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  2. Physiology (Board Review Series)
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Fourth Edition, Library of Congress Cataloging-in-Publication Data. Costanzo, Linda S., Physiology/Linda S. Costanzo. —5th ed. p. ; cm. —( Board. Views 15MB Size Report. DOWNLOAD PDF · BRS Physiology, 5th Edition ( Board Review Series). Read more BRS Neuroanatomy, 4th Edition · Read more. Physiology Cases and Problems FOURTH EDITION Physiology Cases and BRS Physiology. 5th ed. Baltimore: Lippincott Williams & Wilkins;

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Brs Physiology 4th Edition Pdf

DownloadBrs physiology 4th edition pdf free. Free Download e-Books exe 21 02 06 PM CMS TrialDirector Compound Media Storage If there are. Yeah, reviewing a book physiology linda costanzo 4th edition could build up your close BRS physiology pdf is considered one of the best short book of. BRS_physiology_4th_ - Free ebook download as PDF File .pdf) or read book online BRS Physiology Cases and Problems BRS - Pharmacology 4th Ed. pdf.

The subject matter of physiology is the foundation of the practice of medicine, and a firm grasp of its principles is essential for the physician. It is a concise review of key physiologic principles and is intended to help the student recall material taught during the first and second years of medical school. BRS Physiology 6th edition It is not intended to substitute for comprehensive textbooks or for course syllabi, although the student may find it a useful adjunct to physiology and pathophysiology courses. The material is organized by organ system into seven chapters. The first chapter reviews general principles of cellular physiology. Difficult concepts are explained stepwise, concisely, and clearly, with appropriate illustrative examples and sample problems. Numerous clinical correlations are included so that the student can understand physiology in relation to medicine.


It is not intended to substitute for comprehensive textbooks or for course syllabi, although the student may find it a useful adjunct to physiology and pathophysiology courses.

The material is organized by organ system into seven chapters. The first chapter reviews general principles of cellular physiology. The remaining six chapters review the major organ systems—neurophysiology, cardiovascular, respiratory, renal and acid-base, gastrointestinal, and endocrine physiology.

Difficult concepts are explained stepwise, concisely, and clearly, with appropriate illustrative examples and sample problems. Numerous clinical correlations are included so that the student can understand physiology in relation to medicine. An integrative approach is used, when possible, to demonstrate how the organ systems work together to maintain homeostasis. More than illustrations and flow diagrams and more than 50 tables help the student visualize the material quickly and aid in long-term retention.

These ques- tions, many with clinical relevance, require problem-solving skills rather than straight recall. Clear, concise explanations accompany the questions and guide the student through the correct steps of reasoning.

The questions can be used as a pretest to identify areas of weakness or as a post-test to determine mastery. Special attention should be given to the Comprehensive Examination, because its questions integrate several areas of physiology and related concepts of pathophysiology and pharmacology. Without normal parasympathetic innervation, the receptors are up-regulated i.

Thus, when an exogenous cholinergic agonist e. When a healthy person stands up suddenly, blood pools in the veins of the legs, and there is a transient decrease in arterial blood pressure. This decrease is only transient because it is detect- ed and immediately corrected by relexes involving the sympathetic and parasympathetic ner- vous systems baroreceptor relex. For this relex to occur, information about blood pressure must be relayed from baroreceptors in the carotid sinus to speciic brainstem centers.

These brainstem centers orchestrate an increase in sympathetic outlow to the heart and blood vessels and a decrease in parasympathetic outlow to the heart Fig. The sympathetic and para- sympathetic effects include an increase in heart rate and contractility, which combine to pro- duce an increase in cardiac output; constriction of arterioles, with a resultant increase in total peripheral resistance; and venoconstriction, which increases venous return to the heart. These effects, in combination, restore arterial pressure to its normal set-point value.

The responses occur so quickly that healthy persons are unaware of them, or may be briely aware of an increase in heart rate. Responses of the baroreceptor relex to a decrease in mean arterial pressure. Pa, arterial pressure; TPR, total peripheral resistance.

Garcia, the baroreceptor relex was severely impaired because of central damage to the sympathetic and parasympathetic nervous systems. When he stood up, his arterial pressure fell orthostatic hypotension and could not be corrected by autonomic relexes. He felt dizzy and fainted because the sustained decrease in arterial pressure caused a decrease in cerebral blood low.

Support stockings constrict the veins in the legs and prevent the venous pooling of blood that initiates an orthostatic decrease in blood pressure. Aldosterone secreted by the adrenal cortex and its analogues increase the reabsorption of Na in the kidney and thereby increase both extracellular luid volume and blood volume.

Because most of the blood volume is contained in the veins, an increase in total blood volume leads to an increase in venous blood volume and venous return, which produces an increase in cardiac out- put and arterial pressure.

