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CardioRespiratory Year 1 > Physiology - The Heart as a Pump > Flashcards

Physiology - The Heart as a Pump Flashcards

1
Q

What are the two circulations

A
  • Systemic

- Pulmonary

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2
Q

Describe the mechanism of action of the systemic system

A

left heart, contraction of the left ventricle pumps blood into the aorta goes around the body

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3
Q

Describe the mechanism of action of the pulmonary system

A

right heart contraction of right ventricle pumps blood into the pulmonary arteries goes round the lungs

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4
Q

What is the same in both circulations

A
  • cardiac output

- if this did not happen blood would accumulate into one circulation and be removed from another

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5
Q

Describe the pressure in the systemic circulation

A
  • The left side of the heart pumps blood into the systemic circulation through the aorta
  • The blood pressure in the systemic circulation has to be kept high so efficient distribution of the blood to different organs can occur
  • Blood flow to organ is determined by the construction of muscles with the small arteries that lead into that organ
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6
Q

Describe the pressure in the pulmonary circulation

A
  • Right heart pumps blood into the pulmonary circulation through he pulmonary artery
  • No high pressure is needed here as there is no distribution of blood to different organs is needed, only lungs are involved
  • Lungs have lower pressure because the pulmonary vascular resistance is much lower than the systemic vascular resistance
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7
Q

Why is the pulmonary arterial pressure lower

A
  • Because the total vascular resistance in the pulmonary vascular bed is lower than that in the systemic circulation
  • If the pulmonary vascular resistance is lower than a lower pressure is needed from the right heart to push the cardiac output through the pulmonary vessels
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8
Q

describe how the structure of the systemic and pulmonary arteries have been influenced by the pressure in there systems

A
  • Systemic arteries – moderate size, thick muscular walls - more resistance, - higher pressure
  • Pulmonary arteries – large diameter, thin elastic walls- less resistance, low pressure
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9
Q

How is blood pressure measured

A
  • Measured in terms of ml of mercury
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10
Q

How is gas pressure measured

A
  • Measured in kPA
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11
Q

What does starlings law state

A
  • Ventricular contractile force increased with increased end diastolic volume
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12
Q

what does Starlings law mean

A
  • This means that the heart when working normally pumps out the from the ventricles whatever volume is delivered to the atria
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13
Q

What is the end diastolic volume

A
  • The end diastolic volume is the largest diameter of the heart during diastole
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14
Q

explain starlings law of the heart

if more blood is delivered…

A
  • If more blood is delivered then the ventricle expands and has a greater diameter, this causes it to contract more strongly therefore it is pumping more strongly with more force
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15
Q

What is the definition of preload

A
  • This is the degree of stretching experienced by the ventricle and the end of diastole
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16
Q

Explain preload and how it is linked to starlings law

A
  • Preload is proportional to the end diastolic volume (EDV), it determines the EDV
  • Therefore it determines the stroke volume
  • It links to starlings law as an increase in the preload makes the heart contract more strongly and therefore expel the extra volume so an increased preload results in an increase stroke volume and an increase in cardiac output
  • E.g. exerice increases preload which results in an increase of cardiac output
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17
Q

What is the limitation of Starlings law

A
  • If the ventricle expands beyond a certain volume it fails leading to heart failure
  • Heart failure is when the ventricles are overstretched and weakened
  • This is when starling law fails
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18
Q

describe the mechanism underlying starlings law

A
  • Cardiac muscle is striated and its contractile mechanism involves actin and myosin filaments
  • The filaments have excess overlap at rest and stretching increases the amount of overlap of actin and myosin filaments and therefore increases the force of contraction
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19
Q

what are the consequences of starlings law

A
  • Ventricular contractile force increases in proportion to end diastolic volume
    Important feature
    The two ventricles eject the same volume of blood – balances the output of the two sides of the heart and prevents blood accumulating in the pulmonary or systemic circulations
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20
Q

Why is an enlarged heart a problem

A
  • A heart with enlarged ventricles where there is no corresponding increase in ventricular wall thickness will contract more weakly than a smaller heart as the muscle fibres are stretched beyond starlings law so starling mechanism no longer works
  • A larger end-diastolic volume produces a smaller stroke volume
  • This causes heart failure
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21
Q

what is stroke volume

A
  • Stroke volume is the volume of blood pumped out of the heart per beat.
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22
Q

In a normal healthy adult what should the stroke volume be

A

70ml (at rest)

23
Q

Stroke volume is…

A

not always the same as EDV ), as there is always some blood left in the ventricle at the end of systole. This blood makes up the residual volume.
- In a typical heart, the EDV is about 120 mL and the ESV about 50 mL. The difference in these two volumes, 70 mL is therefore the stroke volume.

