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Exam Prep MCQs > Cardiovascular Physiology 1 > Flashcards

Cardiovascular Physiology 1 Flashcards

1
Q

What effect does hyperkalaemia have on cardiac output?

A

Negative ionotropic effect

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2
Q

What effect does SVR have on cardiac output?

A

Decreases cardiac output through increasing afterload

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3
Q

When is aortic blood flow lowest?

A

Start of diastole

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4
Q

When is aortic pressure highest?

A

Mid systole

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5
Q

How much can atrial contraction account for ventricular filling?

A

At rest it is normally closer to 20%, but increases to as much as 40% with tachycardia.

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6
Q

When does the QRS complex occur in the cardiac cycle?

A

The QRS complex occurs immediately before isovolumetric contraction.

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7
Q

What are the body’s responses to acute haemorrhage?

A
  • increased ADH secretion
  • initially increased sympathetic activity but when blood volume is critically depleted, peripheral sympathetic drive falls steeply
  • reduced baroreceptor discharge
  • increased glucagon release
  • reduced hydrostatic capillary pressure causes fluid to enter capillaries from the interstitium
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8
Q

How much does PVR fall at birth?

A

By >80%

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9
Q

WHy does SVR of the neonate increase after birth?

A

Intense vasoconstriction of umbilical vessels

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10
Q

Why does left atrial pressure rise after birth in the neonate?

A

Due to increased pulmonary blood flow

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11
Q

When should the ductus arteriosus close by?

A

48hrs.

High PaO2 appears to initiate closure.

Prostaglandins maintain patency.

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12
Q

When does the foramen ovale fuse?

A

48hrs after birth

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13
Q

What factors increase movement of fluid out of capillaries?

A
  • increased capillary hydrostatic pressure
  • increased interstitial colloid osmotic pressure
  • reduced interstitial hydrostatic pressure
  • reduced colloid osmotic pressure
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14
Q

What wave is caused by atrial filling during ventricular systole?

A

The v-wave

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15
Q

What would elevate the a-wave?

A

Tricuspid stenosis

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16
Q

What are canon waves?

A

Large a-waves corresponding to atrial contraction against a closed tricuspid valve.

Seen in complete heart block or junctional arrhythmias

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17
Q

Why are cardiac ventricular muscle cells impermeable to negatively charged ions?

A

These include proteins, sulphates and phosphates which thus remain intracellularly and contribute to the negative RMP.

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18
Q

How long does the depolarization plateau potential last for in cardiac ventricular muscles?

A

About 200ms.

Due to Calcium influx via slow L-type calcium channels

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19
Q

How much does hypoxia increase coronary blood flow by?

A

2-3 fold

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20
Q

What % of cardiac output is coronary blood flow at rest?

A

5%

250ml/min

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21
Q

How is coronary blood flow regulated?

A

Aortic pressure provides the main driving force for coronary blood flow and this pressure is controlled by baroreceptor reflexes

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22
Q

How long does transmission through the atrium and AV node to the ventricular myocardium take?

A

0.2 ms

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23
Q

What is the preferential route of transmission from right to left atrium?

A

Via Bachmann’s bundle

(aka anterior interatrial band)

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24
Q

What allows the myocardium to contract as a single unit?

A

Gap junctions located at the intercalated disc and allow electrical impulses to propagate freely.

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25
Q

At the onset of the Valsalva manouvre, what happens?

A

Arterial pressure rises due to increased intrathoracic pressure on the aorta

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26
Q

After the initial rise in BP, what happens in the valsalva manoevre?

A

The BP then falls due to effects of raised intrathoracic pressure on venous return.

This ismore pronounced in the hypovolaemic.

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27
Q

What are heart rate changes mediated by in the valsalva manoeuvre?

A

Pressure changes are detected by BAROreceptors

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28
Q

What would cause an abset bradycardia after termination of the valsalva?

A

Autonomic neuropathy will result in absense of HR changes, but this would only be seen in 20% of long standing diabetics.

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29
Q

How does valsalva affect the intensity of heart murmurs?

A

Increases mitral regurg but all the rest are decreased.

30
Q

What happens to the fetal circulation at birth?

A

Pulmonary vascular resistance falls markedly as the lungs expand and fill with air. This decreases pulmonary artery pressures and increases blood flow to the left atrium.

Umbilical vessels constrict and placental circulation ceases resulting in increased systemic vascular resistance and arterial pressure. Left atrial pressure becomes higher than right atrial pressure and this closes the foramen ovale.

Blood flow in the IVC falls.

31
Q

What pressure does the first breath generate at birth?

A

-50cm H2O

32
Q

What happens if the neonate is hypoxic after birth?

A

Favours right to left shunt.

This increases pulmonary vascular resistance and hence a persistent fetal circulation.

33
Q

What stimuli will cause a persistent fetal circulation?

A
  • hypoxia
  • hypercarbia
  • acidosis
  • hypothermia
34
Q

What can a pulmonary artery floatation catheter measure?

A

Left atrial pressure (wedge pressure)

35
Q

Does LVEDP determine myocardial O2 consumption?

A

Yes, raised LVEDP increases myocardial work and therefore O2 requirement

36
Q

How will LVEDP be affected by aortic regurgitation?

