Cvs 2: The Cardiac Cycle And Embryology Of The Heart

Front 1

Describe the basic circulation of the heart

Back 1

- The systemic circulation is in series with the pulmonary circulation
- Atria are thin-walled reservoir
- Ventricles are muscular pumping chambers
- Valves control the inflow and outflow of the ventricles
- The left mitral valve has only 2 cusps rather than 3 to better withstand the high pressure that it is under
- Pulmonary veins drain into the left atrium
- Left atrium drains into left ventricle through the mitral valve
- Left ventricle pumps out of the aorta through the aortic valve
- SVC and IVC return blood to the right atrium
- Right atrium flows into the right ventricle through the tricuspid valve
- Right ventricle flows into the pulmonary arteries through the pulmonary valve

Front 2

Describe the mitral valve

Back 2

- Papillary muscles are an integral part of the LV
- They help the mitral valve to close with their chordae tendineae to prevent regurgitation
- Consequenty, mitral repair is preferred to replacement as the muscle is useless otherwise → atrophy, and it is less thrombogenic

Front 3

Describe the conduction of action potential through the heart

Back 3

- Conduction of action potential:
1. Depolarization is initiated in the SA node
2. Depolarization spreads through adjacent atrial work cells causing atrial systole in both atria
3. At the AV node the wave of depolarization is delayed by approximately 0.1s so that the atria can contract fully
4. Conduction continues through the bundle of His and its left and right bundle pathways. These are very fast conduction pathways
5. Numerous subendocardial Purkinje fibres distribute the impulse to the work cells in the endocardium
6. Adjacent work cells then continue the spread to the epicardiu to depolarise the whole ventricle

Front 4

What is the sinuatrial node?

Back 4

- All parts of the heart a capable of causing a heart beat
- The sinoatrial node has the highest intrinsic firing rate, and therefore controls heart rate
- The SA node is located in the posterior wall of the right atrium.
- The SA node is the cardiac pacemaker and is responsible for initiating the depolarization and subsequent contraction of the whole heart

Front 5

What is a chronotropic agent?

Back 5

- An agent that increases (positive chronotrope) or decreases (negative chronotrope) the heart rate

Front 6

What is an inotropic agent?

Back 6

- An agent that increases (positive inotrope) or decreases (negative inotrope) the force of contaction

Front 7

What is heart rate and what is its typical value?

Back 7

- Beats per minute
- Typically 60-70bpm

Front 8

What is stroke volume and giveits typical value?

Back 8

- Volume (ml) ejected by each ventricle per heart beat
- Typically ~70ml

Front 9

What is cardiac output and give its typical value?

Back 9

- Cardiac output is the product of heart rate and stroke volume
- Typically ~ 5l/min

Front 10

Define systole and diastole

Back 10

- The period when the ventricles relax is called diastole and takes ~700ms
- The period when the ventricles cotract is called systole and takes ~300ms
- To increase the heart rate the length of diastole (but not systole) becomes shorter

Front 11

Describe ventricular filling

Back 11

- Within diastole
- g,a
- Lasts 0.5s
- AV valves are open and arterial valves are closed
- Ventricular pressure falls, then slowly rises and ventricular volume increases
- The atria and ventricles are relexed initially and there is passive filling of the ventricles
- The volume continues until a neutral ventricular volume is reached
- Further filling, driven by venous pressure, causes the ventricle to distend, causing the ventricular pressure to rise
- Contraction of the atria further increases the filling of the ventricles - but really only 'tops-up' what is already there (only 15-20% of ventricular filling at rest)
- The volume now in the ventricle is termed the end-diastolic volume

Front 12

Describe isovolumetric contraction of the heart

Back 12

- During systole
- Lasts 0.05s
- b
- AV valves are closed and arterial valves are closed
- Rapid rise in ventricular pressure
- Ventricular volume is constant
- The contraction of the ventricles increases ventricular pressure
- Ventricular pressure rises above arterial pressure, thereby closing the AV valves and creating a closed chamber
- As contraction proceeds, wall tension increases, causing a rapid rise in ventricular pressure
- The rise of pressure is a measure of cardiac contractility

Front 13

Describe ejection of the cardiac cycle

Back 13

- Duration = 0.3 seconds
- c & d (not the aortic pressure should be lower than the ventricular pressure as blood is moving downhill and a pressure gradient is needed)
- AV valves closed
- Arterial valves open
- Ventricular pressure rises, thanslowly falls
- Ventricular volume decreases
- Ventricular pressure rises aboe arterial pressure, opening the arterial valves
- This causes a rapid initial rise in the arterial pressure, and then the pressure starts to fall as the contraction fades
- The momentum of the blood prevents immediate valve closure, even when the ventricular pressure falls below arterial pressure
- Eventually the arterial valves close, creating a brief dicrotic notch as the walls of the vessels elastically return
- Note: the ventricle does not empty completely - at rest it remains 50% full, which can be used to increase stroke volume if necessary

