Cardiovascular System Flashcards

(53 cards)

1
Q

What is the pericardial sac made of?

A

1) Fibrous pericardium
2) Serous pericardium - split into parietal and visceral (continuous membrane)

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2
Q

What are the 3 walls of the heart wall?

A

1) Epicardium - outer
2) Myocardium
3) Endocardium

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3
Q

What are the heart chambers?

A

1) Right atrium
2) Left atrium
3) Right ventricle
4) Left ventricle

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4
Q

How does blood flow in the heart and to/from the body?

A

1) Body to the right atrium
2) Right ventricle to the lungs
3) Lungs to left atrium
4) Left ventricle to body

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5
Q

What is the function of the heart valves?

A

1) Allow blood to flow in 1 direction only
2) Open and close in response to pressure difference

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6
Q

How is heart blood flow controlled?

A

1) Pressure changes reflect alternating contraction/relation of heart
2) Blood moves along pressure gradients (high to low) through any available opening
3) Pressure changes cause valves to open/close - keep blood flowing in 1 direction

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7
Q

What are the 7 events in the cardiac cycle?

A

1) Atrial systole
2) Isovolumetric contraction
3) Rapid ejection
4) Reduced ejection
5) Isovolumetric relaxation
6) Rapid ventricular filling
7) Reduced ventricular filling

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8
Q

What happens in atrial systole?

A

1) Atrium contracts
2) Increase in atrial pressure (‘a’ wave)
3) Tops off ventricle with blood
4) Contraction finished before ventricle contracts

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9
Q

What happens in isovolumetric contraction?

A

1) Interval between AV (atrioventricular valve) closing and opening of semilunar valves
2) AV valve closes when ventricular pressure exceed atrial pressure - 0.03s
3) Ventricle pressure increases but volume does not change

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10
Q

What happens in rapid ejection?

A

1) Ventricle contraction causes pressure to exceed aorta and pulmonary artery pressure - semilunar valves open
2) Blood enters arteries increasing pressure to a peak
3) Right ventricular contraction pushes AV valve into atrium (‘c’ wave)

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11
Q

What is reduced ejection?

A

1) Ventricular pressure fall and blood flow decreases
2) Ventricular pressure drops below artery pressure - blood begins to flow back, closing semilunar valves

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12
Q

What happens during isovolumetric relaxation?

A

1) Throughout 3-5 atria filling with blood (‘v’ wave)
2) Ventricle pressure continues to fall
3) Ventricular volume at a minimum - ready to be filled

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13
Q

What happens during rapid ventricular filling?

A

1) Atria pressure exceeds ventricle pressure and AV valves open
2) Ventricular volume increases rapidly as blood flows from atria

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14
Q

What happens during reduced ventricular filling?

A

Ventricular volume increases more slowly until nearly full

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15
Q

What are the heart’s arteries called?

A

Coronary arteries, surface vessels - epicardial

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16
Q

What are the coronary arteris affected by?

A

Are narrow and affected by atherosclerosis - can lead to myocardial infarction (heart attack)

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17
Q

What is the role of coronary veins?

A

Remove deoxygenated blood from myocardium

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18
Q

How does a myocardial infarction happen?

A

1) Caused by blockages of coronary arteries
2) Macrophages ingest cholesterol and other lipids - forming fatty streaks below endothelial lining of larger arteries
3) As streak grows - forms lipid core
4) Lipid core grows with local smooth muscle cell division creating bulging plaque
5) Plaque develops hard, calcified regions and fibrous collagen caps
6) Rupturing of cap initiates a clot - myocardial infarction

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19
Q

What are the features of a cardiomyocyte?

A

1) Sarcomeres join end-to-end forming myofibrils
2) Irregular smooth sarcoplasmic reticulum
3) Sarcomeres in close association with T-tubules
4) Intercalated disc where cells interlock - contains desmosomes and gap junctions

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20
Q

What is the role of desmsomes?

A

Prevents adjacent cells pulling apart during contraction

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21
Q

What is the role of the gap junction?

A

Ion-permeable passage allowing the stimulating impulse to move continuously cell to cell

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22
Q

What is the role of T-tubules?

A

Invagination of sarcolemma conducts impulses to deeper cell regions

23
Q

What is the role of the sarcoplasmic reticulum?

A

Specialised SER surrounding myofibrils and stores Ca2+

24
Q

What is the role of cardiac myofibrils?

A

Contractile filaments (actin and myosin) slide past each other during contraction

