Week 2 Flashcards
(100 cards)
1
Q
- List the general processes that use ATP in the working heart.
A
Cellular processes (25%) and cross-bridging to produce contractions (75%, 50% of which is due to isovolumetric contraction)
2
Q
- State the phase of the cardiac cycle in which the most energy is expended, and which cardiac variable the amount of that energy use is most dependent upon.
A
Most energy is spent in the isovolumetric phase of contraction, cardiac afterload being a major determinant of myocardial oxygen consumption
3
Q
- Explain what feature of the ventricular pressure-volume loop represents “stroke work,” list the two general ways that stroke work can be increased, and note which of those two mechanisms are more costly in terms of myocardial oxygen consumption.
A
Stroke work is equal to the area enclosed by the left ventricle pressure- volume loop. Stroke work is increased wither by an increase in stroke volume or by an increase in afterload, an increase in afterload being the most costly parameter to change
4
Q
- Describe the effects of increasing heart rate and increasing myocardial contractility on the oxygen requirements of the heart, and explain which of these changes is the most efficient way to increase cardiac output.
A
Increasing heart rate and myocardial contractility increase the oxygen requirements of the heart. The most efficient way to increase cardiac output is with a low heart rate and high stroke volume.
5
Q
- List three noninvasive techniques that are used to evaluate electrical function, valve function, and mechanical pumping action of the heart.
A
Electrocardiographic record, auscultation of the chest, echocardiography
6
Q
- Draw a stereotypical electrocardiogram trace showing one beat of the heart, label the three major wave features, and explain what electrical events are indicated by those waves and the intervals/segments that interconnect them.
A
P wave is depolarization of the atria, the QRS complex is ventricular depolarization and T wave the ventricular repolarization; PR segment/ interval indicates the time takes for an action potential to spread through the atria and the AV node; ST segment follows the QRS complex is a phase of no rapid changes in membrane potential; the QT interval roughly approximates the duration of the ventricular myocyte depolarization and thus the period of ventricular systole
7
Q
- Explain the electrical conventions that create Lead’s I, II, and III of Einthoven’s triangle, specifying which end of each lead is negative (reference electrode) and which end is positive (recording electrode) for each lead.
A
Lead II between right arm (-) and left leg(+); Lead I between right arm (-) and left arm (+); lead III between left arm (-) and left leg (+). When a lead registers, if charge is flowing from (-) to (+) then the lead read up will deflect upward, whereas the converse is also true
8
Q
- Explain how a moving wave of depolarization can be represented by a net electrical dipole that can be detected by electrodes on the surface of the body, and list the two factors that determine the magnitude of the dipole.
A
A net electrical dipole describes the net direction of the charge separation on the AP wavefront, each dipole being oriented in the direction the local wave is traveling. Extracellular fluid conducts these net dipoles to be detected on the surface of the skin. The magnitude of the dipole is determined by how many cells are depolarizing at the same time as well as the consistency of the orientation between individual dipoles.
9
Q
- Demonstrate how a net dipole simultaneously is recorded as electrical voltage in different ECG Leads, using an example where one lead shows a negative voltage difference and the other two leads show a positive voltage difference. Explain how the voltage in a given lead is affected when the dipole is oriented perpendicular or parallel to that lead.
A
the more parallel the dipole is to the lead poles, the greater the magnitude of the voltage on the trace, if the dipole is in the same orientation as – to + then it will appear positive voltage.
10
Q
- Describe the nature of the cardiac dipole while an action potential is traveling through the AV node, and how that event appears on the ECG.
A
The P wave terminates when the depolarization reaches the non-muscular border between the atria and the ventricles and the number of individual dipoles becomes very small. The number of cells in the AV node is so small that it does not register on the EKG
11
Q
- Draw a figure showing how the net cardiac dipole changes during the spread of depolarization through the ventricle, and show how that spread would appear when viewed by Leads I, II, and III.
A
just do it.
12
Q
- List the components of an idealized ECG recording that are typically isoelectric.
