Differentiate between the systemic and pulmonary circulations
- Systemic: left heart, systemic arteries, capillaries, and veins
- Pulmonary: right heart, pulmonary arteries, capillaries, and veins.
Cardiac output
rate at which blood is pumped from either ventricle
Venous return
rate at which blood is returned to the atria from the veins
equation for velocity
v=Q/A (flow/area)
equation for flow
Q=ΔP/R (change in pressure/radius)
equation for resistance
R=8ηl/πr4 (viscosity*length/radius of vessel)
-radius of vessel is most important and causes biggest change
series resistance
-arrangement of blood vessels in a specific organ. The blood will flow into organ from an artery digressing into arteriole, into capillary, into venule, until it drains out to major vein. The total resistance of the system is equal to the sum of each individual resistance.
parallel resistance
- distribution of blood flow among the major arteries branching from aorta and the collected at the vena cava’s. The resistance in parallel arrangement is less than any of the individual resistances
- flow through each organ is fraction of total blood flow, which allows for no loss of pressure, and mean pressure in each major artery will be similar to mean pressure in aorta. When adding a resistance to circuit, the total resistance will decrease. When adding resistance to one of individual vessels, the total resistance will increase.
Compliance
- volume of blood vessel can hold at given pressure.
- greater in veins which is why they can hold more
Local (intrinsic) control of blood flow
- autoregulation
- active hyperemia
- reactive hyperemia
Autoregulation
maintenance of a constant blood flow to an organ in the face of changing arterial pressure. Seen in kidneys, brain, heart, and skeletal muscle.
Active hyperemia
blood flow to an organ is proportional to its metabolic activity. If metabolic activity increases, then blood flow will increase proportionately.
-due to increase in heat, BPG, CO2
Reactive hyperemia
increase in blood flowin responseto orreactingto a prior period of decreased blood flow. For example, increase in blood flow to an organ that occurs following a period of arterial occlusion. During the occlusion, an O2debt is accumulated. The longer the period of occlusion, the greater the O2debt and the greater the subsequent increase in blood flow above the preocclusion levels. The increase in blood flow continues until the O2debt is “repaid.”
Neural (extrinsic) control of blood flow
involves thesympathetic innervationof vascular smooth muscle in some tissues. The density of such sympathetic innervation varies widely from tissue to tissue.
steps involved in the excitation-contraction coupling of the cardiac myocyte cell
- depolarization spreads to the interior of the cell via the T tubules.
- Entry of Ca2+into the myocardial cell produces an increase in intracellular Ca2+concentration. This triggers the release ofmoreCa2+from stores in the sarcoplasmic reticulum through ryanodine receptors.
- Ca2+binds totroponinC,which binds to tropomyosin which is moved out of the way, and the interaction of actin and myosin can occur. Actin and myosin bind,cross-bridgesform and then break, the thin and thick filaments move past each other, and tension is produced.
- Actin and myosin bind forming cross bridge. Cross-bridge cycling, fueled by adenosine triphosphate (ATP), continues as long as intracellular Ca2+concentration is high enough to occupy the Ca2+-binding sites on troponin C.
- Tension produced by myocardial cells.
types of smooth muscle
- unitary
- multiunit
Unitary (single unit) smooth muscle
Smooth muscle contracts in a coordinated fashion because the cells are linked bygap junctions. Gap junctions are low-resistance pathways for current flow, which permit electrical coupling between cells.
Multiunit smooth muscle
Each muscle fiber behaves as a separate motor unit (similar to skeletal muscle), and there is little or no coupling between cells.
Collaterals
-allow for continued blood flow with blockage in main artery
Relaxation of Myocardial cells
- The SR will self-regulate and draw back a majority of the Ca2+, excess will leave the membrane through exocytosis
- The reuptake of Ca causes tropomysin to block the actin binding site and the cell can no longer contract
Contractility through sympathetic stimulation
- NE will bind to beta receptors, cause AC to activate cAMP which activates PKA.
- PKA will phosphorylate:
- L-type ligand gated channel and ryanodine for faster intracellular release of Ca2+ (quicker contraction)
- Troponin C and phopholambam for faster reupatke of Ca2+(quicker relaxation)
Contractility through stretching
- stretching of myocyte allows for more cross bridges to form which increases contraction
- this is intrinsic mechanism
Contraction of smooth muscle cell
- Depolarization opens up voltage-gated Ca channels in SR, flow into cell. Additional mechanisms can be used to increase intracellular concentration of Ca through IP3 and ligand gated through hormones and neurotransmiters.
- Intracellular Ca2 binds calmodulin
- Calmodulin binds myosin-light-chain-kinase
- MLCK phosphorylates the myosin light chain changing the confirmation of its head and allowing it to gain access to the ATPase
- Myosin head binds actin in cross bridge and contracts
Relaxation of smooth muscle
- Larg + O2 = NO + cit in endo membrane
- NO diffuses into smooth muscle, activates GC– GTP to cGMP–activates myosin light chain phosphatase–dephosphorylates myosin light chain–causes relaxation