24
Q

What is after load

A
  • This is the effective flow impedance (resistance) of the aorta and large arteries.
25
Q

what is compliance

A

the reciprocal of after load

26
Q

an increased after load decreases…

A

the cardiac output

27
Q

what determines the after load

A

flow impedance

28
Q

Explain the after load

A
  • The resistance of the aorta to fluid flow depends on the diameter and the elasticity of the tissue.
  • In a heartbeat, pressure is constantly rising and falling
  • The reciprocal of afterload is compliance.
  • The higher the compliance of the aorta the lower the afterload, and thus the less work the heart has to do to generate a cardiac output so increased cardiac output.
  • In older people, the elasticity of the aorta declines, as elastic tissue is lost from the wall and replaced with collagen. This process is increased by smoking. Therefore, the afterload increases.
  • The greater the afterload, the longer the period of isovolumetric contraction of the ventricle before the aortic valve opens and the shorter the duration of ejection, and so the smaller the stroke volume and the larger the end-systolic (residual) volume.
  • An increased afterload DECREASES Cardiac output
  • Flow impedance determines the afterload
29
Q

What is isovolumetric contraction

A
  • This is an event that occurs early systole when the ventricles contract with no corresponding volume change this is because all the heart valves are closed
30
Q

What does inotropy mean

A

this means force

- This is the contractility (force of contraction) of the ventricular muscle

31
Q

an increase in contractility will…

A

decrease the residual volume and therefore increase stroke volume at a given end diastolic volume

32
Q

What can isotropy vary to

A
  • This can vary due to the influence of neuronal and hormonal factors
33
Q

What are the factors that increase contractility

A
  • Increased blood calcium levels
  • Beta adrenergic agonists (eg adrenaline)
  • Drugs which stimulate calcium entry into myocardium (eg levosimendan)
  • Cardiac glycosides (eg digoxin)
  • Insulin
  • Glucagon
34
Q

Name the heart valves and their structure

A
  • Right atrio-ventricular = tricuspid - more efficient with lower pressures in right hand side of the heart
  • Left atrio-ventricular = mitral bicuspid - more efficient when closing when you have higher pressure in the left side of the heart
  • Aortic and pulmonary are also tricuspid
  • Pulmonary = pulmonary artery valve – semilunar valve
  • Aorta = Aortic valve – semilunar valve
35
Q

there is no valve between…

A

between vena cava and right atrium and no valve between pulmonary vein and left atrium

36
Q

Describe the anatomy of the heart vavles

A
  • Kept in position when closed by the chordae tendineae these are fibrous tendons and these are attached to papillary muscles
  • Papillary muscles are the first thing that contract and pull on the chordae tendineae this push’s the valves up and closes them this happens during systole
  • the chordae hold the valves against the pressure of the contracting ventricles
37
Q

describe the cardia cycle stage

A

Artial systole
1. atrial systole begins – atrial contraction forces a small amount of blood into the relaxed ventricles
2. atrial systole ends and atrial diastole begins
Then you have ventricular systole this starts with
1. isovolumetric contraction
2. ventricular contraction this is the first stage of ventricular systole – ventricular contraction pushes the AV valves closed but does not create enough pressure for the semilunar valves to open
3. ventricular ejection, this is the second stage – ventricular pressure rises and is larger than that in the arteries, the semilunar valves opens and causes the injection of the stroke volume into the artery
then you have relaxing
1. isovolumetric relaxation – this is start of ventricular diastole – the ventricles relax and pressure drops, the blood flows back against the cusps of semilunar valves and forces them closed, blood flows into the relaxed atria
2. ventricular filling – this is the end of ventricular diastole – all chambers are relaxed and the ventricles fill passively

