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Year 1 Body Systems > Cardiology Physiology > Flashcards

Cardiology Physiology Flashcards

(70 cards)

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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
What happens to the longitudinal and horizontal and circumferential filaments during systole?
Longitudinal filament shortening | Horizontal and circumferential filament thickening
26
In which 2 ways can heart rate be increased?
1) Sympathetic innervation | 2) Adrenaline - beta 1 agonism
27
In which 2 ways can stroke volume be increased?
1) Increase pre load 2) Sympathetic input - prolonged opening of Ca2+ channels, enhances calcium action in excitation/contraction coupling mechanisms
28
What happens to the LVEF of a failing heart?
Decreases
29
What is the physiological LVEF and the LVEF in exercise?
Physiological LVEF - 50-75% | LVEF in exercise - can reach 90%
30
Why would ischaemia and viral infection/alcohol lead to a heart which contracts with less force?
Ischaemia - scarred myocardium | Viral infection/alcohol - wall thinning
31
In heart failure how does you body try to compensate for the weaker contraction of the heart and what does this lead to?
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
What 3 treatments would be given to a patient with heart failure and pulmonary oedema?
1) High flow O2 2) Morphine - relax pulmonary vessels to reduce preload and relieving pain 3) Furosemide - diuretic
33
How is preload measured?
End diastolic volume using an echocardiogram
34
What 6 ways can stroke volume be increased?
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
What is the bowditch effect?
Another curve, up to a point, increased heart rate = increased force of contraction
36
What organs does the parasympathetic nervous system have no effect on?
Adrenal glands and kidneys
37
What are the 4 effects of SNS on heart?
1) positive chonotropy - SA node 2) positive dromotropy - AV node 3) positive inotropy - atria and ventricles 4) positive lusitropy - atria and ventricles
38
What are the actions of RAAS (ie. angiotensin II, aldosterone and vasopressin)?
``` ANGIOTENSIN II Vasoconstriction Increased Na+ and H2O retention Vasopressin release Aldosterone release ALDOSTERONE Increased Na+ and H2O retention VASOPRESSIN Increased water retention ```
39
What are the PNS actions on the heart?
1) negative chonotropy - SA node 2) negative dromotropy - AV node 3) negative inotropy - Only ATRIA - no effect on ventricles
40
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?
1) Causes kidneys to release renin 2) Causes vasoconstriction 3) Acts directly on the heart to increase heart rate and stroke volume
41
How does the renal juxtaglomerular system work?
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
Where are baroceptors located and how do they control BP?
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
What is the anaerobic threshold in cardiopulmonary exercise testing?
Time when anaerobic respiration begins
44
What does cardiopulmonary exercise testing measure?
O2 consumption at rest and during exercise
45
What are the 6 consequences of uncontrolled hypertension?
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
Where the cardiovascular center located in the brain?
Medulla oblongata of the brain stem - region known as the tractus solitarius
47
What are the 4 inputs to the cardiovascular center in the brain?
1) Higher brain centers 2) Proprioreceptors - monitor joint movements 3) Baroreceptors - monitor blood pressure 4) Chemoreceptors - monitor blood acidity
48
What are the outputs from the CV center in the brain?
1) Vagus nerves - heart (decreased rate) | 2) Sympathetic nerves - heart (increased rate and contractility) and blood vessels (vasoconstriction)
49
What is orthostatic or postural hypotension?
Decreased BP on standing
50
Which 2 hormones lead to increased BP through increasing cardiac rate and contractility?
Epinephrine | Norepinephrine
51
What 4 hormones lead to increased BP through vasoconstriction?
1) Angiotensin 2 2) Vasopressin 3) Norepinephrine 4) Epinephrine
52
What 2 hormones lead to increased circulatory volume and thus increase in BP?
1) Vasopressin | 2) Aldosterone
53
What hormone leads to decreased circulatory volume and thus a decrease in BP?
1) Atrial natiuretic peptide
54
What structures can pass through fenestrated capillaries and where are they found?
Small, lipophillic molecules | Intestinal villi, endocrine glands, kidney glomeruli
55
What substances can pass through sinusoidal capillaries and where are they found?
Red blood cells and large hydrophillic molecules | Liver, bone marrow and spleen
56
What is Starling's law of the capillaries?
Hydrostatic pressure out and osmotic pressure in At arterial end net pressure is out At venous end net pressure is in
57
What are the 3 types of blood flow?
1) laminar flow 2) Turbulent flow 3) Single file flow
58
What is the flow in the aorta?
Pulsating laminar flow during early systole | Turbulence during peak velocity of flow
59
Why is velocity of blood lowest in capillaries?
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
What 3 parameters determine resistance?
1) Length of blood vessel 2) Radius of the vessel 3) Viscocity of blood
61
The levels of what 4 substances rise in the blood during exercise and cause local vasodilation by relaxation of vascular smooth muscle?
1) H+ 2) CO2 3) K+ 4) Adenosine (ATP-ADP-AMP-Adenosine)
62
Why does NO have a protective effect against thrombosis?
Causes relaxation of vascular smooth muscle and thus vasodilation reducing blood pressure It makes the blood less prone to clotting
63
By what process is increased NO formed in endothelial cells during exercise?
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
Why is NO given in GTN spray to relieve angina?
Causes vascular smooth muscle relaxation and thus vasodilation
65
Why does atheroma formation occur frequently at arterial junctions?
These are stress points | They have high flow rates and more turbulent flow in these regions
66
What are the 3 main stages of atheroma formation?
1) Endothelial damage 2) Uptake of LDL particles, adhesion and infiltration of macrophages 3) Smooth muscle proliferation and formation of a fibrous cap
67
What 4 factors promote atheroma formation?
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
What causes proliferation of smooth muscle and deposition of collagen in a atheromatous plaque?
Growth factors are released by the damaged endothelium which cause proliferation of smooth muscl and deposition of collagen
69
What forms a fibrous cap over an atheromatous plaque and why is the fragility increased?
Collagen forms a fibrous cap | Fragility is increased because of calcification of the plaque
70
What triggers the formation of a thrombus in atheroscelrosis?
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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