The Heart

Question 1

How does the Langendorff heart allow for in vivo experimentation?

Answer 1

The heart is removed from an animal, blood vessels are severed. Heart is then perfused via aorta with a nutrient rich oxygenated solution. Backwards pressure causes aortic valve to shut, forces the solution into coronary arteries. This allows the cardiac muscle to continue beating for hours after removal from the animal.
Allows addition of drugs via the perfusate solution to see the effects on the heart, without complications of in vivo experimentation.

Question 2

Describe the pathway of electrical impulse through the heart

Answer 2

The sino atrial node spontaneously depolarises. This electrical signal moves across the atria to the atrioventricular node. It then moves down the septum and into the bundle of His, and from there it reaches the Purkinje fibres. This action causes the ventricles to contract from the bottom upwards.

Question 3

What are cells in the myocardium capable of?

Answer 3

All capable of showing spontaneous electrical activity in suitable conditions. This means that they are all potential pacemaker cells.

Question 4

Which is the dominant pacemaker?

Answer 4

The SA node. Has the highest frequency of 100/s.

Question 5

Which pacemaker is the AV node?

Answer 5

It is the secondary pacemaker. Takes role of SAN if it fails. Frequency of 40-60/s.

Question 6

What are tertiary pacemakers?

Answer 6

Anything below the AVN with a low frequency. This is the bundle of His and Purkinje fibres. Frequency of 30-40/s. Can still work is AVN fails.

Question 7

What is the ectopic pacemaker?

Answer 7

Group of excitable cells that causes a premature heartbeat separate to the normal function of the SAN.
Chronic occurrence can lead to tachycardia (fast heart beat), bradycardia (slow heart beat) or ventricular fibrillation.

Question 8

What property of cardiac muscle allows rapid, coordinated contraction?

Answer 8

The fact that cardiac muscle forms a syncytium (fusion of two or more cells in a cytoplasmic mass) means that contraction is coordinated along the whole length of cardiac muscle.

Question 9

Describe 5 features of cardiomyocytes

Answer 9

1) Fibres that branch and allow electrical waves to spread through the muscle.
2) Centrally located nuclei in each cell.
3) Intercalated discs that are the sites of attachment between cells.
4) T-tubules that carry the action potential to myocytes.
5) Sarcoplasmic reticulum that contains Ca2+, its release leads to contraction of the cardiac muscle (binds to troponin which uncovers the tropomyosin from actin binding sites).

Question 10

State a similarity between the action potential in the SAN and AVN.

Answer 10

Both action potentials show a fast depolarisation, then a plateau phase at the peak of the curve, then repolarisation of the cell.

Question 11

State 2 differences between the action potential in the SAN and AVN.

Answer 11

1) There is a second plateau phase in the ventricle that is not present in the SAN action potential. This is because it takes time for the Ca2+ channels to open and for the influx of ions to cause a contraction. The outward movement of K+ from the membrane means the membrane potential becomes positive at a slower rate.
2) The resting membrane potential is not as stable in the SAN than the ventricles. This is because repolarisation is followed immediately by another spontaneous depolarisation in the SAN (due to hyper polarisation in the SAN).

Question 12

Outline phase 0 in the action potential in the heart

Answer 12

Fast depolarisation of the membrane when the Na+ channels open, large influx of Na+ into the cell. Larger influx in the ventricles.
In excitatory cells that generate an action potential the influx depends on Ca2+ influx not Na+. (Means that rate of action potential is slower, outward K+ movement also slows down rate of depolarisation).
Once membrane reaches potential of 0mV it goes slightly above (overshoot period) and this triggers Na+ channels to close.
L-type Ca2+ channels open when the membrane potential is greater than -40mV. This is a small influx of Ca2+ down it concentration gradient.

Question 13

Outline phase 1 in the action potential in the heart

Answer 13

Small repolarisation of membrane due to closure of L-type Ca2+ channels, with the movement of K+ out of cells and Cl- into cells.
Only occurs in ventricle action potential as the ventricles contract (Ca2+ needed for contraction), the SAN doesn’t contract.

Question 14

Outline phase 2 in the action potential in the heart

Answer 14

Plateau that occurs during influx of Ca2+. The L-type Ca2+ open so there is a constant inward flow of Ca2+. At the same time K+ moves out of the cell down a concentration gradient.
These oppose each other so depolarisation occurs slowly. (More Ca2+ enters than K+ leaves).
Only occurs in ventricles as contraction only occurs here.

