-
pericardial sac
- envelops heart
- visceral and parietal layer
- pericadial cavity - lubricating fluid
- decrease friction
-
pericarditis fibrinosis
- thick layer of fibrin in pericardial cavity b/c of infection
- (cow eats nail and it punctures heart)
-
purpose of heart
TRANSPORT - gas, heat, hormones, cells, water, minerals
-
when blood leaves organs
blood pressure is lower even in the lungs
-
arteries have how much pressure
HIGH = arteries
-
veins have how much pressure
LOW = veins
-
heart is 1 functional unit
2 separate pumps
-
heart skeleton
base of heart, all vales attached, fibrous, chondric, and osseous (cattle)
-
semilunar valves
3 valves
-
-
-
role of the atrium is to
fill ventricles
-
Systole
- AV closed
- ventricles contract
- semilunar open
- blood to system
-
diastole
- AV open
- ventricles relaxed
- semilunar valves closed
-
contraction
- shift down for atria filling
- shift up for ventricle filling
-
-
ventricle filling
shift up
-
atria
- systole and diastole
- shorter
- begin and end before ventricle
-
atrial systole
- ventricle relaxed
- atria contraction completes filling of ventricle
-
ventricular systole
- increase in blood pressure
- all valves closed
- isovolmetric contraction
- diastole
-
isovlometric contraction
ventricular systole
-
ventricle pressure higher that aortic/pulmonary
causes ejection
-
ventricle diastole
- decrease in blood pressure
- all valves open
- isovolmetric relaxation
-
isovolmetric relaxation
ventricle diastole
-
atria high pressure than ventricle
- AV valves open
- passive filling
-
ventricle pressure in diastole
- lower than atria
- aortic valve closed
-
ventricle pressure in systole
- higher that atria
- AV valves closed
-
aortic valves are closed till
- ventricle pressure is higher than aortic
- ejection to system
-
stroke volume
- difference between end diastolice volume and end systolic volume
- volume of blood ejected during systole
-
end systolic volume
- decrease in ventricle blood volume
- end of systole
-
End Diastolic volume
- max volume of cardiac cycle
- ventricles fill till end of diastole
-
catacholamines
increase heart rate
-
-
parasympathetic
all of heart w/o ventricles
-
-
-
dromotropic
- speed of conduction
- atria only
-
inotropic
- force of contraction
- atria only
-
norepi
- steeper diastolic depolarization
- increase Na
- decrease K
- increase heart rate
-
acetyl
- flatter diastolic depolarization
- increase K
- decrease Ca
- lower heart rate
- negative tropic effects on heart
-
fight or flight
no parasympthetic
-
sym and para
- sym - day
- para - night
- equal influence of both SA node intrinsic rate wins
-
increase in contration
- exercise
- increase stroke volume and end diastolic colume
- digitalis, isoprotenerol, norepi
-
decrease in contration
- propanol - Beta antagonist
- barbituate - anaesthesia
-
pacemaker cells
- cant contract
- generate Action potenital
- no stable membrane potential
-
-
intrinsci rates of pacemakers
- SA - 70
- AV - 40- 50
- bundle of his, branches and purkinji 25 - 40
-
SA node fires
- AP runs through heart and resets all pacemakers
- self excitation - increase permability to Na and K
-
pacemaker potenial or prepotential
- diastole
- slow depolarization between AP
-
-
membrane potential of pacemaker ions
-
AV node depolarizing
- still depolarizing when AP arrives from SA
- increase deplarization to threshold to generate the AP
-
Auxilary pacemaker
nerve complete their pacemaker potential b/c faster pacemeaker dominates
-
Action potential
atrium depolarizes, AP reaches AV node before all of atrium depolarizes
-
AV node delay
- frequency filter
- atria then ventricle depolarize
- atria pump into ventricle
-
SA AP
.22 sec to ventricle deplarization to contaction
-
size of heart
- relation to body
- small heart higher heart rate
-
heart rate
- more exersize - decreases
- reptiles - warmer body temp increase heart rate
-
wave of ECG
one positive or negative deflection
-
segment of ECG
distance/ time between 2 waves
-
interval of ECG
consists of one or more waves and segments
-
ECG
- AP - wave of depolarization (has direction)
- number of cells depolarizes increase to max then decrease in number of cells
- direct corallation between strength of electrical signal and number of depolarized cells
-
max record potential
- can't exceed max generated potential
- can be lower
-
depolarization direction
direction of depolarization in realtion to direction of measument
-
electrical potential
- ionic differences in Extra cellular fluid = electircal potential
