CVS Session 2 - Cardiac Cycle and Control of Cardiac Output Flashcards Preview

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Flashcards in CVS Session 2 - Cardiac Cycle and Control of Cardiac Output Deck (42):

Distinguish between systemic and pulmonary circulation.

The right side of the heart pumps blood to the lungs i.e. pulmonary circulation and the left side to the body i.e. systemic circulation.


Briefly outline the contraction of the heart muscle.

- The myocardium consists of individual specialised muscle cells joined by low electrical resistance connections.

- The contraction of each cell is produced by a rise in intracellular calcium concentration triggered by an all or none electrical event in the cell membrane - the action potential.

- The cardiac action potential is very long, so over most of the heart a single action potential will produce a sustained contraction of the cell lasting about 200 - 300 ms.

- Action potentials spread from cell to cell, so at each heart beat all the cells in the heart normally contract.


Define the terms systole and diastole.

The period when the myocardium is contracting is known as SYSTOLE. The period of relaxation between contractions is DIASTOLE.


What is the cardiac cycle?

The cardiac cycle is the sequence of pressure flow changes and valve operations that occur with each heartbeat.


Briefly outline the cardiac cycle.

- As the ventricular muscle relaxes (i.e. early diastole), the intraventricular pressure falls, and the atrioventricular valves (tricuspid and mitral) open as atrial pressure exceeds ventricular.

- The atria have been distended by continuing venous return during the preceding systole, so initially blood is forced rapidly from the atria into the ventricles - the 'rapid filling' phase.

- Filling of the ventricles continue throughout diastole, at a steadily decreasing rate until the intraventricular pressure rises to match atrial pressure.

- Atrial systole is the contraction of the atria, which forces a small extra amount of blood into the ventricles.

- The ventricles then contract 'isovolumetrically' and intraventricular pressure rises rapidly until it exceeds the diastolic pressure in the arteries, when the outflow valves open.

- There is then a period of rapid ejection of blood, and both intra ventricular and arterial pressure rise to a maximum.

- Towards the end of systole, intra ventricular pressure falls and once it is below the arterial pressure, the outflow valves close.


Outline the conduction system.

- Pacemaker cells in the sinoatrial node are specialised cardiac myocytes and generate an action potential.

- Activity spreads over atria – atrial systole.

- Reaches the atrioventricular node and delayed for ~ 120 ms. The signal is delayed to prevent simultaneous atrial and ventricular contraction.

- From the AV node, the 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.


Outline abnormal valve function.

- Stenosis occurs when the valve doesn’t open enough and there is a resultant obstruction to blood flow when then valves normally open.

- Regurgitation occurs when the valve doesn’t close all the way and there is a resultant back leakage when the valve should be closed.


Outline aortic valve stenosis (causes, sounds, consequences)

- Causes:

I. Degenerative (senile calcification/fibrosis)

II. Congenital (bicuspid form of valve)

III. Chronic rheumatic fever –inflammation-commissural fusion


- Sound: Crescendo-decrescendo murmur


- Consequences: less blood can get through the valve

I. Increased LV pressure - LV hypertrophy

II. Left sided heart failure - syncope, angina

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Outline aortic valve regurgitation (causes, sounds, consequences)

- Causes:

I. Aortic root dilation (leaflets pulled apart)

II. Valvular damage (endocarditis rheumatic fever)


- Sound: Early decrescendo diastolic murmur


- Consequences: LV hypertrophy

I. Blood flows back into LV during diastole which increases stroke volume

II. Systolic pressure increases

III. Diastolic pressure decreases

IV. Bounding pulse (head bobbing, Quinke’s sign)

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Outline mitral valve regurgitation (causes, sounds, consequences)

- Causes:

I. Chordae tendineae & papillary muscle normally prevent prolapse in systole. Myxomatous degeneration can weaken tissue leading to prolapse.

II. Damage to papillary muscle after heart attack

III. Left sided heart failure leads to LV dilation which can stretch valve.

IV. Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation.


