Cardiac Cycle

Question 1

Difference between resistance and capacitance vessels?

Answer 1

Resistance- arteries, arterioles etc. Restrict blood flow to drive supply to hard to perfuse areas of the body.
Capacitance vessels- veins/venuoles - enable system to vary amount of blood pumped around the body.

Question 2

Define systole and diastole for the ventricles

Answer 2

Systole- contraction and ejection of blood from the ventricles
Diastole - relaxation and filling of ventricles

Question 3

Describe the valves in the right side of the heart

Answer 3

Tricuspid valve - between the right atria and ventricle (deoxy). Pulmonary valve- between the right ventricle and the pulmonary artery (carries deoxy blood to lungs).

Question 4

Describe the valves in the left side of the heart

Answer 4

Mitral valve from left atria to ventricle (bicuspid), aortic valve between right ventricle to aorta- carries oxygenated blood.

Question 5

Define stroke volume

Answer 5

The amount of blood ejected by each ventricle with each beat of the heart (70ml at rest).

Question 6

Briefly describe the process of how a heart receives an action potential and contracts

Answer 6

Cells act in response to an action potential in membrane. Action potential causes a rise in intracellular calcium. AP! Action potentials triggered by spread of excitation from cell to cell. (Relatively long 280ms).

Question 7

The semi lunar cusps are?

Answer 7

Right - pulmonary valve left- aortic valve

Question 8

What physiological features prevent the inversion of the tricuspid and mitral valve upon systole?

Answer 8

Cusps of the valves attach to papillary muscles via cordae tendineae.

Question 9

What appearance would the aortic valve have when the mitral valve is open?

Answer 9

Aortic valve is shut.

Question 10

Describe the conduction system that allows the heart to contract

Answer 10

Pacemaker cells are found in the sinoatrial node and generate an action potential.
Activity spreads over the atria- atrial systole.
Reaches the atrioventricular node and is stored for 120ms
Excitation travels down the septum and spreads through ventricular myocardium from endocardium (inner) to epicardium (outer)
Ventricle contracts from the apex up, forcing blood through the aortic and pulmonary valves.

Question 11

If the heart rate increases does diastole or systole get shorter and why?

Answer 11

Diastole shorter because more rapid filling of heart, systole is the same as ventricles still take the same amount of time to fill and contract.

Question 12

Recall the 7 phases of the cardiac cycle

Answer 12

Atrial contraction, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, reduced filling, atrial contraction.

Question 13

Atrial contraction account for what percentage of atrial filling?

Answer 13

Approximately 10% (only tops up the last amount- atrial kick), atria mostly filled by the tricuspid and mitral valves opening and blood flowing in.

Question 14

Describe the features we would see on a wiggers diagram with atrial contraction. (Electrocardiogram, left ventricular volume, left atrial pressure)

Answer 14

electrocardiogram - p wave signals atrial depolarisation and contraction.
Left atrial pressure - rises due to contraction (A wave).
Left ventricular volume- EDV end diastolic volume - ventricular volume is maximal (pressure is not as no ventricular contraction yet to increase pressure).

Question 15

Describe the features of isovolumetric contraction with reference to a wiggers diagram

Answer 15

QRS on electorcardiogram shows the depolarisation and contraction of the ventricles.
Left ventricle pressure increases hugely.
The pressure in the left ventricle is greater than that in the atria so the mitral and tricuspid valves snap shut. All valves now closed.
atrial pressure increases slightly due to closing of the mitral valve - creates a C wave.

Question 16

What is the S1 sound made by?

Answer 16

The mitral and tricuspid valves closing (LUB).

Question 17

Describe features of rapid ejection

Answer 17

Begins when intraventricular pressure is greater than the aorta, this causes the aortic valve to open.
Blood volume in ventricles decreases.
Pressure in aorta increases (not more than ventricles, otherwise valve would shut).
X descent as there is a slight reduction in atrial pressure due to pulling on the atrioventricular valves. (Transient change in pressure).

