CRS Flashcards
Functions of nasal cavity?
CONDUCT/PREPARE inspired air:
Warm/moisten/filter/mucous traps particles to swallow
HEAT EXCHANGERS for cooling brain: Cooled venous blood passes via rete mirabalis and cools arterial blood going to brain (warm-blooded adaptation)
OLFACTION:
Olfactory epithlium on caudal regions of turbinates
Nasal cavity landmarks?
Dorsally/laterally: facial bones
Ventrally: hard palate
Rostrally: nostrils (external nares).
Caudally: pharynx / ethmoid bone
What are Nares?
= nostrils
Actual meatus/hole
Surrounded by: hairless skin
Supported by: nasal cartilages (lateral nasal cartilage- dorsal and ventral- forms nostril opening and attached to septum)
BOVINE nostrils?
Surrounded by smooth hairless nasolabial plate
Stratified/cornified epithelium on surface
nasolabial (serous) glands create moisture
CARNIVORE nostrils?
Nasal plate: divided by median groove (philtrum)
Lateral nasal gland: secretes
SUIDAE nostrils?
Small on snout
Highly sensitive
Os rostrale: BONE- strengthens pig’s nose for digging with it
Large mucous production
AVES nostrils?
Slit openings- not diving birds
Operculum (some birds): Overhanging bony flap
Choana: allow wide communication between nasal cavity and pharynx
EQUINE nostrils?
Cartilage:
No ventral cartilage
Incomplete cartilaginous ring= distensible nostrils
Alar cartilages (plate and horn)= form comma-shaped nostrils (ventral TRUE nostril, dorsal FALSE nostril on outside- Skin lined diverticulum, within nasoincisive notch)
SEE diagram
Nostril muscles?
NOSTRIL DILATION: Levator nasolabialis Caninus Transversus nasi (Mainly important in horses) INNERVATION: Facial nerve VASCULATURE: Facial artery
NOTE: facial nerve paralysis due to innervation by SAME nerve
What is the nasal vestibule?
(Beyond nares)
= opening of nasal cavity
Contains: opening of nasolacrimal duct (connects eye to nose) on ventral surface
(DOGS) Receives: nasal gland secretions
Nasal bones?
DORSAL Frontal bones Nasal bones LATERAL Lacrimal bones Zygomatic bones Incisive bones Maxilla VENTRAL Palatine bones Maxilla Incisive bone Vomer CAUDAL Ethmoidal bone SEE diagrams
Nasal cavity position?
Cavity between: nares and cribiform plate of ethymoid bone
Rostral: nares
Caudal: Choane (paired caudal openings of nasal cavity)
SEE diagram
Nasal cavity divisions?
Divisions: INITIALLY: by nasal septum FURTHER: scrolls of turbinate bone form nasal conchae (increase SA, highly vascular structure, evolved in mammals/birds for endothermy) NOTE: The hard palate evolved at the same time (allows suckling e.g. breathing and ingesting milk) BALANCE between: Airflow resistance Defence mechanisms Warming/moistening Olfaction
Dog= complex Horse= simple (high oxygen demand)
What are nasal conchae?
Consist of turbinates covered by nasal mucosa
Scrolled up
(hollow space= reduces weight of head)
Nasal conchae shapes?
Rostral region: a.) Basal lamella Spiral lamella Recessus (coomunicates with nasal meatus) b.) Basal lamella Spiral lamella Bulla Cellulae
Caudal region:
Conchal sinus
Fusion with neighbouring bones (forms complete hollow chamber)
SEE diagram
Turbinate groups?
(Delicate scrolls) ECTOTURBINATES In frontal sinus Dogs: 6, horses: 20-30 ENDOTURBINATES In nasal cavity 5-6 1 and 2 form dorsal/middle conchae Attached to cribriform plate caudally MAXILLOTURBINATES In nasal cavity Paired Attached to maxiall medial walls Forms ventral concha
Equine turbinates?
1st endoturbinate- forms dorsal conchal sinus (conchus)
2nd endoturbinate- forms middle conchal sinus (conchus)
3rd/4th/5th grouped as ethymoidal surface
Maxillotubinate: originates from maxilla, bony support for ventral concha (contains ventral conchal sinus/conchus)
Made by different parts of turbinate bones
SEE diagram
Nasal conchae?
DORSAL concha
MIDDLE concha (horse/pig= short, dogs/ruminants= longer)
VENTRAL concha
SEE diagram
Nasal conchae divide nasal cavity into 3 separate passages: dorsal/ventral (runs into common)/middle meatus
SEE diagram
Equine meatus?
SIMPLE
4 nasal meatus: DORSAL meatus to olfactory mucosa MIDDLE meatus to paranasal sinuses VENTRAL meatus to pharynx COMMON meatus to pharynx SEE diagram
Canine turbinates?
MORE COMPLEX than equine
(Increase SA for exchange and heat control)
Large frontal sinus (not part of airflow)
Respiratory epithelium?
Pseudostratified columnar epithelium
Nasal epithelium?
VESTIBULE=
Transition from Stratified squamous epithelium (mucous membrane)
NASAL CAVITY= Respiratory epithelium
THEN caudodorsal part of ethmoidal conchae= Olfactory epithelium
NOTE: specialised region of vomer= vomeronasal organ
NOTE: Pseudostratified columnar epithelium= respiratory epithelium
Nasal epithelium?
VESTIBULE=
Transition from Stratified squamous epithelium (mucous membrane)
NASAL CAVITY= Respiratory epithelium
THEN caudodorsal part of ethmoidal conchae= Olfactory epithelium
NOTE: specialised region of vomer= vomeronasal organ NOTE: Pseudostratified columnar epithelium with cilia and goblet cells= respiratory epithelium
Nasal mucosa?
Respiratory mucosa= covers most parts of nasal cavity
Mucosa= epithelium and Lamina propria (basement membrane, contains mucous and serous glands)
Features of respiratory epithelium?
- Pseudostratified columnar
- Goblet cells (produce mucous)
- Ciliated (capture)
Observable in micrographs=
Mucous/serous glands/thin-walled veins-easily damaged
SEE diagram
Microanatomy= Top: Respiratory epithelium Middle: lamina propria (contains: capillary net, nasal glands, venous cavernous bodies, artery) Bottom: Periosteum, vein SEE diagram
Respiratory epithelium functions?
- ) Air flow regulation- by erectile tissue
- ) Cleaning- by cilia
- ) Humidification- evaporator
- ) Warming- variable blood perfusion
- ) Protection- reflex e.g. sneeze
3.) and 4.) cool brain and retain water from expiratory air in some species e.g. camels
Explain what occurs during olfaction?
Ethmoturbinates: (extend rostrally from ethmoid bone)
Covered with respiratory epithelium
Contain olfactory sensory neurones
Sniffing alters airflow: brings air into contact with ethmoturbinates
Olfactory region structure?
Olfactory regions:
Contain non-motile cilia-like structures
Specific neurones which allow exposed dendrite onto mucosal surface- detect chemicals and pass signals through to brain
Completed via cranial nerve 1 (olfactory nerve)- passes through cribiform plate (sieve-like structure at front of brain)- many holes which allow bundles of nerves (axons collect in bundles in lamina propria) from olfactory region to get to brain (olfactory lobe)
1 area of the body where neurones can regenerate (due to neural stem cells)
OVERVIEW:
Cilia-like structures detect chemicals -> pass signals back through cribiform plate via the olfactory nerve and to the brain
What is the vomeronasal organ?
= accessory olfactory sense organ
Location: contained within hard palate
paired, blind ending ducts originating from the incisive ducts, which connect nasal and oral cavities. Within these=
UNIQUE chemoreceptors:
role in pheromone detection
Lip-curling: (Flehmen in horses)- lift upper lip so air flows over vomeronasal organ to detect pheromones in air
Describe resistance to nasal airflow?
Resistance= length/radius^4 (INDIRECTIONALLY proportional i.e. ½ radius= 16x more resistance)
ALSO resistance to flow is affected by direction change
LINK: Anaesthesia- choose appropriately-sized tube (radius of tube may be too small- high resistance for animal to move gas to keep it alive)
Small changes in airway diameter makes big different in air resistance
Compromised airway in brachiocephalic dogs- narrow diameter
Turbulent= high resistance, laminar= lower resistance
EQUINE:
Obligate nasal breathers (soft palate structure makes mouth-breathing hard)
Flow aided by:
- ) Ram air into nostrils
- ) Straighter head-neck-thorax alignment
Compromise flow and air preparation
Less complex turbinates reduce resistance
Describe the paranasal sinuses?
