Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Week 9 > Control of CV system > Flashcards

Control of CV system Flashcards

1
Q

functions of the CV system

A

transport of nutrients, O2 and waste products around the body
transfer of heat (generally core to skin)
buffers body pH
transport of hormones
- adrenaline from adrenal glands
assists in response to infection
assists in formation of urine
- filtration and circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the relative thickness of the RV wall and explain why

A

thin because blood not under a large amount of pressure
(in contrast, LV wall is thicker as it has to generate systolic BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are chordae tendineae

A

‘heart strings’
inelastic cords of CT that control the movement of valves
- works with papillary muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the clinical relevance of valves

A

septal defects
calcification of valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how do septal defects effect heart function

A

ASD, VSD - efficiency reduces (due to mixing of oxygenated and deoxygenated blood
long-term structural changes (RV may increase wall thickness to compensate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does calcification of valves affect heart function

A

aortic valve - LV hypertrophy leading to heart failure (may be able to detect using stethoscope)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

heart sounds

A

sound one - AV valves closing
sound two - sound of pulmonary (P2) and aortic (A2) valves closing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are Korotkoff sounds

A

sounds (whoosh) produced by flow of blood in the Brachial artery
- used for measuring blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what could a third heart sound be an indicator of

A

oscillation of blood flow into the ventricle, tensing of chordae tendineae or various disease states (HF or valve defects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does the cardiac cycle consist of (basic)

A

systole and diastole of atria and ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does the cardiac cycle consist of (complex)

A

isometric contraction
rapid ejection phase
reduced ejection phase
isometric relaxation
rapid ventricular filling
slow ventricular filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what happens in isometric contraction

A

early systole
ventricles contract with no change in blood volume
forced AV valves shut -> ‘lub’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what happens in the rapid ejection phase

A

semilunar valves open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens in reduced ejection phase

A

marks the beginning of ventricular polarisation , decrease in ventricular pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what happens in isometric relaxation

A

ventricular pressure < aortic/ pulmonary pressures
aortic/ pulmonary valves close -> ‘dub’ (A2 and P2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens in rapid ventricular filling

A

augmented by ventricular suction / ventricular untwisting -> muscle fibres return to slack length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what happens in slow ventricular filling

A

diastasis (atrial/ ventricular pressures increase slowly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what happens in atrial systole

A

atrial depolarisation -> atrial contraction (a wave)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the EDV

A

end diastolic volume
120mls on each side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the SV

A

stroke volume
amount of blood ejected from heart per beat
can be increased under certain circumstances - Stirling’s law

21
Q

what is CO and how is it calculated

A

cardiac output
CO = SV x HR
normally 5L/ min (each side)

22
Q

what makes the heart beat

A

impulses generated within the SAN are spread over the atria followed by the ventricles
- delay made though the AVN
- spreads down septum and contracts from bottom

23
Q

what is the natural rate of the heart

A

100 bpm
- body keeps HR artificially low

24
Q

role of the SAN

A

has the fastest intrinsic rate so determines HR

25
Q

role of AVN

A

slows conduction and can act as a secondary pacemaker if required

26
Q

pacemaker cells

A

SAN
AVN
Purkinje fibres
- interdigitate with myocytes to spread impulse across ventricles
- excitation contraction (EC) coupling

27
Q

clinical relevance of pacemaker cells

A

arrythmias
bundle branch block (BBB)
atrial fibrillation

28
Q

what are arrythmias

A

e.g. ectopic beats, tachycardia, bradycardia, fibrillation (AF/ VF)
problems with conduction of impulse across the heart lead to aberrant HR -> often the result of ischaemic damage to the tissue

29
Q

what is a BBB

A

bundle branch block
heart block
- primary, secondary, tertiary

30
Q

what is the relevance of atrial fibrillation

A

can lead to blood clot formation

31
Q

what is an ECG

A

detects phasic change in potential difference between two electrodes
- on surface of heart or on limbs
- recorded on oscilloscope/ computer/ paper