- Sound: Holosystolic murmur


- Consequences: As some blood leaks back into the LA, this increases preload as more blood enters LV in subsequent cycles, can cause LV hypertrophy.

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Outline mitral valve stenosis (causes, sounds, consequences)

- Main cause: Rheumatic fever

I. Commissural also fusion of valve leaflets

II. Harder for blood to flow from L.A > L.V.


- Sound: Snap as valve opens, Diastolic rumble


- Consequences: Increased LA pressure

I. Pulmonary oedema, dyspnea, pulmonary hypertension: RV hypertrophy

II. LA dilation: atrial fibrillation --> thrombus formation, oesophagus compression --> dysphagia

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What are heart sounds?

- Heart Sounds: The preceding events are associated with sounds which are often used to assess the state of the heart.

- Sound is produced by sudden acceleration and deceleration of structures or by turbulent flow.


What are the first and second heart sounds?

In a normal heart, there are always two sounds. Two others may be audible.

- First heart sound: As the A-V valves close oscillations are induced in a variety of structures, producing a mixed sound with crescendo-descendo quality - 'lup'.

- Second heart sound: As the semi-lunar outflow valves close oscillations are induced in other structures including the column of blood in the arteries. This produces sound of shorter duration, higher frequency and lower intensity than the first - 'dup'.

- A third sound may be heard early in diastole, and a 4th sound is sometimes associated with atrial contraction.


What are murmurs?

In exercise, turbulent flow generates 'murmurs' in normal individuals, but at rest murmurs are associated with disturbed flow, say through a narrowed valve, or back flow through an incompetent valve.


What are the 7 phases of the cardiac cycle?

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How else can the cardiac cycle be split?

Two phases:

- Systole

I. Isovolumetric contraction

II. Rapid Ejection

III. Reduced Ejection


- Diastole

I. Isovolumetric relaxation

II. Rapid filling

III. Reduced filling

IV. Atrial contraction

When the heart rate increases, systole stays the same but it's diastole which gets shorter.


Outline Phase 1: Atrial Contraction

- LAP: Atrial pressure rises due to atrial systole. This is called the "A wave".

- LVV: Atrial contraction accounts for final ~10% of ventricular filling. This value varies with age and exercise.

- ECG: P wave in signifies onset of atrial depolarisation.

- At the end of Phase 1, ventricular volumes are maximal: termed the End-Diastolic Volume (EDV) typically ~120 ml.

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Outline Phase 2: Isovolumetric Contraction

- Mitral valve closes as intraventricular pressure exceeds atrial pressure.

- LVP: Rapid rise in ventricular pressure as ventricle contracts.

- LAP: Closing of mitral valve causes the "C wave" in the atrial pressure curve.

- LVV: Isovolumetric since there is no change in ventricular volume (all valves are closed)

- ECG: QRS complex signifies onset of ventricular depolarisation

- Phonocardiogram: Closure of mitral valves results in the first heart sound.

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Outline Phase 3: Rapid Ejection

- AP: Ejection begins when the intraventricular pressure exceeds the pressure within the aorta. This causes the aortic valve to open.

- LAP: Atrial pressure initially decreases as the atrial base is pulled downward as the ventricle contracts. This is called the "X descent".

- LVV: Rapid decrease in ventricular volume as blood is ejected into aorta.

- Blood continues to flow into the atria from their respective venous inputs. The atrioventricular valves are closed but the outflow valves are open.

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Outline Phase 4: Reduced Ejection

- LVP: Repolarisation of the ventricle leads to a decline in tension and the rate of ejection begins to fall.

- LAP: Atrial pressure gradually rises due to continued venous return from the lungs. This is called the "V wave".

- ECG: Ventricular repolarisation depicted by the T-wave.

- The atrioventricular valves are closed but the outflow valves are open.

