Lab 3 - Sheep Heart Flashcards
link between pulmonary trunk and aorta
adult: ligamentum arteriosum (fibrous bridge)
fetus: ductus arteriosus (carried blood from pulm trunk to aorta)
flap between LA and RA
adult: fossa ovalis
fetus: foramen ovale
visceral pericardium
aka epicardium
- can’t move around (stuck to heart)
- made of mesothelial cells
appearance of fat
- at body temp. (37º): snotty
- out of body: hard
appearance of diaphragm
- muscular (dark red)
- hard
- fibrous
- different to rats
thin walls =>
low pressure
head orientation
cranial
tail orientation
caudal
bellyside orientation
ventral
backside of body orientation
dorsal
frontside on horizontal plane
anterior
backside on horizontal plan
posterior
pulmonary trunk
- most ventral great artery
- thick, rubbery/elastic, opaque (cream-coloured)
left anterior vena cava
- blood from head + forelegs (+ right anterior vena cava)
- several cardiac veins drain into here
posterior vena cava
blood from hind legs
right atrium shape in humans vs sheep
humans: vertical/ long
sheep: horizontal
great vein appearance
almost invisible as the thin and membranous walls have collapsed after death
clues for orientation
1) pulmonary trunk
- only in ventral view
2) interventricular sulcus
- present/absence (lateral)
- diagonal (ventral)
- vertical (dorsal)
3) apex/LV
- left (dorsal)
- right (ventral)
4) shape of heart
- flat on dorsal
- round on ventral
5) auricle
- sit/flop in ventrally
blood always goes
DOWN pressure gradient
brachiocephalic trunk
- provide for forearm/limbs + head
- first trunk of aorta
why did the ductus arteriosus close
after birth due to smooth muscle contraction (vasoconstriction) + oxygen meaning blood to lungs (less resistance)
pressure in right atrium
~5 mm Hg
- low pressure system (lung circulation)
two parts of atria
1) main part: smooth internal wall for laminar flow (no turbulance/loss of energy)
2) atrial appendage (auricle): trabeculated for 3D flow/contraction
- different origins in developing embryo
pressure in left atrium
~8 mm Hg
LV:RV thickness ratio
3:1
LV:RV pressure ratio
5:1
pressure in LV
(0-8) - 120 mm Hg
pressure in RV
(0-5) - 27 mm Hg
moderator band
- red
- made of muscle not CT
- contains Purkinje (modified cardiac muscle) fibres
- shortcut as too late for electrical signal to go to last papillary
tricuspid valve
soft and transparent but strong
chordae tendineae
heart strings
- tough white connective tissue cords
why does LV not have a moderator band
more extensive purkinje network + larger/stronger papillary/chordae tendineae as LV must withstand more pressure to prevent valve inversion
+ LV more trabeculated than RV
heart sounds
due to turbulance of blood not flaps clapping together
- first sound: heard near apex
- second sound: heard near base
pulmonary valve
3 semilunar valves/flaps
flaps of mitral valve are
larger than tricuspid valve flaps
mitral valve during diastole
open
- chordae tendineae: loose
- papillary muscle: relaxed
mitral valve during systole
closed
- chordae tendineae: tight
- papillary muscle: contracted
infarction (dead tissue) near papillary muscle =>
papillary muscle doesn’t contract
=> chordae tendineae relaxed
=> valve doesn’t close
=> blood -> atria not aorta
=> heart attack
aortic valve during systole
open + cover coronary ostea => blood can’t enter
coronary ostea
opening to coronary arteries
aortic valve during diastole
close + blood enter coronary artery
coronary arteries
supply heart
cardiac veins
- drain deoxygenated blood into RA (flow into left anterior vena cava)
- pinprick holes/pores on wall of RA
fossa ovalis
- translucent membrane in interatrial septum
- remnant of foramen ovale
foramen ovale
- allows blood to cross from RA to LA
- flap on the left side of septum
closure of foramen ovale
at birth: increased LA volume => increased LA pressure and when LA P > RA P => flap closed => sealed by connective tissue growth around edges
first heart sound is due to closure of
mitral/tricuspid valves
second heart sound is due to closure of
aortic/pulmonary valves
consequences of rupture of papillary muscle
inlet valve doesn’t close properly => blood flows back into atria
potential cause of papillary muscle rupture
ischemia => insufficient oxygen/blood flow => myocardial infarction
ischemia
lack of blood to tissues in blood
why do outlet valves not require chordae tendineae
cusps remain stable due to cusp shape (semilunar) when valve closes
blood through ductus arteriosus
90% of blood due to low resistance
blood through lung capillaries in fetus
10% of blood
- lung not functioning
- surrounded by amniotic fluid => high resistance => hard for RBC to flow through
- only small amount of blood for lung growth
ductus arteriosus
- large fetal vessel
- carried blood from pulmonary trunk to aorta
blood through lung capillaries in adults
100% of blood
- air in lungs => drastically decrease resistance to blood flow
if ductus arteriosus doesn’t close properly
blood shunted into pulmonary trunk since aortic P > pulmonary trunk P => more blood to lungs, less to body
if foramen ovale doesn’t close
blood goes from LA -> RA => more blood to lungs, less to body
interventricular septum
made of muscular tissue
patent
open/unobstructed vessel; failing to close
