cardiovascular Flashcards
purpose cardiovascular sys
- delivery O2, nutrients, hormones, enzs
- removal waste products + heat
what is present in thorax
- heart
- distal airways + lungs
- thoracic oesophagus
- thymus
- bvs
- lymph nodes + lymphatic vessels
label key parts + brief descr how articulate
13 ribs, each articulate w vertebra, 1st 9 connect sternum, rest to each other in costal arch except last = floating rib
where is heart located w/in thorax
bet lungs, ventral to hilus (root of lungs)
general lung anatomy
lungs, divided lobes, each fed by 1 secondary bronchus, divided lobules
RIGHT: 4 lobes - cranial, middle, caudal, accessory
* no middle in horses
LEFT: 2 lobes - cranial (further divided cranial + caudal portions), caudal
pleura
serous mem lining thorax, lining lungs - visceral adherant lung surface then parietal layer w serous fluid in pleural cavity between
* no friction, no sticking + gen neg press force lungs open
* parietal = diaphragmatic, costal + mediastinal (covers other organs in midline)
all connected
pericardium
invaginated serous mem sac containing heart w visceral + parietal layers sepped serous fluid (easy movement of heart) create potential space
layers heart wall
- endocardium = smooth inner lining
- myocardium = muscle
- epicardium = visceral pericardium
relative position heart + its parts
sits midline w apex deviated slightly to left
* base cranial + dorsal to apex
* right side cranial + to right of left
parts heart w pathway blood
lungs -> pulmonary vein -> left atrium -> mitral AV valve -> left ventricle -> aortic semilunar valve -> aorta -> tissues -> caudal/cranial vena cava -> right atrium -> tricuspid AV valve -> right ventricle -> pulmonic SL valve -> pulmonary artery -> lungs
all bvs enter/leave at base
coronary circulation
supplies heart muscle w blood - coronary arteries to, great cardiac vein from
5% of circulation
heart septums
interatrial = thin muscular wall
interventricular = v muscular, acc part left ventricle
structure AV valves
have fibrous cusps - parts that ‘open + close’
* mitral has 2
* tricuspid has 3 - that can vary in dogs
supported by fibrous skeleton to maintain structure
atrial appendage
= auricle - extra section to each atrium that also fills + empties
order systole + diastole
- atria fill passively, press increases so AV valves open
- ventricles fill passively, then atria contract to complete emptying + AV valves close = atrial systole
- ventricles contract but all valves closed = isovolumetric ventricular contraction
- press increases enough for SL valves open, ventricles still contracting = ventricular systole
- SL valves close, ventricles relax = isovolumetric ventricular relaxation
- AV valves open again, ventricles begin fill = ventricular diastole
systole = emptying, diastole = filling
isovolumetric contraction/relaxation why?
press in chamber has be increased before valves open - if all valves closed then vol constant
pressure volume loop
graph diagram thing
what causes heart sounds
generally
movement blood = blood turbulence as it bounces off surfaces
normal heart sounds causes
S1 = blood rebounding in ventricles after AV valves close
* also as it accelerates in aorta after aortic valve opens
S2 = blood decelerating in great blood vessels after SL valves close
marking start + end ventricular systole
abnormal heart sounds
S3 = blood flowing into ventricle under press heard due reduced compliance ventricle wall in early diastole
* due heart failure in smallies
S4 = ‘stiff’ (impaired relaxation) ventricle wall causes increased force atrial contraction
murmurs caused blood turbulance due anything disturbing normal bloodflow
S3 + S4 normal in horses due larger heart, ‘gallop rhythm’ in smallies
auscultation heart dogs
LEFTSIDE RIB SPACES
* pulmonic valve = 3
* aortic valve = 4
* mitral AV valve = 5
RIGHT SIDE RIB SPACES
* tricuspid valve = 4/5
how is heart cycle driven elec activity
v simplified pathway
stims muscles contract rhythmically
1. initial impulse gened sinoatrial node
2. passed AV node + conducted slowly give atria time contract fully + empty
3. passed bundle of His
4. passed Purkinje fibres, then stim all ventricle muscle contract at once
function valve
ensure blood flow correct direction by opening + closing according press changes
structure valves
made cusps that open/close due press changes - 2 @ mitral, 3 @ tricuspid (not dogs - 2 main, other commissural)
structure around AV valves
chordae tendinae attach free edge cusps, preventing inversion into atria - attached papillary muscles ventricle walls but DONT control opening/closing
annulus fibrosus
fibrous skeleton structure surrounding all valves to support + electrical insulation bet atria + ventricles
therefore all valves at same level w/in heart
what is incompetence in relation to valves + what does it cause
failure close properly -> blood flows wrong direction (= regurgitation) -> congestion + heart failure
what is stenotic valve + what does it cause
= narrowed -> harder blood pass through -> more work for heart + greater press in chambers
function systemic cardiovascular sys
maintenance equilibrium bet blood plasma + interstitial fluid
what are caps + how does structure vary depending tiss supplying
vessels of exchange
* v active tiss = at leat 1 in contact every cell, less active = greater dist okay
* varying permeability walls depending function
therefore more active tiss can tolerate greater blood press
layers vessel walls
- tunica intima - inside layer endothelial cells - e.g. continuous w endocardium
- tunica media - elastic + smooth musc depending function - e.g. arteries thicker
- tunica adventitia = CT
* thick artery walls = need own blood supply = small bvs in adventitia = vasa vasorum
caps only have tunica intima
elastic vs muscular arteries
diff amounts these tissues as obvious - elastic near heart withstand + maintain press, muscular further
still cont other type tiss, just mostly x or y type
path arteries to cap bed
arteries -> smaller arteries -> arterioles (thinner layer smooth musc) -> precapillary/terminal arterioles (no elastic) -> caps
all bloodflow due press differences, maintained by increasing cross-sectional area as so many more caps than initial arteries
precapillary sphincter zone
at precapillary arterioles w intermittent smooth musc cells - regulate blood flow to caps
how is high press gened arterial sys
- forceful contraction ventricle
- elastic recoil arteries
why slow movement blood through caps
- time exchange nutrients, waste products, etc
- time to reach equilibrium
how do veins maintain blood flow towards heart
- internal press grad
- external press from muscles
- valves if blood pulled wrong direction by gravity to prevent backflow
what are arterial + venous systems referred to as
arterial = pressure reservoir of circulation - press stored here
venous = vol reservoir circulation - majority blood found here
collateral circulation defn
diff pathways to same tiss from side branches in artery in case blockage main trunk
* extra branches can accomodate increase flow
parts collateral circulation
anastomoses = joining these 2 parts
1. interarterial
2. intervenous
3. arteriovenous - muscular wall to act as sphincter (circular muscles open + close passages to reg flow substances)+ move blood, skips cap bed
retia = network bvs used slow blood supply (+ cooling)
end arteries
