cardiovascular system Flashcards
describe the general structure of the heart
surrounded by a protective, fluid-filled sac - the pericardium
has four chambers, two atria and ventricles
AV valves - tricuspid R, mitral L
SL valves - pulmonary and aortic
the right atrium receives deoxygenated blood from the systemic system etc…
describe the structure and function of valves
they prevent backflow
AV valves are connected to cardiac wall by chordae tendinae and papillary muscles
SL valves have three small fibrous nodules that come together to close
describe the layers of the heart wall
from outside-in:
1) Epicardium - made up of connective tissue and elastic fibres, produces pericardial fluid to reduce friction
2) Myocardium - thickest, made with collagen fibres, it’s involuntary striated muscle
3) Endocardium - smooth endothelial cells, has elastic fibres and some smooth muscle
describe all the areas of conducting cells in the heart
SAN = primary pacemaker
internodal tracts = between the two nodes
AVN = can actually take over as pacemaker if SAN is damaged
Bundle of His = with right and left bundle branches going to the two ventricles, which branch into purkinje fibres
the atria and ventricles are made up of mostly ehat cell?
contractile cells - APs lead to contraction and generate force
what are the four currents of the heart?
include what they do and where
1) Na+ current - largest, causes rapid depolarisation in the A and V muscle and the purkinje fibres
2) Ca2+ current - depolarisation, SAN and AVN, results in contraction of all cardiomyocytes
3) K+ current - repolarisation of all cardiomyocytes
4) Funny current - K+ and Na+ mix, inward current causing hyperpolarisation?, SAN, AVN + PF
on graphs for SAN and ventricular muscle, what does the electrical diastolic phase show in terms of currents?
calcium, potassium and funny current cause pacemaker activity (it’s the shallow part on the graphs)
what connects muscle fibre cells in the heart and why?
what structure is important in maintaining integrity?
what structure allows for a wave-like syncytium?
intercalated discs connect muscle cells so they can work in sync and ensure a good ejection of blood
desmosomes between these discs are important for integrity
gap junctions allowing AP propagation from cell to cell
how do T-tubules result in excitation-contraction coupling?
include details on muscle contraction
T tubules are deep invaginations in the sarcolemma, when wave of depolarisation passes along they ensure it is relayed to the core of the cell, resulting in Ca2+ release at the z line of the sarcomere
the T tubules interact with the sarcoplasmic reticulum via a dyad
the cytosolic Ca2+ (from T tubules) activates channels on sarcoplasmic reticulum to cause calcium induced calcium release - this Ca2+ binds to troponin C which releases troponin I, causing muscle contraction
what’s the difference in T tubules in contractile cells compared to the pacemaker and conducting cells?
L-type Ca2+ channels in T tubules release Ca2+ in contractile cells
T-type Ca2+ channels in pacemaker and conducting cells
the cardiac cycle has seven phases, what are they and what is happening in each one
Atrial systole (section A):
atria contract, AV valves open, ventricles fill further with blood (a lot of blood fills without contraction)
Isovolumetric ventricular contraction (section B):
PF activate, ventricles contract (systole)
AV valves close (sound 1)
Pressure increases hugely
Rapid ventricular ejection (section C):
V pressure exceeds aortic so SL valves open causing rapid blood ejection
MOST of the stroke volume is ejected
V vol decreases and arterial pressure increases
Atria begin to fill so atrial pressure inc, slowly
Reduced ventricular ejection (section D):
Ventricle are repolarised so are no longer contracting so pressure decreases
SL valves are open as blood is still being ejected but slower, so vol is still decreasing
Arterial volume is decreasing (as blood is elastically pushed to all other arteries)
Isovolumetric ventricular relaxation (section E):
After Vs fully repolarise, the Vs relax, so V pressure decreases
SL valves close as arterial pressure exceeds V pressure (sound 2)
Rapid ventricular filling (section F):
Atrial pressure exceeds ventricular, AV valves open
Ventricles benign to fill rapidly, vol increases but pressure remains low as no contraction
Reduced ventricular filling (section G):
LONGEST PHASE, last bit of the ventricles filling
what causes the 4 sounds of a heart beat?