32
Q

what is an ECG useful for

A

diagnosis of arrythmias, post MI damage, congenital/ iatrogenic abnormalities

33
Q

what are the stages of an ECG

A

P wave - atrial depolarisation
QRS complex - ventricular polarisation (septum upwards)
T-wave - ventricular repolarisation
- atrial polarisation hidden by QRS complex on graph
P-R interval - delay through AVN
S-T interval - plateau phase of AP (ventricle repolarisation)

34
Q

clinical relevance of ECG results
(look over diagram in control of CV system notes)

A

atrial fibrillation
- no distinguishable P wave (atria not contracting properly)
ventricle fibrillation
- mess; patient will die quickly
secondary heart block
- AVN not firing correctly
VT
- RR waves much closer together
-> tachycardia
myocardial infarction (STEMI)
- ST interval plateau above baseline

35
Q

process of SAN AP

A

1- SAN nerve cell depolarizes - becomes more +ve, -30mV ish
- if K+ permeability increases, longer time to threshold = fewer BPM so HR decreases (action of ACh from vagus nerve)
- if Ca2+ permeability increases, shorter time to threshold (Action of (nor)adrenaline
2- Ca2+ then moves in (slow leak) (does normal job of Na+)
3- K+ channels start opening and K+ moves out

36
Q

what makes SAN exhibit automaticity

A

reduced permeability to K

37
Q

what happens to HR if K+ permeability increases

A

longer time to threshold = fewer BPM
action of ACh from vagus nerve

38
Q

what happens to HR if Ca2+ permeability increases

A

shorter time to threshold = higher BPM
action of (nor)adrenaline

39
Q

process of Purkinje AP

A

rapid depolarisation due to Ca2+ influx
plateau occurs cause Ca2+ is going in and K+ is going out
increased the length of AP
- refractory period
- decreases likelihood of arrythmias

40
Q

contraction of cardiac muscle

A

Ca2+ enters into cardiac muscle cells; tiggers contractions
exterior of the myocyte
sarcoplasmic reticulum inside cell
‘calcium-induced calcium release’
allows a greater contraction for a small Ca2+ movement (amplifier)

41
Q

clinical relevance of process of contraction of cardiac muscle

A

some drugs used in HF increase intracellular Ca and/ or increase myofilament sensitivity - increases contraction and output from the failing heart
digoxin drug (cardiac cell excitation-contraction-relaxation (builds up to Ca to produce stronger contraction)

42
Q

how does an increase in SV increase HR

A

if the heart is filled with more blood, it will exert more pressure on the walls of the ventricle
- the increased pressure stretches it more
- elastic potential -> leads to a stronger contraction
- therefore, when the heart has a larger SV, the contraction is stronger
- prevents the ESV (end systolic volume) from increasing

43
Q

types of androreceptors

A

exist in A and B forms with subtypes of each

44
Q

what type of androreceptor is major in the heart

A

B1 on nodal tissue, conducting system and myocardium

45
Q

what does B1 androreceptor do

A

bind to NorA released by sympathetic nerves but also circulating adrenaline

46
Q

what response dose B1 create

A

positive ionotropy (force of contraction)
positive chronotropy (increase HR)
positive lusitropy (increase in speed of relaxation)
positive dromotropy (speed of conduction)

47
Q

what is the clinical relevance of B1 androreceptor

A

beta-agonist used an short-term support in cardiogenic shock, arrest etc.
isoprenaline (B1 and B2 agonist) used for asthma - a good idea??
- accidentally also increases the action of the heart while dilating the airway (isoprenaline)
- lead to death in some patients

48
Q

which two areas of the heart does the vagus nerve terminate in

A

right vagus - SAN
left vagus -> AVN
release of ACh activates M2 receptors which reduces HR - increased K+ permeability

49
Q

clinical relevance of vagus nerve terminations in the SAN/ AVN

A

vagolytic drugs (atropine) can be used to increase HR in bradycardic patients
you can stimulate the vagal reflex by breath holding, diving reflex etc.

Week 9 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions