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Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

What is the equation for MABP?

A

((2 x diastolic pressure) + systolic pressure)/3

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2
Q

What is a different equation for MABP?

A

diastolic pressure + 1/3 (systolic - diastolic)

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3
Q

What is the normal range of MABP?

A

70-105 mmHg

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4
Q

What is the minimum MABP required for perfusion of coronary arteries, brain and kidneys?

A

60 mmHg

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5
Q

What effect does sympathetic stimulation have on the arterioles and veins?

A

Vasoconstriction

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6
Q

Which system controls the short term regulation of mean arterial blood pressure?

A

The baroreceptor reflex

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7
Q

Where are the baroreceptors?

A

Aortic arch

Carotid sinus

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8
Q

Which nerves do the baroreceptor signals travel in to reach the brain and where in the brain do they go?

A

CN IX and CN X

Medulla

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9
Q

How do the baroreceptors respond to a decrease in blood pressure?

A

Decrease firing from baroreceptors
Decrease vagal activity, so sympathetic activity increases
Heart rate and stroke volume increase ergo cardiac output increases
Vasocontriction occurs, so TPR increases
Venoconstriction occurs, so venous return increases and SV increases

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10
Q

How do the baroreceptors respond to an increase in blood pressure?

A 
Increase firing from baroreceptors
Increase vagal activity
HR decreases, SV decreases, CO decreases
Vasodilatation occurs, so TPR decreases
Venodilatation occurs, so venous return decreases and SV decreases
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11
Q

Which receptor regulates the contraction of vascular smooth muscle?

A

L-type Ca2+ channels

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12
Q

What molecule does the calcium-calmodulin compound activate?

A

Myosin light chain kinase

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13
Q

What does myosin light chain kinase do that allows contraction?

A

Phosphorylates, and thus activates, myosin light chain

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14
Q

What effect does phosphorylation of MLCK have on it?

A

Inactivates it

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15
Q

Which enzyme dephosphorylates phosphorylated MLC?

A

Myosin-LC-phosphatase

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16
Q

What molecule activates myosin-LC-phosphatase and this stimulates relaxation?

A

cGMP

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17
Q

Where are the electrical signals of the heart generated?

A

Within the heart itself - pacemaker cells of the sinal atrial node

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18
Q

Where is the SA node located?

A

In the upper right atrium close to where the SVC enters the right atrium

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19
Q

What is the term given to the state where the heart is controlled by the sinal atrial node?

A

Sinus rhythm

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20
Q

What is the pacemaker potential?

A

The potential that must be taken to threshold potential to generate an action potential in the SA node

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21
Q

What generates the pacemaker potential?

A

It is slow depolarisation caused by a decrease in potassium efflux and a slow sodium influx

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22
Q

What is the “funny current”?

A

The slow sodium influx of the pacemaker potential

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23
Q

What causes the rising phase of the action potential?

A

Activation of voltage gated Ca2+ channels

Rapid influx of Ca2+

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24
Q

What is the falling phase of the action potential caused by?

A

Potassium efflux

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25
Q

Which junctions spread electrical excitation from cell to cell?

A

Gap junctions

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26
Q

Where is the AV node located?

A

At the base of the right atrium, just above the junction between atria and ventricles

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27
Q

What is the only point of electrical contact between atria and ventricles?

A

AV node

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28
Q

What structures allow the spread of the action potential to the ventricles?

A

The bundle of His

Perkinje fibres

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29
Q

What is the resting potential of the ventricular muscle cell?

A

-90mV

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30
Q

What is the rising phase of the ventricular muscle action potential caused by?

A

Fast sodium influx

This is phase 0

31
Q

What is phase 1 of the ventricular muscle action potential caused by?

A

Closure of Na+ channels

K+ efflux

32
Q

What is phase 2 or the “plateau” phase of the ventricular muscle action potential caused by?

A

Ca2+ influx

33
Q

What is phase 3 of the ventricular muscle action potential caused by?

A

Closure of Ca2+ channels

K+ efflux

34
Q

What is phase 4 of the ventricular muscle action potential?

A

Resting membrane potential

35
Q

What autonomic influence dominates control of the heart under normal resting conditions?

A

Vagal tone

36
Q

What effect does vagal stimulation have on the slope of the pacemaker potential?

A

Decreases the slope of the pacemaker potential - takes longer to reach threshold

37
Q

What is the p wave of the ECG?

A

Atrial depolarisation

38
Q

What is the QRS complex of the ECG?

