The Heart as a Pump

Question 0

What is the difference b/n absolute refractory period and relative refractory period?

Answer 0

ARP: is another name for the effective refractory period where the muscle has begun to relax but it is impossible to evoke another AP.
RRP: the muscle is even more relaxed and another AP can evoked BUT it will be weak and conduct slowly.

Question 1

Define effective refractory period (ERP)?

Answer 1

The time before any other AP can be evoked.

Question 2

Why is the cardiac AP much longer than other cell types?

Answer 2

Because of a formation of a plateau due to:
1) L-type Ca channels-drive Vm toward ECa =120mV
(1) is balanced by
2) Delayed Rectifier K channels-drive Vm toward EK=-95mV
As a result of this plateau the refractory period is long and comparable to the period of contraction

Question 3

What would happen if there was tetanic summation in cardiac mm?

Answer 3

Cardiac mm will seize up in a tetanic contraction and not be able to relax, thus will not allow the ventricles to refill=death.

Question 4

Label ERP and RRP in Figure 1.1

Answer 4

pp. 4

Question 5

T/F Cardiac mm must be electrically excited to contract.

Answer 5

T.

Question 6

Explain the process of excitation-contraction in cardiac mm.

Answer 6

Electrical excitation leads to mechanical response: AP travel to T-tubule opening voltage gated L-type Ca channels (DHPR).
1) Ca influx
2) CICR (Ca induced Ca release) from SR
=Increase in intracellular [Ca]=> Contraction

Question 7

What determines the force developed by contracting cardiac mm?

Answer 7

1) Length of the Fibers
2) Inotropic State
3) Afterload

Question 8

What is the name of the effect that describes “the force of contraction of the cardiac mm is proportional to its initial length”?

Answer 8

Frank-Starling Effect

Question 9

T/F Changes in contractility are of a d/f origin from changes in force resulting from length changes.

Answer 9

T.

Question 10

What are 2 possible causes of the Frank-Sterling Effect?

Answer 10

1) Change in lateral spacing b/n thick (myosin) and thin (actin) filaments that favor greater force development
2) Increased sensitivity of myofilaments to Ca

Question 11

Define Inotropic state (IS).

Answer 11

is the contractility of cardiac mm as a function of the intracellular [Ca] present in the myoplasm.

Question 12

Describe the pathway of how increased intracellular [Ca] leads to contraction.

Answer 12

Figure pp. 8

Question 13

T/F Change in IS is somewhat dependent on changes in fiber length.

Answer 13

F. Change in IS is completely independent from change in fiber length (although both determine the output of the heart).
NOTE: 2 identical mm fibers can contract with d/f force if they start @ d/f lengths. BUT 2 fibers with d/f force of contraction at the same starting length have fundamentally d/f properties.

Question 14

T/F Frank-Sterling Effect is an inherent property of the mm in the absence of extrinsic effectors.

Answer 14

T. While IS is the force of contraction due to increase in intracellular [Ca]. IS independent of initial length.

Question 15

What affects IS?

Answer 15

1) Ca in myoplasm
2) # of functional myocytes
3) Coronary supply of O2 (which affects the # of functional myocytes)

Question 16

Define Afterload.

Answer 16

is the pressure against which the heart pumps.

Question 17

When the afterload (MAP) is higher what happens to stroke volume?

Answer 17

Stroke Volume gets smaller.

Question 18

What is homeometric autoregulation?

Answer 18

Homeometric autoregulation is increased force of contraction and a partial restoration of SV. It happens when afterload increases and leads to decreased ejection and increased end systolic volume. This leads to increased end diastolic volume after refilling of the ventricle and increased ventricular stretch (increased fiber length and contraction) before next beat.

Question 19

Briefly describe the events happening during cardiac cycle.

Answer 19

pp. 144
Ventricular Systole
Ventricular Diastole

Question 20

What are the 1st and 2nd heart sounds related to?

Answer 20

The 1st heart sound is related to the closing of the AV valve.
The 2nd heart sound is related to the closing of the semilunar valves.

Question 21

What does the pattern of deflection (P-wave, QRS-complex, and T-wave) in the ECG during the cardiac cycle signify?