Question 15

Outline phase 3 in the action potential in the heart

Answer 15

Repolarisation of the membrane. L-type Ca2+ channels close, and movement of K+ out of the cells decreases the membrane potential. Na+ and Ca2+ returned to the extracellular environment through Na+/K+ATPase pumps that use energy to move 3Na+ out for 2K+ into the cell.
Overall effect restores there membrane potential.

Question 16

Outline phase 4 in the action potential in the heart

Answer 16

Resting membrane potential of the cell. This is not stable in the SAN due to constant leak of K+ through inward rectifier channels.
This causes hyper polarisation in those cells. The hyper polarisation is a trigger for the spontaneous depolarisation of the SAN.
The Na+ and Ca2+ channels are closed.

Question 17

How can the rate of spontaneous depolarisation in the SAN be changed?

Answer 17

1) The rate of reaching the threshold is changed by presence of either more or less ions in the cell, therefore more/less ions have to move into the cell to cause the depolarisation. The less steep the spontaneous depolarisation, (longer it takes to reach threshold) the later the action potential, therefore heart rate will be lower.
Threshold reached faster = tachycardia
Threshold reached slower = bradycardia

2) The threshold itself can be increased or decreased. Ion channels in the cells of the SAN can be altered to open at a different threshold value (not -40mv). The greater the threshold the more depolarisation needed to reach threshold, longer it takes for action potential to occur, results in a slower heart rate.

3) The resting potential of the cell can be changed. The ion channels in the membrane of SAN cells can be altered to change the resting potential. If resting potential is lowered then more depolarisation needs to occur for threshold to be reached. Will take longer for action potential to be made, so heart rate is lowered.

Question 18

What is myosin?

Answer 18

Thick filaments with globular heads spaced along the length. Contains ATPase to help the detachment of myosin heads from the actin. ADP required for attachment of myosin to actin.

Question 19

What is actin?

Answer 19

Thin filament consisting of 2 strands arranged as a alpha helix. Has binding sites for myosin heads.

Question 20

What is tropomyosin?

Answer 20

Double helix structure that lies in the grooves of actin filaments. In its resting state it prevents contraction by covering the binding sites so myosin head cannot bind to the actin.

Question 21

What is troponin?

Answer 21

Complex located between actin and myosin.
When bound to actin and activated by Ca2+ ions it causes a conformational change in tropomyosin, which causes it to uncover the actin binding sites so contraction can occur.

Question 22

What are the 3 parts of troponin and their functions?

Answer 22

TnT = structural part of troponin
TnC = part of molecule where Ca2+ binds to cause the conformational change in tropomyosin
TnI = part of molecule that inhibits myosin from binding to actin, this moves away after the conformational change of tropomyosin.

Question 23

What are the 2 sources of Ca2+ that can cause contraction of cardiac muscle?
(in skeletal muscle only intracellular Ca2+ from the sarcoplasmic reticulum causes contraction)

Answer 23

1) Extracellular Ca2+ from the sarcolemma. T-tubule has L-type Ca2+ channels that allow Ca2+ to enter the cell.

2) Intracellular Ca2+ from the sarcoplasmic reticulum. When an action potential is detected from the T-tubules it causes Ca2+ to be released from the SR Ca2+ storage.

Question 24

What is the definition of excitation-contraction coupling?

Answer 24

It is the process of converting an electrical stimulus (action potential) to a mechanical response (contraction).

Question 25

Outline the first stage of EC coupling (combining action potential and contraction)
CONTRACTION

Answer 25

Action potential initiated by cells in the SAN and AVN.
Action potential travels along sarcolemma and T-tubules. This causes extracellular Ca2+ to enter cell through L-type Ca2+ channels. Ryanodine receptors on the sarcoplasmic reticulum detect this increase. As a result more Ca2+ is released from the SR. This therefore leads to intracellular Ca2+ levels increasing.
This Ca2+ can now cause contraction of the cardiac muscle by binding to TnC.

Question 26

Outline the second stage of EC coupling (combining action potential and contraction)
RELAXATION

Answer 26

Ca2+ ions have to be removed from the sarcoplasm in order to stop the contraction.
Two ways calcium levels return to base level.
1) Efflux - the Na+/Ca2+ exchanger in the sarcolemma and the Ca2+ ATPase pump both pump out Ca2+ ions from the sarcoplasm.

2) Re-uptake into SR - some Ca2+ is taken back into the sarcoplasmic reticulum. If the heart rate increases this uptake also has to occur at a faster rate.

