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MRCEM Physiology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

The atria are separated from the ventricles by a band of fibrous connective tissue called what?

A

The annulus fibrosus

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2
Q

Blood flows from the right atria to the right ventricle through which valve?

A

Tricuspid valve

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3
Q

Blood flows from the left atria to the left ventricle through which valve?

A

Mitral valve

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4
Q

The walls of the heart are formed mainly of what?

A

Myocardium

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5
Q

What is the name of the inner surface of the heart, which provides an anti-thrombogenic surface?

A

Endocardium

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6
Q

What is the name of the outer surface of the heart?

A

Epicardium

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7
Q

What is the name of the thin fibrous health that the heart is enclosed in?

A

Pericardium

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8
Q

What is the average stroke volume of the heart at rest?

A

About 70ml/beat

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9
Q

What is the definition and formula for cardiac output?

A

The volume of blood pumped out of the heart via the aorta per minute.
Cardiac output = stroke volume x heart rate
Usually around 5L/minute are rest in humans

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10
Q

What is the term for the difference between systolic and diastolic blood pressure?

A

Pulse pressure

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11
Q

What is the formula for mean arterial pressure (MAP)?

A

MAP = DP + 1/3(SP-DP)

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12
Q

What is the MAP at the start of the arterioles?

A

About 65mmHg

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13
Q

What is MAP on the arterial side of capillaries?

A

About 25mmHg

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14
Q

What is the MAP on the venous side of capillaries?

A

About 15mmHg

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15
Q

What is the MAP in the vena cava at the level of the heart (central venous pressure)?

A

Usually close to 0mmHg

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16
Q

What effect does sympathetic stimulation have on the heart?

A

Increases cardiac output by increasing heart rate, contractility and CVP. Increased blood pressure by increasing total peripheral resistance (TPR) and cardiac output.

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17
Q

What effect does parasympathetic stimulation have on the heart?

A

Marked decrease in heart rate (negative chronotropic effect) but only a slight decrease in heart muscle contractility (negative inotropic effect) as parasympathetic ventricular innervation is sparse.

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18
Q

Mean Arterial Pressure (MAP) = Cardiac output (CO) x what?

A

Total peripheral resistance (TPR)

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19
Q

What 2 places are arterial baroreceptors located and which nerves travel from them to the medulla where the activity of the autonomic nervous system is coordinated?

A

Carotid sinus - afferent nerves travelling via the glossopharyngeal nerve.
Aortic arch - afferent nerves travelling via the vagus nerve.

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20
Q

A decrease in MAP, such as in postural hypotension and haemorrhage has what effect on baroreceptor firing, in order to increase MAP?

A

Decreases baroreceptor firing to cause increase in heart rate, cardiac contractility and central venous pressure (CVP)

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21
Q

How is the Frank-Starling curve affected by preload?

A

Increase in preload causes a rightwards shift along the curve and a decrease in preload causes a leftward shift along the curve

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22
Q

How is the Frank-Starling curve affected by contractility?

A

Increases in contractility shifts the curve upwards and to the left. Decreases in contractility shifts the curve downwards and to the right.

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23
Q

How is the Frank-Starling curve affected by afterload?

A

Increase in afterload shifts the curve downward and to the right and a decrease in afterload shifts the curve upwards and to the left.

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24
Q

Cardiac muscle contracts when which intracellular ion rises?

A

Ca2+ (>100nmol/L)

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25
Q

In relaxation of cardiac muscle, about 80% of Ca2+ is rapidly pumped back into the sarcoplasmic reticulum by Ca2+ ATPase pumps. The Ca2+ that entered the cell during the action potential is transported out of the cell primarily by the Na+/Ca2+ exchanger in the membrane which pumps one Ca2+ ion out in exchange for what?

A

3 Na+ ions in, using the Na+ electrochemical gradient as an energy source

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26
Q

What is the Treppe effect?

