Cardiovascular System

Question 1

Preload and its influence on cardiac function

Answer 1

The end diastolic volume, determined by central venous pressure. Affects stroke volume/cardiac output. If high CO is high.

Question 2

Afterload and its influence on cardiac function

Answer 2

The force against which left ventricle pumps to eject blood into the aorta. Determined by aortic pressure. Affects stroke volume and cardiac output because valves only open when ventricular pressure is higher than aortic. If high enough cardiac output can be lower, but in normal range it has no effect to to control mechanisms.

Question 3

Starling’s Law

Answer 3

The energy released during contraction depends on initial fiber length

Question 4

2 mechanisms that explain Starling’s law

Answer 4

1. Cross bridge theory: when sarcomere length is more stretched more space for it contract. 2. Calcium sensitivity in troponin C increases (specific to cardiac muscle).

Question 5

Cardiac contractility

Answer 5

The strength of contraction for a given preload and afterload.

Question 6

Effects of the noradrenaline (sympathetic NS) on cardiac contractility

Answer 6

increases contractility by stimulating B1 and some B2 adrenergic receptors. It does this by shortening the funny current time.

Question 7

Effect of adrenaline and noradrenaline (sympathetic) on pacemaker action potential

Answer 7

1. Increases funny current 2. faster rate of diastolic depolarisation 3. faster heart rate

Question 8

Effects of parasympathetic stimulation (acetylcholine on pacemaker action potentials

Answer 8

1. Decrease funny current 2. A slower rate of diastolic depolarization 3. Slower heart rate

Question 9

Plateau phase of the cardiac action potential. When it starts and how it is maintained.

Answer 9

Starts at the inactivation of the sodium channels. It plateaus because ‘long’ refractory period’. Maintained by Calcium inward current and the relatively slow opening of K channels out.

Question 10

As heart rate increases, length of action potential…

Answer 10

decreases

Question 11

Why the cardiac action potential is so long (2 reasons)

Answer 11

1. Prevent tetany 2. Protect against arrhythmias

This is done by having a longer ABSOLUTE refractory period.

Question 12

2 theories about the cardiac clocks and what they are.

Answer 12

1. Membrane clock -> cyclical changes in ionic currents within the membrane 2. Calcium clock -> cyclical release of CA from intracellular stores

Question 13

Why funny current is funny, and a drug that blocks this, and which cells in the heart display this.

Answer 13

inward current activated when the membrane potential gets more negative. ivabradine

Displayed by AV nodal cells SA nodal cells and bundle of his. NOT atria and ventricle cells

Question 14

Protein channels in gap junctions and proteins they are made of.

Answer 14

Connexons (hemi-channels) made up of connexins.

Question 15

Anisotropic conduction

Answer 15

electrical impulses travel easier along fibers than across them because there are a lot of connexons at the end of cells, not many on their side.

Question 16

(use image of ECG for this) Explain points PQRST

Answer 16

P: Atrial Depolarization Q: Depolarisation of septum (moves towards the heart) R: Depolarisation of ventricles (towards apex) S: Depolarisation of ventricle (through Purkinje fibres away from apex) T: Repolarisation of the ventricle

Question 17

(use image of ECG intervals for this) Explain the intervals of the ECG: PQ, QRS, QT, ST and associated pathologies

Answer 17

PQ: AV nodal delay (AV block) QRS: Ventricular conduction velocity (bundle branch block) QT interval: Ventricular action potential duration (long GT syndrome) ST: heterogeneity of ventricular polarisation (myocardial infarction)

Question 18

2 methods calcium is removed from the cytosol causing relaxation

Answer 18

1. SERCA - active transport of CA into SR stores. 2. smaller amount of calcium via Na/Ca exchanger

Question 19

Chronotropy and effects of positive/ negative chronotropes

Answer 19

Heart rate. Positive increase, negative decrease.

Question 20

Inotropy, effects of positive/ negative inotropes.

Answer 20

The strength of contraction. Positive increase, negative decrease.

Question 21

Lusitropy, effects of positive/ negative lusitropes.

Answer 21

The rate of relation. Positive increase, negative decrease.

Question 22

Examples of positive chronotopes.

Answer 22

adrenaline, noradrenaline (increase heart rate)

Question 23

Examples of negative chronotropes

Answer 23

acetylcholine (decrease heart rate)

Question 24

B1 adrenoreceptor pathway

Answer 24

B1 agonist - activated adenyl cyclase - activate cAMP - activate protein kinase A (PKA) - ativate proteins

Question 25

Proteins activated by protein kinase A (PKA) in cardiac muscle)

Answer 25

L type Calcium channels Ryanodine receptors ATPase subunits (SERCA, Na/Ca exchanger) Troponin I and C Membrane and calcium clocks

Question 26

What is the myogenic response in blood vessels?

Answer 26

An increase in pressure within a blood vessel causes vasoconstriction due to the stretch-activated calcium receptors. A decrease in pressure causes vasodilation.

Question 27

Effect of Nitric Oxide (NO) on smooth muscle cell.

Answer 27

1. NO released from endothelial cell 2. guanylate cyclase activated and causes GTP -\> cGMP 3. cGMP goes and causes calcium reuptake

Question 28

Channels involved in NO mediated vasodialtion

Answer 28

SERCA smooth ER Calcium ATPase PMCA plasma membrane Calcium ATPase Voltage gated calcium channel (deactivated)

Question 29

Smooth muscle contraction pathways

Answer 29

1. Phospholipase C activated causing PIP2 to DAG and IP3. 2. IP3 causes opening of ryanodine receptors in SR. 3. DAG causes opening of receptor gated Sodium/ Potassium gated channel. 4. Sodium causes membrane depolarization spread to other cells and the opening of Voltage-gated calcium channels.

Question 30

Mechanism of endothelium-derived hyperpolarisation

Answer 30

1. vasodilating substance binds to a receptor on the endothelial cell, causing an increase in Ca within the cell. 2. Ca activated K channels open and channel flows out, causing hyperpolarisation of endothelial cell. 3. Wave of hyperpolarisation spreads to smooth muscle via gap junction and relaxation.

Question 31

End diastolic and end systolic volume of ventricles

Answer 31

End diastolic volume: 120 ml End systolic volume: 70 ml

Question 32

Effect of total peripheral resistance on blood pressure.

Answer 32

Increases blood pressure

Question 33

Control of resistance in the microcirculation

Answer 33

Smooth muscle regulated locally, allowing for finer localised control

Question 34

Control of the vascular system by the ANS: which receptors are involed in the SNS and PNS

Answer 34

SNS: alpha 1 receptors (can raise TPR) PNS: nMuscarinic and NANC

Question 35

Adrenaline vs noradrenaline receptors they activate and effect they have

Answer 35

Question 36

Stenosis

Answer 36

Narrowing of arteries due to atherosclerosis (buildup of plaques)

Question 37

Venous pressure label

Answer 37

Question 38

Describe the cardiac cycle in terms of movement of ions

Answer 38

Question 39

effect of Epoxyeicosatrienoic acids, activation of beta1, PGI2 and adenosine receptors on smooth muscle cell

Answer 39

relaxation

Question 40

Describe additional mechanisms that reduce drastic changes in blood flow due to changes in pressure. (metabolite whashout and reactive hyperanaemia)

Answer 40

Metabolite washout: metabolites around vascular beds help to dilate the vessels and an increase in blood flow will wash them out so vessel will contract. Reactive hyperanaemia: increased muscle metabolism causes a release of vasoconstricting substances (adenosine, K+ lactic acid, H+...)

Question 41

Clotting process

Answer 41