Case 2- factors that effect heart contraction

Question 1

Hypercalcaemia

Answer 1

High Ca+ concentration in the blood, you have increased force contractions as you have a more sustained depolarisation. If you have raised systolic calcium levels, the calcium ATPase pumps become saturated meaning they can’t remove them all meaning the muscle can not relax. This can cause a cardiac arrest in sytole. Short QT interval, shortening of ST segment

Question 2

Hypernatremia

Answer 2

High Na+ concentration in the blood. More sodium will enter cardiac tissue and we get a slight depolarisation making it more excitable. It is more likely to meet the threshold as its slightly more positive then it should be. More sodium will enter the cell when the sodium channels open. The rate of depolarisation, amplitude and duration of action potential will all increase. As its more excitable it may fire out of sync with the rest of the heart which could cause arrhythmia

Question 3

Hyperkalaemia

Answer 3

High K+ concentration. Decrease the K gradient across the cell membrane, this will reduce K efflux. The cell is initially more excitable as its nearer the threshold potential, as its slightly depolarised as there is more K+ within the cell. Causes conduction problems as the Na+ channel cannot reset as repolarisation isn’t happening, meaning it cannot generate another action potential upstroke. Can cause a cardiac arrest in diastole and death. Reduced P waves and unusual T waves (peaked).

Question 4

Hypomagnesia

Answer 4

Low Mg levels. The Na/K ATPase is Mg dependent so without it you have K depletion and Na retention. Mg depletion can be from diuretic use and is associated with arrhythmias and sudden death. As it upsets the electrolyte balance either side of the membrane, it may fire out of sync. A short PQ and QRS, there will be a shortening of the QT and a negative T wave

Question 5

Strove volume

Answer 5

The amount of blood pumped per ventricle

Question 6

Cardiac output

Answer 6

The volume pumped per ventricle per minute

Question 7

Venous return

Answer 7

The volume of blood returning to the heart, VR should equal CO

Question 8

What is cardiac output controlled by

Answer 8

Stroke volume and heart rate. Stroke volume depends on how strong the contractions are which is dependent of the length-tension relationship of muscle fibres as well as their strength. Heart rate is controlled by the sympathetic and parasympathetic nerves.

Question 9

What does preload depend on

Answer 9

The degree of stretch in the ventricles due to end diastolic pressure, it is dependent on EDV (end diastolic volume). Changes in stroke volume are dependent on resting ventricular muscle fibre length (preload).

Question 10

Ejection fraction

Answer 10

The percentage of blood that left the ventricle, its always under 100%

Question 11

Mechanisms is which venous return changes in exercise

Answer 11

• Skeletal muscle pump- skeletal muscle contractions increase, this squeezes the blood in the veins.
• Increases rate and depth of ventilation- this enhances thoracic and abdominal negative pressure when the thoracic wall stretches out. This draws venous blood into the thoracic cavity meaning venous return increases.
• Vasoconstriction of small veins- caused by sympathetic nerves. Increases pressure and helps suck blood back to the lungs. Vasodilation in areas of the body where blood flow in needed

Question 12

Mechanisms that boost cardiac output in exercise

Answer 12

• Atrial booster pump= caused by increased venous return which stretches the atrial wall so that there are more forceful atrial contractions. This compensates for the shorter diastole during exercise.
• Increased ventricular suction during diastole- after the ventricle contracts and pushes blood in the aorta a backpressure is created which helps suck blood from the atria
• Increased myocardial contractility- the ventricular wall stretches, also caused by noradrenaline and adrenaline release.
• Increased heart rate- due to the sympathetic nervous system. Begins at the onset of exercise.

Question 13

What happens to the cardiac cycle during exercise

Answer 13

Heart rate may increase by a factor of 3 and stroke volume increases by 50%. Cardiac cycle is shortened, diastole is shorter then systole

Question 14

Effects of exercising regularly

Answer 14

• Cardiac muscle increases
• Skeletal muscle mass increases- this will cause more capillaries to develop to improve the blood supply to the muscles, there is reduced diffusion distance and increased oxygen delivery
• Cardiac physiological changes- EDV increases (up to 200ml) so there is increased ventricular return this causes stroke volume to increase. Heart rate will be lower. Maximum heart rate does not significantly change but because stroke volume is bigger cardiac output will be higher.

Question 15

Beneficial effects of exercise on CVS

Answer 15

Lowers blood pressure, improves endothelial function, improves circulation, improves lipid metabolism

Question 16

Starling forces of the heart

Answer 16

The force of contraction is proportional to the initial fibre length in diastole. An increase in blood returning to the heart, or filling pressure increases EDV (end diastolic volume). This stretches the cardiac muscle and produces a more forceful contraction.

Question 17

Cross bridges formed with a low preload (empty chamber)

Answer 17

Actin and myosin overlap is not optimal because fibre length is small, the sarcomere length is minimal, reduces ability to contract.

Question 18

Cross bridges formed with a full ventricle (high preload)

Answer 18

There is some stretching of ventricular muscle, optimum cross bridge formation is possible. Sarcomere length, as well as actin and myosin overlap is optimal. There is an increased affinity of Troponin C to Ca+2. Maximum force produced

Question 19

Cross bridges formed with an overfull heart (heart failure)

Answer 19

Actin and myosin are physically separated. This prevents interaction. A reduced force is generated

Question 20

How epinephrine affects the heart

Answer 20

1) Epinephrine is released from the adrenal medulla and binds to beta1 receptors on myocardial contractile cells activating cAMP resulting in phosphorylation of voltage gated Ca+2 channels.
2) The open time of these channels increase, there is more calcium ion entry from the extracellular space (ECF).
3) Causes increased calcium stores in the SR and more Ca+2 release.
4) This causes more powerful contractions.
5) The cAmp second messenger also causes the phosphorylation of phospholamban.
5) This causes increases activity of the calcium- ATPase pump in the sarcoplasmic reticulum.
6) Ca+2 is removed from the cytosol faster meaning there is more Ca+2 stores in the SR. It also means the time of Ca-troponin binding is shorter so the contractions are shorter

Question 21

How norepinephrine effects the heart

Answer 21

Has the same effect as epinephrine but is released from sympathetic neurons