Cardiovascular Systems Physiology and Pathophysiology VII Flashcards
Illustrates that cardiac function is dependent upon venous pressure; whereby, all other things equal, as venous pressure rises cardiac output will increase
The cardiac function curve (also known as a Starling or Frank-Starling curve)
Will result in the formation of a new (so-called higher or lower) cardiac function curve
Changes in inotropic state
Notice that the cardiac and venous function curves intersect, showing cardiac function at a given
Venous pressure
In the acute response to increased cardiac SNS tone what affects would this have on a cardiac and venous function curve?
Cardiac output increase and venous pressure decreases
What will be the result if venous pressure increase but cardiac output does not increase?
Edema
There are different ways the cardiovascular system can respond to achieve a new operating point. These can include changes in
Vasomotor tone, intravascular volume, and/or cardiac contractility
In other words, alterations in vasomotor tone, cardiac function, and the regulation of intravascular volume status via the kidneys cooperate to maintain
Cardiovascular homeostasis
While exercising, there is a linear increase in pulse rate and systolic blood pressure with increased
Exercise intensity
Remains stable or may even fall slightly with increasing exercise intensity
-This is due to the production of vasodilators within the active skeletal muscles
Diastolic BP
One of the indicators of cardiac dysfunction is a
Fall in systolic BP during exercise
What are the neurons that mediate the control mechanisms for the cardiorespiratory response during exercise?
Class IV unmyelinated C fibers
Lactic acid accumulation in muscle causes the central nervous system to release
Endorphins
Blunts the respiratory response limiting unnecessary O2 utilization and lactate production by the respiratory muscles
Endorphin release
Two central phases are involved in the cardiovascular response to exercise. These are called the
Anticipatory and participatory phases
When exertion is planned, cortical centers prepare
the cardiovascular system for the impending increased demand, i.e.
You get excited
Then, neural tracts from the cortical centers activate SNS cardioacceleratory and vasomotor centers within the
Medulla
What happens to SNS efferent tone during the anticipatory phase?
It is upregulated
During the exercise-induced cardiac cycle in a healthy heart, what happens to
- ) EDV
- ) ESV
- ) EDV is increased
2. ) ESV is decreased
Increased EDV and decreased ESV during exercise corresponds to
Increased SV (i.e. enhanced pumping efficiency)
During this positive inotropic state, EDV and EDP are
Elevated
During exercise, the SNS signals the adrenal medulla to secrete
Adrenergic catecholamines
Catecholamines cause which three things?
- ) Vasoconstriction in less metabolically active tissues (a1 receptors)
- ) Vasodilation in active muscle and skin (B2 receptors)
- ) Stimulate HR via cardiac B1 receptors
SNS-induced vasoconstriction is part of a two-fold mechanism that increases venous return during exercise. The second mechanism results from
Increased rate of ventilation
In response to increased ventilation, the pressure difference between the chest and gut is
-establishes a favorable gradient for venous return
Increased
Within active skeletal muscle, net vasodilation is predominantly controlled by
Vasoactive metabolites
In contrast, the microvasculature within the less active skeletal muscle and visceral tissues (e.g., splanchnic beds) undergoes
Net vasoconstriction
To allow more blood to be delivered during periods of increased metabolic demand, chronic regular exercise stimulates
Angiogenesis in skeletal muscle
The point at which the generation of lactic acid exceeds the removal capacity
Anaerobic threshold
In exercise that is intense enough to exceed the anaerobic threshold, the accumulation of lactic acid can result in
-further drives ventilation
Mild acidosis
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
With the progression of heart failure, the heart is unable to sustain sufficient
Perfusion pressure
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
This results in the accumulation of intravascular volume and eventually shifts in fluid balance which lead to the formation of
Peripheral and pulmonary edema
Can cause all sorts of problems in cardiac function including electrical properties, Ca2+ handling, and cell survival
Ventricular remodeling
Most often associated with signs and symptoms of fluid overload due to increased venous pressure (e.g., edema and hepatic congestion)
Right heart failure
Most often associated with nocturia and shortness of breath (chiefly exertional dyspnea)
Left heart failure
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)
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
Increase vasomotor tone
An-II and AVP
Increase renal retention of Na+
Aldosterone and to some degree An-II
Increases renal retention of H2O
AVP
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
Are often preserved in diastolic heart failure
Ejection fraction and cardiac output
Systolic function is maintained in patients with
Diastolic heart failure
The problem with diastolic heart failure resides with improper diastolic filling due to
Increased ventricular wall stiffness and/or impaired relaxation
Because of this, at a given LVV, LVP is elevated; if elevated enough, what can form?
Pulmonary congestion, dyspnea, and edema
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
Results from impaired ventricular contractility and/or pressure overload
Systolic heart failure
Systolic ejection, and thus ejection fraction, is impeded in
Systolic heart failure
In systolic heart failure, since the ejection fraction is reduced, what is increased?
End diastolic pressures
In systolic heart failure, preload is by definition increased, and initially this enables the Frank-Starling mechanism to maintain
Stroke volume
The increase LVP seen in systolic heart failure is translated to the
LA and ultimately the pulmonary veins