A
PR and ST intervals are typically isoelectric, the PR being when depolarization is traveling through the AV node and the ST interval when all the ventricular cells are in their plateau
13
Q
- Explain why the T-wave is typically broader than, and in the same direction as, the R wave in a Lead II recording.
A
Typically the ventricular depolarization occurs in a less unified way where the dipoles created are not in a similar direction. It is in the same direction because the cells that depolarized first are the first to repolarize and therefore demonstrate a repolarization in the opposite direction (opposite direction and opposite charge mean same dipole) and same positive deflection
14
Q
- From a sample recording of a QRS complex, be able to determine the mean electrical axis of ventricular depolarization by the method you learn in our ECG workshop.
A
Mean electrical axis: the orientation of the cardiac dipole during the most intense phase of ventricular depolarization, used to determine whether the ventricular depolarization is proceeding over normal pathways
15
Q
- Draw a figure that shows the convention by which the angle (in degrees) of electrical axis is reported, and define left axis deviation and right axis deviation. (Note: use the ranges taught in the workshop rather than in the textbook).
A
The downward direction is designated 90+, and anywhere in the patients left hand quadrant is considered normal
16
Q
- Describe how the augmented unipolar limb leads (aVR, aVL, and aVF) are measured, and state their orientation (in degrees) on the standard axes.
A
Between right arm and aVR, left arm and aVL and left leg and aVF, these leads describe additional “perspectives” defined by drawing a line from the center to vertices of Einthoven’s triangle with (-) in the center and (+) at the vertices the leads together can be considered a hexaxial reference system for observing the cardiac vectors in the frontal
17
Q
- Describe how the precordial limb leads (V1-V6) are measured, and describe the electrical orientation (“view”) of each of those leads.
A
12 unipolar leads that look at the electrical system in the transverse plane, the indifferent leads are formed by electrically connecting the limb electrodes, the electrical orientation the this view is of the transverse plane with the first 6 leads forming a central point of reference
18
Q
- List the criteria that are used to define an ECG trace as being a normal sinus rhythm with respect to the following variable: Frequency, QRS duration, PR interval duration, QT interval duration and P-wave occurrence.
A
Frequency of QRS complex is 1/s, the shape of the QRS is normal for lead II and duration is less than 120 milliseconds, each QRS complex is preceded by a P wave of proper configuration , indicating SA node origin of excitation, PR interval Is less than 200 milliseconds, indicating proper delay through AV node, the QT interval is less than half the P-T interval, indicating normal ventricular repolarization and there are no extra P waves, indicating that no AV nodal conduction block is present; deviation of ST segment from isopotential baseline is indicative of cardiac ischemia
19
Q
- Define tachycardia and bradycardia.
A
Tachycardia, excessively fast HR limiting the time for cardiac filling between beats and bradycardia, excessively slow HR, which is inadequate to support sufficient cardiac output or decreases the coordination of myocyte contraction, which will reduce stroke volume
20
Q
Normal sinus rhythm
A
typical EKG discussed earlier
21
Q
Supraventricular tachycardia
A
occurs when the atria are abnormally excited and drive the ventricles at a very fast pace
22
Q
First degree heart block
A
the only electrical abnormality is unusually slow conduction through the AV node
23
Q
Second-degree heart block
A
some but not all atrial impulses are transmitted through the AV node to the ventricle, impulses are blocked in the AV node if the cells of the region are still in a refractory period form a previous excitation
24
Q
Third degree block
A
no impulses are transmitted through the AV node, atrial and ventricular rate are completely independent, and ventricle output can be slowed significantly
25
Atrial fibrillation
complete loss of normally close synchrony of the excitation and resting phases between individual atrial cells, cells in different areas of the atria depolarize, repolarize and are excited again randomly ** no P wave is present, can lead to blood clots
26
Right and Left bundle branch blocks
leads to reentrant conduction pathway, less synchronous ventricle depolarization and wider QRS complex
27
Premature ventricular contraction
ectopic focus starts an independent ventricular contraction, often followed by a compensatory beat which can affect the filling volume of the ventricles
28
Ventricular tachycardia
ventricles are beating at a high rate, often by an ectopic center (very serious condition, can lead to inefficient filling of ventricles)
29
Long QT syndrome with torsades des pointes
a result of delayed ventricular myocyte repolarization which maybe due to inappropriate opening of sodium channels or prolonged closure of K channels during the AP plateau phase, when QT interval is greater than 50% of cycle length which can occur with ventricular electrical complexes cyclically varying in amplitude around the baseline and can deteriorate rapidly into ventricular fibrillation
