemma => decreased inotropic state Ischaemia and heart failure negative inotropic influences. They reduce the ability of the heart to generate force

Answer 56

Action Potential duration ↑ AP plateau length –> ↑ calcium influx so increased calcium release –> ↑ inotropic state External Ion Concentrations ↑ external calcium –> ↑ influx because increased gradient –> ↑inotropic state Lower external sodium —> slows sodium calcium exchange —> calcium accumulates inside –> ↑ inotropic state Heart rate increased heart rate—> more calcium entry due to more action potentials —> less time for calcium removal —-> Ca2+ accumulation –> ↑ inotropic state Calcium removal is depended on the time that the channels have to get it out of the cells. The amount of calcium that comes in changes with rate because the number of openings of the channels changes as well with rate. Neurotransmitters Adrenaline and nor adrenaline - SNA, act through beta receptors Mainly through activation of G-protein pathways adrenergic agonist Cause phosphorylation of calcium channels making them be open for longer Phosphorylation of phospholamban - increased rate of pump to remove calcium, so that relaxation can occur faster, decreased inotropic state Cholinergic muscarinic agonist (PNS) Reduction of [Ca2+]i decreased inotropic state Hormones and Drugs Xanthines (eg. caffeine) Prevents cAMP breakdown —> increased inotropic state Cardiac Glycosides (eg. digoxin - short term, the underlying damage continues to accumulate) Inhibit Na+/K+ pump so there is an accumulation of Na inside the cell. Diminished Na+ gradient. Slow Na+/Ca2+ exchange . Ca2+ accumulation inside cell. Increased inotropic state Calcium channel blockers (eg. verapamil) reduce Ca2+ entry across sarcolemma => decreased inotropic state Ischaemia and heart failure negative inotropic influences. They reduce the ability of the heart to generate force

Question 57

stroke volume = __ -__

Answer 57

SV = End diastolic volume - end systolic volume

Question 58

Cardiac output = __x__

Answer 58

CO = Heart rate x Stroke volume

Question 59

Preload = —— —– —–

Answer 59

End diastolic volume or pressure

Question 60

Preload is the degree of —- of the muscle just before ——. It determines the —— overlap (length - tension relation) and length dependent activation. As preload increase stroke volume —— and maximum potential pressure ——.

Answer 60

Preload is the degree of stretch of the muscle just before contraction. It determines the filament overlap (length - tension relation) and length dependent activation. As preload increases, stroke volume increases and maximum potential pressure increases.

Question 61

What is Stroke Work?

Answer 61

Work = Pressure x Volume Work = MAP x SV

Question 62

What is inotropic state?

Answer 62

Influencing muscular contractility: increasing or decreasing the force of muscular contractions

Question 63

High blood pressure causes death by ——- —— disease or ——– There is a —— relationship between your risk of death and your systolic pressure - the higher your systolic pressure the ——- the risk of coronary artery disease or stroke. So the lower the BP the better it is

Answer 63

High blood pressure causes death by coronary artery disease or stroke There is a linear relationship between your risk of death and your systolic pressure - the higher your systolic pressure the greater the risk of coronary artery disease or stroke. So the lower the BP the better it is

Question 64

Big arteries have a high —— component and are very ——-. Therefore the —– helps to buffer the big swings in —— when the heart is —— and ——-, allowing the flow in the rest of the body to be continuous. Arterioles - all the blood vessels that are leading up to the ——- and end ——, controlling the blood flow to the particular organs depending on its ——. The high component of —– muscle allows this to happen by regulating the —— size and thus ——-. The high ——- means that you will see a big drop in ——– in that area. Capillaries - ——— thin wall Venules - connect ——- to bigger ——–. Veins ——– of the blood is stored here. High —— tissue, floppy, —— wall to lumen ratio although the wall is —- compared to arterioles, ——– muscle - can control the —— in the veins but because of the large ——– and the pressure is —– that doesn’t change the ——– much. If you squeeze a vein it will push the blood back to the heart, increasing —— but not changing ———.

Answer 64

Big arteries have a high elastic component and are very stretchy. Therefore the aorta helps to buffer the big swings in pressure when the heart is ejecting and relaxing, allowing the flow in the rest of the body to be continuous. Arterioles - all the blood vessels that are leading up to the capillaries and end organs, controlling the blood flow to the particular organs depending on its need. The high component of smooth muscle allows this to happen by regulating the lumen size and thus resistance. The high resistance means that you will see a big drop in pressure in that area. Capillaries - endothelium thin wall Venules - connect capillaries to bigger veins. Veins - most of the blood is stored here. High elastic tissue, floppy, thin wall to lumen ratio although the wall is thick compared to arterioles, smooth muscle - can control the resistance in the veins but because of the large capacity and the pressure is low that doesn’t change the pressure much. If you squeeze a vein it will push the blood back to the heart, increasing preload but not changing pressure.