ALL have: 1.) FRONTAL and 2.) MAXILLARY
1.) FRONTAL sinus=
Position: between nasal and cranial cavities
usually drains into ethmoidal meatus (different in HORSE)
2.) MAXILLARY sinus=
Position: caudolateral aspect of upper jaw, around cheek teeth (molars and premolars)
Species variance (e.g. horses have 2 separate regions with no communication between them)
OTHER= palatine, sphenoid, lacrimal
Describe the paranasal sinuses?
= ventilated spaces connected to nasal cavity (usually middle meatus)
ALL have: 1.) FRONTAL and 2.) MAXILLARY
1.) FRONTAL sinus=
Position: between nasal and cranial cavities
usually drains into ethmoidal meatus (different in HORSE)
2.) MAXILLARY sinus=
Position: caudolateral aspect of upper jaw, around cheek teeth (molars and premolars)
Species variance (e.g. horses have 2 separate regions with no communication between them)
OTHER= palatine, sphenoid, lacrimal CATTLE= palatomaxillary BIRDS= Infraorbital HORSES= more complex due to long skull
Development of sinuses?
7
Functions of sinuses?
Voice (resonation)
Brain insulation/cooling
Lightweight
Insertions surfaces for teeth
EQUINE paranasal sinuses (more complex):
How many sinuses does a horse have and what are they?
SEVEN Caudal maxillary sinus (and Rostral) Dorsal conchal sinus (and Ventral) Ethmoidal sinus Frontal sinus PS (Sphenopalatine sinus)
What are the cardio-respiratory functions?
TRANSPORT O2/CO2 Nutrients Heat Hormones Waste HOMEOSTASIS pH, osmolarity, etc. Infection OTHER Generate pressure (renal)
2 main features of cardiac cycle?
NOTE: usually refer to ventricles BUT also have systole/diastole
SYSTOLE (1/3 of cycle)
Ventricular contraction (CO)
LUB
DIASTOLE (2/3 of cycle)
Ventricular relaxation
(ventricles fill)
DUB
Time between lub/dub
What is the lub/dub sound generated by?
Ventricles contract-
atrioventricular valves close- flow through heart is stopped- heart/assoc. structures vibrate (NOT just valves themselves making the noise)
Time between lub dub= ventricles contracting (other time= relaxation and refilling)
Semilunar valves closing generates second heart sound
Feel pulse at same time as listening to heart: helps to identify ventricular systole
Clinical examination is VERY important (rang of what is ‘normal’ is very big)
2 main features of cardiac cycle?
NOTE: usually refer to ventricles BUT also have systole/diastole
SYSTOLE (1/3 of cycle)
Ventricular contraction (CO)
LUB
DIASTOLE (2/3 of cycle)
Ventricular relaxation
(ventricles fill)
DUB
Time between lub/dub= ventricles contracting (other time= relaxation and refilling)
Semilunar valves closing generates second heart sound
What is the lub/dub sound generated by?
Ventricles contract-
atrioventricular valves close- flow through heart is stopped- heart/assoc. structures vibrate (NOT just valves themselves making the noise)
NOTE: Feel pulse at same time as listening to heart: helps to identify ventricular systole
Clinical examination is VERY important (range of what is ‘normal’ is very big)
Function of the heart?
PUMP Cardiac output (/min) Stroke volume (/beat) Other pumping mechanisms DISTRIBUTION Unidirectional flow Constriction/dilation Vital organs Cardiac valves Vascular valves
What is stroke volume?
What is cardiac output?
SV=
end diastolic volume- end systolic volume
CO (important determinant in blood pressure)=
SV*HR
Blood pressure/flow to different organs?
Flow to different areas: determined by physiological circumstances (e.g. after eating= more flow to gut BUT less to skeletal muscles)
RENAL SYSTEM
Rely on certain perfusion pressure to function
Components of vascular system?
ARTERIES From heart VEINS To heart PORTAL VEINS Between 2 capillary beds CAPILLARIES Diffusion
Capillary bed= network of capillaries (oedema forms here when heart fails)
Heart imaging and failure?
Compensatory systems activated to maintain blood pressure if failure occurs
Angiostrongylus: ‘heart worm’ becoming more common
Radiography
Echocardiography
Avian cardiovascular system?
EFFICIENT
Metabolic demands
O2 for thermoregulation
LARGE CARDIAC SIZE (comparatively)
Large cardiac output primarily due to high heart rate
NOTE: heart size fluctuates- increase before migration (increase in athletes)
Avian cardiovascular system?
EFFICIENT
Metabolic demands
O2 for thermoregulation
LARGE CARDIAC SIZE (comparatively)
Large cardiac output primarily due to high heart rate
END OF SYSTOLE= almost completely empty
NOTE: heart size fluctuates- increase before migration (increase in athletes)
Avian cardiovascular system?
EFFICIENT
Metabolic demands
O2 for thermoregulation
LARGE CARDIAC SIZE (comparatively)
Large cardiac output primarily due to high heart rate
END OF SYSTOLE= almost completely empty
VENTRICLES=
LEFT ventricle: wall is 3x thicker, muscular bars on interior, forms entire apex
RIGHT ventricle: thin-walled
HEART LOCATION/SIZE= Comparatively large Ventral midline Enclosed by L/R liver lobes No diaphragm- pressure changes in air sacs instead
HEART STRUCTURE=
4 chambers: L/R atrium/ventricle
Valves:
NOTE: heart size fluctuates- increase before migration (increase in athletes)
Where are the valves of the heart?
Atrioventricular:
a. ) Tricuspid-
b. ) Bicuspid valve
Avian cardiovascular system?
EFFICIENT
Metabolic demands
O2 for thermoregulation
LARGE CARDIAC SIZE (comparatively)
Large cardiac output primarily due to high heart rate
END OF SYSTOLE= almost completely empty
VENTRICLES=
LEFT ventricle: wall is 3x thicker, muscular bars on interior, forms entire apex
RIGHT ventricle: thin-walled
HEART LOCATION/SIZE= Comparatively large Ventral midline Enclosed by L/R liver lobes No diaphragm- pressure changes in air sacs instead
HEART STRUCTURE=
4 chambers: L/R atrium/ventricle
Valves: Left AV valve (3 leaflets), right AV valve (muscular flap, no chordae tendinae)
RENAL PORTAL SYSTEM
NOTE: heart size fluctuates- increase before migration (increase in athletes)
Where are the valves of the heart?
Atrioventricular valves:
a. ) Tricuspid- between R atrium/R ventricle
b. ) Bicuspid (mitral) valve- between L atrium/L ventricle
Semi-lunar valves:
a. ) Aortic- left ventricle/aorta
b. ) Pulmonary- right ventricle/pulmonary artery
AVIAN cardiovascular system?
EFFICIENT
Metabolic demands
O2 for thermoregulation
LARGE CARDIAC SIZE (comparatively)
Large cardiac output primarily due to high heart rate
END OF SYSTOLE= almost completely empty
VENTRICLES=
LEFT ventricle: wall is 3x thicker, muscular bars on interior, forms entire apex
RIGHT ventricle: thin-walled
HEART LOCATION/SIZE= Comparatively large Ventral midline Enclosed by L/R liver lobes No diaphragm- pressure changes in air sacs instead
HEART STRUCTURE=
4 chambers: L/R atrium/ventricle
Valves: Left AV valve (3 leaflets), right AV valve (muscular flap, no chordae tendinae)
RENAL PORTAL SYSTEM (regulated by portal valve)
In all non-mammalian vertebrates
Receives blood from caudal body- drains hind limbs SO drugs injected into hind limbs are metabolised (go through kidneys) before general circulation (reaching veins)
NOTE: heart size fluctuates- increase before migration (increase in athletes)
FISH circulatory system?
CIRCULATION
Single circulation: gills-body-heart
HEART
Simple, linear (not divided into chambers, ventral aorta with several aortic arches)
NOTE: similar structure to developing mammalian heart
FISH circulatory system?
CIRCULATION
Single circulation: gills-body-heart
HEART
Simple, linear (not divided into chambers, ventral aorta with several aortic arches)
NOTE: similar structure to developing mammalian heart
SEE DIAGRAM OF HEART
Developing mammalian heart?
5 zones of primitive tube: SEE DIAGRAM (top to bottom) Arterial trunk/truncus arteriosus Bulbus cordis Ventricle (B and V primitive ventricle) Atrium Sinus venosus
FISH circulatory system?
