Cardiac physiology (Block 3)

Question 1

Drugs and the Heart

Answer 1

Drugs can affect the efficiency for the heart pump (HR, force of contraction, rhythm, etc)
Drugs can affect blood vessels (altering blood pressure, etc)

Question 2

Average weight of human adult heart

Answer 2

250-350g

Question 3

Approx size dimensions of human adult heart

Answer 3

12cm long by 9cm wide

Question 4

Typical resting heart rate

Answer 4

60-80 bpm

Question 5

Typical HR during exercise

Answer 5

140-180 bpm

Question 6

How much blood is on average pumped by the heart?

Answer 6

70ml per heartbeat
5L per minute

Question 7

Anatomically, the heart consists of what tissues?

Answer 7

Endocardium
Myocardium
Epicardium
Pericardium

Question 8

What is endocardium made of?

Answer 8

Endothelial cells

Question 9

What is myocardium made of?

Answer 9

Specialised muscle cells called myocytes

Question 10

What is epicardium composed of?

Answer 10

A thin layer of mesothelioma cell and connective tissue

Question 11

What is pericardium?

Answer 11

A fibrous sac that encloses the heart

Question 12

Myocardium structure

Answer 12

Cardiac muscle is striated, BUT:
single nucleus
under autonomic control
all cardiac cells contract together (skeletal - selective recruitment of motor units)
high oxygen demand
structure permits coordinated contraction (acts as a syncytium)
Cardiac myocytes do not regenerate

Question 13

Automaticity

Answer 13

Ability to initiate an electrical impulse

Question 14

Excitability

Answer 14

Ability to respond to an electrical impulse

Question 15

Conductivity

Answer 15

Ability to transmit an electrical impulse from one cell to another

Question 16

Physiology of cardiac conduction

Answer 16

Cardiac electrical activity is the result of ion movement across the cell membrane. In resting state, cardiac muscles cells are polarised (an electrical difference exists between the negatively charged inside of the cell and the positively charged outside of the cell membrane)

Question 17

Sinoatrial (SA) node

Answer 17

Primary pacemaker of the heart
Located at the junction of the superior vena cava and the right atrium
15mm long x 5mm wide
Cells spontaneously depolarise ~100 times per min

Question 18

Atrioventricular (AV) node

Answer 18

Impulses from SA node are conducted to AV node
AV node co-ordinates incoming electrical impulses after slight delay
Relays the impulse via His/Purkyne fibres to the ventricles

Question 19

Sinus rhythm

Answer 19

Normal heartbeat rhythm

Question 20

Atrial arrhythmia

Answer 20

Without rhythm

Question 21

Action potential

Answer 21

The pattern of repolarisation and depolarisation

Question 22

What does the Nernst equation predict?

Answer 22

Predicts where the electrochemical gradient will balance
** write equation in notes bc you can’t type it here

Question 23

Key cardiomyocyte pump

Answer 23

Na/K pump

Question 24

Key cardiomyocyte transporter

Answer 24

Na/Ca exchanger

Question 25

Drug action of the SA node

Answer 25

SAN contains autorhythmic fibres that initiate an action potential (100-110 per minute) • Nerve impulses from the autonomic nervous system (ANS) and hormones (e.g. adrenaline) modify the timing and strength of each heartbeat, but they do not establish the fundamental rhythm. • Vagus nerve innervates SA node, reducing rate to 60-80bpm (through acetylcholine action on muscarinic receptors) • Higher (>100 bpm) = tachycardia; Lower (<50 bpm) = bradycardia • Acetylcholine decreases slope of phase 4 and therefore extends time to reach threshold ( through increased K+ efflux, reduced Ca++ and Na+ influx) • Atropine will block effect of acetylcholine • Sympathetic activity releases noradrenaline (norepinephrine), increasing bpm (reduced vagal tone) via action at -adrenoreceptors

Question 26

Non-pacemaker action potentials

Answer 26

Non-pacemaker cells have true resting potential (phase 4) e.g. ventricular myocytes, Purkinje cells • Depolarisation to -70mV (from an incoming action potential) causes rapid influx of Na+ (phase 0) • Partial repolarisation occurs as the Na+ current is inactivated (Phase 1) and transient K+ efflux • Slow Ca++ influx (plateau phase 2) via slow L-type calcium channels (open at ~ -40 mV) • Repolarization (phase 3) is caused by increased K+ efflux and decreased influx of Na+ and Ca++ • Phase 4 - resting state

Question 27

Phases of non-pacemaker action potentials

Answer 27

0 Depolarisation (Na+ channels open: fast) 1 Early repolarisation (Na+ channels close, some K+ efflux) 2 Plateau (Ca++ influx: slow) 3 Repolarisation (K+ out) 4 Resting (restoration of normal ionic balance by pumps)

Question 28

Refractory periods in non-pacemaker cells

Answer 28

The refractory period of cardiac muscle is dramatically longer than that of skeletal muscle. • This prevents tetanus from occurring and ensures that each contraction is followed by enough time to allow the heart chamber to refill with blood before the next contraction.

Question 29

ARP

Answer 29

Absolute Refractory Period During this time a second stimulus will not cause any response

Question 30

ERP

Answer 30

Effective refractory period After the end of of the ERP a second stimulus will cause a propagated action potential

Question 31

ECG

Answer 31

Electrocardiogram (ECG) is measured from electrodes placed on the skin It therefore shows a summation of cardiac electrical activity Changes in the ECG are used to diagnose heart disrhythmias

Question 32

Properties of cardiac muscle

Answer 32

Excitation of the heart is triggered by intrinsic electrical impulse rather than neural transmitters. Contraction of the heart is triggered by elevation of intracellular calcium influx.

Question 33

Myocyte contraction

Answer 33

Excitation-contraction coupling (ECC) causes myocyte contraction in phase 2 of action potential • L-type Ca++ channels in sarcolemma open. Calcium influx then activates ryanodine receptors (RyR) on sarcoplasmic reticulum (SR), increasing intracellular Ca++ from 10-7 to 10-5M • Ca++ binds troponin C, changing its conformation and allowing myosin-actin cross-bridging and contraction • At the end of phase 2, Ca++ is sequestered by an ATP-dependent calcium pump (SERCA, sarco-endoplasmic reticulum calcium-ATPase) m influx.