What does SNS-dependent vasoconstriction result in in 1. ) Arterioles 2. ) Venules

1. ) Increased TPR 2. ) Does not effect TPR but enhances venous return

Cardiovascular Systems Physiology and Pathophysiology VI Flashcards by Joel Glotfelty

Defined as the presence of a severe and constricting pain

Angina

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Severe and constricting pain that occurs within the chest and is due to ischemia

Angina pectoralis

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The discomfort associated with angina pectoralis is usually

Retrosternal (can radiate to shoulders, neck, backand/or jaw)

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The pathogenesis of the signs and symptoms of angina pectoris is explained by ischemia within one or more regions of the

Ventricular myocardium

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A specific form of angina, and results from a fixed narrowing of one or more coronary vessels; generally due to atheromatous plaque formation

Chronic stable angina

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With chronic stable angina, as cardiac demand is upregulated (such as after exercise or a big meal) O2 supply an not meet demand, which sets a cascade of events in place leading to

Impaired LV function

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Characterized by an increase in LV diastolic pressure and LV wall tension, which collectively overburden the already O2 starved myocytes

Chronic stable angina

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Signs and symptoms of stable angina result from impeded O2 delivery, and include

Diffuse retrosternal tightness and pressure

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Physical exam during an episode of chronic stable angina would likely reveal

Elevated BP and an S4 gallop (due to decreased LV compliance)

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Would show horizontal or downsloping ST depression and T wave inversions or flattening over ischemic regions

ECG of stable angina

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What can be used to treat and manage angina?

Vasodilators and negative inotropic agents

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What are some common vasodilators that could be used to treat angina?

) Nitroglycerine

2. ) Ca2+ channel blockers such as: amlodipine, diltaizem, and verapamil

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What are some negative inotropic agents that could be used to treat angina?

Beta bockers and Ca2+ channel antagonists

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Each decrease Ca2+ current in the SA and AV nodes

Beta blockers and Ca2+ channel antagonists

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Drug to treat angina that impairs the late Na+ current that is present in cardiomyocytes which helps to restore NCX activity

Ranolazine

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In angina, there is a prolonged phase of terminal Na+ current. This impedes NCX function and results in increased intracellular Ca2+ which promotes a state of increased

LV wall tension(thus increasing O2 demand)

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The only blood vessels that do not contian any form of vascular smooth mucle

Capillaries

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Innervate predominantly the microcirculatory beds within the GI, genito-urinary, respiratory, salivatory, ocular, and cerebral tissues

PSNS efferents

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PSNS-induced changes in vascular resistance in

the aforementioned do not translate into significant alterations in

Systemic BP

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PSNS activity is not traditionally associated with antagonizing SNS vasoconstriction to lower BP Instead, PSNS activity enables more localized changes in blood flow in order to aid in

Tissue metabolism

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SNS fibers innervate

Arteries, arterioles, venules, and veins

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By and large, SNS fibers induce vasoconstriction via

Norepinephrine and a1 receptors

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SNS is typically responsible for the interplay between vasoconstriction and dilation. However, in some tissue beds, vasodilation can be induced by

-ex skeletal muscle

B2 adrenergic receptors

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What does SNS-dependent vasoconstriction result in in

) Arterioles
) Venules

) Increased TPR

2. ) Does not effect TPR but enhances venous return

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Increased venous return increases

Cardiac output

A large bed which receives about 25% of CO and can accommodate upwards of 20% of total blood volume

Splanchnic circulation (that within the gut)

Highly endowed with a1 adrenoreceptors when compared to other venous beds - extremely sensitive to any increase in SNS tone - contains high compliance veins

Splanchnic circulation

Venoconstriction of the splanchnic venous tissues results in mobilization of venous blood volume from this bed for

Venous return to the RA

Collectively increases arterial BP by increasing TPR and upregulating venous return and cardiac output

SNS

Graded by the amount and type of neurotransmitter that is released in response to the efferent signal

SNS stimulation

In response to initial efferent tone, post-ganglionic SNS fibers release norepi, and norepi which activates -provides an early phase for a low degree of vasoconstriction

Type a1 adrenergic receptors

As the efferent signal increases to moderate intensities, the noradrenergic system is complemented by the release of

ATP

Acts as a neurotransmitter since is stimulates post-junctional purinoreceptors

ATP

Together, cause a greater stimulation of smooth muscle contraction than would occur in the presence of norepi alone

Norepinephrine and ATP

What happens in the event of intense efferent SNS tone?

Norepinephrine secretion is elevated -ATP secretion ceases NP-y secretion is stimulated

Binds and activates so-called Y receptors on the pot-junctional smooth muscle membrane and functions as a synergist to norepinephrine

NP-Y

A potent vasoconstrictor that is synthesized from the renal hormone, renin, via a multi-step process

Angiotensin-II (An-II)

Acts through a receptor mediated process to stimulate vasoconstriction -also can bind SNS post-ganglionic pre-junctional receptors to stimulate Norepinephrine secretion

An-II

Receptors that are coupled to the release of norepinephrine and are activated in the face of chronically elevated epinephrine

Pre-junctional B2 receptors

Therefore, in the case of extreme SNS activity, both epi and norepi can directly and indirectly stimulate vasoconstriction to markedly increase

TPR

The spontaneous rhythmic contraction of small resistance vessels within the microcirculation

Vasomotion

The vascular endothelium is a very metabolically active tissue, and the continuous release of nitric oxide by the vascular endothelium sets the

Basal vascular smooth muscle tone

What are the 4 major vasoactive factors?

Thrombin, ACh, seratonin, and shear stress

Allows the intermittent flow of blood through the capillary network

Vasomotion

Generally sets the rate of vasomotion within a given capillary bed

O2 usage by the tissues

For example what effect would the sustained contraction of skeletal muscle i.e. the relatively O2-depleted environment of the skeletal muscle cause?