S1 – “lub” caused by the closing of the AV valves
S2 – “dub” caused by the closing of semilunar valves
S3 – linked with flow of blood into the ventricles
S4 – linked with atrial contraction
what is an ECG and how does it work?
detects movement of ions in depolarisation/repolarisation as they create an electrical current
this extracellular current is an instantaneous vector so can be picked up by external electrodes, usually use 3 electrodes but there are 15
describe what a typical ECG trace looks like
small rise = P wave
after a little bit there’s a small dip = Q
massive rise = R
dip = S
makes this massive spike called the QRS complex
little break than another small wave = T wave
what do the sections of the ECG trace indicate?
The P wave indicates atrial depolarization, the QRS complex consists of a Q wave, R wave and S wave and represents ventricular depolarization
what is blood made up of?
plasma (ECF high in protein)
erythrocytes (RBCs)
leukocytes
platelets
what is the hematocrit?
centrifuge a blood sample, there’ll be loads of RBCs at the bottom
Height of the RBCs/Total height
what is in plasma?
its a watery solution of electrolytes, plasma proteins, carbs and lipids
most common proteins are:
albumin (1st)
fibrinogen (involved in clotting)
globulins
other coagulation factors
how are the principle proteins of the plasma viewed?
using gel electrophoresis, you can even turn your gel 90 degrees and apply a current again to separate further
erythrocytes - describe their structure in detail and why it is the way it is
no nucleus, biconcave to maximise SA:V ratio
has the membrane protein glycophorin, working with other proteins like spectrin, to anchor the cytoskeleton to the membrane - this is because RBCs experience a lot of pressure and need anchoring to maintain integrity
function of RBCs?
O2 from lungs to systemic system, CO2 from tissues to lungs
buffering acids and bases too
what are the three kinds of granulocytes (a class of white blood cell)?
neutrophils - phagocytose bacteria
eosinophils - combat parasites and viruses
basophils - release histamines, heparin the anticoagulant, and peroxidases
aside from granulocytes, what other kind of WBC are found in the blood?
monocytes - macrophages and dendritic cells (phagocytosis)
lymphocytes - B and T cells
describe the structure and contents of platelets
no nuclei
they have lysosomes, peroxisomes and mitachondria
alpha granules - these contain Von Willebrand Factor, fibrinogen which is CF 1, and CF 5
dense core granules - ATP, ADP, Ca, serotonin
platelet receptors on external coat
inner skeleton made of bands of microtubules
in platelets
1) why do dense core granules have serotonin?
2) what do the circumferential bands of microtubules do?
serotonin is uses to recruit other platelets
the tubulin microtubules maintain shape, and alter it upon activation
explain how platelets work in a negative feedback loop
platelets are produced by cells in the bone marrow called megakaryocytes
production of megakaryocytes is stimulated by TPO (thrombopoietin)
they then make platelets
platelets have thrombopoietin receptors as well, so as they increase in m=number, more TPO is occupied by platelet receptors, less is available to activate megakaryocyte production
as a result platelet levels go down, TPO is no longer all trapped up by platelet receptors and so can stimulate megakaryocyte production etc…
explain how velocity works in a blood vessel
think of blood as flowing concentric layers
outer layer experiences the most friction from the stationary vessel wall, so is the slowest, the layer beneath experiences friction from this slow moving outer layer, so is a little slow too (but not as much)
the central layer is the fastest
what factors influence blood viscosity?
viscosity = resistance to the sliding of shearing fluid layers
haematocrit (more red blood cells = higher viscosity)
fibrinogen plasma concentration
vessel radius
linear velocity
temeprature
what is a normal haematocrit value?
35% - 50%
explain what plasma skimming is and how it is prevented
red blood cells tend to accumulate at the centre of a blood vessel
so when a vessel branches, it takes more plasma than RBCs, lowering it’s haematocrit
to prevent this, a t branching points there is a small invagination of the vessel wall known as an arterial cushion
what is tank trading (RBCs)?
in small blood vessels, RBCs actually rotate their membranes, meaning two adjacent cells spin the plasma in order to keep themselves away from the blood vessel edges
blood flow is usually laminar and has a parabolic profile
how does turbulent flow occur?
when flow/velocity is really high
profile is no longer parabolic it becomes blunted
occurs when the radius is large and velocity is high - like in the aorta and during exercise
how does turbulence have clinical improtance?
it can be heard and is therefore used to detect murmurs