- occurs during de and repolarization
-
0 mV
- at resting
- stale depolarization state
- no difference in ECF
-
size of item and angle
view size of an item depends on the view of the angle
-
record potential
depends on the location of depolarization and placement of electrodes
-
vector
points from depolarized to nonpolarized area
-
electrode reads
left to right
-
Zero
vector measuring plane are vertical to each other then independently of the actual magnitude of potenital difference
-
einthoven
- equilateral triangle
- 3 different values of same vector
- only use 2 planes
-
cardiac vector
main ptoential difference in heart electrode orientation determines how much of the cardiac vector is measured
-
III lead
- use 2 and 3
- third plane
- max strenght
- recorded size of vector is different compared to other leads
-
animal shape influence on ECG
- different size and shapes of animals influence ECG
- don't make equilateral triangle
- same function (PQRST)
-
Goldberg
- 2 connected electrodes
- stonger signal, better
- inverted 45 degrees b/c of heart
- augmented voltage (aV + right, left or foot)
- aVr, aVl, aVf
- aVr - 1 electrode on right, 2 connected in series on left
-
wilsons
- leads placed on chest close to heart
- increased detail
-
P wave
atria depolarize and AV node
-
PQ segment
depolarization of AV node (bundle of his)
-
PQ interval
atria depolarization to begining of ventricle depolarization
-
QRS
depolarization of ventricle
-
ST segment
- ventricle still depolarized
- no electical change = no signal
-
T wave
- ventricle repolarizes
- only repolarization
- atria repolarize earlier but to small to see in ECG
-
R and S wave
can be missing
-
no P wave
- no SV node
- AV node is the pacemaker
-
amplified standard
- 5 or 10 mm per mV
- slower - better idea of rhythmic events and reveal random events
- higher - more detail
-
duration
- P wave .6
- PR .13
- QRS .05
- QT .19-.23
-
ECG provides
- only partial info about mechanical events in heart
- can be calculated and compared to standard values
-
ECG also provides
- only projections to the 3 planes (not actual vector)
- vector can be reconstructed from projections
- vector changes value and direction during cycle
- depolarization of atria and ventricle, reoplarization of ventricle bein and end at zero
-
vectorcardiogram 3 loops
- 1. P
- 2. QRS
- 3. T
- QRS largest loop
-
resting state
no signal, ECG baseline, cardiogram just a dot
-
Vectorcardiogram
- segments are not shown
- b/c heart is completely depolarized or repolarized
- dots where circles intersect
- normal - larger diameter of ellipse almost verticle
-
Valves
- not source of heart sounds
- help generate source of sound from oscillation of blood and vibrations of muscles and valves
-
murmurs
- 1. extracardiac events - fibrinous pericaditis - rubbing of heart and pericardium
- 2. altered valves - stenosis or insuficiencey
- 3. abnormal openings - ductus arteriosus, foramen ovale, ventricle septum defect
-
Auscultation
- PAM (bi) left side
- tri - right side
-
1st heart sound
- loudest
- systole
- AV closed
- venticle contract
- QRS
-
2nd heart sound
- diastole
- semilunar valves close
- after T wave
-
3rd heart sound
- in rushing blood from atria
- between T and P
-
4th heart sound
- contaction of atria
- P wave
-
stages of murmurs
- 1. hard to hear
- 2. soft but definit
- 3. low to moderate
- 4. loud
- 5. very loud (audible all over chest and palpate "thrill")
- 6. very loud even when stethoscope not in contact w/wall "thrill"
-
murmurs are from
- abnormal heart sounds
- abnormalities of physical heart sounds
- additional abnormal noises
-
stenosis
aquired congenitally undersized valves = developmental
-
insufficiency
leakage at closure from disease
-
Stenosis
- systole - semilunar valves
- Diastole - AV valves
-
insufficiency
- systole - AV valves
- diastole - semilunar vlaves
-
Mitral(bi) insufficiency
- begining at QRS and ends at T wave (end systole)
- AV valves closed - leaky systolic murmur
-
mital stenosis
diastolic murmur "hic up"
-
aortic insufificency
extended diastole murmur
-
aortic stenosis
systolic murmur
-
machinery murmur
- PDA -patent ductus arterious
- systolic and diastolic murmur
- caused by stenosis and insufficency
- always a sound
-
Fetus
- higher pressure on right side of heart (switch when foramen ovale closes)
- higher resistance through collasped lung - ductus arteriosus
- lower resistance through placenta - ductus venosus
-
PDA
continuous murmur sound
-
patent foramen ovale
murmur quiet b/c atrial pressure is low
