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Physiology > Cardiovascular teach > Flashcards

Cardiovascular teach Flashcards

1
Q

cardiac conduction

A 
SAN
AVN
Bundle of His
Left bundle branch
Right bundle branch
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2
Q

What does the AV node do?

A

gate in the firewall between atria and ventricles
slows conduction - 100ms
allows time for atrial emptying
protects ventricles from atrial tachyarrhythmias
affected by autonomic NS

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3
Q

what do Purkinje fibres do?

A

depolarise from in to out - opposite of perfusion

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4
Q

how many stages are there in the cardiac myocyte action potential?

A

0-4

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5
Q

what are the stages of a cardiac myocyte action potential

A

0 - rapid depolarisation, Na+ fast channels open and there is sodium ion influx, some Ca2+ helps via T-type
1 - +20mV repolarisation, previous channels close and K+ channels open causing outflow of K+
2 - Ca2+ l-type channels open causing repolarisation to slow down and causes a plateau
3 - Ca2+ l-type channels close and only K+ channels are open so only K+ outflow and rapid repolarisation
4 - at resting potential K+ channels are closed

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6
Q

cardiac myocyte action potential

A

100 times longer than normal nerve due to l-type calcium ion channels and the involvement of calcium ions
this means there can be adequate ventricular contraction
there is a prolonged refractory period
allowing for ion channel inactivation
prevents tetany

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7
Q

what does the antiport system do?

A

to sustain the intracellular/ extracellular gradient it exchanges Ca2+ for Na+

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8
Q

pacemaker cells

A

specialised cells in the atria
can be found all over the atria but have the highest concentration in the SA node
they fire automatically without stimulation

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9
Q

shape of pacemaker action potential

A

similar to a nerve action potential but still involves calcium t-type and l-type channels and slow Na+ channels

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10
Q

pacemaker action potential

A

fires without stimulation

this is because of the consciously open leaky Na+ ion channels

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11
Q

normal heart rate

A

100bpm

but is continuously regulated by parasympathetic and sympathetic nervous system maintaining it at 70bpm

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12
Q

cardiac cycle

A

pressure in the left heart is greater then that of the right heart

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13
Q

right atrium pressure =

A

central venous pressure = JVP

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14
Q

diastole

A

phase of the heartbeat when the heart muscle relaxes and allows the chambers to fill with blood

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15
Q

systole

A

contraction of the heart muscles to eject blood

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16
Q

what is average pressure in aorta?

A

120/70mmHg

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17
Q

what is isovolumetric contraction?

A

ventricles contract so there is an increase in pressure

all valves are closed so no blood can escape so the volume stays the same

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18
Q

ventricular ejection

A

ventricular pressure>arterial pressure
aortic and pulmonary valves open
blood is expelled out of the ventricles down its pressure gradient

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19
Q

what is isovolumetric relaxation?

A

the ventricles relax decreasing the pressure
all valves are closed so no blood can escape so the volume is the same
arterial pressure>ventricular pressure>atrial pressure

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20
Q

ventricular filling

A

atrial pressure is increased so tricuspid and mitral valves open
blood flows down its pressure gradient from the atria into ventricles

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21
Q

cardiac output

A

heart rate x stroke volume

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22
Q

what factors affect the cardiac output?

A

preload
afterload
contractility
heart rate

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23
Q

what is preload?

A

increases with increased venous return to the heart
increased end diastolic volume = increased contractility
this means a greater stroke volume

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24
Q

starling’s law

A

length force relationship

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25
Q

what limits cardiac output?

A

myocardial connective tissue

pericardial sac - cardiac tamponade

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26
Q

afterload

A

pressure at which the heart needs to pump against

the higher this pressure in the systemic or pulmonary circulation the more work the heart needs to do

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27
Q

what increases afterload?

A

hypertension
aortic stenosis/ regurgitation
inadequate perfusion to kidneys

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28
Q

what happens when there is a reduction in contractility?

A

a reduction in the ventricles ability to contract would result in a reduction in cardiac output

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29
Q

what factors affect contractility?