no collateral circulation = only supply of oxed blood to a tiss
* blocked = no blood supply to tiss (ischaemia) -> infarction + necrosis
loads in brain
thoroughfare channels
caps straight to middle cap bed, missing most of it
blood directed here by precap sphincter zone
cap endothelium structure
- intercellular cleft = gap junction for diff water soluble mols
- tight junctions can seal endothelial layer - brain has continuous to only allow Na+ + water
* other mols would have to fac diff across - fenestrations = area w thinner mem endothelial cells or no cells (renal glomerulus)
* where v active substance (prots, H2O soluble, new bcs) transfer
constructed diff depending situation
sinusoids
type cap w thin walls + large diameter (blood through slowly) + discontinuous endothelium for free communication blood plasma + surrounding tiss
* lots liver + BM + arteriovenous
diapedesis is + example
diffusion movement cells out lumen post-cap venules
* how wbcs into circulation into tiss to fight infection
label left lateral aspect heart
label right lateral aspect heart
when does coronary circulation occur
during ventricular diastole bc systole = wall contracting = vessels squished + v little blood movement
where do coronary arteries arise from
from aortic bulb
* caudosinistral sinus -> left coronary artery
* cranial sinus -> right coronary artery
main branches = circumflex + interventricular
supplying walls respective ventricles
how does blood return heart from coronary circulation
- great cardiac vein -> coronary sinus in right atrium
- Thebesian veins = small veins directly draining all 4 chambers
descr aortic arch - main branches aorta
diagram
bigger species = left subclavian artery branches off brachiocephalic trunk, not distinct
which veins return blood to cranial vena cava
- internal + external jugular from head
- cephalic from cranial chest + forelimb
- auxillary + subclavian from forelimb + some intercostal
- vertebral
- internal thoracic
- azygous from ribcage (ruminants + pigs)
veins leading caudal vena cava
diagram
what do we take thoracic radiographs for
- respiratory disease
- cardiovascular disease (esp Congestive Heart Failure)
- staging neoplasia (uncontrolled, abnormal growth)
* looking for mastasis (2 malignant growths) in lungs - trauma
why do tumours often spread to lungs
all blood has to go thru cap bed at lungs - can’t be bypassed
* tumour cell likely be seived out + remain in lungs
what to remember when taking thoracic radiograph to examine lungs
take at peak inspiration - can be gently inflated via anaesthetic breathing sys
1st priority for radiography
patient 1st - need to stabilise to sedate/anaesthetise b4 radiograph
* prioritise right here + now to stabilise - diagnosis irrelevant if dead
which position best view for lungs
ventrodorsal as lungs closest to plate
* tiss closest to plate most accurately repped
how should you position for dorsoventral/ventrodorsal
sternum + thoracic vertebrae superimposed
attenuate defn
blocks the beam - opp to expose
what to consider when positioning for lateral
left + right ribs superimposed - less blocking image
how many views to take
always at least 1 more orthagonal (perpendicular)
* see where is dorsal to ventral + left to right to exact position as structures superimposed - 3D thing, 2D image
for lungs ideally both lateral as lower less inflated than upper
heart more accurately depicted in R lateral = good cardiac silhouette
BUT MONEY
which position don’t use if in respiratory distress
ventrodorsal as shouldn’t be laid on their back
which view is best for heart
dorsoventral as heart closest plate (by sternum)
why do we say we see cardiac silhouette on thoracic radiograph
what’s visible is heart in pericardial sac w fluid inside - might be excess fluid that bigger, not larger heart
label position heart chambers
label heart chambers
label lung lobes
not visible in radiography but should know positions so can identify where mass etc located w/in lungs
label lung lobes
label lung lobes
how to tell if RL or LL view thoracic radiograph
RL = crura diaphragm align = smooth round curve
LL = diaphragm crura diverge = Y shape at dorsal aspect
how to tell if DV or VD view thoracic radiograph
VD = diaphragmcrura superimposed so triple hump appearance
DV = diaphragm is a smooth curve
basic sims + diffs bet circulatory systems
- same vol blood each side
- vol + flow rates L + R ventricles similar
- press L + R ventricles v diff
hydrostatic press
press exerted by fluid on its container, altered by changing vol fluid or size cont, e.g. diameter bvs
this is the press we refer to in aorta, ventricles etc
how is HP in caps altered
no smooth musc so can’t change diameter to alter press themselves
arterioles supplying cap bed vasoconstrict = blood arriving slower = press in caps decreases (+ vice versa)
bulk flow def
movement fluid by means HP diff - v fast over long distances
perfusion press
press needed for blood to move along bv
diff in press bet any 2 pts along
P(inlet) - P(outlet)
what does it mean if a tiss is well perfused
good blood flow
osmotic press
drive for water to move into a sol by osmosis, exerted by osmotic particles (e.g. solutes)
plasma oncotic press
= prot/colloid osmotic press, constant through circulation, altered by disease
* tendency water move into caps by osmosis from ISF due higher conc plasma prots exerting osmotic press
water moves area low oncotic press to high
bulk flow across vessels caused by?
transmural HP diff = exchange bet blood plasma + ISF across cap wall
* bulk flow in = absorption
* bulk flow out = filtration (HP higher in than out so water vessel -> ISF down press grad)
Starling’s law caps
net movement water bet caps + ISF depends balance hyd press + oncotic press diffs across cap wall
net press = (P(cap) - P(ISF)) - (O(cap) - O(ISF))
pos answer = water filtered out, neg = water absorbed in
how does filtration + absorption change along cap
- HP decreases along cap length as fluid moves out
- OP constant
therefore most filtration at start, absorption by end
normally overall filtration > absorption
oedema
failure of lymphatic sys to remove excess fluid from ISF + return it to circulation, due problem w sys or too much fluid filtered out caps causes this = swollen ankles etc
fairly common
how is arterial supply arranged + why
in parallel - arteries -> 1 cap sys -> venous -> heart so all caps receive oxed blood + change/block/damage 1 no affect others
gut to liver + hypothalamus to pituitary gland (to comm) in series
how are pulmonary + systemic circulation arranged
in series = blood has to pass through 1 to get to other = change in 1 affects other
cardiac output
vol blood pumped by 1 ventricle in a min - same L + R
CO = stroke vol * heart rate (CO = SV * HR)
HR increase too much = can’t fill properly = less effective
EDVV, ESVV + SV
End Diastolic Ventricular Volume = vol in ventr at end diastole
End Systolic Ventricular Volume = vol ventr at end systole - don’t empty completely w each contraction
Stroke vol = EDVV - ESVV = vol blood ejected into artery w each contraction
right SV = left SV - in series so handle same vol blood
ejection fraction
and what measures
prop available blood in ventricle that was ejected - measure systolic function heart
as percentage
what affects SV
EDVV + ESVV
what affects EDVV
- diastolic filling time - more time fill = more full
- preload
- compliance = stretchiness ventricle wall
