Flashcards in 11.29 B Deck (71):
Normal extracellular potassium concentration is roughly what?
3.5 - 5 mEq/liter
Hypokalemia is characterized by depressed (intracellular/extracellular) potassium levels.
Hypokalemia and hyperkalemia both have what effect on resting membrane potential in cardiac muscle?
they depolarize resting membrane potential
Although both hyperkalemia and hypokalemia depolarize resting membrane potential they have differing effects on what?
Hypokalemia and hyperkalemia promote what state, one of hyper or hypoexcitability?
hypoexcitability due to the diminished sodium current they are responsible for
What happens to the QRS complex when the sodium current is diminished?
it has a smaller magnitude and becomes widened
What happens to stroke volume when the QRS complex is widened?
it decreases and there is a corresponding drop in MAP
What happens to the nernst potential and conductance of potassium in a hyperkalemic state?
- increased potassium conductance
- more positive nernst potential
What happens to the nernst potential and conductance of potassium in a hypokalemic state?
- decreased potassium conductance
- more negative nernst potential
What happens to the duration of the ventricular action potential in a hypokalemic state?
it is prolonged due to reduced potassium current
What happens to the duration of the ventricular action potential in a hyperkalemic state?
it is shortened due to increased potassium current
Why does potassium current decrease in a hypokalemic state?
because the decreased potassium conductance outweighs the more negative potassium nernst potential
Why does potassium current increase in a hyperkalemic state?
because the increased potassium conductance outweighs the more positive potassium nernst potential
Describe the series of changes that happen in hypokalemia?
- diminished extracellular potassium levels
- decreased potassium conductance and more negative potassium nernst potential
- conductance change is more significant
- decreased potassium current
- longer ventricular action potential duration
What happens to heart rate in a hypokalemic state?
it increases to a tachycardic state
Why does hypokalemia lead to tachycardia?
due to a decrease in potassium current, MDP is more positive and phase 4 is steeper in the SA node, leading to more frequent depolarization
Why is hyperkalemia not always associated with bradychardia despite an increase in potassium current?
the baroreflex kicks in, increasing sympathetic firing and the heart rate
What are the effects of hyperkalemia and hypokalemia on heart rate?
- hypokalemia always leads to tachycardia
- hyperkalemia should lead to bradycardia but is sometimes controlled by the baroreflex
Hypokalemia and hyperkalemia have the same effects on ___ current and different effects on ____.
- same on sodium
- different on potassium
A U wave is characteristic of what medical problem?
Flaccid paralysis is a good indicator of what?
a potassium disturbance
What happens to the T wave in hyperkalemia?
it is increased, spiked
A spiked T wave is indicative of what potrassium disturbance?
How is hypokalemia treated?
a slow infusion of IV potassium based on a calculation of total body water
What are the four ways in which hyperkalemia is treated?
- calcium gluconate
- sodium bicarbonate
How does calcium gluconate help treat hyperkalemia?
it recovers resting sodium channels by shifting the sodium channel inactivation curve such that more inactivation gates will reopen during repolarization
Why is calcium gluconate only a temporary treatment for hyperkalemia?
because it restores excitability without resetting the resting depolarization
How does sodium bicarbonate help treat hyperkalemia?
by indirectly enhancing the Na-K pump
How does sodium bicarbonate indirectly enhance the Na-K pump?
by increasing sodium influx via the Na-H exchanger
How does insulin help treat hyperkalemia?
by directly stimulating the Na-K pump to move extracellular potassium into the cell
Which directly stimulates the Na-K pump, insulin or sodium bicarb?
How does lasix help treat hyperkalemia?
it enhances potassium excretion by the kidney
Which is a later onset, longer duration treatment for hyperkalemia, sodium bicarb or insulin?
insulin has a later onset and longer duration
How does high extracellular calcium alter the sodium inactivation and activate gate curves?
it shifts both to the right
High extracellular calcium normally does what to excitability?
it diminishes excitability
If high extracellular calcium normally diminishes excitability, why is it used to treat hyperkalemia?
because the shift in the inactivation gate curve is more significant and has a greater effect than does the simulatenous shift of the activation gate curve, which normally accounts for the diminished excitability it elicits
How does sodium bicarb indirectly treat hyperkalemia?
it increases pH, thus changing the proton gradient that drives the Na-H exchanger, thus changing the sodium graident that controls the K-Na exchanger
What is the key difference between the action potential changes associated with hypoxia and those associated with ischemia?
there is no change in phase 4 resting membrane potential in hypoxia
How does hypoxia affect the cardiac action potential?
