Z-Pathophys Of Cardiac Arrhythmias

Front 1

What are all cardiac arrhythmias disturbances of? (one of two things -or both)

Back 1

1. disturbances of impulse formation
2. disturbances of conduction

Front 2

What are the three basic mechanisms responsible for cardiac arrhythmias?

Back 2

1. automaticity (enhanced or depressed)
2. triggered activity
3. re-entry of excitation

Front 3

What is automaticity?

Back 3

The ability of a pacemaker cell to spontaneously reach threshold and generate a regenerative action potential.

Front 4

VIP
What are four mechanisms that cause arrhythmias due to altered automaticity?

Back 4

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.

Front 5

Describe the cellular mechanism in which automaticity can be altered by HYPOKALEMIA.

Back 5

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

Front 6

Describe the cellular mechanism in which automaticity can be altered by STRETCH of heart.

Back 6

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)

Front 7

Give an example of what stretch can do to the rate of the heart.

Back 7

After an MI a patient can get a ventricular aneurysm that stretches the heart. This aneurysm may enhance pacemaker activity of subendocardial Purkinje fibers.

Front 8

Describe the cellular mechanism in which automaticity can be altered by ISCHEMIA.

Back 8

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.

Front 9

On an ECG what is ischemia responsible for?

Back 9

S-T segment changes associated with ischemia or infarction.

Front 10

What does hypokalemia do to:
1. action potential duration
2. pacemaker rate
3. pacemaker rate arrhythmias

Back 10

1. increase action pot duration
2. increases pacemaker rate
3. increases pacemaker arrhythmias

Front 11

Six possible causes of tachycardia and premature beats:

Back 11

1. hypokalemia
2. fever
3. drugs
4. sympathetics (norepi)
5. hyperthyroidism
6. ischemia (current of injury acts like a stimulus)

Front 12

Define an DAD:

Back 12

A transcient subthreshold depolarization that FOLLOWS (and is triggered by) a preceding action potential. These result from abnormal elevated INTRACELLULAR Ca.

Front 13

Describe the process of generation of an DAD:

Back 13

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!

Front 14

What are four possible causes of DAD's?

Back 14

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

Front 15

What is an EAD?

Back 15

A transient depolarization that occurs DURING the later part of the action potential plateu (phase 2) or final repolarization (phase 3)

Front 16

What happens to ion movement during ischemia?

Back 16

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.

Front 17

What do EAD's do to action potential length? How does this show up on an EKG?

Back 17

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!

Front 18

What underlies Torsades de Pointes?

Back 18

This is a ventricular tachycardia caused by EAD's

Front 19

What are five causes of EAD's?

Back 19

1. medications - quinidine
2. hypokalemia (longer AP's)
3. slow heart rate
4. acidosis (occurs in ischemia)
5. prolonged q-t syndrome

Front 20

What is re-entry of excitation?

Back 20

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.

Front 21

What are the three requirements for reentry of excitation?

Back 21

1. geometry of a conduction loop
2. slow conduction
3. unidirectional block which protects heart from repolarizing

Front 22

What are three methods of therapy in re-entry of excitation?

Back 22

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

Front 23

Describe the differences in EKG findings in first, second, and third degree block.

Back 23

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

Front 24

What is one of the major things that the duration of the QRS complex depends on?

Back 24

Mass of the ventricular myocardium

Front 25

How does reentry of excitation occur in Wolfe-Parkinsons White syndrome? What is seen on the EKG?

Back 25

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.

Front 26

What can reentry of excitation cause?

Back 26

1. atrial fibrilation
2. supraventricular tachycardia
3. ventricular tachycardia
4. premature atrial beat