what affects ESVV
- afterload
- contractility = how good ventr at contracting + ejecting contents (efficacy in time, e.g. same vol out less time)
what happens if EDVV increases too much
w/in normal limits fine, but too much = heart wall overstretched = damaged + loses contractility
what is preload
filling press ventr = atrial press = venous press = EDVV
how to increase preload
increase vol and/or press in venous sys + so atria by:
* reducing perfusion to non-essential tiss - reduce space blood occupies = increase press
* respiratory + skeletal pump push blood thru + increase press
* increase overall blood vol
action respiratory + sk pump during exercise
SK: contracts + relaxes to compress veins + pump contents towards heart, increasing venous return
RESP: in breathing diaphragm compresses cranial abdominal veins to push blood to heart
* distension thoracic veins in inspiration = blood from abdominal veins drawn into central circulation
ALL TO INCREASE EDVV
what happens if veins compressed too much
persistent increase in H press = fluid leaks out, e.g. into permeable pleura, + forms oedema
effect preload on EDVV
EDVV increases then plateaus as ventricles limit in how far can stretch - max capacity ~90ml
* elastic tiss stretched to max so continue = damage myocardium, decreasing contractility
effect EDVV on SV
- increase EDVV = more blood available for ventricle dispel
- AND stretching cardiac musc cells = increase Ca2+ release = increase contractility = decrease ESVV = SV
- BUT massive EDVV = cardiac musc overstretched + damaged + loses contractility = increase ESVV
increasing EDVV = SV increases until plateaus + eventually decreases
heterometric autoregulation
what, why, how
maintaining same SV both sides heart so blood no accumulate either one
* increase preload side X = increase EDVV = increase SV = increase bloodflow = increase preload side Y…
works bc in series
compliance
ability ventricle walls stretch - change vol achieved for given change press (preload)
change in vol/change in press
v compliant = lil change preload, big change vol
affect big preload on compliance
CT in ventricle reaches elastic limit = stiffer + won’t take more vol
example disease affecting ventricle compliance + consequence
dilated cardiomyopathy = decrease compliance = need higher preload maintain same SV
how heart rate affects CO
- more contractions per min (CO=HRxSV)
- decreases diastolic filling time = less filling = lower EDVV = lower SV
so despite CO=HRxSV, CO no increase in proportion HR
lusitropy
ability relax
how diastolic filling time maintained w high HR
under physiological stress = flight/flight, exercise
symp NS responds:
* increase contractility = decrease ESVV = increase SV (increase EF)
* decrease length systole = relatively longer diastole = better EDVV
difference response increased HR physiological stress + disease
pathological tachycardia (or pacemaker) = length systole preserved = at higher HR CO decreases
why is ventricular filling divided 2 stages
rapid filling, atrial press drops to near ventr press, so rate drops
reduced filling (diastasis), then atrial systole to complete filling
what causes valves close
press area entering exceeds press area leaving = slight backflow blood = valve closes
why 2 stages ventricular ejection
- rapid ejection as blood under high press
- reduced ejection as rate decreased as ventricular press past peak systolic
how does importance atrial systole vary
higher HR = atrial systole responsible higher % ventr filling (less is passive)
* atrial fibrillation = atria no contract properly - fine at rest but during exercise no
how is contractility altered
- symp autonomic NS increases it to decrease ESVV
- increases w mild musc stretch as w physiological preload increase
afterload + response when increased
w press-vol loop for increased afterload
resistance arteries ventr has overcome pump blood out = aortic/pulmonic press (increase = increase ESVV)
increase = heart gens more press in isovolumetric contraction to overcome press, open SL valves + maintain CO
where is greatest resistance to flow
arterioles as narrower = higher press, more resistance
* caps narrower but so many more that net resistance cap bed < arteriole
so arterioles control distrib blood thru cap beds + so organ systems by varying resistance
vascular resistance
measure how compliant vessel is - high resist = low compliance
== perfusion press/bloodflow
Poiseuille’s law
resistance varies inversely w 4th power radius - small change radius = big change resist
what affects vascular resistance
- length bv - can’t change
- radius bv - wider = lower resistance bc press lower
by what + how is vascular resistance modified
ANS + hormones
* vasoconstriction = vessels narrow = afterload increases…
symp NS response to exercise
increase CO:
* increase contractility
* increase HR (but decrease systole preserve EDVV)
* vasoconstriction to increase preload
plus breathing heavier + moving = action respiratory + sk musc pumps
total peripheral resistance (TPR)
net resistance whole circulation - arterioles contrib most
(mean aortic press - mean vena caval press)/CO
* caval press negligible so:
TPR = mean aortic press/CO
why arterial press approx same rest + exercise
Pa = bp = TPR * CO
exercise = TPR decreases due dilation
= CO need increase maintain bloodflow essential organs (cardiac musc + brain) due increase in blood use sk musc
ALSO = bvs non-essential organs constrict
bp needs be maintained to ensure adequate perfusion organs
hyper/hypotension
- increased bp - usually systemic arterioles constricted = increased TPR = hypertrophy cardiac musc as works overcome afterload + maintain CO (elderly cats)
- decreased bp - due significant haemorrhage, anaesthesia
hypertrophy
increase + growth musc cells
how is bp repped
shows graph change over time (don’t learn)
systolic/diastolic = 120/80mmHg
pulse press
systolic press (Ps) - diastolic press (Pd)
bc press in arteries pulsatile (up + down)
what is systolic press
in systole blood ejected aorta/pulm art at high press - press in vessel rises to systolic press
what is diastolic press
SL valve closed + heart in diastole = press in aorta/pulm art decreases to diastolic press
what affects pulse press
increase
- SV
- aortic compliance
- HR
- TPR
increase, decrease (bigger afterload), decrease (bigger EDVV), increase
how increase pulse press
- increase SV
- decrease aortic compliance (increase afterload)
- decrease HR (increase EDVV + longer diastole = more blood out = lower diastolic press)
- increase TPR (increase afterload from vasoconstriction)
all to increase press gened by heart from contraction
how to dissect to see right side heart
dressing forceps through cranial vena cava out caudal vena cava, cut between them then down into right atrium + atrial appendage then all way round along interventricular septum (not into), + out cutting through pulmonary trunk
how to dissect to see left side heart
scalpel into edge wall left ventricle then scissors in to cut down to apex + up through atrium + atrial appendage. then cut out aorta (= through everything else)
what is tracheal bifurcation
where trachea divides into left + right primary bronchi
what are the heart surfaces
left lateral = auricular surface = left atrium + ventr on right, apex bottom to the right, can see right auricle peaking over top left + right ventricle curves over from the right a bit.
