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Week 9 > Control of CV system > Flashcards

Control of CV system Flashcards

(49 cards)

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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

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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

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3
Q

what are chordae tendineae

A

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

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4
Q

what is the clinical relevance of valves

A

septal defects
calcification of valves

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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)

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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)

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7
Q

heart sounds

A

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

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8
Q

what are Korotkoff sounds

A

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

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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)

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10
Q

what does the cardiac cycle consist of (basic)

A

systole and diastole of atria and ventricles

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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

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12
Q

what happens in isometric contraction

A

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

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13
Q

what happens in the rapid ejection phase

A

semilunar valves open

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14
Q

what happens in reduced ejection phase

A

marks the beginning of ventricular polarisation , decrease in ventricular pressure

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15
Q

what happens in isometric relaxation

A

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

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16
Q

what happens in rapid ventricular filling

A

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

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17
Q

what happens in slow ventricular filling

A

diastasis (atrial/ ventricular pressures increase slowly)

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18
Q

what happens in atrial systole

A

atrial depolarisation -> atrial contraction (a wave)

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19
Q

what is the EDV

A

end diastolic volume
120mls on each side

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20
Q

what is the SV

Study These Flashcards
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

Study These Flashcards
A

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

22
Q

what makes the heart beat

Study These Flashcards
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

Study These Flashcards
A

100 bpm
- body keeps HR artificially low

24
Q

role of the SAN

Study These Flashcards
A

has the fastest intrinsic rate so determines HR

25
role of AVN
slows conduction and can act as a secondary pacemaker if required
26
pacemaker cells
SAN AVN Purkinje fibres - interdigitate with myocytes to spread impulse across ventricles - excitation contraction (EC) coupling
27
clinical relevance of pacemaker cells
arrythmias bundle branch block (BBB) atrial fibrillation
28
what are arrythmias
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
what is a BBB
bundle branch block heart block - primary, secondary, tertiary
30
what is the relevance of atrial fibrillation
can lead to blood clot formation
31
what is an ECG
detects phasic change in potential difference between two electrodes - on surface of heart or on limbs - recorded on oscilloscope/ computer/ paper
32
what is an ECG useful for
diagnosis of arrythmias, post MI damage, congenital/ iatrogenic abnormalities
33
what are the stages of an ECG
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
clinical relevance of ECG results (look over diagram in control of CV system notes)
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
process of SAN AP
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
what makes SAN exhibit automaticity
reduced permeability to K
37
what happens to HR if K+ permeability increases
longer time to threshold = fewer BPM action of ACh from vagus nerve
38
what happens to HR if Ca2+ permeability increases
shorter time to threshold = higher BPM action of (nor)adrenaline
39
process of Purkinje AP
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
contraction of cardiac muscle
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
clinical relevance of process of contraction of cardiac muscle
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
how does an increase in SV increase HR
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
types of androreceptors
exist in A and B forms with subtypes of each
44
what type of androreceptor is major in the heart
B1 on nodal tissue, conducting system and myocardium
45
what does B1 androreceptor do
bind to NorA released by sympathetic nerves but also circulating adrenaline
46
what response dose B1 create
positive ionotropy (force of contraction) positive chronotropy (increase HR) positive lusitropy (increase in speed of relaxation) positive dromotropy (speed of conduction)
47
what is the clinical relevance of B1 androreceptor
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
which two areas of the heart does the vagus nerve terminate in
right vagus - SAN left vagus -> AVN release of ACh activates M2 receptors which reduces HR - increased K+ permeability
49
clinical relevance of vagus nerve terminations in the SAN/ AVN
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)

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