Teleost
CIRCULATION Single circulation: gills-body-heart HEART Simple, linear (not divided into chambers, ventral aorta with several aortic arches) Structure: SEE DIAGRAM 1: Single dorsal aorta, runs into paired dorsal aortae, aortic arch comes off this, ventral aorta runs parallel to dorsal aorta, heart attached to dorsal aorta Flow: SEE DIAGRAM 2
NOTE: similar structure to developing mammalian heart
Developing mammalian heart?
5 zones of primitive tube: SEE DIAGRAM 3: (top to bottom) Arterial trunk/truncus arteriosus Bulbus cordis Ventricle (B and V primitive ventricle) Atrium Sinus venosus
Tetrapods
FROGS AND TOADS
Systemic arch
NOT dual-chambered BUT do have L/R aortic arch
SEE DIAGRAM 4
Anuran heart
SEE DIAGRAM 5
Frogs and toads
Fairly linear but development of valves and other structures
Recapitulation
Theory of recapitulation
Embryological parallelism
Haeckel “Ontogeny recapitulates phylogeny”
Ontogeny (the developmentof theembryofromfertilizationto gestation or hatching), goes through stages representing the stages of the evolution of the animal’s remote ancestors (phylogeny).
THEORY: Changes mammalian heart goes through represents stages of evolution
Largely discredited now BUT was supported strongly by Haeckel
Circulatory system functions?
TRANSPORT Nutrient Waste O2 and CO2 Heat Hormones PROTECTION Carries WBC and Ig HOMEOSTASIS pH, ions, fluid volume PRESSURE
Circulation of blood?
TWO PUMPS IN SERIES Pulmonary circuit: Pulmonary artery Arterioles Capillaries Pulmonary veins
Systemic circuit Aorta Arteries Arterioles Capillaries Venules Systemic veins
Circulation of blood?
TWO PUMPS IN SERIES
(If 1 side fails= serious implications on other side)
Pulmonary circuit: From bottom left to top left Pulmonary artery Arterioles Capillaries Pulmonary veins
Systemic circuit: From top right to bottom right Aorta Arteries Arterioles Capillaries Venules Systemic veins
Where are the valves of the heart?
Atrioventricular valves:
a. ) RIGHT AV= Tricuspid- between R atrium/R ventricle (3 cusps BUT often only has 2 cusps)
b. ) LEFT AV= Bicuspid (mitral) valve- between L atrium/L ventricle (2 cusps)
Semi-lunar valves:
a. ) RIGHT SEMILUNAR= Aortic- left ventricle/aorta (3 cusps)
b. ) LEFT SEMILUNAR= Pulmonic- right ventricle/pulmonary artery (3 cusps)
Chordae tendinae:
connect papillary muscles (in ventricles) to tricuspid/ bicuspid valves
Size and position of the heart across species?
How can it be accessed during surgery?
Position= essentially the same in all species
Ventral border of lungs
Laterally: lungs
Cranially: thymus
Caudally: diaphragm
In mediastinum, divides L and R pleural cavities
On midline BUT greater proportion of heart on L side
Apex= sits in sternum
Atria= Form base- dorsal (where great vessels come out)
R ventricle= cranial to L
Relatively larger in small species
Mass increases with training
Gap between lung lobes on both sides allows access to the heart (CARDIAC NOTCH)
Developing mammalian heart?
5 zones of primitive tube: SEE DIAGRAM 3: (top to bottom) Arterial trunk/truncus arteriosus Bulbus cordis Ventricle (Bulbus cordis and primitive ventricle) Atrium Sinus venosus
Primitive tube begins to ‘snap off’ into different sections
Sinus venosus doesn’t survive in mammals but does in reptiles– venous system bringing blood into primitive atria (becomes 2 atria that we know)
Bulbus cordis and primitive ventricle form the 2 ventricles
Truncus arteriosus becomes aorta and pulmonary artery
Heart structure?
Ventricles:
R= cranial to left
Paraconal groove cranially
Subsinuosal groove caudally
Atria:
Form base- blind appendages ('auricles')
Coronary groove:
Runs around heart- main trunks of coronary run in this groove3 grooves of the heart>
Coronary groove
Subsinuosal groove
Paraconal groove
Relative positions of right and left sides of the heart?
‘Fist’ analogy
Left atrium= middle/back of heart
Right ventricle wraps around front of left ventricle
What is the pericardium?
= Sac surrounding the heart- prevents distension, equlises output of 2 sides of heart Inner: VISCERAL layer of perichardium Attached to surface of heart (= epicardium) Outer: PARIETAL layer of perichardium No significant lumen Small amount of fluid in healthy animal (Contiguous with BV adventitial layer) Ligaments: Sterno-pericardial ligament Phrenico-pericardial ligament
SEE DIAGRAM 6
Right atrium:
Structure?
Position?
Features?
23-27
Left atrium:
Position?
Features?
Position:
Dorsal and caudal, under tracheal bifurcation (trachea splits into 2 main stem bronchi)
Features:
Pulmonary veins- enter in groups into 2 or 3 sites
Scar of valve of f.ovale
Right ventricle:
Structure?
Position?
Features?
Structure:
Crescentic in section
Does not go to apex of heart (left ventricle does)
Position:
Wraps around LV, cranial and to the right
Features:
Pulmonary artery- cranial and L of aorta
Trabecula septomarginalis- within R ventricle, septum- outer wall
NOTE: Trabecula septomarginalis is shown in ultrasound of heart- could be confused with pathological issue
3 grooves of the heart?
Coronary groove
Subsinuosal groove
Paraconal groove
FIBROUS cardiac skeleton functions?
Separates atria/ventricles
Insulation- AV bundle
Ruminants: ossa cordis (bone in this region for support)
Describe cardiomyocytes?
Large, cylindrical cells Striated myofibrils (LIKE skeletal) Short, branched fibres (UNLIKE skeletal) Central nuclei (UNLIKE skeletal- peripheral) Many mitochondria Actin-myosin function (LIKE skeletal)
Right atrium:
Structure?
Position?
Features?
Collects deoxygenated blood via cranial and caudal vena cava
Roof of atrium= contains intervenous tubercule- diverts blood from vena cavae to right ventricle
Sino-atrial node (in wall of R atrium)= origin of electrical activity
Coronary sinus= main blood vessel draining the heart- brings deoxygenated blood back from myochardium
Azygous vein- R or L= bring s deoxygenated blood back from other parts of the body
Fossa ovalis= remnants of interatrial foramen ovale which is open in the foetus and allows movement from R to L
SEE DIAGRAMS/GROUP OF IMAGES 12
Describe cardiomyocytes: Structure?
Function?
Training effects?
Repair?
STRUCTURE: Large, cylindrical cells Striated myofibrils (LIKE skeletal) Short, branched fibres (UNLIKE skeletal) Central nuclei (UNLIKE skeletal- peripheral) Many mitochondria Actin-myosin function (LIKE skeletal)
FUNCTION:
Excitable
Functional (electrical) syncitium
Structure facilitates fast AP passage: T-tubules, Sarcoplasmic reticulum
NOTE: Revise sarcomere structure and function
TRAINING/OVERLOAD: Myocyte hypertrophy (NOT increased cell NUMBER)
REPAIR:
Previously: thought that if damaged, cannot regenerate
BUT: increasing evidence that there are cells that lead to regeneration
Infusing stem cells into myochardium may be possibpe- particularly in human medicine (would allow myochardial regeneration which could be used for people who have suffered from a heart attack)- some interest in veterinary medicine
Explain coronary circulation?
L and R coronary arteries (L>R)
Arise from: coronary sinus (above aortic valve)
Perfusion: during ventricular diastole
Great cardiac vein- coronary sinus
How is blood pushed through the valves?
In diastole, vortexes of blood form which then pushes blood through the valves
Functions of cardiac valves?
=Generate unidirectional flow
1.) Ventricular diastole: blood enters the 2 ventricles
Most ventricular filling occurs immediately after valves open (2/3s of filling occur very quickly)
Valves start to close: atria contract to complete ventricular filling BUT contribution of atria to ventricular filling is very small- on Wigger’s diagram most of the blood in the ventricles goes in early during diastole
Atria are important in vigorous exercise in athletes- Racehorses may suffer from atrial disease
SUMMARY:
In ventricular diastole= AV valves open and blood enters 2 ventricles, semilunar valves are closed
2.) As soon as ventricular systole occurs- AV valves close but aortic/pulmonary valves don’t open until pressure in L and R ventricles exceed pressure in aorta and pulmonary artery
Once ventricular pressure exceeds aorta/pulmonary artery pressure: semilunar valves open and blood ejected into aorta/pulmonary artery
Heart begins to contract, there is a period when all 4 valves are shut- see Wigger’s diagram
3.) AS ventricles relax (at end of systole): semilunar valves shut and S2 heard
Period when all 4 valves are shut: pressure in ventricles hasn’t dropped below pressure in atrial. Once ventricular pressure drops below atrial pressure: AV valves open AND cycle begins again
NOTE: Isovolume-contraction and isovolume-relaxation should be noted on Wigger’s diagram (times when all 4 valves are shut)
FIBROUS cardiac skeleton functions?