Question 65

Capacitance A measure of the —– to —— relationship over the entire P/V curve. Reflects the storage capacity of the vessels. Capacitance = Change in ——/change in ——- Veins = capacitance vessels - they can store large amounts of blood volume with little change in ——. When they —— large quantities of blood are transferred to the heart thereby increasing ——- —–. About —- of your blood volume is held in the veins and — is held in the arteries. (ratio = 3:1)

Answer 65

Capacitance A measure of the volume to pressure relationship over the entire P/V curve. Reflects the storage capacity of the vessels. Capacitance = Change in volume/change in pressure Veins = capacitance vessels - they can store large amounts of blood volume with little change in pressure. When the constrict large quantities of blood are transferred to the heart thereby increasing cardiac output. About ⅔ of your blood volume is held in the veins and ⅓ is held in the arteries. (ratio = 3:1)

Question 66

Compliance The ability to hold —- at a certain —–. Initially the relationship in veins is very —— so they are very compliant. When they are about 300 times their initial volume then the ——– starts to rise and the compliance starts to ——–. Arteries are more linear across the whole range of pressures. They are ——-, dont have the —— and don’t ——– the same as the veins. As a result they have ——— compliance, so their ability to —- their volume is not as good as a vein at their working pressure Compliance doesn’t effect the MAP

Answer 66

The ability to hold volume at a certain pressure. Initially the relationship in veins is very steep so they are very compliant. When they are about 300 times their initial volume then the pressure starts to rise and the compliance starts to decrease. Arteries are more linear across the whole range of pressures. They are stiffer, dont have the elastin and don’t collapse the same as the veins. As a result they have decreased compliance, so their ability to increase their volume is not as good as a vein at their working pressure Compliance doesn’t effect the MAP

Question 67

What are the values of normal mean arterial BP, systolic BP (max) and diastolic BP (minimum)?

Answer 67

MAP = 100 mmHg systolic = 120 mmHG diastolic = 90 mmHg

Question 68

MAP=__+ __(__-__)

Answer 68

MAP= Pd+ 1/3 (Ps - Pd)

Question 69

Pulse pressure = (__-__)

Answer 69

PP= Ps-Pd

Question 70

Aortic compliance and pulse pressure. During —— the aorta stretches to absorb the blood. Blood will continue to flow in ——- due to the aorta being —— out in ——-. Therefore the ——– pressure is going to be relatively ——. The more compliant large blood vessels are the —- the pulse pressure. If the aorta is compliant it stretches and absorbs the volume of blood then the pressure isn’t going to be too high. If the aorta can’t stretch and absorb the volume of blood the pressure is going to be high. Someone with a stretchy aorta (healthy) will have a not too high systolic and diastolic pressure. Therefore will have a —- pulse pressure Someone who doesn’t have a stretchy aorta (not healthy) will not be able to —— the volume of blood, so the —— pressure is going to be high, but because the blood is not absorbed the —— pressure is going to be lower. This means that this person will have a —– pulse pressure

Answer 70

During systole the aorta stretches to absorb the blood. Blood will continue to flow in diastole due to the aorta being stretched out in systole. Therefore the diastolic pressure is going to be relatively high. The more compliant large blood vessels are the smaller the pulse pressure. If the aorta is compliant it stretches and absorbs the volume of blood then the pressure isn’t going to be too high. If the aorta can’t stretch and absorb the volume of blood the pressure is going to be high. Someone with a stretchy aorta (healthy) will have a not too high systolic and diastolic pressure. Therefore will have a small pulse pressure Someone who doesn’t have a stretchy aorta (not healthy) will not be able to absorb the volume of blood, so the systolic pressure is going to be high, but because the blood is not absorbed the diastolic pressure is going to be lower. This means that this person will have a high pulse pressure

Question 71

Pulse pressure —— with age due to ——- compliance. As a result of a decrease in compliance systolic pressure ——— and diastolic pressure may ——–. A less compliant aorta will result in a —– pulse pressure.

Answer 71

Pulse pressure increases with age due to decreased compliance. As a result of a decrease in compliance systolic pressure increases and diastolic pressure may decrease. A less compliant aorta will result in a larger pulse pressure

Question 72

Increasing stroke volume delivered to the aorta increases arterial pulse pressure. Systolic pressure increases in exercise because the stroke volume has increased. The more volume that comes out the higher the pressure will be. Has the compliance changed?

