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How do cardiac AP differ from skeletal muscle AP
Cardiac AP: Automaticity, conductivity (from cell to cell), excitability (long refractory duration); NO TETANY
What are HCN/funny channels
Pacemaker current; activated by HYPERpolarization enhanced by sympathetic and adrenaline suppressed by vagus
What are the phases of cardiac AP generation
Phase 0: Depolarization → Phase 1: Initial repolarization → Phase 2: Plateau → Phase 3: Rapid repolarization → Phase 4: Resting potential
What occurs during each phase of cardiac AP generation
Phase 0: Depolarization → Na enter cell; Phase 1: Na channel close, K channel open and K leaves; Phase 2 → L type Ca channel allow Ca in, K goes out (both are balance; Phase 3 → Ca channel close, another K channel open; Phase 4 → Na/K pump and Na/Ca exchange
What causes tetany
Hypocalcemia → More Na enters cell than normal → More depolarization → Tetany
What happens in myocardial CONTRACTIOn
Phase 2 (plateau) → Ca enters → Activates RyR2 in SR → Ca release → Cross bridge
What is the RyR2
Ca gated Ca channel found in SR → Supplies Ca to cardiomyocytes → Rhythmic Depolarization
What happens in myocardial RELAXATION
Ca reabsorb into SR and Ca channel close → Thin filament deactivate → No more cross bridge → SERCA transports Ca back into SR
Why is a long refractory period important for heart cells
PREVENTS tetany from happening
What is the supranormal period
Period where the membrane is very sensitive to AP potential activation → Occurs at end phase of refractory period
What is Frank Starling curve
Force/tension in a muscle fiber depends on the extent the fiber is stretched (Tension = F/unit length)
What is the consequence of overactive or underactive muscle
Overactive → Actin myosin overlap and shorten muscle → Tension and force decrease; underactive → muscle is stretched too much and tension decrease
What is inotropic agent
An agent that can increase (positive) or decrease (negative) contractability of the heart
What substances are positive and negative inotropic
Positive: NorE; negative: Beta blockers
How can inotropic agent be used for heart failure
Heart failure from poor contractability → Positive inotropic increase contractability of heart
How can inotropic agent be used for ischemia
Ischemia = O2 demand > supply of O2 → Treatment is to DECREASE O2 demand → NEGATIVE inotropic agent decrease heart workload and energy
How can inotropic agent by used for low BP
Positive inotropic increase contractability of heart = increases heart rate
How can inotropic agent be used for tachycardia
Negative inotropic reduce HR