1. see above; depriving tissues of O2 can lead to cell damage and/or cell death; cardiac cells are non-regenerative and are replaced with a patch of fibrous connective tissue – this diminishes pumping efficiency and the normal functioning capabilities of the heart drop
2. diastole – rest, systole – pump
3. see pg 380; diastole: the atria fill with blood, the A.V. valves open and the ventricles fill to about 80% while semilunar valves are still closed…

atrial systole: atria pump blood to ventricles, they fill to 100%…
atrial diastole: atria start filling with blood again, and
ventrical systole: AV valves shut, SL valves open, blood goes to either the lungs or the body

4. Cardiac muscle contractions are different than skeletal muscle contractions because they involve V-Ca++ gates! An AP is fired in the following steps: V-Na+ gates open first, sodium rushes in, V-Ca++ gates open and stay open, causing a plateau of depolarization inside the cell, V-K+ gates open and the rest of the AP steps follow; the plateau phase guarantees that another AP won’t fire before the contraction is done, therefore preventing tetanus
5. nodal tissue is made up of specialized cardiac muscle cells with an unstable resting membrane potential – a constant leakage of ions lets the sinoatrial (SA) nodes fire APs on its own~ setting a pace at about 70 APs/minute (or 70 beats/min)
6. AP spreads through the atria first, they contract, then the AP reaches the second node (AV node) that follows the lead of the sinoatrial node, delays signal to the ventricles, allows completion of the atrial contractions, and it relays the signal down specialized conduction fibers called Perkinje fibers- they spread the AP into the ventricles