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Outline Phase 5: Isovolumetric Relaxation

- AP: When intraventricular pressure falls below aortic pressure, there is a brief backflow of blood which causes the aortic valve to close. "Diacritic notch" in aortic pressure curve caused by valve closure.

- LVP: Although rapid decline in ventricular pressure, volume remains constant since all valves are close. Hence, isovolumetric relaxation.

- LVV: End systolic volume (ESV) EDV - ESV = stroke volume, typically ~80ml - Phonocardiogram: Closure of aortic and pulmonary valves results in second heart sound (S2)

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Outline Phase 6: Rapid filling.

- LAP: Fall in atrial pressure that occurs after opening of mitral valve is called the 'Y-descent"

- LVP: When the intraventricular pressure falls below atrial pressure, the mitral valve opens and rapid ventricular filling begins.

- Phonocardiogram: ventricular filling normally silent. However, third heart sound (S3) sometimes present. S3 heart sound is normal in children but can be a sign of pathology in adults.

- Atrioventricular valves are open but outflow valves are closed.

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Outline Phase 7: Reduced Filling.

- LVV: 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 ~75-80% full by the end of phase 7.

- The atrioventricular valves are open but the outflow valves are closed.

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What is cardiac output?

- Cardiac output: The volume pumped per minute by the left heart.

- As the pumping is intermittent, it is the product of the volume ejected per cardiac cycle - stroke volume and the number of cycles per minute - the heart rate. Both may vary.


How is end diastolic volume determined?

End diastolic volume is determined by the filling of the heart. During diastole, the ventricles fill as the venous pressure drives blood into them. As they fill so the passive stretch of the ventricular wall causes intra ventricular pressure to rise, until it matches venous pressure, when no more filling will occur. Within limits, the higher the venous pressure, the more the ventricle will fill in diastole.


How is stroke volume determined?

Stroke volume is determined by how much the ventricle contracts during systole. All myocardial cells normally contract, so active tension is changed by factors which act directly upon individual myocardial cells. These factors may be mechanical or chemical.


Define preload, afterload and total peripheral resistance.

- Afterload: The load the heart must eject blood against (roughly equivalent to aortic pressure)

- Preload: Amount the ventricles are stretched (filled) in diastole – related to the end diastolic volume or central venous pressure.

- Total peripheral resistance: sometimes referred to as systemic vascular resistance – resistance to blood flow offered by all the systemic vasculature.


What are the effects of changing total peripheral resistance?

- If TPR falls and CO is unchanged

I. Arterial pressure will fall

II. Venous pressure will increase


- If TPR increases and CO is unchanged

I. Arterial pressure will increase

II. Venous pressure will fall


What are the effects of changing cardiac output?

- If CO increases and TPR is unchanged

I. Arterial pressure will increase

II. Venous pressure will fall.


- If CO decreases and TPR is unchanged

I. Arterial pressure will fall

II. Venous pressure will rise


Outline the changes in demand for blood.

- The heart must meet changes in demand for blood.

- If the tissues need more blood the arterioles and precapillary sphincters will dilate.

- Therefore, peripheral resistance falls.

- The heart needs to pump more so that arterial pressure does not fall and venous pressure doesn’t rise.

- The heart ‘sees’ changes in this demand as changes in arterial blood pressure(aBP) and central venous pressure (CVP).

- The heart responds to changes in CVP and aBP by INTRINSIC and EXTRINSIC mechanisms.


Outline the principles of preload and afterload.

- Because of the operation of the valves in the heart the mechanical forces acting on the myocardium are different in diastole and systole.

- In diastole, the ventricle is connected to the veins, so venous pressure determines the end diastolic stretch or 'preload' on the myocardium.

- Once systole begins the ventricles are isolated from the veins but connected to the arteries, and the force necessary to expel blood into the arteries or the 'afterload' determines what happens during systole.

- Preload and afterload may vary independently.

