Basic Science (still to finish)

Question 1

What are pacemaker potentials?

Answer 1

 There are rhythmically discharging cells in the SA and AV
 After each action potential (impulse) these cells gradually depolarise to their firing level again → this intrinsic post-impulse depolarising tendency is called prepotential (or pacemaker potential).
 The absence of Na+ in the generation of pacemaker action potentials means they do not have the same sharp, depolarising spike that other cardiac cells have.

Question 2

What is the normal resting pacemaker membrane potential?

Answer 2

-60mV

Question 3

Describe the steps in generation of pacemaker activity?

Answer 3

1. IK begins at the peak of the impulse, caused by K+
   efflux via K+ channels, and leading to repolarisation. (Phase 3)
2. K+ efflux decays (↓I K ). At the same time Ih begins, caused by the opening of a ‘funny’ channel that permits Na+ as well as dropping K+ permeability below baseline, causing the prepotential to begin. (Phase 4)
3. ICaT begins, in which transient (T) Ca2+ channels complete the prepotential.
4. I Ca L begins, in which long-lasting (L) Ca2+ channels bring the impulse. (Phase 0)
   o There is no phase 1 or 2 in pacemaker cells

Question 4

Describe the effect of sympathetic stimulation on pacemaker potentials

Answer 4

Sympathetic (noradrenergic) stimulation (via β 1 receptors):
 ↑cAMP facilitates opening of Ca2+ channels, ↑I Ca → faster
depolarisation phase of the impulse

Question 5

Describe the effect of vagal stimulation on pacemaker potentials

Answer 5

Vagal (cholinergic) stimulation (via M 2 muscarinic receptors) has two complimentary responses that ↓ firing rate:
 G-protein mediated opening of special K+ channels, leads
to accentuated I K (called I KACh ) → hyperpolarisation.
 ↓cAMP slows opening of Ca2+ channels, leading to delayed
ICa

Question 6

Describe the speard of cardiac excitation

Answer 6

 Route is: SA node → Internodal atrial pathways → AV node → Bundle of His → Purkinje fibres
 There is an AV nodal delay of ~ 0.1s, due to slow conduction in the AV node
o This is lengthened by vagal stimulation, and shortened by sympathetic stimulation
 The pattern of ventricular depolarisation is: Left septum → Right septum → Down to apex → Along the ventricular walls → Endocardial to epicardial → Posterobasal left ventricle, pulmonary conus (right) and uppermost septum

Question 7

What does each ECG interval mean

Answer 7

Question 8

ECG changes seen in hyperkalaemia?

Answer 8

Question 9

ECG changes in hypokalaemia?

Answer 9

Question 10

Describe the his bundel electrogram

Answer 10

Question 11

Describe late diastole in the cardiac cycle?

Answer 11

 Late diastole
o Mitral and tricuspid (i.e. atrioventricular = AV) valves open → Blood flows into atria and ventricles passively down pressure gradient
o Aortic valve and pulmonary (i.e. semilunar = SL) valves are closed
o Pressure in ventricles low - 70% of ventricular filling (Phase 5) occurs during diastole

Question 12

Describe atrial systole as part of the cardiac cycle?

Answer 12

 Atrial systole (Phase 1)
o Atria contract → Some additional blood into ventricles
 Also narrows orifices of SCV and IVC, but no valves exist → Some regurgitation into SVC and IVC occurs (JVP’s a wave)

Question 13

What does each JVP wave correspond to?

Answer 13

 Transmitted waves from atrial pressure changes into the great veins. The 3 characteristic waves:

1. a wave: caused by atrial systole and regurgitation of blood into SVC
2. c wave: due to isometric contraction of RV and bulging tricuspid valve pushing on the atrium
3. v wave: the result of atrial pressure build up against a closed tricuspid valve

 Respiratory fluctuations also affect JVP waves:
o Inspiration: ↓ Intrathoracic pressure → ↓ Venous pressure
o Expiration: ↑ Intrathoracic pressure → ↑ Venous pressure
 Clinical information from JVP:
o Tricuspid insufficiency: giant c wave with each ventricular systole
o Complete heart block: a waves are not synchronous with radial pulse; giant a wave (‘cannon wave’) with every atrial
contraction that occurs while tricuspid valve is closed
o Distinguishing atrial from ventricular extrasystoles: atrial premature beats produce an a wave, but ventricular premature
beats do not.

Question 14

What does the S1 heart sound correspond to?

Answer 14

S1: Low, slightly prolonged ‘lub’, caused by vibrations due to the sudden closure of mitral and tricuspid (AV) valves at the start
of ventricular systole

Question 15

What does S2 heart sound correspond to?

Answer 15

S2: High, shorter ‘dub’; caused by vibrations associated with the closure of the aortic and pulmonary (SL) valves just after the end
of ventricular systole

Question 16

What does S3 heart sound correspond to?

Answer 16

S3: Soft, low-pitched; heard about ⅓ of the way through diastole in many normal young individuals probably due to vibrations from the period of rapid ventricular filling (inrush of blood)
o “SLOSH…ing-in”

Question 17

What does S4 heart sound correspond to?

Answer 17

S4: can sometimes be heard immediately before S1; rarely heard in normal adults; due to ventricular filling, can be heard when
atrial pressure is high or the ventricle is stiff (e.g. ventricular hypertrophy)
o “a-STIFF…wall”

Question 18

What are the three ways to measure CO?

Answer 18

Question 19

Describe factors that control cardiac output?

Answer 19

Question 20

Describe frank-starling law

Answer 20

Question 21

What factors reduce end diastolic volume?

Answer 21

Question 22

Describe the pressure-volume loop

Answer 22

Question 23

What is myocardial contractility affected by?

Answer 23