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Year 1 Body Systems > Cardiology Physiology > Flashcards

Cardiology Physiology Flashcards

1
Q

Action potential in the T tubules of cardiac myocytes triggers calcium entry in which 2 ways?

A

1) L type channels - voltage sensitive Ca2+ channels

2) Calcium induced calcium release - Calcium released from SR

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2
Q

What protein does calcium interact with to induce contraction?

A

Troponin

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3
Q

What is the resting potential and threshold potential of pacemaker cells?

A 
Resting = -60mV
Threshold = -40mV
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4
Q

What is the resting potential and threshold potential of cardiac myocytes?

A 
Resting = -90mV
Threshold = -65mV
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5
Q

What is the TFR of a cardiac myocyte?

A

ARP (absolute refractory period) + RRP (relative refractory period)

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6
Q

In an ECG what direction does the depolarisation go in a +ve and -ve deflection?

A

Towards an electrode = +ve deflection

Away from an electrode = -ve deflection

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7
Q

What are Einthoven’s 6 leads?

A 
RA, LA, LA 
Lead I - LA -RA
Lead II - LL-RA
Lead III - LL-LA
Augmented limb leads (recorded with respect to 0)
aVR = RA 
aVL = LA
aVF = LL
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8
Q

What are Virchows leads?

A

Chest leads (V1-V6) Unipolar leads recorded with respect to 0

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9
Q

What leads is the electrical axis of the heart to do with?

A

Einthovens’s leads

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10
Q

What is the electrical axis of the heart?

A

Max current produced by an ECG - normally lead II (60 degrees) but can be anywhere between -30 and 90 degrees (einthoven’s leads)

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11
Q

What would left deviation (-150 - -30) and right deviation (+90 - -150) tell you?

A

Left deviation - left ventricular hypertrophy

Right deviation - right ventricular hypertrophy

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12
Q

What is the left ventricular axis and which leads is it to do with?

A

To do with Virchows leads

Max current generated by ECG - towards V6

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13
Q

What are the 4 phases of the heart beat?

A

1) Diastolic ventricular filling (passive phase followed by active phase when atria contract)
2) Isovolumic contraction (semilunar valves closed by ventricles contracting)
3) Systolic ejection ( 2nd phase of ventricular systole - ventricles contracting and blood ejecting - during this phase atria relax and fill with blood)
4) Isovolumic relaxation (ventricles relax, semilunar valves close, atria continue to fill)

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14
Q

What is cardiac power and how is it calculated?

A

Rate of work done by the heart

Cardiac power = pressure x flow rate

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15
Q

What is EDV?

A

End diastolic volume

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16
Q

What is ESV?

A

End systolic volume

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17
Q

How is stroke volume calculated?

A

EDV - ESV

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18
Q

How is ejection fraction (LVEF) calculated?

A

SV/EDV

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19
Q

What is the main source of ATP for the heart?

A

Free fatty acids

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20
Q

What does the difference between LV and aortic pressure tell us?

A

The extent of aortic stenosis

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21
Q

What is V (blood velocity)?

A

Distance travelled per particle per unit of time

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22
Q

What is the equation linking pressure, blood flow and resistance?

A

Pressure = blood flow x resistance

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23
Q

What is the difference between the action potential in cardiac and skeletal muscle and what is the purpose of this difference?

A

Presence of plateau caused by Ca2+ ions in the cardiac myocyte action potential
Maintains contractile period during depolarisation

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24
Q

What happens to the troponin tropmyosin complex during systole?

A

Calcium binds to troponin, troponin-tropomyosin complex moves and myosin can now dock onto the exposed binding sites

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25
Q

What happens to the longitudinal and horizontal and circumferential filaments during systole?

A

Longitudinal filament shortening

Horizontal and circumferential filament thickening

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26
Q

In which 2 ways can heart rate be increased?

A

1) Sympathetic innervation

2) Adrenaline - beta 1 agonism

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27
Q

In which 2 ways can stroke volume be increased?

A

1) Increase pre load
2) Sympathetic input - prolonged opening of Ca2+ channels, enhances calcium action in excitation/contraction coupling mechanisms

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28
Q

What happens to the LVEF of a failing heart?

