Cardiovascular Flashcards
define stressed volume?
volume of blood contained in the arteries
arteries are under the highest pressure in the vasculature
where can we find the highest resistance to blood flow?
why?
Arterioles
they have a lot of smooth muscle which is tonically active (innervated by sympathetic adrenergic nerve fibers)
what adrenergic R can we find in the arterioles in the skin and splanchnic vasculature?
what is the consequences?
a1-Adrenergic -> contraction -> decrease in diameter of the arteriole -> increase the resistance to blood flow
which vessels have large capacitance and why?
veins
bcs their walls contain much less elastic tissue than arteries
equation for the relationship btw velosity, flow and crossectional area
V=Q/A
what two factors eefect the blood flow through a blood vessel?
- pressure difference
2. resistance of the vessel
equation for the relationship btw flow, pressure and resistance?
Q=P/R
mL/min
direction of blood flow is allways from:
high pressure to low pressure
what will higher resistance do to flow?
inversley prop. higher resistance -> decreased flow
define TPR
the resistance of the entire systemic vasculature
how can we measure TPR?
we can put cardiac output instead of flow in the Q=P/R equation
and the difference in pressure btw Aorta and Vena Cava
what does compliance describes?
the volume of blood the vessel can hold at a given pressure
compliance equation
C=V/P
C- Compliance (mL/mmHg)
V- Volume (mL)
P- Pressure (mmHg)
SA node BPM
60-80 BPM
sinus rythm
what is the reason for the delay 0.1 sec in the AV node conduction?
- less amount of Gap Junction
2. diameter is smaller (slower conductance)
connection btw nodal cells
Gap Junction
funny channels function
allow slow leaking into the cell of Na+
resting membrane potential of nodal cells
around -60 mV
T-type channels are for ___ and open at ___
Ca++
-55 mV
threshold point in the nodal cells
-40 mV
which channel opens when the membrane otential reaches the threshold?
L-type Ca++ channels
what happens to the contractile cells when the nodal cells reach depolarization (at +40mV)?
how?
positive cations moves from the nodal cells into the contractile cells through the Gap Junction
define intercalated disks
Desmosomes+Gap Junction
btw nodal and contractile cells
resting membrane potential of the contractile cells in the heart
around -85 mV / -90 mV
threahold potential of the contractile cells in the heart
-70 mV
upon entering of cations from the nodal cells and reaching the threshold, which channels are stimulated?
voltage gated Na+ channels open
what happens after voltage gated Na+ channels open and Na+ ions get inside the contractile cell?
- also L Type Ca++ are open (slowly)
- K+ ch open (K+ goes out -> repolerize the cell to 0 mV)
what does the repolirization of the cell to 0mV causes?
L Type Ca++ are open faster and allows many Ca++ get inside the cell. in the same time K+ leave the cell
what causes the platau in the contractile cell membrane potential?
L Type Ca++ are open -> many Ca++ get inside the cell. in the same time K+ leave the cell
describe Ca++ induce Ca++ release mechanism
Ca++ is in the cells due to L -Type Ca++ channels -> Ca binds RYR-2 on the Sarcoplamic Reticulum -> RYR-2 opens its channel -> Ca leave the Sarcoplamis Reticulum to the cell
describe the contraction mechanism itself of the contractile cells of the heart
Ca++ binds Troponin -> changes the shape of Tropomyosin -> Myosin head can now interact with the Actin
[over all Ca++ induces the cross-bridging]
how does the contraction terminates?
- L type Ca ch stop working
- antipoter of H+/Ca++ using ATP to give back the Ca++ ions to the Sarcoplasmic Reticulum
- Na/Ca antiporter on the Sarcoplasmic Reticulum
what R can we find on the nodal cell of the heart?
B1 Adrenergic R (NE/N) -symp NS
M2-R (Ach) - para symp
action of B1 Adrenergic R on the nodal cell
activates Gs GPCR -> cAMP increases -> pKA activates -> phoshorylation of L-Type Ca channels and other proteins -> Ca enters the cell BLA BLA BLA -> increased HR
action of M2-R on the nodal cell
activates Gi GPCR -> B and Gamma subunits of Gi open K+ chennels -> K+ move out -> Hyperpolarization -> decreased HR
** A subunit -> cAMP decrease