right lateral = atrial surface = right ventricle top right + right ventr bottom right curling round side,
how is heart oriented in animal bod
- auricular surface on left of thorax
- atrial surface on right of thorax
- left side w ventricle etc caudal
- right side w ventricle etc (where curves) cranial
- base of heart dorsal
- apex of heart ventral
- axis of heart craniocaudally angled
interventricular grooves
coronary grooves w coronary arteries in
auricular surface = paraconal
atrial surface = subsinuosal
what is left azygous vein
pigs + ruminants: drainage directly from body into coronary sinus - everyone else only have 1 azygous vein
muscular ridges visible in walls heart
stregthening walls atria + auricles = pectinate muscles
ventr = trabeculae carnae
reduce suction inside to keep resistance low so don’t have to gen more press to pull walls apart
names of cusps in AV valve
septal + parietal, plus angular in tricuspid (not dogs)
external distinguishing bet species lungs
- dogs + cats have more clear, divided lobes than ruminants - move more so lobes need be able move over each other
- horses don’t have middle lobe
- pigs have v little lobe division but marbling CT bet lobules visible
thorax dissection general process
- cut along sternum + up each side to veterbrae
- skin it
- cut away muscles + brachius plexus + through skin to remove forelimb completely
- cut away muscle layers, expose all ribs
- cut out 2nd, 4th w 5th, 7th w 8th ribs
- have an explore
jugular furrow - what + where
runs down neck, where fur changes direction, houses external jugular vein
where does heart sit
ribs
under ribs 4 + 5
where is pulmonic valve located
LHS under rib space 3rd
where is aortic valve located
LHS under 4th rib space
where is mitral valve located
LHS under 5th rib space
where is tricuspid valve located
RHS under 3rd/4th/5th rib space
variable
other name xiphoid process
xiphisternum
dorsal epaxial muscles
at top thorax
* latissimus dorsi
* fan-shaped serratus ventralis
* serratus dorsalis
2 muscles on cranial side thorax
- scalenus (top) involved inspiration, attached 1st few ribs
- rectus thoracis (more circular below) involved inspiration, running w tendon of rectus abdominis musc
intercostal muscles
- external run caudoventrally
- internal underneath run cranioventrally
where do vessels run on ribs
run along caudal border of rib
phrenic nerve
runs suspended in mediastinum to innervate diaphragm
one each side
where pleura bends back on itself
- costomediastinal recess
- costodiaphragmatic recess
- cupula pleura extends beyond 1st rib
basic features foetal CV sys
- starts to develop when at 3 layer stage - b4 that simple diffusion enough to meet needs
- umbilical veins bring oxed blood from allantois (extra-embryonic mem)
- vitelline veins bring nutrition from yolk sac
- cardinal veins bring blood from rest of embryo
- pulm sys not functional - lungs collapsed so bvs squished = high resistance, high afterload, not much blood thru - ox from placenta
arteries same names take blood back to same place
why is blood in foetal circ less oxed than adult
- deoxed blood from RV in pulm art into aorta through ductus arteriosus
- deoxed blood from pulm veins (lil bit) in LA mixes w oxed blood from RA
1st stage CV sys development
- cells splanchnic mesoderm organised form blood islands of haemangioblast cells
- stim surrounding mesenchymal cells form endothelial + smooth musc cells form walls around
- blood islands start join, forming start vessel structures
- small vessels coalesce form larger vessels that comm = dorsal aortae
uses cell signalling
structure heart before bits start join
- cardiogenic plate -> cardiac tube later
- neural plate
- coelom (L+R) - fuses w neural plate form coelemic cavity (horseshoe), extends round heart -> pericardial cavoty
foetal position heart + implications
where head will be - folding = moves dorsally to thorax but recurrent laryngeal nerve hooked round ductus arteriosus = goes down to chest then back up to brain
* vulnerable damage by turning neck
formation cardiac tube from cardiogenic plate
- -> endocardial tube w L + R limbs
- moves dorsal to neural plate
- 2 limbs coalesce
- -> cardiac tube = primitive heart, simple pump
fusion cardiac tube to make caterpillar
- dorsal aortae fuse either end cardiac tube horseshoe (w folding asw)
- vitelline veins fuse other end
- dorsal aortae fuse caudally (opp end from vitelline veins)
- 1st aortic arches form where cardiac tube joined dorsal aortae -> 1 dorsal aorta w aortic arches in between
- cardiac tube folds form structure w 5 parts
structure cardiac tube + what each part becomes later
caterpillar stage, on pic
formation AV canals
forms rubber ducky as sinus venosus + bulbus cordis kinked up - still 1 tube
endocardial cushions from mesenchymal cells form bet single atrium + ventr, grow in from each side + fuse form septum intermedium sep AV canal into 2 (L+R)
mesenchymal cells
multipotent stem cells bet endocardium + myocardium
formation ventricles
primordial ventricular septum forms bet dilated section bulbus cordis + foetal ventr (together were common ventr)
* interventricular foramen remains until defferential cellular proliferation closes
formation atria
- septum primum grows down towards intermedium, leaving hole (foramen primum) - blood sinus venosus -> LA
- programmed cell death = 2nd opening forms more dorsally = foramen secundum (+ 1st closes)
- septum secundum grows down just to right, stopping before intermedium = gap
leaves 2 septums overlapping w hole allowing oxed blood RA -> LA but not back (no-return valve) so when born + press higher LA blood no other way = FORAMEN OVALE
where is sinus venosus found w/in devloping atria + why
RA wall bc it grew + expanded to form it, hence smooth lining (was lining of sinus venosus)
* sinus venosus also forms SA node + coronary sinus
why is lining of atrial appendages lumpy
developed from foetal atrium as it split in 2
how do pulm veins develop in foetal heart
bud out developing LA, join lungs - expansion generally forms smooth lining LA
how do AV valves form
- mesenchymal proliferation on edge apertures endocardial cushions forming septum intermedium
- cavitation musc beneath cusps
- attached muscular strands from free ventr walls3. strands diff replace musc tiss w CT = chordae tendinae attached papillary musc
where is pacemaker located throughout foetal heart development
- caudal part cardiac tube - whole tube contracting together
- right limb sinus venosus
- becomes SAN once RA forms - annulus fibrosis = atr + ventr electrically isolated
sepping aorta + pulm art
sep conus cordis (non-dilated part bulbus cordis) + truncus arteriosus
1. sub-endocardial thickenings along division bet them = bulbar ridges
2. fuse = aorticopulmonary septum (spiral)
how SL valves form
at origin trunks mesenchymal tiss proliferates + ridges remodelled form CT covered endothelium = cusps
aortic arches
6 pairs that form - some disappear, some permanent:
3 -> carotid arteries
4 left -> arch of aorta
4 right -> right subclavian
6 -> pulm arts + ductus arteriosus
how do all veins join
- vitelline incorps drainage gut + passes thru liver = hepatic sinusoids
- vitelline + umbilical anastomose on L + R (sep) = common drainage
- shunt bet left umbilical + cranial part right common drainage = venus ductosus
purpose ductus venosus
mostly bypass liver as not using it or gut
what forms cranial vena cava
cranial cardinal vein - after anastomosis R + L
L cranial cardinal also coronary sinus
what happens w caudal cardinal vein
-> subcardinal, drains kidneys -> caudal vena cava (w cranial vitelline)
-> supracardinal, drains dorsal wall; R -> azygous
anastomoses bet subcardinal + supracardinal
ductus arteriosus where + why
bet pulm trunk + aorta to take deoxed blood -> aorta + no flow to lungs (collapsed)
* bc press higher pulm art as lungs collapsed
* joins after coronary arteries + brachiocephalic trunk so relatively high oxed blood -> brain + cardiac musc
Eustachian valve
at mouth entry vena cava to RA, directing blood to foramen ovale to LA to aorta to bod
what changes at birth
- umbilical arteries contract = no blood flow neonate -> placenta
- umbilical veins contract = venous blood to neonate - 30% blood vol so no cut too early
- when rupture arteries undergo elastic recoil to prevent haemorrhage
what do umbilical artery + vein become after birth
- umbilical artery -> round ligament of bladder
- umbilical vein -> round ligament of liver
how does foramen ovale close
breathe in = lungs open + pulm caps open = big drop resistance to flow pulm circ = drop resistance pulm art = drop RV afterload + increased pulm blood flow = increase LA venous return = bigger preload LA = bigger LA press = septum primum pushed against secundum + closed
* fibrosis over time = permanent, + fossa ovalis remnant left (fibrous indent)
how does ductus arteriosus close
birth = press aorta increases bc higher output LV, + press pulm art decreases as less resistance from lungs so flow would reverse = smooth musc duct constricts = flow stopped
* then CT proliferates cause permanent closure = now ligamentum arteriosum
what happens if ductus arteriosus no close
press higher aorta than pulm trunk = reverse flow
* oxed blood to lungs + need to maintain press + take it to bod
* pulm circ overloaded - poss pulmonary oedema from congestive heart failure
* constant flow so constant murmur = machinery murmur
how does ductus venosus close
smooth musc contracts = flow stopped + diverted to hepatic circ = liver sinusoids perfused
permanent w/in 2-3 weeks
aortic stenosis
valve no form properly + narrowed = increased resistance = increased afterload = difficult ventr push out blood = hypertrophy = reduced vol = can’t fill as much + press overload + heart failure
* not enough blood through = pass out lots (syncope)
* arrythmia (abnormal heart rhythm)
* systolic heart murmur left 4th
varying degrees severity
ventricular septal defect
septum no completed = blood left -> right down press grad = sound on right
* overload RV = overload pulm circ, increased return LA = left vol overload….