A

Decreases

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29
Q

What is the physiological LVEF and the LVEF in exercise?

A

Physiological LVEF - 50-75%

LVEF in exercise - can reach 90%

30
Q

Why would ischaemia and viral infection/alcohol lead to a heart which contracts with less force?

A

Ischaemia - scarred myocardium

Viral infection/alcohol - wall thinning

31
Q

In heart failure how does you body try to compensate for the weaker contraction of the heart and what does this lead to?

A

1) SNS overactivates
2) RAAS kicks in
Both these measures increase the pre load and the LV stretch exceeds physiological levels - go onto descending limb of the curve

32
Q

What 3 treatments would be given to a patient with heart failure and pulmonary oedema?

A

1) High flow O2
2) Morphine - relax pulmonary vessels to reduce preload and relieving pain
3) Furosemide - diuretic

33
Q

How is preload measured?

A

End diastolic volume using an echocardiogram

34
Q

What 6 ways can stroke volume be increased?

A

1) Increased central venous pressure - increased by increased circulatory volume
2) Decreased venous compliance
3) Increased atrial filling or contraction
4) Decreased heart rate - prolongs diastole and filling
5) Increased ventricular compliance - more can get in
6) Increased aortic or pulmonary pressure - need more blood to generate enough pressure to open valves

35
Q

What is the bowditch effect?

A

Another curve, up to a point, increased heart rate = increased force of contraction

36
Q

What organs does the parasympathetic nervous system have no effect on?

A

Adrenal glands and kidneys

37
Q

What are the 4 effects of SNS on heart?

A

1) positive chonotropy - SA node
2) positive dromotropy - AV node
3) positive inotropy - atria and ventricles
4) positive lusitropy - atria and ventricles

38
Q

What are the actions of RAAS (ie. angiotensin II, aldosterone and vasopressin)?

A 
ANGIOTENSIN II
Vasoconstriction
Increased Na+ and H2O retention
Vasopressin release
Aldosterone release 
ALDOSTERONE
Increased Na+ and H2O retention
VASOPRESSIN
Increased water retention
39
Q

What are the PNS actions on the heart?

A

1) negative chonotropy - SA node
2) negative dromotropy - AV node
3) negative inotropy - Only ATRIA - no effect on ventricles

40
Q

Epinephrine is released into the blood from the adrenal medulla in response to sympathetic innervation what 3 effects does it have in terms of the cardiovascular system?

A

1) Causes kidneys to release renin
2) Causes vasoconstriction
3) Acts directly on the heart to increase heart rate and stroke volume

41
Q

How does the renal juxtaglomerular system work?

A

Macula densa cells in the distal convaluted tubule located next to the glomerulus sense a drop in NA concentration (lower transglomerular pressure - less filtered out - indicates BP) and signals to granular cells to secrete renin

42
Q

Where are baroceptors located and how do they control BP?

A

Carotid sinuses and aortic arch
Decreased arterial pressure - decreased firing - increase in sympathetic tone and decrease in parasympathetic tone
Increased arterial pressure - increased firing - decrease in sympathetic tone and increase in parasympathetic tone

43
Q

What is the anaerobic threshold in cardiopulmonary exercise testing?

A

Time when anaerobic respiration begins

44
Q

What does cardiopulmonary exercise testing measure?

A

O2 consumption at rest and during exercise

45
Q

What are the 6 consequences of uncontrolled hypertension?

A

1) Stroke - hameorrhagic/ischaemic
2) LV hypertrophy - diastolic dysfunction, AF, heart failure
3) Hastened atherosclerosis
4) Vascular disease - coronary, peripheral, arterial
5) Retinopathy
6) Renal failure

46
Q

Where the cardiovascular center located in the brain?

A

Medulla oblongata of the brain stem - region known as the tractus solitarius

47
Q

What are the 4 inputs to the cardiovascular center in the brain?

A

1) Higher brain centers
2) Proprioreceptors - monitor joint movements
3) Baroreceptors - monitor blood pressure
4) Chemoreceptors - monitor blood acidity

48
Q

What are the outputs from the CV center in the brain?