Question 27

Outline the third stage of EC coupling (combine action potential and contraction)
REPOLARISATION

Answer 27

The refractory period is the time from phase 0 to the next possible depolarisation of a myocyte.
Cardiomyocytes have a longer refractory period than other muscle cells due to the long plateau from slow Ca2+ channels (allows time for the ventricles to empty and refill before the next contraction).

Question 28

What is the ERP (effective refractory period)?

Answer 28

Period of time where no new action potential can be triggered. The channels responsible for action potentials occurring are inactivated. Between phase 0 and 3.

Question 29

What is the RRP (relative refractory period)?

Answer 29

Potential for new action potentials with a lower amplitude to be triggered. Can lead to arrhythmias and heart beat will not be consistent. Between phase 3 and 4.

Question 30

What is the heart rate controlled by?

Answer 30

1) Controlled by the autonomic nervous system. Sympathetic = increases heart rate
Parasympathetic = decreases heart rate
Sympathetic nervous system can also regulate contractile force by directly innervating ventricular cardiomyocytes.

Question 31

What neurotransmitters are linked to sympathetic stimulation of ventricular myocytes?

Answer 31

Catecholamines
Epinephrine
Norepinephrine
These are coupled G protein receptors to the production of cAMP.

Question 32

Outline the regulation of contraction

Answer 32

Protein kinase A phosphorylates all the components of the introductory unit (calcium influx channels and calcium release channel).
Therefore increased sympathetic stimulation will increase the production of cAMP through the G protein coupled neurotransmitters. This activates more protein kinase A, so an increased number of components for Ca2+ ion channels are formed. This means more Ca2+ can enter the sarcomere, so the strength of the contraction will be greater as more Ca2+ can bind to troponin so tropomyosin is more likely to undergo its conformational change to expose the actin binding sites.

Question 33

Outline the regulation of relaxation

Answer 33

Protein kinase A also regulates the Ca2+ removal units. These are the sarcoplasmic reticulum Ca2+/ATPase reuptake pumps.
This pumps Ca2+ into the SR against their concentration gradient.
Ca2+ can also be removed from the cell through the Ca2+ATPase pump or the Na+/Ca2+ exchanger.

Phospholamban has an inhibitory function on the SRCa2+ATPase pumps. If it is not interacting with the pump then Ca2+ can enter the sarcoplasmic reticulum.
When phospholamban is phosphorylated by Protein Kinase A it can no longer interact with the pump so it detaches. This allows more Ca2+ to be pumped into the SR.
Shows that drugs that actively detach phospholamban from the SR pump can help to increase reuptake of Ca2+ ions (if a patient is not able to relax heart muscle).

Question 34

Describe thefunctionoftheNa+ channels present in the SAN and the ventricle

Answer 34

SAN = Ifunny channel
Responsible for spontaneous depolarisation and hyper polarisation of the membrane (excess K+ ions leaving the cell). This channel can be pharmacologically manipulated with drugs to control heart rate, as this will control how fast action potential can occur. (More hyper polarisation means slower heart rate).

Ventricle = Fast voltage dependent channels
Responsible for the large peak in the action potentials.

Question 35

What are the Ca2+ channels present in the SAN and ventricle?

Answer 35

SAN = L-type and T-type
Ventricle = L-type
L-type channels are less sensitive (takes more depolarisation for an action potential) and T-type channels are high sensitivity with a low threshold (doesn’t need much for an action potential to occur).

Question 36

Describe the K+ channels present in the SAN and ventricle

Answer 36

Both have = Inwardly rectifying , Delayed rectifier, ATP sensitive, Acetyl-choline sensitive channels.

Question 37

Describe the Cl- channels present in the SAN and ventricle

Answer 37

Only present in the ventricle!
Voltage dependant Cl- channels that move into cell due to concentration gradient.

Question 38

Name 2 receptor targets of Na+ receptors

Answer 38

Lidocaine, Procainamide

Question 39

Name 2 receptor targets of Ca2+ receptors

Answer 39

Verapamil, Nifedipine

Question 40

Name 2 receptor targets of K+ receptors

Answer 40

Dofetelide, Ibutilide

Question 41

Define what channelopathies are

Answer 41

Channelopathies are mutations in ion channels (usually K+ and Na+) that cause action potential generation.
Cannot see any problems with heart but these mutations cause 85% of sudden death syndromes.
Mutations of these ion channels are usually selected against in embryonic stages.
Can be diagnosed using an electrocardiodiagram.
Diseases such as long QT syndrome and idiopathic ventricular fibrillation can be caused by this.