A

The muscle tension increases in a graded manner that to some looks like a set of stairs. This tension increase is called trip, a condition where muscle contractions become more efficient.

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27
Q

In cardiac muscle, the intercalated discs provide structural attachments between myocytes to distribute force, known as what?

A

Desmosomes

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28
Q

Regarding conduction of the heart, the heartbeat is initiated by what?

A

Spontaneous depolarisation of the sinoatrial node (SAN), a region of specialised myocytes in the right atrium

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29
Q

The wave of depolarisation from then sinoatrial node is prevented from reaching the ventricles directly by what?

A

Annulus fibrosus

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30
Q

Where is the atrioventricular node (AVN) located?

A

Between the right atrium and right ventricle, near the atrial septum.

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31
Q

The sinoatrial node is the primary pacemaker of the heart and will normally discharge at a rate of 60-100bpm. What is the secondary pacemaker of the heart and how often does it discharge?

A

Atrioventricular node. Discharges at about 40-60bpm.

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32
Q

If the sinoatrial node and atrioventricular node both fail to function, what other structures may become the pacemaker and how often do they discharge?

A

The left and right bundle of His and the Purkinje fibres produce a spontaneous action potential at a rate of 20-40bpm.

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33
Q

What is the resting potential of the sinoatrial node (SAN)?

A

About -60mV

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34
Q

What is the threshold potential when an action potential is initiated in the sinoatrial node?

A

About -40mV

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35
Q

The upstroke of the sinoatrial node action potential is slow as it is not due to the activation of fast Na+ channels like cardiac myocytes, but instead what type of channels?

A

Slow L-type Ca2+ channels

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36
Q

Name 2 chronotropic agents and the effect they have on the action potential of the sinoatrial node (SAN)?

A

Noradrenaline (sympathetic neurotransmitter) is a positive chronotrope and causes a faster rate of decay and thus heart rate.
Acetylcholine (parasympathetic neurotransmitter) is a negative chronotrope and lengthens the time to reach threshold and decreases heart rate

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37
Q

What are inotropes?

A

Factors that affect intracellular Ca2+ and hence cardiac contractility

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38
Q

Noradrenaline is a positive inotrope, how does it work?

A

It binds to β1-adrenoceptors on the membrane and causes increased Ca2+ entry via L-type channels during the action potential and thus increases Ca2+ release.

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39
Q

Cardiac glycosides (e.g. digoxin) act as a positive inotrope, negative chronotrope, how does it work?

A

Slows the removal of Ca2+ from the cell by inhibiting the membrane Na+ pump which generates the Na+ gradient required for driving the export of Ca2+; consequently the removal of Ca2+ from the myocyte is slowed and more Ca2+ is available inside the myocyte for the next contraction.

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40
Q

What is the main reason acidosis is negatively inotropic?

A

Largely because H+ competes for Ca2+ binding sites

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41
Q

Atrial depolarisation causes what on an ECG?

A

P wave (initiation of atrial contraction)

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42
Q

True or false: Most ventricular filling occurs during atrial contraction

A

False - atrial contractions only contributes around 15-20% of the final ventricular volume as most occurs passively in diastole due to venous pressure

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43
Q

End-diastolic volume (EDV) is usually around what?

A

120-140ml

44
Q

What causes the QRS complex on an ECG?

A

Ventricular depolarisation

45
Q

What cause the T wave on an ECG?

A

Ventricular repolarisation

46
Q

In the cardiac cycle, what causes the first heart sound?

A

Caused by closure of the AV (mitral and tricuspid) valves at the start of systole

47
Q

In the cardiac cycle, what causes the second heart sound?

A

Closure of the semilunar (aortic and pulmonary) valves

48
Q

In the cardiac cycle, what causes the third heart sound?

A

Rapid flow of blood from the atria into the ventricles during the ventricular filling phase during early diastole. This is normal in children, but in adults is associated with disease such as ventricular dilation.

