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cardiovascular Flashcards

1
Q

purpose cardiovascular sys

A
  • delivery O2, nutrients, hormones, enzs
  • removal waste products + heat
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2
Q

what is present in thorax

A
  • heart
  • distal airways + lungs
  • thoracic oesophagus
  • thymus
  • bvs
  • lymph nodes + lymphatic vessels
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3
Q

label key parts + brief descr how articulate

A

13 ribs, each articulate w vertebra, 1st 9 connect sternum, rest to each other in costal arch except last = floating rib

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4
Q

where is heart located w/in thorax

A

bet lungs, ventral to hilus (root of lungs)

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5
Q

general lung anatomy

A

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

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6
Q

pleura

A

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

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7
Q

pericardium

A

invaginated serous mem sac containing heart w visceral + parietal layers sepped serous fluid (easy movement of heart) create potential space

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8
Q

layers heart wall

A
  1. endocardium = smooth inner lining
  2. myocardium = muscle
  3. epicardium = visceral pericardium
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9
Q

relative position heart + its parts

A

sits midline w apex deviated slightly to left
* base cranial + dorsal to apex
* right side cranial + to right of left

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10
Q

parts heart w pathway blood

A

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

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11
Q

coronary circulation

A

supplies heart muscle w blood - coronary arteries to, great cardiac vein from

5% of circulation

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12
Q

heart septums

A

interatrial = thin muscular wall
interventricular = v muscular, acc part left ventricle

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13
Q

structure AV valves

A

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

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14
Q

atrial appendage

A

= auricle - extra section to each atrium that also fills + empties

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15
Q

order systole + diastole

A
  1. atria fill passively, press increases so AV valves open
  2. ventricles fill passively, then atria contract to complete emptying + AV valves close = atrial systole
  3. ventricles contract but all valves closed = isovolumetric ventricular contraction
  4. press increases enough for SL valves open, ventricles still contracting = ventricular systole
  5. SL valves close, ventricles relax = isovolumetric ventricular relaxation
  6. AV valves open again, ventricles begin fill = ventricular diastole

systole = emptying, diastole = filling

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16
Q

isovolumetric contraction/relaxation why?

A

press in chamber has be increased before valves open - if all valves closed then vol constant

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17
Q

pressure volume loop

graph diagram thing

A
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18
Q

what causes heart sounds

generally

A

movement blood = blood turbulence as it bounces off surfaces

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19
Q

normal heart sounds causes

A

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

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20
Q

abnormal heart sounds

A

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

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21
Q

auscultation heart dogs

A

LEFTSIDE RIB SPACES
* pulmonic valve = 3
* aortic valve = 4
* mitral AV valve = 5

RIGHT SIDE RIB SPACES
* tricuspid valve = 4/5

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22
Q

how is heart cycle driven elec activity

v simplified pathway

A

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

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23
Q

function valve

A

ensure blood flow correct direction by opening + closing according press changes

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24
Q

structure valves

A

made cusps that open/close due press changes - 2 @ mitral, 3 @ tricuspid (not dogs - 2 main, other commissural)

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25
Q

structure around AV valves

A

chordae tendinae attach free edge cusps, preventing inversion into atria - attached papillary muscles ventricle walls but DONT control opening/closing

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26
Q

annulus fibrosus

A

fibrous skeleton structure surrounding all valves to support + electrical insulation bet atria + ventricles

therefore all valves at same level w/in heart

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27
Q

what is incompetence in relation to valves + what does it cause

A

failure close properly -> blood flows wrong direction (= regurgitation) -> congestion + heart failure

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28
Q

what is stenotic valve + what does it cause

A

= narrowed -> harder blood pass through -> more work for heart + greater press in chambers

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29
Q

function systemic cardiovascular sys

A

maintenance equilibrium bet blood plasma + interstitial fluid

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30
Q

what are caps + how does structure vary depending tiss supplying

A

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

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31
Q

layers vessel walls

A
  1. tunica intima - inside layer endothelial cells - e.g. continuous w endocardium
  2. tunica media - elastic + smooth musc depending function - e.g. arteries thicker
  3. tunica adventitia = CT
    * thick artery walls = need own blood supply = small bvs in adventitia = vasa vasorum

caps only have tunica intima

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32
Q

elastic vs muscular arteries

A

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

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33
Q

path arteries to cap bed

A

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

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34
Q

precapillary sphincter zone

A

at precapillary arterioles w intermittent smooth musc cells - regulate blood flow to caps

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35
Q

how is high press gened arterial sys

A
  • forceful contraction ventricle
  • elastic recoil arteries
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36
Q

why slow movement blood through caps

A
  • time exchange nutrients, waste products, etc
  • time to reach equilibrium
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37
Q

how do veins maintain blood flow towards heart

A
  1. internal press grad
  2. external press from muscles
  3. valves if blood pulled wrong direction by gravity to prevent backflow
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38
Q

what are arterial + venous systems referred to as

A

arterial = pressure reservoir of circulation - press stored here
venous = vol reservoir circulation - majority blood found here

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39
Q

collateral circulation defn

A

diff pathways to same tiss from side branches in artery in case blockage main trunk
* extra branches can accomodate increase flow

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40
Q

parts collateral circulation

A

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)

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41
Q

end arteries

A

no collateral circulation = only supply of oxed blood to a tiss
* blocked = no blood supply to tiss (ischaemia) -> infarction + necrosis

loads in brain

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42
Q

thoroughfare channels

A

caps straight to middle cap bed, missing most of it

blood directed here by precap sphincter zone

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43
Q

cap endothelium structure

A
  1. intercellular cleft = gap junction for diff water soluble mols
  2. tight junctions can seal endothelial layer - brain has continuous to only allow Na+ + water
    * other mols would have to fac diff across
  3. 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