vascular ring anomalies
wrong aortic arch persisted can cause bits to remain in wrong places, e.g. oesophagus stuck = food can’t go down + regurgitate + it stretches - won’t return normal
how does cardiac musc contract together
cells branch w intercalated discs cont gap junctions bet them for cations move thru + depol next cell - all v fast so cells contract together + musc acts functional syncytium
how does heart beat + control
pacemaker cells have automaticity = spontaneously depol so ANS innervation only to change HR + rhythm (contractility)
* symp via cardiac nerves
* parasymp via vagus nerve
what in heart is responsible initial a pot
SAN as has pacemaker cells that depol faster than AVN
ectopic pacemaker
if cardiac myocyte damaged cells can become pacemaker - enough together can gen own a pot, still conducted through heart but wrong way = arrhythmias
* often hear heartbeat but no feel pulse
pathway a pot thru heart
- SAN free wall RA gens a pot, travels cell-cell across atria = contract at once
- annulus fibrosus = no pass to ventr + coalesce at AVN
- conduction slowed as narrow fibres AVN so time to pass thru = gap bet atr + ventr systole
- passed bundle of His (AV bundle) traversing annulus fibrosus
- 2 paths down interventricular septum (L+R)
- L bundle branch into anterior + posterior fascicles to supply thick wall LV
- both sides divide branching Purkinje fibres w super fast conduction so ventr contract as unit from apex to base
R bundle branch has lil offshoot to free ventr wall = septomarginal band
how is cardiac musc a pot diff from sk musc
long plateau phase during contraction so not another a pot gened = time relaxation b4 contract again + no temporal summation
* sk musc wants contract + stay contracted, e.g. hold something - continuous contraction = tetany
how is a pot gened in cardiac musc cell
resting mem pot = K+ channs open, moving out = neg
1. fast Na+ channs open = Na+ in = depol
2. fast Na+ close = cell starts repol
3. K+ close + Ca2+ open via 2nd messenger sys - slow = slight repol on graph
4. Ca2+ in from t-tubules = Ca induced Ca release from SR
5. = pos intracellular + cell contracts
6. Ca2+ close, K+ open = K+ out + Ca2+ pumped back SR (Ca2+ATPase) + ECF in exchange Na+ = repol to resting mem pot
how is long plateau phase in cardiac musc cells caused
fast Na+ channs absolute refractory period until cell almost back to resting mem pot = musc forced relax + specialised Ca2+ channs stay open long keep inside pos
how is atrial a pot shorter
- Ca2+ channs open less time
- K+ channs closed less time
- shorter refractory period = shorter less flat plateau
what is pacemaker pot
pacemaker cells no have stable resting mem pot - after repol mem pot slowly rises back to threshold = pacemaker pot
how is pacemaker pot gened
- ‘funny’ Na+ channs closed during a pot, open when ends for slow gradual depol
- K+ channs open at end a pot + slowly start close to let less K+ out cell
- Ca2+ open as Na+ close = faster depol for actual a pot
NO FAST NA+ CHANNS = slow a pot
why does AVN have longer refractory period
narrower fibre diameter - so ventre no beat too soon + elec impulse no circle back to atria
how does symp NS increase contractility
longer opening Ca2+ channs
what does electrocardiogram do
records elec activity of heart by comparing voltage at pos electrode w V at neg electrode
* plots voltage (Y axis) against time (X)
* bc elec activity heart conducted to skin bc bod = bag salty water
what makes ECG upward or downward deflection
atrial depol = cations in + surface neg
atria at rest = surface pos
a pot towards pos electrode = more pos charges near pos electrode = upward deflection + vice versa
no pot diff bet electrodes = graph at baseline (0)
what do waveforms on ECG rep
P = atrial depol
QRS = ventr depol
T = ventr repol
which direction does a pot flow make P wave
R -> L = upwards wave
which way does a pot flow make all parts QRS complex
Q = early depol, L->R = down
R = full depol, R->L + massive LV wall = tall up
S = late depol, charge to 0 or down depending where depol ends
which was does a pot flow make T wave
unpredictable so can go up or down
where are ECG leads located w charges
diagram
bipolar leads have pos + neg poles
augmented unipolar leads measure elec pot bet pos electrode 1 limb + avg other 2
why do we use lead II most
most closely matches normal electrical axis heart = overall direction a pot
how to assess HR from ECG
- avg R-R interval then maths to HR
- no. PQRST complexes in 3 or 6 secs then multiply
how to assess rhythm using ECG
how consistent are R-R intervals
* regular = sinus rhythm
what does tall P wave mean
P pulmonale = RA enlargement (bigger elec pot diff)
what does wide P wave mean
P mitrale = LA enlargement (longer atrial depol so more time)
what does tall R wave mean
ventr enlargement (bigger elec pot diff)
what does wide R wave/wide QRS complex mean
LV enlarged w hypertrophy - depol taking longer
bradycardia
slow HR
tachycardia
fast HR
regularly vis irregularly irregular rhythm
regularly = R-R interval varying in repeatable pattern
irregularly = no pattern - coordination flow a pots thru heart lost
* e.g. atrial fibrillation = atria fluttering + AVN transmitting a pots as fast as poss but kinda random
how is bp maintained normally (no extreme changes)
metabolic autoregulation by altering flow to tiss by vasodil/constrict (changing vascular resistance) - intrinsic control to match blood flow to tiss metabolic rate
* O2 = vasoconstrictor
* CO2, lactic acid, K+ in ISF = vasodilator
flow to brain, coronary + working sk maintained - essential tissues
explain active hyperaemia
increased metabolic rate = increased O2 in tiss = vasoconstrict artierioles = decreased bloodflow to caps = fewer open = less O2 to tiss + less waste removed = stimulus for vasocnstrict removed = vasodilate etc until bloodflow matches metabolic rate
* increased bp + increased perfusion tiss
how do intrinsic controls deal w complete interruption blood flow essential tiss
O2 depleted + build up waste products conts significantly enough thatflow reestablished to above normal short time until waste gone + O2 debt repaid, then returned normal = reactive hyperaemia
paracrine intrinsic control is?