Answer 72

No

Question 73

Diastolic pressure is determind by the ability of blood to flow ——–. This in turn is dependent on —— —- —— and — ——. Slow heart rate = ——- diastole = blood pressure continues to —- for longer = diastolic pressure ——- High resistance downstream = ——– for blood to flow forward = ——- diastolic pressure During exercise the ——– pressure increases due to increased ——- ——-. The —– pressure decreases because the ——– decreases to allow more blood flow to the organs. This is why sometimes the mean pressure doesn’t change much during exercise. If its cold then the diastolic pressure goes up during exercise

Answer 73

Diastolic pressure is determind by the ability of blood to flow forward. This in turn is dependent on total peripheral resistance and heart rate. Slow heart rate = longer diastole = blood pressure continues to decrease for longer = diastolic pressure decreases High resistance downstream = harder for blood to flow forward = increased diastolic pressure During exercise the systolic pressure increases due to increased stroke volume. The diastolic pressure decreases because the resistance decreases to allow more blood flow to the organs. This is why sometimes the mean pressure doesn’t change much during exercise. If its cold then the diastolic pressure goes up during exercise

Question 74

Q Arterial pressure regulation Different mechanisms dominate in blood pressure control over different time scales. Short term - nerual reflexes such as baroreceptors, chemoreceptors and the CNS ischemic response. Minutes to hours - hormonal (Angi ll) and fluid shifts Hours to days - blood volume regulation via renal mechanisms. Can you control blood pressure without baroreceptors?

Answer 74

Yes

Question 75

Arterial baroreceptor reflex The carotid baroreceptors are in the ——– ——- with their nerve endings locating in the ———–. They sense ——– in the arteries. The —– ——- nerve goes into the ———— nerve up to the—— in the brain The receptors respond to ——– changes not ——— changes. ———– changes can result in the baroreceptors moving to the new mean pressure. If the arteries can’t —— then even if the pressure increases the baroreceptors can’t fire. Increase in arterial pressure results in an ——– in baroreceptor firing due to increased ———. This causes an ——– in PNS which decreases —— —–, therefore decreases —- —-and a ——— in SNS due to the —— inhibiting the —— which results in decreased —- and ——–. There is decreased —– —— and decreased vascular ——— resulting in a ——– arterial pressure.

Answer 75

Arterial baroreceptor reflex The carotid baroreceptors are in the carotid sinus with their nerve endings locating in the adventitia. They sense stretch in the arteries. The carotid sinus nerve goes into the glossopharyngeal nerve up to the NTS (nucleus tractus soltarius) in the brain The receptors respond to sudden changes not gradual changes. Gradual changes can result in the baroreceptors moving to the new mean pressure. If the arteries can’t stretch then even if the pressure increases the baroreceptors can’t fire. Increase in arterial pressure results in an increase in baroreceptor firing due to increased stretch. This causes an increase in PNS which decreases HR, therefore decrease CO and a decrease in SNS due to the CVLM inhibiting the RVLM which results in decreased HR and vasodilation. There is decreased cardiac output and decreased vascular resistance resulting in a decreased arterial pressure.

Question 76

What is the equation for blood flow?

Answer 76

Blood flow (Q) = change in pressure (P) / resistance (R)

Question 77

Blood flow to tissues is controlled in relation to tissue ——.

Answer 77

Needs

Question 78

When talking about the whole body blood flow = —– —–

Answer 78

cardiac output

Question 79

To increase blood flow increase the —— of the blood vessel, or ————.

Answer 79

To increase blood flow increase width of blood vessel, or vasodilate

Question 80

Blood flow determines —— —- and —— —–

Answer 80

Blood flow determines heart rate and stroke volume

Question 81

Pressure Change in pressure = ___ x _____ MAP = —- x —- Anything that increases , —- —, —— —– or ——– will increase pressure Change in pressure = —— usually in theory because —– pressure is minimal so it can be ignored. If cardiac output increases during exercise resistance decreases to maintain the same mean arterial pressure

Answer 81

Pressure Change in pressure = blood flow x Resistance MAP = CO x TPR Anything that increases , blood flow, cardiac output or resistance will increase pressure Change in pressure = MAP usually in theory because venous pressure is minimal so it can be ignored. If cardiac output increases during exercise resistance decreases to maintain the same mean arterial pressure

Question 82

Resistance in series

Answer 82

Rtotal = R1 + R2+ R3...