Any drug that would further antagonize either sympathetic or parasympathetic activity e. Recall that nicotinic receptors are present on postsynaptic neurons in both sympathetic and parasympathetic ganglia.

Use the information provided in Table 2—1 to answer the questions.

Physiology (Board Review Series)

Part of the challenge in answering these questions will be in deciding which information you need in order to perform each calculation. Good luck! Mean arterial pressure is not the simple average of systolic and diastolic pressures. Why not? How is mean arterial pressure estimated? From the information given in Table 2—1, calculate the mean arte- rial pressure in this case. Calculate the stroke volume, cardiac output, and ejection fraction of the left ventricle.

Calculate cardiac output using the Fick principle. What is the deinition of total peripheral resistance TPR? Which equation describes the relation- ship between TPR, arterial pressure, and cardiac output? What is the value of TPR in this case? How is pulmonary vascular resistance calculated? What is the value of pulmonary vascular resis- tance in this case? Compare the calculated values for pulmonary vascular resistance and TPR and explain any difference in the two values.

What information, in addition to that provided in Table 2—1, is needed to calculate the resistance of the renal vasculature? If the diameter of the aorta is 20 mm, what is the velocity of aortic blood low? Would you expect the velocity of blood low in systemic capillaries to be higher than, lower than, or the same as the veloc- ity of blood low in the aorta? Systemic arterial pressure is not a single value because arterial pressure varies over the course of each cardiac cycle.

Its highest value is systolic pressure, which is measured just after the blood is ejected from the left ventricle into the aorta i. Its lowest value is diastolic pressure, which is measured as the blood lows from the arteries into the veins and back to the heart i. Mean arterial pressure cannot be calculated as the simple average of systolic and diastolic pres- sures because averaging does not take into account the fact that a greater fraction of each cardiac cycle is spent in diastole approximately two-thirds than in systole approximately one-third.

Thus, mean arterial pressure is closer to diastolic pressure than to systolic pressure. Figure 2—1 shows an arterial pressure tracing over a single cardiac cycle. The difference between systolic pres- sure and diastolic pressure is called pulse pressure. Systemic arterial pressure during the cardiac cycle. Although this approach is impractical, the mean arterial pressure can be determined by measur- ing the area under the arterial pressure curve. Alternatively, the mean arterial pressure can be esti- mated as follows: These calculations concern the cardiac output of the left ventricle.

The basic relationships are as follows: It is calculated as the product of stroke volume determined to be 70 mL and heart rate. Heart rate is not given in Table 2—1, but it can be calculated from the R-R interval. The R-R interval is the time elapsed from one R-wave to the next Fig.

It is also called cycle length i. ECG measured from lead II. The interval between R-waves is the cycle length. As shown in Question 2, we calculate cardiac output as the product of stroke volume and heart rate.

However, we measure cardiac output by the Fick principle of conservation of mass. The Fick principle for measuring cardiac output employs two basic assumptions: This relationship can be stated mathematically as follows: To ind the appropriate values in the table, recall that systemic arterial blood is equivalent to pulmonary venous blood.

Chapter 2 Cardiovascular Physiology 53 4. TPR is the collective resistance to blood low that is provided by all of the blood vessels on the sys- temic side of the circulation. These blood vessels include the aorta, large and small arteries, arteri- oles, capillaries, venules, veins, and vena cava. Most of this resistance resides in the arterioles. The fundamental equation of the cardiovascular system relates blood low, blood pressure, and resistance.

Blood low is analogous to current low, blood pressure is analogous to voltage, and hemodynamic resistance is analogous to electrical resistance. Thus, the equation for blood low is: In solving this problem, it may be helpful to visualize the organization and cir- cuitry of the cardiovascular system Fig.

Circuitry of the cardiovascular system. Inlow pressure to the systemic circulation is aortic pressure, and outlow pressure from the systemic circulation is right atrial pres- sure. In Question 1, the mean aortic pressure was calculated as 96 mm Hg, which is also approxi- mately the value of mean arterial pressure. The right atrial pressure is given in Table 2—1 as 2 mm Hg. Resistance R , which represents TPR, is: We need to know the values for pulmonary blood low cardiac output of the right ventricle and the pressure difference across the pulmonary circulation.

To determine the pulmonary blood low, it is necessary to understand that the left and right sides of the heart operate in series i. The pressure difference across the pulmonary circulation is inlow pressure minus outlow pressure.

The inlow pressure is mean pulmonary artery pressure 15 mm Hg , and the outlow pressure is left atrial pressure 5 mm Hg. Thus, pulmonary vascular resistance is: How is this possible? No, because pulmonary pressures are also much lower than systemic pressures. Thus, pulmonary blood low can be exactly equal to systemic blood low because pulmonary vascu- lar resistance and pressures are proportionately lower than systemic vascular resistance and pres- sures.

