Cardiovascular teach Flashcards
cardiac conduction
SAN AVN Bundle of His Left bundle branch Right bundle branch
What does the AV node do?
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
what do Purkinje fibres do?
depolarise from in to out - opposite of perfusion
how many stages are there in the cardiac myocyte action potential?
0-4
what are the stages of a cardiac myocyte action potential
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
cardiac myocyte action potential
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
what does the antiport system do?
to sustain the intracellular/ extracellular gradient it exchanges Ca2+ for Na+
pacemaker cells
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
shape of pacemaker action potential
similar to a nerve action potential but still involves calcium t-type and l-type channels and slow Na+ channels
pacemaker action potential
fires without stimulation
this is because of the consciously open leaky Na+ ion channels
normal heart rate
100bpm
but is continuously regulated by parasympathetic and sympathetic nervous system maintaining it at 70bpm
cardiac cycle
pressure in the left heart is greater then that of the right heart
right atrium pressure =
central venous pressure = JVP
diastole
phase of the heartbeat when the heart muscle relaxes and allows the chambers to fill with blood
systole
contraction of the heart muscles to eject blood
what is average pressure in aorta?
120/70mmHg
what is isovolumetric contraction?
ventricles contract so there is an increase in pressure
all valves are closed so no blood can escape so the volume stays the same
ventricular ejection
ventricular pressure>arterial pressure
aortic and pulmonary valves open
blood is expelled out of the ventricles down its pressure gradient
what is isovolumetric relaxation?
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
ventricular filling
atrial pressure is increased so tricuspid and mitral valves open
blood flows down its pressure gradient from the atria into ventricles
cardiac output
heart rate x stroke volume
what factors affect the cardiac output?
preload
afterload
contractility
heart rate
what is preload?
increases with increased venous return to the heart
increased end diastolic volume = increased contractility
this means a greater stroke volume
starling’s law
length force relationship
what limits cardiac output?
myocardial connective tissue
pericardial sac - cardiac tamponade
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
what increases afterload?
hypertension
aortic stenosis/ regurgitation
inadequate perfusion to kidneys
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
what factors affect contractility?
sympathetic nervous system - noradrenaline or adrenaline on Beta 1 receptors
Hormonal - circulating adrenaline
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
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
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
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
What is the atrial reflex
Bainbridge reflex
adjusts heart rate on venous return
stretch receptors in right atrium
increases sympathetic activity to the heart
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
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
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
calculating BP
mean arterial blood pressure = cardiac output x systemic vascular resistance
how is BP regulated?
neurological
humoral
neurological regulation of BP
autonomic NS
short-term regulation
influences cardiac output and vascular resistance
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
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
what happens in the nerve system when there is increased BP?
- increase in BP causes stimulation of the baroreceptors and glossopharyngeal and vagus nerve innervation to the medulla oblongata
- increased parasympathetic activity from the medulla oblongata to the SAN in heart via vagus nerve
- reduces HR and reduces cardiac output
- reduction of sympathetic activity so heart rate decreases further and there is vasodilation of blood vessels, reducing systemic vascular resistance.
what happens in the nerve system when there is decreased BP?
- fall in BP causes a reduction in baroreceptor stimulation so there is less innervation of the glossopharyngeal and vagus nerves
- there is an increased sympathetic and decreased parasympathetic response from the cardioregulatory and vasomotor centre of the brain
- increased sympathetic activity increases HR, increases cardiac output and vasoconstriction, increasing systemic vascular resistance
- decreased parasympathetic activity, decreasing HR
hormonal regulation of BP
long term
when there is a decrease in BP renin released from juxtaglomerular cells
starts RAAS
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
RAAS
renin-angiotensin-aldosterone system
what to do when clinic BP = or over 140/90mmHg
offer ABPM or HBPM
following ABPM or HBPM if <135/85mmHg
not hypertensive
monitor
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
following ABPM or HBPM if > or = 150/95mmHg
stage 2 hypertension
treat all patients, regardless of age
Treatment options for hypertension
ACE inhibitors angiotensin receptor blockers/ ARBs Ca2+ channel blockers Thiazide-like diuretic Loop diuretic
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
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
angiotensin receptor blockers
usually end with -sartan
e.g. losartan
usually used as an alternative to ACE inhibitors should its side effects become intolerable
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
How do Ca2+ channel blockers work?
