Cardiac Cycle And Cardiac Output- Veterinary

Front 1

R side of Heart

Back 1

- Low Pressure system
- R Atrium collects deoxygenated blood from the cranial & caudal vena cava and conducts it into the R Ventricle through the R Atrioventricular Valve (Tricuspid)
- The R Ventricle then pumps blood through the Semi-lunar Valve ( pulmonic ) into the pulmonary artery

Front 2

L side of Heart

Back 2

- Left atrium collects oxygenated blood from the pulmonary veins and conducts it through the L AV valve (Mitral) and into the L Ventricle
- L Ventricle then pumps the blood through the Semi-lunar ( Aortic) valve into the Aorta

Front 3

Diastole

Back 3

- Ventricle filling time
- Atria are emptying and acting as conduits and the AV valves are open

Front 4

Early Diastolic Filling

Back 4

- At beginning of diastole, bl. flows rapidly from the atria into the relatively empty ventricles

Front 5

S3

Back 5

- The end of early diastolic filling causes a vibration in the ventricle wall that can be heard in horses or diseased hearts of dogs & cats
- S3 Gallop

Front 6

S4

Back 6

- During LATE DIASTOLIC FILLING
-the atria contract, squeezing more blood into and already full ventricle
- This causes heart sound S4 gallop, normal in horses

Front 7

Systole

Back 7

- At the end of diastole, the ventricle begins to contract

Front 8

S1

Back 8

- pressure in Ventricle rises > exceeds pressure w/in atrium, > AV VALVES SNAPS SHUT
- Ventricle continues to contract

Front 9

S2

Back 9

- AV and Semilunar valves are closed, pressure w/in ventricle rapidly rises, but ventricular volume stays the same
- When intraventricular volume pressure exceeds pressure in pulmonary artery or aorta, the semi-lunar valves open and blood rapidly exits ventricle
- VENTRICLE RELAXES AND SEMI-LUNAR VALVES SNAP SHUT
-heard as S2, marks onset of diastole

Front 10

Cardiac Output

Back 10

Volume of Bl. ejected by heart in one minute

Front 11

Stroke Volume

Back 11

Volume of Bl. ejected from ONE ventricle during systole

Front 12

Heart Rate

Back 12

Number of cardiac cycles in one minute

Front 13

Cardiac Output =

Back 13

Heart Rate X Stroke Volume

Front 14

Stroke Volume =

Back 14

End diastolic volume - End systolic volume

Front 15

Myocardium blood supply

Back 15

- The myocardium obtains most of it's OWN blood supply via the coronary circulation during DIASTOLE

Front 16

P Wave

Back 16

- Specialized cells w/in SA node initiate an impulse that is conducted across the Atria resulting in atrial systole of late diastolic filling

Front 17

PQ Interval

Back 17

- Impulse conducted rapidly to AV node where it is STORED MOMENTARILY to ensure that ALL of the Atrial myocardium has depolarized.
- This delay is known as PQ interval

Front 18

Annulus Fibrosus

Back 18

- The framework on which the heart valve leaflets are attached
- insulates the atria electrically from the ventricles, ensuring that ventricles can only contract via and impulse that has travelled through AV node, only when atria have emptied as much as possible through open AV valves

Front 19

Bundle of His

Back 19

- Carries the electrical impulse from the AV node to the Purkinje Fibres of the Ventricles

Front 20

Purkinje Fibres

Back 20

- Branching pathways of specialized conducting fibres
- conduct rapidly and depolarize myocardial cells as they go before they eventually terminate

Front 21

QRS Complex

Back 21

- The depolarization of the ventricles forms the QRS complex

Front 22

T Wave

Back 22

- Final phase of the ECG
- Results from ventricular Re- Polarization
- can be positive, negative, or biphasic in Veterinary Medicine

Front 23

Electrical Phases of Cardiac Cycle

Back 23

- Electrical activity always just slightly precedes the associated mechanical response, referred to electromechanical delay
- Electrical current via the flow of ions initiates, propagates, and regulates cardiac contraction

Front 24

Resting Membrane Potential

Back 24

- An electrical potential difference that exists across the plasma membrane of most animal cells

Front 25

The Resting Membrane Potential Exists for 2 reasons =

Back 25

- a semi-permeable membrane which fairly freely allows potassium to diffuse in and out of the cell, but not sodium

- a sodium/potassium ATPase pump that helps maintain the potential by pumping out 3 sodium ions and pumping in 2 potassium ions.
This in itself creates negative charge across the cell membrane

Front 26

Cardiac Cell Properties - EXCITABILITY

Back 26

- all cardiac cells can be stimulated to conduct or contract by electrical impulse

Front 27

Cardiac Cell Properties - AUTOMATICITY

Back 27

- All cardiac cells have the ability to create and electrical impulse themselves! but inherent rate varies according to TYPE of cell
- SA node = fastest, normal creators of cardiac impulse
- AV node- slower
- Purkinje cells, slowest

Front 28

Cardiac Cell Properties - OVERDRIVE SUPPRESSION

Back 28

- The automaticity of cardiac cells can be suppressed by other cells depolarizing at faster rates
- SO, normally AV, Purkinje and myocardial cells do NOT depolarize spontaneously because they are being made to depolarize FASTER than their own inherent rate by the SA NODE
- if SA node fails due to disease, the next fastest autonomic cells will take over, ie the AV nodal cells

Front 29

Cardiac Cell Properties - CONDUCTIVITY

Back 29

- All cardiac cells conduct and electrical impulse to adjacent cells, done via local depolarization

Front 30

Cardiac Cell Properties - REFRACTORINESS

Back 30

- Once a cell has depolarized, it will remain refractory to further stimulation for a certain period of time
- this is vital to ensuring electrical current spreads through heart in an ordered fashion, and prevents Fatal Tetany of the myocardium

Front 31

Cardiac Cell Properties - EXCITATION/CONTRACTION COUPLING

Back 31

- When myocardial cell is depolarized, it will contract
- this is due to inflow of Ca+ ions into the cell that triggers the release of more Ca+ w/in the cell that binds to Troponin C and initiates contraction

Front 32

7 Basic Deterimants of Cardiac Output

Back 32

1- Heart Rate- CO= HR X SV

2- Contractility- inherent ability of the ventricles to contract for a fixed amount of blood within them

3- Preload- amount of blood that enters the ventricle

4- Afterload- resistance against which the ventricle has to contract to expel blood

5- Elasticity

6- Hypertrophy- thickening of heart muscle, decreases elasticity, occurs when heart tries to cope with volume overload

7- Leaks- leaky valves, blood flowing the wrong direction