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44
Q

sinusoids

A

type cap w thin walls + large diameter (blood through slowly) + discontinuous endothelium for free communication blood plasma + surrounding tiss
* lots liver + BM + arteriovenous

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45
Q

diapedesis is + example

A

diffusion movement cells out lumen post-cap venules
* how wbcs into circulation into tiss to fight infection

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46
Q

label left lateral aspect heart

A
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47
Q

label right lateral aspect heart

A
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48
Q

when does coronary circulation occur

A

during ventricular diastole bc systole = wall contracting = vessels squished + v little blood movement

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49
Q

where do coronary arteries arise from

A

from aortic bulb
* caudosinistral sinus -> left coronary artery
* cranial sinus -> right coronary artery

main branches = circumflex + interventricular

supplying walls respective ventricles

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50
Q

how does blood return heart from coronary circulation

A
  1. great cardiac vein -> coronary sinus in right atrium
  2. Thebesian veins = small veins directly draining all 4 chambers
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51
Q

descr aortic arch - main branches aorta

diagram

A

bigger species = left subclavian artery branches off brachiocephalic trunk, not distinct

left subclavian actually after brachiocephalic trunk
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52
Q

which veins return blood to cranial vena cava

A
  • internal + external jugular from head
  • cephalic from cranial chest + forelimb
  • auxillary + subclavian from forelimb + some intercostal
  • vertebral
  • internal thoracic
  • azygous from ribcage (ruminants + pigs)
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53
Q

veins leading caudal vena cava

diagram

A
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54
Q

what do we take thoracic radiographs for

A
  1. respiratory disease
  2. cardiovascular disease (esp Congestive Heart Failure)
  3. staging neoplasia (uncontrolled, abnormal growth)
    * looking for mastasis (2 malignant growths) in lungs
  4. trauma
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55
Q

why do tumours often spread to lungs

A

all blood has to go thru cap bed at lungs - can’t be bypassed
* tumour cell likely be seived out + remain in lungs

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56
Q

what to remember when taking thoracic radiograph to examine lungs

A

take at peak inspiration - can be gently inflated via anaesthetic breathing sys

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57
Q

1st priority for radiography

A

patient 1st - need to stabilise to sedate/anaesthetise b4 radiograph
* prioritise right here + now to stabilise - diagnosis irrelevant if dead

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58
Q

which position best view for lungs

A

ventrodorsal as lungs closest to plate
* tiss closest to plate most accurately repped

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59
Q

how should you position for dorsoventral/ventrodorsal

A

sternum + thoracic vertebrae superimposed

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60
Q

attenuate defn

A

blocks the beam - opp to expose

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61
Q

what to consider when positioning for lateral

A

left + right ribs superimposed - less blocking image

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62
Q

how many views to take

A

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

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63
Q

which position don’t use if in respiratory distress

A

ventrodorsal as shouldn’t be laid on their back

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64
Q

which view is best for heart

A

dorsoventral as heart closest plate (by sternum)

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65
Q

why do we say we see cardiac silhouette on thoracic radiograph

A

what’s visible is heart in pericardial sac w fluid inside - might be excess fluid that bigger, not larger heart

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66
Q

label position heart chambers

A
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67
Q

label heart chambers

A
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68
Q

label lung lobes

A

not visible in radiography but should know positions so can identify where mass etc located w/in lungs

note: caudal lung lobes overlap diaphragm
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69
Q

label lung lobes

A
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70
Q

label lung lobes

A
accessory sits on midline bet 2 caudal lobes
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71
Q

how to tell if RL or LL view thoracic radiograph

A

RL = crura diaphragm align = smooth round curve
LL = diaphragm crura diverge = Y shape at dorsal aspect

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72
Q

how to tell if DV or VD view thoracic radiograph

A

VD = diaphragmcrura superimposed so triple hump appearance
DV = diaphragm is a smooth curve

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73
Q

basic sims + diffs bet circulatory systems

A
  • same vol blood each side
  • vol + flow rates L + R ventricles similar
  • press L + R ventricles v diff
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74
Q

hydrostatic press

A

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

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75
Q

how is HP in caps altered

A

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)

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76
Q

bulk flow def

A

movement fluid by means HP diff - v fast over long distances

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77
Q

perfusion press

A

press needed for blood to move along bv
diff in press bet any 2 pts along
P(inlet) - P(outlet)

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78
Q

what does it mean if a tiss is well perfused

A

good blood flow

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79
Q

osmotic press

A

drive for water to move into a sol by osmosis, exerted by osmotic particles (e.g. solutes)

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80
Q

plasma oncotic press

A

= 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

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81
Q

bulk flow across vessels caused by?