25
How does contraction of the heart happen?
1) Sinoatrial node initiates sequence - anatomical pacemaker, causing atrial muscles to contract 2) AP - depolarisation travels through internodal pathway to AV node 3) Conduction delayed in AV node to allow completion of atrial contraction continuing through Bundle of His, bundle branches and Purkinje Fibres resulting in ventricle contraction
26
How are action potentials generated in the cardiovascular system?
1) By autorhythmic cells 2) Wave of depolarisation spreads to contractile cells via gap junctions
27
Why is the resting membrane potential said to be -ve?
1) Transport proteins embedded in sarcolemma control movement of ions in (Na+, Ca2+) and out (K+) the cell 2) At rest, there is a voltage difference across membrane (membrane potential) 3) Outside cell is relatively +ve to inside
28
What is pacemaker potential?
1) Slow influx of Na+ 2) Reduced efflux of K+ 3) Membrane potential becomes less -ve generating pacemaker potential
29
What is depolarisation in autorhythmic cells?
1) Voltage gated (-40mV) Ca2+ channels open 2) Fast influx Ca2+ 3) Reversing membrane potential
30
What is repolarisation in autorhymic cells?
1) Depolarisation triggers opening of voltage gated K+ channel - rapid K+ efflux 2) Ca2+ actively pumped out of cell 3) Na+/K+ ATPase also pumps Na+ out and K+ in
31
What are contractile cells?
1) Rely on autorhythmic cells to generate APs 2) Contain sarcoplasmic reticulum (SR) - acts as Ca2+ storage 3) SR Ca2+ membrane transport proteins help regulate cytoplasmic [Ca2+] 4) Plasma membrane also has Ca2+ channels - different from those in SR
32
What is depolarisation in contractile cells?
1) Positive ions move through gap junction from depolarise autorhythmic cell 2) Creates small voltage change - initiates depolarisation 3) Voltage change stimulates opening of fast Na+ channels 4) Results in depolarisation for an AP
33
What is the plateaux in contractile cells?
1) Depolarisation triggers opening of slow Ca2+ channel (PM and SR) 2) K+ efflux begins 3) Ca2+ influx briefly balances K+ efflux 4) Ca2+ initiates contraction
34
What is repolarisation in contractile cells?
1) Ca2+ channels close while more K+ channels open - rapidly repolarising membrane 2) Then channels (PM and SR) remove Ca2+ and Na+/K+ pump restores balance
35
What is the first heard sound (S1)?
1) Represented by lubb 2) Relatively lower pitched
36
What is the 2nd heart sound?
1) Represented by dupp 2) Relatively higher pitched
37
What is the result of abnormal heart sounds?
1) Faulty valves 2) Heart murmur - blood leaking through valve when closed
38
What is the equation for cardiac output?
Cardiac output (CO/Q) = Stroke volume (SV x Heart rate (HR)
39
What it stroke volume?
Volume of blood pumped per ventrticle each time heart contracts (ml/beat)
40
What is cardiac output?
Volume of blood pumped by either ventricle every minute (ml/min)
41
How does heart rate and stroke volume vary?
1) Athlete - higher SV; lower HR 2) Non-athlete - lower SV; higher HR
42
What is intrinsic regulation of the heart?
1) Cardiac muscle fibre force of contraction is related to 'stretch' 2) Greater stretch - greater force of contraction 3) Volume of blood that returns to heart (venous return) determines degree of ventricles wall stretch at end of diastole - preload
43
What is Starling's Law of the heart (increase)?
1) Increase preload (venous return) 2) Increased force contraction 3) Increased SV 4) Increased CO
44
What is afterload in the intrinsic regulation of the heart?
1) Back pressure from aorta to left ventricle 2) Hypertension results in elevated aortic pressure 3) To force blood out of left ventricle, stronger contraction required - eventually lead to heart failure 4) Afterload influences CO less than preload
45
What are 2 types of extrinsic regulation of the heart?
1) Nervous 2) Chemical
46
What effect does sympathetic innervation have on the SA node?
1) Increases Hr 2) Increases SV
47
How does parasympathetic innervation effect the SA node?
Decreases HR
48
What are baroreceptors?
1) Pressure sensitive mechanoreceptors that respond to changes in arterial pressure 2) Located in aortic arch (blood to body) and carotid sinus (carotid artery) 3) Change in blood pressure causes change in baroreceptor stretch and change in rate of APs 4) Connected to centres in medulla oblongata by afferent neurons
49
What is the response to increase in blood pressure?
1) Increases parasympathetic innervation (vagus nerve) of SA node to decrease HR 2) Decrease in sympathetic innervation of SA node decreases HR and SV
50
How does the renin-angiotensin system affect blood pressure?
1) Adrenaline and noradrenaline release renin into the blood stream 2) Renin binds to angiotensinogen (inactive plasma protein synthesised in liver released into circulation) - converts angiotensinogen into active angiotensin I 3) Passing through the lung capillaries - angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II 4) Angiotensin II is a potent vasoconstrictor - raises blood pressure in body's arterioles
51
What is the effect of aldosteron in blood pressure?
1) Angiotensin II stimulates release of aldosterone - promoting retention of Na+ and H2O by kidneys by reabsorption of sodium through tubules 2) As sodium moves into blood stream, H2O follows by osmosis 3) Reabsorbed H2O increases blood volume - increasing blood pressure
52
What are the short term effects of osmolarity on blood pressure?
1) Increased osmolarity excites 'thirst centres' in hypothalamus 2) Thirst centres stimulate individual to drink more H2O and rehydrate blood and extracellular body fluids 3) Blood osmolarity, volume and pressure are restored
53
What is the long term effect of osmolarity on blood pressure?
1) Hypothalamus 'thirst centre' sends signal to posterior pituitary to release ADH 2) ADH stimulates kidney to resorb more H2O from urine 3) ADH promotes reabsorption of H2O from kidney, stimulating increase of H2O channels in DCTs and CDs 4) Aquaporins aid movement of H2O from urine into blood - decreasing osmolarity, increasing blood volume and pressure