CVS Flashcards

1
Q

Features of cardiac muscle

A
Striated 
Involuntary 
Extensive branching
Intercalated disc 
Gap junctions
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2
Q

Role of intercalated disc in cardiac muscle

A

Present at Z line
Increases cell to cell cohesion
Heart is a mechanical synctium

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3
Q

Role of gap junctions in cardiac muscle

A

At z line

Heart is a functional synctium

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4
Q

Difference between skeletal muscle and cardiac muscle

A

Sk muscle - c muscle
T-tubule- at A-I junction- at Z line,wider
SR. - well developed- less developed
DHPR - voltage sensor- voltage gated ca Channel
Source of Ca- SR- SR+ ECF
Removal of SR Ca- SERCA - SERCA+ Na/K antiport
Phospholamban-absent-present

(See your notes)

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5
Q

Name the modified contractile cells that have pacemaker potential

A

SA node

AV node

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6
Q

Modified contractile cells (conducting tissue) that have plateau potential

A

Internodal tracts
Bundle of His
Bundle branches
Purkinje fibres

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7
Q

Fastest conducting tissue

A

Purkinje fibres 4 m/s

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8
Q

Which is the slowest conducting tissue and why

A

AV node 0.05 m/S
Small diameter
Very few gap junctions

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9
Q

What is the advantage of AV node delay

A

Atria contract ahead of ventricles

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10
Q

Advantages of having a plateau potential in cardiac muscle

A

Prolonged ARP

cardiac muscle cannot be tetanized

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11
Q

What happens during plateau phase in cardiac muscle

A

K efflux Ca influx (slow Ca channel/slow Na-Ca channel)

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12
Q

What happens in depolarisation in pacemaker potential cardiac muscle

A

Ca influx through CaL channels

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13
Q

What is pre-potential phase in pacemaker potential (cardiac muscle)

A

Slow and spontaneous depolarisation till firing level

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14
Q

What does pre-potential phase start with (cardiac muscle)

A

Decrease K efflux

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15
Q

What does opening of F channels do

A

F ‘funny’ channels permit movement of both Na and K but movement of Na predominates

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16
Q

Main reason for reaching the prepotential phase (level becoming positive)

A

Ca influx through CaT channels

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17
Q

Effect of sympathetic discharge on pacemaker potential

A

Increase heart rate (know how)

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18
Q

Effect of parasympathetic discharge on pacemaker potential

A

Dual action

Decreased heart rate

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19
Q

What is the intrinsic rate of discharge of SAN

A

100/min

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20
Q

What is the resting heart rate

A

70-80/min

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21
Q

What is the heart rate of transplanted heart

A

100/min

As there is no sympathetic or parasympathetic discharge

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22
Q

Why do athletes have bradycardia at rest and what is the advantage

A

Very high resting vagal tone
Adv-high cardiac reserve

Cardiac reserve = maximum CO- basal CO

23
Q

Sympathetic and parasympathetic effect on force of contraction do heart

A

Sympathetic-increases force

Parasympathetic-no effect (no vagus to ventricles)

24
Q

At what seconds does conduction reach AVN,leave AVN,leave bundle of his (not too sure of the question is right)

A

Reach AVN- 0.03s (duration 0.03s)
Leave AVN-0.12s (duration 0.09s)
Leave bundle of His 0.15s (duration 0.03s)

25
Q

When does the conduction reach endocardium and epicardium in heart

A

Endo-0.18-0.19s

Epi-0.21-0.22s

26
Q

Ventricular depolarisation direction

A

Septum-endo-epi

27
Q

Ventricular repolarisation direction

A

Epi-endo

28
Q

What are the types of blood vessels present in the heart and eg

A
Wind Kessel vessels-aorta,large arteries
Resistance vessel-arterioles
Exchange vessels -capillaries 
Capacitance vessels-venues,veins,vena Cava
Shunt vessels -AV anastomoses
29
Q

What’s re the determinants of DBP

A

Elastic recoil of aorta and large arteries

TPR

30
Q

What is known as the seat of peripheral resistance

A

Arterioles

31
Q

Which vessels respond to local metabolised

A

Exchange vessels

32
Q

Decreased pO2 causes vasodilation by what mechanism

A

ATP dependent K channels

33
Q
Decreases pO2 (hypoxia) causes vasodilation everywhere except?
And what is the mechanism
A

Lungs (vasoconstriction)

Sensitive K channels

34
Q

Increase sympathetic discharge in resistance vessels causes what

A

Increased resistance

35
Q

Why does resting skeletal muscle blood flow increase during exercise

A

Due to release of local metabolised

Exchange vessels respond

36
Q

Increases sympathetic discharge causes what in capacitance vessels

A

Increases venous return

37
Q

Where are shunt vessels present (eg) and what is it’s function

A

Earlobes
Fingertips

Function- temperature regulation

38
Q

What are the hemodynamics laws applicable to CVS

A

1.Flow=deltaP/R
2.velocity of flow ~ 1/cross section area
V1A1=V2A2
3.Hagen poisuille law (know the formula in terms of resistance and flow)
4.laminar and turbulent flow (reynold’s number)
5.La place’s law

39
Q

Resistance in woods unit is

A

R= deltaP(mm Hg)/flow (L/min)

40
Q

Resistance in R units (PRU)

A

R= delta P (mm Hg)/flow (ml/sec)

41
Q

Maximum velocity in

a) aorta
b) capillaries

A

Aorta

Total surface area
Aorta= 4.5 sq cm
Capillaries= 4500 sq cm

42
Q

In terms of hagen poisuille law what kind of circulation will anemia have

A

Anemia-viscosity low

Flow ~ 1/eta
Therefore hyper dynamic circulation

43
Q

In terms of hagen poisuille law what kind of circulation will a vessel with larger radius have

A

Larger radius
Flow ~ radius

More flow

44
Q

What is Reynolds number and what is it’s significance

A

Reynolds number = rhoDV/eta

> 3000- turbulent
<2000-laminar
2000-3000-transitional flow

45
Q

La place’s formula for cylinder and sphere

A

If wall thickness (W) is significant
T=
Cylinder = Pr/W (artery)
Sphere = Pr/2W(ventricle)

If wall thickness is not significant
T=
Cylinder=Pr (capillaries)
Sphere=Pr/2(alveoli)

P-pressure
r-radius

46
Q

Korotkoff sounds can be related to which hemodynamic rules of CVS

A

Reynolds number high (due to less radius during cuffing)

Turbulence therefore sound heard

47
Q

Cardiac cycle time

A

0.8 s

48
Q

Atrial systole and atrial diastole timings

A

Atrial systole 0.1s

Atrial diastole 0.8s

49
Q

Ventricular systole and diastole timing

A

Ventricular systole - 0.3s

Ventricular diastole-0.5s

50
Q

Phases of cardiac cycle

A

0.3s
Isovolumetric contraction
Rapid ejection
Slow ejection

0.5s
Isovolumetric relaxation 
1st Rapid filling 
Diastasis
2nd Rapid filling 

KNOW THE WHOLE THING
VERY IMPORTANT

51
Q

What and when is S1 due to

A

Onset of ventricular systole

Closure of AV valve

52
Q

What and when is S2 due to

A

End of ventricular systole

Closure of semilunar valves

53
Q

What and when is S3 due to

A

Due to rapid flow of blood from atria to ventricle

During first rapid filling phase

54
Q

What and when is S4 due to

A

Second rapid filling phase

Coincides with AS