AREA - area per unit volume is determined by capillary density
DIFFUSION RESISTANCE - affected by the nature of the molecule, the barrier and the capillary density
CONCENTRATION GRADIENT - the large the gradient the faster the diffusion rate, to maintain concentration gradient flow must be sufficient
SUPPLY & DEMAND - increasing metabolism > increased flow this is know as the perfusion rate.
what must the CVS supply to the different tissues of the body?
brain -750 ml/min
kidney - 1200 ml/min
heart - 300-1200 ml/min
skeletal muscle - 1000-16000 ml/min
skin - 200-2500ml/min
gut - 1400 -2400ml/min
in total - 5 - 25 l/min
how is blood flow regulated?
arterioles - resistance vessels
veins - capacitance vessels
structure of large arteries?
elastic to permit recoil > maintaining blood pressure during diastole
tunica intima: endothelium, narrow subendothelium with discontinuous elastic lamina
tunica media: 40-70 fenestrated elastic membranes with smooth muscle cells and collagen between lamellae
tunica adventitia: thin layers of fibroelastic connective tissue containing vasa vasorum, nerves and lymphatics
structure of muscular medium arteries?
tunica intima: endothelium, thick subendothelium - with internal elastic lamina
tunica media: 40 layers of smooth muscle joined by gap junctions to give co-ordinated contraction
tunica adventitia: thin layer of firbroelastic connective tissue with some vasa vasorum, nerves and lymphatics
structure of arterioles?
endothelium wrapped in smooth muscle cells
tunica adventitia is layers of fibroblasts
structure of meta-arterioles?
the smooth muscle is not continuous and instead forms pre-capillary sphincters
structure of capillaries?
what are the three types of capillaries?
single layer endothelium and basement membrane
pericytes are a branching outer layer that divide into smooth muscle cells and fibroblasts
there are three types of capillaries: fenestrated, sinusoids and continuous
continuous are most common and have tight cell junctions
fenestrated are found in the gut, endocrine glands and glomerulus
sinusoids are found in the liver, spleen and bone marrow they allow cells to move between blood and tissue
structure of venules?
post capillary venules are just endothelium and pericytes they are more permeable than capillaries
venules contain valves and gradually accumulate smooth muscle fibres which are the start of the tunica media
structure of medium veins?
tunica intima: thin
tunica media: 2-3 layers of smooth muscle cells
tunica adventitia: well developed
structure of large veins?
thin walls more connective tissue than muscle
larger diameter then associated arteries
well developed aadventitia
what are ateriovenous shunts?
miss out capillaries
what are vasa vasorum?
small blood vessels that supply large blood vessels with blood
what are venacomitantes?
veins that accompany arteries helping with blood temperature and return to the heart
what are varicose veins?
swollen enlarged veins
caused by dysfunctional valves which allow back flow of blood
describe the location of the heart
inferior middle mediastinum
between the sternum and the oesophagus
describe the pericardium
inner serous layer which itself is formed of an inner visceral layer and an outer perital layer - between these layers is a space with a few drops of lubricating fluid
there is then also a outermost fibrous layer
describe the features of cardiac muscle
3 layers - endocardium, myocardium, epicardium
low electrical resistance between the cells of the myocardium means they all contract together during systole
what are the pacemaker cells
found in the SA node control the rate of the heart
describe the cardiac cycle
at rest the pacemaker cells in the SA node produce approximately one action potential per second
this produces a short atrial systole followed by a longer ventricular systole (280ms)
this is followed by diastole (700 ms)
in diastole the ventricles relax and the pressure falls causing opening of the AV valves - blood can then flow from the atria into the ventricles throughout diastole
atrial systole pushes the remaining blood into the ventricles and then about 150 ms the ventricles contract - the rise in pressure forcibly closes the AV valves and once the pressure exceeds the diastolic pressure in the arteries the outflow valves open
what are the normal heart sounds?
s1 - lup - closure of AV valves at start of ventricular systole
s2 - dup - closure of outflow valve at the end of systole
draw the Jugular Venous Pressure
a = atrium contracting tricuspid valve open
c = small back flow into atrium as ventricle contracts
x = atrium relaxing then filling
v = atrium tense and full
y = tricuspid valve open
what are the normal pressures in the RA, LA, RV, LV, the pulmonary artery and the aorta
RA = 0-8mmHg
LA = 1-10 mmHg
RV = 15-30/0-8
LV = 100-140/1-10
pulmonary artery = 15-30/4-12
aorta = 100-140/60-90
where does the left anterior descending coronary artery supply?
anterior left ventricle
some right ventricle
where does the left circumflex artery supply?
posteriorlateral left ventricle
where does the right coronary artery supply?