A

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)

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82
Q

Starling’s law caps

A

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

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83
Q

how does filtration + absorption change along cap

A
  • HP decreases along cap length as fluid moves out
  • OP constant

therefore most filtration at start, absorption by end

normally overall filtration > absorption

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84
Q

oedema

A

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

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85
Q

how is arterial supply arranged + why

A

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

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86
Q

how are pulmonary + systemic circulation arranged

A

in series = blood has to pass through 1 to get to other = change in 1 affects other

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87
Q

cardiac output

A

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

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88
Q

EDVV, ESVV + SV

A

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

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89
Q

ejection fraction

and what measures

A

prop available blood in ventricle that was ejected - measure systolic function heart

as percentage

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90
Q

what affects SV

A

EDVV + ESVV

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91
Q

what affects EDVV

A
  • diastolic filling time - more time fill = more full
  • preload
  • compliance = stretchiness ventricle wall
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92
Q

what affects ESVV

A
  • afterload
  • contractility = how good ventr at contracting + ejecting contents (efficacy in time, e.g. same vol out less time)
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93
Q

what happens if EDVV increases too much

A

w/in normal limits fine, but too much = heart wall overstretched = damaged + loses contractility

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94
Q

what is preload

A

filling press ventr = atrial press = venous press = EDVV

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95
Q

how to increase preload

A

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

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96
Q

action respiratory + sk pump during exercise

A

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

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97
Q

what happens if veins compressed too much

A

persistent increase in H press = fluid leaks out, e.g. into permeable pleura, + forms oedema

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98
Q

effect preload on EDVV

A

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

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99
Q

effect EDVV on SV

A
  1. increase EDVV = more blood available for ventricle dispel
  2. AND stretching cardiac musc cells = increase Ca2+ release = increase contractility = decrease ESVV = SV
  3. BUT massive EDVV = cardiac musc overstretched + damaged + loses contractility = increase ESVV

increasing EDVV = SV increases until plateaus + eventually decreases

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100
Q

heterometric autoregulation

what, why, how

A

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

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101
Q

compliance

A

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

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102
Q

affect big preload on compliance

A

CT in ventricle reaches elastic limit = stiffer + won’t take more vol

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103
Q

example disease affecting ventricle compliance + consequence

A

dilated cardiomyopathy = decrease compliance = need higher preload maintain same SV

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104
Q

how heart rate affects CO

A
  1. more contractions per min (CO=HRxSV)
  2. decreases diastolic filling time = less filling = lower EDVV = lower SV

so despite CO=HRxSV, CO no increase in proportion HR

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105
Q

lusitropy

A

ability relax

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106
Q

how diastolic filling time maintained w high HR

under physiological stress = flight/flight, exercise

A

symp NS responds:
* increase contractility = decrease ESVV = increase SV (increase EF)
* decrease length systole = relatively longer diastole = better EDVV

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107
Q

difference response increased HR physiological stress + disease

A

pathological tachycardia (or pacemaker) = length systole preserved = at higher HR CO decreases

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108
Q

why is ventricular filling divided 2 stages

A

rapid filling, atrial press drops to near ventr press, so rate drops
reduced filling (diastasis), then atrial systole to complete filling

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109
Q

what causes valves close

A

press area entering exceeds press area leaving = slight backflow blood = valve closes

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110
Q

why 2 stages ventricular ejection

A
  1. rapid ejection as blood under high press
  2. reduced ejection as rate decreased as ventricular press past peak systolic
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111
Q

how does importance atrial systole vary

A

higher HR = atrial systole responsible higher % ventr filling (less is passive)
* atrial fibrillation = atria no contract properly - fine at rest but during exercise no

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112
Q

how is contractility altered

A
  1. symp autonomic NS increases it to decrease ESVV
  2. increases w mild musc stretch as w physiological preload increase
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113
Q

afterload + response when increased

w press-vol loop for increased afterload

A

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

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114
Q

where is greatest resistance to flow

A

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

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115
Q

vascular resistance

A

measure how compliant vessel is - high resist = low compliance

== perfusion press/bloodflow

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116
Q

Poiseuille’s law

A

resistance varies inversely w 4th power radius - small change radius = big change resist

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117
Q

what affects vascular resistance

A
  1. length bv - can’t change
  2. radius bv - wider = lower resistance bc press lower
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118
Q

by what + how is vascular resistance modified

A

ANS + hormones
* vasoconstriction = vessels narrow = afterload increases…

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119
Q

symp NS response to exercise

A

increase CO:
* increase contractility
* increase HR (but decrease systole preserve EDVV)
* vasoconstriction to increase preload

plus breathing heavier + moving = action respiratory + sk musc pumps

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120
Q

total peripheral resistance (TPR)

A

net resistance whole circulation - arterioles contrib most

(mean aortic press - mean vena caval press)/CO
* caval press negligible so:
TPR = mean aortic press/CO

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121
Q

why arterial press approx same rest + exercise

A

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

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122
Q

hyper/hypotension

A
  1. increased bp - usually systemic arterioles constricted = increased TPR = hypertrophy cardiac musc as works overcome afterload + maintain CO (elderly cats)
  2. decreased bp - due significant haemorrhage, anaesthesia
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123
Q

hypertrophy

A

increase + growth musc cells

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124
Q

how is bp repped

shows graph change over time (don’t learn)

A

systolic/diastolic = 120/80mmHg

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125
Q

pulse press

A

systolic press (Ps) - diastolic press (Pd)

bc press in arteries pulsatile (up + down)

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126
Q

what is systolic press

A

in systole blood ejected aorta/pulm art at high press - press in vessel rises to systolic press

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127
Q

what is diastolic press

A

SL valve closed + heart in diastole = press in aorta/pulm art decreases to diastolic press

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128
Q

what affects pulse press

increase

A
  • SV
  • aortic compliance
  • HR
  • TPR

increase, decrease (bigger afterload), decrease (bigger EDVV), increase

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129
Q

how increase pulse press

A
  • 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

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130
Q

how to dissect to see right side heart

A

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

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131
Q

how to dissect to see left side heart

A

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)

