Cardiac Cycle

Front 1

Law of LaPlace

Back 1

P = T/r
ventricular pressure
T tension in the ventricular wall
r radius of ventricle

Front 2

Preload

Back 2

end dyastolic volume that determines the resting or passive ventricular muscle tension

Front 3

Afterload

Back 3

aortic pressure, because is the pressure that the left ventricle must overcome to circulate blood

Front 4

ventricular filling

Back 4

filling increases radius, small changes in pressure and tension

Front 5

isovolumetric contraction

Back 5

increases tension, increases pressure, NO change in radius

Front 6

isovoumetric relaxation

Back 6

radius constant
tension decreased
pressure falls
AV valves open ----> V. filling

Front 7

Cardiac Output

Back 7

amount of blood pumped by the heart at any given amount of time.

Front 8

Formula for Cardiac Output

Back 8

CO= Stroke Vol X HR

Front 9

Heart beat is equal to

Back 9

arterial pulse rate

Front 10

Increase heart rate will affect the stroke vol...

Back 10

decreased because the heart spends less time in dyastole

Front 11

in increased heart rate, carciac output...

Back 11

increases, because the heart compensates for the decrease in stroke volume by increasing the cardiac output

Front 12

what factors can change the cardiac output

Back 12

changes in stroke volume and changes in the heart rate

Front 13

Physiological factors that can change cardiac output

Back 13

Frank Starling law- preload
Afterload
Contractility

Front 14

Purpose of the cardiovascular control mechanisms

Back 14

maintain blood pressure by changing the heart rate, stroke volume, and vascular tone

Front 15

What does the law of Frank Starling States?

Back 15

"the stroke volume increases as ventricular end dyastolic voume increases" - the greater the stretch (preload) the greater the force of contraction and the greater the stroke volume

Front 16

what protective mechanism does the frank starling law provide to the heart

Back 16

it balances the output of the right and left circulations of the heart. this prevents the pooling of blood either in the pulmonary or systemic regions of the circulation.
- the heart pumps out as much blood as it receives-

Front 17

Afterload- and its role in the Frank Starling Mechanism

Back 17

- afterload- its the arterial blood pressure that the heart must overcome to circulate blood.

the greater the afterload the SMALLER the stroke volume.
the smaller the stroke volume- it increases the end systolic volume

Front 18

What triggers the cardiac muscle contraction

Back 18

the arrival of an action potential will increase the Ca++ concentration from: the extracellular fluid
the storage in the sarcoplasmic reticulum

Front 19

how is Ca++ removed from the cytoplasm after contraction

Back 19

2 mechanisms;
- Ca++ ATPasel: back to the SR
- Na/Ca++ exchanger: against the electrochemical gradient uphill- out of the cell

Front 20

what medical condition would be benefit from the use of Na/Ca++ exchanger inhibitors

Back 20

Congestive Heart Failure; because it increases the cytoplasmic Ca++and in turn the force of contraction

Front 21

when would you use Na, K ATPase or Na pump inhibitors.... why

Back 21

in Hypertension bc inhibiting the pump increases Na intracytoplasmic.
The NaCa exchanger transports Na out of the cell an Ca into the cell, when the Na levels increase in the cell the NaCa exchangers slow down. this also increases the Ca++ levels in the cell. Since the cardiac contraction depends on calcium the force of contraction is increased.

Front 22

Mechanism of action of cardioactive glycosides

Back 22

Inhibit the Na+K+ATPase or
Inhibit the Na+pump

Front 23

Physiologic impact of shock in the cardiovascular system

Back 23

- Decrease of Cardiac Output
- Decrease of Blood Pressure
due to decreased circulating blood

Front 24

In what types of shocks would you find a pooling of blood in the large veins

Back 24

Neurogenic
Anaphylactic
Septic
Bc they cause vasodilation unlike hypovolemic shock where fluid leaves the body

Front 25

Sympathetic response to shock

Back 25

Increase HR - Increase contractility- Increased venous tone--- all this to increase cardiac output --- this causes an increase of arterial pressure by the increase in arterial tone

Front 26

what kind of pulse would you find in shock

Back 26

weak and rapid, bc the blood volume is low and the body tries to compensate by increasing HR

Front 27

what condition would cause; systemic arterial pressure decrease - system venous pressure increase

Back 27

Right Heart Failure

Front 28

what nutrient does the heart prefer for production of ATP

Back 28

Ketone bodies, but can also use glucose

Front 29

what part of the cardiac myocites serves as store oxygens

Back 29

Myoglobin

Front 30

it what phase of the cardiac cycle do the AV valves close and why

Back 30

the av valves close at the beginning of ventricular systole to prevent back flow of blood to the atria while the ventricles contract

Front 31

when do the semilunar valves open

Back 31

during ventricular systole

Front 32

T or F, do the ventricles contract at the same time?

Back 32

true

Front 33

this circulation starts at the left ventricle and ends at the right atruim

Back 33

systemic circulation

Front 34

this circulation start at the right ventricle and ends at the left atrium

Back 34

pulmonary circulation

Front 35

at rest 2/3 of the cardiac cycle is in...

Back 35

dyastole

Front 36

when exercising which stage of the cardiac cycle is modified

Back 36

the heart spends less time in dyastole

Front 37

phases of the atrial systole...
start and deflections on EKG

Back 37

starts w SA depolarization- no trace

Front 38

what part of the cardiac cycle represents a P wave

Back 38

atrial depolarization --- it always precedes atrial contraction

Front 39

when does atrial contraction occur...what precedes it

Back 39

it occurs after atrial depolarization and it reflects as an A wave