Question 42

What is the desired effect of anti-arrhythmic and antihypertensive drugs?

Answer 42

1) These drugs are used to inhibit spontaneous action potential generation.
This is done by decreasing the frequency of impulses from the sympathetic nervous system to the SA node.
This results in inhibition of ventricular contraction, so the cardiac output is decreased (heart rate x stroke volume).
This means cardiac work and arterial blood pressure is also reduced.

2) The drugs can also promote vasodilation. This decreases peripheral resistance in the arteries, so decreased arterial blood pressure.

Question 43

What does an electrocardiodiagram do?

Answer 43

ECG’s record the fluctuation of electrical potential in the chest, and this reflects the cardiac action potentials on the surface of the heart.
Only measures potential difference between an active and resting part of the heart. This is because the movement of an action potential creates a potential vector which is connected to the surface of the body by electrolytes.
Measured with electrodes linked to a voltmeter.

Question 44

Explain the different parts of the normal ECG curve

Answer 44

Positive parts of the curve are where an action potential moves towards a positive pole.

First, the atria are activated = positive deflection = P wave

Time delay, electric activity is transferred to ventricles = QRS complex

Repolarisation is still a positive wave as the charge is becoming negative but also moving towards a negative pole. This cancels each other out to form a positive = T wave

Question 45

Fill the gap.
Repolarisation occurs at the places that are ____ to be activated.

Answer 45

Last

Question 46

Describe what happens in deranged EC coupling in heart failure

Answer 46

Overactivation of the sympathetic nervous system leads to hyper polarisation of all parts of the system - one of these include overphosphorylation of ryanodine receptors of the sarcoplasmic reticulum.
This causes them to become more leaky so Ca2+ leaves the SR even when not activated.
This will cause arrthymias as the heart will not be able to relax so will have an increased contractive state. This means the heart will not be able to contract as strongly.

Constant sympathetic activation of protein kinase A leads to less regulation of the SRCa2+/ATPase pump, due to lack of phospholamban binding. This results in less capacity for the SR pump to reuptake Ca2+, so there is less Ca2+ storage in the SR.

However, increased activity of the Na+/Ca2+ exchanger means more Ca2+ is completely removed from the cell so cannot be used for contraction.

Overall this results in deranged Ca2+ signalling and loss of contractile force.

Question 47

Define cardiodynamics

Answer 47

The changes in pressure and volume during the cardiac cycle

Question 48

Define cardiac output

Answer 48

Heart rate x Stroke volume

Question 49

Define ventricular systole

Answer 49

Contraction of the ventricles

Question 50

Define ventricular diastole

Answer 50

Relaxations and dilation of the ventricles

Question 51

Define stroke volume

Answer 51

The volume of blood pumped by the heart in one beat. It is measure as the EDV - ESV.

Question 52

Define the end diastolic volume

Answer 52

The volume of blood in the ventricles when full of blood, before the ventricles contract to move the blood to the aorta. Not much blood is flowing in the coronary arteries.

Question 53

Define the end systolic volume

Answer 53

The volume of blood in the ventricles when all blood has entered the aorta and diastole starts. This is when the aorta has the highest pressure and blood flows to the coronary arteries.

Question 54

Define the ejection fraction

Answer 54

The stroke volume ÷ End diastolic volume
This forms a ratio.
(How much is ejected in each stroke)

Question 55

Name the 4 valves of the heart

Answer 55

Tricuspid, Bicuspid(Mitral), Pulmonary, Aortic

Question 56

When does isovolumetric contraction occur?

Answer 56

Occurs during systole when the ventricles are already full of blood and the ventricle contracts from the base upwards.
There is a large increase in pressure with the same volume of blood.
Leads to ejection of blood out of the heart chamber.

Question 57

When does isovolumetric relaxation occur?

Answer 57

Occurs during diastole when the ventricles are now empty and begin to fill with blood from the atria.
There is a large increase in volume with little changes in pressure.
Leads to the filling pf the ventricles with blood.

Question 58

Are the mitral and tricuspid valves open or closed during isovolumetric contraction/relaxation?

Answer 58

The valves are all closed during these stages of the cardiac cycle.

Question 59

Which stage occurs after atrial systole?

Answer 59

Isovolumetric contraction occurs after atrial systole when the mitral valves close.

Question 60

What stage occurs after isovolumetric relaxation?

Answer 60

The mitral valves open and the ventricles fill up with blood from the atria.

Question 61

What stage occurs before isovolumetric relaxation?

Answer 61

The aortic valve closes.