-
aortic stenosis
- long lub
- first sound in systole
-
mital reguritation
- long and low in lub
- systole
-
aortic reguritation
- long diastole
- 2-4 heart sound
-
mitral stenosis
long and low in 3 and 4 heart sounds durign diastole
-
cardiac electrical abromalities - Excitation
- nomotropis dysfunction
- heterotropic dysfunction
-
nomotropic dysfunctions
- sinus arrhythmia
- sinus tachycardia
- sinus bradycardia
-
sinus arrhythmia (irregular)
- abnormalities in cardiac rythum
- normal in dogs - increase with inspriation and decrease with expiration
-
sinus tachycardia
- increase heart rate
- SA AP rate too high
-
sinus bradycardia
- decrease in heart rate
- SA AP rate too low
-
heterotropic dysfunction
- escape rhythm
- suraventricular extrasystole
- shifting pacemaker
- ventricular diastole
- supraventricular tachycardia
- atrial flutter
- artial fibrillation
- ventricle tachycardia
- ventricle flutter
- ventricle fibrillation
-
escape rhythm
- extreme brachycardia
- AV node rate exceeds SA and takes over
-
Supraventricular Extrasystole
- premature stimulus by atria
- SA no effect
- next systole is normal
- P wave very close to T wave
- waves to close together
-
Shifting pacemaker
- SA fails
- ectopic atrial pacemaker takes over
- b/c increase in vagal tone
- closer to AV node the shorter the PQ segment
-
Ventricular tachycardia
- premature stimulus from heterotropic ventricle
- next systole back to normal
- cant see P wave
- R and L depolarize at same time (from inside out)
-
supraventricular tachycardia
- increase in AP from atria
- P waves differnt shapes b/c several ectopic atrial pacemakers
- normal intervals
-
atrial flutter
- ectopis AP at high rate
- 220 - 350
- regular contractions, pulse rate and strenght
- myocardial infraction
- atria no pumping
-
atrial fibrillation
- ectopic AP at high rate 350-600
- rapid irregular and uncordinated depolarization
- pulse irregular
- no atrial pumping
-
ventricle tachycardia
- no P wave
- R waves from ventricle pacemaker
-
ventricle flutter
- multifocal excitation
- ceases pumping function
- different paper speeds
-
ventricle fibrillation
- mulitfocal excitation
- ceases pumping function
- death
- caused by decrease in blood to myocardium of ventricles
-
Cardiac electical abnormalities
conduction disorders
-
conduction disorders
- AV blocks
- firstm second and third degree
-
AV Block basics
- conditions and rate of conduction of the impluse through AV node and Bundle of His or block entirly
- AP to AV node and bundle of His
- affected by - ishemia (decrease in blood flow)
- compression (smaller diameter, calcification, scar)
- inflammation (infection, fever)
- extreme vagal tone
-
first degree block
- AV conduction slow
- PQ segment very long
-
second degree block
- dropped beat, ventricle does not contract
- SA node work others cant conduct AP
- no QRST interval
-
third degree block
- atrium and ventricle connection broken
- ventricles (bundle branch) cause AP (slower)
- need pacemaker
- atria and ventricles contract at different times
-
Cardiac structureal abnormalities - morphological
Hypertorphy
- of right ventricle
- change in cardiac vector to side effected
- increase muscle tissue = stronger signal = increased R waves
- change in timing of depolarization w/ only one side affected
-
cardiac structural abnormalities - functional
myocardial infraction
- few anastomoses in coranary artery
- embolus will cause occlusion
- decrease in blood to cardiac muscle tissue (dies)
- distorts R wave
- right after Shifter ST segment
-
Technical alterations
- electrical interference
- trembling patient
-
electical interference
- ECG (230 Hz power supply)
- poor lead connections
- regular and same reading over and over
-
trembling patient
skeletal muscle interfer
-
Heart Failure
- not able to adequatly meet body needs b/c of malfunction
- 1. decrease in cardiac output
- 2. damming of blood behind left or right heart
- 3. overload of heart through increased output
-
low heart failure
- 1. compensated heart
- 2. decompensated heart
- 3. bi/unilateral failure
-
compensated heart
- fails but recovers to allow minimum output
- cardiac reserve reduced
-
decompensated heart
- minimum not restored
- compensatory mechanism continue
- leads to death
-
bi/unilateral failure
whole or part of heart fails
-
high output failure
- increase force b/c some bypass of normal circulation
- continuous overload causes heart failure
-
high pressure
increase pressure b/c increased resistance in circulation = heart failure
