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CRS1 > The Heart (incl. ECG) > Flashcards

The Heart (incl. ECG) Flashcards

1
Q

What is the annulus fibrosus?

A

Disk of connective tissue separating atria from ventricles.

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2
Q

What are chordae tendineae? To which 2 structures do they attach?

A

The tendinous chords attached to the free ends of the AV valves at one end, and papillary muscles at the other.

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3
Q

How do the valves open and close?

A

Passively by hydrostatic pressure differences either side of the valve.

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4
Q

What are the papillary muscles and what is their function?

A

Small muscles protruding from the ventricular wall, which prevent the inversion of the AV valves into the atria.

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5
Q

What are intercalated discs and what is their function?

A

The end-to-end attachments between cardiomyocytes, containing numerous gap junctions to allow ions and small molecules to move between cells. Allows myocardium to act like a syncytium.

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6
Q

What are autorhythmic cardiomyocytes?

A

Cardiomyocytes which generate action potentials spontaneously, by undergoing slow depolarisation until the membrane potential reaches threshold level.

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7
Q

Where are autorhythmic cardiomyocytes concentrated?

A

Sinoatrial node (SAN) and throughout the ventricular conduction system.

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8
Q

Explain how contractile cardiomyocytes are stimulated, even though they are not innervated.

A

Depolarisation travels through the gap junctions of the intercalated discs from the autorhythmic cells along the whole myocardium.

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9
Q

Which components make up the ventricular conduction system?

A

The AV node, the Bundle of His and the purkinje fibres.

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10
Q

What is the Bundle of His? What is their function?

A

Group of autorhythmic cardiomyocytes that penetrate the annulus fibrosus and divide into the purkinje fibres.
They carry the wave of depolarisation from the AV node down to the purkinje fibres, to stimulate contraction of the ventricular myocardium.

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11
Q

What is the pacemaker potential?

A

The gradual depolarisation that occurs in autorhythmic cardiomyocytes. The action potential of these cells follows the pacemaker potential, once the threshold potential is reached.

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12
Q

In terms of ion movements, explain how the pacemaker potential, and subsequent action potential, is achieved in autorhythmic cardiomyocytes. (4 steps)

A

1) As the membrane is repolarised, sodium and potassium ‘funny’ channels open. Causing depolarisation.
2) As membrane depolarises, funny channels close and voltage-gated calcium ion channels open, causing an influx of calcium into the cell. Depolarisation continues.
3) As membrane potential approaches the threshold, a different type of voltage-gated calcium channel opens.. Leading to a very large depolarisation. Action potential occurs after threshold has been reached)
4) Action potential is then terminated in this cell by the opening of voltage-gated potassium channels, causing an outflow of potassium.

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13
Q

Which ion influences the action potentials of autorhythmic cardiomyocytes?

A

Ca2+. Sodium ions is involved in the pacemaker potential but not the action potential.

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14
Q

What are ‘funny channels’?

A

Voltage-gated sodium and potassium ion channels, that open when the membrane potential is very negative (more negative on inside).

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15
Q

How does the ANS affect heart rate?

A

It alters the depolarisation rate of autorhythmic cardiomyocytes.

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16
Q

What happens if the SAN is damaged?

A

Other autorhythmic cardiomyocytes will take over, such as those in the ventricular conduction system. The further from the SAN the AP is generated, the slower the heart rate will be.

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17
Q

What is the main difference in the action potential between skeletal muscle fibres and contractile cardiomyocytes?

A

Contractile cardiomyocytes remain depolarised for much longer. (They have a plateau phase)

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18
Q

Explain the 5 phases of the cardiac action potential (phase 0 - 4)

A

0) Very strong, brief depolarisation due to influx of Na+
1) Na+ channels close so membrane repolarises
2) Voltage-gated Ca2+ channels open, creating a plateau.
3) After the plateau repolarisation occurs due to opening of K+ channels (leading to an outflow of K+)
4) The reopened K+ channels maintain the resting potential until another AP reaches the cell.

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19
Q

What is calcium-induced calcium release?

A

Small amount of calcium entering cell from ECF is not sufficient to cause contraction alone, but it does cause the sarcoplasmic reticulum to release even more calcium.

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20
Q

How does epinephrine and norepinephrine increase contractility?

A

1) They bind to Beta-1 receptors on cardiomyocyte membrane,
2) which stimulates adenyl cyclase to activate cAMP.
3) cAMP then causes phosphorylation of calcium ion channels, prolonging their opening so more calcium is present for contraction.

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21
Q

Where do the calcium ions go after the AP has terminated?

A

90% to sarcoplasmic reticulum, 10% to ECF.

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22
Q

What are cardiac glycosides, such as digoxin, are used for? Explain how they work.

A

They slow calcium ion removal from the cell cytosol

So are used to treat heart failure since they increase contractility.

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23
Q

What does the Q wave represent in the ECG? Why is it a negative deflection?

A

Depolarisation of the septum. Negative because direction of depolarisation is left to right.

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24
Q

What does the S wave represent in an ECG?