Front 14

Describe isovolumetric contraction of the heart

Back 14

- During systole
- Lasts 0.05s
- b
- AV valves are closed and arterial valves are closed
- Rapid rise in ventricular pressure
- Ventricular volume is constant
- The contraction of the ventricles increases ventricular pressure
- Ventricular pressure rises above arterial pressure, thereby closing the AV valves and creating a closed chamber
- As contraction proceeds, wall tension increases, causing a rapid rise in ventricular pressure
- The rise of pressure is a measure of cardiac contractility

Front 15

Describe ejection of the cardiac cycle

Back 15

- Lasts 0.3s
- AV valves closed
- Arterial valves open
- c & d
- Ventricular pressure rises, than slowly falls
- Ventricular volume decreases
- Ventricular pressure rises above arerial pressure, opening the arterial valves
- This causes a rapid initial rise in arterial pressire, and then the pressure starts to fall as the contraction fades
- The momentum of the blood prevents immediate closure of the valve, even when the ventricular pressure falls below arterial pressure
- Eventually the arterial valves close, which creates the brief rise in arterial pressure called the dicrotic notch, as the elastic walls of the arteries return
- Note: the ventricle does not empty completely. It usually remains 50% full, and can be used to increase heart value where necessary

Front 16

Describe the isovolumetric relaxation of the cardiac cycle

Back 16

- Lasts 0.08s
- AV valves closed
- Arterial valves closed
- e
- Ventricular pressure rapidly falls
- Ventricular volume is constant
- The relaxation of sarcomeres plus collagen recoil drops the ventricular pressure
- When ventricular pressure falls below atrial pressure, the AV valve open, leading to filling

Front 17

Describe the sounds of the heart and why they occur

Back 17

- 4 possible herat sounds
- S1 = mitral and tricuspid closure
- S2 = aortic and pulmonary valve closure
• These valves don't close at exactly the same time and therefore can be split (this can be heard better when the patient inhales)
- S3 = passive LV filling in early diastole. High blood velocity causes sound from blood turbulance
- S4 = PATHOLOGICAL active (atrial kick) LV filling in late diastole. Found in individuals with impaired ventricular filling e.g. hypoertrohpy, or when a high cardiac output is required, as atrial contraction is needed to produce a high enough cardiac output

Front 18

What is fibrillation?

Back 18

- Fibrillation is chaotic electrical and mechanical activity due to errors in the spread of the heart beat
- The pumping action of the affected chamber is lost

- Atrial fibrillation reduces efficiency of the heart but does not cause a serious problem for cardiac output in the absence of other heart disease
• Blood may be more likely to be trapped in the atrium and clot (thromboembolism), increasing the risk of stroke
• A rippling effect of the muscle occurs, which does not contribute to ventricular filling
• Ventricular activity is affected, producing a characteristic 'irregularly irregular' pulse in rate and volume
• Commonly caused by mitral valve disease, ischaemic heart disease, thyrotoxicosis, hypertension and alcohol

- Ventricular fibrillation results in complete loss of cardiac output and is fatal within minutes unless corrected (electrical defibrillation)

Front 19

Describe how right atrial waveform can be assessed

Back 19

- JVP is the best way of assessment
- JVP indicates right heart pressure, and therefore if raised can be indicative of disease e.g. right heart failure of SVC obstruction
- The waveform can also be observe if the venous pressure is normal, which also can be indicative of various diseases e.g. atrial fibrillation

Front 20

What is pulmonary capillary wedge and what does it measure?

Back 20

- Push a catheter through the venal side into the right ventricle and then into the pulmonary artery. As you continue to push it, it will become lodged as it's so small, stopping the flow of blood
- This allows a measurement of left atrial pressure (as blood it returning to the LA)

Front 21

Describe the differences in pressures in different chambers of the heart during the cardiac cycle

Back 21

Front 22

Describe where you would auscultate for the heart

Back 22

Front 23

What is a murmur?