blocks L-type channels in smooth muscles (arterial walls –> vasodilation) and cardiac muscles
Ca2+ channel blockers
e.g. amlodipine
verampril and dilitiazem are designed to slow depolarisation in the SAN to reduce heart rate
Thiazide-like diuretics
e.g. bendrofluazide
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
Loop diuretics
e.g. Furosemide
used in resistant hypertension
how do loop diuretics work?
inhibits NKCC co-transporter in the ascending loop of henle
very effective natruiresis - sodium excretion in urine
Beta blockers
usually end with -ol
e.g. propanolol
how do beta blockers work?
inhibit beta 1 receptor stimulation
inhibits sympathetic effect on the heart
reduces heart rate and contractility
mineralocorticoid receptor antagonist
blocks aldosterone’s action by inhibiting intracellular action
increased Na+ excretion
decreases extracellular fluid
e.g. spironolactone
Glycosides
e.g. Digoxin
useful in treating AF
side effect is yellow vision and potential arrhythmias
How do glycosides work?
inhibits Na+/K+ pump secondary exchange of Ca2+/Na+ is inhibited increased Ca2+ increase ionotropicity slows a-V conduction
how to treat hypertension in under 55 year olds
- ACE inhibitor
- add calcium channel blocker
- add thiazide diuretic
- if K+ or = add spironolactone. If K+> 4.5 add a higher dose thiazide-like diuretic
- If further therapy not tolerate or ineffective consider alpha or beta blocker
how to treat hypertension in over 55 year olds or people with Afro/ Caribbean origin
- Calcium channel blocker
- add ACE inhibitor
- add thiazide diuretic
- if K+ or = add spironolactone. If K+> 4.5 add a higher dose thiazide-like diuretic
- If further therapy not tolerate or ineffective consider alpha or beta blocker
lead 1
aVR is negative
aVL is positive
lead 2
aVR is negative
aVF is positive
lead 3
aVL is negative
aVF is positive
chest leads
6 leads surrounding the chest
what are the different parts of the ECG trace?
P wave QRS complex T wave P-Q interval S-T segment Q-T interval
P wave
atrial depolarisation
QRS complex
ventricular depolarisation
T wave
ventricular repolarisation
smaller and slower than QRS complex because repolarisation is slower than depolarisation
P-Q interval
time between end of P wave and start of QRS complex
S-T segment
begins at end of S wave and ends at the start of the T wave
Q-T interval
time from start of Q wave to the end of the T wave
how to read an ECG?
rhythm of ventricles rate of ventricles P wave rhythm and rate - atria PR normal duration and constant QRS duration
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
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
hyperkalaemia
raised T waves
QRS widening
hypertrophy
tall QRS
atrial fibrillation
lack of P waves
ventricular fibrillation
haywire ECG
1st degree heart block
all SAN impulses go through ventricles but are delayed
long P-R intervals
Normal QRS
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
3rd degree heart block
no link between P waves and QRS complexes
wide QRS complexes
Bundle branch block
left and right
left BBB
W shape in QRS complex of V1 and M in QRS complex of V6
right BBB
M shape in QRS complex of V1 and W in QRS complex of V6
what is anaemia?
reduced ability to carry oxygen
what causes anaemia?
decreased RBC production
increased blood loss
increased RBC breakdown
anaemia in men
<130g/L
anaemia in women
<120g/L - non pregnant
anaemia in children
<120g/L
types of anaemia
normocytic microcytic macrocytic AND hypochromic normochromic
causes of microcytic anaemia
iron deficiency
anaemia of chronic disease
thalassaemia
sideroblastic
causes of normocytic anaemia
bone marrow failure acute blood loss chronic kidney disease rheumatic disease haemolytic anaemia
causes of macrocytic anaemia
B9 deficiency
B12 deficiency
alcohol and liver disease
drugs - azathiprine and methotrexate
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
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
