Cardiac Cycle Flashcards

1
Q

Where is the sa node located and what is its role

A

Group of cells Found in the walls of the right atrium
Spontaneously produce action potential that travels through the heart via electrical conduction system
Sets rhythm of heart

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2
Q

Role of the av node

A

Electrically connects right atrium and right ventricle delaying impulses so atria have enough time to eject their blood into ventricles before ventricular contraction

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3
Q

Hyperpolarisation

A

Membrane repolarises below threshold, it is unstable

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4
Q

Phases of atrial and ventricular muscle action potentials

A

0-voltage gated sodium channels open , na influx , voltage gated ca channels open slowly
1- sodium channels close , cells begin to repolarise
2-calcium voltage gated channels fully open , calcium influx halts repolarisation, voltage gated potassium channels start to open
3-calcium ion channels close and potassium ion channels open fully, potassium ion efflux
4-stable na/k pump , 3na out 2k in

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5
Q

Electrical conduction of heart stages

A

1-electrical activity generated in SA node spreads out via gap junctions in to atria
2- av node conduction is delayed so there is a correct filling of ventricles
3- conduction occurs through bundle of His into ventricules
4-conduction through purkinje fibres , spreads quickly throughout ventricles

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6
Q

What happens at the p wave

A

Atrial depolarisation and contraction

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7
Q

What happens at the PR segment

A

Av nodal delay

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8
Q

What happens at the QRS complex

A

Ventricular depolarisation contraction, atria are repolarising simultaneously

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9
Q

What happens at the ST segment

A

Ventricles contracting and emptying

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10
Q

T wave

A

Ventricular repolarisation

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11
Q

What happens at the TP interval

A

Ventricles relaxing and filling

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12
Q

What creates pressure changes in the heart chambers

A

Electrical activity is converted into myocardial contractions

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13
Q

What is cardiac diastole

A

Relaxation of heart muscles
Blood returns to the heart and fill the chambers
Low pressure in ventricles, mitral and tricuspid valves open and ventricles fill with blood

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14
Q

Atrial systole

A

Ventricles are in diastole at low pressure
Atrial contraction causes blood to move into relaxed ventricles,
Mitral and tricupsid valve close

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15
Q

Ventricular systole

A

Atrial diastole
Period if isovolumetric contraction
Pressure rises sufficiently, forces open aortic and pulmonary valves
Blood pushed out of ventricles

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16
Q

Left ventricular pressure changes

A

-contraction of left atrium pushes blood into ventricle, pressure of ventricle rises
-mitral valve close
-pressure rises in isovolumetric contraction
-ventricular pressure highe than aortic , aortic valve pushed open blood is ejected from ventricle
-when ventricular pressure is less than aortic , aortic valve close
-isovolumetric relaxation

17
Q

When does isovolumetric contraction occur

A

Ventricular systole

18
Q

Ventricular pressure volume loop

A

-ventricule relaxed , pressure low , volume increased
- mitral valve closes ,ventricles contract , pressure increases
-pressure high enough to force aortic valve to open and blood leaves ventricle
- as ventricle empties ,aortic valve closes so pressure deals

19
Q

What creates the lub sound

A

Close of mitral valve at beginning of ventricular diastole

20
Q

What creates the dub sound

A

Close of aortic valve at end of ventricular systole

21
Q

What causes occasional sound

A

Turbulent blood flow into ventricles

22
Q

Cardiac output

A

CO=HR x SV
Amount of blood ejected from heart per volume

23
Q

What is preload

A

Stretching of heart at rest , increases stroke volume due to starlings law
More blood in = ,more blood out

24
Q

After load

A

Opposes ejection reduces stroke volume due to Laplace law
Opposes contraction that ejects blood from the heart, stress through wall of heart prevents muscle contraction

25
Q

Equation for wall stress

A

Stress = tension / wall thickness

26
Q

How is afterload increased

A

Increasing pressure and radius

27
Q

Why does radius affect wall stress/afterload

A

Small ventricle radius has more wall stress directed to the centre of the chamber so less afterload and better ejection

Large ventricle radius will have less wall stress directed to the centre of the chamber so more afterload and less ejection

28
Q

Acute rises in blood pressure offset by ?

A

-starling law - increased stretch give increases contraction and increased stroke volume
Local positive inotropes eg noradrenaline
Baroreflex - decreased sympathetic tone which decreases blood pressure

29
Q

What causes volume overload

A

The heart doesn’t contract properly, so blood is left in the ventricle

30
Q

Increased pressure or radius leads to

A

Increase in wall stress which opposes ejection

31
Q

How does the heart compensate for wall stress ?

A

Ventricular hypertrophy, greater myocyte size and more sarcomeres , thus increases wall thickness , which decreases wall stress

32
Q

What is the downside of ventricular hypertrophy

A

It requires more energy as more sarcomeres are used so also a greater oxygen, eventually contractility will decrease and produce more heart failure

33
Q

What happens during exercise

A
  • increased venous return , which leads to increased preload and higher EDV
  • the ventricle while eject blood to the same ESV so there is an increase in stroke volume
34
Q

What happens during hypertension

A

Longer time spend in isovolumetric contraction to increase pressure in chamber above that I’m aorta to open the valve
-more energy used and lowers force of contraction which reduces stroke volume and increased esv