Cardiovascular Systems Physiology and Pathophysiology VII

Question 1

Illustrates that cardiac function is dependent upon venous pressure; whereby, all other things equal, as venous pressure rises cardiac output will increase

Answer 1

The cardiac function curve (also known as a Starling or Frank-Starling curve)

Question 2

Will result in the formation of a new (so-called higher or lower) cardiac function curve

Answer 2

Changes in inotropic state

Question 3

Notice that the cardiac and venous function curves intersect, showing cardiac function at a given

Answer 3

Venous pressure

Question 4

In the acute response to increased cardiac SNS tone what affects would this have on a cardiac and venous function curve?

Answer 4

Cardiac output increase and venous pressure decreases

Question 5

What will be the result if venous pressure increase but cardiac output does not increase?

Answer 5

Edema

Question 6

There are different ways the cardiovascular system can respond to achieve a new operating point. These can include changes in

Answer 6

Vasomotor tone, intravascular volume, and/or cardiac contractility

Question 7

In other words, alterations in vasomotor tone, cardiac function, and the regulation of intravascular volume status via the kidneys cooperate to maintain

Answer 7

Cardiovascular homeostasis

Question 8

While exercising, there is a linear increase in pulse rate and systolic blood pressure with increased

Answer 8

Exercise intensity

Question 9

Remains stable or may even fall slightly with increasing exercise intensity

-This is due to the production of vasodilators within the active skeletal muscles

Answer 9

Diastolic BP

Question 10

One of the indicators of cardiac dysfunction is a

Answer 10

Fall in systolic BP during exercise

Question 11

What are the neurons that mediate the control mechanisms for the cardiorespiratory response during exercise?

Answer 11

Class IV unmyelinated C fibers

Question 12

Lactic acid accumulation in muscle causes the central nervous system to release

Answer 12

Endorphins

Question 13

Blunts the respiratory response limiting unnecessary O2 utilization and lactate production by the respiratory muscles

Answer 13

Endorphin release

Question 14

Two central phases are involved in the cardiovascular response to exercise. These are called the

Answer 14

Anticipatory and participatory phases

Question 15

When exertion is planned, cortical centers prepare

the cardiovascular system for the impending increased demand, i.e.

Answer 15

You get excited

Question 16

Then, neural tracts from the cortical centers activate SNS cardioacceleratory and vasomotor centers within the

Answer 16

Medulla

Question 17

What happens to SNS efferent tone during the anticipatory phase?

Answer 17

It is upregulated

Question 18

During the exercise-induced cardiac cycle in a healthy heart, what happens to

1. ) EDV
2. ) ESV

Answer 18

1. ) EDV is increased

2. ) ESV is decreased

Question 19

Increased EDV and decreased ESV during exercise corresponds to

Answer 19

Increased SV (i.e. enhanced pumping efficiency)

Question 20

During this positive inotropic state, EDV and EDP are

Answer 20

Elevated

Question 21

During exercise, the SNS signals the adrenal medulla to secrete

Answer 21

Adrenergic catecholamines

Question 22

Catecholamines cause which three things?

Answer 22

1. ) Vasoconstriction in less metabolically active tissues (a1 receptors)
2. ) Vasodilation in active muscle and skin (B2 receptors)
3. ) Stimulate HR via cardiac B1 receptors

Question 23

SNS-induced vasoconstriction is part of a two-fold mechanism that increases venous return during exercise. The second mechanism results from

Answer 23

Increased rate of ventilation

Question 24

In response to increased ventilation, the pressure difference between the chest and gut is

-establishes a favorable gradient for venous return

Answer 24

Increased

Question 25

Within active skeletal muscle, net vasodilation is predominantly controlled by

Answer 25

Vasoactive metabolites

Question 26

In contrast, the microvasculature within the less active skeletal muscle and visceral tissues (e.g., splanchnic beds) undergoes