A

Ventricular depolarisation masking atrial repolarisation

39
Q

What is the T wave of the ECG?

A

Ventricular repolarisation

40
Q

What is the PR interval of the ECG?

A

AV node delay

41
Q

Whatt is the ST segment of the ECG?

A

Ventricular systole

42
Q

What is the TP interval of the ECG?

A

Diastole

43
Q

How is cardiac muscle described?

A

Striated

44
Q

What causes the striation of the cardiac muscle?

A

Regular arrangement of contractile protein

45
Q

What do desmosomes do?

A

Provide mechanical adhesion between cells

46
Q

What are myofibrils?

A

The contractile units of muscle - each muscle fibre contains many myofibrils

47
Q

What is the name given to the thin protein filaments that cause the lighter appearance in myofibrils and fibres?

A

Actin

48
Q

What is the name given to the thick protein filaments that cause the darker appearance in myofibrils and fibres?

A

Myosin

49
Q

How is cardiac muscle tension produced?

A

Actin sliding on myosin

50
Q

What does force generation in the heart depend upon?

A

ATP-dependant interaction between myosin and actin filaments

51
Q

What covers the binding sites on the actin filaments?

A

Tropomyosin

52
Q

What controls the movement of the tropomyosin from the actin binding sites to allow cross bridge formation?

A

Troponin - calcium binding causes troponin to move the tropomyosin away from the sites

53
Q

Where is calcium stored within muscle cells?

A

Sarcoplasmic reticulum

54
Q

What is the release of Ca2+ from the sarcoplasmic reticulum in cardiac cells dependant on?

A

Extracellular Ca2+

55
Q

When in the ventricular muscle action potential does release of Ca2+ from sarcoplasmic reticulum occur?

A

Phase 2 - influx of Ca2+ released more Ca2+ from SR which activates contraction and generates systole

56
Q

What is the refractory period?

A

A period following an action potential in which it is not possible to generate another action potential

57
Q

What state are the sodium channels in during the plateau phase of the action potential and how does this contribute to the refractory period?

A

The Na+ channels are closed, which is important for the refractory period to occur as phase 0 of the action potential is caused by Na+ opening and fast sodium influx
Ergo, with the Na+ channels closed, the action potential cannot be triggered

58
Q

What state are the potassium channels in during the descending phase of the ventricular muscle action potential and how does this contribute to the refractory period?

A

The K+ channels are open - the membrane cannot be depolarised

59
Q

What is the stroke volume?

A

The volume of blood ejected by each ventricle per heart beat

60
Q

How can the SV be calculated?

A

End diastolic volume - end systolic volume

61
Q

What is the diastolic length of the myocardial fibres determines by?

A

The volume of blood within each ventricle at the end of diastole - i.e. end diastolic volume
The myofibres stretch to accommodate the volume of blood

62
Q

What determines the cardiac preload?

A

End diastolic volume

63
Q

What is the end diastolic volume determined by?

A

The venous return to the heart

64
Q

What does the Frank-Starling mechanism describe?

A

The relationship between venous return, end diastolic volume and stroke volume

65
Q

What does Starling’s law of the heart state?

A

The greater the end diastolic volume, the greater the stroke volume

66
Q

What is the afterload?

A

The resistance into which the heart is pumping

67
Q

How does the Frank-Starling mechanism partially compensate for decreased stroke volume caused by increased afterload?

A

When there is increased afterload, the heart is unable to eject the full stroke volume - this results in increased EDV
The force of contraction increases by the Frank-Starling mechanism to eject full SV

68
Q

Why does ventricular hypertrophy occur in untreated hypertension?

A

The force of contraction rises by the Frank-Starling mechanism to overcome the increased afterload
The heart is doing more work than it can cope with

69
Q

Where is the main site of TPR?

A

Arterioles

70
Q

What is the vasomotor tone?

A

The vascular smooth muscles are partially constricted at rest

71
Q

What causes the vasomotor tone?

A

The tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline

72
Q

What effect does antidiuretic hormone/vasopressin have on vascular smooth muscle?

A

Causes vasoconstriction

73
Q

What role does the intrinsic control of vascular smooth muscles play in metabolism?

A

The control mechanisms match the blood flow of different tissues to their metabolic needs

74
Q

What factors result in vasodilatation?

A 
Decreased local PO2
Increased local PCO2
Increased local H+
Increased extra-cellular K+
Release of: histamine, prostaglandins, bradykinin, NO

Cardiology (15 decks)

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