Cardio Physiology Review

Question 1

Automaticity definition

Answer 1

the ability for a cell or group of cells to initiate an action potential

Question 2

Excitability definition

Answer 2

the ability of a cell to respond to an external electrical stimulus, usually in the form of an action potential

Question 3

conductivity definition

Answer 3

the ability of a cell or region of cells to receive and transmit an action potential

Question 4

dromotropism definition

Answer 4

the ability to alter the rate of electrical conduction

Question 5

refractoriness definition

Answer 5

the inability of a cell to receive and trasmit an action potential

Question 6

Drugs that block K channels do what to heart?

Answer 6

Prolong QRS complex - cant repolarize as fast?

Question 7

Phase 0 ion of AP in nodal tissue is?

Answer 7

Calcium

Question 8

Phase 0 ion of AP in non-nodal cardiac tissue is?

Answer 8

Sodium

Question 9

ERP - effective refractory period of cardiac cycle contains which phases?

Answer 9

0, 1, and to the end of 2

Question 10

APD - action potential duration period of cardiac cycle contains which phases?

Answer 10

ALL - 0, 1, 2, 3 and 4

Question 11

What does a low ERP/APD ratio mean? And how to antiarrhythmics fit into this picture?

Answer 11

• Means that ERP is shorter relative to APD and therefore it is easier for the tissue to be depolarized by abnormal impulses
• Antiarrhythmics prolong the ERP relative to the APD = less chance to have depolarization by an abnormal impulse

Question 12

Two cardiac arrhythmia categories:

Answer 12

1) Disorders of impulse formation

2) Disorders of impulse conduction

Question 13

Disorders of impulse formation

-name the types, describe, and provide example

Answer 13

1) No change in the original pace-maker site - ex) sinus tachycardia
2) Change in original pace-maker site - ex) ectopic foci (premature beats), atrial tachycardia, atrial fib
3) Triggered activities -
a) early after depolarizations (EAD): prolongation of cardiac AP as with slow HR, hypokalemia, or drugs that prolong APD –> could potentially result in an interruption of phase 3 repolarization
b) delayed after depolarizations (DAD): conditions of Ca overload in either intracellular or sarcoplasmic reticulum ex) myocardial ischemia, adrenergic stress, digitalis intoxication, heart failure ==> results in normal AP followed by DAD i.e. a secondary beat or beats can be triggered if the threshold is reached- the higher the HR = the more beats may occur = abnormal rhythm

Question 14

EADs are induced more readily in which cells of heart?

Answer 14

Purkinje cells

Question 15

What is torsades de pointes?

what causes torsades de pointes (TdP)?

Answer 15

• TdP is a common polymorphic ventricular tachycardia seen commonly as a result of long QT interval - TdP is an example of an EAD! = can be caused by slow HR, hypokalemia, or drugs that prolong
• EADs that trigger reentry across the ventricular wall (transmural re-entry) causes TdP;
• usually have a SHORT, LONG, SHORT cycle before the TdP begins

-R on T phenomenon triggers the TdP?

Question 16

Drugs that block potassium channels do what and can have what side effect?

Answer 16

-prolong Q-T interval and can cause TdP

Question 17

Disorders of impulse conduction

• what is it?
• name the types, what it means, and give example(s)

Answer 17

• involve abnormality in the propagation of impulses in the cardiac tissues
  ex) 1) AV nodal block
  2) Re-entry - one of the most common mechanisms of tachycardia. existence of conduction routes with different conduction velocities
  a) AVNRT - AV nodal reentrant tachycardia

Question 18

AV nodal block

• types
• what kind of heart disorder?

Answer 18

1st degree = increased PR interval
2nd degree = not all P-waves pass through (P-waves without QRS)
3rd degree = no P-QRS relationship at all

-disorder of impulse conduction

Question 19

AV nodal reentrant tachycardia

• affects who?
• how does it happen?

Answer 19

• most common cause of paroxysmal regular narrow complex tachycardia.
• Affected individuals are usually young and healthy with no organic heart disease
• individual has to conduction paths from atria, slow and fast, usually only the fast conducts because slow is inefficient. Anyway, if this individual has a premature depolarization of the atria then when it reaches the fast pathway the fast is in refractory so the impulse takes the slow path. By the time it gets to the junction of fast, slow and His-bundle, part of impulse takes His and the other part goes back up the fast pathway depolarizing = circus movement

Question 20

What is the most common junctional tachycardias?

Answer 20

AVRNT

Question 21

Atrial flutter is a result of ?

Answer 21

a reentry circuit in the atrium

Question 22

What is the response rate in atrial flutter (what does ECG look like?)? what does this mean?

Answer 22

response rate is 3:1… for every 3 impulses you get one contraction from the atria and the system

Question 23

What does ECG look like in AVRNT? What does this mean?

Answer 23

P-waves occur after the QRS bc the signal comes down slow path and activates the ventricles and then goes back up and depolarizes the atria again via the fast path

Question 24

What is accessory pathway mediated SVT? What does it look like on ECG?

Answer 24

• there is a congenital accessory pathway somewhere outside of the usual impulse pathway that sends signal up to the AV node and SA node.
• looks like AVRNT with the P wave after QRS

Question 25

Ventricular re-entry pathway looks like? what is it?

Answer 25

• there is a pathway within the ventricle that occasionally sends a signal back up and to the ventricles again = ventricular tachycardia
• on ECG the QRS interval is wider and larger

Question 26

Consequences of arrhythmias:

Answer 26

1) Compromise of mechanical performance: ventricular strone affected directly = decrease in Cardiac output (CO)
2) Proarrhythmic/arrhythmogenic: arrhythmias untreated = worse arrhythmia develops such as premature ventricular beats develop into a v. tachcardia and a v. tachycardia can develop into v. fibrilation
3) thrombogenesis: arrhythmias facilitate formation of heart thrombi esp if there are endocardial lesions –> may lead to stroke. Atrial flutter and atrial fib are commonly associated with thrombi