Because of the serial arrangement of blood vessels within the lungs i. This question addresses the same issue as Question 6, but as applied to the systemic circulation.

Because of the serial arrangement of blood vessels in the systemic circulation i. Chapter 2 Cardiovascular Physiology 55 8. The principles that were used to determine TPR or to determine pulmonary vascular resistance can also be used to calculate the vascular resistance of individual organs e. Recall how the pressure, low, and resistance relationship was rearranged to solve for resistance: R can also represent the resistance of the blood vessels in an individual organ e.

Actually, none of the exact information needed to calculate renal vascular resistance is available in Table 2—1 or from the previous calculations. Renal arterial pressure is close, but not exactly equal, to the mean arterial pressure that was calculated for the aorta in Question 1. It must be lower in order for blood to low in the right direction, that is, from the aorta to the distal arteries. Like the pressure in any large vein, renal venous pressure must be slightly higher than the right atrial pres- sure.

Because of the parallel arrangement of arteries off the aorta, renal blood low is only a fraction of the total systemic blood low. The velocity of blood low is the rate of linear displacement of blood per unit time: The cross-sectional area can be calculated from the diam- eter of the aorta, which is 20 mm radius, 10 mm. Of course, a single capillary has a smaller radius than the aorta, but all of the capillaries have a larger collective radius and cross- sectional area than the aorta.

This loop shows the relationship between left ventricular pressure in mm Hg and left ventricular volume in mL over a single cardiac cycle. Use Figure 2—4 to answer the following questions. Left ventricular pressure—volume loop. Adapted, with permission, from Costanzo LS. Describe the events that occur in the four segments between numbered points on the pressure— volume loop e.

Correlate each segment with events in the cardiac cycle. According to Figure 2—4, what is the value for left ventricular end-diastolic volume? What is the value for end-systolic volume?

What is the approximate value for stroke volume? What is the approximate value for ejection fraction? Which portion, or portions, of the pressure—volume loop correspond to diastole? To systole? Which portions of the pressure—volume loop are isovolumetric?

At which numbered point does the aortic valve open? At which numbered point does the aortic valve close? At which numbered point does the mitral valve open?

At which numbered point, or during which segment, would the irst heart sound be heard? At which numbered point, or during which segment, would the second heart sound be heard? Superimpose a new pressure—volume loop to illustrate the effect of an increase in left ventricular end-diastolic volume i.

What is the effect on stroke volume? Superimpose a new pressure—volume loop to illustrate the effect of an increase in contractility. What is the effect on end-systolic volume? What is the effect on ejection fraction?

Superimpose a new pressure—volume loop to illustrate the effect of an increase in aortic pressure i. Figure 2—4 shows a single left ventricular cycle of contraction, ejection of blood, relaxation, and illing to begin another cycle.

This igure can be used to describe the events as follows. During this phase, the ventricle which was previously illed from the atrium is contracting. Contraction causes a steep increase in ventricular pressure.

However, because the aortic valve is closed, no blood is ejected and left ventricular volume remains constant i. The ventricle is still contracting, causing ven- tricular pressure to increase further. The aortic valve is now open, and blood is ejected from the left ventricle, which causes ventricular volume to decrease. The left ventricle relaxes, and ventricular pressure decreases.

Both the aortic and the mitral valves are closed, and ventricular volume remains constant. The left ventricle is still relaxed, but now the mitral valve is open and the ventricle is illing with blood from the atrium. Because the ventricle is relaxed, the increase in ventricular volume causes only a small increase in ventricular pressure.

End-diastolic volume is the volume present in the ventricle after illing is complete, but before any blood is ejected into the aorta. Therefore, end-diastolic volume is present at points 1 and 2 approximately mL. End-systolic volume is the volume that remains in the left ventricle after ejection is complete, but before the ventricle ills again i.

Stroke volume is the volume ejected during systole ventricular ejection. Thus, stroke volume is represented by the width of the pressure—volume loop, or approximately 70 mL mL — 70 mL. Ejection fraction is stroke volume expressed as a fraction of end-diastolic volume i.

Diastole is the portion of the cardiac cycle when the ventricle is relaxed i. Systole is the portion of the cardiac cycle when the ventricle is contracting. By deinition, isovolumetric portions of the ventricular cycle are those in which ventricular volume is constant i. The aortic valve opens at point 2, when ventricular pressure exceeds aortic pressure.

Opening of the aortic valve is followed immediately by ejection of blood and a decrease in ventricular volume. The aortic valve closes at point 3, and ejection of blood ceases. The mitral valve the atrioventricular valve of the left heart opens at point 4, and ventricular illing begins.

