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Cardiovascular teach Flashcards

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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
what limits cardiac output?
myocardial connective tissue | pericardial sac - cardiac tamponade
26
afterload
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
27
what increases afterload?
hypertension aortic stenosis/ regurgitation inadequate perfusion to kidneys
28
what happens when there is a reduction in contractility?
a reduction in the ventricles ability to contract would result in a reduction in cardiac output
29
what factors affect contractility?
sympathetic nervous system - noradrenaline or adrenaline on Beta 1 receptors Hormonal - circulating adrenaline
30
how does adrenaline increase contractility?
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
31
what is ejection fraction?
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
32
what is the clinical importance of ejection fraction?
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
33
regulation of heart rate
neuronal and endocrine regulation Increase HR - noradrenaline/ adrenaline on sympathetic beta 1 receptors or hormonal adrenaline Decrease HR - parasympathetic via muscarinic 2 receptor
34
What is the atrial reflex
Bainbridge reflex adjusts heart rate on venous return stretch receptors in right atrium increases sympathetic activity to the heart
35
how does the sympathetic nervous system affect heart rate?
``` 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 ```
36
how does the parasympathetic nervous system affect heart rate?
``` 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 ```
37
Beta 1 receptor blockage
``` 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 ```
38
calculating BP
mean arterial blood pressure = cardiac output x systemic vascular resistance
39
how is BP regulated?
neurological | humoral
40
neurological regulation of BP
autonomic NS short-term regulation influences cardiac output and vascular resistance
41
humoral regulation of BP
``` aldosterone adrenaline ADH/ vasopressin atrial and brain natriuretic protein Angiotensin II Short and long term regulation influences vascular resistance and blood volume ```
42
how is BP regulation neurologically?
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
what happens in the nerve system when there is increased BP?
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
what happens in the nerve system when there is decreased BP?
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
hormonal regulation of BP
long term when there is a decrease in BP renin released from juxtaglomerular cells starts RAAS
46
when is renin released?
- 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
RAAS
renin-angiotensin-aldosterone system
48
what to do when clinic BP = or over 140/90mmHg
offer ABPM or HBPM
49
following ABPM or HBPM if <135/85mmHg
not hypertensive | monitor
50
following ABPM or HBPM if > or = 135/85mmHg
``` 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
following ABPM or HBPM if > or = 150/95mmHg
stage 2 hypertension | treat all patients, regardless of age
52
Treatment options for hypertension
``` ACE inhibitors angiotensin receptor blockers/ ARBs Ca2+ channel blockers Thiazide-like diuretic Loop diuretic ```
53
ACE inhibitors
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
how do ACE inhibitors work?
inhibit angiotensin converting enzyme which reduces aldosterone production and reduces increase in BP from RAAS angiotensin converting enzyme converts angiotensin I to II
55
angiotensin receptor blockers
usually end with -sartan e.g. losartan usually used as an alternative to ACE inhibitors should its side effects become intolerable
56
how do ARBs work?
similar mechanism to ACE by blocking angiotensin II receptors to block its action and reduce RAAS's influence on increasing BP
57
How do Ca2+ channel blockers work?
blocks L-type channels in smooth muscles (arterial walls --> vasodilation) and cardiac muscles
58
Ca2+ channel blockers
e.g. amlodipine | verampril and dilitiazem are designed to slow depolarisation in the SAN to reduce heart rate
59
Thiazide-like diuretics
e.g. bendrofluazide
60
How do thiazide-like diuretics work?
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
Loop diuretics
e.g. Furosemide | used in resistant hypertension
62
how do loop diuretics work?
inhibits NKCC co-transporter in the ascending loop of henle | very effective natruiresis - sodium excretion in urine
63
Beta blockers
usually end with -ol | e.g. propanolol
64
how do beta blockers work?
inhibit beta 1 receptor stimulation inhibits sympathetic effect on the heart reduces heart rate and contractility
65
mineralocorticoid receptor antagonist
blocks aldosterone's action by inhibiting intracellular action increased Na+ excretion decreases extracellular fluid e.g. spironolactone
66
Glycosides
e.g. Digoxin useful in treating AF side effect is yellow vision and potential arrhythmias
67
How do glycosides work?
``` inhibits Na+/K+ pump secondary exchange of Ca2+/Na+ is inhibited increased Ca2+ increase ionotropicity slows a-V conduction ```
68
how to treat hypertension in under 55 year olds
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
how to treat hypertension in over 55 year olds or people with Afro/ Caribbean origin
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
lead 1
aVR is negative | aVL is positive
71
lead 2
aVR is negative | aVF is positive
72
lead 3
aVL is negative | aVF is positive
73
chest leads
6 leads surrounding the chest
74
what are the different parts of the ECG trace?
``` P wave QRS complex T wave P-Q interval S-T segment Q-T interval ```
75
P wave
atrial depolarisation
76
QRS complex
ventricular depolarisation
77
T wave
ventricular repolarisation | smaller and slower than QRS complex because repolarisation is slower than depolarisation
78
P-Q interval
time between end of P wave and start of QRS complex
79
S-T segment
begins at end of S wave and ends at the start of the T wave
80
Q-T interval
time from start of Q wave to the end of the T wave
81
how to read an ECG?
``` rhythm of ventricles rate of ventricles P wave rhythm and rate - atria PR normal duration and constant QRS duration ```
82
NSTEMI
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
STEMI
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
hyperkalaemia
raised T waves | QRS widening
85
hypertrophy
tall QRS
86
atrial fibrillation
lack of P waves
87
ventricular fibrillation
haywire ECG
88
1st degree heart block
all SAN impulses go through ventricles but are delayed long P-R intervals Normal QRS
89
2nd degree heart block
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
3rd degree heart block
no link between P waves and QRS complexes | wide QRS complexes
91
Bundle branch block
left and right
92
left BBB
W shape in QRS complex of V1 and M in QRS complex of V6
93
right BBB
M shape in QRS complex of V1 and W in QRS complex of V6
94
what is anaemia?
reduced ability to carry oxygen
95
what causes anaemia?
decreased RBC production increased blood loss increased RBC breakdown
96
anaemia in men
<130g/L
97
anaemia in women
<120g/L - non pregnant
98
anaemia in children
<120g/L
99
types of anaemia
``` normocytic microcytic macrocytic AND hypochromic normochromic ```
100
causes of microcytic anaemia
iron deficiency anaemia of chronic disease thalassaemia sideroblastic
101
causes of normocytic anaemia
``` bone marrow failure acute blood loss chronic kidney disease rheumatic disease haemolytic anaemia ```
102
causes of macrocytic anaemia
B9 deficiency B12 deficiency alcohol and liver disease drugs - azathiprine and methotrexate
103
what causes a reduction in contractility?
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
what does sympathetic stimulation do in the heart?
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

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