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PCS > Unit 2: Heart > Flashcards

Unit 2: Heart Flashcards

1
Q

how are cardiac myocytes connected? discuss the cell junctions found

A

intercalated discs - work as syncytium

  • gap junctions: allow rapid depolarisation
  • desmosomes: stop separating of cells during contraction by binding filaments
  • fascia adherens - anchor for actin
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2
Q

what is the name of the ligament that connects heart to diaphragm?

A

pericardiophrenic

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3
Q

what is the effect of parasympathetic innervation of the heart?

A

right vagus nerve innervates SA node - slows heart rate (negative chronotropy)
left vagus nerve innervates AV node - decreased conduction velocity (decreased slope of pacemaker potential so longer intervals between successive AP - longer to reach threshold)

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4
Q

what is the effect of sympathetic innervation of the heart?

A

increase heart rate - positive chronotropy
increase conduction velocity
increased force of contraction - positive inotropy

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5
Q

describe the durations of the cardiac cycle

A

atrial systole - 0.1s
ventricular systole - 0.3s
diastole - 0.4s

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6
Q

what occurs in atrial systole?

A

atria contract increase in ventricular volume

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7
Q

what two stages of ventricular systole?

A

isovolumetric contraction - AV closes but semilunar valves are not yet open - increased ventricular pressure
ejection - semilunar valves open -eject 2/3 of blood

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8
Q

what are the two stages of ventricular diastole?

A

isovolumetric relaxation - semilunar valves close

filling - AV valves open

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9
Q

what is end-diastolic volume?

A

volume of blood that fills ventricle before systole

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10
Q

what are the heart sounds associated with?

A

1st - lub closure of AV valve
2nd - dub - closure of semilunar valves
3rd - early diastole - rapid filling
4th - atrial contraction

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11
Q

what does dicrotic notch represent?

A

backflow of blood into ventricles after closure of valves

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12
Q

what do the ECG waves represent?

A 
P - atrial depolarisation
QRS complex - ventricular depolarisation
Q - interventricular septum
R -from apex of ventricle
S - passing up towards atria (base) 
T - ventricular repolarisation (Of outermost cells)
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13
Q

how will 1st degree heart block appear on ECG?

A

prolonged PR intervals

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14
Q

how will 2nd degree heart block appear on ECG?

A

dropped beats (QRS)

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15
Q

how will 3rd degree heart block appear on ECG?

A

regular P and R waves but they are independent of each other

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16
Q

explain the electrical activity of the heart

A

depolarisation in SA node - wave spreads across cells and to left atrium via Bachmunn’s bundle so atria contract simultaneously
waves passes through internodal tracts to reach AV node - there is 0.1s delay to allow atria to fully contract so blood moves in co-ordinated way
AV node has slower conduction velocity because cells have smaller diameter and wave passes through bundle of His to purkinje fibres
purkinje fibres sends electrical signals to ventricular myocytes via gap junctions to allow ventricles to contract upwards

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17
Q

what is the pacemaker potential?

A

resting potential of SA node
- change in potential- funny current - slow current = gradual depolarisation by non-selective voltage-gated cation channel - HCN channel

18
Q

how does sympathetic stimulation affect pacemaker potential?

A

slope more steep - threshold reached quicker - shorter intervals between successive AP

19
Q

what happens to ECG with atrial fibrillation?

A

no defined P wave/ irregular RR intervals

20
Q

describe the stages of ventricular action potential

A

0 - when cardiac myocytes hit threshold
1 - Potassium channels open voltage gated channels
2 - Balance of voltage gated potassium channels balanced by calcium channels = plateau
3 -Voltage gated potassium channels are open
4 - Baseline negative state - resting potential

21
Q

what is considered tachycardia/ brachycardia?

A

tachy: >100
brachy: <100

22
Q

what is frank starling relationship?

A

increase in stretch = increase in venous return - increase strength of contraction
(ensure output of ventricles closely matched)

23
Q

what is haematocrit values?

A

ratio of volume of red blood cells: volume of blood

higher ratio - higher viscosity - more resistance - decreased blood flow

24
Q

what is the biggest determinant of poiseulle’s law?

A

radius Q is proportional to r^4

25
Q

what is the difference between laminar and turbulent flow?

A

laminar - parallel layers

turbulent - differnt directions ie. aortic arch/ atheroscelerosis

26
Q

what is mean arterial pressure?

A

diastolic pressure + 1/3(pulse pressure)

27
Q

what is pulse pressure?

A

difference between systolic and diastolic pressure

28
Q

what is perfusion pressure?

A

arterial - venous pressure

29
Q

what is blood flow equation?

A

blood flow = perfusion pressure/ vascular resistance

30
Q

what is cardiac output?

A

heart rate x stroke volume

31
Q

how is cardiac output calculated using fick’s principle?

A

oxygen uptake/ CaO2 - CvO2

oxygen content of arterial blood - venous blood

32
Q

what is cardiac index?

A

cardiac output / body surface area

33
Q

what is ejection fraction?

A

stroke volume/ end diastolic volume

34
Q

what is preload?

A

initial stretching of ventricular walls prior to contraction

35
Q

how does adrenaline increase contractility?

A

binds to B2 adrenoreceptors - cAMP -PKA phosphorylates L-type calcium channels - more cross-bridge cycling

36
Q

how does caffeine increase heart contractility?

A

blocks action of phosphodiesterase - cAMP levels remain high - more calcium ions - increased contractility

37
Q

digitalis is an example of positive inotropic agent explain its mechanism

A

inhibits sodium-potassium ATPAse so build up of soidum in cell causes reversal of Na+Ca2+ exchanger - calcium pumped in sodium pumped out - increased calcium - increased contractility

38
Q

give examples of negative inotropic agents

A

beta blocker - propanolol / calcium blocker - verapamil

39
Q

what is lusitropy?

A

change in rate of relaxation

40
Q

what two processes support positive lusitropy?

A

phospholamban - phosphorylated by PKA no inhibitory effect on Ca2+-ATPase so speeds uptake of calcium
troponin - phosphorylated by PKA - speeds up calcium uptake from dissociation of calcium from myofilaments

41
Q

what is afterload?

A

load that heart must eject blood against - affected by hypertension - decreases ejection time so increased end systolic volume

42
Q

what is the effect of myocardial ischaemia?

A

increased preload - more stretch in wall - heart performs more work when pumping from distended ventricles so coronary arteries cannot meet demands

PCS (29 decks)

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