30
Ventricular fibrillation
various areas of the ventricle are excited and contract asynchronoysly
31
90. Write the Fick equation and, given appropriate data, use it to calculate cardiac output.
tissue substance rate/ substance consumed = flow; requires invase methods to obtain measurements (venous blood requires mixing by heart to get adequate measurement
32
91. Describe the echocardiography imaging technique, and explain how it can be used to determine the ejection fraction.
Eco uses sound waves which come in contact with substances of varying densities and the reflection of the waves off those substances are reflected back to a computer and interpreted by that computer to make an image of the heart and its vessels. Eco can be used to find the end diastolic volume, which is used to calculate ejection fraction (EF = SV/EDV)
33
92. Write the equation for ejection fraction, and state the range and mean value observed in people with normal cardiac contractility.
EF= SV/ EDV, range 55-87% with the mean at 67%; ejection fraction is useful in estimating contractility
34
93. Describe how the end-systolic pressure-volume relationship can be used to determine myocardial contractility.
use one of the imaging techniques to measure ESV (measured based on the insicura or rebound on the aortic valve) and measure ESP via the arterial pressure next to the aortic valve - that gives you a data point. you can draw a line from point to origin and the slope of that will give you contractility. Higher contractility = a leftward shift of the curve (like the hand on a clock going in reverse), lower c = rightward shift
35
94. Draw pressure volume loops comparing the function of a normal heart, a failing heart with depressed contractility (untreated), and the failing heart after a treatment that reduces arterial blood pressure.
in an untreated heart, there is reduced contractility and less ability to fight the atrial pressure so that leads to reduces EF and SV(taller/skinnier curve), if you treat by decreasing arterial pressure, you will increase the pumping abilities of the heart and increase EF and SV
36
95. With regard to valve function, define “stenosis” and “insufficiency,” and explain how the different effect these two abnormalities have on ventricular chamber remodeling.
Stenosis is narrowing (or does not open fully) of the valves and since this narrowing leads to extra force required to move fluid through the valve, it can lead to ventricular hypertrophy insufficiency relates to valves that do not close completely and leads to regurgitation of the valves, leading to a greater volume load on the ventricle. Stenoic SL valves cause increased thickness of walls of the upstream chamber; insufficient valves tend to cause an increase in “volume work” and dilation of chambers
37
Aortic stenosis
a much greater pressure is required by the ventricular contraction to overcome the extra obstruction of the stenoic valve and would lead to a whistling sound between the lub and the dup (systolic murmur)
38
Mitral stenosis
a much greater left atrial pressure (leading to pulmonary edema and SOB) leading to a whistling between the dup and the lub (diastolic murmur)
39
Aortic insufficiency (aka regurgitation, incompetence)
aortic pressure falls much faster and farther than normal so it is normally low and EDV and pressure are also elevated, leads to a gurgling diastolic murmur
40
Mitral insufficiency (aka regurgitation, incompetence)
causes an increase in left atrial pressure as excess fluid re-enters the atria from the ventricle and results in a gurgling systolic murmur (common to hear both an insufficiency and stenosis)
41
97. Describe the force that causes one-way flow of blood through the peripheral vasculature.
The pressure difference between the aorta and vena cava is such that blood flows from high pressure to lower pressure
42
98. Write the equation that determines the rate of convective transport of a substance (X) through the cardiovascular system.
