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CDL301 Cardiovascular Pharmacology > Lecture 4 Physiology of the Heart III > Flashcards

Lecture 4 Physiology of the Heart III Flashcards

1
Q

The main coronary arteries are the first branches of the aorta T or F

A

T

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2
Q

Describe how coronary arteries project over and perfuse the heart

A

The coronary arteries run over the surface of the heart and then perforate into the muscle itself

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3
Q

What is unusual about the perfusion by the coronary arteries

A

The coronary blood flow occurs during diastole. In systole the vessels are squashed by the contracting cardiac muscle

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4
Q

Anything increasing left ventricular end diastolic pressure will have what effect on coronary artery perfusion

A

Anything increasing LVEDP will diminish perfusion of the coronary arteries

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5
Q

What can be said about the relationship between cardiac output and coronary oxygen consumption

A

Oxygen consumption increases in parallel to cardiac output. Cardiac output can increase 7-fold during exercise and similarly oxygen consumption increases 7/8-fold during exercise

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6
Q

Recall the equation for cardiac oxygen delivery

A

Oxygen delivery = arterial oxygen concentration x coronary blood flow

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7
Q

Using the equation and in theory what two aspects can be changed in order to increase oxygen delivery to the coronary arteries

A

Can increase the arterial oxygen concentration or increase the coronary blood flow or both

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8
Q

Why is it that the primary determinant of oxygen delivery to the heart is coronary blood flow and not arterial oxygen concentration

A

There is relatively little oxygen dissolved in blood plasma and so arterial oxygen concentration is mainly determined by the oxygen bound to haemoglobin. Ordinarily there is little change in the oxygen content of arterial blood with oxygen saturation remaining high at around 98%

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9
Q

What is the standard arterial systolic pressure

A

120mmHg

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10
Q

What is the standard arterial diastolic pressure

A

80mmHg

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11
Q

Why is the standard arterial diastolic pressure not 0mmHg

A

Diastolic pressure is not 0mmHg in the arteries because of the closed aortic valve. Without the aortic valve the diastolic pressure would drop to zero and you wouldn’t be able to perfuse the coronary arteries.

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12
Q

What is the dicrotic notch

A

The dicrotic notch is a secondary upstroke in the descending part of an arterial blood pressure trace. This corresponds to the transient increase in aortic pressure upon closure of the aortic valve

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13
Q

Pressures in the aorta indicative of all the arteries of the body T or F

A

T

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14
Q

How does the systolic pressure of the ventricles compare to the arterial systolic pressure

A

The systolic pressure in the ventricles should be exactly the same as the aorta around 120mmHg. This is because at this point the aortic valve offers no resistance to flow and hence anything generated in the ventricle will be reflected in the aorta

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15
Q

How does the diastolic pressure of the ventricles compare to the arterial diastolic pressure

A

It’s a lot less. As the ventricles contract they expel the blood so that upon relaxation in diastole there is nothing to support much pressure

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16
Q

What is the approximate value of ventricular diastolic pressure

A

Roughly 5-8mmHg

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17
Q

What feature of the arterial and ventricular pressures causes the perfusion of the coronary arteries

A

The difference in arterial diastolic pressure and left ventricular end diastolic pressure is what causes the perfusion of the coronary arteries

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18
Q

Which ventricular pressure is considered when talking about the perfusion of the coronary arteries

A

The left ventricular pressure

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19
Q

What three factors can change coronary flow

A

Physical factors (pressure gradients) local metabolites and nervous/humoral factors

20
Q

Draw a diagram depicting the arterial and left ventricular pressures in diastole and systole highlighting the region where coronary flow occurs

A

See completed diagram below – coronary flow window indicated in yellow

21
Q

What changes increase the window of coronary blood flow perfusion

A

Increases in the time between systole and diastole and increases in the difference in diastolic pressure between the aorta and ventricles

22
Q

What are the effects of tachycardia on coronary perfusion

A

Tachycardia disproportionately reduces the time of diastole which in turn decreases coronary perfusion

23
Q

What are the effects of a raised LVEDP on coronary perfusion

A

Raised left ventricular end diastolic pressure decreases the difference in diastolic pressure which in turn decreases coronary perfusion

