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Phys Pharm I > the heart > Flashcards

the heart Flashcards

1
Q

what is the effect of sympathetic nerves on the heart?

A
  • increased heart rate (+ve chronotropy)
  • increase in contractility (+ve ionotropy)
  • increase in speed conduction through the AV node
  • increase in automaticity
  • decrease in cardiac efficiency
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2
Q

what is automaticity?

A

the tendency of non-pacemaker regions to initiate action potentials

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3
Q

what is the effect of parasympathetic nerves on the heart?

A
  • decrease in heart rate and automaticity
  • decrease in contractility of atria
  • slows conduction through the AV node
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4
Q

why is the heart rate slower than intrinsic rate of the SA node when at rest?

A

due to maintained parasympathetic activity known as vagal tone

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5
Q

what is Kv?

A

a delayed rectifier voltage-activated potassium channel it inactivates slowly with time at a negative potential

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6
Q

what is the significance of Kv?

A

the decay in outward K+ current permits inward depolarising currents to become dominant

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7
Q

when is If current activated?

A

during hyperpolarisation. contributes to generation of depolarisation due to Na+

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8
Q

why does cardiac efficiency decrease as B-adrenoceptor activation increases?

A

B-adrenoceptor activation switches metabolism towards fatty acids, requiring more O2

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9
Q

how does sympathetic stimulation of the SA node increase rate?

A

cAMP acts directly on If channels to increase their activity. this increases the rate of pacemaker depolarisation
PKA phosphorylates L-type Ca2+ channels, increasing their activity. this lowers threshold for the AP

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10
Q

what is the effect of parasympathetic stimulation of the heart?

A

ACh binds to M2 muscarinic receptors coupled to Gai, this results in decreased adenylyl cyclase activity, decreased cAMP production and decrease in heart rate. small decrease in ventricular contraction

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11
Q

what is isovolumetric contraction?

A

when the ventricle contracts without a change in pressure, as the aortic valve has just opened and blood flows into the aorta under high pressure

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12
Q

define cardiac output

A

volume of blood heart pumps in a given time

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13
Q

how can you calculate cardiac output using the Fick principle?

A

CO = Vo2 / (Cv-CA)

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14
Q

what is the frank starling mechanism?

A

increasing venous return leads to increased left ventricular end diastolic pressure, causing an increase in stroke volume. increase in venous return increases blood pumped out of the ventricle

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15
Q

what is the basis for the Frank Starling mechanism?

A

force of contraction in cardiac muscle fibre is proportional to its initial length due to FILAMENT OVERLAP and CALCIUM SENSITIVITY

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16
Q

what is meant by filament overlap?

A

when the sarcomere is below 2uM in length, actin overlaps, this interferes with cross-bridge formation

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17
Q

what is cardiac contractility?

A

an index of the contractile performance of the heart

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18
Q

what is involved with an increase in cardiac contractility?

A

increase in pressure and an increase in rate of contraction

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19
Q

how does sympathetic stimulation affect cardiac contractility?

A

noradrenaline, adrenaline and cardiac glycosides increase contractility

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20
Q

what are the roles of the heart?

A

supplying o2, nutrients to cells and removing CO2 and waste products
regulating pH balance of extracellular fluid and osmotic balance

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21
Q

what causes valves in the heart to close?

A

transient reversal of flow

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22
Q

what is aortic root velocity during ventricular filling?/

A

the aortic valve is closed

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23
Q

how do you calculate cardiac output?

A

measure [O2] in pulmonary artery and [O2] in pulmonary vein. CO = Vo2/Cv-Ca

24
Q

what is the effect of sympathetic activity on cardiac efficiency?

A

decrease due to B-adrenergic activation, metabolism switches towards fatty acid oxidation, which requires more oxygen

25
Q

what are the characteristics of SA node cells?

A
  • no stable resting potential
  • rising phase of potential depends on Ca2+ influx
  • falling phase depends on K+ exit via voltage activated channels
26
Q

what difference between a ventricular cell and SA node cell is responsible for the difference in depolarisation slope?

A

SA nodes have very little inward rectifying K current. there is a slow depolarisation slope because there are many voltage gated potassium channels which are slow to close

27
Q

what is the effect of NCX in pacemaker cells?