-
cardiac output and artial pressure (preload) related
-
increase tissure demand = increased cardiac output
-
increase blood = increased atrial pressure and better ventricle filling time
-
longer muscle fibers
increased for and pumps more blood
-
max cardiac output
max heart rate and stroke volume
-
min cardiac output
- determined by tissues
- blood volume needed for maintenance
- 5 liters at rest
-
Cardiac reserve
- number of times heart increases output from resting level
- max-min = ___/min = cardiac reserve
-
heart failure
- decrease in contractility
- cardiac output drops below min
- causes blood to back up in stria and increase atria pressure
- increase sympathetic stimulation to strengthen heart muscle
- heart recovers over time (5-7 wks)
-
Kidney
- cardiac output min not maintained the kidney retains water and NaCl to increase blood volume and increase atrail pressure
- begins a few min after and lasts till pressure is normal
-
pumping ability reduced to 40-50%
- decrease from normal pumping ability
- benefits better systemic filling = decrease resistance, increase in preload
- cardiac output goes back to normal
-
pumping ability reduced to 25-45%
- fluid retention is detrimental
- overstreching of heart leads to increased weakening
- kidney cant regulate NaCl and water - fluid retention - edema (lung) - death
-
heart repair
- immediately
- new collateral blood supply
- nercrotic tissue = scar tissue
- undamaged muscle tissue hypertorpy
- 5-7 wk
- muscles at fringe may be functional again
-
cardiac reserve and different heart compensated heart failure
- meets needs of tissue at expense of increased atrial pressure
- little cardiac reserve left (increase preload causes no change in cardiac output (graph more horizontal)
- heavy exercise usually causes immediate return of symptoms
-
decompensated heart failure
- heart to weak to supply kidney (return NaCl and water) excessively
- causes blood volumes to increase beyond physiological limits - edema - overstreching - diliation of ventricles - death
- sympathetic strengthening does not work also
-
cardiac edema and ventricle dialtion cause
- weaker heart
- decrease output
- weaker heart
-
unilateral heart failure
- left side more likely then causes right side failure
- back up into pulmonary veins - increase pressure
- need 10mmHg for gas exchange and is now to high
- right pressure increases in pulmonary artery
- pulmonary edema - elveolar edema
-
high output edema
- heart forced to pump more blood to tissues additional volume = heart failure
- caused by - arterio-venous shunts, decrease reisitance to blood flow
- 1. PDA
- 2. ventricle septum defect
- 3.tetroloy of Fallot
- 4. low resistance to blood flow
-
PDA
- ductus arteriosus to bypass lung
- blood flow : left ventricle - lung - left ventricle if does not leave after birth
- heat has to pump increased volume - left ventricle gets larger
- if large (PDA) peripheral tissue does not receive required blood
-
ventricle septum defect
- heart contracts part of left ventricle blood goes through septum into right ventricle
- increase workload of left ventricle and causes enlargement
- thickening and dilation of cardiac meuscle
- rigth dilates muscle walls get thinner
-
tetrology of fallot
- 1. aorta connceted to both ventricles
- 2. ventricle septum defct b/c of aortic valve
- 3. stenotic pulmonary valve/artery, less space for this to develop b/c aorta in its place
- 4. hypertorphy of right ventricle - b/c more pressure needed to pump blood to lung (stenosis of pulmonary)
-
low resistance to blood flow
- arterioles - regulates blood flow and depends on metabloism of tissue, increased tissue metabolism then arterioles dilate
- controled by sympathetic of ANS
- malfunction = dilation - to much blood to tissue
- BERBERI - decrease Vit B b/c decrease in artery tone, heart has to pump more to maintain pressure
-
BeriBeri
- decrease in vit B (thiamine)
- b/c decrease in arteriole tone
- edema
- wobbly and trembling
- "walking like a sheep"
- heart pumps volume to maintain pressure
- low resistance blood flow
-
high pressure heart failure
- heart has to continuosly increase blood pressure = hypertorphy of muscle tissue (fibers grow in diameter)
- pericardium can't expand much to muscle fibers expand into the heart
- chamber gets smaller - thickness gets bigger
- increase heart rate and pressure - decrease in blood volume
- increase rate and increase pressure = increased workload = failure
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