The irst heart sound corresponds to closure of the atrioventricular valves. This closure occurs at the end of ventricular illing, at the beginning of isovolumetric contraction. Thus, the irst heart sound occurs at point 1. The second heart sound corresponds to closure of the aortic valve, at point 3. End-diastolic volume preload is the volume of blood contained in the ventricle just before contrac- tion.

Therefore, an increase in ventricular end-diastolic volume e. In Figure 2—5, point 1 shifts to the right to represent the increased end-diastolic volume. The Frank—Starling relationship for the ventricle states that the greater the end-diastolic volume, the greater the stroke volume.

Therefore, without any change in contractility, an increase in end-diastolic volume causes an increase in stroke volume, as evidenced by increased width of the pressure—volume loop. Effect of an increase in preload on the left ventricular pressure—volume loop. Contractility inotropy is the intrinsic ability of myocardial ibers to develop tension at a given muscle length i.

When contractility is increased e. As a result, stroke volume increases Fig. Because ejection fraction is stroke volume expressed as a fraction of end-diastolic volume, if stroke volume increases and end-diastolic volume is unchanged, ejection fraction must have increased.

Effect of an increase in contractility on the left ventricular pressure—volume loop. Afterload is the pressure against which the ventricles must eject blood. Afterload of the left ventricle is aortic pressure. To open the aortic valve and eject blood, left ventricular pressure must increase to a level greater than aortic pressure.

Thus, if afterload increases, the left ventricle must work harder than usual to overcome this higher pressure. Figure 2—7 shows the consequences of an increase in afterload.

Because of the increased afterload, stroke volume is compromised, more blood remains in the left ventricle after ejection, and end- systolic volume is increased. Because stroke volume decreases and end-diastolic volume is unchanged, ejection fraction must have decreased. Effect of an increase in afterload on the left ventricular pressure—volume loop.

One morning, she awakened from a deep sleep and realized that she was more than an hour late for work. She panicked, momentarily regretting her late-night socializing, and then jumped out of bed. Briely, she felt light- headed and thought she might faint. As she walked toward the bathroom, she noticed that her light-headedness dissipated. The rest of her day was uneventful.

When Joslin moved rapidly from a supine lying position to a standing position, there was a brief, initial decrease in arterial pressure that caused her light-headedness. Describe the sequence of events that produced this transient fall in arterial pressure.

Why did the decrease in arterial pressure cause Joslin to feel light-headed? Describe the speciic effects of this relex on heart rate, myocardial contrac- tility, TPR, and capacitance of the veins. What receptors are involved in each of these responses? How does each component of the relex e. It may help to write the equation that relates arterial pressure, cardiac output, and TPR. In addition to the relex correction of blood pressure, the fact that Joslin walked to the bathroom helped return her arterial pressure to normal.

How did walking help? Orthostatic hypotension is the phenomenon whereby arterial pressure decreases when one stands up. When a person suddenly moves from a supine lying position to a standing position, blood pools in the veins of the legs. Because the capacitance, or compliance, of the veins is high, they can hold large volumes of blood. This pooling decreases venous return to the heart, which decreases cardiac output by the Frank—Starling mechanism. The Frank—Starling mechanism describes the relationship between venous return and cardiac output.


Increases in venous return lead to increases in end- diastolic volume. Up to a point, increases in end-diastolic volume lead to increases in cardiac out- put. Conversely, decreases in venous return lead to decreases in cardiac output.

Because arterial pressure is affected by the volume of blood in the arteries, a decrease in cardiac output i. When Joslin stood up quickly, she felt light-headed because a brief period of cerebral ischemia occurred as a result of the decrease in arterial pressure.

The autoregulatory range for cerebral blood low is 60 to mm Hg. In other words, cerebral blood low is maintained constant as long as arte- rial pressure is greater than 60 mm Hg and less than mm Hg. When Joslin stood up, her arterial pressure briely decreased below this critical autoregulatory range. As a result, cerebral blood low decreased, and she felt light-headed. Baroreceptors located in the carotid sinus and the aortic arch sensed the decrease in arterial pressure. The baroreceptor relex then orchestrated a series of compensatory responses, including increased sympathetic outlow to the heart and blood vessels.

There are four consequences of this increased sympathetic outlow: Chapter 2 Cardiovascular Physiology 67 4.

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Cardiovascular responses in a person moving suddenly from a supine to a standing position. The increased heart rate and contractility combined to produce an increase in cardiac output. The increased cardiac output caused an increase in arterial pressure. The increased arteriolar constriction produced an increase in TPR, which also increased the arterial pressure.