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132
Q

what is tracheal bifurcation

A

where trachea divides into left + right primary bronchi

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133
Q

what are the heart surfaces

A

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,

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134
Q

how is heart oriented in animal bod

A
  • 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
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135
Q

interventricular grooves

A

coronary grooves w coronary arteries in
auricular surface = paraconal
atrial surface = subsinuosal

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136
Q

what is left azygous vein

A

pigs + ruminants: drainage directly from body into coronary sinus - everyone else only have 1 azygous vein

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137
Q

muscular ridges visible in walls heart

A

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

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138
Q

names of cusps in AV valve

A

septal + parietal, plus angular in tricuspid (not dogs)

139
Q

external distinguishing bet species lungs

A
  • 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
140
Q

thorax dissection general process

A
  • 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
141
Q

jugular furrow - what + where

A

runs down neck, where fur changes direction, houses external jugular vein

142
Q

where does heart sit

ribs

A

under ribs 4 + 5

143
Q

where is pulmonic valve located

A

LHS under rib space 3rd

144
Q

where is aortic valve located

A

LHS under 4th rib space

145
Q

where is mitral valve located

A

LHS under 5th rib space

146
Q

where is tricuspid valve located

A

RHS under 3rd/4th/5th rib space

variable

147
Q

other name xiphoid process

A

xiphisternum

148
Q

dorsal epaxial muscles

A

at top thorax
* latissimus dorsi
* fan-shaped serratus ventralis
* serratus dorsalis

149
Q

2 muscles on cranial side thorax

A
  1. scalenus (top) involved inspiration, attached 1st few ribs
  2. rectus thoracis (more circular below) involved inspiration, running w tendon of rectus abdominis musc
150
Q

intercostal muscles

A
  1. external run caudoventrally
  2. internal underneath run cranioventrally
151
Q

where do vessels run on ribs

A

run along caudal border of rib

152
Q

phrenic nerve

A

runs suspended in mediastinum to innervate diaphragm

one each side

153
Q

where pleura bends back on itself

A
  • costomediastinal recess
  • costodiaphragmatic recess
  • cupula pleura extends beyond 1st rib
154
Q

basic features foetal CV sys

A
  • 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

155
Q

why is blood in foetal circ less oxed than adult

A
  1. deoxed blood from RV in pulm art into aorta through ductus arteriosus
  2. deoxed blood from pulm veins (lil bit) in LA mixes w oxed blood from RA
156
Q

1st stage CV sys development

A
  1. cells splanchnic mesoderm organised form blood islands of haemangioblast cells
  2. stim surrounding mesenchymal cells form endothelial + smooth musc cells form walls around
  3. blood islands start join, forming start vessel structures
  4. small vessels coalesce form larger vessels that comm = dorsal aortae

uses cell signalling

157
Q

structure heart before bits start join

A
  • cardiogenic plate -> cardiac tube later
  • neural plate
  • coelom (L+R) - fuses w neural plate form coelemic cavity (horseshoe), extends round heart -> pericardial cavoty
158
Q

foetal position heart + implications

A

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

159
Q

formation cardiac tube from cardiogenic plate

A
  • -> endocardial tube w L + R limbs
  • moves dorsal to neural plate
  • 2 limbs coalesce
  • -> cardiac tube = primitive heart, simple pump
160
Q

fusion cardiac tube to make caterpillar

A
  1. dorsal aortae fuse either end cardiac tube horseshoe (w folding asw)
  2. vitelline veins fuse other end
  3. dorsal aortae fuse caudally (opp end from vitelline veins)
  4. 1st aortic arches form where cardiac tube joined dorsal aortae -> 1 dorsal aorta w aortic arches in between
  5. cardiac tube folds form structure w 5 parts
161
Q

structure cardiac tube + what each part becomes later

caterpillar stage, on pic

A
162
Q

formation AV canals

A

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)

163
Q

mesenchymal cells

A

multipotent stem cells bet endocardium + myocardium

164
Q

formation ventricles

A

primordial ventricular septum forms bet dilated section bulbus cordis + foetal ventr (together were common ventr)
* interventricular foramen remains until defferential cellular proliferation closes

165
Q

formation atria

A
  1. septum primum grows down towards intermedium, leaving hole (foramen primum) - blood sinus venosus -> LA
  2. programmed cell death = 2nd opening forms more dorsally = foramen secundum (+ 1st closes)
  3. 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

166
Q

where is sinus venosus found w/in devloping atria + why

A

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

167
Q

why is lining of atrial appendages lumpy

A

developed from foetal atrium as it split in 2

168
Q

how do pulm veins develop in foetal heart

A

bud out developing LA, join lungs - expansion generally forms smooth lining LA

169
Q

how do AV valves form

A
  1. mesenchymal proliferation on edge apertures endocardial cushions forming septum intermedium
  2. cavitation musc beneath cusps
  3. attached muscular strands from free ventr walls3. strands diff replace musc tiss w CT = chordae tendinae attached papillary musc
170
Q

where is pacemaker located throughout foetal heart development

A
  1. caudal part cardiac tube - whole tube contracting together
  2. right limb sinus venosus
  3. becomes SAN once RA forms - annulus fibrosis = atr + ventr electrically isolated
171
Q

sepping aorta + pulm art

A

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)

172
Q

how SL valves form

A

at origin trunks mesenchymal tiss proliferates + ridges remodelled form CT covered endothelium = cusps