Question 83

Resistance in series:

Answer 83

1/Rtotal = 1/R1 + 1/R2 + 1/R3...

Question 84

Approx relative resistances

Answer 84

RA = 20 Ra = 50 Rc = 20 Rv = 6 RV = 4

Question 85

Mean velocity equation

Answer 85

Q = v x A

Question 86

Jean Poiseuille flow

Answer 86

as radius increases, the flow increases and pressure decreases

Question 87

Resistance to blood flow

Answer 87

Resistance is proportional to: The tube length (L) The viscosity of fluid (n) and inversely proportional to the radius raised to the fourth power.

Question 88

Determinants of blood viscosity

Answer 88

Temperature - gets thicker as it gets colder Haematocrit - as Hct rises so does viscosity Shear rate (velocity) - viscosity increases as cells aggregate Vessel diameter - in very small blood vessels there is an apparent decrease in viscosity

Question 89

Assumptions of Poiseuilles equation

Answer 89

steady laminar flow rigid straight tube Newtonian fluid

Question 90

Changing pressure in BV

Answer 90

Increasing pressure: Distension of blood vessel Reduced resistance Increased blood flow Decreasing pressure Reduced stretch of vessels Increased resistance Decreased blood flow

Question 91

What is CCP

Answer 91

Critical closing pressure - the internal pressure at which a blood vessel collapses and closes completely

Question 92

Endothelium and shear stress

Answer 92

As flow increases, shear stress increases causing: NO release and vasodilation potentially damaging endothelium

Question 93

Factors resulting in turbulence

Answer 93

High fluid densities Large tube diameter High flow velocities Low fluid viscosities

Question 94

Reynolds number

Answer 94

Helps predict fluid flow patterns. An increase in diameter, increase in velocity or decrease in viscosity will lead to increase in Re. Turbulent flow exceeds 2000 of Reynold number

Question 95

Change in pressure =

Answer 95

P = CO x R

Question 96

Driving pressure

Answer 96

The pressure gradient between two points. The driving pressure governs blood flow

Question 97

Transmural Pressure

Answer 97

The pressure across the vessel wall

Question 98

Hydrostatic Pressure

Answer 98

Dependent on gravity

Question 99

Transmural equation

Answer 99

P = Pi - Po

Question 100

Laplace Equation

Answer 100

T = (P*r)/wall thickness

Question 101

Hypertension contributions

Answer 101

ANG II, VGF, endothelin, oxidative stress increases wall tension and cause remodelling to thicker, stiffer walls with smaller lumen

Question 102

Aneurysm

Answer 102

Thinning of vessel wall Radius increases Wall tension increases Bursts!

Question 103

Describe the effect of gravity on blood pressure

Answer 103

Blood pressure drops as height increases

Question 104

Sympathetic activity on vascular resistance

Answer 104

NE released from sympathetic terminals binds to a1-adrenoceptors leading to vasoconstriction.

Question 105

Vasodilation

Answer 105

Occurs in response to epinephrine released from adrenal medulla which activates B2-adrenergic receptors

Question 106

A1-adrenoceptors

Answer 106

Linked to G-protein receptors that activate smooth muscle contraction through IP3 pathway.

Question 107

B2-adrenoceptors

Answer 107

Act via cAMP to inhibit myosin light chain kinase, inhibiting contraction. Salbutamol is an agonist and used for asthma

Question 108

Factors promoting dilation

Answer 108

Decreased O2 Increased CO2 and H+ Lactic acid Adenosine, prostaglandins and nitric oxide (NO) from endothelial cells Rising K+ and H+ in interstitial fluid Histamine Elevated temps

Question 109

Reactive hyperaemia

Answer 109

Blood flow is restored after a brief occlusion above pre-occlusion levels for a period and is driven by metabolites

Question 110

Vaping

Answer 110

Leads to impaired vascular function

Question 111

Myogenic autoregulation

Answer 111

Ca2+ influx by stretch channels leads to depolarisation. If pressure increases, vessel constricts normalizing flow.

Question 112

Blood pressure control in exercise

Answer 112

Exercise increases sympathetic activity and decreases parasympathetic activity, increasing HR, CO, contractility and blood pressure.