Increase in vasomotion

Microcirculation consists of what 5 components?

1. ) Arterioles 2. ) Metarterioles 3. ) Pre-capillaries 4. ) Capillaries 5. ) Venules

Blood PO2 is elevated (98 mmHg) as the RBCs enter the microcirculation through the

Arterioles

As red blood cells move from capillaries to venules to enter the venous circulation, PO2 is relatively

Low (40 mmHg)

The important functions of the microcirculation are

Exchange of blood gases and delivery of nutrients

Surrounded by a sheet of smooth muscle, and therefore can be constricted/dilated in response to the SNS and other stimuli

Arterioles

Also contain smooth muscle; however, the smooth muscle is more localized as rings of smooth muscle fibers

Metarterioles

Forms the junction between metarterioles and capillaries -serves as a modulator to flow within the microcirculation bed

Pre-capillary sphincter

The link between the capillary bed and veins -contain relatively little smooth muscle when compaired to arterioles

Venules

The plasma pressure in venules is very

Low

Movement of fluids and (small) molecules between capillaries and surrounding tissues occurs via small openings that are present between adjacent endothelial cells called

Slit pores

In the brain, the slit pores are very small and therefore only allow the passage of

H2O and very small molecules

This cytoarchitecture within the brain microvasculature is referred to as the

Blood-brain barrier

The slit pores within certain microvessels in the liver are

Large

The primary mechanism of exchange that occurs between capillaries and the interstitial space

Diffusion

Diffusion of aqueous material occurs through

Slit-pores and aquaporins

Lipid soluble molecules don't travel through pores but rather traverse the plasma membrane. Some examples are

CO2, O2, phospholipids, and steroid hormones

For the purposes of understanding microcirculation fluid dynamics, fluid movement consists of which two processes?

1. ) Filtration | 2. ) Reabsorption

Are in constant opposition in the capillary bed

Filtration and resorption

Physical forces within the lumen and interstitium that determine in which direction the fluid will move

Starling forces

What are the 4 primary fluid forces encountered in microcirculation?

1. ) Hydraulic pressure (Capillary pressure, Pcap) 2. ) Interstitial fluid pressure (Pif) 3. ) Colloid osmotic pressure (oncotic pressure) 4. ) Interstitial colloid osmotic pressure

Caused by the concentration of charged serum proteins

Colloid osmotic pressure

High colloid osmotic pressure tends to draw fluid

In the absence of other forces, high colloid osmotic pressure would result in

Increased diffusion (resorption) of H2O into capillaries

At the entrance to the capillary network, forces cause a net outward movement of fluid. This outward movement is known as

Filtration

Within the capillaries at the entrance of the capillary network, what are the characteristics of 1. ) Hydraulic pressure (Capillary pressure, Pcap) 2. ) Interstitial fluid pressure (Pif) 3. ) Colloid osmotic pressure (oncotic pressure) 4. ) Interstitial colloid osmotic pressure

1. ) Relatively high 2. ) Negative 3. ) Robust 4. ) Modest

Hence, filtration occurs primarily at the

Arterial feed of a capillary bed

What are the pressure characteristics at the venous end of the capillary bed?

Colloid osmotic pressure higher than the other three combind

Therefore, what occurs primarily at the venous end of a capillary bed?

Absorption (resorption)

When considering the mean net force (filtration versus reabsorption) of the capillary network, the general trend is

Filtration is favored over resorption

The concept of net filtration over resorption is referred to as the

Starling Equilibrium

The buildup of interstitial fluid

Edema

The removal of the net fluid accumulation from the interstitium is accomplished by the

Lymphatic system

Reabsorption of excess fluid and some other molecules occurs via the

Lymphatic system

Ultimately, fluids are returned to the blood plasma via a network of lymphatic ducts that empty into the

Subclavian veins

Besides the need for increased O2, other factors that can influence the rate of flow within the microcirculation are

Nutrients, metabolic by-products such as adenosine, CO2, and H+

When considering the acute response, the primary determining factor for enhancing vasomotion is

Decreased O2 relative to demands

What happens by default when O2 tissue concentrations fall?

CO2 level is raised by default

The phenomenon of the intracellular mechanisms that signal the production and/or release of vasodilators by tissues in response to increased CO2 levels

Autoregulation

Examples of important vasodilators that we need to know are

Adenosine, CO2, H+, K+, Lactic acid, and histamine

Can result when PO2 in the cerebral microcirculation drops

Coma

Regulations of cerebral microcirculation is dependent upon

Blood PCO2

Alterations in PCO2 stimulate coordinated responses in

Cerebral vasomotion

In actuality, changes in PCO2 initiate a cascade of events that result in alterations in -Causes vasomotor events in the brain

H+

Cardiac output has to equal

Venous return

The venous function curve illustrates vascular (venous) behavior based upon the relationship between

1. ) RAP (venous pressure, X-axis) | 2. ) Cardiac output (Y-axis)

Venous and cardiac function curves show that as cardiac output increases, venous pressure (RAP)

Decreases

Venous and cardiac function curves also show that increases in venous pressure (RAP) have what effect?

Upregulate cardiac output

Venous vasomotor tone and intravenous volume affect

Cardiac Output

Enhances cardiac output by lowering resistance to flow within the venous system

Vasodilation

Impedes cardiac output by increasing resistance to flow within the venous system

Vasoconstriction

Increases cardiac output because there is more plasma available for venous return and thus cardiac output

Increased venous volume

It is critical to keep in mind that viewing an isolated | venous function plot, without the cardiac function curve is

Pointless

In other words, the whole purpose of the venous and cardiac function curves is to show the interdependent relationship between

Venous and cardiac function