Transport rate= flow x concentration
43
99. List the four factors that determine the rate of diffusion of a substance between capillary blood in the interstitial fluid, and write them in the equation that determines diffusion rate.
Variables that determine the rate of diffusion are: permeability of the membrane, surface area of exchange, the concentration gradient and the thickness of the membrane (diffusion distance)
44
100. List the anatomical features of capillaries that maximize the ability to exchange substances between the blood and interstitial fluid.
Capillary tube walls are very thin and allow for diffusion across themselves very easily, have a small diameter, may pores and are present in huge numbers (great surface area)
45
101. Contrast the diffusion pathway across capillary walls of lipid-soluble substances like O2 and CO2 with small water-soluble molecules like ions and glucose.
Lipid-soluble substances can diffuse across the cell wall easily (occurring at any point in the capillary wall) while polar substances have a much lesser permeability and it is proposed that they move through pores
46
102. Name a class of molecules that are in high concentration in the plasma but have a very low permeability through the capillary wall.
Plasma proteins like albumin
47
103. List three physiological roles that endothelial cells play in addition to being the barrier to exchange between the blood and ISF.
Epithelial cells convert certain circulating hormones to their active forms, they produce substances that are involved in blood clotting (angioplasty can kill endothelia and cause contraction) and can produce vasoactive substances that act on smooth muscle cells that surround them to influence arteriolar diameter
48
104. With regard to capillary function, define “filtration” and “reabsorption.”
Net fluid movement out of capillaries is referred to as filtration, and fluid movement into capillaries is called reabsorption; net flow can help maintain circulating blood volume, allow intestinal fluid absorption, cause tissue edema and form saliva, sweat and urine
49
105. List and describe the two categories of pressures that influence transcapillary fluid movement.
Both hydrostatic and osmotic pressure influence transcapillary fluid movement, hydrostatic pressure is what keeps blood moving through vessels and osmotic pressure is its opposing force, keeping plasma in the capillaries to accommodate the density of plasma proteins dissolved in the blood (specially named oncotic pressure)
50
106. Write out the mathematical relationship that determines net filtration pressure at capillaries (aka, the Starling hypothesis), and define each of the 5 variables in the equation.
Net filtration pressure (NFP) is the tendency for fluid to move. Net filtration pressure = k[(pc-pi) (πc-πi)] Pc is the hydrostatic pressure of the intracapillary fluid, πc is the oncotic pressure of intracapillary fluid, Pi and πi are the hydrostatic and oncotic pressures for the interstitial fluid; (important variable K, fluid permeability, is close to one for leaky capillaries, and close to 0 for tight capillaries). Postive NFP means net filtration, negative NFP means net reabsorption
51
107. Explain what occurs when the Starling forces are unbalanced at capillary beds, using the examples of tissue histamine release and hemorrhage-induced hypotension.
Normally NFP is very small ~0 with a very small net filtration. When histamine is released into the blood, it causes increased capillary permeability, which allows plasma proteins to enter the interstitial space and cause a disruption in the balance of oncotic pressure, increased diameter also means increased capillary pressure. Hemorrhage-induced hypotension would lead to greatly reduced hydrostatic pressure and also increased recovery of fluid from capillary beds
52
108. Describe the anatomy and physiology of the system that prevents the accumulation of large, osmotic molecules in tissue interstitial fluid spaces.
The lymphatic system represents a pathway by which large molecules reenter the circulating blood. Lymph vessels are very porous and collect large particles, carried in lymph (accompanying interstitial fluid) and flows through lymph nodes before reentering the circulation via the thoracic duct (2.5L/day) Back up is exemplified in filariasis, blockage of lymph by parasite causing edema.
53
109. For a series of vessels of differing diameter arranged in series, describe the relationship between flow, pressure and resistance.
In series, the resistances of vessels of varying diameter are additive so the equation is just slightly adjusted as Q = ΔP/ (sum of Resistances), the fluid that flows through each element in a given time must be a constant volume. Pressure will decrease over any element, and decrease the greatest when it flows through elements with the greatest resistance. Remember, given a constant flow, velocity of flow varies inversely with radius.