locally acting chems that alter flow rate in response local environ
what happens in response increased blood flow velocity
- endothelial cells sheared due increased velocity = release NO = vasodilator
- parasymp neurones release NO + ACh - stims more release NO from endothelial
intrinsic paracrine controls
response local irritation
- prostacyclin (prostaglandin I2) from endothelial cells = vasodilation + decrease platelet aggregation
- histamine from mast cells = vasodilation (mediated NO) + increased cap perm
- bradykinin from globulins = vasodilation (mediated NO = due its release)
intrinsic paracrine controls
response endothelial damage
= actual cut
- endothelin 1 release = vasoconstriction
- thromboxane A2 from platelets = vasocon + platelet aggregation
intrinsic paracrine control
relationship intrinsic + extrinsic blood flow controls
intrinsic usual management + maintenance bp + always happening at essential tissues but in times extreme change bp extrinsic take over to disrupt flow to non-essential tiss
ischaemia - what is, why happens + normal response
reduced blood flow to tiss due longterm mechanical compression vessels, e.g. sustained contraction sk musc from weightlifting
* causes pain + reduces strength musc contraction = bod trying stop contraction
* reflex to increase arterial bp so increase perfusion press musc (increases workload heart)
infarction + necrosis
tiss damage + cell death due ischaemia
e.g. from badly applied bandage
how do coronary arteries ensure maintained bloodflow during exercise
low resistance so even w increased HR + contractility + shorter diastole still enough bloodflow to card musc
risk to pulmonary vessels w anaesthesia
caps bet alveoli v compliant = easily compressed if too much air into alveoli + expand = increased resistance = increased pulm art press (allows maintain flow to extent) = increased afterload RV, decreased blood pulm veins = decreased preload LA… ischaemia, infarction
extrinsic control + what would happen w/o
overwhelm intrinsic control + temporarily compromise non-essential tiss in order maintain flow essential
otherwise increase flow working sk = less blood available others = accumulate waste = vasodilate = bp drop in loop uncontrollable
how extrinsic control works
CNS coordinates using ANS, controlled CV centre in medulla oblongata maintain CO + then alter TPR if necessary to keep art bp w/in normal limits
how is baroreflex started
- baroreceptors = stretch receptors to sense bp as stretch affected internal press
- sending constant, regular a pots to CV centre
- increase/decrease bp = inc/dec frequency a pots
- frequency detected CV centre + compared ref val so change detected + response ilicited
its immediate = 1st act in response change bp
where are barorecptors + why
- aortic arch to detect changes in press to bod
- carotid sinuses to check vessels supplying brain
baroreflex response to drop bp
vice versa for increase
- increase symp output
* inc HR by inc firing SAN = inc CO
* inc contractility = inc CO
* faster conduction = inc CO
* peripheral vasocon = inc preload, inc TPR - dec parasymp output = more vasoconstr + inc HR
bc Pa = CO*TPR
renin-angiotensin-aldosterone sys (RAAS)
dec bp = inc sym activity due baroreflex = renin released juxtaglomerular apparatus cells kidney = angiotensinogen -> angiotensin I in liver -> angiotensin II in lungs (by angotensin converting enz (ACE))
angiotensin causes:
1. aldosterone from adrenal gland = Na+ + H2O retention kidney
2. ADH from pit gland = kidney conserve H2O + more vasocon
3. hypothalamus inc sensation thirst = drink more
4. vasocontr in own right
more water = inc blood vol = inc bp
Starling’s law caps
vasoconstr arterioles = dec bloodflow caps = dec HP in caps = HP diff more outwheighed OP diff = more fluid retained/reabsorption = inc blood vol
* would dec plasma OP but liver prods more prots to balance
what governs long term regulation bp
kidney as based relationship art bp + urine excretion + sets ref val for CV centre for baroreflex - CNS can change, e.g. higher during fight/flight
* therefore maintenance reliant normal renal function
psychological overrides bp control
emotional state bypasses CV centre + overrides baroreflex
1. how fight/flight causes complete symp NS activation
2. vasovagal syncope = fear/excitement cause dec symp activity, inc parasymp = vasodil = dec bp = no cerebral bloodflow = faint
lymphoid sys
sys thin-walled vessels that drain fluid from tiss thru series nodes
* blind-ending caps coalesce larger vessels
* eventually empty into major systemic veins in thorax
lymphoid tissues
- nodes
- spleen
- thymus
- mucosa-associated lymphoid tiss
- lymphocytes (B+T cells)
- plasma cells
chyle
lymph once passed thru gut so conts lipid from SI villiin form chylomicrons (too big enter blood caps)
white
roles lymphatic sys
- removal excess water from ISF to maintain fluid balance
- removal infectious agents + dead cells
- antigen presentation - present foreign mats to IS, it decides whether mount response = management ID
- movement lymphatic cells
- transport some prots
- transport dietary lipids from gut
structure lymphatic vessels
- thin walls
- endothelium tunica intima, media, adventitia w some CT
- discontinuous BM caps = more permeable than blood caps
- caps begin blind-ended, into 2-3 trunks that open into great veins at junction neck
- large vessels some sm musc
- larger have valves
look like veins histologically
lymph node structure
pig lymph node structure
what happens at lymph nodes
- foreign mat removed phagocytes
- fresh lymphocytes recruited from cortex
all lymph passes thru at least 1
lymphocentre defn
grp few relatively large lymph nodes
* horses + pigs = lots little
lymphocentres of head
- retropharyngeal
- parotid
- mandibular
drain all structures head
lymphocentres neck
- superficial
- deep cervical
drain neck, superficial part cranial trunk, top forelimbs
lymphocentres forelimb
axillary (armpit)
* drains deep structures whole limb + superficial structures distal limb
thorax lymphocentres
- dorsal thoracic
- ventral thoracic
- mediastinal
- bronchial
drains contents + walls thorax
lymphocentres abdomen
- lumbar
- coeliac
- cranial mesenteric
- caudal mesenteric
drain loin area (inc repro tract) + abdominal contents
hindquarter lymphocentres
- popliteal
- ischial
- deep inguinal
- superficial inguinal
- iliosacral
drain hindlimb, abdominal wall + pelvis
which lymph nodes are palpable - dog
on diagram
palpable lymph nodes - cat
palpable lymph nodes ox
prescapular + prefemoral
palpable lymph nodes horse
submandibular
which LNs visible radiograph
enlarged thoracic
which LNs visible ultrasound
enlarged abdominal
main duct pathways
diagram for ref
- L + R tracheal ducts from retropharyngeal nodes drain head + proximal forelimb
- L tracheal -> thoracic duct
- R tracheal -> R lymphatic duct (drains R thorax) (joins thoracic)
- mediastinal from heart
- tracheobronchial from lungs
- lumbar ducts (hind) -> cisterna chyli -> thoracic duct
cisterna chyli
collection vat w drainage all structures hind area
only 1 lymphatic drainage pathway?
