HOM > Cardiac function > Flashcards

Cardiac function Flashcards

(43 cards)

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1
Q

phonocardiogram

A

listening to the chest wall to assess the heart

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2
Q

what should you hear in a phonocardiogram?

A

“lub” - AV valve closure
“dub” - semi-lunar valve closure

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3
Q

what are “gallops” in phonocardiograms?

A

a third sound such as a “lub-dup-dup” or a “lub-lub-dup” due to out of time semilunar valve or AV valve closure, respectively

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4
Q

abnormal phonocardiogram sounds

A
  • gallops
  • clicking
  • whooshing
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5
Q

what does whooshing mean in a phonocardiogram?

A

murmurs caused by the leaking of blood through an incompletely closed valve (valvular incompetence)

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6
Q

what does ECG stand for?

A

electrocardiography

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7
Q

waves and segments of an ECG

A
  • P wave
  • PQ segment
  • QRS complex
  • ST segment
  • T wave
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8
Q

P wave

A

corresponds with atrial depolarisation

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9
Q

QRS complex

A

corresponds to ventricular depolarisation

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10
Q

T wave

A

corresponds to ventricular repolarisation

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11
Q

why is atrial repolarisation not shown on an ECG?

A

it is masked by the QRS complex

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12
Q

R-R interval

A

accurate measure of heart rate

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13
Q

what does a long Q-T segment mean?

A
  • inherited channelopathies
  • mutations in myocardial Na+ and K+ channels (affecting repolarisation)
  • can also be a side effect of some drugs
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14
Q

Anrep effect

A

autoregulation method in which myocardial contractility increases with afterload

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15
Q

what causes the Anrep effect?

A
  • sustained myocardial stretch activates tension dependent Na+/H+ exchangers
  • increased [intracellular Na+]
  • reduces the Na+ gradient exploited by the sodium-calcium exchanger and stops them from working effectively
  • Ca2+ accumulate intracellularly and are uptaken by SR via SERCA pumps
  • calcium-induced calcium release increased
  • contractile force increases in attempt to increase stroke volume and cardiac output to maintain tissue perfusion
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16
Q

EDV

A

end diastolic volume - volume of blood left at the end of passive cardiac filling

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17
Q

ESV

A

end systolic volume - volume of blood left in the heart at the end of the ejection phase

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18
Q

afterload

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A

peripheral resistance

19
Q

preload

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A

cardiac filling pressure

20
Q

what happens if afterload and heart rate are maintained constant whilst preload is increased?

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A
  • greater volume of blood ejected against the same resistance
  • cardiac output increases due solely to an increase in stroke volume (heart is paced at a constant rate)
  • left ventricular and aortic pressures increase
  • ventricles stretch and EDV increases (Frank-Starling mechanism)
21
Q

what happens when preload and heart rate are maintained constant but afterload increases?

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A
  • same volume of blood being pumped against a greater resistance
  • left ventricular and aortic pressure increase
  • stroke volume and cardiac output initially fall
  • this increases ESV (more blood left due to less being forced out)
  • ventricle walls stretch and increase cardiac output (Frank-Starling mechanism)
22
Q

Frank-Starling law

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A
  • greater preload, greater contractile force, greater stroke volume/cardiac output
  • heart automatically adjusts its output to meet changing demands for blood flow
  • maintains cardiac output and blood pressure
23
Q

blurt the cardiac cycle around graph

24
Q

where do the sympathetic and parasympathetic branches of the autonomic nervous system to the heart originate from?

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A

cardiovascular centre in the medulla oblongata

25
which sympathetic nerves affect the heart? where do they come from? where do they go to?
- cardiac accelerator nerves - from thoracic region of spinal cord - to the SAN and AVN and most portions of the myocardium
26
what do the cardiac accelerator nerves release? what do they bind to?
- noradrenaline - binds to beta 1 receptors on cardiomyocytes
27
what does noradrenaline do to the heart?
- increases frequency of contraction at SAN (positive chrono-tropic effect) - increases contractility of ventricles (positive inotropic effect)
28
positive chrono-tropic effect
increased frequency of contraction at SAN (caused by binding of noradrenaline to beta 1 receptors)
29
positive inotropic effect
increased contractility of ventricles (caused by noradrenaline binding to beta 1 receptors)
30
which parasympathetic nerves affect the heart? where do they go to?
- right and left vagus nerves - SAN, AVN and atrial myocardium
31
what do the left and right vagus nerves release? what does it bind to?
- acetylcholine - binds to muscarinic receptors at SAN, AVN and atrial myocardium
32
what does acetylcholine do to the heart?
- reduces heart rate (negative chrono-tropic effect) - little to no effect on contractility of the ventricles in most species
33
negative chrono-tropic effect
reduced heart rate (caused by acetylcholine binding to muscarinic receptors in the SAN, AVN and atrial myocardium)
34
why is there no negative inotropic effect?
little to none parasympathetic (vagus) nerves innervate the ventricles so there is little affecting their contractility
35
chronotropic effects
effects on heart rate
36
inotropic effects
effects on ventricle contractility
37
which hormone has chronotropic or inotropic effects? where is it secreted from? what does it bind to? where does it act? what does it do?
- adrenaline - released from adrenal medulla - binds to beta 1 receptors - positive chronotropic effects - positive inotropic effects
38
why is it important to have endocrine as well as neuronal control of the heart?
endocrine control is longer-lasting so can maintain neurally-mediated sympathetic effects such as increased heart rate and ventricle contractility
39
initial membrane potential of the SAN
approx -60mV
40
pacemaker potential
spontaneous slowly increasing potential of the SAN from membrane potential to threshold (approx -60mV to -40mV)
41
nodal cells threshold
approx -40mV
42
what determines the time taken to reach threshold in nodal cells?
slope of the pacemaker potential
43
what does sympathetic stimulation do to the slope of the pacemaker potential?
increases gradient of slope to decrease the time taken to reach threshold and increase heart rate
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