54
110. Contrast how resistance to blood flow is determined in blood vessels arranged in parallel with how resistance to blood flow is determined in blood vessels arranged in series.
Resistance is calculated by adding the reciprocals of all the systems, in general, the more parallel systems that a circuit contains, the lower the overall resistance due to the increased total cross-sectional area; therefore, although an individual capillary may have a very high resistance, the overall resistance of the system will be much lower.
55
111. Explain the distinction between blood flow, and blood flow velocity, using the units of each quantity to reinforce your explanation.
Flow will be the same at all points but the velocity varies inversely with the local cross-sectional area. Blood flow is the total volume flowing by a point in a given time (flow= volume/time) and blood flow velocity is the speed at which a fluid flows past a point (linear velocity = flow/ cross-sectional area)
56
112. Describe the variation in flow velocity in the arteries, arterioles, capillaries, venules and veins.
Flow velocity is greatest in larger vessels such as the arteries and veins and much slower in the smaller vessel, the arterioles, venules and especially the capillaries, which is important for exchange with the blood.
57
113. Describe the laminar flow pattern that occurs during blood flow in normal vessels, and explain what occurs to this pattern when blood flows through an excessively narrowed segment of a vessel; use the term “bruits” in your explanation.
Laminar flow in normal vessels is streamlined and orderly where the velocity profile can be described with a parabola, the speed at the edges of the vessel being the least and the speed being greatest at the center of the vessel. If liquid is forced to go through a diameter that is too small, it causes disruption of the laminar flow of the fluid, mixing the fluid traveling at different speeds and turbulent blood flow. Turbulent blood causes sounds called briuts and can be a sign of a pathological condition.
58
114. Rank the following vessels according to the volume of blood they contain at any given moment in a health adult: Arteries, Arterioles, Capillaries, Venules, Veins.
veins and venules, arteries, capillaries, arterioles
59
115. Draw a graph that shows how the mean pressure changes in the systemic circuit as blood flows through arteries, arterioles, capillaries, and veins.
mean pressure is greatest in arteries, decreases the most in arterioles and then decreases slowly as it returns back to the heart
60
116. Draw a graph showing how the total vascular resistance varies in arteries, arterioles, capillaries and veins.
resistance rises moving from arteries to arterioles and the decreases until it reaches the heart, the greatest vascular resistance occurs in the arterioles
61
117. Explain how the total peripheral resistance (TPR) would be different if systemic organ systems were arranged in series rather than in parallel.
If systemic organs were in series, their total resistance would be much greater (the resistance of the vessels would be additive) Bonus: arteriole dilation decreases pressure in the arteries and increases pressure in the capillaries, where the opposite is also true—net arteriole radius determines the TPR which is an important determinant of mean artery pressure
62
118. Draw a graph the demonstrates the difference in compliance in the arterial compartment vs the venous compartment.
both arteries and veins are compliant (veins most compliant), which mean they are prone to stretch with applied pressure but arteries are elastic and resist the compliant stretching whereas veins are not as elastic. Compliance is change in volume over change in pressure.
63
119. Describe a scenario that demonstrates the effect of high venous compliance on circulating blood volume during postural changes, and explain how active venous constriction influences that effect.
High venous compliance causes results in an increase in venous volume when a person goes from sitting to standing because there is greater pressure of gravity pulling blood downwards. This can greatly decrease the blood pressure. This process can be countered by active venous constriction of smooth muscle by sympathetic innervation.
64
120. Describe how the elasticity of arteries contributes to blood flow in the systolic and diastolic phases of the cardiac cycle.
The elasticity of arteries allows them to act as a pressure reservoir (2/3 total pressure) between beats of the heart. The recoil of the arteries during diastole is what pushes blood through the vessels. Elasticity of arteries maintain a fairly stable pressure and flow of blood to the systemic circulation. With aging, there is less compliance and less elasticity so there is an increase in systolic pressure and decrease in diastolic pressure.
