1. Depolarization wave from SA node contracts atria from top down
2. Atrioventricularnode (AV) intercepts signal from nodal tissues in atria, delays signal to allow atrial contraction to maximize ventricular filling, relays depolarization wave to AV bundle (Bundle of His)
3. BundleofHis (a.k.a. AV bundle) at junction of atria and ventricles, A-V bundle branches carry impulse to apex of heart
4. Purkinjefibers carry impulse to ventricular myocardium, Depolarization wave from apex up, Ventricle contracts from bottom up
Slower contraction speed than skeletal muscle, fewer myofibrils
All-or-none response
Slow refractory period, 9X longer than skeletal muscle, Plateau effect - slow Ca+2 channels allow slow leak of calcium, Counteracts K+ outflow, Extends into relaxation phase, Insures time for ventricles to fill, No summation, voltage-gated K+ channels cause rapid repolarization
The more the cardiac fibers stretch, the stronger the contraction, More blood will be pumped out with greater filling, Less filling, lighter contraction, Regulates for different end diastolic volumes, Allows adjustment for right vs. left ventricle
Elastic arteries - large, dampen shock of ventricular systole, recoil to propel blood forward
Muscular arteries - medium, regulate bloodpressure, respond to vasomotor commands, thick tunica media
Arterioles - smallest arteries, lead into capillaries, pre-capillary sphincter
Capillary bed - area of majority of gas & nutrient exchange via diffusion, extensive branching, ~5% of blood, more filtration at arteriole end, osmotic return at venule end
Friction generated by blood as it moves past the vessel walls, Flow = pressure / resistance, ↑diameter by 2 = cut resistance in half, ↓ diameter by 2 = ↑ resistance by 2
If we combine ALL capillaries the total cross section is greater than that of any other vessel type, Low resistance, lowest flow rate = ↑ diffusion time