Answer 26

Net vasoconstriction

Question 27

To allow more blood to be delivered during periods of increased metabolic demand, chronic regular exercise stimulates

Answer 27

Angiogenesis in skeletal muscle

Question 28

The point at which the generation of lactic acid exceeds the removal capacity

Answer 28

Anaerobic threshold

Question 29

In exercise that is intense enough to exceed the anaerobic threshold, the accumulation of lactic acid can result in -further drives ventilation

Answer 29

Mild acidosis

Question 30

Abnormal levels of neurohormonal factors (e.g., angiotensin II, aldosterone, norepi/epi, vasodilators, vasopressin, and cytokines), age, genetics, environmental influences, and coexisting conditions can contribute to

Answer 30

Heart failure

Question 31

With the progression of heart failure, the heart is unable to sustain sufficient

Answer 31

Perfusion pressure

Question 32

As renal perfusion is compromised, the collective of Na+ and water conservatory hormones are secreted inducing a

Answer 32

"Salt avid" state of Na+ and water retention

Question 33

This results in the accumulation of intravascular volume and eventually shifts in fluid balance which lead to the formation of

Answer 33

Peripheral and pulmonary edema

Question 34

Can cause all sorts of problems in cardiac function including electrical properties, Ca2+ handling, and cell survival

Answer 34

Ventricular remodeling

Question 35

Most often associated with signs and symptoms of fluid overload due to increased venous pressure (e.g., edema and hepatic congestion)

Answer 35

Right heart failure

Question 36

Most often associated with nocturia and shortness of breath (chiefly exertional dyspnea)

Answer 36

Left heart failure

Question 37

If a sick heart cannot sustain enough cardiac output to maintain sufficient MAP, the low pressure baroceptor system will trigger the SNS resulting in the CV effects of heightened SNS tone with the mobilization of the

Answer 37

Renin-angiotensin (An-II)-aldosterone system and arginine vasopressin (AVP)

Question 38

The goal of this integrated response is an attempt to raise pressure by

Answer 38

Accelerating heart rate and contractility, increasing vasomotor tone, and causing renal retention of Na+ and H2O to increase plasma volume

Question 39

Increase vasomotor tone

Answer 39

An-II and AVP

Question 40

Increase renal retention of Na+

Answer 40

Aldosterone and to some degree An-II

Question 41

Increases renal retention of H2O

Answer 41

AVP

Question 42

At best this cooperation will enable a meager increase in cardiac output above that in noncompensated heart failure, at the expense of inordinate fluid retention leading to increased right atrial pressure with

Answer 42

Peripheral and/or pulmonary edema

Question 43

Are often preserved in diastolic heart failure

Answer 43

Ejection fraction and cardiac output

Question 44

Systolic function is maintained in patients with

Answer 44

Diastolic heart failure

Question 45

The problem with diastolic heart failure resides with improper diastolic filling due to

Answer 45

Increased ventricular wall stiffness and/or impaired relaxation

Question 46

Because of this, at a given LVV, LVP is elevated; if elevated enough, what can form?

Answer 46

Pulmonary congestion, dyspnea, and edema

Question 47

Translate into increased stroke work and elevated cardiac energy demand which can cause the common presenting symptoms of poor exercise tolerance and shortness of breath

Answer 47

Aberrant filling pressure in diastolic heart failure

Question 48

Results from impaired ventricular contractility and/or pressure overload

Answer 48

Systolic heart failure

Question 49

Systolic ejection, and thus ejection fraction, is impeded in

Answer 49

Systolic heart failure

Question 50

In systolic heart failure, since the ejection fraction is reduced, what is increased?

Answer 50

End diastolic pressures

Question 51

In systolic heart failure, preload is by definition increased, and initially this enables the Frank-Starling mechanism to maintain

Answer 51

Stroke volume

Question 52

The increase LVP seen in systolic heart failure is translated to the

Answer 52

LA and ultimately the pulmonary veins