65
121. Describe the technique for measuring systolic and diastolic blood pressure with a blood pressure cuff (sphygmomanometer) and stethoscope, explaining the relationship between cuff pressure, blood vessel patency, and the arterial pressure profile.
Stethoscope is placed over the brachial artery of the arm. A cuff is inflated until it reaches pressures well over the systolic pressure, which collapses the vessels in the arm. Air is bled from the cuff until the it reaches a pressure equal to the systolic pressure, the vessels will be partially patent and produce Korotkoff sounds due to turbulent flow of the partially occluded vessels. When the pressure in the cuff reaches systolic pressure or below, no sounds can be heard over the brachial artery, as the vessels are again fully patent.
66
122. Starting with the basic equation relating blood flow to pressure and resistance (Q=∆P/R), derive the fundamental equation of cardiovascular physiology underlying how mean arterial blood pressure is determined (not calculated or measured, but determined).
Flow defined in the whole circuit is equal to cardiac output, change in pressure is analogous to difference between mean arterial pressure and central venous pressure (~0) and resistance is analogous to total peripheral resistance. This equation can be represented by CO= Mean arterial pressure/ TPR. Rearranged, mean arterial blood pressure is determined by the product of cardiac output and total peripheral resistance.
67
123. Given systolic and diastolic blood pressure, calculate the mean arterial blood pressure.
Mean arterial pressure is approximately equal to diastolic pressure plus one third of the difference between systolic and diastolic pressures; Mean arterial pressure = CO x TPR. All changes in mean arterial pressure result from changes in either CO or TPR (Mean aterial pressure = Pd + 1/3 (Ps-Pd))
68
124. Define “pulse pressure,” and list the variables that influence the magnitude of the pulse pressure.
Arterial pulse pressure is the systolic pressure minus the diastolic (difference in pressure between when the heart is contracting and when it is relaxed). Variables that affect pulse pressure include: pressure of a vessel determined by the vessel’s volume and compliance. Pulse pressure is calculated by dividing stroke volume by compliance. Increase in pressure during systole is proportional to the stroke volume and inversely proportional to compliance
69
125. Draw and explain a graph that demonstrates the factors underlying the typical difference in pulse pressure between a 20-year-old and a 70-year-old patient.
Pulse pressure increases due to decreased compliance, plain old arterial pressure and volume can increase with age but not due to artery compliance but rather to arteriole changes that increase TPR
70
126. Name the type of blood vessel in which regulation of smooth muscle contraction controls the distribution to different tissues to match their individual physiological needs.
arterioles
71
127. Name the type of blood vessel in which regulation of smooth muscle contraction controls the distribution of blood volume and cardiac filling.
veins and venules
72
128. Name the type of blood vessel that has no smooth muscle associated.
capillaries
73
129. Define “vascular tone.”
Term that characterizes the general contractile state of a vessel or a vascular region, arteriolar tone implies a decrease in arteriolar vessel diameter and venous tone causes increased cardiac filling
74
130. Describe the basal tone of the vasculature in a resting individual (is it low, intermediate, or high?) and explain the functional reason for this typical state.
Intermediate. Basal tone exists somewhere between complete relaxation and maximum contraction which establishes a baseline from which arteriolar tone can be regulated as well as contributing to arterial blood pressure (via TPR)
75
131. Explain the effect of local tissue oxygen levels on arteriolar tone in systemic organs.
In nearly all vascular beds, exposure to low oxygen reduces arteriolar tone and vasodilation
76
132. List the chemical alterations that occur in metabolically active tissue that can regulate the tone of arteriolar smooth muscle.
Tissue levels of carbon dioxide, H+ and K+ due to increased metabolism cause arteriolar dilation. Tissues may also release adenosine (from ATP), which is a potent vasodilator agent.
77
133. Detail the mechanism by which endothelial cells influence the tone of adjacent arteriolar smooth muscle, and list some chemical agents known to activate this pathway.