AV & SA nodes
where does the posterior descending coronary artery supply?
describe simply the formation of the CVS during foetal development
Cephalocaudal folding brings heart into chest region
Lateral folding creates primative heart tube from fusion of endocardial tubes - this tube is suspended in a cavity by a membrane that degenerates
The tube receives blood supply from the caudal pole and begins to pump blood around the first aortic arch into the dorsal aorta
The tube continuous to elongate and on day 23 looping begins - (cephalic portion bends ventrally,
caudally and to the right AND caudal portion bends dorsally, cranially and to the left)
This creates the cardiac loop by day 28
Looping occurs so that the primordium of the RV is by the outflow tract and the primordium of the LV is by the inflow tract and the atrium is dorsal to the bulbus
After looping the atrium and ventricle communicate by the atrioventricular canal
The L and R horns are equal in size but venous return switches to the R – L reseeds and R horn is absorbed enlarging the atria
The RA develops from the sinous venosus and the primordial atrium. The LA develops from a small part of the primitive atrium and the proximal part of the pulmonary vessels
Once looping has occurred we need septation to have two pumps in series
Septation of the atrioventricular canal – growth of endocardial cushins
Atrial septation – septum primum grows down towards endocardial cushins, the gap is called the ostium primum, before it closes apoptosis forms the ostium secundum to replace it. The septum secundum then grows up leaving a crescent shape whole at the bottom called the foramen ovale (fossa ovalis after birth)
Ventricular septation – the muscular septum grows up forming most of the septum the membranous septum is made of CT and grows down from the cushins
Septation of the outflow tract – endocarcial cushins form in the truncus arteriosus as the grow they twist around each other forming a spiral septum
what is different in foetal circulation?
what must happen at birth?
lungs are non functional
oxygenated blood come via the placenta from the mother
blood comes via liver > RA > LA > LV > body
some blood goes into the RV so the muscle can develop but it by-passes the lungs using the ductus arteriosus
at birth the ductus arteriosus, RtoL shunt and the ductus venosus must all close
describe 4 acyanotic congenital heart defects
ASD - osteum secundum defect/patent foramen ovale/ primum atrial defect > increase pulmonary blood flow > RV volume overload > right heart failure - fixed splitting of s2
contraction of vascular and visceral smooth muscle
some endocrine and exocrine secretions
force and rate of heart contraction
describe the sympathetic innervation of the heart
SYPATHETIC - post ganglionic cardiac nerve from the sympathetic trunk innervates the SA & AV nodes and the myocardium . release of NA acts on B1 receptors inc. HR and force of contraction (in cAMP > phosphorylation of Ca channels > inc Ca entry > inc force of contraction) + increases slope of pacemaker potential
describe the parasympathetic innervation of the heart
PARASYMPATHETIC - 10th cranial nerve/vagus nerve synapses in wall of the heart with SA and AV nodes the post ganglionic cells release ACh with acts on M2 receptors > dec HR (-ve chronotrophic) and dec AV node conduction velocity. it also slows pacemaker potential by opening K channels via cAMP.
what affects can the ANS have on the vasculature?
most vessels = sympathetic innervation, A1 receptors sympathetic output normal = vasomotor tone, dec = dilation, inc = constriction
the property of a fluid that resists the force tending to cause the fluid to flow, the higher the viscosity the lower the velocity
what is poiseulles law?
resistance is proportional to rxrxrxr
why does it matter that blood vessels are connected together?
reduces the resistance of the capillaries as there are so many in parallel
why are distensible vessels useful?
as the vessel stretches the resistance falls
as the pressure drops the vessel collapses causing a cease in blood flow before the pressure reaches zero
what happens to the pressures in the arteries during the cardiac cycle?