Question 62

What stage occurs after isovolumetric contraction?

Answer 62

The aortic valve opens.

Question 63

What is on the x axis and y axis on a PV loop?

Answer 63

Volume is on the x axis and Pressure is on the y axis.

Question 64

Where is the end diastolic volume on the PV loop?

Answer 64

On the bottom right, where the volume of the ventricle is high and the pressure is low. (post diastole)

Question 65

Where is the end systolic volume on the PV loop?

Answer 65

On the top left, where the volume of the ventricle is low and the pressure is high. (post systole)

Question 66

Which direction does the blood flow in the PV loop?

Answer 66

From the bottom right upwards in systole the, from the top right downwards in diastole.

Question 67

Describe the sequence of events occurring in a PV loop

Answer 67

1) Just before ventricular contraction it is end diastolic volume, the ventricles are full and pressure is low. (Bottom Right)

2) Then isovolumetric occurs where the pressure increases with the same volume in the ventricles.

3) When the pressure exceeds the pressure in the aorta, the systole causes the aortic / pulmonary valves to open and forces blood into the aorta. This decreases the volume of blood and slightly decreases the pressure. This is end systolic volume.

4) Then isovolumetric relaxation occurs where the ventricles relax and pressure decreases, with the ventricles being empty. (Top Left)

5) During diastole the atria slowly fill up with blood. This does not increase the pressure, but only the volume of the ventricles. This complete the loop/

Question 68

What is the diastolic arterial pressure?

Answer 68

The is the pressure in the arterioles when the blood from the ventricles is being forced into the aorta.
This means it is measured when the ventricular blood pressure exceeds the aortic blood pressure.
(After end diastolic volume)

Question 69

What is the systolic arterial pressure?

Answer 69

This is the pressure in the arterioles when the blood has all been forced into the aorta.
It is measures as the peak of the PV loop as it is the maximum pressure reached.
(Before end systolic volume)

Question 70

What is the difference between the systolic arterial pressure and diastolic pressure called?

Answer 70

The Pulse Pressure.

Question 71

Define stroke work

Answer 71

The measure of the force of the output of the heart for the given distance the blood moves in the body.

Question 72

What measurement is given by the area of the PV loop?

Answer 72

The stroke work

Question 73

What is a principle of the ventricles that allows calculation of all PV loops?

Answer 73

Ventricles will expand accordingly when there is an increase in the volume of blood entering the heart.

Question 74

Describe the end diastolic pressure volume relationship

Answer 74

This is when the pressure in the ventricle is measured when it is relaxed and is being filled with blood.
The pressure gradually increases, forming a curved line.

Question 75

Describe the end systolic pressure volume relationship

Answer 75

This is when the ventricle contracts when the ventricle is full of blood. This forms a linear relationship as the pressure increases as the volume of blood in the ventricles is increased.

Question 76

Do all PV loops fit between the curved line of end diastolic pressure volume relationship and the linear end systolic pressure volume relationship>

Answer 76

Yes!
Those are the physiological boundaries of the contraction and filling of the ventricles.

Question 77

What is preload?

Answer 77

This is the passive tension in the myocardial fibres at end diastolic volume.
It is the wall stress on the ventricles.

Question 78

How do you calculate wall stress?

Answer 78

Pressure x Resistance
÷
2 x Wall Resistance

Question 79

How does the initial stretch of the cardiomyocytes affect the tension produced by the fibre?

Answer 79

If the cardiomyocyte is stretched more, then the tension produced will also be greater.
This means the end diastolic volume is also the fibre length of the cardiomyocyte at contraction.

Question 80

How does the Frank-Starling law explain preload?

Answer 80

Means that as a larger volume of blood enters the ventricle, the blood will stretch the walls of the ventricle more.
Greater expansion of the cardiomyocyte fibres results in increased force of contraction.
This means more blood can be pumped into the aorta in systole.

Question 81

Why is the Frank-Starling law regarding preload useful to the contraction of the heart?

Answer 81

It allows the balance of the outputs of the right and left ventricles.

Question 82

How does the PV loop change when the preload is increased?

Answer 82

The PV loop shifts to the right as the volume in the ventricle has increased.
The stroke volume also increases.

Question 83

What is the most important determinant of preload?

Answer 83

Central venous pressure

Question 84

How does central venous pressure affect preload?

Answer 84

The volume of blood in the vein influences the filling of the heart.
The greater the central venous pressure, the greater the passive flow into the atria, therefore more filling of there ventricles.
This then increases the stroke volume and cardiac output.