24
Q

What are the effects of reduced arterial diastolic pressure on coronary perfusion

A

Decreased arterial diastolic pressure decreases the difference in diastolic pressure which in turn decreases coronary perfusion

25
Q

What is meant by autoregulation

A

Autoregulation is the ability of an organ to maintain a constant blood flow despite changes in perfusion pressure

26
Q

Describe the changes in blood flow and resistance that is seen as a result of autoregulation in response to a fall in perfusion pressure in the heart

A

Because flow is proportional to perfusion pressure a drop in perfusion pressure will result in the blood flow also dropping. Interestingly because the blood vessels are capacitive there is an initial small increase in resistance. However autoregulation in the heart means that resistance then decreases. This acts to restores the flow back up due to the inverse relationship between resistance and flow. This flow is then maintained despite the reduced pressure

27
Q

What events can case a drop in perfusion pressure

A

Heart attack septic shock haemorrhaging

28
Q

How is the drop in resistance in the heart in response to a drop in blood flow detected and mediated by the heart during autoregulation

A

In response to a decrease in flow the heart detects the decrease in pO2 reaching it and then triggers the generation of metabolites to causes vasodilatation. Vasodilation in turn decreases the resistance of the vessel

29
Q

Which is the most important mechanism of day-to-day control of coronary flow

A

Vascular control through the release of metabolites and mediators

30
Q

What evidence lead to the indication that local mediators must be responsible for the vascular control of coronary perfusion

A

In response to hypoxia there is a marked coronary vasodilatation in situ but not in isolated coronary arteries in vitro. This implies that the vasodilation is not a property of the coronary arteries themselves

31
Q

Which it the main metabolite responsible for vascular control of coronary blood flow

A

Adenosine

32
Q

Which it the metabolites released during anaerobic respiration are responsible for additional vascular control of coronary blood flow

A

K+ CO2 H+ and lactic acid

33
Q

Outline the neural and hormonal control of coronary blood flow

A

In the large vessels there are α-adrenoceptors that cause vasoconstriction. Similarly in smaller vessels there are β2-adrenoceptors that cause vasodilatation

34
Q

The heart is an exocrine organ T or F

A

F – it is an endocrine organ

35
Q

Which natriuretic peptide comes from the atria

A

ANP

36
Q

Which natriuretic peptide comes from the brain and ventricles

A

BNP

37
Q

Which natriuretic peptide comes from the endothelium

A

CNP

38
Q

What causes natriuretic peptide release

A

Natriuretic peptides are released by stretching of the atrial and ventricular muscle cells. This can happen in raised atrial or ventricular pressures but is also caused by volume overload. Often granules in the atrial appendage respond to stretch and release ANP

39
Q

What are the effects of natriuretic peptides

A

Increase renal excretion of sodium (natriuresis) and water (diuresis) relax vascular smooth muscle increase vascular permeability and inhibit the release or actions of aldosterone angiotensin II endothelin and ADH

40
Q

ANP causes vasodilation what is the exception to this rule and the significance of it

A

ANP causes dilation of the afferent arteriole in the glomerulus however also causes constriction of the efferent arteriole. This acts to increase perfusion to the glomerulus which in turn increases filtration and GFR. Hence there is increased excretion of excess plasma volume particularly Na+ and water

41
Q

Natriuretic peptide pathway antagonises RAAS system T or F

A

T

42
Q

How can natriuretic peptides be used in diagnosis of heart conditions

A

Patients in heart failure will have raised BNP levels. There is a diagnostic blood test that detects these elevated blood BNP – diagnostic test

43
Q

What is the name of the enzyme that metabolises natriuretic peptides

A

Neutral Endopeptidase (NEP neprilysin)

44
Q

How have natriuretic peptides been used to develop new therapeutics in the treatment of heart failure

A

NEP inhibition increases levels of natriuretic peptides. A combination therapy using sacubitril a neprilysin inhibitor along with valsartan an angiotensin II blocker has been developed to treat heart failure

45
Q

What is the name given to the treatment that comprises of sacubitril given in combination with valsartan

A

Entresto

CDL301 Cardiovascular Pharmacology (17 decks)

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