CVS Flashcards
Features of cardiac muscle
Striated Involuntary Extensive branching Intercalated disc Gap junctions
Role of intercalated disc in cardiac muscle
Present at Z line
Increases cell to cell cohesion
Heart is a mechanical synctium
Role of gap junctions in cardiac muscle
At z line
Heart is a functional synctium
Difference between skeletal muscle and cardiac muscle
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)
Name the modified contractile cells that have pacemaker potential
SA node
AV node
Modified contractile cells (conducting tissue) that have plateau potential
Internodal tracts
Bundle of His
Bundle branches
Purkinje fibres
Fastest conducting tissue
Purkinje fibres 4 m/s
Which is the slowest conducting tissue and why
AV node 0.05 m/S
Small diameter
Very few gap junctions
What is the advantage of AV node delay
Atria contract ahead of ventricles
Advantages of having a plateau potential in cardiac muscle
Prolonged ARP
cardiac muscle cannot be tetanized
What happens during plateau phase in cardiac muscle
K efflux Ca influx (slow Ca channel/slow Na-Ca channel)
What happens in depolarisation in pacemaker potential cardiac muscle
Ca influx through CaL channels
What is pre-potential phase in pacemaker potential (cardiac muscle)
Slow and spontaneous depolarisation till firing level
What does pre-potential phase start with (cardiac muscle)
Decrease K efflux
What does opening of F channels do
F ‘funny’ channels permit movement of both Na and K but movement of Na predominates
Main reason for reaching the prepotential phase (level becoming positive)
Ca influx through CaT channels
Effect of sympathetic discharge on pacemaker potential
Increase heart rate (know how)
Effect of parasympathetic discharge on pacemaker potential
Dual action
Decreased heart rate
What is the intrinsic rate of discharge of SAN
100/min
What is the resting heart rate
70-80/min
What is the heart rate of transplanted heart
100/min
As there is no sympathetic or parasympathetic discharge
Why do athletes have bradycardia at rest and what is the advantage
Very high resting vagal tone
Adv-high cardiac reserve
Cardiac reserve = maximum CO- basal CO
Sympathetic and parasympathetic effect on force of contraction do heart
Sympathetic-increases force
Parasympathetic-no effect (no vagus to ventricles)
At what seconds does conduction reach AVN,leave AVN,leave bundle of his (not too sure of the question is right)
Reach AVN- 0.03s (duration 0.03s)
Leave AVN-0.12s (duration 0.09s)
Leave bundle of His 0.15s (duration 0.03s)
When does the conduction reach endocardium and epicardium in heart
Endo-0.18-0.19s
Epi-0.21-0.22s
Ventricular depolarisation direction
Septum-endo-epi
Ventricular repolarisation direction
Epi-endo
What are the types of blood vessels present in the heart and eg
Wind Kessel vessels-aorta,large arteries Resistance vessel-arterioles Exchange vessels -capillaries Capacitance vessels-venues,veins,vena Cava Shunt vessels -AV anastomoses
What’s re the determinants of DBP
Elastic recoil of aorta and large arteries
TPR
What is known as the seat of peripheral resistance
Arterioles
Which vessels respond to local metabolised
Exchange vessels
Decreased pO2 causes vasodilation by what mechanism
ATP dependent K channels
Decreases pO2 (hypoxia) causes vasodilation everywhere except? And what is the mechanism
Lungs (vasoconstriction)
Sensitive K channels
Increase sympathetic discharge in resistance vessels causes what
Increased resistance
Why does resting skeletal muscle blood flow increase during exercise
Due to release of local metabolised
Exchange vessels respond
Increases sympathetic discharge causes what in capacitance vessels
Increases venous return
Where are shunt vessels present (eg) and what is it’s function
Earlobes
Fingertips
Function- temperature regulation
What are the hemodynamics laws applicable to CVS
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
Resistance in woods unit is
R= deltaP(mm Hg)/flow (L/min)
Resistance in R units (PRU)
R= delta P (mm Hg)/flow (ml/sec)
Maximum velocity in
a) aorta
b) capillaries
Aorta
Total surface area
Aorta= 4.5 sq cm
Capillaries= 4500 sq cm
In terms of hagen poisuille law what kind of circulation will anemia have
Anemia-viscosity low
Flow ~ 1/eta
Therefore hyper dynamic circulation
In terms of hagen poisuille law what kind of circulation will a vessel with larger radius have
Larger radius
Flow ~ radius
More flow
What is Reynolds number and what is it’s significance
Reynolds number = rhoDV/eta
> 3000- turbulent
<2000-laminar
2000-3000-transitional flow
La place’s formula for cylinder and sphere
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
Korotkoff sounds can be related to which hemodynamic rules of CVS
Reynolds number high (due to less radius during cuffing)
Turbulence therefore sound heard
Cardiac cycle time
0.8 s
Atrial systole and atrial diastole timings
Atrial systole 0.1s
Atrial diastole 0.8s
Ventricular systole and diastole timing
Ventricular systole - 0.3s
Ventricular diastole-0.5s
Phases of cardiac cycle
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
What and when is S1 due to
Onset of ventricular systole
Closure of AV valve
What and when is S2 due to
End of ventricular systole
Closure of semilunar valves
What and when is S3 due to
Due to rapid flow of blood from atria to ventricle
During first rapid filling phase
What and when is S4 due to
Second rapid filling phase
Coincides with AS