38
Q

when is atrial contraction is used

A
  • not essential for normal cardiac output at rest
  • the elastic recoil of the ventricular walls as they enlarge during diastole can suck the blood into the ventricles without the need of atrial contraction
    but…
  • during exercise Atrial contraction is necessary to fill the ventricles this si because the diastole is shortened with the increase in heart rate the atria give blood extra push causing it to move into the ventricles
39
Q

what is atrial fibrillation

A
  • asynchronous contraction of the atria

- detected only by the patient feeling dizzy or breathless during exercise

40
Q

describe the valve sequences

A
  • at the start of systole just as the left ventricle starts to contrac thte mitral valve closes then pressure rises above the diastolic causing aortic valve to open
  • at the end of systole pressure the ventricle pressure decreases and aortic valves closes, when pressure is near 0 the mitral valve opens
41
Q

Describe heart sounds

A
  • Heart sounds are due to turbulent flow of blood when the valves close in the heart
  • First heart sound – AV valves close (tricuspid and mitral)
  • Second heart sound – aortic and pulmonary valves close
  • Splitting of the first heart sound is an asynchronous closure of the tricuspid and mitral valves
  • There are minor heart sounds such as S3 and S4 not as important as first 2, S3 due to the tuberlent flow during rapid filling of the ventricles during early diastole, may also be heard in adults with heart disease showing damage to the heart vavles
  • S4 – heard immesidately before the first heart sound and is due to the tuberlent flow in the ventricle during late filling, this is a sign of decreased ventricular compliance
  • S3 and S4 can be called gallops – these are sounds that are associated with diastolic filling – can be recorded and amplified of a phonocardiogram
42
Q

What are the 5 areas for listening to the heart

A

All people enjoy time magazine

  • Aortic right 2nd intercostal space
  • Pulmonic left 2nd intercostal space
  • ERB’s point – left 3rd intercostal space
  • Tricuspid – lower left sternal border 4th intercostal
  • Mitral – left 5th intercostal medial to midclavicular line
43
Q

What are the minor heart sounds

A

S3 and S4

44
Q

What is S3 due to

A

due to the tuberlent flow during rapid filling of the ventricles during early diastole, may also be heard in adults with heart disease showing damage to the heart vavles

45
Q

What is S4 due to

A

– heard immesidately before the first heart sound and is due to the tuberlent flow in the ventricle during late filling, this is a sign of decreased ventricular compliance

46
Q

What is S3 and S4 called

A

gallops

- these are sounds that are associated with diastolic filling, this can be recorded and amplified of a phonocardiogram

47
Q

how is the jugular Venus pulse created

A
  • No valves between vena cava and right atrium or the pulmonary veins and the right atrium
  • Flow is low pressure that if a valve was put in place this would increase the resistance to flow
  • significantly increase the resistance to flow. As there are no valves, when the right atrium contracts a backpressure occurs in the jugular vein. This creates the juglar venus pulse
48
Q

what are the three peaks in the Venus pulse

A

a
c
v

49
Q

describe the three peaks in the Venus pulse

A
  • a is due to the atrial contraction just before the tricuspid valve closes
  • c wave due to the pressure rising in the atrium after the tricuspid closes as the valve bulges back into the atrium
  • v occurs as the valve bulges again as the ventricle reaches the peak of contraction
50
Q

what are three ways for Venus return to the heart

A

1) One-way valves in the veins. As muscles in the limbs and abdomen contract they squeeze the blood in the veins and it is propelled upwards to the heart. Lack of muscle activity in the legs can lead to pooling and stasis of blood in the legs, which can lead to clot (thrombus) formation.
2) Muscular pumps; the contractions of muscles in limbs squeeze veins, an, in conjunction with the one way valves, this propels blood back to the heart.
3) Thoraco-abdominal pump. During inspiration, pressures in the thoracic cavity are reduced, pulling blood into the inferior vena cava. On exhalation thoracic pressures increase and this blood is forced into the right atrium.

51
Q

what does Venus return do

A

These work to increase Venus return to match the increase in cardiac output therefore it determines the preload

52
Q

veins have …

A

anastomoses to enable alternative pathways for blood to return to the heart

53
Q

Why is repairing venus drainage less important that restoring material supply

A

veins have alternative pathways for blood to return to the heart as many anastomoses
- Small veins can also enlarge rapidly to cope with a greatly increased flow

54
Q

describe how the throaco - abdominal pump works

A

Inspiration

  • Thoracic cavity expands
  • Intra-thoracic pressure falls
  • Abdominal cavity is compressed
  • Intra-abdominal pressure rises
  • Blood moves to IVC

expiration

  • Thoracic cavity is compressed
  • Intra-thoracic pressure rises
  • Blood moves to the right atrium

CardioRespiratory Year 1 (28 decks)

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