Answer 21

P-wave: atrial depolarization (contraction, systole)
QRS-complex: ventricular depolarization (contraction, systole)
T-wave: ventricular repolarization (relaxation, diastole)

Question 22

How much blood fills the left ventricle during diastole? How much of it is ejected as SV during systole?

Answer 22

135mL, and 70mL respectively.

The ventricle never completely empties.

Question 23

What is the ejection fraction for the left ventricle?

Answer 23

50% (It ejects 50mL of it 135mL of blood).

Question 24

What is the maximum pressure developed in systole of the left and right ventricle?

Answer 24

It is 120 mmHg for the left and 20mmHg for the right ventricle.

Question 25

T/F The right heart beats at the same time as the left hear and the amount of blood ejected from each ventricle is the same.

Answer 25

T. The events making up the cardiac cycle are the same in the right and left hearts BUT the absolute pressures are different.

Question 26

How can we represent the cardiac cycle as a pressure-volume loop?

Answer 26

By simultaneously measuring ventricular pressure and ventricular volume during a cardiac cycle.

Question 27

Explain left ventricle diastole, systole, mitral and aortic valve (closure and opening) and isovolumetric contraction and relaxation using the pressure-loop diagram.

Answer 27

PP. 10

The diagonal line passing through C is a representation of the current inotropic state of the heart.

Question 28

What is the equation for cardiac output (CO)?

Answer 28

CO=HRxSV (Causal relationship)
SV=CO/HR (NOT causal relationship)
HR-Heart rate
SV-Stroke volume

Question 29

What is the physiologically dominant determinant of cardiac output?

Answer 29

Heart Rate.
NOTE: HR controlled by ANS. The SA node has both sympathetic and parasympathetic inputs=> cause HR to vary physiologically over a wide range.

Question 30

What is the range of HR and SV?

Answer 30

HR: 40-180/min. Normal resting HR=70 beats/min
SV: 75-110ml. Resting and recumbent= 85-90ml,
Resting and standing=75-80ml,
Strenuous exercise=105-110ml

Question 31

What are the factors that affect SV?

Answer 31

Preload
Afterload
Inotropic State

Question 32

What are other names for preload (filling) and afterload?

Answer 32

Preload-EDV/EDP (End diastolic volume/ End diastolic pressure)
Afterload-Mean Arterial Pressure (MAP)

Question 33

What is the most potent determinant of SV?

Answer 33

Preload/Filling (EDV/EDP)

Question 34

What results from increased end diastolic volume (preload)?

Answer 34

Increased preload stretches the walls of the ventricles and increases the length of the cardiac mm fibers. This causes increased force of contraction and thus increased SV as the ventricle contracts.
FIGURE pp 13 presentation.
NOTE: cardiac mm prevent mm from stretching to lengths where force begins to decrease to any great extent.

Question 35

How does the IS affect the SV?

Answer 35

directly related to SV BUT as physiological responses occur the role of IS is to increase SV when preload decreases for some reason (this will be clear when we study reflexes).

Question 36

How does afterload affect SV?

Answer 36

It is qualitatively always a factor (it is inversely related to SV) BUT its quantitative effect is only significant when MAP is very high (or when MAP decreases from a high value).

Question 37

What are the 2 functions that the heart serves as a pump?

Answer 37

1) Flow out of the heart that ultimately perfuses tissues

2) The heart produces gradient that causes tissue perfusion

Question 38

What is the general paradigm for controlling flow to organ systems?

Answer 38

1) Pressure is maintained as a constant which drives flow

2) Resistance is varied to control flow to individual organ systems and tissues to meet their needs

Question 39

Look at the case presented:

Answer 39

At the end of the presentation. Understand how the condition leads to increased IS and SV…

Question 40

Looking at the pressure-volume loop. What will happen to the volume at A and D when an aortic stenosis is present? Figure pp. 10

Answer 40

During Isovolumetric contraction and relaxation the aortic pressure is higher than the ventricular pressure. If the valve is not closed (insufficient) blood will move from the aorta to the ventricles. That is volume at A and D will move to the right.