SEE DIAGRAM 7
Separates atria/ventricles
Supports valve cusps
Cattle: sometimes bone in this region for support- ossa cordis
Insulates electrically the atria from the ventricles
Only one place for electrical activity to get from atria to ventricles= through atrioventricular node- but of wiring connects atria and ventricles (Otherwise it can not pass between the 2)
Describe the myocardoum?
Epicardium:
is the visceral pericardium (continuous with adventitial layer of blood vessels)
NOTE: Often a lot of fat associated with outside of heart
Myocardium:
bulk formed by cardiomyocytes
branches of coronary vessels supplying myocardium
Endocardium:
(lining ventricles) continuous with lining of blood vessels
SEE DIAGRAM 8
Intercalated discs
Stair-like intercellular junctions: on tread of stair= robust connections called desmosomes which stops cell tearing itself apart when muscle contracts
Gap junctions on up-side of stair which allows electrical activity to move from cell to cell
Individual cardiomyocytes BUT because of the way they’re connected, the entire myocardium tends to function as one thing- functional syncytium SO contraction occurs and electrical activity travels from cell to cell very quickly (ventricles can contract synchronously)
SEE DIAGRAM 9 AND 10 (can see this with electron microscopy) AND 11
Explain coronary circulation?
L and R coronary arteries (L>R)
Arise from: coronary sinus (above aortic valve)
Perfusion: during ventricular diastole
Great cardiac vein- coronary sinus
How is blood pushed through the valves?
In diastole, vortexes of blood form which then pushes blood through the valves
Where can you hear the different sounds of the heart?
APEX: hear first sound louder
Move up to BASE: hear second sound louder
What is the contractile function of the heart controlled by?
Electrical conduction- from cell to cell and through specialised conduction tissue
Originates from: spontaneously electrical pacemaker cells
What is membrane potential (Vm)?
= Electric potential difference between the cytosol and extracellular fluid
How does Vm vary between cell types?
ALL cells have Vm Specific to cell type Skeletal muscle -90 mV (-0.09 V) Neurones -70 mV (-0.07 V) Red blood cell -30 mV (-0.03 V) Duracell -1500 mV (-1.5 V) NOTE: minus sign= inside of cell is negative compared to its outside
How is membrane potential achieved?
DIFFUSION: causes ionic imbalance which polarise membrane
ACTIVE TRANSPORT: maintains membrane potential
How is resting membrane potential achieved?
Plasma membrane:
Virtually impenetrable to large organic anions (usually proteins)
K+ permeability > Na+/Ca2+/Cl+ permeability
Organic anions (usually proteins) within cell cytosol are too large to pass through membrane= cell is negatively charged SO draws in positively charged potassium ions which move into cell down electrical gradient SO greater concentration of potassium ions inside cell SO potassium ions move out of cell down concentration gradient BUT anions can not leave cell SO negative resting membrane potential- excess negative intracellular charge is attracted to cell membrane SO as more K+ ions leave cell, negative charge of interior becomes great enough to attract K+ back into the cell SO concentration gradient= electrical gradient (only 1 K+ will enter as 1 K+ leaves) NOTE: complete equilibrium does not occur as Na+ is attracted to negative interior and moves down concentration gradient
How is resting membrane potential achieved?
Plasma membrane:
Virtually impenetrable to large organic anions (usually proteins)
K+ permeability > Na+/Ca2+/Cl+ permeability
Organic anions (usually proteins) within cell cytosol are too large to pass through membrane= cell is negatively charged SO draws in positively charged potassium ions which move into cell down electrical gradient SO greater concentration of potassium ions inside cell SO potassium ions move out of cell down concentration gradient BUT anions can not leave cell SO negative resting membrane potential- excess negative intracellular charge is attracted to cell membrane SO as more K+ ions leave cell, negative charge of interior becomes great enough to attract K+ back into the cell SO concentration gradient= electrical gradient (only 1 K+ will enter as 1 K+ leaves) NOTE: complete equilibrium does not occur as Na+ is attracted to negative interior and moves down concentration gradient If only passive forces were involved: ion conc. in/out cell would equalise BUT active transport maintains low intracellular Na+ conc. and high intracelullar K+ conc.
Diffusion along con. gradient, movement along electrical gradient, pumping across membrane
Resting potentials arise as a result of:
- ) Selectively permeable membranes
- ) Large organic anions
- ) Ion channels (SO K+ ions fluxes generate polarised cell)
- ) Active transporters maintaining electrical gradients, despite diffusion gradients
How is resting membrane potential maintained?
(If only passive forces were involved: ion conc. in/out cell would equalise BUT active transport maintains low intracellular Na+ conc. and high intracelullar K+ conc.)
= Maintained by Na=/K= ATPase pump:
3 Na+ ions pumped out, 2 K+ pumped in
(Uses a lot of energy)
Other pumping mechanisms: a.) Na+ / Ca2+ Antiporter Removes Calcium ions from cytosol Energy obtained by sodium passing down electrochemical gradient 3 sodium for 1 calcium
b.) Ca2+ ATPase pump
SEE DIAGRAM
What is resting membrane potential?
= product of potassium conc. either side of cell membrane
Can be predicted by Nernst equation (do not need to learn/memorise this equation)
Differs in different organs
Cardaic RMP: -90mV
Neuronal RMP: -60mV
Why id depolarisation important in cardiac cells?
Depolarisation can result in action potential being generated
Skeletal muscles need nerve to contract, myogenic cells do not need this- intrinsic ability to contract by themself
Basic structures of the heart?
Which 2 major features allow efficient functioning?
Chamber pump
4 chambers
Wall of heart: mainly myocardium with inner endocardium layer
2 sets of valves in the heart
Valves
Coordinated contraction of myocardium
Basic order of electrical activity flow through the heart?
SAN node- atria- delayed by cardiac skeleton- AVN- ventricles
28-29
Excitable cells and the cardiac action potential
How does cardiac depolarisation in contractile cells occur?
Depolarisation arises when CATIONS enter polarised cell
AP occurs in sinoatrical node (due to increase in membrane permeability of Na+)
What is threshold potential?
= membrane potential of which a cell must be depolarised in order to elicit an action potential (ALL or NOTHING event)
Plateau stage= important in this A.P
34
Excitable cells and the cardiac action potential
Explain the different phases of a cardiac action potential?
Cardiac AP is initiated by depolarisation IF threshold potential is reached
PHASE ZERO (rapid depolarisation) At threshold potential (approx. -60mV): Voltage-sensitive (FAST) Na+ channels open quickly and increased Na+ conductance of membrane Inward current caused by opening of fast Na+ channels (positive feedback- many more Na+ channels open) becomes large enough to overcome outward current through K+ channels, resulting in a very rapid upstroke T-type (transient) Ca2+ channels open at membrane potentials of - 70mV to -40mV, causing Ca2+ influx
PHASE 1 (incomplete repolarisation) Depolarisation of ~0.5ms inactivates the Na+ channels – stops fast inward Na+ current. K+ ions leave the cell via transient outward channels Cell does NOT fully repolarise yet as Ca2+ channels open and the opening of the K+ channel is transient
PHASE 2 (plateau phase) Ca2+ enters the cell via L-type (L=long lasting) Ca2+ channels which are activated slowly when the membrane potential is more positive than ~ -35mV. These channels do not inactivate rapidly like Na+. Reduced K+ outward current continues. Calcium entry during the plateau is essential for contraction; blockers of L-type Ca2+ channels (e.g. verapamil) reduce force of contraction.
PHASE 3 (rapid repolarisation) Ca2+ influx declines and the K+ outward current becomes dominant, with an increased rate of repolarisation.
PHASE 4 (electrical diastole)
resting membrane potential is restored.
Active pumps relocate sodium, potassium and calcium.
(Once repolarised, there is a resting phase)
L-type= long-lasting T-type= short-lasting (transient)
SEE DIAGRAM 14
SEE DIAGRAM 15
How are cardiac action potentials different to the events which occur in skeletal muscles?