173
Q

aortic arches

A

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

174
Q

how do all veins join

A
  1. vitelline incorps drainage gut + passes thru liver = hepatic sinusoids
  2. vitelline + umbilical anastomose on L + R (sep) = common drainage
  3. shunt bet left umbilical + cranial part right common drainage = venus ductosus
175
Q

purpose ductus venosus

A

mostly bypass liver as not using it or gut

176
Q

what forms cranial vena cava

A

cranial cardinal vein - after anastomosis R + L

L cranial cardinal also coronary sinus

177
Q

what happens w caudal cardinal vein

A

-> subcardinal, drains kidneys -> caudal vena cava (w cranial vitelline)
-> supracardinal, drains dorsal wall; R -> azygous

anastomoses bet subcardinal + supracardinal

178
Q

ductus arteriosus where + why

A

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

179
Q

Eustachian valve

A

at mouth entry vena cava to RA, directing blood to foramen ovale to LA to aorta to bod

180
Q

what changes at birth

A
  1. umbilical arteries contract = no blood flow neonate -> placenta
  2. umbilical veins contract = venous blood to neonate - 30% blood vol so no cut too early
  3. when rupture arteries undergo elastic recoil to prevent haemorrhage
181
Q

what do umbilical artery + vein become after birth

A
  • umbilical artery -> round ligament of bladder
  • umbilical vein -> round ligament of liver
182
Q

how does foramen ovale close

A

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)

183
Q

how does ductus arteriosus close

A

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

184
Q

what happens if ductus arteriosus no close

A

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

185
Q

how does ductus venosus close

A

smooth musc contracts = flow stopped + diverted to hepatic circ = liver sinusoids perfused

permanent w/in 2-3 weeks

186
Q

aortic stenosis

A

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

187
Q

ventricular septal defect

A

septum no completed = blood left -> right down press grad = sound on right
* overload RV = overload pulm circ, increased return LA = left vol overload….

188
Q

vascular ring anomalies

A

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

189
Q

how does cardiac musc contract together

A

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

190
Q

how does heart beat + control

A

pacemaker cells have automaticity = spontaneously depol so ANS innervation only to change HR + rhythm (contractility)
* symp via cardiac nerves
* parasymp via vagus nerve

191
Q

what in heart is responsible initial a pot

A

SAN as has pacemaker cells that depol faster than AVN

192
Q

ectopic pacemaker

A

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

193
Q

pathway a pot thru heart

A
  1. SAN free wall RA gens a pot, travels cell-cell across atria = contract at once
  2. annulus fibrosus = no pass to ventr + coalesce at AVN
  3. conduction slowed as narrow fibres AVN so time to pass thru = gap bet atr + ventr systole
  4. passed bundle of His (AV bundle) traversing annulus fibrosus
  5. 2 paths down interventricular septum (L+R)
  6. L bundle branch into anterior + posterior fascicles to supply thick wall LV
  7. 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

194
Q

how is cardiac musc a pot diff from sk musc

A

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

195
Q

how is a pot gened in cardiac musc cell

A

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

196
Q

how is long plateau phase in cardiac musc cells caused

A

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

197
Q

how is atrial a pot shorter

A
  • Ca2+ channs open less time
  • K+ channs closed less time
  • shorter refractory period = shorter less flat plateau
198
Q

what is pacemaker pot

A

pacemaker cells no have stable resting mem pot - after repol mem pot slowly rises back to threshold = pacemaker pot

199
Q

how is pacemaker pot gened

A
  • ‘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

200
Q

why does AVN have longer refractory period

A

narrower fibre diameter - so ventre no beat too soon + elec impulse no circle back to atria

201
Q

how does symp NS increase contractility

A

longer opening Ca2+ channs

202
Q

what does electrocardiogram do

A

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

203
Q

what makes ECG upward or downward deflection

A

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)

204
Q

what do waveforms on ECG rep

A

P = atrial depol
QRS = ventr depol
T = ventr repol

205
Q

which direction does a pot flow make P wave

A

R -> L = upwards wave

206
Q

which way does a pot flow make all parts QRS complex

A

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

207
Q

which was does a pot flow make T wave

A

unpredictable so can go up or down

208
Q

where are ECG leads located w charges

diagram

A

bipolar leads have pos + neg poles
augmented unipolar leads measure elec pot bet pos electrode 1 limb + avg other 2

209
Q

why do we use lead II most

A

most closely matches normal electrical axis heart = overall direction a pot

210
Q

how to assess HR from ECG

A
  1. avg R-R interval then maths to HR
  2. no. PQRST complexes in 3 or 6 secs then multiply
211
Q

how to assess rhythm using ECG

A

how consistent are R-R intervals
* regular = sinus rhythm

212
Q

what does tall P wave mean

A

P pulmonale = RA enlargement (bigger elec pot diff)

213
Q

what does wide P wave mean

A

P mitrale = LA enlargement (longer atrial depol so more time)

214
Q

what does tall R wave mean

A

ventr enlargement (bigger elec pot diff)

215
Q

what does wide R wave/wide QRS complex mean

A

LV enlarged w hypertrophy - depol taking longer

216
Q

bradycardia

A

slow HR

217
Q

tachycardia

A

fast HR

218
Q

regularly vis irregularly irregular rhythm

A

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

219
Q

how is bp maintained normally (no extreme changes)

A

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

220
Q

explain active hyperaemia

A

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

221
Q

how do intrinsic controls deal w complete interruption blood flow essential tiss

A

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

222
Q

paracrine intrinsic control is?