Question 113

Coupling factors

Answer 113

Preload and afterload are in part dependent on vascular function = coupling factors

Question 114

Cardiac output equations

Answer 114

CO = SV x HR CO = change in P / TPR

Question 115

Cardiac output curve

Answer 115

Plateau determined by heart strength (contractility x HR) Cardiac output is dependent on venous return (preload)

Question 116

Determinants of venous return

Answer 116

Dependent on pressure gradient (Pa - Pv) and vascular resistance Venous return = (Pa-Pv)/R Pv = right atrial pressure and is dependent on degree of filling (blood volume and venous capacitance)

Question 117

Normal values for Pa and Pv

Answer 117

Pa = 100 Pv = 0

Question 118

Normal value for Cardiac output

Answer 118

6L/min

Question 119

What happens to Pa and Pv if CO = 0

Answer 119

Pa drops to 0 and Pv will go up to equalize at 7mmHg

Question 120

Systemic filling pressure

Answer 120

Pressure gradient is dependent on cardiac output. Increasing cardiac output will increase arterial and reduce right atrial pressure

Question 121

Mean systemic filling pressure (MSF)

Answer 121

Pressure in the system when cardiac output = 0 MSF usually about 7mmHg

Question 122

Vascular function curve (Venous Return)

Answer 122

1. As right atrial pressure increase venous return decreases (due to pressure gradient) 2. Venous return = 0 once right atrial pressure = mean systemic filling pressure 3. The plateau is caused by large vein collapsing as they enter the chest if the pressure is lower than atmospheric 4. Usual right atrial pressure is 0-2mmHg, resulting in a venous return of about 5L/min

Question 123

Blood volume and MSFP

Answer 123

5000mL - 7mmHg MSFP 4000mL - 0 mmHg MSFP

Question 124

MSFP and venous compliance (sympathetic tone)

Answer 124

Increasing blood volume of increasing sympathetic stimulation dramatically increases MSFP

Question 125

Effect of filling pressure on venous return

Answer 125

change in P = Change in V / C At any given right atrial pressure, as MSFP increases, venous return increases Increased blood volume = increased PSF Decreased capacitance (increased venous tone) = PSF

Question 126

Vascular resistance and filling pressure

Answer 126

Increased SNA leads to increased vascular resistance and increased venous tone, increasing PSF

Question 127

Cardiac function curve

Answer 127

Increased sympathetic stimulation results in increased CO at any filling pressure due to increase in inotropy and HR

Question 128

Guyton Analysis

Answer 128

At steady state: CO = Venous return e.g Blood tranfusion Increase in mean systemic filling pressure = increase in venous return = increase cardiac output at higher RA pressure

Question 129

Venous return factors

Answer 129

Increased venous tone (increased filling pressure) Increased resistance (decreasing slope on CO against PRa)

Question 130

Lying to standing

Answer 130

Immediately on standing venous return is decreased due to venous pooling. Sympathetic stimulation increases it

Question 131

Exercise

Answer 131

Sympathetic stimulation - increased MSFP as a result of decreased capacitance. Decrease in systemic resistance and increased ventilation and muscle pumps assist venous return

Question 132

Cycle of heart failure

Answer 132

Myocardial injury -> decreased ventricular performacne -> decreased cardiac output -> increased sympathetic activity -> Vasoconstriction, Na & h20 retention -> increased demand on the heart -> myocardial injury

Question 133

Treating heart failure

Answer 133

Diuretics - reduce venous pressure (RAP), reduce oedema - but will reduce output ACE inhibitors/ARB - vasodilation, reduces remodelling, reduce blood volume Beta blockers - reduce energy demand by reducing cardiac function (also reduces chance of arrhythmias)

Question 134

Relation with HR and SNA

Answer 134

Similar As HR drops, SNA drops as HR increases, SNA increases

Question 135

Sympathetic pathway neurotransmitter and receptor

Answer 135

Norepinephrine and Adrenergic receptor

Question 136

Parasympathetic pathway neurotransmitter and receptor

Answer 136

Acetylcholine and muscarinic receptor

Question 137

Parasympathetic and sympathetic fibres

Answer 137

p = short S = long

Question 138

Varicosity

Answer 138

Vesicle containing neurotransmitter and mitochondrion

Question 139

Nucleus tractus solitarius

Answer 139

Receive input from baro and chemo receptors

Question 140

Rostro-ventro-lateral medulla

Answer 140

Origin of all sympathetic output

Question 141

Heart rate and respiration before exercise

Answer 141

Increases before the onset of exercise

Question 142

Blood pressure after ischemic stroke

Answer 142

Increases Post-stroke hypertension is driven by the sympathetic nervous system

Question 143

Consequences of high blood pressure after stroke

Answer 143

Haemorrhage Oedema Arrhythmias Reperfusion injury