A

sympathetic nervous system - noradrenaline or adrenaline on Beta 1 receptors
Hormonal - circulating adrenaline

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30
Q

how does adrenaline increase contractility?

A

binds to beta 1 receptor - GPCR which activates adenyl cyclase which causes ATP to be converted into cAMP which activates protein kinase. Causes l-type calcium ion channels to open and so calcium moves into the cell. Also activates release of calcium from the sarcoplasmic reticulum and activates other effects that increase contractility by causing smooth muscle contraction

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31
Q

what is ejection fraction?

A

a measure of the ventricles ability to contract
essentially what % of the blood in the ventricle is ejected
ratio of the stroke volume to end diastolic volume
EF = SV/EDV

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32
Q

what is the clinical importance of ejection fraction?

A

measure of the ability of the ventricle to contract
>75% could indicate hypertrophic cardiomyopathy
40-55% abnormal but maybe clinically insignificant
<40% - heart failure, can be very low

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33
Q

regulation of heart rate

A

neuronal and endocrine regulation
Increase HR - noradrenaline/ adrenaline on sympathetic beta 1 receptors or hormonal adrenaline
Decrease HR - parasympathetic via muscarinic 2 receptor

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34
Q

What is the atrial reflex

A

Bainbridge reflex
adjusts heart rate on venous return
stretch receptors in right atrium
increases sympathetic activity to the heart

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35
Q

how does the sympathetic nervous system affect heart rate?

A 
increases HR
increases membrane permeability to Na+ 
Na+ travels across the membrane faster
so reduces depolarisation time
resting membrane potential is increased 
easier to reach the threshold potential
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36
Q

how does the parasympathetic nervous system affect heart rate?

A 
decreases HR 
Reduced membrane permeability to Na+ 
increased membrane permeability to K+
reduces the frequency of impulses
increasing depolarisation time
lowers the resting membrane potenial
harder to reach the membrane potential
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37
Q

Beta 1 receptor blockage

A 
less cAMP being formed
reduced Ca2+ release
reduced contractility
reduces HR
you get a reduce sympathetic innervation
so reduced membrane permeability to Na+
reduced renin secretion via B1 inhibition of juxtaglomerular cells
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38
Q

calculating BP

A

mean arterial blood pressure = cardiac output x systemic vascular resistance

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39
Q

how is BP regulated?

A

neurological

humoral

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40
Q

neurological regulation of BP

A

autonomic NS
short-term regulation
influences cardiac output and vascular resistance

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41
Q

humoral regulation of BP

A 
aldosterone
adrenaline
ADH/ vasopressin
atrial and brain natriuretic protein 
Angiotensin II
Short and long term regulation
influences vascular resistance and blood volume
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42
Q

how is BP regulation neurologically?

A

arterial baroreceptors in aortic arch and carotid sinus continuously monitor BP
these are mechanoreceptors that input into the cardiovascular centre of medulla oblongata
the aortic arch baroreceptors innervate the vagus nerve
the carotid sinus baroreceptors innervate glossopharyngeal nerve

43
Q

what happens in the nerve system when there is increased BP?

A
  1. increase in BP causes stimulation of the baroreceptors and glossopharyngeal and vagus nerve innervation to the medulla oblongata
  2. increased parasympathetic activity from the medulla oblongata to the SAN in heart via vagus nerve
  3. reduces HR and reduces cardiac output
  4. reduction of sympathetic activity so heart rate decreases further and there is vasodilation of blood vessels, reducing systemic vascular resistance.
44
Q

what happens in the nerve system when there is decreased BP?

A
  1. fall in BP causes a reduction in baroreceptor stimulation so there is less innervation of the glossopharyngeal and vagus nerves
  2. there is an increased sympathetic and decreased parasympathetic response from the cardioregulatory and vasomotor centre of the brain
  3. increased sympathetic activity increases HR, increases cardiac output and vasoconstriction, increasing systemic vascular resistance
  4. decreased parasympathetic activity, decreasing HR
45
Q

hormonal regulation of BP

A

long term
when there is a decrease in BP renin released from juxtaglomerular cells
starts RAAS

46
Q

when is renin released?