Question 18

Features of reduced ejection?

Answer 18

Repolarisation in ventricles leads to a decline in tension, ejection rate begins to fall. T wave (electrocardiogram) shows the depolarisation. Atrial pressure gradually rises due to controlled venous return from the lungs ‘v wave’.

Question 19

Features of isovolumetric relaxation?

Answer 19

When the intraventricular pressure falls below the pressure in the aorta the aortic (pulmonary if right) close due to a brief backflow of blood from aorta. Closing of valves = S2 DUB noise. A diachronic notch is a slight rise in aortic pressure as aortic valve closes.
*Rapid decline in ventricle pressure but not volume (both the mitral/tricuspid and aortic/pulmonary valves are closed.

Question 20

Explain the features of rapid filling

Answer 20

when intraventricular pressure falls below the atrial pressure the mitral valve (AV valves open) and rapid ventricular filling begins. Fall in atrial pressure due to opening of valves = Y descent. Ventricular filing normally silent (unless a child), if hear in adult can be pathology (LUB DUB DUB).

Question 21

What is the term used when the rate of ventricular filling slows down as ventricle reaches its relaxed volume.

Answer 21

Diastasis

Question 22

By end of phase 7 (reduced filling) how full are the ventricles with blood?

Answer 22

90%

Question 23

Features of reduced filling?

Answer 23

Rate of filling slows down (diastisis) as ventricle reaches inherent relaxed volume. Further filling is driven by venous pressure.

Question 24

Medical term for when a valve doesn’t open enough?

Answer 24

Stenosis

Question 25

Medical term when valve doesn’t close all the way?

Answer 25

Regurgitation (back leakage when valve should be closed)

Question 26

Which side of the heart has the highest incidence of pathologies?

Answer 26

Left as it is under higher pressure

Question 27

causes of aortic valve stenosis? <1cm2

Answer 27

• degenerative (senile calcification/ fibrosis)
• Congenital (bicuspid form of valve)
• Chronic rheumatic fever - inflammation- commissural fusion (valve leaflets fuse together)

Question 28

Clinical prognosis for someone with aortic valve stenosis and no treatment?

Answer 28

Less blood through valve —> increased LV pressure —> LV hypertrophy
Less blood through valve —> left sided heart failure (not able to pump enough systemic blood around circulation) and either angina (if coronary arteries not enough blood to heart- angina) or syncope (syncope is fainting if brain not getting enough blood)
Shear stress —> Microangiopathic haemolytic anaemia - occurs as blood forced via narrow opening @ high pressure - shear stress on RBC - break.

Question 29

Causes of aortic valve regurgitation?

Answer 29

• Aortic root dilation (leaflets pulled apart)

- valvular damage (endocarditis rheumatic fever)

Question 30

What occurs in aortic valve regurgitation?

Answer 30

Blood flow back into LV in diastole,increases SV, systolic pressure increases, lower diastolic pressure, bounding pulse, (head bobbing, Quinke’s sign- bed of nails red/pale in synchrony with heart), LV hypertrophy.

Question 31

Causes of mitral valve regurgitation?

Answer 31

1.MI - damage to papillary muscles, cause valve prolapse(forced back open in systole)
2.left sided heart failure —> LV dilation which stretches valve
3. Rheumatic fever - leaflet fibrosis - disrupts seal formation
4. Myxomatous degeneration (jelly valve = prolapse)
Means:
Blood leaks back to left atrium, increases preload of heart and can cause LV hypertrophy.

Question 32

Causes mitral valve stenosis

Answer 32

Rheumatic fever primary cause

Question 33

Impact of mitral valve stenosis?

Answer 33

—>Fusion of leaflets, harder for blood to flow LA—> LV
Increased LA pressure - pulmonary oedema, pulmonary hypertension, dyspnea (shortness breath). RV hypertrophy
—> LA dilation - atrial fibrillation - thrombus formation
—>LA dilation - oesophagus-compression - dysphagia (swallowing issues).