8.6 Cardiovascular Physiology Flashcards

1
Q

Pacemaker and conducting system:

A

Pacemaker: initiates contraction
[SA node dictates when an action potential is fired, triggering atrial systole.]
Conducting system: ensures optimal expulsive contraction of ventricles.

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2
Q

Key components and origin of the 3-lead ECG.

A

enables viewing along all the different axes.
Lead I: right→ left arm (+ve electrode on left arm) good at detecting atrial contraction.
Lead II: right arm→ left leg (+ve on leg) good at detecting spread of excitation through septum towards apex.
Lead III: left arm→ left leg (+ve on leg) good at detecting spread across right atrium.

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3
Q

P, QRS, T waves.

A

(SEE IMAGE)

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4
Q

Role of papillary muscles in valve function.

A

Valve leaflets are anchored within the papillary muscles within the wall of the heart by thin and tough structures called chordae tendinae.

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5
Q

1st and 2nd heart sounds.

A

Due to valves closing.

Lub- happens slightly after Q wave- marks isovolumetric contraction at start of ventricular systole.
Dub- happens towards end of T wave- marks isovolumetric relaxation at start of ventricular diastole.

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6
Q

Cardiac cycle:

A

Ventricular diastole- muscle is relaxed (repolarised). Ventricular systole- muscle is contracting (during AP depolarisation).

Phase 1: (ventricular diastole) isovolumetric phase/ both AV valves are closed. Relaxation takes time, BP in ventricles and aorta is falling.

Phase 2: (ventricular diastole) elastic recoil phase, heart has an intrinsic tendency to recoil. Hence volume increases and blood is sucked in given that pressure inside ventricle is reduced beneath atrial pressure→ leads to filling phase.

Phase 3: (atrial systole) atria get excited- happens due to AP travelling in right and then left atria. This causes a contractile response, increasing pressure in atria and is sufficiently large to allow blood to flow down pressure gradient through AV valve.

Phase 4: (ventricular systole) isovolumetric phase= ventricular pressure increases between atrial pressure and arterial pressure.

Phase 5: (ventricular systole) ejection phase- soon followed by further increase in pressure due to inertia of ventricular muscle, eventually going beyond arterial pressure, allowing the semi-lunar valves to open, lifting the arterial pressure.

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7
Q

Jugular venous pulse in relation to central venous pressure.

A

Jugular venous pressure provides an indirect measure of central venous pressure. It is too low to feel but can see on a stretched neck (3× per second).

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8
Q

Physiological significance of the Frank-Starling mechanism.

A

the greater the filling of a cardiac chamber, the greater the individual myocardial fibres are stretched and hence the greater the subsequent force of contraction.

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9
Q

Concept of pre-load (CVP):

A

CVP: measured before entering atrium. No valve in atrium means whatever happens in atria will happen in CVP.

rises when…
• atrium contract
•AV valve shuts (valves bulge back into atria, producing a small pressure increase)
• atrium fills with blood.

falls when…
•atria relax
•AV valve opens.

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10
Q

Determinants of cardiac output.

A

cardiac output= stroke volume× heart rate

Thus can alter force of contraction (INOTROPY)

1) Change cell length: Starling’s Law
2) Cardiac nerves and circulating hormones acting on myocardial cells.

& can alter frequency of contraction (CHRONOTROPY):
1) Cardiac nerves and circulating hormones acting on myocardial cells.

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11
Q

What is an ECG showing?

A

ECG is measuring a wavefront of depolarisation (the part which drags the current).

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12
Q

Pressure and volume changes in cardiac cycle in relation to the ECG:

A

P wave: atrial depolarisation
QRS complex: Ventricular depolarisation.
R wave: where septum is filled with excitation which spreads across ventricles towards apex.
[Ventricular action potential spans from QRS to T wave. Ventricular muscle is massive hence very big dipole, big deflection.]
T wave: ventricular repolarisation.

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13
Q

relative conduction velocities in parts of the conducting system.

A

SA node initiates heart beat. Excitation spreads rapidly to atria which are 1 continuous electrical compartment. Excitation reaches AV node and is delayed by 0.1 secs. To prevent excitation going other routes have annulus fibrosus- this electrically insulates atria from ventricles and travels around whole heart. Excitation spreads rapidly through bundle of His towards apex. Large Purkinje fibres ensures a rapid spread across the ventricle wall.

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14
Q

What is an ECG showing?

A

ECG is measuring a wave front of depolarisation (the part which drags the current). ECG produces a big deflection if it’s a large wave front that’s moving rapidly.

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15
Q

Jugular venous pulse in relation to the cardiac cycle:

A

(SEE IMAGE)

A wave- due to atrial systole
C wave- due to tricuspid valve closure bulging into atrium
X descent- atria relax, AP in atria is over-repolarising
V wave- due to atria filling (during ventricular systole)
Y descent- due to tricuspid opening

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16
Q

Concept of after-load (aortic pressure):

A

Aortic pressure follows the ventricular pressure when semilunar valve is open with a slight delay but when you close the semilunar valves, the aortic and ventricular pressures become uncoupled. Pressure in ventricle dips down to zero whilst valve closure prevents aortic pressure falling towards zero.

17
Q

Functions of the circulation: systemic and pulmonary divisions.

A

:)

18
Q

Distribution of cardiac output to main organs of the body.

A

:)

19
Q

Relation between flow velocity and total cross-sectional area of vessel bed.

A

(SEE IMAGE) Cross-sectional area widens massively at capillaries. Branching slows blood velocity- GOOD- capillaries is where exchange happens.

20
Q

Blood volume and its distribution with respect to vessel type.

A

:)

Majority of blood held in systemic veins- useful: reservoir for blood.

21
Q

Effect of vessel radius on its resistance to flow.

A

:)

22
Q

Anomalous viscosity of blood.

A

:)

23
Q

Fluid balance across capillaries (Starling forces).

A

:)