what would happen if they had rigid walls?
arteries stretch during systole and recoil during diastole maintaining an even pressure
if the walls were rigid then pressure would be very high in systole and zero in diastole
what is reactive hyperaemia?
if the circulation to a part of the body is cut off for a short amount of time when blood flow is restored there is a massive increase in to this area for a short amount of time while metabolites (H, K, adenosine) which cause vasodilatation are washed away once they are washed away the SM of the BV can constrict again
what is autoregulation?
if supply pressure changes the flow to the tissue changes
this alters metabolite concentration
this alters arteriole resistance
thus correct blood flow to the tissue is maintained
draw a diagram of typical arterial pressure in a cardiac cycle
what happens when CO stays the same but TPR falls?
arterial pressure DOWN
venous pressure UP
what happens when CO stays the same but TPR rises?
arterial pressure UP
venous pressure DOWN
what happens when CO rises but TPR stays the same?
arterial pressure UP
venous pressure DOWN
what happens when CO falls but TPR stays the same?
arterial pressure DOWN
venous pressure UP
what is CO?
CO = STROKE VOLUME X HEART RATE
what factors affect CO?
ventricular filling: starlings law more in = more out
force of contraction - can be increased by sympathetic activity
what is starlings law?
stretched muscle contracts harder so if more blood is put into the heart by high venous pressure the harder it will contract and the higher the stroke volume will be
what happens when we eat a meal?
vasodilation around the gut
fall in TPR
rise in venous pressure therefore fall in arterial pressure
the high venous pressure > increase in CO - Starlings law
low arterial pressure triggers SNS > Inc HR
what happens when we have changes in HR?
if HR increases initially with no other change
venous pressure falls
so SV falls
so CO is normalised
- the heart is controlled by the circulation
what happens when we exercise?
massive increase in demand and muscle pumping > inc venous return
the increase in venous pressure is a problem as it tends to overfill the heart
overfilling is prevented by a rise in heart rate as soon as exercise begins from the brain
what happens when we stand up?
blood pools in superficial leg veins
central venous pressure falls
so starlings law causes CO to fall
- this doesn't work because both arterial and venous pressure have changed in the same direction
SPECIAL MECHANISM - baroreceptors increase HR as venous pressure falls and TPR increases by minimising perfusion to the skin and gut this defends the arterial pressure
this helps arterial pressure but further lowers venous pressure
to raise venous pressure the vessels constrict and fluid moves from extracellular into circulation
what happens when we have a longer term increase in blood volume?
blood volume is controlled by the kidney
if blood vol is increased for days
venous pressure increases
arterial pressure increases
TPR increases > further rises in arterial pressure > high BP
what is heart rate dependant on?
heart rate is dependant upon the ANS
baroreceptors in the carotid sinus and aortic arch detect stretch and send messages to the medulla
bainbridge reflex = if venous pressure rises HR rises
draw a graph and describe what happens in myocardial cells that causes the heart to contract
in diastole the cell membrane potential is most permeable to K so the membrane potential is close to Ek at around -80mV
spread of activity raises the cells to threshold by an initial depolarisation this opens voltage gated Na channels so equilibrium moves towards Ena
Na channels are quickly inactivated but by this point the Ca channels are open
Ca channels cause a large influx of Ca causing contraction they remain open for the rest of systole and when they close K channels open
draw a graph and describe what happens in pacemaker cells that causes the heart to contract
pacemaker cells are normally found in the SA node
the spontaneously generate APs
the dont have fast Na channels so the upward stroke is dependant on Ca channels that also close quickly
they have a feature called pacemaker potential - the membrane depolarises at a steady rate until it reaches threshold - HR is dependant on the steepness of the pacemaker potential
what drugs can we use to treat arrhythmias?