A

locally acting chems that alter flow rate in response local environ

223
Q

what happens in response increased blood flow velocity

A
  • endothelial cells sheared due increased velocity = release NO = vasodilator
  • parasymp neurones release NO + ACh - stims more release NO from endothelial

intrinsic paracrine controls

224
Q

response local irritation

A
  • 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

225
Q

response endothelial damage

= actual cut

A
  • endothelin 1 release = vasoconstriction
  • thromboxane A2 from platelets = vasocon + platelet aggregation

intrinsic paracrine control

226
Q

relationship intrinsic + extrinsic blood flow controls

A

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

227
Q

ischaemia - what is, why happens + normal response

A

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)

228
Q

infarction + necrosis

A

tiss damage + cell death due ischaemia

e.g. from badly applied bandage

229
Q

how do coronary arteries ensure maintained bloodflow during exercise

A

low resistance so even w increased HR + contractility + shorter diastole still enough bloodflow to card musc

230
Q

risk to pulmonary vessels w anaesthesia

A

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

231
Q

extrinsic control + what would happen w/o

A

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

232
Q

how extrinsic control works

A

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

233
Q

how is baroreflex started

A
  1. baroreceptors = stretch receptors to sense bp as stretch affected internal press
  2. sending constant, regular a pots to CV centre
  3. increase/decrease bp = inc/dec frequency a pots
  4. frequency detected CV centre + compared ref val so change detected + response ilicited

its immediate = 1st act in response change bp

234
Q

where are barorecptors + why

A
  • aortic arch to detect changes in press to bod
  • carotid sinuses to check vessels supplying brain
235
Q

baroreflex response to drop bp

vice versa for increase

A
  1. 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
  2. dec parasymp output = more vasoconstr + inc HR

bc Pa = CO*TPR

236
Q

renin-angiotensin-aldosterone sys (RAAS)

A

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

237
Q

Starling’s law caps

A

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

238
Q

what governs long term regulation bp

A

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

239
Q

psychological overrides bp control

A

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

240
Q

lymphoid sys

A

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

241
Q

lymphoid tissues

A
  • nodes
  • spleen
  • thymus
  • mucosa-associated lymphoid tiss
  • lymphocytes (B+T cells)
  • plasma cells
242
Q

chyle

A

lymph once passed thru gut so conts lipid from SI villiin form chylomicrons (too big enter blood caps)

white

243
Q

roles lymphatic sys

A
  • 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
244
Q

structure lymphatic vessels

A
  • 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

245
Q

lymph node structure

A
246
Q

pig lymph node structure

A
247
Q

what happens at lymph nodes

A
  • foreign mat removed phagocytes
  • fresh lymphocytes recruited from cortex

all lymph passes thru at least 1

248
Q

lymphocentre defn

A

grp few relatively large lymph nodes
* horses + pigs = lots little

249
Q

lymphocentres of head

A
  • retropharyngeal
  • parotid
  • mandibular

drain all structures head

250
Q

lymphocentres neck

A
  • superficial
  • deep cervical

drain neck, superficial part cranial trunk, top forelimbs

251
Q

lymphocentres forelimb

A

axillary (armpit)
* drains deep structures whole limb + superficial structures distal limb

252
Q

thorax lymphocentres

A
  • dorsal thoracic
  • ventral thoracic
  • mediastinal
  • bronchial

drains contents + walls thorax

253
Q

lymphocentres abdomen

A
  • lumbar
  • coeliac
  • cranial mesenteric
  • caudal mesenteric

drain loin area (inc repro tract) + abdominal contents

254
Q

hindquarter lymphocentres

A
  • popliteal
  • ischial
  • deep inguinal
  • superficial inguinal
  • iliosacral

drain hindlimb, abdominal wall + pelvis

255
Q

which lymph nodes are palpable - dog

on diagram

A
256
Q

palpable lymph nodes - cat

A
257
Q

palpable lymph nodes ox

A

prescapular + prefemoral

258
Q

palpable lymph nodes horse

A

submandibular

259
Q

which LNs visible radiograph

A

enlarged thoracic

260
Q

which LNs visible ultrasound

A

enlarged abdominal

261
Q

main duct pathways

diagram for ref

A
  1. L + R tracheal ducts from retropharyngeal nodes drain head + proximal forelimb
  2. L tracheal -> thoracic duct
  3. R tracheal -> R lymphatic duct (drains R thorax) (joins thoracic)
  4. mediastinal from heart
  5. tracheobronchial from lungs
  6. lumbar ducts (hind) -> cisterna chyli -> thoracic duct
262
Q

cisterna chyli

A

collection vat w drainage all structures hind area

263
Q

only 1 lymphatic drainage pathway?

A

several alternative so disaster + need tie one of, or one blocked, it’s okay bc lymph will find another way

264
Q

why need know lymph drainage pathway

A

pathway provides route metastasis neoplastic diseases that cause tumour growth
* know routes = accurate disease staging + planning surgery

265
Q

embryology lymphatic sys

A
  1. 6 lymph sacs
  2. develop into LNs (except cisterna chyli)
  3. comms vessels arise bet LNs as mesenchymal cells infiltrate
    * bet jugular sacs + cisterna chyli = thoracic duct

atarts after CV sys established

266
Q

names lymph sacs foetus

A
  • paired jugular
  • paired iliac
  • retroperitoneal
  • cisterna chyli

last 2 drain viscera

267
Q

how does spleen develop + overall purposes

A

from mesoderm - v vascular organ w lymphoid functions but also stores rbcs

268
Q

where is thymus

A

cranial mediostinum

269
Q

how does thymus develop

A
  1. arises endoderm + mesoderm
  2. initially paired organ, gives off buds
  3. grow down neck + invade mediostinum
  4. form single organ extending to pericardium
  5. replaced adipose tiss over time
270
Q