A

1) Vagus nerves - heart (decreased rate)

2) Sympathetic nerves - heart (increased rate and contractility) and blood vessels (vasoconstriction)

49
Q

What is orthostatic or postural hypotension?

A

Decreased BP on standing

50
Q

Which 2 hormones lead to increased BP through increasing cardiac rate and contractility?

A

Epinephrine

Norepinephrine

51
Q

What 4 hormones lead to increased BP through vasoconstriction?

A

1) Angiotensin 2
2) Vasopressin
3) Norepinephrine
4) Epinephrine

52
Q

What 2 hormones lead to increased circulatory volume and thus increase in BP?

A

1) Vasopressin

2) Aldosterone

53
Q

What hormone leads to decreased circulatory volume and thus a decrease in BP?

A

1) Atrial natiuretic peptide

54
Q

What structures can pass through fenestrated capillaries and where are they found?

A

Small, lipophillic molecules

Intestinal villi, endocrine glands, kidney glomeruli

55
Q

What substances can pass through sinusoidal capillaries and where are they found?

A

Red blood cells and large hydrophillic molecules

Liver, bone marrow and spleen

56
Q

What is Starling’s law of the capillaries?

A

Hydrostatic pressure out and osmotic pressure in
At arterial end net pressure is out
At venous end net pressure is in

57
Q

What are the 3 types of blood flow?

A

1) laminar flow
2) Turbulent flow
3) Single file flow

58
Q

What is the flow in the aorta?

A

Pulsating laminar flow during early systole

Turbulence during peak velocity of flow

59
Q

Why is velocity of blood lowest in capillaries?

A

Velocity = Flow rate/cross sectional area
Flow rate must be the same throughout circulation
Capillaries have the largest cross sectional area and thus the lowest velocity

60
Q

What 3 parameters determine resistance?

A

1) Length of blood vessel
2) Radius of the vessel
3) Viscocity of blood

61
Q

The levels of what 4 substances rise in the blood during exercise and cause local vasodilation by relaxation of vascular smooth muscle?

A

1) H+
2) CO2
3) K+
4) Adenosine (ATP-ADP-AMP-Adenosine)

62
Q

Why does NO have a protective effect against thrombosis?

A

Causes relaxation of vascular smooth muscle and thus vasodilation reducing blood pressure
It makes the blood less prone to clotting

63
Q

By what process is increased NO formed in endothelial cells during exercise?

A

1) Increased blood flow through capillaries
2) Ca2+ moves into endothelial cell
3) Ca2+ causes the conversion of Larginine to NO
4) NO moves into vascular smooth muscle and causes relaxation

64
Q

Why is NO given in GTN spray to relieve angina?

A

Causes vascular smooth muscle relaxation and thus vasodilation

65
Q

Why does atheroma formation occur frequently at arterial junctions?

A

These are stress points

They have high flow rates and more turbulent flow in these regions

66
Q

What are the 3 main stages of atheroma formation?

A

1) Endothelial damage
2) Uptake of LDL particles, adhesion and infiltration of macrophages
3) Smooth muscle proliferation and formation of a fibrous cap

67
Q

What 4 factors promote atheroma formation?

A

1) Sheer stress - hypertension
2) Toxic damage, chemicals - cigarette smoke
3) High levels lipids - familial hypercholesterolaemia, diabetes
4) Viral or bacterial infection - chlamydia pneumoniae

68
Q

What causes proliferation of smooth muscle and deposition of collagen in a atheromatous plaque?

A

Growth factors are released by the damaged endothelium which cause proliferation of smooth muscl and deposition of collagen

69
Q

What forms a fibrous cap over an atheromatous plaque and why is the fragility increased?

A

Collagen forms a fibrous cap

Fragility is increased because of calcification of the plaque

70
Q

What triggers the formation of a thrombus in atheroscelrosis?

A

Rupture of fibrous cap exposes collagen and TF to the blood which triggers the formation of a thrombus

Year 1 Body Systems (17 decks)

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