49
Q

In the cardiac cycle, what causes the fourth heart sound?

A

Filling of an abnormally stiff ventricle in atrial systole, during late diastole

50
Q

What happens during the a wave in the JVP waveform during cardiac cycle?

A

Occurs due to the right atrial contraction during atrial systole (end diastole)

51
Q

What happens during the c wave in the JVP waveform during cardiac cycle?

A

Occurs due to the bulging of the tricuspid valve into the right atrium during right isovolumetric ventricular contraction - during isovolumetric contraction (early systole)

52
Q

What happens during the x descent in the JVP waveform during cardiac cycle?

A

Occurs due to a combination of right atrial relaxation, the downward displacement of the tricuspid valve during right ventricular contraction, and the ejection of blood from both the ventricles - during rapid ventricular ejection (mid systole)

53
Q

What happens during the v wave in the JVP waveform during cardiac cycle?

A

Occurs due to right atrial filling from venous return - ventricular ejection and isovolumetric relaxation (late systole)

54
Q

What happens during the y descent in the JVP waveform during cardiac cycle?

A

Occurs due to opening of the tricuspid valve and the subsequent rapid inflow of blood from the right atrium to the right ventricle - during ventricular filling (early diastole)

55
Q

What is the resting potential of ventricular myocytes?

A

About -90mV

56
Q

What is the threshold potential of a myocyte for an action potential to be initiated?

A

About -65mV

57
Q

In ventricular myocytes, when fast voltage-gated Na+ channels are activated, a Na+ influx depolarises the membrane rapidly to what?

A

About +30mV

58
Q

In ventricular myocyte action potential, what causes the plateau phase?

A

The initial depolarisation activates voltage-gated Ca2+ channels (slow L-type channels, threshold approximately -45mV) through which Ca2+ floods into the cell. The resulting influx od Ca2+ prevents the cell from depolarisation and causes a plateau phase for around 250ms until the L-type channels inactivate.

59
Q

In ventricular myocyte action potential, what causes depolarisation?

A

Activation of voltage-gated K+ rectifier channels and a K+ efflux.

60
Q

What is different about atrial myocyte action potentials compared to ventricular myocyte?

A

More triangular action potential (less plateau)

61
Q

What is different about Purkinje fibres action potentials compared to ventricular myocyte?

A

Spike at the peak of the upstroke reflecting a larger Na+ current that contributes to their fast conduction velocity.

62
Q

What percentage of the total blood volume do veins contain at any one time?

A

About 70%

63
Q

Most vasoconstrictors bind to what, which mediate elevation in intracellular Ca2+ leading to vascular smooth muscle contraction?

A

G-protein coupled receptors

64
Q

Name 4 vasoconstricting agents?

A

Endothelin-1
Thromboxane A2
Angiotensin II
Noradrenaline (alpha 1-receptors)

65
Q

Most types of vascular smooth muscle do not generate action potential, so how is entry of Ca2+ vacillated?

A

Depolarisation is graded, allowing graded entry of Ca2+

66
Q

How do most endogenous vasodilators work?

A

Cause relaxation by increasing cyclic guanosine monophosphate (cGMP) (e.g. nitric oxide) or cyclic adenosine monophosphate (cAMP) (e.g. prostacyclin, beta-adrenergic receptor agonists) which activate protein kinase causing substrate level phosphorylation.

67
Q

Name 4 vasodilating agents?

A

Nitric oxide
Prostacyclin
Beta-agonists
Calcium-channel blockers

68
Q

How are Prostacyclin (PGI2) and thromboxane A2 (TXA2) synthesised?

A

Synthesised by the cyclooxyrgenase pathway from arachidonic acid, which is made from membrane phospholipids by phospholipase A2

69
Q

In addition to central control of blood pressure, tissues can regular their own blood flow to match their requirements via which 3 mechanisms?

