Cardiovascular Physiology Flashcards
heart cells
- atrial and ventricular cells ~ 99% of heart’s mass
- cells will not contract unless signal is sent
how are heart cells electrically connected
via gap junctions - low resistance electrical pathway for cell:cell conduction
atrioventricular septum
- fibrous tissue that electrically isolates left and right side of the heart - non conducting tissue
- all the heart valves are in this septum
duration of nerve/skeletal muscle AP vs myocardium AP
how does SNS and PNS impact duration
2-3 msec is hundreds of msec and is variable –> sympathetic stimulation shortens duration and parasympathetic lengthens durations
5 phases of action potential in working myocardium (review diagram page 13 slide 1)
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
nodal cells
sympathetic and/or parasympathetic innervation?
- <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
does working myocardium receive sympathetic or parasympathetic innervation?
- myocardial muscle (NOT nodal cells) receives only sympathetic innervation for contractions
nodal cell action potential
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
increasing heart rate changes to currents
what hormones cause this?
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
what causes the unstable resting membrane potential in nodal cells?
funny current! both K and Na ions move through
during diastole, what can you say about working myocardial cells
they are electrically silent
what is the pacemaker region and why?
SA node has the highest density of funny channels
- has the fastest rate of depolarization and sets the pace
comparing action potential conduction velocities
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
leads
3 limb leads
3 augmented limb leads
6 precordial leads in horizontal plane
excitation contraction coupling (ECC)
which phase of the action potential?
- 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
how can we change the force of contraction?
skeletal muscle:
1. recruit more muscle fibres
2. summation and tetanus
cardiac muscle:
- release more Ca2+
- change the sensitivity of troponin-C to Ca2+
key points of vascular system
- 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
pulse pressure
systolic pressure - diastolic pressure
mean arterial pressure
- constant pressure required to produce the same flow
- required for adequate perfusion of the organs
- approximation: diastolic pressure + 1/3 pulse pressure
where is the largest pressure drop
(and what are they known as?)
across the arterioles (they are thus referred to as the resistance vessels
venous valves
- in lower part of the body
- muscles pump blood up the veins, and valves cose to prevent backflow
is blood flow laminar or turbulent
mostly laminar
which is more compliant?
veins/arteries
veins - thinner walls
baroreceptors
- 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
cardiac output
+ ejection fraction
- 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%
what is HR regulated by
ANS and hormones
what is SV regulated by
- 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
heart valves
- tricuspid: RA to RV
- pulmonary: RV to pulmonary arteries
- mitral: LA to LV
- aortic: LV to aorta
aortic and pulmonary are semilunar valves (SLAP)
what is valve operation controlled by
pressure differences!
wiggers diagram
go through tricky bits on slide 2 pg 17
end diastolic pressure volume relationship
compliance = V/P
increased compliance:
- systolic heart failure
- decreases slope
- ventricle increases diameter
decreased compliance
- hypertension
- ventricular wall thickens
- increased P/V slope
end systolic pressure volume relationship
look at slides 20-26 for diagrams!
