Intro 2

Question 1

What is stroke volume?

Answer 1

ml of blood pumped per beat

Question 2

How is heart muscle adapted for contraction?

Answer 2

-Discrete cells but interconnected electrically -Cells contract in response to action potential in membrane -Action potential causes a rise in intracellular calcium -Cardiac action potential relatively long – lasts for durations of a single contraction of heart (~280 ms) -Action potentials are triggered by spread of excitation from cell to cell

Question 3

How is back flow prevented in heart valves?

Answer 3

-Valves have cusps, which are pushed open to allow blood flow and close together to seal and prevent backflow. -Cusps of mitral and tricuspid valves attach to papillary muscles via chordae tendineae. Prevents inversion of valves on systole.

Question 4

Describe the electrical conduction system in the heart

Answer 4

Pacemaker cells in sinoatrial node generate an action potential

-Activity spreads over atria

– atrial systole

• Reaches the atrioventricular node and delayed for ~ 120 ms
• From a-v node excitation spreads down septum between ventricles
• Next spreads through ventricular myocardium from inner (endocardial) to outer (epicardial) surface
• Ventricle contracts from the apex up forcing blood through outflow valves

Question 5

What are the seven stages of the cardiac cycle?

Answer 5

1) Atrial Contraction 2) Isovolumetric Contraction 3) Rapid Ejection 4) Reduced Ejection 5) Isovolumetric Relaxation 6) Rapid Filling 7) Reduced Filling

Question 6

Describe Phase 1 (Atrial Contraction)

Answer 6

-Atrial pressure rises due to atrial systole. This is called the “A wave” -Atrial contraction accounts for final ~10% of ventricular filling. This value varies with age and exercise -P wave in ECG signifies onset of atrial depolarisation. -At the end of Phase 1 ventricular volumes are maximal: termed the End-Diastolic Volume (EDV) (Typically ~120 ml)

Question 7

Describe Phase 2 (Isovolumetric Contraction)

Answer 7

-Mitral valve closes as intraventricular pressure exceeds atrial pressure. -Rapid rise in ventricular pressure as ventricle contracts -Closing of mitral valve causes the “C wave” in the atrial pressure curve -Isovolumetric since there is no change in ventricular volume (all valves are closed) -QRS complex in ECG signifies onset of ventricular depolarisation. -Closure of the mitral and tricuspid valves results in the first heart sound (S1).

Question 8

Describe Phase 3 (Rapid Ejection)

Answer 8

-Ejection begins when the intraventricular pressure exceeds the pressure within the aorta. This causes the aortic valve to open. -Atrial pressure initially decreases as the atrial base is pulled downward as ventricle contracts. This is called the “X descent” -Rapid decrease in ventricular volume as blood is ejected into aorta

Question 9

Describe Phase 4 (Reduced Ejection )

Answer 9

-Repolarization of ventricle leads to a decline in tension and the rate of ejection begins to fall -Atrial pressure gradually rises due to the continued venous return from the lungs. This is called the “V wave” -Ventricular repolarization depicted by T-wave of ECG

Question 10

Describe Phase 5 (Isovolumetric Relaxation)

Answer 10

-When intraventricular pressure falls below aortic pressure, there is a brief backflow of blood which causes the aortic valve to close -“Dicrotic notch” in aortic pressure curve caused by valve closure -Although rapid decline in ventricular pressure, volume remains constant since all valves are closed. Hence isovolumetric relaxation -End systolic Volume (ESV) EDV-ESV = Stroke volume (Typically ~80ml) -Closure of the aortic and pulmonary valves results in the second heart sound (S2).

Question 11

Describe Phase 6 (Rapid Filling)

Answer 11

-Fall in atrial pressure that occurs after opening of mitral valve is called the “Y-descent” -When the intraventricular pressure falls below atrial pressure, the mitral valve opens and rapid ventricular filling begins. -Ventricular filling normally silent. However, third heart sound (S3) sometimes present. S3 heart sound is normal in children but can be sign of pathology in adults

Question 12

Describe Phase 7 (Reduced Filling)

Answer 12

Rate of filling slows down (diastasis) as ventricle reaches its inherent relaxed volume. Further filling is driven by venous pressure. At rest the ventricles are ~90% full by the end of phase 7.

Question 13

In terms of pressure, what is the difference between the systemic and pulmonary circulation?

Answer 13

Systemic is high pressure and pulmonary is low pressure.

Question 14

Define afterload

Answer 14

load that heart must eject blood agains

Question 15

Define preload

Answer 15

amount ventricles are stretched (filled) in diastole (related to end diastolic volume or central venous).

Question 16

Define total peripheral resistance

Answer 16

Resistance to blood flow by systemic vasculature

Question 17

What are the effects of arteriolar contraction on venous pressure and arterial pressure?

Answer 17

• decreased venous pressure
• increased arterial pressure

Question 18

Describe the relationship between cardiac output and total peripheral resistance

Answer 18

If CO unchanged and TPR falls- increased venous pressure and decreased arterial pressure

If CO increased and TPR is constant- increased arterial pressure and decreased venous pressure

Cardiac output must increase to meet demand of tissues. If higher demand, precapillary sphincters are dilated, TPR is decreased. Cardiac output increases to maintain arterial and venous pressures.

Question 19

What is the relationship between cardiac output and stroke volume?

Answer 19

Cardiac output = stroke volume x heart rate

Question 20

Define the pressure principles that describes ventricular filling

Answer 20

In diastole, ventricles are isolated from arteries. Ventricles fill until walls stretch enough to produce intraventricular pressure equal to venous pressure. Therefore, higher venous pressure equates to greater heart filling (ventricular compliance).

Question 21

What is the Frank-Starling Law of the heart?

Answer 21

Stretching heart fibres contract harder. More filling equates to harder contraction and greater stroke volume (upto a limit).

Note that if fibres are stretched too far, sarcomeres become too short and filament overlap interferes with contraction. Also fibres become more sensitive to calcium as they get stretched.

It is an intrinisic mechanism of the heart ensuring that arterial and venous systems maintain the same output

Question 22

Define contractility

Answer 22

Force of contraction for a given fibre length.

It can be influenced by extrinsic factors such as sympathetic stimulation and circulating adrenaline.

Question 23

What is the effect of increased arterial pressure on stroke volume?

Answer 23

Increased TPR means reduced stroke volume, as pressure in aorta has increased (aortic impedance)