A

produce an inward current

28
Q

what maintains the ventricular membrane potential?

A

held close to Ek by a large inward rectifier K current

29
Q

why does a ventricular action potential have a long plateau?

A

balance of inward Ca and outward K+ currents

30
Q

how does a rise in intracellular calcium concentration trigger contraction?

A

calcium binds troponin C, which acts through troponin-tropomyosin complex associated with the actin filament to allow myosin heads to attach to form cross-bridges

31
Q

how are T-tubules in the SR of cardiac myocytes functionally organised?

A

1- APs travel down T-tubule
2- depolarisation activates VG Calcium channels
3- rise in intracellular calcium activates RYR to release more calcium

32
Q

what is meant by calcium induced calcium release?

A

raised calcium activates RYR which are calcium activated calcium channels, permitting further release

33
Q

how do L-type calcium channels close?

A

in response to inactivation and repolarisation

34
Q

what is the role of SERCA?

A

transports Ca back into the SR, this is an electrogenic pump

35
Q

what is the baroreceptor reflex?

A

increase in arterial pressure -> increased activity in afferent nerves -> medullary centres decrease sympathetic activity

36
Q

what are the effects of the baroreceptor reflex?

A

when pressure is high, system responds to:

  • reduce HR and contractility
  • reduce CO
  • reduce contractile tone in blood vessels to reduce peripheral resistance
37
Q

what does arterial pressure depend on?

A

cardiac output and peripheral resistance

38
Q

what type of drug is atropine?

A

muscarinic receptor antagonist

39
Q

how do muscarinic receptor antagonists work?

A

oppose the effect of ACh acting at muscarinic receptors to slow the heart. results in HR increase

40
Q

what do cardiac glycosides do?

A

increase intracellular calcium and contractile force, decreasing the heart rate

41
Q

what are the actions of cardiac glycosides?

A

1- Na/K ATPase inhibition to raise intracellular Ca2- and force
2- slowing of the hear rate and conduction through the AV nodes, increasing parasympathetic activity
3- can cause arrhythmias

42
Q

what is the main use of cardiac glycosides? why?

A

heart failure associated with atrial fibrillation

  • slows AV node conduction to slow ventricles, allowing time for filling
  • increase contractile force
  • increased cardiac output
43
Q

why does most coronary blood flow occur during diastole?

A

during isovolumetric contraction, pressure in ventricle wall exceeds that in the aorta

44
Q

what controls coronary blood flow?

A

local vasodilators

45
Q

what is the effect of adenosine?

A

increased K+ efflux
decrease in pH
decrease in pO2

46
Q

what are the three types of angina?

A

1- stable angina
2- unstable angina
3- variant angina

47
Q

why does cardiac ischaemia cause angina?

A

pain is caused by substances released in ischaemia e.g. K+, H+, adenosine, bradykinin, prostaglandins

48
Q

what are the aims of anti-anginas drugs?

A
  • decrease pain

- increase exercise tolerance

49
Q

what are the actions of anti-anginal drugs?

A
  • decrease cardiac workload and decrease oxygen demand

- improve O2 delivery by dilating coronary arteries

50
Q

why are B-blockers effective for angina?

A

by limiting sympathetic drive, they increase the efficiency of the heart, resulting in decreased work and oxygen consumption, more supply to coronary arteries

51
Q

how do nitrovasodilators work?

A

cause vasodilation of coronary arteries and collateral vessels. reduce cardiac output and workload.

52
Q

what is the mechanism behind nitrovasodilators?

A

NO binds haem group of guanylyl cyclase, activates PKG

53
Q

what are the affects of PKG activation?

A
  • inhibits Ip3 induced calcium release
  • activates K channels by phosphorylation to hyper polarise them and reduce Ca2+ entry
  • induces Ca desensitisation of contractile machinery to cause relaxation
54
Q

what are the effects of L-type calcium channel blockers?

A

in cardiac muscle - decrease force of contraction and oxygen consumption
in smooth muscle - decrease in force of contraction to cause vasodilation

55
Q

what is verapamil?

A

an L-type calcium channel blocker with primarily cardiac effects

56
Q

what is diltiazem?

A

a calcium channel blocker

57
Q

what is nifedipine?

A

an L-type calcium channel blocker of dihydropyridine variety

Phys Pharm I (11 decks)

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