A
  • a low BP is detected in kidneys by baroreceptors
  • a decrease in sodium by macula densa in kidneys
  • sympathetic innervation of the beta 1 receptors
47
Q

RAAS

A

renin-angiotensin-aldosterone system

48
Q

what to do when clinic BP = or over 140/90mmHg

A

offer ABPM or HBPM

49
Q

following ABPM or HBPM if <135/85mmHg

A

not hypertensive

monitor

50
Q

following ABPM or HBPM if > or = 135/85mmHg

A 
stage 1 hypertension
treat if younger than 80 and:
- target organ damage
- established cardiovascular disease
- renal disease
- diabetes
- 10-year cardiovascular risk equivalent to 20% or greater
51
Q

following ABPM or HBPM if > or = 150/95mmHg

A

stage 2 hypertension

treat all patients, regardless of age

52
Q

Treatment options for hypertension

A 
ACE inhibitors
angiotensin receptor blockers/ ARBs
Ca2+ channel blockers
Thiazide-like diuretic
Loop diuretic
53
Q

ACE inhibitors

A

Angiotensin converting enzyme inhibitors:

  • end with -pril
  • e.g. ramipril
  • main side effect is dry cough likely due to bradykinin build up
  • look out for cough after hypertension diagnosis as it could be caused by starting the ACE Inhibitor
54
Q

how do ACE inhibitors work?

A

inhibit angiotensin converting enzyme which reduces aldosterone production and reduces increase in BP from RAAS
angiotensin converting enzyme converts angiotensin I to II

55
Q

angiotensin receptor blockers

A

usually end with -sartan
e.g. losartan
usually used as an alternative to ACE inhibitors should its side effects become intolerable

56
Q

how do ARBs work?

A

similar mechanism to ACE by blocking angiotensin II receptors to block its action and reduce RAAS’s influence on increasing BP

57
Q

How do Ca2+ channel blockers work?

A

blocks L-type channels in smooth muscles (arterial walls –> vasodilation) and cardiac muscles

58
Q

Ca2+ channel blockers

A

e.g. amlodipine

verampril and dilitiazem are designed to slow depolarisation in the SAN to reduce heart rate

59
Q

Thiazide-like diuretics

A

e.g. bendrofluazide

60
Q

How do thiazide-like diuretics work?

A

block Na+ absorption in kidney bu inhibiting the Na+/Cl- co-transporter
increases urine output which reduces blood volume
can cause vasodilation by reducing Ca2+ sensitivity in smooth muscles

61
Q

Loop diuretics

A

e.g. Furosemide

used in resistant hypertension

62
Q

how do loop diuretics work?

A

inhibits NKCC co-transporter in the ascending loop of henle

very effective natruiresis - sodium excretion in urine

63
Q

Beta blockers

A

usually end with -ol

e.g. propanolol

64
Q

how do beta blockers work?

A

inhibit beta 1 receptor stimulation
inhibits sympathetic effect on the heart
reduces heart rate and contractility

65
Q

mineralocorticoid receptor antagonist

A

blocks aldosterone’s action by inhibiting intracellular action
increased Na+ excretion
decreases extracellular fluid
e.g. spironolactone

66
Q

Glycosides

A

e.g. Digoxin
useful in treating AF
side effect is yellow vision and potential arrhythmias

67
Q

How do glycosides work?

A 
inhibits Na+/K+ pump 
secondary exchange of Ca2+/Na+ is inhibited
increased Ca2+ 
increase ionotropicity 
slows a-V conduction
68
Q

how to treat hypertension in under 55 year olds

A
  1. ACE inhibitor
  2. add calcium channel blocker
  3. add thiazide diuretic
  4. if K+ or = add spironolactone. If K+> 4.5 add a higher dose thiazide-like diuretic
  5. If further therapy not tolerate or ineffective consider alpha or beta blocker
69
Q

how to treat hypertension in over 55 year olds or people with Afro/ Caribbean origin

A
  1. Calcium channel blocker
  2. add ACE inhibitor
  3. add thiazide diuretic
  4. if K+ or = add spironolactone. If K+> 4.5 add a higher dose thiazide-like diuretic
  5. If further therapy not tolerate or ineffective consider alpha or beta blocker
70
Q

lead 1

A

aVR is negative

aVL is positive

71
Q

lead 2

A

aVR is negative

aVF is positive

72
Q

lead 3

A

aVL is negative

aVF is positive

73
Q

chest leads

A

6 leads surrounding the chest

74
Q

what are the different parts of the ECG trace?

