CARDIO Flashcards
Describe the general structure of a cardiac myocyte..
type of straited muscle fibre
complex arrangement with branched structure whereby adjacent cells are linked by intercalated discs and gap junctions - to support quick ionic diffusion and spread of AP.
elongated structure - 100um x 20um
single nucleus centrally located
many mitochondria - aerobic respiration
membrane - invaginations T tubules - spread AP to centre of cell, increase S.A for ion channels
Sarcoplasmic reticulum for calcium storage - ryanodine receptors and SERCA to coordinate release and re-uptake.
associated with dense capillary bed - aerobic respiration
difference between cardiac and skeletal muscle
cardiac - more mitochondria, gap junctions, denser capillary bed , single nucleus
skeletal - multinucleated, triad T tubule with SR, ryanodine 1 receptors
both straited
explain the macroscopic arrangement of cardiac muscle that adapts it to function…
looped and helical overlapping muscle structure arranged to contract and expel blood in correct direction e.g. ventricles up into arteries.
what is the function of the intercalated disc?
provides electrical and metabolic continuity between myocytes
gap junctions = connexons = pore = fast spread of AP to allow coordinated contraction
structural integrity provided by desmosome junction complex - anchoring of cytoskeleton of 2 cells - increases strength during contraction
describe the structure of a sarcomere..
this is the contractile unit of a muscle cell.
consists of thick and thin filaments containing myosin and actin respectively
M line in the middle
bound by 2 Z lines
thin filament consists of actin (protein polymer) strands. Encircling this is tropomyosin and troponin complex of T,I and C.
thick filament consists of myosin filaments and their heads.
many organised in parallel and connected to cytoskeleton of the cell. means that during contraction when actin is pulled across myosin, the sarcomere shortens and this is transmitted throughout the whole cell, shortening the muscle fibre.
what is the function of troponin
troponin consists of 3 subunits - T, I and C
this is involved in sensing Ca within myocyte as a result of AP and moving tropomyosin away from actin-myosin binding site on actin.
hence plays a role in excitation- contraction couple
Troponin C bind Ca
Troponin T binds tropomyosin
I - unclear role.
what receptors exist in the heart?
adrenoceptors - B1 predominantely (B2 on coronaries)
muscarinic receptors - M2
others
glucagon GPCR Gs
Adenosine
histamine receptors - chronotropy and ionotropy
dopamine receptors - coronary vasculature (D1)
non-receptors but may be targetted by drugs = L type Ca channels,
describe the cardiac cycle…
divided into diastole and systole - usually 2/3 of the time spent in diastole, although this shortens with increased HR
which are further divided into 5 stages.
DIASTOLE
* isovolumetric relaxation - immediately after systole i.e. dicrotic notch position. all valves closed, atrial fill.
* ventricular filling phase - AV valve opens, SL closed. atria emptying into ventricles.
SYSTOLE
* atrial contraction - remaining 20% atria empty
* isovolumetric contraction - both valves closed, pressure builds up.
* ejection phase - SL valves open , blood ejected into aorta, initially rapid, then slows
draw a pressure - time curve to describe valvular changes and events during cardiac cycle…
1 - atrial systole (AV are open)
2 - AV valves close
3 - Isovolumetric contraction - rapid rise in ventricular pressure
4 - SL valves open + rapid ejection- continued rise in ventricular pressure but starts to curve round. aortic pressure rises as blood ejected out.
5 - reduced ejection
6 - SL close + isovolumetric relaxation - back flow in aortic - dicrotic notch
7 - rapid filing, AV open
important to label axis - x axis -0.2ms at start of contraction to 0.5ms at the end. cycle in total 0.8ms
pressures in aorta = 120/80
LA = 8-10mmJg
LV = 120- 0mmHg
start by drawing ventricular curve first, then aortic, then atrial.
what are the pressures of the right side of the heart…
RA = 0 to 4mmHg
RV = 25/0mmHg
Pulmoanry artery 25/10mmHg
draw a volume time curve for LV
1 - atrial sysole - remaining 20% enters
2 - isovolumetric contraction - no change in volume
3 - ejection phase - drop in volume
4 - isovolumetric relaxation
5 - diastole and filling phase
volume from 50 to 130
thus SV 80ml
time = 0.8ms in total
contraction = 0.2-0.5 ms
describe the JVP waveform
a = atrial contraction
c = tricuspid valve closes and isovolumetric contraction bulges tricuspid upwards
x descent = ejection phase, draws blood out, pulling heart and atria down
v wave = atrial filling against closed tricuspid
y descent = tricuspid valve opens and atria empty
pressure 4-12mmHg
normal JVP max around 8-12mmHg
time 0.8ms
describe the changes in the aortic pressure graph
pressure ranges 80-120mmHg
aortic valve opens at end of isovolumetric contraction and begining of ejection phase
blood ejected into aorta - increases pressure.
eventually aortic pressure extends ventricle
delay in closure of the valve since kinetic energy of blood driving it forwards
eventually back flow and closure of SL valve - dicrotic notch as it causes elastic recoil from stretch of this back flow.
aortic pressures gradually drop until next contraction, as blood leaves aorta to systemic circulation.
what do the different heart sounds correspond to?
1 = AV valve closure
2 = SL valve closure
slight splitting in inspiration - left side closes before right due to negative thoracic pressure, holding right side open for longer.
other heart sounds
3rd = blood flow in ventricular filling due to tensing of chordae tendinae. normal in children, athletes
4th = blood hitting a stiff ventricle in atrial systole- pathological - HTN, aortic stenosis.
when might a 3rd heart sound be pathological?
dilated ventricle e.g. congestive HF
where are heart sounds heard?
aortic = 2nd intercostal space, right side sternum, radiates to carotids
pulmonary = 2nd intercostal, left side
tricuspid = 4th intercostal, left side
mitral = apex = 5th intercostal mid clav line
what causes pathological splitting of heart sounds?
normally split in inspiration where left side closes first.
may be reversed e.g. systemic HTN, aortic stenosis, aortic regurgitation
may be exagerated e.g. mitral regurg, pulmonary stenosis, pulmonary artery HTN
what are the effects of HR on the cardiac cycle
shortening of diastole
some shortening of systole
draw and explain a pressure -volume loop
volume on x
pressure on y
1= ESV - around 50ml
2 = ventricular filling phase
3 = EDV = 130 ml
4 = isovolumetric contraction
5 = ejection phase - SV 80ml
6 = isovolumetric relaxation
how is venticular stroke work calculared?
pressure x volume
i.e. area inside curve
describe the end diastolic and end systolic pressure volume relationship…
as EDV increases, i.e. increased preload, further stretch of myocytes and SV increases. results in a wider PV loop
can plot the EDV vs pressure on a graph ..
can see gradual increase in EDV without significant increase in pressure and this allows for SV to be matched. eventually theres a sharp rise. The steeper the gradient, the less compliant the heart, i.e. HTN, cardiomyopathy
for ESV curve - as volume in heart at end of systole increases, so does pressure. the steeper this relationship, the better the contractility i.e. a good heart will remain maximally contracted at end of systole and increase pressure, whereas weak heart will stretch with added volume, reducing efficiency of contraction.
draw P-V curve for increased preload, afterload and contractility …
Ea represents afterload
the curve sits between these lines
what happens to PV loop in IHD
IHD will result in areas that bulge out with contraction due to scarring.
hence not a straight curve - will be slanted to the left
also loss of diastolic function - hence the EDV curve more steep
loss of ionotrophy - ESV curve shallower
overall reduced SV