how does fluid move into lymph

A
  1. net filtration from blood caps into ISF bc HP diff > OP diff most length caps
  2. bulk flow into lymph caps (low press) - remove ISF to prevent formation oedema down HP grad
271
Q

how does lymphatic sys maintain HP grad for bulk flow in from ISF

A
  • 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
272
Q

causes lymph flow

A
  1. HP grad -> venous sys
  2. external press sk musc
  3. sm musc walls larger lymphatic vessels
  4. valves prevent backflow

more on top HP grad as grad slow so movement slow

273
Q

oedema vs effusion

A

oedema = fluid in interstitial space
effusion = free fluid w/in cavity

274
Q

what causes failure lymphatic drainage

A
  • 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
275
Q

effect ANS on heart

A

incr/decr HR + contractility

276
Q

where does symp NS exit CNS

A

preganglionic fibred from thoracolumbar spinal segments, then postganglionic from sympathetic ganglia C5-T3

277
Q

symp ganglia combining

A

C7-T3 combine make stellate ganglion (large)
C5 + C6 make middle cervical ganglion

278
Q

where does parasymp NS originate

A

craniosacral = from brainstem + sacral spinal segments
* cranial nerve X (vagus) runs caudally + supplies thoracic viscera

279
Q

result on vessels symp + parasymp

A

symp = vasoconstriction, but coronary + working sk dilate
parasymp = genital + coronary dilate, + inhibition symp

280
Q

effector organ receptor parasymp on bvs

A

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

281
Q

effector organ receptor parasymp heart

A

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

282
Q

symp effector organ receptors bvs

A
  1. α1 + α2 adrenergic vasoconstrict arterioles incr TPR, decr bloodflow non-essent, divert -> cardiac + working sk
  2. α1 + α2 adrenergic vasoconstrict veins abdom so more venous blood towards heart = incr proload + CO
  3. β2 adrenergic vasodilate coronary + sk musc arterioles = incr bloodflow = incr O2
  4. M3 cholinergic from SYMP NEURONES = sk musc arterioles vasodilate = incr sk musc bloodflow = incr O2
283
Q

effector organ receptors symp heart

A

β1 adrenergic on cardiac myocytes
* incr HR
* incr conduction
* shorter refractory period (shorter systole, preserve diastole)
* incr contractility

== incr CO

284
Q

what do adrenergic receptors respond to

A

circulating (nor)adrenaline from adrenal gland (= widespread response) + noradrenaline from presynaptic neurone

285
Q

effect exercise on bod + so requirements for heart

A
  • incr requirements O2 delivery + removal waste prods
  • incr heat production by tissues

need incr CO + prioritise tissues

286
Q

systems manage bp during exercise

A
  1. metabolic autoreg bloodflow - match bloodflow to metabolic rate so vasodil working musc
  2. psychogenic response = brain incr symp activity, decr parasymp = incr CO + incr TPR
  3. exercise reflex
  4. baroreflex
  5. sk musc + respiratory pumps
287
Q

exercise reflex

A

joint + musc receptors = specialised nerve endings assess exercise intensity + feedback to ANS to modify response (symp vs parasymp)

feedback sys

287
Q

respiratory pump

A

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

288
Q

skeletal pump

A

rhythmic contractions sk musc squeeze venous contents -> heart = incr preload

289
Q

hypovolaemic shock is + possible causes

A

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

290
Q

how is hypovolaemia detected

A

atrial vol receptors + arterial baroreceptors

291
Q

body responses hypovolaemia

A
  • 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
292
Q

affect whole blood loss on PCV + TP

A
  1. initially unchanged as prop cells etc same
  2. as fluid replaced blood diluted so reduce (become anaemic)
  3. BM replaces cells w/in few weeks
  4. prot synth liver replaces prots in few days
293
Q

forward heart failure + signs

= systolic failure

A

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

294
Q

dilated cardiomyopathy

= DCM

A

heart musc wall thin + stretched = can’t contract effectively = SV low

295
Q

backwards heart failure

= congestive heart failure (CHF)

A

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

296
Q

results pulmonary oedema

A
  1. incr resp rate = tachypnoea
  2. resp difficulty = dyspnoea
  3. decr efficiency O2 exchange = decr blood oxygenation (-> myocardial hypoxia) = decr myocardial function
297
Q

endogenous

A

w/in body

298
Q

endogenous compensation for heart disease

A

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)

299
Q

problems incr atrial press

A

atrial stretch = reduced atrial systole

300
Q

problem caused by RAAS

A

long exposure aldosterone = cardiac musc fibroses + changes shape –> myocardial remodelling

301
Q

decompensation bc why?

A

compensation mechs heart disease end up being problem - symp activation supposed be temporary

302
Q

problems w prolonged vasoconstriction

(in compensation)

A
  1. reduction perfusion organs like kidneys = irreversible nephron damage -> renal failure = decr filtration = build up electrolytes + waste prods (toxic) = azotaemia
    * leads uraemia (decr myocardial contractility)
  2. increased afterload asw
  3. decr GI perfusion = intestine mucosa ischaemic = no barrier bac intestine -> blood (=-> sepsis + ulcers)
303
Q

what happens if small oedema

A

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

304
Q

natriuretic peptides are?