A 
P wave
QRS complex
T wave
P-Q interval
S-T segment 
Q-T interval
75
Q

P wave

A

atrial depolarisation

76
Q

QRS complex

A

ventricular depolarisation

77
Q

T wave

A

ventricular repolarisation

smaller and slower than QRS complex because repolarisation is slower than depolarisation

78
Q

P-Q interval

A

time between end of P wave and start of QRS complex

79
Q

S-T segment

A

begins at end of S wave and ends at the start of the T wave

80
Q

Q-T interval

A

time from start of Q wave to the end of the T wave

81
Q

how to read an ECG?

A 
rhythm of ventricles
rate of ventricles
P wave rhythm and rate - atria
PR normal duration and constant
QRS duration
82
Q

NSTEMI

A

non ST elevation myocardial infarction
better prognosis than STEMI as it is potentially reversible
ischaemic damage is subendocardial - not full thickness of the heart wall
Coronary arteries are on the outside so perfusion starts from the epicardium into the endocardium
so if the clot resolves quickly the ischaemic damage can be reversed/ limited to some of the inner wall
ST depression

83
Q

STEMI

A

ST elevation myocardial infarction
irreversible damage
same issue as NSTEMI - lack of perfusion
ischaemic damage starts deep in the heart wall and climbs outwards
STEMIs have the damage to the full thickness of the muscle wall
expect ST elevation

84
Q

hyperkalaemia

A

raised T waves

QRS widening

85
Q

hypertrophy

A

tall QRS

86
Q

atrial fibrillation

A

lack of P waves

87
Q

ventricular fibrillation

A

haywire ECG

88
Q

1st degree heart block

A

all SAN impulses go through ventricles but are delayed
long P-R intervals
Normal QRS

89
Q

2nd degree heart block

A

partial blockage
P-R intervals get longer with each wave until it misses a QRS then resets
or
P-R intervals area constant with sudden losses of QRS

90
Q

3rd degree heart block

A

no link between P waves and QRS complexes

wide QRS complexes

91
Q

Bundle branch block

A

left and right

92
Q

left BBB

A

W shape in QRS complex of V1 and M in QRS complex of V6

93
Q

right BBB

A

M shape in QRS complex of V1 and W in QRS complex of V6

94
Q

what is anaemia?

A

reduced ability to carry oxygen

95
Q

what causes anaemia?

A

decreased RBC production
increased blood loss
increased RBC breakdown

96
Q

anaemia in men

A

<130g/L

97
Q

anaemia in women

A

<120g/L - non pregnant

98
Q

anaemia in children

A

<120g/L

99
Q

types of anaemia

A 
normocytic
microcytic
macrocytic
AND
hypochromic
normochromic
100
Q

causes of microcytic anaemia

A

iron deficiency
anaemia of chronic disease
thalassaemia
sideroblastic

101
Q

causes of normocytic anaemia

A 
bone marrow failure
acute blood loss
chronic kidney disease
rheumatic disease
haemolytic anaemia
102
Q

causes of macrocytic anaemia

A

B9 deficiency
B12 deficiency
alcohol and liver disease
drugs - azathiprine and methotrexate

103
Q

what causes a reduction in contractility?

A

this can be from a reduction in cardiac muscle’s ability to contract caused by a weak, flabby ventricle
or can be a reduction in the compliance of the cardiac wall caused by a stiff, fibrotic ventricle

104
Q

what does sympathetic stimulation do in the heart?

A

sympathetic stimulation increases Na+ permeability in SAN which speeds up the rate of reaching threshold to fire and increases HR
sympathetic stimulation alters the phosphorylation of contractile proteins which increase the force of contractions

Physiology (46 decks)

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