several alternative so disaster + need tie one of, or one blocked, it’s okay bc lymph will find another way
why need know lymph drainage pathway
pathway provides route metastasis neoplastic diseases that cause tumour growth
* know routes = accurate disease staging + planning surgery
embryology lymphatic sys
- 6 lymph sacs
- develop into LNs (except cisterna chyli)
- comms vessels arise bet LNs as mesenchymal cells infiltrate
* bet jugular sacs + cisterna chyli = thoracic duct
atarts after CV sys established
names lymph sacs foetus
- paired jugular
- paired iliac
- retroperitoneal
- cisterna chyli
last 2 drain viscera
how does spleen develop + overall purposes
from mesoderm - v vascular organ w lymphoid functions but also stores rbcs
where is thymus
cranial mediostinum
how does thymus develop
- arises endoderm + mesoderm
- initially paired organ, gives off buds
- grow down neck + invade mediostinum
- form single organ extending to pericardium
- replaced adipose tiss over time
how does fluid move into lymph
- net filtration from blood caps into ISF bc HP diff > OP diff most length caps
- bulk flow into lymph caps (low press) - remove ISF to prevent formation oedema down HP grad
how does lymphatic sys maintain HP grad for bulk flow in from ISF
- low press
- prot uptake from ISF (bc more perm) = dec oncotic press ISF = inc diffusion ISF -> lymphatics
- inc lymph flow = inc prot uptake = inc ISF vol = lymph sys takes up more prot = inc lymphatic absorption water + dec OP ISF so less filtration water out plasma
causes lymph flow
- HP grad -> venous sys
- external press sk musc
- sm musc walls larger lymphatic vessels
- valves prevent backflow
more on top HP grad as grad slow so movement slow
oedema vs effusion
oedema = fluid in interstitial space
effusion = free fluid w/in cavity
what causes failure lymphatic drainage
- disease lymphatic sys
- capacity lymphatic sys overwhelmed - proding so much ISF (congestive heart failure)
- derangement HP grad - venous press high = fluid can’t go out lymphatic sys = stuck = fluid build up ISF
effect ANS on heart
incr/decr HR + contractility
where does symp NS exit CNS
preganglionic fibred from thoracolumbar spinal segments, then postganglionic from sympathetic ganglia C5-T3
symp ganglia combining
C7-T3 combine make stellate ganglion (large)
C5 + C6 make middle cervical ganglion
where does parasymp NS originate
craniosacral = from brainstem + sacral spinal segments
* cranial nerve X (vagus) runs caudally + supplies thoracic viscera
result on vessels symp + parasymp
symp = vasoconstriction, but coronary + working sk dilate
parasymp = genital + coronary dilate, + inhibition symp
effector organ receptor parasymp on bvs
M3 cholinergic = slight vasodilation coronary + genital arterioles
* ACh from parasymp presyn neurone
* incr coronary bloodflow, counteracting symp effect that reduces coronary bloodflow too far - don’t want heart musc under-perfused
effector organ receptor parasymp heart
M2 cholinergic
* cardiac myocytes (mainly SAN + AVN) - decr HR, decr conduction, longer refractory period, decr contractility = decr CO
* act on symp nerve endings ventr cells to inhibit release noradrenaline = decr symp effect = decr CO
symp effector organ receptors bvs
- α1 + α2 adrenergic vasoconstrict arterioles incr TPR, decr bloodflow non-essent, divert -> cardiac + working sk
- α1 + α2 adrenergic vasoconstrict veins abdom so more venous blood towards heart = incr proload + CO
- β2 adrenergic vasodilate coronary + sk musc arterioles = incr bloodflow = incr O2
- M3 cholinergic from SYMP NEURONES = sk musc arterioles vasodilate = incr sk musc bloodflow = incr O2
effector organ receptors symp heart
β1 adrenergic on cardiac myocytes
* incr HR
* incr conduction
* shorter refractory period (shorter systole, preserve diastole)
* incr contractility
== incr CO
what do adrenergic receptors respond to
circulating (nor)adrenaline from adrenal gland (= widespread response) + noradrenaline from presynaptic neurone
effect exercise on bod + so requirements for heart
- incr requirements O2 delivery + removal waste prods
- incr heat production by tissues
need incr CO + prioritise tissues
systems manage bp during exercise
- metabolic autoreg bloodflow - match bloodflow to metabolic rate so vasodil working musc
- psychogenic response = brain incr symp activity, decr parasymp = incr CO + incr TPR
- exercise reflex
- baroreflex
- sk musc + respiratory pumps
exercise reflex
joint + musc receptors = specialised nerve endings assess exercise intensity + feedback to ANS to modify response (symp vs parasymp)
feedback sys
respiratory pump
exercise = movement muscs thoracic cavity - diaphragm + ribcage
1. squished liver = blood out to caudal vena cava to heart = incr preload = incr ventr filling = incr EDVV = incr SV + incr CO + incr bp
2. movement diaphragm inspiration = incr abdom press = further emptying abdom veins = incr preload
3. incr depth resp = central veins (jugular, subclavian, femoral) distended (swell) + blood drawn abdom veins -> central circ = incr preload
skeletal pump
rhythmic contractions sk musc squeeze venous contents -> heart = incr preload
hypovolaemic shock is + possible causes
decr vol circulating blood = acute drop mean arterial press (bc decr preload = decr CO)
1. haemorrhage = loss whole blood - water, cells, prots
2. severe dehydration
3. sequestration blood, e.g. gut torsion
how is hypovolaemia detected
atrial vol receptors + arterial baroreceptors
body responses hypovolaemia
- baroreflex
- splenic contraction (capsule sm musc) replace lost vol + cells bc spleen blood higher % rbcs than normal
- starling’s law caps = decr HP caps due vasoconstriction = fluid ISF -> caps = incr circulating blood vol (limited dropping OP bc fluid reabsorbed no prots)
- RAAS
affect whole blood loss on PCV + TP
- initially unchanged as prop cells etc same
- as fluid replaced blood diluted so reduce (become anaemic)
- BM replaces cells w/in few weeks
- prot synth liver replaces prots in few days
forward heart failure + signs
= systolic failure
failure of output = decr CO = decr mean arterial press = decr perfusion
* cold extremities
* weak pulse
* slow cap refill time (mucous mems take long refill + pale)
* vasovagal syncope
* lethargic + exercise intolerant
causes backward
dilated cardiomyopathy
= DCM
heart musc wall thin + stretched = can’t contract effectively = SV low
backwards heart failure
= congestive heart failure (CHF)
can’t cope preload due excessive preload + failing heart
= incr atrial press
= incr venous press
= incr cap H press
= fluid -> ISF = oedema
e.g. due degenerative valve disease = contracts bit blood back atrium
results pulmonary oedema
- incr resp rate = tachypnoea
- resp difficulty = dyspnoea
- decr efficiency O2 exchange = decr blood oxygenation (-> myocardial hypoxia) = decr myocardial function
endogenous
w/in body
endogenous compensation for heart disease
maintain CO + bp
1. baroreflex
2. RAAS
3. Starling’s mech - decr CO = venous + atrial press incr = incr preload = incr EDVV = incr CO (for lil bit then oedema)
problems incr atrial press
atrial stretch = reduced atrial systole
problem caused by RAAS
long exposure aldosterone = cardiac musc fibroses + changes shape –> myocardial remodelling
decompensation bc why?
