Foley-Intro To Cardiac Physiology

Front 1

basic flow equation

Back 1

flow=pressure difference/resistance

Front 2

Factors in resistance

Back 2

length and viscosity add to resistance
radius is inversely proportional

Front 3

What is the biggest factor in resistance?

Back 3

radius-it is calculated to the 4th power in the equation, so small change will have big impact

Front 4

actual flow equation

Back 4

change in pressure X (pi radius to the 4th power/8 length viscosity)
understand concepts

Front 5

What is cardiac output

Back 5

cardiac output = stroke volume X heart rate

Front 6

The contractions of individual cardiac muscle cells must occur at regular intervals and be synchronized (not arrhythmic).
The valves must open fully (not stenotic).
The valves must not leak (not insufficient or regurgitant).
The muscle contractions must be forceful (not failing).
The ventricles must fill adequately during diastole.

Back 6

requirements for effective heart pumping

Front 7

What does Starling's law describe?

Back 7

as ventricular diastolic blood volume increases, stroke volume will increase (and in turn, cardiac output will increase)

Front 8

How is the heart controlled?

Back 8

autonomic nervous system-sympathetic and parasympathetic systems
limited parasympathetic innervation of the ventricles

Front 9

What happens to the total cross sectional area of the blood vessels?

Back 9

increases as it goes from aorta to arteries to arterioles to capillaries, then decreases from capillaries to venules to veins
cross sectional area changes due to changes in total number of vessels for each class

Front 10

Why is the cross sectional area so large in capillaries?

Back 10

large cross sectional area decreases pressure and blood flow, allowing for more exhange and diffusion in capillaries

Front 11

Small Na permeability causes the resting potential to be slightly more positive than the K equilibrium potential for the cells

Back 11

cardiac muscle resting potential

Front 12

What do the phases mean in fast response action potentials?

Back 12

Phase 0-intial depolarization (up to +20-30mV)
1-slight return toward 0 mV (right after peak)
2-plataeu (prolonged depolarization)
3-repolarization
4-resting potential

Front 13

What causes the phase responses?

Back 13

Phase 0-Na permeability
Phase 1-Drop in Na after increase
Phase 2-reduced K permeability; increased Ca (Ca-slow release channels)
Phase 3-Increased K and decreased Ca

Front 14

What's the difference between fast response action potentials and slow response action potentials (pacemaker cells)?

Back 14

Pacemaker cells have phase 4 spontaneous depolarization
In slow response action potentials, fast Na remain closed at all times

Front 15

How does phase 4 spontaneous depolarization work?

Back 15

Slight increase of Na permeability (funny Na channels)
K channels decrease permeability
T type Ca channels increase Ca permeability

Front 16

How does slow response action potential repolarization work?

Back 16

drop in Na and Ca
rise in K

Front 17

How can fast response action potential be changed to slow response?

Back 17

anything that messes up the Na permeability (closes fast Na channels):
High levels of extracellular K
Low 02
Low blood flow (arterial restriction)

Front 18

Cardiac muscle conduction mechanisms and speed

Back 18

Cardiac muscle conducts action potential from cell to cell
conduction rate is related to the difference in potentials between cells (larger potential difference=faster conduction)

Front 19

Why does the conduction slow in the AV node?

Back 19

to allow for the ventricles to fill before they contract

Front 20

What is the effect of autonomics on pacemaker cells?

Back 20

they effect the length of time it takes for spontaneous phase 4 depolarization to occur
Sympathetics-shorten time (faster depolarization)
parasympathetics-lengthen time (slower depolarization