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32 Cards in this Set
- Front
- Back
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What does the SA node, SNS, PNS contribute to resting HR? What is the final outcome? |
SA node: +100 BPM SNS: +10 BPM PNS: -40 BPM 72 BPM |
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Inward Rectifying K+ Channel |
Fairly fast, though work like other VG K+ channels. Opens in response to other inward ion current.(Mainly in phase 2) There is some delay behind other VG K+ channels. Helps repolarize the cell back to normal. Closes when tissue rests in phase 4. |
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The # of fast Na+ channels is directly related to what? |
the slope of phase 0 |
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What are the transient Outward Channels? |
contribute to phase 1 by allowing outward current of K+, this caps how high the depolarization of phase 0 can get. Only in fast tissue. |
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L-type Ca+ channel |
Both in slow and fast tissue. Contributes to phase 2 in the AP in extending the plateau. Inactivation the beginning of phase 3. Can be affected by intracellular activity of signalling enzymes. (PKA makes it more sensitive to depolarization or stay open longer) |
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Delayed Rectifying K+ Channels |
Very similar to inward recitfying channels. Opens later, in phase 3. Enhanced by increased Ca++ inside the cell. |
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ATP Sensitive K+ Channels |
Looks at how much ATP is around. Normal lvls = closed Low lvls = opened (dropping membrane potential) -Slows things down to conserve energy -lowers HR |
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Adenosine Mediated K+ channels |
Looks at adensosine lvls. (Extracellular) high lvls = open -slows down the heart |
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What does it mean to have high adenosine lvls? |
means there's not much oxygen |
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What does adenylyl cyclase do? What receptors stimulate it and deactivate it? |
Make cAMP Activate: Beta Deactivate: Parasympathetic and Adenosine |
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How does adenosine leave the cell? |
via aquaporins |
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How long does it take to rebuild adenosine levels? What happens when you have no adenosine? |
Takes a 1/2 hour to make 1% of adenosine that is found in the Heart Mitochondria can't phosphorylate anything. |
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ACh activated K+ Channel |
Muscarinic receptor. Mostly on nodal tissue. Hyperpolarizes Vrm in a vagal stimulation. Shortens phase 2 and drops the slope of phase 4, for longer depolarization, drops overall depolarization and phase 0 is less steep. |
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"Funny" Channels |
Main focus is Na+ channels. Determines HRin nodal tissue. Open during hyperpolarization at -55mV, at beginning of phase 4. Makes it faster to reach threshold potential. |
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When Ca++ increases in the blood, what happens to Na+ permeability? |
It drops |
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Stokes Adams |
If nodal tissue is not working, it is the time it takes for ventricular tissue to depolarize. After the first self depolarization, each subsequent depolarization does not take as long. |
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How is ventricular tissue depolarized? |
It is turned on by its neighbor. It does not usually wait for self-depolarization. It is quickly depolarized by a quick, high stimulus that is hidden in the upstroke. |
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What happens if it take a long time to reach threshold? |
Your slope looks crappy and your action potential looks short. |
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What are the causes of arrhythmia? |
-General anesthesia -Local Anesthetics -Hyperventilation -Intubation -Vagal Tone -Surgical Site -Cardiac disease -Cessation of B-Blockers -Placement of c-line -Physical manipulation of the heart |
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How does general anesthesia create arrhythmias? |
The effects on the autonomic system make it more sensitive to beta agonists. |
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What does ketamine do? |
It blocks the reuptake of catecholamines, works like an antidepressant. |
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How do local anesthetics create arrhythmias? |
there are sympathetic chains that lie right in front of the spinal cord. When you place medication on the spine, you might also knock out the sympathetic chains and cause bradycardia. |
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How can hyperventilation cause arrhythmias? |
by dropping CO2, you drop the acidity. This will drop the body's K+ lvls. As H+ leaves cells, K+ replaces it. |
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How does intubaton cause arrhythmias? |
Sensory feedback in the upper respiratory system. |
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How does vagal tone cause arrhythmias? |
parasympathetic system causes bradycardia and heart block. |
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How does the surgical site cause arrhythmias? |
The 5 and dime reflex, is when the dental and facial surgery interfere with CN V and the feed back to the brain stimulates the CN X and the patient gets decreased BP, HR, CO, and MAP. |
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How does the cessation of B-blockers cause arrhythmias? |
System will be more responsive/sensitive to Beta-agonist. Messing with a system that has had a lot of negative feedback adjustment made. |
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Class I Anti-Arrhythmics |
Caine drugs: Fast Na+ Channel Blockers Not effective on HR. Manipulates phase 0(decrease slope) and drops Vmax. Shifts whole AP over. Less Ca+ comes into cell. |
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How does lidocaine need to be given? Explain. |
Iv or topical. It's broken down by the liver, so it needs to bypass liver, so no oral. |
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Class 2 Anti-Arrhythmics: Beta Blockers |
Alters phase 4 slope to decrease HR. Be careful of pts with low HR More time in plateau phase Resets are slower Changes length of phase 2. |
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Class 3 Anti-Arrhythmics: K+ Blockers |
Amiodarone is typically listed here, but falls into all the categories. Manipulates phase 3, longer for heart to reset. Good for tachycardia. May or may not effect refractory period. |
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Class 4 Anti-Arrhythmic: Ca++ channel blocker |
decrease workload on ventricle, Ca++, Afterload, blood vessel tone. Does not affect phase 4 much in nodal tissue(Na+ leak channels primary determinant). Affects phase 0 in SA node. Affect conduction speed in nodal tissue. Affects phase 2 in ventricular tissue. |
