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BMEG 350 > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

heart cells

A
  • atrial and ventricular cells ~ 99% of heart’s mass
  • cells will not contract unless signal is sent
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2
Q

how are heart cells electrically connected

A

via gap junctions - low resistance electrical pathway for cell:cell conduction

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3
Q

atrioventricular septum

A
  • fibrous tissue that electrically isolates left and right side of the heart - non conducting tissue
  • all the heart valves are in this septum
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4
Q

duration of nerve/skeletal muscle AP vs myocardium AP

how does SNS and PNS impact duration

A

2-3 msec is hundreds of msec and is variable –> sympathetic stimulation shortens duration and parasympathetic lengthens durations

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5
Q

5 phases of action potential in working myocardium (review diagram page 13 slide 1)

A

phase 0 = voltage-gated Na+ channel:
- inward Na+ current
- fast activation and fast inactivation

phase 1 = voltage-gated K+ channel:
- transient outward K current
- fast activation and inactivation

phase 2 = voltage gated Ca+ channel:
- inward Ca current
- slow activation and inactivation
- plateau phase of action potential

phase 3 = voltage gated K+ channel
- outward K current
- slow activation and inactivation
- different from phase 1 channel

phase 4 = voltage gated K channel
- opens during repolarization and closes during depolarization

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6
Q

nodal cells

sympathetic and/or parasympathetic innervation?

A
  • <1% of heart’s mass
  • spontaneously active
  • includes SA and AV nodes, bundle of His, bundle branches and Purkinje fibres
  • firing rate: SA node > AV node > bundle of His and bundle branches > Purkinje fibres
  • internodal pathways are NOT spontaneously active - cells may have more gap junctions to speed conduction
  • nodal cells have sympathetic (increased HR) and parasympathetic (decreased HR) innervation
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7
Q

does working myocardium receive sympathetic or parasympathetic innervation?

A
  • myocardial muscle (NOT nodal cells) receives only sympathetic innervation for contractions
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8
Q

nodal cell action potential

A

phase 0: voltage gated Ca channel
- same as in myocardium
- inward CA current

phase 3: voltage gated K channel
- same as in myocardium
- outward K current

phase 4: voltage-gated Na and K channel = FUNNY CURRENT
- permeable to both Na and K
- opens as the membrane repolarizes and closes as it depolarises
- aka pacemaker potential

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9
Q

increasing heart rate changes to currents

what hormones cause this?

A

noradrenaline and adrenaline increase currents:
- funny current: slope of phase 4 increases, threshold reached earlier, heart rate increases
- K current: repolarization is faster in ALL cells, which shortens the duration of the action potential in every cell

acetylcholine has opposite effect

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10
Q

what causes the unstable resting membrane potential in nodal cells?

A

funny current! both K and Na ions move through

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11
Q

during diastole, what can you say about working myocardial cells

A

they are electrically silent

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12
Q

what is the pacemaker region and why?

A

SA node has the highest density of funny channels
- has the fastest rate of depolarization and sets the pace

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13
Q

comparing action potential conduction velocities

A

determinants:
1. size of cells: purk > bundle of His > ventricle~atria > nodes
2. number of gap junctions

purk: 4m/s
bundle of His: 2 m/s
ventricular and atrial muscle: 0.5 m/s
nodal cells: 0.05 m/s

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14
Q

leads

A

3 limb leads
3 augmented limb leads
6 precordial leads in horizontal plane

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15
Q

excitation contraction coupling (ECC)

which phase of the action potential?

A
  • Ca enters cell through voltage gated channels on the t-tubule portion of the dyad but there isn’t enough of it to produce a significant contraction
  • so, it binds to RyR2 (type II ryanodine receptor), which releases more Ca2+ stored in the SR to cause a contraction!
    —> Ca induced Ca release (CICR)
  • happens at PHASE 2
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16
Q

how can we change the force of contraction?

A

skeletal muscle:
1. recruit more muscle fibres
2. summation and tetanus

cardiac muscle:
- release more Ca2+
- change the sensitivity of troponin-C to Ca2+

17
Q

key points of vascular system

A
  • arterial walls are much thicker and less compliant than veins
  • at rest 70% of blood is in veins
  • SNS activation produces vasoconstriction
  • PNS activation produces vasodilation
  • capillaries have no smooth muscles
  • every cell in the body is usually no more than 2-3 cell lengths away from a capillary
18
Q

pulse pressure

A

systolic pressure - diastolic pressure

19
Q

mean arterial pressure

A
  • constant pressure required to produce the same flow
  • required for adequate perfusion of the organs
  • approximation: diastolic pressure + 1/3 pulse pressure
20
Q

where is the largest pressure drop

(and what are they known as?)

A

across the arterioles (they are thus referred to as the resistance vessels

21
Q

venous valves

A
  • in lower part of the body
  • muscles pump blood up the veins, and valves cose to prevent backflow
22
Q

is blood flow laminar or turbulent

A

mostly laminar

23
Q

which is more compliant?

veins/arteries

A

veins - thinner walls

24
Q

baroreceptors

A
  • stretch receptors embedded in the arterial wall in the carotid sinuses and aortic arch
  • MAP rises = SNS activation goes does and PNS activation goes up –> less constriction and more dilation of vessels
25
Q

cardiac output

+ ejection fraction

A
  • principle measure of pump function
  • CO (L/min) = heart rate (beats/min) x stroke volume (L/beat)
    ~5 L/min at rest
  • ejection fraction is ~55-75%
26
Q

what is HR regulated by

A

ANS and hormones

27
Q

what is SV regulated by

A
  • preload: wall tension before contraction - usually measured by end diastolic pressure
  • afterload: wall tension during systole - usually measured by MAP
  • contractility: max force developed during systole
28
Q

heart valves

A
  • tricuspid: RA to RV
  • pulmonary: RV to pulmonary arteries
  • mitral: LA to LV
  • aortic: LV to aorta
    aortic and pulmonary are semilunar valves (SLAP)
29
Q

what is valve operation controlled by

A

pressure differences!

30
Q

wiggers diagram

A

go through tricky bits on slide 2 pg 17

31
Q

end diastolic pressure volume relationship

A

compliance = V/P
increased compliance:
- systolic heart failure
- decreases slope
- ventricle increases diameter
decreased compliance
- hypertension
- ventricular wall thickens
- increased P/V slope

32
Q

end systolic pressure volume relationship

A

look at slides 20-26 for diagrams!

BMEG 350 (14 decks)

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