Lecture 1

Question 1

Microfibrils

Answer 1

Bundles of protein filaments

Question 2

Intercalated disks

Answer 2

contain desmosomes that transfer force form cell to cell

Question 3

Gap junctions

Answer 3

allow electrical signals to pass rapidly form cell to cell

Question 4

Mitochondria

Answer 4

occupy 1/3 of the cell volume of a contractile cardiac fiber

Question 5

types of ion channels

Answer 5

1) Leakage channels 2) Voltage gated channels 3) Ligand gated channels 4) Mechanically gated channels

Question 6

Leakage channels

Answer 6

gates randomly alternate between open and closed positions

some are always open, K+ leak channels cause nerve an muscle cell membrane to be more permeable to K+ than to Na+

Question 7

Voltage gated channels

Answer 7

open in response to c change in membrane potential Na+, K+, Ca++

Question 8

Ligand gated channels

Answer 8

open and close in response to specific chemical stimulus; nicotinic cholinergic receptor open when acetylcholine binds to it

Question 9

Mechanically gated channels

Answer 9

open or close in response to mechanical

action; sensory receptors

Question 10

P wave

Answer 10

SA depolarization, action potential begins in atria

Question 11

QRS complex

Answer 11

ventricular depolarization

Question 12

T wave

Answer 12

ventricular repolarization

Question 13

ST segment

Answer 13

period during ventricular depolarization (plateau)

Question 14

U wave

Answer 14

due to repolarization of the papillary muscle

Question 15

P - R interval

Answer 15

time taken from first atrial depolarization to first ventricular depolarizatio

Question 16

Q wave

Answer 16

the first downward deflection of the QRS and may or may not be present

Question 17

Wolff-Parkinson-White Syndrome


AV Re-entrant Tach

Answer 17

• premature atrial impulse blocks in the accessory pathway (bundle of Kent) • on reaching the accessory pathway the impulse re-enters the atrium
• re-enters the ventricle via the AV node and becomes self-sustaining
• short P-R interval, prolonged QRS (slurred upstroke)
• treatment: drugs that prolong refractoriness

Question 18

Myocardial Ischemia


Answer 18

obstruction of blood flow in myocardium by partial or complete blockage of a coronary artery
• sudden severe blockage may lead to a myocardial infarction, heart attack
• serious abnormal heart rhythm arrhythmia • Acidosis
• Catecholamine release
• Efflux of K+ from myocyte to ECS • Intracellular Ca2+ accumulation

Question 19

Heart Failure

Answer 19

The body tries to compensate for the heart’s reduced pumping ability by:
• retaining salt and water to increase the amount of blood in the bloodstream • increasing the heart rate
• increasing the size of the heart

Question 20

Arrhythmias


Answer 20

dysfunctions in current flow that cause abnormalities in impulse formation, and conductance in the myocardium

Question 21

Sinus rhythm

Answer 21

generated by SAN

Question 22

Bradycardia

Answer 22

heart rate <60 beats/min

Question 23

Tachycardia

Answer 23

heart rate >100 beats/min

Question 24

Ventricular Tachycardia

Answer 24

arising in ventricles, life threatening

Question 25

Supra-ventricular

Answer 25

above the ventricles (i.e. in atria)

Question 26

Atrial flutter

Answer 26

rapid, regular beating of atria

Question 27

Fibrillation

Answer 27

very rapid, irregular beating, A-Fib, V-Fib

Question 28

Block

Answer 28

failure of conduction

Question 29

Anti-arrhythmic Drugs: Vaughan Williams classification

Answer 29

Class I: Na+ channel antagonists, slow conduction velocity
Ia: intermediate rate
Ib: fast rate
Ic: slow rate

Class II: ß-adrenergic receptor antagonists, blunt sympathetic effects

Class III: K+ channel antagonists, increase APD

Class IV: Ca2+ channel antagonists, affect primarily SA and AV nodes

Class V: Cl- channel antagonists