cardio physiology

• envelops heart
• visceral and parietal layer
• pericadial cavity - lubricating fluid
• decrease friction

• thick layer of fibrin in pericardial cavity b/c of infection
• (cow eats nail and it punctures heart)

TRANSPORT - gas, heat, hormones, cells, water, minerals

blood pressure is lower even in the lungs

HIGH = arteries

LOW = veins

2 separate pumps

base of heart, all vales attached, fibrous, chondric, and osseous (cattle)

3 valves

• 3 valves
• tricuspid

• 2 valves
• bicuspid
• mitral

fill ventricles

• AV closed
• ventricles contract
• semilunar open
• blood to system

• AV open
• ventricles relaxed
• semilunar valves closed

• shift down for atria filling
• shift up for ventricle filling

shift down

shift up

• systole and diastole
• shorter
• begin and end before ventricle

• ventricle relaxed
• atria contraction completes filling of ventricle

• increase in blood pressure
• all valves closed
• isovolmetric contraction
• diastole

ventricular systole

causes ejection

• decrease in blood pressure
• all valves open
• isovolmetric relaxation

ventricle diastole

• AV valves open
• passive filling

• lower than atria
• aortic valve closed

• higher that atria
• AV valves closed

• ventricle pressure is higher than aortic
• ejection to system

• difference between end diastolice volume and end systolic volume
• volume of blood ejected during systole

• decrease in ventricle blood volume
• end of systole

• max volume of cardiac cycle
• ventricles fill till end of diastole

increase heart rate

whole heart

all of heart w/o ventricles

• excitibility
• atria only

• heart rate
• ventricles

• speed of conduction
• atria only

• force of contraction
• atria only

• steeper diastolic depolarization
• increase Na
• decrease K
• increase heart rate

• flatter diastolic depolarization
• increase K
• decrease Ca
• lower heart rate
• negative tropic effects on heart

no parasympthetic

• sym - day
• para - night
• equal influence of both SA node intrinsic rate wins

• exercise
• increase stroke volume and end diastolic colume
• digitalis, isoprotenerol, norepi

• propanol - Beta antagonist
• barbituate - anaesthesia

• cant contract
• generate Action potenital
• no stable membrane potential

• 1 on right
• 2 on left

• SA - 70
• AV - 40- 50
• bundle of his, branches and purkinji 25 - 40

• AP runs through heart and resets all pacemakers
• self excitation - increase permability to Na and K

• diastole
• slow depolarization between AP

• -40
• causes them to close

• -60
• Na more than K

• still depolarizing when AP arrives from SA
• increase deplarization to threshold to generate the AP

nerve complete their pacemaker potential b/c faster pacemeaker dominates

atrium depolarizes, AP reaches AV node before all of atrium depolarizes

• frequency filter
• atria then ventricle depolarize
• atria pump into ventricle

.22 sec to ventricle deplarization to contaction

• relation to body
• small heart higher heart rate

• more exersize - decreases
• reptiles - warmer body temp increase heart rate

one positive or negative deflection

distance/ time between 2 waves

consists of one or more waves and segments

• 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

• can't exceed max generated potential
• can be lower

direction of depolarization in realtion to direction of measument

• ionic differences in Extra cellular fluid = electircal potential
• occurs during de and repolarization

• at resting
• stale depolarization state
• no difference in ECF

view size of an item depends on the view of the angle

depends on the location of depolarization and placement of electrodes

points from depolarized to nonpolarized area

left to right

vector measuring plane are vertical to each other then independently of the actual magnitude of potenital difference

• equilateral triangle
• 3 different values of same vector
• only use 2 planes

main ptoential difference in heart electrode orientation determines how much of the cardiac vector is measured

• use 2 and 3
• third plane
• max strenght
• recorded size of vector is different compared to other leads

• different size and shapes of animals influence ECG
• don't make equilateral triangle
• same function (PQRST)

• 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

• leads placed on chest close to heart
• increased detail

atria depolarize and AV node

depolarization of AV node (bundle of his)

atria depolarization to begining of ventricle depolarization

depolarization of ventricle

• ventricle still depolarized
• no electical change = no signal

• ventricle repolarizes
• only repolarization
• atria repolarize earlier but to small to see in ECG

can be missing

• no SV node
• AV node is the pacemaker

• 5 or 10 mm per mV
• slower - better idea of rhythmic events and reveal random events
• higher - more detail

• P wave .6
• PR .13
• QRS .05
• QT .19-.23

• only partial info about mechanical events in heart
• can be calculated and compared to standard values

• 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

• 1. P
• 2. QRS
• 3. T
• QRS largest loop

no signal, ECG baseline, cardiogram just a dot

• segments are not shown
• b/c heart is completely depolarized or repolarized
• dots where circles intersect
• normal - larger diameter of ellipse almost verticle