arrhythmias can be tachycardia, bradycardia, atria flutter, atrial fibrillation, ventricular fibrillation
they can be caused by: ectopic pacemaker activity due to a damaged area of myocardium,
4 classes of dugs:
1. voltage dependant Na channel blockers - lidocaine - prevents after depolarisations but allows normal HR used after MI if patient shows signs of ventricular tachycardia to prevent VF
2. B blockers - atenalol - blocks SNS acting on B1 receptors in the heart > decrease slope of pacemaker potential > dec HR - used after MI to prevent VF reduces O2 requirement of the heart, can also be used to treat slow conductance of the AV node or used in hyperthyroid to reduce affects on the heart
3. K channel blockers - prolong AP by lengthening ARP - used to treat tachycardia associated with Wolff-Parkinson-White syndrome
4. Ca channel blockers - dec slope of pacemaker potential, dec AVN conductance, dec force of contraction, cause coronary and peripheral vasodilation
what drugs can we use to treat heart failure?
the idea is the reduce the force of contraction, reduce CO, reduce tissue perfusion and oedoma
1. cardiac glycosides - digoxin - block Na/K-ATPase causing a rise in intracellular Na this reduces the effect of NCX and thus more Ca is stored in the SR +ve inotrphic affect and also reduce HR
2. ACE inhibitors
4. B blocker
what drugs can we use to treat angina?
reduce workload of the heart - B blockers, Ca channel antagonists, organic nitrates
improve blood supply to the heart - organic nitrates, Ca channel antagonists
what drugs can we use to treat hypertension?
Ca channels antagonists
A1 adrenoceptor antagonists
what anti-thrombotic drugs are there and when would we use them?
used in AF, acute MI, mechanical valves
heparin - inhibits thrombin
warfrin - antagonises vit K
asprin - anti platelet
describe an ECG
where do the leads go?
what views do the leads give?
RA-On the right arm, avoiding thick muscle.
LA-In the same location that RA was placed, but on the left arm this time.
RL-On the right leg, lateral calf muscle
LL-In the same location that RL was placed, but on the left leg this time.
V1-In the fourth intercostal space (between ribs 4 & 5) just to the right of the sternum (breastbone).
V2-In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum.
V3-Between leads V2 and V4.
V4-In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line (the imaginary line that extends down from the midpoint of the clavicle (collarbone)).
V5-Horizontally even with V4, but in the anterior axillary line. (The anterior axillary line is the imaginary line that runs down from the point midway between the middle of the clavicle and the lateral end of the clavicle; the lateral end of the collarbone is the end closer to the arm.)
V6-Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line is the imaginary line that extends down from the middle of the patient's armpit.)
what would you look for on an ECG?
Draw a normal ECG
what would you see on the ECG of a patient with a MI after:
a) 1 hour
b) 24 hours
a) st elevation
b) inverted t waves
c) pathological q waves
what is 1st degree heart block and what would you see on the ECG?
not itself a problem but may indicate CAD, electrolyte disturbance ...
prolonged PR interval
what is 2nd degree heart block and what would you see on the ECG?
some atrial impulses not conducted to the ventricles
mobitz type 1: progressive lengthening of PR intervals and then a failed conduction
mobitz type 2: most beats are conducted but occasional missing QRS complex
2:1, 3:1... more P waves than QRS complexes
What is 3rd degree heart block and what would you see on the ECG?
no conduction from atria to ventricles can be caused by MI or fibrosis of bundle of His pacemaker required
no relationship between P and QRS
What is RBBB and what would you see on the ECG?
bundle branch block no conduction is carried down right side but left is as usual causes a M in lead v1 and a W in lead v6
may indicate atrial septal defect
what is LBBB and what would you see on the ECG?
v1 = W
v6 = M
may also be t wave inversion
may indicate aortic stenosis, ischaemic disease or possibly an MI
what is 2:1, 3:1, 4:1 and what would you see on the ECG?
multiple P waves for each QRS complex
what are ventricular ectopic beats?
abnormal random QRS can be any shape
if occur early in t wave of a proceeding beat can lead to VF
what is atrial fibrillation?
atrial muscle contracts independantly of the SA node
no p waves
irregular base line
normal shaped QRS
what is ventricular fibrillation?
muscle fibres contract independantly
describe the features of the pulmonary circulation
the lung have two circulations
the bronchial circulation - part of the systemic and the pulmonary circulation
the pulmonary circulation works with low resistance and low pressures
low resistance is due to short wide vessels lots of capillaries and little smooth muscle in the arterioles