Finally, venoconstriction led to decreased capacitance of the veins, which increased venous return to the heart and increased the cardiac output by the Frank—Starling mechanism. As Joslin walked toward the bathroom, the muscular activity compressed the veins in her legs and decreased venous capacitance i. This compression, combined with sympathetic venoconstriction, increased venous return to the heart and cardiac output.

She believes in the impor- tance of a healthy lifestyle and was intrigued when the division of cardiology recruited healthy female volunteers for a study on the cardiovascular responses to exercise. Cassandra met the study criteria i.

Cassandra then walked on the treadmill for 30 min at 3 miles per hour. Her blood pressure and heart rate were monitored continuously, and her arterial and venous PO2 were measured at the end of the exercise period Table 2—2. To set the stage for the following questions, describe the cardiovascular responses to moderate exercise, including the roles of the autonomic nervous system and local control of blood low in skeletal muscle.

What was her cardiac output for the control and exercise periods, respectively? Of the two factors that contribute to cardiac output stroke volume and heart rate , which factor made the greater contribution to the increase in cardiac output that was seen when Cassandra exercised, or do these factors have equal weight? What is the signiicance of the observed change in pulse pressure? Why was the systolic pressure increased during exercise?

Why did the diastolic pressure remain unchanged? However, at the peak of exercise, her skin was lushed and very warm to the touch. What mechanisms were responsible for these changes in skin color and temperature as the exercise progressed? Arterial and venous PO2 were measured before and after exercise. Explain why venous PO2 decreased but arterial PO2 did not. The major mechanism for providing this additional O2 is increased blood low to the exercising skeletal muscle and the myocardium.

In principle, blood low in an organ can be increased in two ways: During exercise, both of these mechanisms are utilized: Figure 2—9 summarizes these responses.

Cardiovascular responses to exercise. At the initiation of exercise, muscle mechanoreceptors and chemoreceptors trigger relexes that send afferent signals to the cerebral motor cortex. The cerebral cortex then directs responses that include increased sympathetic outlow to the heart and blood vessels. The increase in contractility results in increased stroke volume. Together with increased heart rate, this increased stroke volume produces an increase in cardiac output.

Increased venous return is an essential component of the response to exercise; it provides the increased end-diastolic volume that is needed to produce the increase in cardiac output Frank—Starling mechanism. In addition to these central responses that are orchestrated by the sympathetic nervous system, local responses occur in skeletal and cardiac muscle to increase their blood low. These metabolites produce vasodilation of skeletal muscle arterioles, thereby increasing the local blood low.

This local vasodilation in skeletal muscle is so prominent that it is responsible for an overall decrease in total peripheral resistance TPR. If these local responses in skeletal muscle did not occur, TPR would have increased as a result of sympathetic vasoconstriction.

Local responses also dominate in the myocardium, where they are primarily mediated by adenosine and decreased PO2 and cause vasodilation and increased coronary blood low. Recall the calculations of pulse pressure and mean arterial pressure from Case During exercise, her pulse pressure increased to 85 mm Hg mm Hg — 60 mm Hg. You may wish to add this data on pulse pressure and mean arterial pressure to the data provided in Table 2—2.

Cardiac output is the product of stroke volume and heart rate, as discussed in Case During exercise, her cardiac output increased dramatically to Again, you may wish to add these values to the data in Table 2—2. To determine whether stroke volume or heart rate made the greater contribution to the increase in cardiac output, it is helpful to evaluate the observed changes on a percentage basis.

In other words, during exercise, how much did cardiac output, stroke volume, and heart rate change as a percentage of their control values? Thus, cardiac output increased by 8. Thus, the dramatic increase in cardiac output has two components, increased stroke volume and increased heart rate, and the increase in heart rate is the more signiicant factor.

To understand what this change means, consider what the pulse pressure represents. Because of the large amount of elastic tissue in the arterial walls, they are relatively stiff and noncompliant. Compliance is the inverse of elas- tance.

Therefore, during systole, when blood is rapidly ejected from the left ventricle into the sys- temic arteries, arterial pressure increases rapidly from its lowest value diastolic pressure to its highest value systolic pressure. The magnitude of this increase in pressure i. The explanation for the increase in systolic pressure is the same as the explanation for the increase in pulse pressure: On the other hand, diastolic pressure was decreased, which may be surprising.

However, think about what diastolic pressure represents: Because of the decrease in TPR during exercise, diastolic pressure can decrease. Furthermore, increased cardiac output was a major mechanism for increasing O2 delivery during exercise. Therefore, had Cassandra been taking propranolol, her exercise tolerance would have been signii- cantly reduced.