- For purely mechanical reasons therefore:

I. Rises in venous pressure lead to increased stroke volume.

II. Falls in total peripheral resistance lead to increased stroke volume.


Explain the effect of increasing arterial pressure on stroke volume.

- Afterload is the pressure that the heart has to pump against – this is the pressure in the aorta (aortic impedance)

- Arterial (aortic) pressure is increased when the peripheral resistance is increased – this makes it harder for the heart to pump out

- Increased TPR also reduces venous pressure and therefore reduces filling of the heart.

- Over time you can get an inappropriate increase in arterial pressure. The heart will have to work harder.


Referring to the profile of pressure changes in the internal jugular vein, identify the component areas 

A = atrial contraction 

C= tricuspid valve closure

V = passive atrial filling (ventricular contraction)

X = atrial diastole

Y = atrial emptying 

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Outline the concept of resistance. 

- The pressure that the blood exerts drops as it flows through ‘a resistance’

- The arterioles offer the greatest resistance

- Constriction of the arterioles increases the resistance. This will cause pressure in the capillaries and on the venous side to fall but will cause pressure on the arterial side to rise.


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Explain the Frank-Starling Law of the Heart 

- Otto Frank and Ernest Starling demonstrated that stretching the ventricles by increasing the filling of the heart increased the force of contractions.

- Frank – Starling law of the heart: the more the heart fills, the harder it contracts (up to a limit)

- The harder the heart contracts, the bigger the stroke volume.

- An increase in venous pressure will fill the heart more – how much the ventricles fill depends on the compliance.

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Discuss the length tension curve for cardiac muscle.

- If sarcomere length is too short, filament overlap interferes with contraction

- In cardiac muscle, you also get an increase in calcium sensitivity as muscle fibres are stretched

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Explain how the Starling Law of the heart ensures that both sides are balanced. 

- The increased stroke volume with increased filling of the heart is an INTRINSIC control mechanism 

- It ensures that both sides of the heart pump maintain the same output. 

- The pulmonary and systemic circulations operate in series. I.e. The sample volume of blood pumped to the body must also be pumped to the lungs. 

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Outline Ventricular Filling.

- In diastole, the ventricle is isolated from the arteries. 
- The ventricle fills until the walls stretch enough to produce an intraventricular pressure equal to the venous pressure. 
- The higher the venous pressure, the more the heart fills. 
- The relationship is illustrated in the Ventricular Compliance Curve
- Compliance can be increased or decreased in disease states 

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Outline contractility and force of contraction.

- Contractility is the force of contraction for a given fibre length 

- A change in contractility is seen as a change in the slope of the Starling Curve 

- An increase in contractility will increase the force of contraction for a given left EDP 

- Extrinsic factors such as sympathetic stimulation and circulating adrenaline can increase contractility 

- Reducing sympathetic stimulation will reduce contractility. 

- The force of contraction of the ventricle always varies with preload, but the slope of this relationship - the contractility can be affected by neurotransmitters, hormones, or drugs acting on the myocardium. 

- Noradrenaline and adrenaline increase contractility – a 'positive inotropic' effect. So, increases in sympathetic activity will increase stroke volume at a given preload and afterload. 


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Explain how the CVS responds to eating a meal: local vasodilation in the gut.

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Explain how the CVS responds to standing up.

- Standing up causes ‘pooling’ of blood in legs due to effect of gravity on a column of liquid.

- Now both arterial and venous pressure have changed in the same direction.

- Cannot adjust be intrinsic mechanisms.

- Baroreceptor reflex and autonomic nervous system increase heart rate AND increase TPR.

- If reflexes don’t work you get postural hypotension.


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Explain how the CVS responds to exercise 

Initially muscle pumping and venoconstriction returns more blood to the heart.

- Later decreased TPR also increases venous return.
-  Very early response of increased heart rate (decrease parasympathetic drive, increase sympathetic drive).
- Increased contractility (increased sympathetic drive)

Note: increased venous pressure alone would move ventricular function to the top (flat) part of the Starling curve

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