Cardiovascular System Flashcards Preview

Physiology of Systems > Cardiovascular System > Flashcards

Flashcards in Cardiovascular System Deck (42)
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1
Q

Preload and its influence on cardiac function

A

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

2
Q

Afterload and its influence on cardiac function

A

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.

3
Q

Starling’s Law

A

The energy released during contraction depends on initial fiber length

4
Q

2 mechanisms that explain Starling’s law

A
  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).
5
Q

Cardiac contractility

A

The strength of contraction for a given preload and afterload.

6
Q

Effects of the noradrenaline (sympathetic NS) on cardiac contractility

A

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

7
Q

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

A
  1. Increases funny current 2. faster rate of diastolic depolarisation 3. faster heart rate
8
Q

Effects of parasympathetic stimulation (acetylcholine on pacemaker action potentials

A
  1. Decrease funny current 2. A slower rate of diastolic depolarization 3. Slower heart rate
9
Q

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

A

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.

10
Q

As heart rate increases, length of action potential…

A

decreases

11
Q

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

A
  1. Prevent tetany 2. Protect against arrhythmias

This is done by having a longer ABSOLUTE refractory period.

12
Q

2 theories about the cardiac clocks and what they are.

A
  1. Membrane clock -> cyclical changes in ionic currents within the membrane 2. Calcium clock -> cyclical release of CA from intracellular stores
13
Q

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

A

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

14
Q

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

A

Connexons (hemi-channels) made up of connexins.

15
Q

Anisotropic conduction

A

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.

16
Q

(use image of ECG for this) Explain points PQRST

A

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

17
Q

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

A

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)

18
Q

2 methods calcium is removed from the cytosol causing relaxation

A
  1. SERCA - active transport of CA into SR stores. 2. smaller amount of calcium via Na/Ca exchanger
19
Q

Chronotropy and effects of positive/ negative chronotropes

A

Heart rate. Positive increase, negative decrease.

20
Q

Inotropy, effects of positive/ negative inotropes.

A

The strength of contraction. Positive increase, negative decrease.

21
Q

Lusitropy, effects of positive/ negative lusitropes.

A

The rate of relation. Positive increase, negative decrease.

22
Q

Examples of positive chronotopes.

A

adrenaline, noradrenaline (increase heart rate)

23
Q

Examples of negative chronotropes

A

acetylcholine (decrease heart rate)

24
Q

B1 adrenoreceptor pathway

A

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

25
Q

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

A

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

26
Q

What is the myogenic response in blood vessels?

A

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

27
Q

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

A
  1. NO released from endothelial cell
  2. guanylate cyclase activated and causes GTP -> cGMP
  3. cGMP goes and causes calcium reuptake
28
Q

Channels involved in NO mediated vasodialtion

A

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

29
Q

Smooth muscle contraction pathways

A
  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.
30
Q

Mechanism of endothelium-derived hyperpolarisation

A
  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.
31
Q

End diastolic and end systolic volume of ventricles

A

End diastolic volume: 120 ml

End systolic volume: 70 ml

32
Q

Effect of total peripheral resistance on blood pressure.

A

Increases blood pressure

33
Q

Control of resistance in the microcirculation

A

Smooth muscle regulated locally, allowing for finer localised control

34
Q

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

A

SNS: alpha 1 receptors (can raise TPR)

PNS: nMuscarinic and NANC

35
Q

Adrenaline vs noradrenaline receptors they activate and effect they have

A
36
Q

Stenosis

A

Narrowing of arteries due to atherosclerosis (buildup of plaques)

37
Q

Venous pressure label

A
38
Q

Describe the cardiac cycle in terms of movement of ions

A
39
Q

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

A

relaxation

40
Q

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

A

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+…)

41
Q

Clotting process

A
42
Q
A