Cutaneous blood low exhibits a biphasic response to exercise. Blood low is shunted away from the skin, and the skin is cool. As exercise progresses, body temperature increas- es secondary to increased O2 consumption, and sympathetic centers controlling cutaneous blood low in the anterior hypothalamus are inhibited.

This selective inhibition of sympathetic activity produces vasodilation in cutaneous arterioles. As a result, warmed blood is shunted from the body core to venous plexus near the skin surface, as evidenced by redness and warmth of the skin. To help meet the increased demand for O2, her skeletal and cardiac muscles extracted more O2 from arterial blood.

In the respiratory portion of your course, you will appreciate that this increased O2 extraction is accom- plished by a right shift of the O2—hemoglobin dissociation curve [Fig. Right shifts of this curve are produced by increased temperature, increased Pco2, and decreased pH, all of which are conse- quences of an increased metabolic rate.

A right shift facilitates unloading of O2. Thus, in addition to increased blood low, which delivered more O2 to the exercising muscles, more O2 was extracted from the blood. O2—hemoglobin dissociation curve. Dashed line shows right shift of the curve. Chapter 2 Cardiovascular Physiology 73 Now for a puzzling question. No, not if O2 exchange in the lungs restored the PO2 of the blood to its normal arterial value of mm Hg. Mixed venous blood enters the right side of the heart and is pumped to the lungs for oxygenation.

This blood then left the lungs through the pulmonary veins, entered the left side of the heart, and became systemic arterial blood. You may be correctly thinking that people with lung diseases that interfere with O2 diffusion might not be able to restore their arte- rial PO2 to the normal value of mm Hg, especially during exercise, when more O2 is extracted by the exercising tissues. Over the years, the pressures of the job have taken their toll. Hanna has smoked two packs of iltered cigarettes a day for 40 years.

He is 5 feet, 9 inches tall. He recently separated from his wife of 35 years and is dating a much young- er woman. Suddenly realizing how out of shape he had become, he made an appointment for a physi- cal examination.

The physician heard a continuous abdominal bruit sound. Because of Mr. After receiving the results, the physician ordered an additional test called a differential renal vein renin. His differential renal vein renin left to right was 1. The test results were consistent with left renal artery stenosis. A balloon angioplasty was performed immediately to clear the occlusion. He was ordered to stop smoking, follow a low-fat diet, exercise regularly, and undergo periodic physical examinations.

How did occlusion of Mr. How did the increase in plasma renin activity cause an elevation in Mr. The differential renal vein renin measurement involves determining the renin level in venous blood from each kidney.

In healthy persons, the renal vein renin level from each kidney is approximately the same; therefore, the ratio of left to right renin is 1. Hanna, this ratio was elevated to 1. Although it is not apparent, the elevation of the ratio actually had two components: Why was renin secretion increased in the left kidney and decreased in the right kidney? The abdominal bruit was caused by turbulent blood low through the stenosed narrowed left renal artery.

Why did narrowing of the artery cause renal blood low to become turbulent? If the balloon angioplasty was not successful, Mr. Hanna would be treated with an angiotensin- converting enzyme ACE inhibitor e.

What is the rationale for using ACE inhibitors to treat hypertension caused by renal artery stenosis? Atherosclerotic disease caused occlusion narrowing of Mr. Increased quantities of renin, secreted by Mr. The renin—angiotensin II—aldosterone system. TPR, total peripheral resistance. Renin is an enzyme that catalyzes the conversion of angiotensinogen renin substrate to angioten- sin I. Angiotensin I is then converted, primarily in the lungs, to angiotensin II, which has several bio- logic actions.

The second action of angiotensin II is to cause vasoconstriction of arterioles; this vasoconstriction increases the TPR.

Hanna, the increase in blood volume which increased venous return and cardiac output combined with the increase in TPR to produce an increase in his arterial pressure. Hanna had renovascular hypertension, in which his left kidney incorrectly sensed low arterial pressure.

Because his left renal artery was stenosed, there was a decrease in left renal perfusion pres- sure that activated the renin—angiotensin II—aldosterone system and produced an increase in arterial pressure above normal.

Chapter 2 Cardiovascular Physiology 77 3. In the question, you were told that the ratio of left to right renin was elevated for two reasons: Based on the earlier discussion, it is relatively easy to state why left renal renin secretion was increased: But how can we explain decreased renin secretion by the right kidney?

The answer lies in the response of the normal right kidney to the increased arterial pressure that resulted from stenosis of the left renal artery. The right kidney sensed increased arterial pressure and responded appropri- ately by decreasing its renin secretion.

Narrowing of the left renal artery resulted in turbulent blood low, which made a sound called a bruit. The probability of turbulence is given by the Reynolds number: In general, a Reynolds number greater than 2, predicts turbulence.