= decomp

A

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

305
Q

what do natriuretic peptides cause

A
  1. Na loss at kidney
    * lose water w sodium = reduce water retention
  2. peripheral vasodilation
  3. reduce renin + aldosterone
306
Q

what does history consist of

A
  • signs noticed - eat, drink, toilet, activity, demeanour, vomit, weight, lame
  • duration
  • progression
  • general - ownership, vacc, worming, feeding
  • medical history - illness + treatment
307
Q

general exam

A
  1. observe
  2. watch walk
  3. history
  4. hands off exam inc resp rate
  5. hands on exam - head onwards
  6. peripheral pulses
  7. lymph nodes
  8. rectal temp
308
Q

ascites

A

free fluid in abdomen

309
Q

things check for clinical exam

A
  • body condition
  • mm colour + CRT
  • HR + rhythm, association w pulse
  • heart + lung sounds
  • thoracic percussion
  • evidence ascites, oedema, organomegaly
  • jugular distension
310
Q

what testing for bloods

A
  • 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
311
Q

when do we take electrocardiograms

A
  • collapse/seizure
  • episodic weakness
  • arrhythmia
  • pulse deficits = non-conducted beats, pulse no match HR
312
Q

normal arterial bp

A

120/80
systolic bp/diastolic bp

systolic higher bc diastole passive so flow w no press behind it

313
Q

how measure bp

A
  1. put bit on end paw (takes reading)
  2. inflate cuff proximal to occlude bloodflow
  3. when sound stops slowly start deflate
  4. as soon as sound back read bp = blood returning, systolic bp

often just shows systolic

314
Q

vertebral heart score

A

measure long axis + short axis + count how many vertebrae measure
* enlarged cardiac silhouette = cardiomegaly

315
Q

hilus

A

== root = where vessels enter + leave organ

316
Q

how distinguish bet enlarged pericardium + enlarged heart

A

enlarged pericardium = sharper line radiograph (bc not moving, heart moving in fluid) + can’t hear heart sounds as well

317
Q

how perform echocardiography

A
  1. ultrasound machine probe conts crystals - elec current causes them change shape + emit ultrasound
  2. bounced back to probe when hits impenetrable surface
  3. receives echo + crystals change shape again, create elec signal + machine converts to pic made white pixels black background
318
Q

where place probe for echocardiogram

A

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

319
Q

echogenicity

A

amount something relects untrasound waves

320
Q

acoustic shadow

A

white area w shadow beneath on echocardiogram when area not penetrable + all waves bounced simultaneously

321
Q

info from echocardiogram

A
  • chamber size
  • wall thickness
  • valve thickness
  • systolic + diastolic function
  • visualise lesions on heart
322
Q

right parasternal long axis 4 chamber view

most common view

A

pericardium = bright white bc bouncing back lots of beam
blood = black bc fluid

things closest probe at top

323
Q

right parasternal short axis view - mid ventricle

A

probe same position as long axis view just turned 90 degrees

324
Q

right parasternal short axis view - heart base

A

diameter LA ~ diameter aortic valve = view used identify LA enlargement

325
Q

left parasternal view

A
326
Q

M mode on ultrasound

as opposed B mode

A

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

327
Q

Doppler ultrasound

A

colour view show flow blood towards + away probe
* look for incompetent valve, turbulence, flow wrong way

328
Q

how assess systolic function using ultrasound

A
  1. measure LV internal diameter at peak diastole (LVIDd) + systole (LVIDs)
  2. divide difference (ejection fraction by LVIDd
    == fractional shortening (%)
    == % by which diameter reduces
    measure contractility

compare to normal for breed

329
Q

how should speed entry blood into ventricles differ

A

faster during passive filling (atrial diastole) than systole as greater press grad
* if not then indicative delayed ventr relaxation (= early diastolic dysfunction)

330
Q

oedema vs effusion

A

oedema = fluid into ISF (ISF incr)
effusion = free fluid in body cavity

331
Q

diff bet structure sk + cardiac musc

A

sk = no branching, parallel
cardiac needs branching to organise uniform contraction

sk = nuclei at peripheral
cardiac = nuclei internal

332
Q

nervi vasorum

A

nerves w/in walls vessels (in tunica adventitia)

333
Q

what is present only in elastic arteries

A
  • external elastic mem bet tunica adventitia + media
  • internal elastic mem bet media + intima
334
Q

sub-sections endocardium

A
  1. endothelium = surface simple squamous epithelial lining
  2. sub-endothelium = layer dense CT cont elastic + collagen fibres, maybe some sm musc
  3. sub-endocardium = loose CT (elastic + collagen), maybe bvs, lymph, adipose + Purkinje fibres in ventr
335
Q

CT in myocardium

A
  • loose stroma w rich cap bed
  • continuous w CT in adjacent layers (sub-endocardium) + epicardium)
336
Q

cardiac skeleton

A

layer CT sepping contractile musc cells atria + ventr - prevent direct spread depol
* atr + ventr myocardium insert on each side

  1. fibrous rings around valves
  2. triangular CT bet valves
  3. fibrous part interventricular septum
337
Q

what is cardiac skeleton made up from diff species

A

pigs + cats = dense irregular CT
dogs = fibrocartilage
horses = hyaline cartilage
large ruminants = bone

338
Q

layers epicardium

A
  1. sub-epicardium = loose CT w lots elastic fibres, lots bvs, nerves
  2. mesothelium covers surface
339
Q

how is microscopic structure portal veins different other veins

A

carry blood 1 cap bed to other = need gen press move it along = thick muscular wall

340
Q

metarterioles

A

small vessels w discontinuous layer sm musc to control blood flow thru specific cap beds

341
Q

difference bet lymphatic + blood caps

A

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

342
Q

what type endothelium forms epicardium

A

cuboidal

NSF (22 decks)

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