Cardiac Output

Question 1

What are the autonomic influences on the SA node?

Answer 1

1. Parasympathetic Nervous System
2. Sympathetic stimulation

Question 2

What is the role of parasympathetic nervous system in cardiac output?

Answer 2

Reduces rate of action potential in the SA node and ultimately decreasing heart rate.

Question 3

What mechanism in the PNS reduces heart rate?

Answer 3

Enhanced K+ permeability

Question 4

What are the effects of enhanced K+ permeability in reducing heart rate?

Answer 4

1. Hyperpolarisation of SA node as membrane becomes more negative due to more K+ ions leaving the cell. As a result, resting potential is further away from threshold thus increasing the time needed to reach threshold.
2. Decreases rate of SA node’s spontaneous depolarisation, prolonging the time required for membrane potential to reach threshold. Ach inhibits the cAMP pathway and inward movement of Na+ through funny channels and Ca2+ through T-type channels. This results in SA node firing and reaching threshold less frequently, reducing heart rate
3. Decreased AV node excitability prolonging transmission of impulses to the ventricles even longer than the usual AV nodal delay
4. Parasympathetic stimulation of atrial contractile cells shorten plateau phase of action potential by reducing slow, inward current carried by Ca2+, weakening atrial contraction

Question 5

What is the role of sympathetic stimulation on the heart?

Answer 5

Increases the rate of action potentials in the SA node and ultimately increases heart rate

Question 6

What are the mechanisms that increase heart rate?

Answer 6

1. Increased rate of depolarisation so that threshold is reached more rapidly, through greater inward movement of Na+ through funny channels and Ca2+ through T-type calcium channels, allowing more frequent action potentials
2. Reduced AV nodal delay by increasing conduction velocity due to slow inward Ca2+ current
3. Speeds up spread of action potential throughout specialised conduction pathway
4. Increase contractile strength so that the heart beats more forcefully, pumping out more blood. This is due to the increased Ca2+ permeability through prolonged opening of L-type Ca2+ channels, increasing Ca2+ influx which strengthens contraction by intensifying Ca2+ participation in excitation-contraction coupling.
5. Increases speed of contraction by allowing greater influx of Ca2+ through L-type channels
6. Speeds up relaxation by enhancing the SERCA pump that removes Ca2+ from the cytosol.

Question 7

What are the controls that influence stroke volume?

Answer 7

1. Intrinsic control related to the extent of venous return
2. Extrinsic control by factors originating outside the heart

Question 8

Explain the intrinsic control of stroke volume

Answer 8

• A direct correlation between EDV and SV (increased EDV means increased SV)
• Depends on frank starling law (the length-tension relationship of cardiac muscle)

Question 9

Explain the frank starling law

Answer 9

• The heart normally pumps out, during systole, the amount of blood returned to it during diastole. Therefore, increased venous return results in increased SV.
• Increase in cardiac muscle length moves it closer to the optimal length, increasing the contractile tension of the heart on the following systole.
• The main determinant of cardiac muscle fiber length is the degree of diastolic filling. The greater the diastolic filling, the larger the EDV, the more the heart is stretched, the longer the cardiac fibers before contraction

Question 10

What are the advantages of the length-tension relationship?

Answer 10

1. Equalises output between left and right sides of the heart as blood pumped out by heart is equally distributed between pulmonary and systemic circulation. When the right side of the heart has a larger SV, more blood enters the pulmonary circulation. This results in increased venous return to the left side of the heart, causing it to contract more forcefully for the blood to enter the systemic circulation.
2. When a large CO is needed like during exercise, venous return is increased by SNS, constricting the veins to drive blood forward and by the contracting muscles compressing the veins, which squeezes more blood toward the heart. This results in increased EDV and automatically increases SV.

Question 11

Mechanism of the cardiac length-tension relationship

Answer 11

• When the cardiac muscle fiber stretches, myofilaments are pulled closer together side by side.
• Distance between the thick and thin filaments reduce and more cross-bridge interactions between myosin and actin take place when Ca2+ pulls the troponin-tropomyosin complex away from the actin’s cross-bridge binding sites.
• The sensitivity of the myofilament to Ca2+ increases.

Question 12

What is the extrinsic control of stroke volume?

Answer 12

• Sympathetic stimulation and epinephrine increases the heart contractility.
• The heart contracts more forcefully and squeezes out a greater percentage of the blood it contains, leading to more complete ejection. This is a result from the increased Ca2+ influx that is triggered by epinephrine and norepinephrine. Extra cytosolic Ca2+ allows myocardial fibers to generate more force through greater cross-bridge cycling.