Initially, the relationship between blood vessel size and turbulence is puzzling. Diameter d is in the numerator. Recall the equation for velocity of blood low from Case Thus, velocity, which appears in the numerator of the Reynolds number equation, is inversely correlated with radius to the sec- 2 ond power r.

Diameter, which also appears in the numerator, is directly correlated with radius to the irst power. In other words, because of the greater second-power dependence on velocity, the Reynolds number increases as vessel radius decreases. The reason why angiotensin-converting enzyme ACE inhibitors such as captopril successfully lower arte- rial pressure in renovascular hypertension should be evident from the pathogenesis of the elevated blood pressure.

Angiotensin II caused the increase in arte- rial pressure, both directly by vasoconstriction and indirectly through the actions of aldosterone. Blocking the production of angiotensin II by inhibiting ACE activity interrupts this sequence of events. Regulation of Blood Pressure Mavis Byrne is a year-old widow who was brought to the emergency room one evening by her sister. Early in the day, Mrs.

Byrne had seen bright red blood in her stool, which she attributed to hemor- rhoids. She continued with her daily activities: However, the bleeding continued all day, and by dinnertime, she could no longer ignore it.

Byrne does not smoke or drink alcoholic beverages. She takes aspirin, as needed, for arthritis, sometimes up to 10 tab- lets daily. In the emergency room, Mrs. Byrne was light-headed, pale, cold, and very anxious. Table 2—3 shows Mrs. A colonoscopy showed that the bleeding came from her- niations in the colonic wall, called diverticula. When arteries in the colon wall rupture, bleeding can be quite vigorous. By the time of the colonoscopy, the bleeding had stopped spontaneously.

Because of the quantity of blood lost, Mrs. Byrne received two units of whole blood and was admitted for observa- tion. The physicians were prepared to insert a bladder catheter to allow continuous monitoring of urine output. However, by the next morning, her normal color had returned, she was no longer light-headed, and her blood pressure, both lying and standing, had returned to normal. No additional treatment or monitoring was needed.

What is the deinition of circulatory shock? What are the major causes?

After the gastrointestinal blood loss, what sequence of events led to Mrs. Why was Mrs. If central venous pressure and pulmonary capillary wedge pressure had been measured, would you expect their values to have been increased, decreased, or the same as in a healthy person? What is hematocrit? Why was her skin pale and cold? How was the saline infusion expected to help her condition?

Why did the physicians consider monitoring her urine output? In this regard, why was it dangerous that Mrs. Byrne had been taking aspirin? Had her blood loss been more severe, Mrs. Byrne might have received a low dose of dopamine, which has selective actions in various vascular beds. In cerebral, cardiac, renal, and mesenteric vascular beds, dopamine is a vasodilator; in muscle and cutaneous vascular beds, dopamine is a vasoconstrictor.

Why is low-dose dopamine helpful in the treatment of hypovolemic shock? Shock or circulatory shock is a condition in which decreased blood low causes decreased tissue perfusion and O2 delivery. Untreated, shock can lead to impaired tissue and cellular metabolism and, ultimately, death. In categorizing the causes of shock, it is helpful to consider the components of the cardiovascu- lar system that determine blood low to the tissues: Shock can be caused by a failure of, or deicit in, any of these com- ponents.

Hypovolemic shock occurs when circulating blood volume is decreased because of loss of whole blood hemorrhagic shock , loss of plasma volume e. Cardiogenic shock is caused by myocardial impairment e. Mechanical obstruction to blood low can occur anywhere in the circulatory system and cause a local decrease in blood low. Neurogenic shock e. Septic or anaphylactic shock involves increased iltration across capillary walls, which leads to decreased circulating blood volume. Byrne had a gastrointestinal hemorrhage and lost a signiicant volume of whole blood.

How did this blood loss lead to decreased arterial pressure? Although it is tempting to picture blood pouring out of the arteries as the direct cause of her decreased arterial pressure, this explanation is an over- simpliication. A number of intervening steps are involved. Recall that because the capacitance of the veins is high, most of the blood volume is contained in the veins, not in the arteries. Therefore, when a hemorrhage occurs, most of the blood volume that is lost comes from the veins.

A decrease in venous volume leads to a decrease in venous return to the heart and a decrease in end-diastolic volume preload. A decrease in end-diastolic volume leads to a decrease in cardiac output by the Frank—Starling mechanism the length—tension relationship for the ventricles. A decrease in cardiac output leads to a decrease in arterial pressure, as expressed by the familiar relationship: Thus, after blood loss, the fundamental problem is decreased venous volume and venous return, leading to decreased cardiac output.

In textbooks, you will see references to illing pressure, venous illing pressure, or cardiac illing pressure. All of these terms refer to the relationships between venous volume, venous return, cardiac output, and ultimately arterial pressure.