Na+ channels open & close quickly and membrane begins to repolarise (1)
Repolarisation interrupted due to 2 things that don’t happen in skeletal muscle:
a.) Some K+ channels close
b.) Many Ca2+ channels open
This keeps the cell in a depolarised state
48
Excitable cells and the cardiac action potential
What is the significance of the long cardiac action potential?
50-51
Excitable cells and the cardiac action potential
CNS to skeletal muscle?
CNS- single somatic motor nerve fibre -> skeletal muscle
4-5
AUTONOMIC NS
6
AUTONOMIC NS
2 branches of autonomic nervous system and their functions?
Sympathetic NS= fight/flight
Parasympathetic= rest/digest
Explain sympathetic NS?
ADD SLIDE 16
Pre-ganglionic cell body in grey matter of spinal cord
Thoracolumbar spinal cord (species variation in thoracic/lumbar segments)
Short pre-ganglionic nerve fibres: synapse with many post-ganglionic fibres
In a nu,ber of ganglia, alongside spinal cord
Ganglia in a chain each side of spinal cord
More ganglia than segments
= widespread response due to many post-ganglionic fibres
SEE DIAGRAM 16
Endocrine association
Pre-ganglionic fibres to medulla of adrenal gland
NO post-ganglionic fibre
COMPLETE SLIDE 16
8-9
AUTONOMIC NS
Explain parasympathetic NS?
ADD SLIDE 20
Pre-ganglionic cell body in grey matter of brain stem
Pre-ganglionic cell body in grey matter of sacral spinal cord (CHECK)
Cranio-sacral
Fibres leave CNS in cranial nerves: III, VII. IX, X (vagus nerve- supplies fibres to most of thorax and abdomen)
ADD SLIDE 20
More localised action than sympathetic system
No endocrine association
NOTE: Thoraco lumbar= sympathetic, cranio-sacra;= parasympathetic
11
AUTONOMIC NS
12
AUTONOMIC NS
Explain sympathetic NS?
ADD SLIDE 16
Pre-ganglionic cell body in grey matter of spinal cord
Thoracolumbar spinal cord (species variation in thoracic/lumbar segments)
Short pre-ganglionic nerve fibres: synapse with many post-ganglionic fibres
In a nu,ber of ganglia, alongside spinal cord
Ganglia in a chain each side of spinal cord
More ganglia than segments
SEE DIAGRAM 16
= widespread response due to many post-ganglionic fibres
Endocrine association
Pre-ganglionic fibres to medulla of adrenal gland
NO post-ganglionic fibre
COMPLETE SLIDE 16
NOTE: Sympathetic NS can work on smooth muscle of airways to open them up
NEED TO DO SLIDE 22 ONWARDS
AUTONOMIC NS
AUTONOMIC NS
Slide 22 onwards
AUTONOMIC NS
Slide 22 onwards
AUTONOMIC NS
Slide 22 onwards
AUTONOMIC NS
Slide 22 onwards
What types of cells can myocytes be divided into?
‘Work’ cells with STABLE resting Vm
Pacemaker (autorhythmic) cells with UNSTABLE Vm
What are autorhythmic cells?
Modified, non-contractile cells located in discrete cardiac regions
Spontaneously generate APs
Slowly depolarise until threshold value reached- these depolarisations= most rapid in SA node (reaches threshold potential first)
What is the function of the Sinoatrial Node?
Resting Vm?
Threshold potential?
What is spontaneous decay?
What controls rate of depolarisation and how?
In right atrium wall
Reaches THRESHOLD potential FIRST
Controls rhythm of WHOLE heart
Membrane potential drifts towards threshold to generate AP which is then propagated throughout myocardium
Resting Vm= -60mV
Threshold potential= -40mV
Spontaneous decay:
Sodium channels OPEN- not fast type, If, Ib
Membrane permeability for K+ gradually falls
AS Vm approaches -40mV: low threshold Ca2+ channels open
Rate of sodium entry= controls rate of depolarisation (i.e. heart rate)
SOME neurotransmitters/drugs increase If sodium channels= increase rate of spontaneous depolarisation= increase HR
These neurotransmitters/drugs= chronotropic agents (atropine, adrenaline)
SO: sodium flowing in faster= faster depolarisation rate
NOTE: Sodium If channel= funny channel, Ib= background
Action of Chronotropic agents?
Neurotransmitters/drugs that increase If sodium channels= increase rate of spontaneous depolarisation= increase HR
Examples: atropine, adrenaline
What is the function of the Sinoatrial Node?
Resting Vm?
Threshold potential?
What is spontaneous decay?
What controls rate of depolarisation and how?
In right atrium wall
Reaches THRESHOLD potential FIRST
Controls rhythm of WHOLE heart
Membrane potential drifts towards threshold to generate AP which is then propagated throughout myocardium
Resting Vm= -60mV
Threshold potential= -40mV
Spontaneous decay:
Sodium channels OPEN- not fast type, If, Ib
Membrane permeability for K+ gradually falls
AS Vm approaches -40mV: low threshold Ca2+ channels open
Rate of sodium entry= controls rate of depolarisation (i.e. heart rate)
SOME neurotransmitters/drugs increase If sodium channels= increase rate of spontaneous depolarisation= increase HR
These neurotransmitters/drugs= chronotropic agents (atropine, adrenaline)
SO: sodium flowing in faster= faster depolarisation rate
NOTE: Sodium If channel= funny channel, Ib= background
SEE DIAGRAM 26
Function of the Atrioventricular node?
(Similar to SA node)
Acts as pacemaker in absence of SAN
Depolarises more slowly- slows conduction through the heart AND results in short pause between atrial/ventricular contraction
What does the conduction system consist of?
What is its function?
Features:
Nodal myocytes: impulse generation=
1,) Sinoatrial node
2.) Atrioventricular node
Specialised myocytes: impulse conduction=
3.) Atrioventricular bundle/Bundle of His (comprising trunk, left and right crura)
4.) Purkinje fibres (subendocardial plexus of cardiac conducting fibres)
Functions:
Delay transmission between atria/ventricles
Only connection between atria/ventricles
Allow more rapid conduction of AP’s than is possible through contractile muscle cells- enables simultaneous ventricular myocardium contraction
NOTE:Specialised myocytes conduct electrical impulse across heart- NOT nerves but act similarly to nerves
SEE DIAGRAM 17
SEE DIAGRAM 20
Function of the Atrioventricular node?
(Similar to SA node)
Acts as pacemaker in absence of SAN (auxiliary pacemaker function)
Depolarises more slowly- slows conduction through the heart AND results in short pause between atrial/ventricular contraction- long refractory periods prevent ventricles from contracting too fast (atrial fibrillation) BUT sympathetic action shortens AV delay (shortens AV node refractory period), increasing AV conduction
Innervated by: autonomic nervous system
Autonomic NS: Shortens action potential at AVN and SAN= heart beats faster
Explain co-ordinated contraction/conduction through the heart?
SA node= excitation source
Impulse spreads by branching heart muscle fibres
Excitation wave spreads through atria
AV node= activates ventricular myocardium through specialised conduction system
DELAY at AV node before ventricles because: no delay would mean that blood would be pumped to the apex and not into the inlets (where it should be pumped)
SEE DIAGRAM 19
SEE DIAGRAM 22
What are the Purkinje fibres?
Function?
Rapid conduction tissue:
- Simultaneous ventricular contraction
- From APEX to BASE
Similar to ventricular AP:
- Also retain spontaneous activity as a results of sodium leakage
- Usually suppressed by SAN and AVN
NOTE: If SAN and AV node stops working, purkinje fibres would contract by themselves
SAN is fastest, if damaged then AV node takes over (SAN and AVN over-ride purkinje fibres usually)
What are the Purkinje fibres?
Function?
Rapid conduction tissue:
- Simultaneous ventricular contraction
- From APEX to BASE
Similar to ventricular AP:
- Also retain spontaneous activity as a results of sodium leakage
- Usually suppressed by SAN and AVN
NOTE:
SAN and AV node stops working: purkinje fibres contract by themselves
SAN is fastest, if damaged: AV node takes over (SAN and AVN over-ride purkinje fibres usually)
How do pacemaker cells function?
Spontaneous pacemaker- particular ion channels:
Lack fast Na+ channels
Have Na+ channels that spontaneously open once AP finishes
K+ channels close
Influx of Ca2+ speeds final approach to threshold
Once threshold reached: AP occurs
SEE DIAGRAM 21
Do atria or ventricles beat faster and why?
