Cardiovascular Systems Physiology and Pathophysiology VII Flashcards

1
Q

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

A

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

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2
Q

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

A

Changes in inotropic state

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3
Q

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

A

Venous pressure

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4
Q

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

A

Cardiac output increase and venous pressure decreases

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5
Q

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

A

Edema

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6
Q

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

A

Vasomotor tone, intravascular volume, and/or cardiac contractility

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7
Q

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

A

Cardiovascular homeostasis

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8
Q

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

A

Exercise intensity

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9
Q

Remains stable or may even fall slightly with increasing exercise intensity

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

A

Diastolic BP

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10
Q

One of the indicators of cardiac dysfunction is a

A

Fall in systolic BP during exercise

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11
Q

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

A

Class IV unmyelinated C fibers

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12
Q

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

A

Endorphins

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13
Q

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

A

Endorphin release

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14
Q

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

A

Anticipatory and participatory phases

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15
Q

When exertion is planned, cortical centers prepare

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

A

You get excited

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16
Q

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

A

Medulla

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17
Q

What happens to SNS efferent tone during the anticipatory phase?

A

It is upregulated

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18
Q

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

  1. ) EDV
  2. ) ESV
A
  1. ) EDV is increased

2. ) ESV is decreased

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19
Q

Increased EDV and decreased ESV during exercise corresponds to

A

Increased SV (i.e. enhanced pumping efficiency)

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20
Q

During this positive inotropic state, EDV and EDP are

A

Elevated

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21
Q

During exercise, the SNS signals the adrenal medulla to secrete

A

Adrenergic catecholamines

22
Q

Catecholamines cause which three things?

A
  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
23
Q

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

A

Increased rate of ventilation

24
Q

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

-establishes a favorable gradient for venous return

25
Within active skeletal muscle, net vasodilation is predominantly controlled by
Vasoactive metabolites
26
In contrast, the microvasculature within the less active skeletal muscle and visceral tissues (e.g., splanchnic beds) undergoes
Net vasoconstriction
27
To allow more blood to be delivered during periods of increased metabolic demand, chronic regular exercise stimulates
Angiogenesis in skeletal muscle
28
The point at which the generation of lactic acid exceeds the removal capacity
Anaerobic threshold
29
In exercise that is intense enough to exceed the anaerobic threshold, the accumulation of lactic acid can result in -further drives ventilation
Mild acidosis
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
Heart failure
31
With the progression of heart failure, the heart is unable to sustain sufficient
Perfusion pressure
32
As renal perfusion is compromised, the collective of Na+ and water conservatory hormones are secreted inducing a
"Salt avid" state of Na+ and water retention
33
This results in the accumulation of intravascular volume and eventually shifts in fluid balance which lead to the formation of
Peripheral and pulmonary edema
34
Can cause all sorts of problems in cardiac function including electrical properties, Ca2+ handling, and cell survival
Ventricular remodeling
35
Most often associated with signs and symptoms of fluid overload due to increased venous pressure (e.g., edema and hepatic congestion)
Right heart failure
36
Most often associated with nocturia and shortness of breath (chiefly exertional dyspnea)
Left heart failure
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
Renin-angiotensin (An-II)-aldosterone system and arginine vasopressin (AVP)
38
The goal of this integrated response is an attempt to raise pressure by
Accelerating heart rate and contractility, increasing vasomotor tone, and causing renal retention of Na+ and H2O to increase plasma volume
39
Increase vasomotor tone
An-II and AVP
40
Increase renal retention of Na+
Aldosterone and to some degree An-II
41
Increases renal retention of H2O
AVP
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
Peripheral and/or pulmonary edema
43
Are often preserved in diastolic heart failure
Ejection fraction and cardiac output
44
Systolic function is maintained in patients with
Diastolic heart failure
45
The problem with diastolic heart failure resides with improper diastolic filling due to
Increased ventricular wall stiffness and/or impaired relaxation
46
Because of this, at a given LVV, LVP is elevated; if elevated enough, what can form?
Pulmonary congestion, dyspnea, and edema
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
Aberrant filling pressure in diastolic heart failure
48
Results from impaired ventricular contractility and/or pressure overload
Systolic heart failure
49
Systolic ejection, and thus ejection fraction, is impeded in
Systolic heart failure
50
In systolic heart failure, since the ejection fraction is reduced, what is increased?
End diastolic pressures
51
In systolic heart failure, preload is by definition increased, and initially this enables the Frank-Starling mechanism to maintain
Stroke volume
52
The increase LVP seen in systolic heart failure is translated to the
LA and ultimately the pulmonary veins