Back 23

- Turbulent flow through the heart, which is audible with the stethoscope
- May be caused by:
• High cardiac output (normal heart)
• Leaking valves
• Narrowed valves
• Abnormal connections between cardiac chambers

Front 24

Describe the changes in heart sounds brought about for aortic stenosis

Back 24

- Increased resistance of flow of the aortic valve (which has been narrowed) and turbulent flow through it
- Increases ventricular work
- This increase of work is an example of pressure overload and is also seen in hypertension
- Causes a murmur between S1 and S2 but a normal diastole

Front 25

Describe the differences in sounds of the heart in aortic regurgitation

Back 25

- Systole is normal
- Early diastolic murmur which tails off, so that diastole seems shorter
- Listen for on the left hand side and blood will be flowing in the wrong direction

Front 26

Describe the differences in sounds of the heart in mitral regurgitation

Back 26

- Systolic heart sounds are not completely separate due to regurgitation murmur
- Diastole normal

Front 27

Describe the differences in sounds of the heart in mitral stenosis

Back 27

- Mid to late diastolic murmur
- Systole is normal, and slight gap between S2 and it beginning

Front 28

What is hypertrophy of the heart and why might it occur?

Back 28

- Increase in the size of the heart
- Heart muscle responds toany kind of long-term stres (physiological or pathological) by undergoing hypoertrophy
- Physiologically may be an adaptive response in athletes e.g. cycling, rowing, weightlifting
- May also be caused by aortic stenosis and after an MI
- Concentric hypertrophy (increase in muscle thickness inwards but not of overall heart) may cause a pressure overload
- Eccentric hypertrophy (increase in lumen and overall size of heart) may cause volume overload, and therefore the apex beat may appear to move around

Front 29

Describe the formation of the heart into a 4 segmented tube

Back 29

- The cardiogenic region is a horse-shoe shaped region derived from the splanchnopleuric mesoderm by a process called vasculogenesis (day 19)
- A network of blood vessels and the blood cells inside them, begins to form in the mesoderm during the 3rd week of development
- Gradually one vessel on each side becomes larger than the rest of the network. These vessels are the 2 endocardial tubes
- Folding of the embryo draws the endocardial tubes together in the midline and positions them ventral to the future head region. The 2 tubes fuse and the 1st primitive heart is formed
- Cardiac muscle differentiates in its wall and it begins to beat around day 21
- Blood enters the heart at the posterior end from the developing network of veins and is pumped out anterior into the arteries, thus establishing a circulation
- As the heart enlarges it changes from a simple tube to one with 4 segments - from posterior to anterior:
1. Sinus venosus
2. Atrium
3. Ventricle
4. Truncus arteriosus

Front 30

The blood flow into the sinus venosus comes from which 3 pairs of vessels?

Back 30

1. Cardinal veins that drain the embryo proper
2. Vitelline veins from the yolk sac
3. Umbilical veins from the placenta
- The umbilical and vitelline veins traverse the liver, which forms within the tissue of the septum transversum

Front 31

Describe the folding of the heart

Back 31

- A cavity, the pericardial cavity forms around the heart
- As the heart grows longer it bends into a loop in order to accomodate to the size of the pericardial cavity
- The sinus venosus and atrium come to lie posterior to the ventricle and truncus arteriosus

Front 32

Describe the formation of the mature ventricles

Back 32

- The superior, inferior, right and left cusions form around the atrioventricular canal
- At the same time the ventricular septum begins to grow up towards the cushions to divide the single ventricle
- Dorsal and ventral endocardial cushions fuse in the middle of the AV canal, forming the AV septum which divides the canal into rigt and left AV openings. The also form the mitral and tricuspid valves
- Also, neural crest cells that form at the level of the 4th and 6th aortic arches populate the forming trucal cushions
- These form the conotruncal cushions and the pulmonary and aortic trunks
- The conotruncal cushions fuse to form the aorticopulmonary septum
- Further along the outflow tract, these cushions are more dorsal and ventral to one another. This change in position is indicative of the spiraling of the aorticopulmonary septum, aorta and pulmonary artery
- Fusion of the outflow tract cushions resuts in the separation of blood flow to their correct constituent parts

Front 33

Describe the formation of the mature atria

Back 33

1. Septum primum grows down from the roof of the common atrium towards the fused endocardial cushions. The ostium primum is the gap between the septum primum and the endocardial cushions (it does not grow all the way down)
2. Septum secundum appears in the roof of the common atrium on the right side of septum primum. The ostium secundum is formed by the rupture of the upper part of septum primum. Ostium primum is closed by the fusion of the septum primum with the AV septum
3. Foramen ovale is the oblique passage between septum primum and septum secundum. Septum primum is a moveable septum, whereas septum secundum is a rigid septum. During the foetal period, septum primum acts like a valve of foramen ovale, letting blood floew from right atrium (high pressure side) to left atrium (low pressure side). This is important as foetal blood flow must still get through from right to left atria.
4. At birth the pressure in the left atrium increases and pushes the septum primum to septum secundum, closing the foramen ovale and forming the interatrial septum. This is a functional closure - the anatomical closure takes 3 months, and may never truely complete. The lowere margin of the septum secundum forms the annulus fossa ovalis. Septum primum forms the fossa ovalis