Question 85

How is preload measured?

Answer 85

Preload is proportional to the end diastolic volume.
The larger the end diastolic volume, the larger the preload.

Question 86

What is after load?

Answer 86

This is the active tension of the myocardial fibres during systole that is needed to overcome the aortic pressure to force blood out of the ventricles.

Question 87

How is after load measured?

Answer 87

Afterload is proportional to the arterial blood pressure, as this is what the heart has to pump against.
Therefore can be measure through the aortic pressure.

Question 88

What will happen in the heart if the systemic blood pressure (after load) increases?

Answer 88

Increase in systemic blood pressure means the heart has to work harder to pump out the same volume of blood against a higher arterial blood pressure.
This means the heart has to increase the strength of the ventricular contraction, however this also decreases the stroke volume and increases the end systolic volume.
This is because the increased after load reduces the velocity of the myocardial fibres shortening and blood ejection. Means some blood will remain in ventricles and not all is ejected.
After a few cycles the heart adapts by increasing the ventricular volume, which brings the stroke volume back to the normal level - but the overall stroke work has still increased.

Question 89

How can sympathetic stimulation affect the contractility of the heart?

Answer 89

Increased sympathetic stimulation increases the inotropic effect on the heart.

Question 90

Which neurotransmitter corresponds to a positive inotropic effect of increasing tension on the heart?

Answer 90

Noradrenaline

Question 91

What is the positive inotropic effect?

Answer 91

This increases the energy of contraction for any resting fibre length or increase in end diastolic volume.
Results in an increase in stroke volume and decrease in end systolic volume(more blood is ejected).

Question 92

How can arterial elasticity be measured?

Answer 92

Ea = End systolic pressure ÷ stroke volume
It is a ratio.

Question 93

How does the PV loop change with an increased inotropic effect?

Answer 93

The end systolic pressure volume relationship gradient increases, as for the same ventricular volume the ventricular pressure is now much greater due to higher contractility.
Means that for the same after load and preload the heart can carry out more stroke work and generates a greater stroke volume.

Question 94

When is it useful to have a positive inotropic effect?

Answer 94

During exercise, when the stroke volume has to combat a higher arterial blood pressure with the same after load and preload.

Question 95

List 3 effects of sympathetic stimulation that result in an increased cardiac output

Answer 95

1) Increased depolarisation of the pacemaker cells -> increased heart rate

2) Increased force of ventricular contraction -> increased stroke volume

3) Increased vasoconstriction -> increased venous return -> increased preload -> increased force of ventricular contraction

Question 96

List 3 effects of parasympathetic stimulation that result in a decreased cardiac output

Answer 96

1) Decreased depolarisation of the pacemaker cells -> decreased heart rate

2) Decreased force of atrial contraction -> decreased preload -> decreased force of ventricular contraction

3) Decreased cardiac output itself -> decreased venous return -> decreased preload

Question 97

What is involved in intrinsic regulation of stroke volume?

Answer 97

The amount of stretch in the myocardial fibres at the end of diastole determines the stroke volume.

Question 98

What is involved in extrinsic regulation of stroke volume?

Answer 98

The activity of the sympathetic nervous system (positive inotropic effects) and the effect of some circulating hormones.

Question 99

Outline the equation linking mean arterial pressure, central venous pressure, cardiac output and systemic vascular resistance

Answer 99

(Mean Arterial Pressure - Central Venous Pressure) = (Cardiac Output x Systemic Vascular Resistance)

Question 100

What factors affect systemic vascular resistance?

Answer 100

Vasoconstriction and Vasodilation, which is determined by the autonomic nervous system.
(Parasympathetic = vasodilation
Sympathetic = vasoconstriction)

Question 101

Why is it bad for the heart rate to be too high or too low?

Answer 101

If the heart rate is too low it will reduce cardiac output.

If the heart rate is too high then not enough blood will be able to fill up the heart during diastole, which decreases the stroke volume, also decreasing cardiac output.

Question 102

How does sepsis and anaphylaxis affect the systemic vascular resistance?

Answer 102

It causes vasodilation, which lower the systemic vascular resistance.

Question 103

Which adrenoreceptors are associated with controlling the vascular tone?

Answer 103

Alpha 1(blood vessels), Alpha 2, Beta 2(bronchial smooth muscle)

Question 104

Which adrenoreceptors are associated with affecting the heart rate?

Answer 104

Beta 1

Question 105

What is the course of action for a patient that is suffering from vasodilation?