• not source of heart sounds
• help generate source of sound from oscillation of blood and vibrations of muscles and valves

• 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

• PAM (bi) left side
• tri - right side

• loudest
• systole
• AV closed
• venticle contract
• QRS

• diastole
• semilunar valves close
• after T wave

• in rushing blood from atria
• between T and P

• contaction of atria
• P wave

• 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"

• abnormal heart sounds
• abnormalities of physical heart sounds
• additional abnormal noises

aquired congenitally undersized valves = developmental

leakage at closure from disease

• systole - semilunar valves
• Diastole - AV valves

• systole - AV valves
• diastole - semilunar vlaves

• begining at QRS and ends at T wave (end systole)
• AV valves closed - leaky systolic murmur

diastolic murmur "hic up"

extended diastole murmur

systolic murmur

• PDA -patent ductus arterious
• systolic and diastolic murmur
• caused by stenosis and insufficency
• always a sound

• 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

continuous murmur sound

murmur quiet b/c atrial pressure is low

• long lub
• first sound in systole

• long and low in lub
• systole

• long diastole
• 2-4 heart sound

long and low in 3 and 4 heart sounds durign diastole

• nomotropis dysfunction
• heterotropic dysfunction

• sinus arrhythmia
• sinus tachycardia
• sinus bradycardia

• abnormalities in cardiac rythum
• normal in dogs - increase with inspriation and decrease with expiration

• increase heart rate
• SA AP rate too high

• decrease in heart rate
• SA AP rate too low

• escape rhythm
• suraventricular extrasystole
• shifting pacemaker
• ventricular diastole
• supraventricular tachycardia
• atrial flutter
• artial fibrillation
• ventricle tachycardia
• ventricle flutter
• ventricle fibrillation

• extreme brachycardia
• AV node rate exceeds SA and takes over

• premature stimulus by atria
• SA no effect
• next systole is normal
• P wave very close to T wave
• waves to close together

• SA fails
• ectopic atrial pacemaker takes over
• b/c increase in vagal tone
• closer to AV node the shorter the PQ segment

• premature stimulus from heterotropic ventricle
• next systole back to normal
• cant see P wave
• R and L depolarize at same time (from inside out)

• increase in AP from atria
• P waves differnt shapes b/c several ectopic atrial pacemakers
• normal intervals

• ectopis AP at high rate
• 220 - 350
• regular contractions, pulse rate and strenght
• myocardial infraction
• atria no pumping

• ectopic AP at high rate 350-600
• rapid irregular and uncordinated depolarization
• pulse irregular
• no atrial pumping

• no P wave
• R waves from ventricle pacemaker

• multifocal excitation
• ceases pumping function
• different paper speeds

• mulitfocal excitation
• ceases pumping function
• death
• caused by decrease in blood to myocardium of ventricles

conduction disorders

• AV blocks
• firstm second and third degree

• 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

• AV conduction slow
• PQ segment very long

• dropped beat, ventricle does not contract
• SA node work others cant conduct AP
• no QRST interval

• atrium and ventricle connection broken
• ventricles (bundle branch) cause AP (slower)
• need pacemaker
• atria and ventricles contract at different times

• 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

• 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

• electrical interference
• trembling patient

• ECG (230 Hz power supply)
• poor lead connections
• regular and same reading over and over

skeletal muscle interfer

• 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

• 1. compensated heart
• 2. decompensated heart
• 3. bi/unilateral failure

• fails but recovers to allow minimum output
• cardiac reserve reduced

• minimum not restored
• compensatory mechanism continue
• leads to death

whole or part of heart fails

• increase force b/c some bypass of normal circulation
• continuous overload causes heart failure

increase pressure b/c increased resistance in circulation = heart failure

increased for and pumps more blood

max heart rate and stroke volume

• determined by tissues
• blood volume needed for maintenance
• 5 liters at rest

• number of times heart increases output from resting level
• max-min = ___/min = cardiac reserve

• 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)

• 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

• decrease from normal pumping ability
• benefits better systemic filling = decrease resistance, increase in preload
• cardiac output goes back to normal

• fluid retention is detrimental
• overstreching of heart leads to increased weakening
• kidney cant regulate NaCl and water - fluid retention - edema (lung) - death

• immediately
• new collateral blood supply
• nercrotic tissue = scar tissue
• undamaged muscle tissue hypertorpy
• 5-7 wk
• muscles at fringe may be functional again

• 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

• 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

• weaker heart
• decrease output
• weaker heart

• 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

• 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

• 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

• 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

• 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)

• 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

• 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

• 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