ATRIAL cells beat faster than ventricles
Similar AP to ventricular BUT shorter plateau: Ca2+ slow channels open and K+ channels closed for shorter period
SO form more APs/min
BEAT faster than ventricles
NOTE: normal atrial cells, NOT SAN/AVN
SUMMARY of automaticity:
a. ) What is spontaneous electrical activity a results of?
b. ) What determines rate of depolarisation?
c. ) Are these cells contractile?
a. ) Spontaneous electrical activity= product of sodium’s inward movement (NOT through fast channels)
b. ) Rate of sodium influx= controls rate of depolarisation
- Ensures dominance (suppression of minor pacemakers- SAN= usually dominant, AV nodal rate is slower, Purkinje rate is even slower)
c. ) These cell types= non-contractile: just maintain automaticity
What is excitation-contraction coupling?
Mechanism by which depolarisation causes contraction
(Covered in MSK for skeletal muscle)
NOTE: long refractory period (plateau) before cells can contract again
SEE DIAGRAM 23
Calcium enters cell during AP’s plateau phase- contributes only 10-20% of calcium required BUT remainder arises from sarcoplasmic reticulum:
- Bound to calsequestrin
- Release activated by: increase in calcium within cell (calcium sensitive release channels (ryanodine receptors))
= Calcium-induced calcium release
SEE DIAGRAM 24
SO: Contraction is a product of calcium in the cell
How is cardiac contraction regulated?
Calcium concentration is sarcolemma Calcium binds to troponin C: - Troponin 1 dissociates from actin - Tropomyosin moves out of actin cleft- exposes binding sites - Myosin can cross bridge actin
Tension is dependent on number of cross links- this is dependent on calcium concentration
(Same as in skeletal muscle)
Cell relaxation?
Calcium ATPase pump:
Pumps calcium into SR and out of cell
Calcium dissociates from troponin
Muscle relaxes
What are the 2 possible autonomic actions at SAN?
- ) SYMPATHETIC
- Innervates all regions of heart (atria and ventricles)
- Release noradrenaline at SA node cells: increase HR
- Increase rate of drift to threshold
- ß-receptor activation: higher/shorter AP’s AND stronger/quicker contractions
- Increases Ca2+ entry
- K+ channels open sooner - ) PARASYMPATHETIC
- Mainly act on SAN/AVN (little direct action on ventricles)
- Release acetylcholine at SA node cells: decrease HR
- Decrease rate of drift to threshold
- Strong anti-sympathetic action on atrial cells
- SA node: decreases rate
- AV node: slow conduction, lengthen refractory period
NOTE: Parasympathetic normally dominant in dog
SEE DIAGRAM 25
Innervation of autonomic nervous system?
SYMPATHETIC
From T2-T4 via mid-cervical and cervico thoracic ganglia to supply SA node + whole myocardium
PARASYMPATHETIC
Vagus to supply SA node and atria
36 AND 37 TO COMPLETE
Pacemaker and cardiac conduction
Explain 2 possible dysfunctions of the conducting system?
CARDIAC ARRHYTHMIAS
Result from: AP or conduction problems
AP: Sinus arrest (sick sinus syndrome)- treatment?
AV node block: various degrees
TACHYARRYTHMIAS
Atrial fibrillation
Ventricular fibrillation
Cardiac action potential diagrams?
SEE DIAGRAMS 26 and 27
ECHO 36 and 37
Pacemaker and cardiac conduction
What affects amount of blood pumped by the heart for each cardiac cycle?
Stroke volume
What affects volume of blood delivered to tissues?
- ) SV
- ) HR
- ) Vascular tone
1 and 2= CO
Co and 3= Blood pressure
What is cardiac output and how is it calculated?
Amount of blood pumped in 1 minute (usually close to total blood volume- blood usually circulates every minute)
At rest: tissue oxygen delivery > oxygen consumption
CO (ml/min)= HR (beats/min) * SV (ml/beat)
What must be matched in cardiac output?
What happens if this is not matched per beat?
Vol. entering lungs= vol. entering circulation
If not matched:
Increases pressure in venous side
Leads to oedema
What is stroke volume determined by and how can it be calculated?
Preload (EDV)
Afterload
Contractility (ESV)
SV= EDV-ESV
What is preload?
What is afterload?
What is contractility?
Preload= End diastolic volume (EDV), intrinsic Afterload= Resistance to ventricular ejection Contractility= Sympathetic NS activity, end systolic volume (ESV), extrinsic (force which heart contracts)
NOTE: EDV= volume of blood at end of diastole
What is preload determined by?
1.) Venous return of blood (i.e. central venous pressure)
- Low: reduced ventricular filling SO reduced SV
- High: increased ventricular filling SO increased SV
(More blood returning= higher preload)
2.) Heart rate: can also affect ventricular filling
SUMMARY: blood coming in from venous system determines preload which determines blood being ejected from heart (i.e. greater stretch on rubber band= greater force coming together again)
SEE DIAGRAM 28
What happens if preload is increased?
What happens if preload is decreased?
Increased pressure= increase SV= increased CO
SEE DIAGRAM 29
Reduced venous return= reduced preload= reduced SV
SEE DIAGRAM 30
What is the Frank-Starling mechanism?
Relationship between preload and stroke volume
(Under normal conditions: increased preload= increased SV, linear relationship under normal conditions)
Increased ventricular muscle stretching= stronger contractile force
BUT over-stretching occurs past a certain point
SEE DIAGRAM 31
What is the length-tension relationship?
(Muscular system) Increased preload= Increased exposure to actin= Increased cross-bridge formation= Increased force of contraction
BUT over-stretching leads to decline in contractile force
SEE DIAGRAM 34
What are the limits of the Frank-Starling mechanism?
1.) Excessive stretching= decreases cross-bridge formation
2.) Laplace’s law: More wall tension is required to generate the same internal pressure in a large sphere than it does in a small one (bigger heart must work harder to achieve same pressure)
(Pressure= tension/radius
SEE DIAGRAM 33
What are the consequences of Laplace’s Law?
As heart fills with blood, muscle is at increasing mechanical disadvantage (i.e. chambers more difficult to empty as greater pressure is needed)
Clinical implications: dilated cardiomyopathy- common cardiac disease in dogs
SLIDE 18
Preload etc.
How do skeletal muscles affect venous return?
Venous return 1- skeletal muscle pump
(SKELETAL MUSCLE PUMP e.g. exercising- increases CO) Contraction of skeletal muscle= Veins compressed= Blood forced to heart= Increased preload SEE DIAGRAM 34
How does respiration affect venous return?
Venous return 2- respiratory pump
Inspiration: - Diaphragm moves caudally - Increases abdominal pressure - Decreases thorax pressure = increased abdominal return of blood SO increased preload SEE DIAGRAM 35
Sympathetic control of venous return?
Venous system= ‘reservoir’ of blood (2/3 of blood in veins, not arteries)
Sympathetic stimulation:
Causes venous vasoconstriction
Increases central venous pressure
INCREASES PRELOAD (= increased SV)
Flow diagram of how increased preload results in an increased stroke volume?
Increased sympathetic activity (OR directly increases venous pressure) Increased blood volume Increased venous pressure Increased venous return Increased EDV Increased stroke volume
Increased skeletal muscle pump (OR directly increases venous pressure) Increased respiratory movements Increased venous pressure Increased venous return Increased EDV Increased stroke volume
Explain stroke volume extrinsic regulation?
COMPLETE WITH SLIDE 23
Preload, afterload and contractility
SYMPATHETIC nervous system= increases contractility
Strength of contraction at any given preload
How can contractility increase stroke volume?
Particular force has particular SV
SO
Increasing force= increase amount of blood ejected= increase SV
SEE DIAGRAM 36
Ventricular contractility:
Effect of sympathetic stimulation?
COMPLETE WITH THE NOTES SECTION OF THE SLIDE
Preload, afterload and contractility
Contractile force increase= enables heart to:
- ) Handle greater pre-load (i.e. greater filling volume)
- ) Empty more completely (i.e. reduces ESV)
- ) Do all of this against increased after=load (increased aortic pressure)
- ) Deliver increased SV (even when increased HR reduces ventricular filling time)
Activation of Beta 1-adenoreceptors:
increase in intracellular cAMP levels
Ventricular contractility:
Effect of parasympathetic stimulation?
