PSIO202 Exam 1 Lecture 4 Flashcards

1
Q

What is a cardiac cycle?

A

All of the events in one heartbeat

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2
Q

What is the length of the average cardiac cycle at rest?

A

0.8 seconds

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3
Q

How is HR related to cycle period (T)?

A

HR=1/T x 60

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4
Q

What does 1/T represent?

A

Frequency (beats per second)

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5
Q

How does flow of ions impact membrane potential in the SA/AV nodes?

A

leak current of Na+ causes slow depol to threshold, increase in Ca++ permeability causes depolarization, and K+ flowing out causes repolarization

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6
Q

Is control of heart rate chronotropic or inotropic?

A

chronotropic

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7
Q

Other than nervous input, what else can modify heart rate?

A

emotions/limbic system, circulating hormones, cortical input, and ion concentrations

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8
Q

Where are the cardiovascular control centers located?

A

caudal medulla

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9
Q

Does the sympathetic nervous system affect HR, contractility, or both? What is the reasoning for this?

A

Both, because it innervates the nodes, atria, and ventricles

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10
Q

Does the parasympathetic nervous system affect HR, contractility, or both? What is the reasoning for this?

A

HR only, because it only innervates the nodes and atria

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11
Q

What is the pathway of sympathetic nervous input on HR? Draw it out.

A

sympathetic neurons from the cardioaccelatory center synapse onto a short preganglionic neuron, release ACh onto the ganglion, along postganglionic neuron synapses onto the SA/AV nodes, atria, and ventricles where norepinephrine is released. NE activates B1 receptors, increase Na+ and Ca++, less permeable to K+, reaches threshold more easily (and doesn’t hyperpolarize as much) which increases heart rate

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12
Q

What is the pathway of parasympathetic nervous input on HR? Draw it out.

A

parasympathetic neurons in the cardioinhibitory centers send axons to the heart in the Vagus nerve (CN X), vagus nerve synapses onto the SA/AV nodes and atrial muscle. Vagus nerve releases ACh onto the cells, increase K+ diffusion out of the cell, lots of hyperpolarization, takes more time for Na+ leak to reach threshold and activate Ca++, longer cycles and slower HR

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13
Q

What ion concentrations affect normal heart function?

A

hypocalcemia: low Ca++, impede crossbridge formation, depress contractility
hypercalcemia: too much Ca++, too much crossbridge formation, spastic contractions and heart irritability
hypernatremia: too much Na+, inhibits Ca++, no crossbridge formation, blocks heart contraction
hyperkalemia: too much K+, super hyperpolarized, leak current of Na+ can’t depolarize to threshold

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