Tissue levels of carbon dioxide, H+ and K+ due to increased metabolism cause arteriolar dilation. Tissues may also release adenosine (from ATP), which is a potent vasodilator agent.
78
134. Detail the mechanism by which shear stress influences vascular smooth muscle tone.
Blood flow related shear stresses also stimulate NO production. Shear stress is normally detected by cilia on cells to measure flow over the cell.
79
135. Describe the myogenic response of vascular smooth muscle, and explain how it could be adaptive in cases where cardiovascular disturbances alter vascular transmural pressure.
After vessel is stretched (by transmural pressure) passively stretch receptors (debated) inherent to the muscle cause the vessel to actively contract (myogenic response). Myogenic response is fundamentally important factor in determining the basal tone of arteries and local flow response
80
136. Define “active hyperemia,” explain when it occurs, and describe the underlying mechanism.
In organs with highly variable metabolism, blood flow response to metabolic rate. For example, skeletal muscle blood flow increases within seconds of the onset of muscle exercise and returns to control shortly after. Underlying mechanisms could include local metabolic vasodilator feedback on arterial smooth muscle.
81
137. Define “reactive (post-occlusion) hyperemia,” explain when it occurs, and describe the underlying mechanism.
Greater than normal blood flow that occurs transiently after the removal of any restriction that has caused a period of lower than normal blood flow. Lower than normal blood flow causes dilation during occlusion and when flow is restored it is excessive for needs and gradually comes down. Both local metabolic and myogenic mechanism may be mechanisms involved.
82
138. Define “autoregulation,” describe the underlying mechanisms, and explain the general function of this phenomenon in maintaining homeostasis.
Except in active and reactive hyperemia, nearly all organs tend to keep their blood flow constant despite variations in arterial pressure. Autoregulatory mechanisms operate in the opposite direction in responses to change in arterial pressure. Mechanisms include vasodilator factor washout, myogenic response, and opposing increased tissue pressure Corrections can slightly overshoot set point and create new set points.
83
139. Describe the distribution of sympathetic vasoconstrictor nerves to the vasculature, and explain the global role they play in cardiovascular regulation.
Sympathetic vasoconstrictor nerves are the backbone of the system for controlling TPR and thus are essential participants in regulating blood pressure. These neural fibers innervate arterioles in all systemic organs. Greater firing of these nerves creates greater tone while less than baseline firing creates vasodialation
84
140. Name the principal neurotransmitters and receptor-type that mediate the function of sympathetic vasoconstrictor nerves.
Sympathetic fibers release norepinephrine which binds to a1- adrenergic receptors on smooth muscle cells. (preganglionic fibers use acetylcholine on nicotinic receptors to propagate signals)
85
141. Differentiate the phenomenon of neurogenic vascular tone from that of basal vascular tone.
Neurogeneic vascular tone is due to the tonic firing of sympathetics that is a component of the their normal baseline state of contraction.
86
142. List some examples of the few tissues that receive parasympathetic vasodilator nerves.
Parasympathetic vasodilator nerves that release achetylcholine are present in the vessels of the brain and heart but their influence seems to be inconsequential. Parasympathetic are present in the vessels of the salivary glands, pancreas, gastric mucosa and external genitalia that allow for vasodialation
87
143. Discriminate between the vascular effects of norepinephrine, moderate levels of circulating epinephrine, and high levels of circulating epinephrine; explain the receptor-mechanisms.
Moderate levels of epi cause vasodialation via B2 where as high levels of epi cause vasoconstriction via a1. (more details >> )Moderate levels of NE and Epi activate cardiac a1 receptors to cause vasoconstriction and sometimes also B2 adrenergic receptors that mediate vasodialation. B2 receptors are more sensitive to EPi than a1 and moderately increased level of circulating epi can cause vasodilation, where as higher level cause a1 receptor mediated constriction
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144. Describe the source, stimulus for secretion, and circulatory effects of vasopressin.