COMPLETE WITH THE NOTES SECTION OF THE SLIDE
Preload, afterload and contractility
Decreased force of contraction
Inhibition of norepinephrine release from sympathetic NS
Activation of M2 muscarinic receptors:
reduce cAMP production
(Cardiac slowing; inhibition of AV conduction)
Contractility:
Pharmacological manipulation?
COMPLETE WITH THE NOTES SECTION OF THE SLIDE
Preload, afterload and contractility
POSITIVE INOTROPES Phosphorylation of Ca2+ channels Faster calcium uptake Sensitisation of Troponin C to calcium = Increased contractility Examples: 1.) Cardiac glycoside (Digoxin) 2.) Beta 1-adrenoceptor agonists SEE DIAGRAM 37
What is afterload?
What us afterload influenced by?
Resistance against which ventricle pumps
(Increased SV= Increased afterload)
Influenced by: pressure of blood in circulation=
affected by vasomotor tone, primarily by arteriolar tone
Venous tone= controls preload
Arteriolar tone= controls afterload
Explain the link between intrinsic and extrinsic control of SV?
Intrinsic control mechanisms:
i.e. normal heart pumps venous return each cycle
Extrinsic mechanisms overcome limits of intrinsic control:
i.e. increased contractility at a given preload
Afterload= limiting factor in SV in diseased animals (e.g. high blood pressure) i.e. afterload has big impact on CO if in diseased state
How are CO, HR and SV all linked?
SEE DIAGRAM 38
CO:
HR and SV
SV:
Preload, afterload and contractility
HR and Preload
Increase SV or increase HR= CO increases
AS HR increases, preload decreases slightly
What is heartrate controlled by?
ADD NOTES SECTION OF THE SLIDE
Preload, afterload and contractility
(INTRINSIC ACTIVITY- SAN)
a.) Controlled by sympathetic and parasympathetic NS:
Tightly regulated to maintain blood pressure: RAPID control
b.) Baroreceptors in carotid artery
High/low blood pressure control?
ADD NOTES SECTION OF THE SLIDE
Preload, afterload and contractility
High blood pressure=
Parasympathetic stimulation SLOWS heart
Low blood pressure=
Sympathetic NS INCREASES HR
INCREASES vascular tone
What is cardiac index?
= The amount of blood pumped per minute per kg of body weight
NOTE: Increased cardiac index= heart must work harder to maintain this, this increased work could lead to some type of failure of the heart
The heart: Metabolic rate? Anaeronic capacity? Blood supply? CO use?
Metabolic rate= very high
Anaerobic capacity= little
Blood supply= very rich
Cardiac output= uses 4-5% of CO it gives out
SLIDE 42
COMPLETE SLIDE
Preload, afterload and contractility
COMPLETE
How is blood pressure calculated?
COMPLETE SLIDE
Preload, afterload and contractility
Blood pressure= CO * Total peripheral resistance
How is blood flow calculated?
Blood flow resistance:
What is resistance proportional to?
Blood flow= pressure difference/resistance
NOTE: pressure difference= between 2 points along vessel
Resistance is proportional to:
Length and Radius^4
NOTE: length of vessel is fixed BUT radius can be changed (power of 4= small change in diameter or radius leads to big difference in resistance SO blood flow. Example: Halving radius decreases by 2^4 (1/16th of the flow by reducing tone by half BUT counteract this by increasing the pressure difference by increasing SV and thus CO)
How is pulse pressure calculated?
What is pulse pressure influenced by?
Pulse pressure= P(systolic) - P(diastolic)
i. e. pressure at systole - pressure at diastole
c. f. MAP= DAP + 1/3 * (SAP-DAP)
Influenced by: Arterial compliance (aorta) Stroke volume Ejection rate (ventricular inotropy) Consistent high pulse pressure 'ages' the heart quicker (important to try and minimise pulse pressure
NOTE:
Arterial compliance= Ability yo accommodate the increase in pulse pressure- aorta is slightly rigid but has some elasticity
Inotropy= force of muscle contraction
More transient afterload= heart must work harder
Summary of CO and blood pressure?
Cardiac Output = SV x HR Stroke Volume influenced by: Preload (venous return), contractility and afterload Intrinsic control (Frank-Starling) Extrinsic control (Sympathetic nervous system)
Heart rate
Sympathetic (increase) and parasympathetic (decrease) NS
Acts via b1 adrenoceptors / M2 receptors
Blood pressure = CO x resistance
Cardiac output
Systemic vascular resistance:
Sympathetic nervous system
Other mechanisms (RAAS)
Increased CO= increased BP
Cardiac contractions and circulation:
- Dogs?
- Humans?
Cardiac partitioning:
- Dogs?
- Humans?
Cardiac contractions and circulation:
a.) 18-19 days – dog
b.) 28 days – humans
(Slow at first, increases when atria and SV form)
Cardiac partitioning:
a. ) 28 days – dog
b. ) 35-49 days – humans
What are the layers that make up the embryo?
Endoderm
Mesoderm
Ectoderm
What does the heart develop from and where does this occur?
(Heart= first organ to undergo functional development)
Heart - cardiogenic plate of mesodermal tissue at head end of embryonic disc
Rapid development and flexion of head cause cardiac disc to lie below head and mouth but cranial to the foregut- must migrate caudally in mammals (doesn’t migrate caudally in iguanas)
Explain the structure of the primitive cardiac tube (before forming the tube structure)?
2 lateral extensions of cardiac disc hollowed out:
Pair of endothelial tubes- soon forms primitive cardiac tube when embryo folds laterally
Lateral extensions of cardiac tube hollow out and form pair of endothelial tubes which fuse- Begins as pair and ends up as one
SEE DIAGRAM 39
Where do vessels join the heart tube (in a developing heart)?
Paired veins enter heart tube from: Trunk (the cardinal system) Liver Yolk sac Placenta (Heart tube is connected to trunk, liver, yolk sac (at this stage) and later it is connected to placenta as placenta develops)
Arterial arches develop and emerge from the upper end
Explain how the different layers of the heart develop
(Inside=) Endocardial tube forms:
ENDOCARDIUM (part of it forms valves)
Cardiac jelly becomes:
Collagen/glycoproteins
Thick mesoderm-myocardium becomes:
Myocardium (myocard contraction, cell migration- septa and valves)
Thin epicardial layer: becomes epicardium (outer cardiac surface)
Explain growth of the primitive tube
Tube grows quicker than rest of embryo AND it is fixed at 2 ends SO it folds
Falls to right: d-looping
Abnormal fall to left: l-looping (leads to apex beat being on right instead of left- CHECK IF LEFT OR RIGHT)
SEE DIAGRAM 40
What happens in the primitive tube once it has completed d-looping?
Begins to bulge (primarily comes to right- due to d-looping)
Ventricles: Bulbus cordis becomes right V, primitive ventricle becomes left C
Aorta and pulmonary artery grow from same position
Chamber: some sits on left, some on right- begins to show how you have 2 atria/2 ventricles (heart has folded but hasn’t separated into 4 chambers yet)
SEE DIAGRAM 41
Blood supply to the heart in the stage following d-looping?
Blood flows:
From: vitelline (from yolk sac) and common cardinal veins, Into: SV
From: SV, To: common atria
From: common atria, To: common ventricle
From: common ventricle, Then: exits heart via TA
How are the cardiac chambers formed?
Partitioning influenced by blood flow:
- ) Form atria
- ) Form atrio-ventricular canal (separates atria/ventricles)
- ) Form Bulboventricular loop (separates the 2 central ventricles)
- ) Form Truncus arteriosus (divides)
- ) Separation of the aorta and pulmonary artery – aorticopulmonary septum - concomittant
NOTE: Folded chamber BUT still not 4 chambers and 4 valves- partitioning is needed
(NOTE: SV is only seen in embryonic heart)
Sinus Venosus development?
RIGHT horn of SV: becomes incorporates into atrial wall (becomes part of atrial appendage- joint seen in some animals)
LEFT horn of SV: not incorporated- coronary sinus
AV cushions development?
COMPLETE
Cardiac embryology
Interatrial septa development- SV?
COMPLETE
Cardiac embryology
Interatrial septa development- SS?
COMPLETE
Cardiac embryology
Explain blood flow into the atria in utero?
Following AV cushions/interatrial septa/interatrial septa development
MAJORITY: From caudal vena cava (at this stage) Aimed at septum primum- pushing to left keeping FO open Blood goes from RA to LA Blood goes from LA to: - LV - Aorta - Body
SMALL VOLUME:
RA to RV to PA to DA to aorta
NOTE: Ductus arteriosus (DA)= stop blood going to lungs as they are not aerated (communication between PA and aorta- needed in utero BUT closes when we are born- do not want blood going from PA into aorta. If it doesn’t close= persistent ductus arteriosus)
What happens to the intra-atrial septa at birth?