Answer 105

The patient will be flushed and warm, need to increase the blood pressure.
Heart rate can be increased in order to increase the cardiac output therefore increase blood pressure.

Question 106

What is the course of action for a patient that is suffering from low cardiac output?

Answer 106

The patient will be cold and clammy, need to increase vascular resistance.
Vasoconstriction can be increased so blood pressure and vascular resistance also increases.

Question 107

Outline the equation that calculates oxygen delivery

Answer 107

Cardiac output x Oxygen content of blood

Question 108

Outline how to calculate the oxygen content of blood

Answer 108

Haemoglobin concentration x percentage oxyhaemoglobin saturation x 1.34(Huffners constant)

Question 109

What is the meaning of 1.34 Huffners constant?

Answer 109

It shows how many mls per gram the haemoglobin can carry if it is fully saturated.

Question 110

List 3 causes of reduced oxygen delivery

Answer 110

1) Reduced cardiac output
2) Decreased oxyhaemoglobin saturation of blood
3) Reduced haemoglobin concentration

Question 111

What could happen if there is inadequate oxygen delivery?

Answer 111

This can cause hypoxia. Blockages to certain parts of the body may increase anaerobic respiration in that area, therefore a rise in lactic acid.

Question 112

How can the cardiac output be increased?

Answer 112

The stroke volume can be increased (increased preload, increased after load).

The heart rate can be increased (increased sympathetic stimulation, decreased parasympathetic stimulation).

Question 113

How can the haemoglobin saturation with O2 be increased?

Answer 113

More oxygen can be given via a face mask.

Question 114

How can the concentration of haemoglobin in the blood be increased?

Answer 114

Through blood transfusion.

Question 115

Define heart failure

Answer 115

When there is reduced heart function, so the heart cannot pump enough blood to maintain the flow to meet the needs of the body at normal pressures.

Question 116

List 6 reasons for heart failure

Answer 116

1) Myocardial infarction - part of heart muscle dies due to lack of blood flow.

2) Abnormal rhythm - electric depolarisation and repolarisation doesn’t occur effectively.

3) Lack of venous return - could be due to excessive bleeding.

4) Obstruction in the pericardium - heart cannot relax in diastole, so cannot fill with blood, meaning that less blood can be expelled in each stroke.

5) Right lung failure - pulmonary arteries damaged, means that heart has to pump with more force, which could cause blood to be pushed to the left side of the heart by accident.

Question 117

Describe the sequence of a decrease of cardiac output

Answer 117

A decrease in cardiac output leads to fluid retention (no hydrostatic pressure in the blood vessels) and an increased sympathetic reflex (nervous system detects a lower heart rate).
This cannot restore the cardiac output enough for renal function, so the renin-aldosterone system causes even more fluid retention (more ENAC channels in the DCT cause more Na+ reabsorption).
This results in decreased venous return to the heart, thereby decreased delivery of oxygen to the tissues.

Question 118

Outline mechanisms that can return the cardiac output back to normal levels

Answer 118

1) Increased renin/angiotensin pathway
2) Increased sympathetic nervous stimulation

3) Increased heart rate and contractility
4) Increased systemic vascular resistance
5) Increased venous return
6) Increased preload
7) Cardiac ischaemia
8) Increase in brain natriuretic peptide
9) Baroreceptor reflex

Question 119

Outline some consequences of heart compensation for heart failure

Answer 119

1) Heart becomes damaged if it tries to beat faster against a higher systemic vascular resistance - increased after load.

2) More O2 supply needed for the myocardium.

3) Lack of stretch in the aortic receptors causes the renin-angiotensin pathway to remain activated. This retains more fluid, which causes more stretch of the heart, resulting in increased output of the heart.

Question 120

How can the heart be protected against damage from compensating for heart failure?

Answer 120

Drugs such as beta blockers can be used to slow down the heart rate or reduce vasoconstriction. (Beta 1 receptors).

Question 121

What is Atrial Natriuretic Peptide?

Answer 121

Peptides released in response to excess stress and pressure on the walls of the heart.

Question 122

List 3 causes of the release of ANP?

Answer 122

1) Natruiresis - presence of Na in the blood, allows the volume of blood to reduce and stress on the heart to reduce.

2) Vasodilation

3) Inhibits renin activation - stops more reabsorption of Na from the DCT.

Question 123

What Brain Natriuretic Peptide?

Answer 123

Peptides released in response to stress in the ventricular cardiac muscle cells.

Question 124

Define hypovolaemia

Answer 124

When there is a decreased volume of circulating blood in the body.