A

Autoregulation
Metabolic factors
Local hormones (autocoids)

70
Q

Autoregulation is the ability to maintain a constant blood flow despite variations in blood pressure. What range of blood pressure can it do this in?

A

50-170mmHg

71
Q

What are the 2 main methods contributing to autoregulation local control of blood flow?

A
  1. Myogenic mechanism - arterial contractions in response to stretching of the vessel wall, probably due to activation of smooth muscle stretch-activating Ca2+ channels. Reduction in pressure and stretch closes these channels causing vasodilatation.
  2. Locally produced vasodilating factors
72
Q

How does potassium contribute to metabolic hyperaemia (increased blood flow)?

A
  1. K+, released from active tissues in ischaemia, causes vasodilation partly by stimulation the Na+ pump, thus increasing Ca2+ removal from the smooth muscle cells and hyper polarising the cell.
73
Q

Along with potassium what other 3 important factors contribute to metabolic hyperaemia (increased blood flow) and how do they work?

A
  1. CO2 and acidosis cause vasodilation largely through increased nitric oxide production and inhibition of smooth muscle Ca2+ entry.
  2. Adenosine, released from the heart, skeletal muscle and brain during increased metabolism and hypoxia, causes vasodilation by stimulating the production of cAMP in smooth muscles.
  3. Hypoxia - may reduce ATP sufficiently for K+ channels to activate causing hyperpolarisation
74
Q

In local control of blood flow, autocoids are mostly important under certain circumstances. Name 2 examples?

A
  1. In inflammation, local inflammatory mediators such as histamine and bradykinin cause vasodilation and increased permeability of exchange vessels, leading to swelling but allowing access by immune cells to damaged tissues.
  2. In clotting, serotonin and thromboxane A2 released from activated platelets cause vasoconstriction to help reduce bleeding.
75
Q

In lymph nodes, bacteria and other foreign materials are removed by what/

A

Phagocytes

76
Q

In the lymphatic system, fluid which is not reabsorbed by capillaries returns via efferent lymphatics and the thoracic duct into which vein?

A

Subclavian veins

77
Q

The capillary wall is very permeable to water. Regarding osmotic pressure and hydrostatic pressure, how does water tend to flow?

A

Osmotic pressure - from low to high
Hydrostatic pressure - from high to low

78
Q

What is Starling’s equation with regards to the net flow of water?

A

(Pc-Pi) - (πp-πi) where (Pc-Pi) is the difference in hydrostatic pressure between the capillary and interstitial space and (πp-πi) is the difference in osmotic pressure between plasma and interstitial fluid.

79
Q

What does a positive value of Starling’s equation mean?

A

There is a net fluid movement out of the cell (filtration).

80
Q

What does a negative value of Starling’s equation mean?

A

There is a net fluid movement into the capillary (absorption).

81
Q

The osmotic force across the capillary wall is largely determined by the concentration of what in the blood?

A

Protein

82
Q

What does the normal capillary hydrostatic pressure typically vary between?

A

35mmHg at the arteriolar end to about 15mmHg at the venous end.

83
Q

What is the interstitial hydrostatic pressure typically?

A

Normally close to 0mmHg (or is slightly negative)

84
Q

What is the total daily net filtration of fluid from the capillaries into the interstitial space?

A

8L

85
Q

The skeletal muscle circulation receives what percentage of cardiac output normally and also during exercise?

A

15-20% normally, may rise to >80% during exercise

86
Q

Capillaries are recruited during exercise by metabolic hyperaemia, caused by the release of what?

A

K+ and CO2 from the muscle and adenosine

87
Q

In the pulmonary circulation, what is the most important mechanism regarding flow?

A

Hypoxic pulmonary vasoconstriction, in which small arteries constrict in response to hypoxia (in contrast to elsewhere in the body)

88
Q

The lungs will maintain optimal ventilation-perfusion matching by diverting blood to areas of the lung that are better ventilated if an ear of the lung is poorly ventilated and the alveolar pressure of oxygen is low. This effect is accentuated by high alveolar PCO2. When is this response unhelpful and why?