ADH is released by poster pituitary gland in response to low blood volume and or high extracellular fluid osmolarity by decreasing water secretion. Vasopressin affects are very potent
89
145. Describe the vascular effect of angiotensin II.
Angiotension II regulates aldosterone release from the adrenal cortex to balance salt and is also a very important vasoconstrictor agent; synthesized in response to low blood volume
90
146. Differentiate the general effect of venous constriction from the general effect of arteriole constriction on the function of the cardiovascular system.
Veins are normally in their dilated state and vasodilators usually have little effect coming form upstream. Because of their thin walls, they are much more susceptible to physical forces ie. External compression is an important determinant of venous volume, which is especially true of veins in skeletal muscle. Constriction of peripheral veins raises central veous pressure and contributes to increased cardiac output. Smooth muscle tone in veins can be increased by sympathetic signaling
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147. With regard to venous function, define “skeletal muscle pump” and explain its role and its mechanism.
Rhythmic contraction of skeletal muscle can cause pumping action of the blood through the valves of veins and helps return blood to the heart during exercise
92
148. List organs in which blood flow is strongly regulated by local metabolic factors, and list other organs in which blood flow is strongly regulated by sympathetic nerve activity.
Strongly regulated by local metabolic factors: brain, heart muscle and skeletal muscle; strongly regulated by sympathetic nerve activity: kidneys, splanchnic organs and skin
93
149. State the approximate percentage range of oxygen extracted from the blood flowing through the coronary vasculature in a resting individual, and explain how homeostasis is maintained when cardiac metabolism is elevated, as in exercise.
Myocardium extracts 70-75% of the oxygen in the blood that passes through it, which is more than any other organ. Increases in myocardial oxygen consumption must be accompanied by appropriate increases in coronary flow, most believe it is the release of adenosine that induces this change
94
150. Describe how coronary vascular resistance changes during systole and diastole, and the implications for blood flow to the endocardial and epicardial myocardium during the cardiac cycle.
The endocardium of the left ventricle is exposed to intraventricular pressure while epicardial surface is exposed only to intrathoracic pressure, systolic compressional forces on coronary vessels are greater in the endocardial layer of the left ventricular wall than in the epicardial layers. Endocardial layers usually make up for this flow during systole, but not when coronary flow is restricted.
95
Why does power lifting exercise sometimes lead to myocardial infarction
thick walls + compression + high HR = No flow
96
Explain the paradox of neural influence on coronary flow
although sympathetic vasoconstrictor neurons exist to cardiac vessels, when sympathetic firing increaes heart rate and contractility, metabolic change causes net vasodilation
97
152. Explain the different effect on blood flow and central venous pressure of rhythmic skeletal muscle contraction/relaxation vs sustained, tetanic contractions of skeletal muscles.
Rhythmic contractions can increase venous return from exercising skeletal muscle increasing cardiac output, but with strong sustained skeletal muscle compressional forces can actually stop muscle blood flow. Blood displaced from skeletal muscle into the central venous pool is an important factor in the hemodynamics of strenuous whole body exercise.
98
153. Explain the relative importance of brain blood flow in terms of the overall function of the cardiovascular system.
Interruption of cerebral blood flow for more than a few seconds leads to unconsciousness; in all situations, measures are taken to preserve adequate blood flow to the brain. Local control dominates and auto regulates blood flow
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154. List the mechanisms by which cerebral blood flow is regulated.
Cerebral blood is regulated almost entirely by local mechanisms. Flow is auto-regulated very strongly and is little affected by changes in arterial pressure unless it falls below about 60mmHg. Cerebral activity in discrete regions is not constant but closely follows the local neuronal activity. Blood CO2 is very influential in blood flow to the brain, high CO2 leads to cerebral vasodilation.
100
155. Explain how hyperventilation causes changes in blood flow that can result in dizziness/confusion/fainting.
Confusion and dizziness are direct results of cerebral vasoconstriction. It appears that this constriction is closely related to the changes in the extracellular H+ due to excess CO2 being blown off.
