Exam I Cardio II Flashcards

1
Q

What is the path the impulse takes after beginning in SA node?

A

Rhythm is set in S-A node. Excitation travels via internodal pathways to A-V node, continues along A-V bundle to left and right bundle branches of Purkinje fibers.

  1. From SA node, impulses radiate out through right atrium.
  2. ‘Bachmann’s bundle’ conducts SA impulse to left atrium.
  3. Excitation proceeds through right atrium on to AV node.
  4. AV node carries excitation into ventricles.

The AV node is situated posterior, on the right side of the interatrial septum.

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2
Q

How is heart rhythm generated? What are the resting potentials of the sinus nodal fiber and the ventricular fiber (why are these important)? What is the function of the If?

A

The sinus cell has a fluctuating resting membrane potential of -55 to -60mV. The ventricular fiber rests at -85 to -90mV. Remember the principle currents underlying the muscle AP are fast Na channels, slow Ca, and K channels. The Na channels produce the rapid depolarization, but quickly become ‘inactivated’ at depolarized membrane potentials.
The resting membrane potential of sinus nodal fiber (-55 to -60mV) keeps the Na channels inactivated. The hyperpolarization does however active a current called If for “funny” current. This allows Na to leak in (and some K to leak out), which slowly depolarizes the cell until it reaches the Ca (Na/Ca Channel) channel threshold.
This supports the faster depolarization, and as it begins to inactivate, the voltage-gated K channels begin to open, repolarizing the cell, and starting the cycle over again.

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3
Q

The delay of impulse conduction at the AV node is due to what and serves what purpose?

A

Delay at A-V node allows artial pumping, slower conduction due to few gap junctions

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4
Q

Where are the Purkinje fibers located? Why do they conduct impulse so fast and for what purpose? Why is it important that they have one-way conduction?

A

Purkinje are specialized muscle fibers, lead from A-V node to ventricles to distribute excitation. High speed comes from size, high gap junction density, and few myofibrils.
Large and fast (1.5 to 4m/sec), allows near synchronous excitation of all ventricle muscle. Note extensive distribution.
Note the time of arrival post-initiation of rhythmic S-A node impulse. Once arrived at A-V node, there is near immediate excitation of entire ventricle mass. Necessary for effective pumping.
‘One-way’ conduction protects against re-entry into atria.

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5
Q

A-V node and purkinje fibers can also show rhythmic discharge, why are they not the pacemaker instead of the SA node? What are ectopic pacemakers?

A

A-V node and purkinje fibers also show rhythmic discharge (40-60bpm), but they discharge slower than S-A node (70-80 bpm), making S-A node the pacemaker.
“Ectopic pacemaker” forms when unusual areas discharges faster than S-A node and takes over (usually in A-V node). If A-V block occurs, then V-A node takes over in 5 to 20 sec.

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6
Q

Why does the faster pace of the SA node make it the “pacemaker”?

A

?

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7
Q

What are the two divisions of the autonomic nervous system? Describe them (how and where they are stimulated, what NT they release and its effects, and overall effects the stimulation have on the heart).

A

The autonomic system is divided in the sympathetic and parasympathetic systems.
Parasympathetic:
Parasympathetic stim comes through the Vagus nerves (the Vagi). Distributed primarily to S-A and V-A nodes, some atrial muscle, little ventricle muscle.
Para sym stim releases Acetylcholine which binds to muscarinic receptors (M2), effects;
Ach increases K permeability, increases leak current. This lowers resting membrane potential, takes longer to reach threshold which causes:
-decrease rate of rhythm at S-A node.
-decrease excitability at A-V junction. (which slows transmission to ventricles).
Para stim slows heart rate, strong stimulation can stop S-A rhythm and/or block A-V node (note ventricular escape).

Sympathetic:
Sympathetic Stim is distributed throughout heart. Stimulation releases norepinephrine, binds to beta receptors (B1) (hence beta-blockers). Effects of stimulation:
1. increase rate of sinus node discharge.
2. increases rate of conduction & excitability in heart tissues.
3. Increases heart rate, strength of contraction.
4. Increase Na & Ca permeability > this results in a higher resting membrane potential in S-A node making it easier to reach threshold, facilitates conduction through A-V node.
B1 antagonists (propranolol) used for hypertension, cardiac arrhythmia.

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8
Q

Identify all the waves of a typical EKG.

A

P wave is beginning of contraction of the atria.
QRS complex is the beginning of contraction of the ventricles.
Atrium relaxes during QRS complex, makes an atrial T wave but is typically obscured by QRS.
The T wave is repolarization of the ventricles.

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