Inotropy

Question 1

What is inotropy also known as?

Answer 1

Myocardial Contractility

Question 2

What is the consequence of compromised cardiac muscle function?

Answer 2

Lower myocardial contractility will result in a lower stroke volume therefore a lower cardiac output

Question 3

What is volume a normal heart pumps out during systole?

Answer 3

The normal heart will pump out the same amount of blood that is pumped into the blood

Question 4

What causes muscle to contract?

Answer 4

Calcium influx

Question 5

Simply explain what happens during calcium induced calcium release

Answer 5

During depolarisation of the cardiac myocyte, L-type calcium channels are opened allowing slow leakage of calcium into the cell, an increase in intracellular calcium is detected by Ryanodine receptors triggering release of calcium from the intracellular calcium store (sarcoplasmic reticulum), contraction then occurs with Ca2+ binding to Troponin,

Question 6

How does re-uptake of calcium occur within the cell?

Answer 6

After contraction ends SERCA receptors on the SR allow Ca ions to re-enter the intracellular calcium store. (energy dependent)

Question 7

How is calcium transported out of the cell after contraction?

Answer 7

Ca2+ATPase in cell membrane pumps out Calcium (energy dependent), Sodium and Calcium exchanged (Ca out of cell, Na into cell)

Question 8

What does a increased concentration of Ca2+ inside the cardiac myocyte cause?

Answer 8

Increased strength of contraction (positive inotropism)

Question 9

Name the 3 Positive Inotropic Effects of Noradrenaline and Adrenaline on the heart

Answer 9

1. Slow Ca2+ channel activation (phosphorylation)
2. Sensitisation of Troponin C to calcium
3. Stimulation of Ca2+ uptake by SR (muscle relaxes quicker)

Question 10

What is the positive inotropic effect of increased sympathetic stimulation?

Answer 10

More stimulation means a larger contractile force at a constant filling pressure (Increased rate of contraction, rate of relaxation and maximal force)

Question 11

What types of regulation can increase stroke work/volume?

Answer 11

Intrinsic or Extrinsic regulators

Question 12

What is intrinsic regulation of stroke work/volume?

Answer 12

Change in filling pressure and muscle resting length (see a movement along a starling curve)

Question 13

What is extrinsic regulation of stroke work/volume?

Answer 13

Neuronal or Hormonal stimulation of the sympathetic nerves that means a movement from one starling curve to another starling curve

Question 14

What is Acetylcholine in the context of inotropes?

Answer 14

Weak negative inotrope in the atria only effecting atrial contractility so, ventricular filling (ihibits cAMP production via g-coupled protein receptor)

Question 15

What factors increase contractility?

Answer 15

Sympathetic drive
Cathecholamines (family of amines that induce neurotransmitters such as adrenaline)
Positive inotropic drugs

Question 16

What factors decrease contractility?

Answer 16

Parasympathetic drive (atria only - weak effect)
Heart Failure
Myocardial Infarction
Hypoxia
Negative inotropic drugs

Question 17

What else influences contractility?

Answer 17

Structural adaptation to long-term alterations in volume or pressure loading of the ventricles
Compensation initially good but eventually detrimental as oxygen demand increases and so does fibrosis

Question 18

Can the failing heart still eject and adequate stroke volume?

Answer 18

Yes, if sympathetic activity is increased or of the end diastolic volume is increased

Question 19

Why is compensation ultimately bad for the cardiac muscle cells?

Answer 19

They have a high oxidative metabolic rate but little anaerobic metabolic capacity (Oxygen debt is detrimental to metabolism)
Oxygen supply must keep pace with cardiac work