A

The base of the left ventricle depolarising. (The base is closest to the annulus fibrosus, opposite to the apex.)

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25
Q

Is it normal to have a negative T wave?

A

Yes - can be positive or negative in domestic animals and be completely normal.

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26
Q

What effect would pronounced right-sided hypertrophy have on an ECG?

A

Negative QRS complex.

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27
Q

What may cause right-sided hypertrophy?

A

Stenotic (narrowed) pulmonary valve - so the right side must work harder to eject blood.

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28
Q

What could cause A) increased aplitude of the QRS complex, and B) decreased?

A

A) Enlargement of one or both ventricles

B) Fluid build-up in pericardial cavity

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29
Q

What could cause increased duration of the QRS complex?

A

Slowing of transmission across ventricles, by damage to purkinje fibres for example. Or ventricular hypertrophy/dilation (APs have further to propagate)

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30
Q

What is 1st degree heart block and how is it caused?

Also what is 2nd and 3rd?

A

1) Elongation of the PQ interval. Caused by reduction in conduction speed of the AVN. (HUSBAND IS LATE)
2) Where not all P waves initiate a QRS complex, due to impaired conduction. (HUSBAND DOESN’T COME BACK EVERY NIGHT)
3) No communication between atria and ventricles, so P waves and QRS complexes seem unrelated. (HUSBAND AND WIFE NOT TALKING ANYMORE)

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31
Q

Why do QRS complexes appear wide and bizarre in 3rd degree heart block?

A

Because the APs are not originating from the SAN, so don’t follow the exact conduction system.

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32
Q

What is respiratory sinus arrhythmia?

A

Heart rate is higher during inspiration. This is perfectly normal in dogs.

33
Q

What is paroxysmal tachycardia? What are the two types? And why are they so serious?

A

When a portion of the heart becomes more excitable than the SAN.
You get supraventricular (atrial) and ventricular
Serious because often caused by a lack of oxygen to that area, and go on to cause fibrillation.

34
Q

What is atrial flutter?

A

Frequent but rhythmical atrial contractions.

35
Q

What is fibrillation? How is it caused? What is the prognosis?

A

Depolarisation in a rapid, irregular and uncoordinated manner. Caused by myocardial infarction. Very often life-threatening if ventricular, less so if atrial.

36
Q

Why is atrial fibrillation less serious?

A

Because atria do not need to contract for the pumping function of the heart to work correctly - ventricles fill passively.

37
Q

What happens in the first third of diastole? And the second?

A

1st) Blood accumulated in atria fills ventricles

2nd) Blood flows directly from vena cavae into ventricles.

38
Q

At which point of diastole do the atria contract? What effect does this have?

A

The final third. This contributes to 20-30% of ventricular filling.

39
Q

Why does the pressure decrease in the arteries during diastole?

A

Because the SL valves are closed (pressure is higher in the arteries than the heart chambers), and blood is flowing away into circulation. So they are losing blood without gaining any.

40
Q

At what point of the ECG does systole begin?

A

After the Q wave.

41
Q

What is isovolumetric contraction?

A

The point when all of the valves are closed, hence volume remains the same but pressure is rising.

42
Q

What causes heart murmurs? List 3 things.

A

When blood leaks back through a leaky valve, or when blood is forced through a stetonic (narrow) valve. Or other causes, such as blood flowing through septal defects.

43
Q

What disease is common in CKCS (Cavvies)?

A

Autoimmune inflammation of the mitral valve.

44
Q

Why is inflammation of the valves degenerative?

A

They become thicker and adhere, sometimes permanently. This leads to backflow of blood, which may cause oedema. (Pulmonary if left side, systemic if right side)

45
Q

Why does blood continue to flow through the arteries during diastole?

A

As the arteries are filled, their elastic walls expand. And when blood stops coming through, they contract again and push the blood through them.

46
Q

What is a phonocardiogram? (PCG)

A

A chart or record of the sounds made by the heart

47
Q

What causes the 4 heart sounds?

A

1) Closure of the AV valves
2) Closure of the SL valves
3) Occurs when blood hits against the wall of the almost empty ventricle after isovolumetric relaxation.
4) Due to jet of bloodflow into ventricles due to atrial contraction.

(Both 3 and 4 are due to ventricular filling, but 3 is in the first third of systole and 4 is in the last.)

48
Q

What is the moderator band? And what is its other name?

A

Muscular band in right atrium from septum to outer wall. Aka trabecula septomarginalis.

49
Q

What is the Os Cordis

A

A bony structure in the annulus fibrosus of cattle and pigs. (Ossifies with age)

50
Q

What are the two types of heart failure?

A

Congenital (present at birth) and acquired

51
Q

Which type of heart failure is surgically correctable?

A

Congenital

52
Q

What is dilated cardiomyopathy (DCM), and which species is it most common in?

A

When the ventricle as a whole is enlarged and weakened. In dogs.

53
Q

What is restrictive cardiomyopathy, and which species is it most common in?

A

When ventricle becomes fibrous and stiff. In cats.