compensation mechs heart disease end up being problem - symp activation supposed be temporary
problems w prolonged vasoconstriction
(in compensation)
- reduction perfusion organs like kidneys = irreversible nephron damage -> renal failure = decr filtration = build up electrolytes + waste prods (toxic) = azotaemia
* leads uraemia (decr myocardial contractility) - increased afterload asw
- decr GI perfusion = intestine mucosa ischaemic = no barrier bac intestine -> blood (=-> sepsis + ulcers)
what happens if small oedema
incr ISF HP = decr filtration = incr lymph flow away = decr ISF prot conc = OP diff against filtration
* but lymph sys gets overwhelmed by fluid vol = oedema builds up
natriuretic peptides are?
= decomp
counteract neg effects compensation + decr blood vol
1. ANP (atrial) released due stretch atria
2. BNP (brain) mainly proded ventr when under stress
ultimately fail. test = indicator myocardial stretch
what do natriuretic peptides cause
- Na loss at kidney
* lose water w sodium = reduce water retention - peripheral vasodilation
- reduce renin + aldosterone
what does history consist of
- signs noticed - eat, drink, toilet, activity, demeanour, vomit, weight, lame
- duration
- progression
- general - ownership, vacc, worming, feeding
- medical history - illness + treatment
general exam
- observe
- watch walk
- history
- hands off exam inc resp rate
- hands on exam - head onwards
- peripheral pulses
- lymph nodes
- rectal temp
ascites
free fluid in abdomen
things check for clinical exam
- body condition
- mm colour + CRT
- HR + rhythm, association w pulse
- heart + lung sounds
- thoracic percussion
- evidence ascites, oedema, organomegaly
- jugular distension
what testing for bloods
- electrolytes - affect flow a pots thru heart = cause cardiac arrhythmias
- thyroxine - hyperthyroidism = hypertrophy ventr musc = tachycardia
- cortisol
- proBNP = precursor BNP, released response cardiac musc stretch - indicative heart failure coming
- cardiac tropnin I incr when damage myocardium
- Ca - affects HR + contractility
when do we take electrocardiograms
- collapse/seizure
- episodic weakness
- arrhythmia
- pulse deficits = non-conducted beats, pulse no match HR
normal arterial bp
120/80
systolic bp/diastolic bp
systolic higher bc diastole passive so flow w no press behind it
how measure bp
- put bit on end paw (takes reading)
- inflate cuff proximal to occlude bloodflow
- when sound stops slowly start deflate
- as soon as sound back read bp = blood returning, systolic bp
often just shows systolic
vertebral heart score
measure long axis + short axis + count how many vertebrae measure
* enlarged cardiac silhouette = cardiomegaly
hilus
== root = where vessels enter + leave organ
how distinguish bet enlarged pericardium + enlarged heart
enlarged pericardium = sharper line radiograph (bc not moving, heart moving in fluid) + can’t hear heart sounds as well
how perform echocardiography
- ultrasound machine probe conts crystals - elec current causes them change shape + emit ultrasound
- bounced back to probe when hits impenetrable surface
- receives echo + crystals change shape again, create elec signal + machine converts to pic made white pixels black background
where place probe for echocardiogram
lateral recumbency = bottom lung collapses lil bit + window see (lie longer = bigger window)
* bc gas impenetrable + lungs in way of heart
* fluid penetrable (shows black) = anechoic
need awake so heart function no affected
echogenicity
amount something relects untrasound waves
acoustic shadow
white area w shadow beneath on echocardiogram when area not penetrable + all waves bounced simultaneously
info from echocardiogram
- chamber size
- wall thickness
- valve thickness
- systolic + diastolic function
- visualise lesions on heart
right parasternal long axis 4 chamber view
most common view
pericardium = bright white bc bouncing back lots of beam
blood = black bc fluid
things closest probe at top
right parasternal short axis view - mid ventricle
probe same position as long axis view just turned 90 degrees
right parasternal short axis view - heart base
diameter LA ~ diameter aortic valve = view used identify LA enlargement
left parasternal view
M mode on ultrasound
as opposed B mode
B mode = 2D image moving real time
M mode = moving graph
* vertical axis = distance
* horizontal axis = time
M used measure contractility - diameter systole vs diastole
Doppler ultrasound
colour view show flow blood towards + away probe
* look for incompetent valve, turbulence, flow wrong way
how assess systolic function using ultrasound
- measure LV internal diameter at peak diastole (LVIDd) + systole (LVIDs)
- divide difference (ejection fraction by LVIDd
== fractional shortening (%)
== % by which diameter reduces
measure contractility
compare to normal for breed
how should speed entry blood into ventricles differ
faster during passive filling (atrial diastole) than systole as greater press grad
* if not then indicative delayed ventr relaxation (= early diastolic dysfunction)
oedema vs effusion
oedema = fluid into ISF (ISF incr)
effusion = free fluid in body cavity
diff bet structure sk + cardiac musc
sk = no branching, parallel
cardiac needs branching to organise uniform contraction
sk = nuclei at peripheral
cardiac = nuclei internal
nervi vasorum
nerves w/in walls vessels (in tunica adventitia)
what is present only in elastic arteries
- external elastic mem bet tunica adventitia + media
- internal elastic mem bet media + intima
sub-sections endocardium
- endothelium = surface simple squamous epithelial lining
- sub-endothelium = layer dense CT cont elastic + collagen fibres, maybe some sm musc
- sub-endocardium = loose CT (elastic + collagen), maybe bvs, lymph, adipose + Purkinje fibres in ventr
CT in myocardium
- loose stroma w rich cap bed
- continuous w CT in adjacent layers (sub-endocardium) + epicardium)
cardiac skeleton
layer CT sepping contractile musc cells atria + ventr - prevent direct spread depol
* atr + ventr myocardium insert on each side
- fibrous rings around valves
- triangular CT bet valves
- fibrous part interventricular septum
what is cardiac skeleton made up from diff species
pigs + cats = dense irregular CT
dogs = fibrocartilage
horses = hyaline cartilage
large ruminants = bone
layers epicardium
- sub-epicardium = loose CT w lots elastic fibres, lots bvs, nerves
- mesothelium covers surface
how is microscopic structure portal veins different other veins
carry blood 1 cap bed to other = need gen press move it along = thick muscular wall
metarterioles
small vessels w discontinuous layer sm musc to control blood flow thru specific cap beds
difference bet lymphatic + blood caps
lymph caps larger + much more permeable - sometimes gaps bet endothelial cells
* outer surface lymph endothelial cells attached by cell adhesion mols to surrounding tiss = held open = constant drainage contents = lower H press = movement in constant
what type endothelium forms epicardium
cuboidal
