The Heart As A Pump Flashcards

1
Q

What are resistance vessels?

A

Arterioles

Restrict blood flow to drive supply to hard to perfume areas of the body

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2
Q

What are capacitance vessels?

A

In venous side

Enable system to vary amount of blood pumped around body

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3
Q

Where is there a greater % of blood low in moderate exercise

A

Much greater in skeletal muscle

Much lower in gut

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4
Q

Describe the nature of the heart as a pump and the pressure in teh 2 circulations

A
  • Two pumps acting in series
  • Systemic circulation = High Pressure
  • Pulmonary circulation = Low pressure
  • Output of left and right sides over time must be equal
  • Atria act as “priming pumps” for ventricles
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5
Q

What is systole?

A

Contraction and ejection of blood from ventricles

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6
Q

What is diastole?

A

Relaxation and filling of ventricles

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7
Q

How much blood is pumped per beat? And what is the approximate vol of blood in the body?

A

~70ml per beat = stoke volume

• At a heart rate of 70 bpm = 4.9 litres blood pumped per minute (i.e. the approximate volume of blood in the body)

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8
Q

Describe the nature of cardiac muscle

A

Discrete cells but interconnected electrically
Each muscle fibre is mutinucleate (many cells joined togetehr - syncitium)
Myocytes closely coupled by gap junctions to make a functional syncitium
Cells contract in response to AP in membrane
Need AP to travel through entire heart so cells need to be electrically coupled to each other (by gap junctions)
Spread unimpeded through myocardium bc gap junctions
Muscle forms figure 8 - ventricles contract from apex upwards in a twisting motion

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9
Q

Describe a cardiac action potential

A

Action potential causes a rise in intracellular calcium
280ms relatively much longer than neuronal
needs to be longer for a smooth beat of the beart - so ventricles contract after atria
Action potentials are triggered by spread of excitation from cell to cell

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10
Q

What is the function of the heart valves?

A
  • Four valves determine pathway of blood flow through heart.
  • Open or close depending on differential blood pressure on each side.
  • Valve cusps 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.
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11
Q

Name the 4 heart valves

A

Tricuspid (right AV)
Mitral (left AV)
Pulmonary (pulmonary artery - right out)
Aortic (Aorta - left out)

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12
Q

How is conduction spread in the heart?

A
  • Pacemaker cells in sinoatrial node generate an action potential - myocardium in origin but with a pacemaker function
  • Activity spreads over atria – atrial systole
  • Reaches the atrioventricular node and delayed for ~ 120 ms so artia contract before ventricles
  • From a-v node excitation spreads down septum between ventricles
  • Next spreads through ventricular myocardium from inner (endocardial) to outer (epicardial) surface through Purkinje fibres
  • Ventricle contracts from the apex up forcing blood through outflow valves
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13
Q

What are the 7 phases of the cardiac cycle

A

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

2 3 & 4 = SYSTOLE
5 6 7 & 1 = DIASTOLE

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14
Q

If the heart rate is increased, e.g in exercise, what happened to the length of the phases of the cardiac cycle?

A

Systole stays the same

Diastole shortens

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15
Q

What is the Wiggers diagram?

A

Graph of pressure against time for the cardiac cycle
Starts at atrial contraction by convention
One beat of heart is one cardiac cycle
Typically plotted for left side. The right side would be similar but at lower pressures

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16
Q

Describe phase 1: atrial contraction

A

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)

17
Q

Describe phase 2: isovolumetric contraction

A

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).

18
Q

Describe phase 3: rapid ejection

A

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
Blood continues to flow into the atria from their respective venous inputs

19
Q

Describe phase 4: reduced ejection

A

Repolarization of ventricle leads to a decline in tension and the rate of ejection begins to fall
Diastole
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

20
Q

Describe phase 5: isovolumetric relaxation

A

When intraventricular pressure falls below aortic pressure, there is a brief backflow of blood which causes the aortic valve to close
Diastole
“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
EDV
End systolic Volume (ESV) EDV-ESV = Stroke volume (Typically ~70-80ml)
Closure of the aortic and pulmonary valves results in the second heart sound (S2).
End of isovolumetric relaxation - ventricles lowest volume (40ml remaining after contraction) - ESV
EDV-ESV=volume of blood ejected from heart during 1 cardiac cycle = STROKE VOUME

21
Q

Describe phase 6: rapid filling

A

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

22
Q

Describe phase 7: reduced filling

A

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.
Initial rapid filling of ventricles - as they finish contracting, suck blood into ventriclesso rapid filling
Later stage slower - reduced filling phase -filled to about 90%

23
Q

What can result from abnormal valve function

A

STENOSIS - valve doesn’t open enough, obstruction to blood flow when valve normally open

REGURGITATION or incompetence or insufficiency - valve doesn’t close all the way, back leakage when valve should be closed

24
Q

What are the causes of aortic valve stenosis

A

• Degenerative (senile calcification/fibrosis)
• Congenital (bicuspid form of valve)
• Chronic rheumatic fever –inflammation- commissural fusion
Causes crescendo-decrescendo murmur

25
Q

What can result from aortic valve stenosis

A

Increase LV pressure -> LV hypertrophy
LEft sided heart failure -> Syncope or angina

Normally aortic valve when open should have an opening of 3-4cm^2
Stenotic valve <1cm^2
Less blood can get through valve

Some patients have a bicuspid aortic valve- can cause stenosis in later life
Rheumatic fever is caused by streptococcal infection - antibodies produced by body can have an autoimmune reaction with body - affects myocardium/valves of hear
Less bld can get through valves
Increases pressur ein LV
Hypertrophy
Ventricles have to do more work
Left sided heart failure
If brain is nt receiving uffient blood - syncope
If coronary arteries not supplying enough blood to heart - angina
Microangiopathic haemolytic anaemia - blood forced though small opening - sheer stress on blood cells themselves - lyse cells - damage to RBCs

26
Q

What are the causes and effects of aortic valve regurgitation?

A

Causes:
• Aortic root dilation (leaflets pulled apart)
• Vlavular damage (endocarditis rheumatic fever)
• Blood flows back into LV during diastole
• Increases stroke volume
• Systolic pressure increases
• Diastolic pressure decreases
• Bounding pulse (head bobbing, Quinke’s sign - nailed flood with colour in time with the heart)
• LV hypertrophy
Causes early decrescendo murmur

27
Q

What is mitral valve regurgitation?

A

• Chordae tendineae & papillary muscle
normally prevent prolapse in systole
• Myxomatous degeneration can weaken tissue leading to prolapse
• Other causes:
• Damage to papillary muscle after heart attack
• Left sided heart failure leads to LV dilation which can stretch valve
• Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation
• As some blood leaks back into LA, this increases preload as more blood enters LV in subsequent cycles/can cause LV hypertrophy

28
Q

What are the causes and effects of mitral valve stenosis?

A
  • Main cause = Rheumatic fever (99.9% cases)
  • Commissural fusion of valve leaflets
  • Harder for blood to flow LA to LV

Increased LA pressure

  • pulmonary oedema, dyspnea, pulmonary mypertension -> RV hypertrophy (as it has to do more work)
  • LA dilation
    - Atrial fibrillation -> thrombus formation
    - Oesophagus compression -> dysphasia