54
Q

What is hypetrophic cardiomyopathy, and which species is it most common in?

A

Heart is very thick walled with a very narrow lumen. Heart itself is the same size. Present in cats.

55
Q

What does the ingestion of wire often cause in cattle?

A

Pericarditis

56
Q

What compensatory mechanisms are in place when heart failure occurs? (3 things)

A

Sympathetic NS
Renin-angiotensis system (RAS)
Cardiac enlargement

57
Q

Name 3 ways in which the sympathetic nervous system affects blood pressure, and state which receptors are acted upon for each.

A

1) Cause vasoconstriction - Alpha-1
2) Increases heart rate - Beta-1
3) Cause kidneys to release renin (for RAS) - Beta-2

58
Q

What is meant by the terms A)inotropic and B)chronotropic?

A

A) Increases contractility

B) Increases heart rate

59
Q

Outline the renin-angiotensin system

A

1) Kidneys are stimulated to release renin by the SNS
2) Renin converts angiotensin to angiotensin I
3) Angiotensin I is then converted to angiotensin II by ACE (angiotensin-converting enzyme), which is found in the lungs.
4) Angiotensin II is a very potent vasoconstrictor

60
Q

Why is the increase of heart rate and contractility an inappropriate response to heart failure in the long-term?

A

The already damaged heart now has to work even harder.

61
Q

Why is vasoconstriction an inappropriate response to heart failure in the long-term?

A

There is an increase in afterload so cardiac output falls even further, the valves leak more and so once again the heart has to work even harder despite being already damaged

62
Q

Why is the retention of salt and water an inappropriate response to heart failure in the long-term?

A

Venous return increases, and so does the pressure in the capillaries. So oedema occurs.

63
Q

Why is cardiac enlargement an inappropriate response to heart failure in the long-term?

A

Oxygen demand is increased, some cells die and scar tissue develops further decreasing contractility.

64
Q

Where would you expect oedema to develop with A) left and B) right sided heart failure?

A

A) Pulmonary oedema

B) Systemic oedema, usually in pleural space or abdomen.

65
Q

What is eccentric hypertrophy?

What is concentric hypertrophy?

A

Eccentric - new sarcomeres are added in-series with existing ones, so ventricles dilate without narrowing lumen. I.e. thickness increases in proportion to the increase in chamber size, so heart becomes very large.

Concentric - Wall thickens while chamber radius does not change, so heart stays the same size and lumen becomes very small. Heart stays the same size. (Think concentric = constrict? Maybe? lol?)

66
Q

Describe class I, class II and class III heart failure. What is the prognosis for each?

A

I is no clinical signs, with small signs of compensation.
II is a mild exercise intolerance and clinical signs showing when exercising.
III is obvious clinical signs even when at rest.
They all progress to the next one, until death. Animal will not get better.

67
Q

Why is digoxin used to treat cardiomyopathies? (explain pharmacological process) What type of drug is digoxin?

A

Because it binds to calcium channels in the sarcolemma, increasing the influx the calcium influx into the muscle fibre.

It is a cardiac glycoside.

68
Q

what does a positive lusitrope do and what types of cardiomyopathies are they used for and why? Give 2 examples of positive lusitropes.

A

Relaxes myocardium. Used to treat hypertrophic/restrictive cardiomyopathies (cats), because the lumen is very narrow so the drugs relax the muscle to widen it a bit.

Examples are calcium channel blockers and beta blockers (blocks SNS from increasing contractility)

69
Q

From which germ layer does the heart develop?

A

Mesoderm.

70
Q

What are the 5 chambers of the primitive heart tube?

A

Truncus arteriosus, Bulbus cordis, Ventricle, Atrium and Sinus venosus. (Tigers are big cats and vultures are silly vaginas) …….

71
Q

What is the A) Vitelline and B) Cardinal circulation?

A

A) Blood flow from embryo to yolk sac and back again.

B) Veins of the foetal body.

72
Q

When the heart tube folds which way does it fall? What is the condition where it falls in the opposite direction?

A

Falls to the right. Dextrocardia is formed, which causes exercise intolerance.

73
Q

What do the two horns of the sinus venosus (left and right) go on to form in the adult heart?

A

Right becomes incorporated into atrial wall and left becomes coronary sinus.

74
Q

Describe the flow of blood in a fish’s cardiovascular system. (e.g. for mammals: Heart -> Lungs -> Heart -> Body -> Heart)

A

Heart -> Gills -> Body -> Heart

75
Q

Define cardiac output. And give its equation.

A

Amount of blood pumped in 1 minute. (stroke volume * Heart rate)

76
Q

Define preload

A

End diastolic volume (vol of blood in heart after diastole)

77
Q

Outline the respiratory pump for venous return.

A

As diaphragm moves caudally, thoracic pressure increases while abdominal pressure decreases. So blood moves down the pressure gradient, towards the heart. (increasing preload)

78
Q

Define afterlaod

A

The resistance against which the ventricle pumps blood.

CRS1 (6 decks)

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