Cardiac function and BP Flashcards

(36 cards)

1
Q

skeletal muscle
(striated)

A
  • muscle cells made up of sarcomeres that contain thick filaments (myosin)
    and thin filaments (actin)
  • shortening of sarcomere occurs via sliding filament mechanism, where actin filaments slide along adjacent myosin filaments
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2
Q

cardiac muscle

A
  • acts like a syncytium
  • a wave of depolarisation os followed by atrial and ventricular contraction
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3
Q

syncytium

A

a single, multi - nucleated cell formed from many fused cells

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4
Q

cardiac excitation

A
  • 1% cardiac cells - with pacemaker activity
  • 99% cardiac cells - contractile function -> within ventricular tissue
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5
Q

SA node

A
  • sinoatrial node - natural pacemaker of the heart
  • a specialised region in the right atrial wall at the junction between the superior vena cava and the right atrium
  • they generate heart beats
  • they don’t have a resting potential
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6
Q

SA Node phases

A

phase 0 : upstroke of action potential is less steep than myocyte
phase
phase 3 : plateau is not sustained
phase 4 : membrane potential deviates from K+ equilibrium potential

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7
Q

cardiac excitation purpose

A

allows atria to contract and empty blood into ventricles

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8
Q

why does excitation spread rapidly down the bundle of His & Purkinje fibres

A

to ensure almost simultaneous activation of ventricular cells

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9
Q

4 events of cardiac excitation

A

only 3 are visible
1. atrial depolarisation (P wave)
2. Ventricular depolarisation (QRS complex)
3. Ventricular repolarisation (T wave)

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10
Q

atrial systole

A

A-V valves open and atria empty blood into ventricles
- atrial excitation and contraction should be complete before onset of ventricular contraction

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11
Q

ventricular systole

A
  1. ventricles contract -> rise in pressure closes A-V valve
  2. pressure in ventricle rises above aortic pressure -> aortic valve opens and blood is ejected from heart
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12
Q

ventricular diastole

A
  1. pressure in ventricles falls below aortic pressure -> aortic valve closes
  2. pressure in ventricles falls below atrial pressure -> AV valve opes and filling begins
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13
Q

stroke volume influences

A
  1. end diastolic volume
  2. aortic pressure
  3. contractility
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14
Q

end diastolic volume (preload)

A
  • resting cardiac muscle stretched prior to contraction
  • venous tone, blood volume, posture, intrathoracic pressure
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15
Q

aortic pressure (after load)

A
  • pressure against which the heart must work to eject blood during systole
  • aortic stiffness, periooheral resistance , blood volume
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16
Q

contractility

A
  • strength and vigour of the heart’s condition during systole at a given preload and after load
  • increased by sympathetic nerve stimulation and circulating catecholamines
  • decreased by hypoxia, acidosis, infarction
17
Q

heart rate influences

A

intrinsic rate
SNS - increase in heart rate
PNS- decrease in heart rate

18
Q

intrinsic rate

A

heart can initiates own heart beat in the absence of any nervous or hormonal control

19
Q

systole

A

heart contracting
systolic blood pressure = 120 mmHg

20
Q

Diastole

A

heart relaxing
bp = 80mmHg

21
Q

what is systolic blood pressure (SBP) determined by

A

stroke volume(StV) -> increases in StV will increase in SBP
aortic elasticity -> decreases in elasticity will also increase SBP

22
Q

Diastolic blood pressure (DBP)

A

pressure within the arteries during the period when the heart is not beating, as the heart fills with blood

23
Q

what is DBP determined by

A
  1. peripheral resistance (TPR) increases in TPR, increase DBP
  2. Aortic elasticity -> decreases in elasticity will decrease DBP
  3. heart rate -> decreases in HR will decrease DBP
24
Q

stroke volume =

A

end diastolic volume - end systolic volume

25
pulse pressure =
systolic BP - diastolic BP
26
mean BP =
diastolic BP + 1/3 pulse pressure
27
resistance =
pressure difference/ flow
28
vasoconstriction relationship w vessel radius
decrease in diameter increased resistance
29
vasodilation relationship w vessel radius
increase in diameter decreased resistance
30
what happens if bp is too low
inadequate supply of oxygen and nutrients to tissues
31
what happens if bp is too high
excessive strain on the heart and increased risk of vascular damage
32
how to effectively control bp
1. effector mechanisms -> ANS 2. pressure sensors -> baroreceptors 3. Central integration -> CNS cardiovascular centres
33
what does sympathetic stimulation lead to
vasoconstriction and increased total peripheral resistance
34
what is a baroreceptor
pressure sensors
35
where are baroceptosr located
located in the walls of major arteries
36
how does the body react to a fall in bp
- sensed by baroreceptors - afferent input to CNS CVS - info centrally integrated - efferent output via ANS - increased sympathetic drive to heart - increase heart rate abdominal TPR