Cardiac Contractility and Events of the Cardiac Cycle

Question 1

What causes L-type dihydropyridine channels to open?

Answer 1

The action potential

depolarisation (?)

Question 2

What happens when L-type dihydropyridine channels open?

Answer 2

– Large influx of [Ca2+]e
• only ~10% contributes to contraction
– Cardiac muscle T-tubules 5x greater in diameter than sk. muscle (25x more volume)
– Cardiac T-tubule mucopolysaccharides sequester Ca2+
DHP activation causes release of Ca2+ from sarcoplasmic reticulum via ryanodine release channels

At resting heart rates, ↑[Ca2+]i due to influx and sarcoplasmic release is insufficient to cause maximal contractile force.

Question 3

Describe the path of Ca++ in cardiac contraction

Answer 3

Ca++ will pass into the myocyte via T tubules (greater diameter than in skeletal muscle so great amount of calcium sequestered there via mucopolysaccharides).

This influx of calcium via L-type dihydropyridine channels will cause release of Ca++ from sarcoplasmic reticulum, which will then pass onto troponin C to form cross links between heads of actin/myosin to cause contraction.
(calcium induced calcium release (CICR))

Ca++ released in relaxation will then pass into sarcoplasmic reticulum via Ca-ATPase pumps on the SR membrane. The rest will be passed out via Ca-ATPase pumps and Na+/Ca++ cotransporters on the sarcolemma

Question 4

How do you impact contractility of the heart?

Answer 4

Sympathetic nervous system having positive inotropic effect via noradrenaline on Beta1 receptors

Question 5

What + where is the effect of the parasympathetic innervation on heart contractility?

Answer 5

– Mostly to SA node
– Innervates atria
– Main effect is ↓rate
– Indirect –ve inotropic effect

Question 6

Describe in detail the impact of the sympathetic nervous system on contractility of the heart (and where this is)

Answer 6

Sympathetic innervation
– Throughout entire heart
– Positive inotropic effect

Noradrenaline on β1 receptors
– ↑[cAMP]i
– Enhances Ca2+ influx
– Promotes storage and release of Ca2+ from sarcoplasmic stores
– therefore ↑contractility
– therefore ↑speed of relaxation

Question 7

What is preload?

Answer 7

The volume of blood in the ventricles prior to contraction

Question 8

Discuss the refractory period of the heart

Answer 8

Cardiac twitches involve all fibers of the myocardium
Can not significantly summate contractions of cardiac muscle
Refractory period due to inactivation of Na+ channels

Skeletal muscle
– Absolute refractory period 1-2ms
– Period of contraction 20-100ms

Cardiac muscle
– Absolute refractory period (ARP) ~245ms
– Relative refractory period (RRP)
– Period of supranormal excitability (SNP)
– Period of contraction 250ms

Question 9

Describe each stage of the cardiac cycle

Answer 9

Atrial systole
Isovolumetric contraction
Ejection
Isovolumetric relaxation
Rapid inflow
Diastasis

Question 10

Discuss the atria as primer pumps

Answer 10

– ~80% of ventricular filling is passive due to normal blood flow
– Atrial contraction ‘tops up’ remaining ~20% volume

Question 11

Discuss the ventricles as pumps

Answer 11

– Isovolumic (isometric) period of contraction
– Period of rapid ejection (1/3) when 70% of stroke volume
ejected
– Period of slow ejection (2/3) when remaining 30% ejected
– Isovolumic (isometric) period of relaxation

Question 12

Discuss blood pressure in the arteries of the systemic circulation

Answer 12

Blood pressure in the arteries oscillates

Systolic blood pressure in the aorta
– ~120 mmHg

Diastolic blood pressure in the aorta
– ~80 mmHg

Question 13

Discuss blood pressure in the arteries of the pulmonary circulation

Answer 13

Pressure in pulmonary circulation is much lower
– Much less resistance to flow
– Right side of heart needs to do less work
– Right ventricle walls contain less muscle mass

Pulmonary systolic pressure
– ~30 mmHg

Pulmonary diastolic pressure
– ~12 mmHg

Question 14

What is ESV?

Answer 14

End systolic volume (ESV)

Volume in ventricle at the end of systole

Question 15

What is EDV?

Answer 15

End diastolic volume (EDV)

Volume in ventricle at the end of diastole

Question 16

What is SV?

Answer 16

Stroke volume (SV)
EDV-ESV. Quantity of blood expelled per beat (L)

Question 17

What is CO?

Answer 17

Cardiac output (CO)
SV x HR. Volume of blood pumped by the heart (L/min)

Question 18

Main Points

Answer 18

Calcium handling in cardiac muscle allows for modulation of contractility
The refractory period of cardiac muscle prevents tetany from occurring
The heart functions as a pulsatile pump that produces oscillations in pressure
COisHRxSV

Question 19

Learning outcomes

Answer 19

To explain how force is produced in cardiac muscle, how it differs from skeletal muscle and how it can be influenced by the extrinsic sympathetic nerves.
To relate the timings of the electrical activity of the heart to the resulting mechanical events of the cardiac cycle.
To interpret cardiac volume/pressure diagrams and state how they differ between the left and right sides of the heart.