A

Global lung hypoxia, at altitude, or in respiratory failure, where it may contribute to the development of pulmonary hypertension and right-sided heart failure (cor pulmonale)

89
Q

What is the main function of the cutaneous circulation?

A

Thermoregulation

90
Q

Arteriovenous anastomoses (AVAs) directly linked arterioles and venues, allowing high blood flow into the venous plexus and thus radiation of head. Where are AVAs mostly found?

A

Hands, feet and areas of the face

91
Q

Temperature is sensed by peripheral thermoreceptors. What coordinates the response?

A

The hypothalamus

92
Q

In cutaneous circulation what is the response when temperatures are low?

A

Sympathetic stimulation of alpha-adrenergic receptors causes vasoconstriction of cutaneous vessels minimising loss of heat. Piloerection traps insulating air.

93
Q

In cutaneous circulation what is the response when temperatures are high?

A

Reduction of sympathetic adrenergic stimulation, causing vasodilation and allowing more blood to flow to the skin and radiate its heat to the environment, whereas activation of sympathetic cholinergic fibres promote sweating and the release of bradykinin, which also causes vasodilation.

94
Q

What percentage of cardiac output does the brain receive?

A

15%

95
Q

The autoregulation of cerebral blood flow can maintain a constant flow for what range of MAP?

A

50-170mmHg

96
Q

Which 2 important metabolic regulators in the brain, with increasing concentration cause vasodilation and a function hyperaemia?

A

CO2 and K+

97
Q

Why can hyperventilation cause fainting?

A

Reduced blood PCO2 and cause fainting due to cerebral vasoconstriction.

98
Q

Capillaries throughout the body vary in their permeability based on the size of their pores. What are the 3 basic types of capillaries and where are they found?

A
  1. Continuous capillaries - found in the skin, lungs, muscles and CNS, are the most selective with low permeability.
  2. Fenestrated capillaries - found in renal glomeruli, endocrine glands and intestinal villi, are more permeable.
  3. Discontinuous capillaries - found in the reticuloendothelial system (bone marrow, liver and spleen), have large gaps between endothelial cells and are permeable to red blood cells.
99
Q

In capillaries, is the endothelial lipid bilayer membrane more permeable to non-polar lipohilic substances (e.g. CO2 and O2) or hydrophilic molecules (e.g. glucose, polar molecules and ions)?

A

More permeable to non-polar lipohilic substances (e.g. CO2 and O2)

100
Q

What is oedema?

A

Swelling of the tissues due to excess fluid in the interstitial space

101
Q

What are the 4 main mechanisms of oedema?

A
  1. Increased capillary hydrostatic pressure.
  2. Decreased plasma oncotic pressure.
  3. Increased capillary permeability (leading to reduced oncotic pressure gradient).
  4. Lymphatic obstruction.
102
Q

Oedema can be caused by increased capillary hydrostatic pressure, what causes this mechanism of oedema?

A

Increased venous pressures e.g. by gravitational forces, volume expanded states, in heart failure or with venous obstruction.

103
Q

Oedema can be caused by decreased plasma oncotic pressure, what causes this mechanism of oedema?

A

Decreased protein concentration in blood e.g. nephrotic syndrome, protein malnutrition, liver failure

104
Q

Oedema can be caused by increased capillary permeability (leading to reduced oncotic pressure gradient), what causes this mechanism of oedema?

A

Proinflammatory mediators or by damage to the structural integrity of capillaries so that they become more ‘leaky’ e.g. in tissue trauma, burns and severe inflammation

105
Q

Oedema can be caused by lymphatic obstruction, what causes this mechanism of oedema?

A

Caused by, for example, filariasis or following lymph node dissection surgery or radiation therapy

MRCEM Physiology (2 decks)

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