A

It’s increased, regurgitant blood re-enters the ventricle increasing volume + pressure

37
Q

What is the formula for compliance of the ventricle? What happens to LVEDP if left ventricular compliance increases?

A

Compliance = volume/pressure

Pressure will be lower for a given volume if compliance increases.

38
Q

Does LVEDP give an index of preload?

A

Yes - the best measure of preload is LVEDV, but this usually correlates with LVEDP

39
Q

What does an increase in right atrial pressure cause?

A
  • increases LVEDV and therefore SV and consequently CO and arterial blood pressure
  • increases type A atrial stretch receptor discharge during atrial systole
  • causes an increase in urine volume due to production of ANP due to atrial stretch receptor stimulation
  • can increase HR via Bainbridge reflex (atrial stretch receptors)
  • can decrease HR via baroreceptor reflex
40
Q

What is lusitropy?

A

Lusitropy is a term that decribes myocardial relaxation.

Catecholamines have a positive lusitropic action (allowing rapid relaxation) whilst hypercalcaemia inhibits relaxation due to incomplete calcium reuptake (an essential process in diastole).

41
Q

Is myocardial relaxation metabolically active?

A

Yes, calcium re-uptake occurs via the sarcoplasmic reticulum

42
Q

Which happens first, left or right atrial contraction?

A

RA contration preceeds LA contraction, however LV contaction precedes RV contraction.

43
Q

Which shortens first with increasing HR - diastole or systole?

A

Diastole shortens first (particularly the slow ventricular filling phase - diastasis)

44
Q

What happens to insulin and glucagon secretion in the first 24hrs after major trauma?

A

Insulin secretion is decreased and glucagon secretion increases briefly

45
Q

What is afterload?

A

Afterload is the tension developed in the LV wall during systole. SVR is however the commonest index of afterload used clinincally, but it is only one component that determines afterload

46
Q

What is the Anrep effect?

A

If afterload increases, SV initially falls.

SV is then (partially) restored by an increase in LVEDV. This is known as the Anrep effect

47
Q

What happens to LVEDV if afterload is increased?

A

LVEDV is increased to restore SV after it’s intial fall

48
Q

What would you expect afterload to be in the failing heart?

A

Afterload is the tension developed in the LV wall during systole and as such can be related to pressure by Laplaces law.

Thus in the failing heart afterload is likely to be low due to low intraventricular pressure.

49
Q

What will afterload be in a dilated ventricle?

A

Using Laplace’s law, the increased radius will increase tension - so afterload will be higher in a dilated ventricle

50
Q

What will afterload be in mitral regurg?

A

Afterload is increased because the left ventricle requires less tension to eject blood through this low pressure pathway

51
Q

What is the hepatic artery a branch of?

A

The coeliac axis

52
Q

What is the ratio between the flow of the hepatic artery and portal vein?

A

There is an inverse ratio

53
Q

Where does 1/3 of hepatic blood come from?

A

Hepatic artery which is a branch of the coeliac axis

54
Q

What mediates mesenteric arteriolar vasodilatation?

A

Beta 2 adrenergic receptors mediate vasodilatation.

55
Q

How does PEEP affect portal blood flow?

A

Portal blood flow does not autoregulate well.

PEEP increases hepatic venous pressure and reduces portal flow.

56
Q

Why is oxygen delivery to the tips of hepatic mucosal villi poor?

A

The countercurrent exchange of oxygen between parallel arterioles and submucosal venules makes O2 delivery to tips of mucosal villi poor

57
Q

What are the major reservoirs of available blood in times of stress?

A

Splanchnic and skin circulations

58
Q

How much of total blood volume does the splanchnic venous system contain?

A

1/3 of total blood volume

59
Q

What is the RMP of myocardial cells?

A

-90 mV

60
Q

Do myocardial cells posess gap junctions?

A

Yes. Gap junctions connect the cytosol of adjacent myocardial cells allowing rapid transmission of electrical signals

61
Q

Where is conduction velocity greatest in cardiac tissue?

A

The bundle branches and Purkinje system

62
Q

When is calcium released within the SR?

A

Released in response to rising intracellular calcium levels

63
Q

What is the blood supply to the SA and AV nodes?

A

Right coronary artery

64
Q

What changes happen in the CVS during moderate exercise?

A
  • cardiac output increases up to 7x normal resting values
  • cerebral blood flow maintained at normal levels
  • increased CO mainly from increased HR
  • CVP doesn’t change until it rises at max exertion
    • this is because increased venous return matches increased CO
  • intravascular volume is decreased due to insensible losses and increased capillary filtration
  • slight rise in haematocrit
65
Q

What does hypokalaemia do to the cardiac muscle?

A

Hypokalaemia makes the cardiac muscle RMP more negative, resulting in it being less excitable but with increased automaticity.

66
Q

How does hypokalaemia affect the QT interval?

A

Increases QT interval

67
Q

How does hyperkalaemia affect the RMP?

A

It brings RMP closer to threshold potential (makes the RMP less negative)

68
Q

What does hypercalcaemia do to the RMP?

A

Makes the threshold potential less negative, decreases conduction velocity and shortens the refractory period.

69
Q

What does hypermagnesemia do to the PR interval?

A

Delays AV conduction/prolongs PR interval

70
Q
A

Exam Prep MCQs (19 decks)

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