Question 125

What occurs during hypovolaemia?

Answer 125

Less blood fills the ventricles during diastole -> Less blood is pumped out from each ventricle -> There is less venous return to each side of the heart

Question 126

What mechanisms can help to act against hypovolaemia?

Answer 126

1) Increased renin/angiotensin pathway -> more fluid retained in bloodstream
The juxtaglomerular apparatus detects reduction of stretch.

2) Increased activation of sympathetic nervous system

3) Increased heart rate and contractility

4) Increased systemic vascular resistance

5) Increased venous return

6) Decreased BNP release to prevent any vasodilation.

Question 127

What do the compensatory mechanisms against hypovolaemia result in?

Answer 127

Results in an increased stroke volume and heart rate, so an increased cardiac output. Reduces end systolic volume.

Increased sympathetic drive increases the systemic vascular resistance and mean atrial blood pressure.

Positive inotropy, chronotropy
Vasoconstriction

Question 128

Outline what happens in the juxtaglomerular apparatus when the renin/angiotensin system is activated

Answer 128

1) Decrease in renal perfusion

2) Release of renin from the kidney

3) Converts angiotensin to angiotensin 1

4) ACE from the surface of pulmonary and renal endothelium converts angiotensin 1 to angiotensin 2

Question 129

What are the effects of activated angiotensin 2 to the circulation?

Answer 129

1) Increased sympathetic stimulation

2) Increased aldosterone secretion from the kidneys

3) Excretion of Na+, Cl-, K+, retention of water

4) Arterial vasoconstriction, increase in blood pressure

5) Increased ADH secretion from the the pituitary gland, so more water retention

Question 130

Define sepsis

Answer 130

Inflammation to organs caused by infection.
Blood vessels become abnormally dilated, so the systemic vascular resistance is very low.
Cardiac output tries to compensate but this is not enough, so mean arterial pressure remains low.
Means that cells cannot take up oxygen very well.

Question 131

What is the compensatory mechanism for sepsis?

Answer 131

The heart increases its stroke volume, which is easy as there is less resistance for the heart to pump against. Sympathetic activation also speeds the heart up and makes its contraction stronger.

Question 132

Define cardiac arrest

Answer 132

When cardiac output is low/nonexistent. No pulse as blood pressure is very low.

Question 133

List 2 shockable causes of cardiac arrest that are shockable

Answer 133

1) Ventricular fibrillation
2) Pulseless ventricular tachycardia

Question 134

List 2 non shockable causes of cardiac arrest that a not shockable

Answer 134

1) Asystole (no electrical activity)
2) Pulseless electrical activity

Question 135

List 4 reasons why it is useful to measure cardiac output

Answer 135

1) Helps to diagnose problems

2) Helps to choose treatments

3) Help to know when to give fluid

4) Helps to measure oxygen delivery

Question 136

How does an oesophageal doppler monitor measure cardiac output?

Answer 136

Probe is inserted into oesophagus which emits ultrasound that bounces back from moving RBCs in the aorta.
This measures the distance travelled by the RBCs, the grater distance means the stroke volume is higher.

However it cannot give a picture of the heart.

Question 137

How does a pulmonary artery catheter measure cardiac output?

Answer 137

Catheter inserted in right atrium through subclavian vein. Cold fluid is inserted, and temperature after it leaves the atrium is measured.
If stroke volume is low the temperature will be high, if stroke volume is high then temperature will be low.

Cannot take pictures but can deliver drugs through it.

Question 138

How does echo cardiography measure cardiac output?

Answer 138

Ultrasound high frequency sound is emitted and reflected back.
Gives information about structure and function, valve function, ejection fraction and if parts of the muscle are not working.

Question 139

How does dye dilution measure cardiac output?

Answer 139

The concentration changes of the dye is measured.
A greater cardiac output will dilute the dye more, so there his a smaller rise in concentration.

Can give drugs and take blood samples.

Question 140

How does pulse contour analysis measure cardiac output?

Answer 140

A catheter is placed inside the artery, the pressure against time is measured. the changes are calculated.
Cannot calculate absolute values, only changes, so needs another method for calibration.

Question 141

Describe the process of continuously giving fluids to a patient

Answer 141

1) Fluids added increases the venous return to the heart.

2) More blood fills up the ventricles, and a greater volume of blood results in a greater force of contraction.

3) Results in a greater cardiac output due to a greater stroke volume.

4) BUT heart cannot be stretched indefinitely, so eventually there graph will plateau and the effectiveness of giving fluid will decrease, until there is no actual benefit.