Cardiovascular Systems Physiology and Pathophysiology VI Flashcards
Defined as the presence of a severe and constricting pain
Angina
Severe and constricting pain that occurs within the chest and is due to ischemia
Angina pectoralis
The discomfort associated with angina pectoralis is usually
Retrosternal (can radiate to shoulders, neck, backand/or jaw)
The pathogenesis of the signs and symptoms of angina pectoris is explained by ischemia within one or more regions of the
Ventricular myocardium
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
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
Characterized by an increase in LV diastolic pressure and LV wall tension, which collectively overburden the already O2 starved myocytes
Chronic stable angina
Signs and symptoms of stable angina result from impeded O2 delivery, and include
Diffuse retrosternal tightness and pressure
Physical exam during an episode of chronic stable angina would likely reveal
Elevated BP and an S4 gallop (due to decreased LV compliance)
Would show horizontal or downsloping ST depression and T wave inversions or flattening over ischemic regions
ECG of stable angina
What can be used to treat and manage angina?
Vasodilators and negative inotropic agents
What are some common vasodilators that could be used to treat angina?
- ) Nitroglycerine
2. ) Ca2+ channel blockers such as: amlodipine, diltaizem, and verapamil
What are some negative inotropic agents that could be used to treat angina?
Beta bockers and Ca2+ channel antagonists
Each decrease Ca2+ current in the SA and AV nodes
Beta blockers and Ca2+ channel antagonists
Drug to treat angina that impairs the late Na+ current that is present in cardiomyocytes which helps to restore NCX activity
Ranolazine
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)
The only blood vessels that do not contian any form of vascular smooth mucle
Capillaries
Innervate predominantly the microcirculatory beds within the GI, genito-urinary, respiratory, salivatory, ocular, and cerebral tissues
PSNS efferents
PSNS-induced changes in vascular resistance in
the aforementioned do not translate into significant alterations in
Systemic BP
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
SNS fibers innervate
Arteries, arterioles, venules, and veins
By and large, SNS fibers induce vasoconstriction via
Norepinephrine and a1 receptors
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
What does SNS-dependent vasoconstriction result in in
- ) Arterioles
- ) Venules
- ) Increased TPR
2. ) Does not effect TPR but enhances venous return
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?
- ) Arterioles
- ) Metarterioles
- ) Pre-capillaries
- ) Capillaries
- ) 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?
- ) 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?
- ) Hydraulic pressure (Capillary pressure, Pcap)
- ) Interstitial fluid pressure (Pif)
- ) Colloid osmotic pressure (oncotic pressure)
- ) Interstitial colloid osmotic pressure
Caused by the concentration of charged serum proteins
Colloid osmotic pressure
High colloid osmotic pressure tends to draw fluid
In
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
- ) Hydraulic pressure (Capillary pressure, Pcap)
- ) Interstitial fluid pressure (Pif)
- ) Colloid osmotic pressure (oncotic pressure)
- ) Interstitial colloid osmotic pressure
- ) Relatively high
- ) Negative
- ) Robust
- ) 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
- ) 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
