Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

26 Cards in this Set

  • Front
  • Back
What are all cardiac arrhythmias disturbances of? (one of two things -or both)
1. disturbances of impulse formation
2. disturbances of conduction
What are the three basic mechanisms responsible for cardiac arrhythmias?
1. automaticity (enhanced or depressed)
2. triggered activity
3. re-entry of excitation
What is automaticity?
The ability of a pacemaker cell to spontaneously reach threshold and generate a regenerative action potential.
What are four mechanisms that cause arrhythmias due to altered automaticity?
1. sino-atrial block - when sinus node stops conducting so ectopic pacemaker must take over (at a slower rate)
2. ectopic pacemaker rate exceeds the sinus node rate - something stimulates the ectopic pacemaker to beat faster than the sinus node
3. sinus rate falls below ectopic pacemaker rate - causes pacemaker rate to take over
4. combination of a decrease in sinus rate and increase in ectopic pacemaker rate - this happens in older people since fibroblasts proliferate in tissue as you get older and can electonically connect to cardiac cells and alter rate.
Describe the cellular mechanism in which automaticity can be altered by HYPOKALEMIA.
Hypokalemia decreases K permiability (increase in membrane resistance) which exaggerates the effects of inward (depolarizing) currents during diastole, causing an increase in slope of the pacemaker potential in ectopic pacemakers. REMEMBER: SA node is relatively resistant to changes in plasma K
Describe the cellular mechanism in which automaticity can be altered by STRETCH of heart.
Stretching of the pacemaker tissue can generate inward (depolarizing) current via non-selective Stretch Activated Channels (SAC), thereby increasing diastolic slope. This mechanism may enhance pacemaker rate or initiate pacemaker activity in nonpacemaker tissue. (just like hypoK)
Give an example of what stretch can do to the rate of the heart.
After an MI a patient can get a ventricular aneurysm that stretches the heart. This aneurysm may enhance pacemaker activity of subendocardial Purkinje fibers.
Describe the cellular mechanism in which automaticity can be altered by ISCHEMIA.
Ischemia generates a current that can act as an inward (depolarizing) current, thereby increasing diastolic slope in nearby pacemaker tissue. In addition, if large enough, current of injury can stimulate working (non-pacemaker) cells to join it an crank out spontaneous activity.
On an ECG what is ischemia responsible for?
S-T segment changes associated with ischemia or infarction.
What does hypokalemia do to:
1. action potential duration
2. pacemaker rate
3. pacemaker rate arrhythmias
1. increase action pot duration
2. increases pacemaker rate
3. increases pacemaker arrhythmias
Six possible causes of tachycardia and premature beats:
1. hypokalemia
2. fever
3. drugs
4. sympathetics (norepi)
5. hyperthyroidism
6. ischemia (current of injury acts like a stimulus)
Define an DAD:
A transcient subthreshold depolarization that FOLLOWS (and is triggered by) a preceding action potential. These result from abnormal elevated INTRACELLULAR Ca.
Describe the process of generation of an DAD:
1. Something causes increased intracellular Ca
2. As a result, there is a spontaneous release of Ca from internal stores which stimulates inward Na/Ca exchange current to depolarize membrane potential causing a DAD.
3. If these DAD's are large enough in amplitude they can reach threshold and cause single or repetitive spontaneous action potentials, single premature beats, or v-tach!
What are four possible causes of DAD's?
1. cardiac glycoside toxicity
2. high concentrations of catecholamines
3. ischemia
4. rapid heart rates - can not cause an overload of intracell Ca but can contribute if you are on meds or have ischemia
What is an EAD?
A transient depolarization that occurs DURING the later part of the action potential plateu (phase 2) or final repolarization (phase 3)
What happens to ion movement during ischemia?
During ischemia, ischemic tissue releases intracellular Ca from the SR into the cytoplasm. This Ca is picked up by the Na-Ca exchanger and causes and inward Na current. This inward current fights to induce and action potential and thus creates a DAD.
What do EAD's do to action potential length? How does this show up on an EKG?
EAD's can increase action potential length. This causes an prolonged Q-T on the EKG. Also EAD's can be induced by interventions that prolong action potential duration. Since EAD's lengthen the AP duration anything else that lengthens the AP duration will predispose the px to an EAD!
What underlies Torsades de Pointes?
This is a ventricular tachycardia caused by EAD's
What are five causes of EAD's?
1. medications - quinidine
2. hypokalemia (longer AP's)
3. slow heart rate
4. acidosis (occurs in ischemia)
5. prolonged q-t syndrome
What is re-entry of excitation?
It is when the heart has an area of "block" where for what ever reason that area can not conduct impulses in one direction. Normally the heart (conducting through a branch pt - picture a triangle) will have their impulses cancelled out at the bottom of the triangle. However, with a block there is nothing to cancel out the impulse on the other side and the impulse swings around and up into the area of block (retrograde). If the refractory period of the block is shorter than the conduction time of the other impulse the impulse is allowed through the block and a reentry arrhythmia will be established.
What are the three requirements for reentry of excitation?
1. geometry of a conduction loop
2. slow conduction
3. unidirectional block which protects heart from repolarizing
What are three methods of therapy in re-entry of excitation?
1. increase refractory period of normal tissue
2. produce a complete block through the damaged region (it won't allow retrograde exitation)
3. enhance conduction through damaged region
Describe the differences in EKG findings in first, second, and third degree block.
1st - P-R interval > 0.2 sec and they are consistant
2nd - lengthened P-R interval (>0.2) with intermittent conduction failure to ventricles in dropped R waves. The P-R intervals can be gradually increasing (Type I) or constantly lengthened (Type II)
3rd - no consistant P-R interval due to complete failure of conduction between atria and ventricles
What is one of the major things that the duration of the QRS complex depends on?
Mass of the ventricular myocardium
How does reentry of excitation occur in Wolfe-Parkinsons White syndrome? What is seen on the EKG?
This form of reentry excitation is anatomically determined. WPW Px have an anatomical reentry circuit called the Bundle of Kent which forms an abnormal connection between the atria and the ventricles.
A characterisitic delta wave (slant of the begining of the QRS) since the impulse, going through the accessory pathway, gets to the ventricle before the AV node does.
What can reentry of excitation cause?
1. atrial fibrilation
2. supraventricular tachycardia
3. ventricular tachycardia
4. premature atrial beat