Week 1- Heart As Pump, Cardiac Output, Heart Sounds

Front 1

Describe excitation-contraction coupling

Back 1

electrical activation of cardiac muscle makes action potential
Ca2+ enters myocytes during plateau phase of action potential

Ca2+ triggers massive release of intracellular CaCa2+ in sarcoplasmic reticulum

Ca2+ triggers myocardial contraction by activating cross-bridge formation between actin and myosin filaments

Front 2

Describe L-Type Calcium Channels

Back 2

Voltage-gated: open when transmembrane potential > -55 mV
•Dihydropyridines, like nifedipine, block channel

Front 3

How does Ca2+ get back in sarcoplasmic reticulum after AP?

Back 3

Ca2+ dependent ATPase pump

Front 4

How does Ca2+ get out of cell after AP?

Back 4

Na+ Ca2+ exchanger. Sodium follows its concentration gradient

Front 5

Major steps of Excitation-Contraction Coupling

Back 5

1. electrical activation of cardiac muscle
2. calcium-induced release of calcium from sarcoplasmic reticulum
3. shortening of contractile elements

Front 6

Steps of interaction between actin and myosin for muscle contraction

Back 6

1. activation of myosin head by ATP hydrolysis
2. cross bridge formation between myosin head and actin filament
3. phosphate release and power stroke
4. ADP release, ATP binding, actin filament release

Front 7

What is systole? What is diastole?

Back 7

systole- period of active contraction
diastole- period of relaxation

Front 8

Hemodynamic differences between right and left heart

Back 8

Left ventricle generates 6 times more
pressure than right!

Front 9

What is the origin of the first heart sound?

Back 9

contraction of the ventricles simultaneously closes the AV valves (tricuspid and mitral relatively simultaneously)

Longer lasting and lower in pitch than second heart sound

Front 10

What is the origin of the second heart sound?

Back 10

Produced when the aortic and pulmonic valves snap closed

Inspiration causes transient increase in RV filling, so pulmonic closure sound is delayed

This causes “physiologic splitting” of S2 with the aortic closure sound

preceding the pulmonic closure sound by 0.04 sec during inspiratio

Front 11

Left Ventricular Contraction Dynamics and Stroke Volume

Back 11

At end diastole, LV volume is maximum and wall is thinner

During systole, myocardial fibers shorten.
LV long and short axes shrink
LV wall thickens
Wringing motion due to helically oriented fibers of epicardium

Front 12

Cardiac Output Equation

Back 12

Cardiac Output = Stroke Volume x Heart Rate

Front 13

Typical stroke volume

Back 13

70 mL

Front 14

Stroke Volume Equation

Back 14

end-diastole volume - end-sistole volume

Front 15

What is the width of the pressure volume loop?

Back 15

Stroke volume

Front 16

What is Ejection Fraction?

Back 16

Stroke Volume/End Diastolic Volume

Front 17

What is the stroke work?

Back 17

The useful mechanical work the heart does on the systemic circulation when it contracts

(mean arterial pressure) - (pulmonary capillary wedge pressure) x Stroke Volume

Front 18

What is cardiac output?

Back 18

The amount of blood pumped by the heart per minute

Front 19

What is venous return?

Back 19

The amount of blood from veins returning to right atrium per minute

Front 20

In a steady state, cardiac output is equal to __ __.

Back 20

venous return

Front 21

What are the four ways to control cardiac output?

Back 21

preload
afterload
myocardial contractility
heart rate

Front 22

What is preload?

Back 22

Force that pre-stretches myofilaments before contraction

Left ventricular Preload is
the intracavity pressure at
end diastole (Ped), which
produces wall stress and
distends the ventricle to its
end-diastolic volume

• This stretches myofibers
that are circumferentially
oriented in the LV midwall,
priming LV for contraction

Front 23

What are the three phases of diastolic filling?

Back 23

First third of diastole is period of rapid diastolic
filling (passive process, flow from LA to LV driven by pressure gradient generated by LV relaxation

– During middle third of diastole, the pressures in
the atria and their respective ventricles
equilibrate, so not much blood flows into the
ventricles during this period of “diastasis”

– During final third of diastole, atrial contraction
occurs, which contributes an additional 20% to
ventricular filling

– Mitral valve closes when LV contracts and LV
pressure rapidly rises above LA pressure

Front 24

frank-starling mechanism- preload dependence of cardiac output

Back 24

relates left ventricular filling pressure with cardiac output

curvilinear relationship

Front 25

What its the subcellular basis for frank-starling mechanism

Back 25

Sarcomere stretch optimizes actin-myosin overlap, which increases force generation and sarcomere shortening

Front 26

End-systolic-pressure-volume relationship

Back 26

Pes = Ees · (Ves - Vo)

End systolic pressure = end systolic elastance * (end systolic volume* Vo)

Ees = Pes/(Ves - Vo)

Front 27

How is preload regulated?

Back 27

Rapid regulation- sympathetic tone. veins are highly distensible, so they have large capacity to store blood. Sympathetic stimulation causes constriction of veins, which increases preload

Slow regulation- renal mechanisms leading to salt and water retention

Front 28

What are the renal mechanisms for regulating preload (start with low cardiac output)

Back 28

low cardiac output --> reduced renal blood flow --> kidney retains Na+ and H20 --> increased intravascular volume --> increased preload

Front 29

What is afterload?
How is ti produced?

How is it regulated?

Back 29

force that resists shortening of the myofilaments during contraction
Afterload is the force resisting LV ejection

produced by interactions between blood
and the vascular wall that impart a resistance to flow

primarily regulated by changes in arterial tone

Front 30

How do you measure afterload in a person?

Back 30

systemic vascular resistance

Front 31

Relate systemic vascular resistance as after load

Back 31

SVR = (MAP – RAP)/CO

systemic vascular resistance = mean arterial pressure - right artrial pressure/ cardiac output

Front 32

CONTROL OF CARDIAC OUTPUT- CONTRACTILITY

Back 32

• Sympathetic stimulation, catecholamines,
and drugs with positive inotropic effects
increase myocardial contractility
• Myocardial ischemia or injury, inhibition of
sympathetic nervous system, and drugs
with negative inotropic effects decrease
myocardial contractility