Flashcards for:
Understanding Heart Rate Regulation Mechanisms

Extrinsic factors adjust the heart rate above or below the intrinsic sinus rhythm.

Hyperpolarization, typically mediated by parasympathetic action, slows down action potential generation, thereby decreasing heart rate.

Sympathetic influence increases contractility and stroke volume, elevating cardiac output and blood pressure through increased crossbridge formation and calcium influx.

Acetylcholine.

Sympathetic stimulation has a positive chronotropic effect (increasing heart rate), while parasympathetic stimulation has a negative chronotropic effect (decreasing heart rate).

Bradycardia is a heart rate less than 60 bpm, typically due to the parasympathetic system's hyperpolarization effects.

During sympathetic stimulation, action potentials occur more frequently.

The sympathetic nervous system releases norepinephrine and epinephrine, binds to Beta-1 adrenergic receptors, activates G stimulatory protein, converts ATP to cyclic AMP, and uses protein kinase A to phosphorylate L-type calcium channels, increasing heart rate.

Beta-1 adrenergic receptors, when activated by sympathetic stimuli, increase heart rate by enhancing calcium entry and depolarization.

The parasympathetic nervous system decreases heart rate by releasing acetylcholine via the vagus nerve, which binds to muscarinic type 2 receptors, activating G inhibitory proteins and causing hyperpolarization.

The absolute refractory period is when no new action potentials can be initiated, whereas the relative refractory period allows for strong stimuli to potentially initiate action potentials, though it is risky.

Tachycardia is caused by increased depolarization due to sympathetic stimulation that raises heart rate above 100 bpm.

Balancing these systems maintains cardiovascular health by ensuring proper heart rate and contractility.

Intrinsic innervation sets the normal sinus rhythm of the heart.

Parasympathetic activity reduces heart rate, which in turn decreases cardiac output.