- limited ATP production
- less calcium channel phosphorylation
- less calcium current
- decrease duration of the action potential
Hypoxia decreases what about the cardiac action potential?
Why does ischemia increase the resting potential of the cardiac cells while hypoxia does not?
because ischemia prevents blood flow and allows extracellular potassium to accumulate, causing local hyperkalemia
Ischemia induces local ____.
Ischemia has what effects on cardiac action potential?
it diminishes excitability by increasing resting membrane potential and it shortens the duration of the AP
Potassium disturbances have what effects on sodium and calcium channels?
it decreases the number of resting sodium channels and does not affect the number of resting calcium channels
Arrhythmias are the result of what?
abnormal impulse generation
Abnormal impulse generation can lead to arrhythmias via what two mechanisms?
- increased automaticity
Arrhythmias can be induced by increased automaticity which can arise from what changes?
- enhanced beta-adrenergic agonists
- decreased potassium conductance (hypokalemia)
- depolarizing current that flows from an ischemic region into adjacent normally polarized tissue
EADs and DADs are limited in their roles for re-entry loops in that they are only...
triggers, they do not sustain the loop
EAD and DAD stand for what?
early after depolarization and delayed after depolarization
EADs are associated with what two ionic changes?
- decreased rate of repolarization from decreased potassium current
- calcium window current due to opening of inactivation gates before activation gates have all closed
If ____ current is suppressed, EADs can occur in late ____ or early ____ due to the _____.
- late phase 2
- early phase 3
- calcium window
EAD production is favored by conditions that do what?
increase the calcium window overlap or prolong action potential repolarization
Cocaine is related to re-entry loops how?
- it blocks potassium rectifier channels and impairs reuptake of NE by sympathetic nerves, increasing the calcium window
- it leaves one susceptible to EADs
Delayed after depolarizations occur when during an action potential?
Delayed after depolarizations occur in what cell population?
EADs occur when during an action potential?
late phase 2 or early phase 3
DADs are associated with what two factors?
- increased cytosolci calcium levels
Why is tachycardia associated with DADs?
because it causes accumulation of calcium within myocytes, which aren't able to pump it out fast enough
Why is increased cytosolic calcium associated with DADs?
the calcium activates a Na/Ca exchanger and a non-specific cation channel, which both allow extracellular ions into the cell, creating a depolarizing current
M cells are unique ventricular cells in that they....
have a longer action potential duration
Ventricular fibrillation results from the development of what?
multiple re-entry loops
What three things are required for reentrant conduction?
- a closed conduction loop
- unidirectional conduction
- an action potential length shorter than the loop length
How does hypertrophy make reentrant conduction more likely?
by increasing the mass of the heart, it makes the conduction loop length longer, making it more likely that an action potential length will be shorter than the loop length
Reentrant loops are more likely when what is true about the cardiac action potential?
conduction velocity is decreased and/or the duration of the AP is decreased
Torsades de Pointes is treated with what?
a beta-aderenergic blocker which decreases potassium current, increasing the AP duration and hopefully interrupting the loop
Long QT syndromes are the result of abnormal ___ channels.
sodium and potassium channels
Short QT syndrome is the result of increased ____.
Brugada syndrome is an inherited arrhythmogenic syndrome caused by what abnormality?
reduced inward sodium current
Catecholaminergic polymorphic ventricular tachycardia is an inherited arrhythmogenic syndrome caused by what abnormality?
decreased ability of SR to control calcium
Atrial fibrillation is an inherited arrhythmogenic syndrome caused by what abnormality?
increased potassium current and impaired gap junctions