Septum Secundum and Septum Primum tightly appose:
- decrease pressure in RA, increase in LA
- now have bood inflow from lungs
NOW called intra-atrial septum (occurs within mins. of birth)
NOTE: apposition BUT not fusion= quite common, esp. in cattle
PFO (persistant foramen ovale)= common in people and cattle (associated with migraines in people)
Truncus arteriosus and bulbus cordis
COMPLETE
Cardiac embryology
Change of orientation of TA
COMPLETE
Cardiac embryology
Interventricular septum
COMPLETE
Cardiac embryology
COMPLETE SLIDE 27
COMPLETE
Cardiac embryology
What is trabeculation?
COMPLETE
Cardiac embryology
Why and when does the interventricular septum close?
Due to growth of atrioventricular cushions- plugs hole
Dogs: 32 days
Humans: 45 days
How do AV valves form?
(Occurs as AV septum forms)
Forms from reshaping and tissue loss within ventricular walls
Ventricle dilates, walls hypertrophy, trabeculation occurs and endodermal cell death
- Strands of cardiac wall mesenchyme from Atrio-ventricular cushions to ventricular wall remain
- Form cusps of atrio-ventricular valves and chordae tendinae
How do the aorta (Ao) and pulmonary artery (PA) form?
Following formation/fusion of truncal ridges: get 3 swellings in walls of Ao and PA trunks (i.e. once truncus arteriosus has separated, there are 3 swellings)
Expand into lumen of each vessel
Very broad BUT then thinning occurs with cellular degeneration (thinning allows thin valves which hold high pressures)
(Congenital abnormalities)
What is the defect when:
1.) Atrio-ventricular cushions and interventricular septum don’t fuse?
- ) Truncal septum deviated to PA side?
- ) Truncal septum fails to develop?
- ) Septum primum and secundum don’t meet or fuse?
- ) Ventricular septal defects
- ) Persistent trncus arteriosus or over-riding aorta
- ) Persistent truncus arteriosus
- ) Persistent foramen ovale
What stages of cardiac development are primitive? (i.e. conserved in phylogenetically old groups)
What are later developments?
Development of atria
SA valves
Development of atrio-ventricular valves
(Development of semi-lunar valves – Ao/PA)
Two ventricles
Truncus arteriosus dividing into Ao and PA
Vena cavae
Explain the structure of a fish’s heart
Simple
1 atrium
1 ventricles
Rudimentary valve (thick) between the atria and ventricle
Conus arteriosus to gills (similar to truncus arteriosus)
Keep sinus venosus
SEE DIAGRAM 42 (3 pictures/parts)
Explain the structure of an amphibian’s heart
2 atria
1 ventricle- functionally but not anatomically divided ( 1 pumping chamber bur can send blood to 2 different parts of the body)
Sino-atrial valves
Sinus venosus
Rudimentary semi-lunar (Ao and PA) valves
Bulbus cordis cushions – form but don’t completely fuse with truncus arteriosus cushions
SEE DIAGRAM 43 (2 pictures/parts)
Explain the structure of a snake’s heart
2 atria
1 ventricle (partial septation i.e. it is PARTLY divided)
Caudal vena cava and 2 Cranial vena cava drain into sinus venosus
Hard to tell difference between sinus venosus and right atrium – is a sinoatrial valve
Paired AV valves (only 1 cusp- not very efficient)
Paired semilunar valves
2 aortic arches -Right aortic arch – bicarotid trunk – then fuses with left aortic arch caudally in midline
Explain the structure of a lizard’s heart
2 atria
2 ventricles (right and left)
Sinus venosus – blood from two anterior vena cavae, hepatic vv and coronary aa
(R and L aortic arches)
One pulmonary vein
Heart position= breed dependent:
- Iguanids – heart sits in thoracic inlet – Heart originates a long way cranially which is reflected in iguanas (heart migrates further back in mammals)
- Monitors – more conventional heart position
Heart originates a long way cranially which is reflected in iguanas where heart sits at thoracic inlet
SEE DIAGRAM 44
Explain the structure of a chelonian’s heart
2 atria
1 ventricle (functionally but not anatomically divided)
Two large carotid-subclavian arterial trunks (more developed arterial trunks than in fish)
Trabeculation has occurred but it hasn’t fused with AV cushions
SEE DIAGRAM 45 (3 pictures/parts)
Explain the structure of a bird’s heart
Relatively larger than mammals and beats faster
Comparatively larger left ventricle
Main structural difference: atrio-ventricular valve= muscular flap (could be argued that it is more efficient)
SEE DIAGRAM 46
SUMMARISE ALL EVENTS OF CARDIAC DEVELOPMENT
Cardiac embryology
ECHO
Why is foetal circulation different to adult circulation?
IT NEEDS TO BE
Fetus ‘breathes’ amniotic fluid (no lung inflation- fetal heart ventricles work in parallel)
Fetus swims in amniotic fluid (Stable temperature- no need to regulate body temoerature, protection)
Fetal blood is oxygen-poor (hypoxaemic)
Fetus receives nutrients parenterally (umbilical cord), not orally/ via gut (oral = enteral feeding )
Fetus has placenta attached (replaces role of lungs)
Fetal kidneys do not need to process waste
NOTE: Lungs are just growing, not really performing as lungs
What is the lung replaced with in a fetus?
LUNG= REPLACED BY PLACENTA (fetus= symbiotic parasite)
Placenta becomes fetal lung:
- Interface for exchange of gases/food/waste
- De novo production of fuel substrates and hormones
- Filtration of potentially toxic substances
Why must maternal and fetal blood be separate?
Maternal side, Decidua basalis
Foetal side, trophoblast, chorionic villi
Different blood types so systems must be kept separate to prevent blood being rejected
SLIDE 6:
EDIT TEXT AND COPY PICTURES
The structure of the placenta. No direct mixing of maternal and foetal blood.
Poorly oxygenated blood from foetus arrives at the placenta from 2 Umbilical Arteries. These divide into Chorionic Arteries and terminate as chorionic villi. These increase exchange surface area. Maternal blood sprays over these chorionic villi exchanging O2, CO2, nutrients and waste products. O2 and nutrient rich blood flows away via thin walled veins that follow the chorionic arteries to the umbilical cord where they converge to form the Umbilical Vein.
How is fetal circulation different to adult circulation?
ADULT FETUS
Fuel storage/detoxification Fat/Muscle/Liver Placenta
Gas Exchange Lungs Placenta
Waste removal Kidneys/Liver Placenta
Fetal circulation has 3 key ‘shunts’
How fetal circulation is different: what are its 3 key shunts?
What is their function?
- ) Ductus venosus
- ) Foramen ovale
- ) Ductus arteriosus
Function:
‘shunt’= a passage or anastomosis between two natural channels such as blood vessels
SEE DIAGRAM 47
Which parts shunt what?
ECHO SLIDE 9
COMPLETE
Fetal stress
COMPLETE
SHUNT 1 of 3 Ductus Venosus Function? Location? Species differences?
Function:
Creates low resistance pathway through liver
Allows 50% blood to bypass liver
Streams blood to foramen ovale
Location:
From umbilical vein to caudal vena cava
Species differences:
Fetal horse: DV is not present
Fetal pig: No shunts are present
SEE DIAGRAM 48 (2 pictures/parts)
Umbilical vein and umbilical arteries?
TWO umbilical arteries: go to placenta
Umbilical vein: goes to fetus
Shunt 2 of 3 Foramen Ovale Function? Location? How is it kept open in fetus? How is patency maintained? What would occur if the FO wasn't present in a fetal heart? How does the FO change this?
COMPLETE USING NOTES SECTION OF THIS SLIDE
Function:
Shunts oxygenated blood straight through RA to LA
Location:
Opening connects RA to LA
Kept open in fetus by:
Pressure differences
Patency maintained by:
High blood flow (blood at high pressure as it comes directly from umbilical vein- most will have bypassed capillary beds of liver)
Kinetic energy of blood in IVC
If FO wasn’t present:
High pressure exit through right side would take blood into pulmonary trunk and to collapsed lung
BUT INSTEAD:
Most of the blood goes to LA though FO then LV to Ao and NOT through LV to lungs
THEREFORE:
Oxygenated blood leaves from pulmonary trunk AND aorta and goes straight up from heart to brain and back to heart.
