Term
| The normal rhythmical impulse of the heart is generated in the ___. |
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Definition
| sinus node aka sinoatrial node aka SA node |
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Term
| The SA node is located ___. |
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Definition
| superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava |
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Term
| Ventricular contraction in the normal heart has a delayed onset of ___ after the atrial contraction. |
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Definition
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Term
| The ___ conduct the impulse from the sinus node to the atrioventricular (A-V) node. |
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Definition
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Term
| The ___ conducts the impulse from the atria into the ventricles |
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Definition
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Term
| The ___ conduct the cardiac impulse to all parts of the ventricles. |
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Definition
| superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava |
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Term
| Does the sinus node tissue contract? |
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Definition
| No, the fibers of this node have almost no contractile muscle filaments |
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Term
| the resting membrane potential of the sinus nodal fiber between discharges has a negativity of about ___, in comparison with ___ for the ventricular muscle fiber. |
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Definition
| negative 55 to negative 60 millivolts / negative 85 to negative 90 millivolts |
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Term
| What is the natural permeability of sinus fibers? |
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Definition
| leaky to sodium and calcium ions, these positive charges neutralize much of the intracellular negativity |
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Term
| What types of channels are gound in cardiac muscle fiber? |
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Definition
| 1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels. |
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Term
| Opening of the ___ channels is responsible for the action potential observed in ventricular muscle |
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Definition
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Term
| Then the plateau of the ventricular action potential is caused primarily by ___ channels |
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Definition
| slower opening of the slow sodium-calcium |
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Term
| At this level of -55 millivolts or less, the fast sodium channels mainly have become ____. |
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Definition
| inactivated, therefore, only the slow sodium-calcium channels can open to cause the action potential. |
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Term
| When the potential reaches a threshold voltage of about ___, the sodium-calcium channels become activated, thus causing the action potential. |
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Definition
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Term
| Why does the leakiness to sodium and calcium ions not cause the sinus nodal fibers to remain depolarized all the time? |
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Definition
| sodium-calciuminflux is inactivated about 100 to 150 milliseconds after the channel opens, then greatly increased numbers of potassium channels openallowing potassium efflux |
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Term
| How is hyperpolarization caued in cardiac muscle? |
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Definition
| potassium channels remain open for another few tenths of a second after negative resting level is reached, temporarily continuing movement of positive charges out of the cell, with resultant excess negativity inside the fiber |
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Term
| The velocity of conduction in most atrial muscle is about ___, but can be as fast as ___, in several small bands of atrial fibers. |
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Definition
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Term
| The anterior, middle, and posterior internodal pathways are bands that ___. |
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Definition
| are located in the atrium, have faster contractility, and terminate in the AV node |
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Term
| The anterior interatrial band passes ___. |
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Definition
| through the anterior walls of the atria to the left atrium |
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Term
| The A-V node is located ____. |
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Definition
| in the posterior wall of the right atrium immediately behind the tricuspid valve |
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Term
| The impulse, after traveling through the internodal pathways, reaches the A-V node about ___ after its origin in the sinus node. |
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Definition
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Term
| There is a delay of ___ in the A-V node itself before the impulse enters the penetrating portion of the A-V bundle, where it passes into the ventricles. |
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Definition
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Term
| A final delay of ___ occurs in the penetrating A-V bundle |
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Definition
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Term
| The total delay in the A-V nodal and A-V bundle system is about ___. |
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Definition
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Term
| There is a total delay of ___ before the excitatory signal finally reaches the contracting muscle of the ventricles. |
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Definition
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Term
| Purkinje fibers transmit action potentials at a velocity of ___. |
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Definition
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Term
| Can action potentials to travel backward from the ventricles to the atria? |
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Definition
| not under normal circumstances |
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Term
| The distal portion of the A-V bundle passes downward in the ventricular septum and divides into ___ in the ___. |
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Definition
| left and right bundle branches that lie beneath the endocardium on the two respective sides of the ventricular septum. |
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Term
| The total elapsed time of transduction from the bundle branches in the ventricular septum to the terminations of the Purkinje fibers is ___. |
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Definition
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Term
| The velocity of transmission in the ventricular muscle fibers themselves is ____. |
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Definition
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Term
| Transmission from the endocardial surface to the epicardial surface of the ventricle requires ___. |
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Definition
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Term
| The total time for transmission of the cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in the normal heart is about ___. |
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Definition
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Term
| Impulse spreads at moderate velocity through the atria but is delayed ___ in the A-V nodal region before appearing in the ventricular septal A-V bundle. |
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Definition
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Term
| The A-V nodal fibers, when not stimulated from some outside source, discharge at an intrinsic rhythmical rate of ___, and the Purkinje fibers discharge at a rate between ___. |
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Definition
| 40 to 60 times per minute / 15 and 40 times per minute |
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Term
| The pacemaker of the heart is the ___. |
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Definition
| the sinus node because its rate of rhythmical discharge is faster than that of any other part of the heart |
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Term
| A pacemaker elsewhere than the sinus node is called an ___. |
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Definition
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Term
| When A-V block occurs a new pacemaker usually develops in the Purkinje system of the ventricles and drives the ventricular muscle at a new rate of ___. |
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Definition
| 15 and 40 beats per minute |
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Term
| What is Stokes-Adams syndrome? |
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Definition
| An AV block of 5 to 20 seconds when the ventricles fail to pump blood- person faints after the first 4 to 5 seconds |
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Term
| Stimulation of the parasympathetic nerves to the heart (the vagi) causes the hormone ___ to be released at the vagal endings. |
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Definition
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Term
| What is the effect of parasympathetic innervation on the heart? |
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Definition
| decreases the rate of rhythm of the sinus node, andt decreased excitability of the A-V junctional fibers between the atrial musculature and the A-V node |
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Term
| What is ventricular stimulation? |
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Definition
| Strong vagal stimualtion causes the ventricles stop beating for 5 to 20 seconds, but then some point in the Purkinje fibers, usually in the ventricular septal portion of the A-V bundle, develops a rhythm of its own and causes ventricular contraction at a rate of 15 to 40 beats per minute. |
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Term
| What does acetylcholine do to potassium channels in the heart? |
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Definition
| it increases the permeability of the fiber membranes to potassium ions, which allows rapid leakage of potassium out of the conductive fibers causing hyperpolarization |
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Term
| In the sinus node, the state of hyperpolarization decreases the resting membrane potential of the sinus nodal fibers to a level of ___. |
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Definition
| negative 65 to negative 75 millivolts |
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Term
| Stimulation of the sympathetic nerves to the heart (the vagi) causes the hormone ___ to be released at the vagal endings. |
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Definition
| increases the rate of sinus nodal discharge, rate of conduction, and level of excitability in all portions of the heart |
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Term
| Stimulation of the sympathetic nerves releases the hormone ___ at the sympathetic nerve endings. |
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Definition
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Term
| What does norepinephrine so to sodium-potassium channels? |
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Definition
| increases the permeability of the fiber membrane to sodium and calcium ions accelerating self-excitation |
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