As a result, end-diastolic volume was further reduced, which led to further reductions in cardiac output and arterial pressure. Asking why Mrs. Essentially, decreased arterial pressure triggers several compensatory mechanisms, including an increase in heart rate, that attempt to restore blood pressure to normal Fig.

Two major mechanisms are activated in response to decreased arterial pressure: In the baroreceptor relex, sympathetic outlow to the heart and blood vessels is increased. As a result, heart rate and contractility increase and cause an increase in cardiac output.

There is arte- riolar constriction, which increases TPR, and there is venoconstriction, which increases venous return. Cardiovascular responses to hemorrhage. Pc, capillary hydrostatic pressure; TPR, total peripheral resis- tance. Therefore, the baroreceptor mechanism was more strongly stimulated, and sympathetic stimulation of the heart and blood vessels including the increase in heart rate was exaggerated.

Central venous pressure is measured in the vena cava. Its value is related to the volume of blood in the veins and is approximately equal to the right atrial pressure. At that point, the catheter senses pulmonary capillary pressure, which is nearly equal to the left atrial pressure. Thus, central venous pressure estimates the right atrial pressure, and pulmonary capillary wedge pressure estimates the left atrial pressure.

The values relect end-diastolic volume, or pre- load, of the right and left ventricles, respectively. Had they been measured, Mrs. Hematocrit is the fraction or percentage of blood volume occupied by red blood cells; the remain- ing fraction of whole blood is plasma, which is mostly water. A decrease in hematocrit can be caused by any number of factors, including blood loss, decreased red blood cell production, increased red blood cell destruction, or an increase in plasma volume without an accompanying increase in red blood cell volume.

But, wait a minute! You may be asking: In the irst hours after hemorrhage, it is true that hematocrit is unchanged. However, as plasma volume is restored as a result of increased aldosterone levels [see the answer to Question 8], increased capillary absorption of luid, and the infusion of saline , plasma volume increases, but red blood cell volume does not. It takes about 7 days for stem cells to become mature red blood cells.

Therefore, Mrs. A decrease in hematocrit is dangerous because red blood cells contain hemoglobin, the O2- carrying protein of blood.

Thus, after a hemorrhage, there are two potentially lethal consequences for O2 delivery to the tissues: As the baroreceptor relex was initiated in response to decreased arterial pressure see Question 4 , sympathetic vasoconstriction of arterioles occurred in many vascular beds, including the skin. Cutaneous vasoconstriction particularly makes sense as it allows the body to increase the arterial pressure and redirect blood low to more vital organs e.

In contrast to hemorrhagic or hypovolemic shock, where the skin is cold and pale, in the early stages of septic shock e. If urinary Na excretion had been measured, it likely would have been decreased. Increased blood volume leads to increased venous return, increased cardiac output, and ultimately, increased arterial pressure. In an attempt to restore venous return and cardiac output, Mrs.

Byrne received an infusion of saline to increase her extracellular luid volume and blood volume. However, vasoconstriction, by increasing resistance, decreases the blood low in the involved organs.

Of particular note is the kidney, where both sympathetic activity and angiotensin II cause arte- riolar vasoconstriction. If unopposed, this vasoconstriction can compromise renal blood low and glomerular iltration rate GFR , producing renal failure and even death.

Thus, had Mrs. Byrne not recovered quickly, it would have been important to monitor her urine output as an indicator of renal perfusion and renal function. Yes, there are! Prostaglandins serve this modulatory role. Both sympathetic activity and angiotensin II cause increased local production of prostaglandin E2 and prostaglandin I2, which are renal vasodilators. Thus, the vasoconstrictive effects of sympathetic activity and angiotensin II are offset by the vasodilatory effects of endogenous prostaglandins.

Renal blood low is thereby protected and maintained in high vasoconstrictor states, such as hem- orrhage. The confounding and potentially harmful issue with Mrs. Byrne was her use of large amounts of aspirin for her arthritis. Aspirin, a nonsteroidal anti-inlammatory drug NSAID , is a cyclooxygenase inhibitor that blocks prostaglandin synthesis. Byrne was at risk for developing renal failure if her ingestion of aspirin prevented the protective, vasodilatory effects of prosta- glandins.

Chapter 2 Cardiovascular Physiology 85 Dopamine, a precursor of norepinephrine, has its own vasoactive properties, as explained in the question. Low doses of dopamine selectively dilate arterioles in critical organs i. In particular, the kidneys, which might otherwise be vasocon- stricted as a result of increased sympathetic activity and angiotensin II, may be spared by the vasodilatory actions of dopamine.

Right Ventricular Failure At the time of her death, Celia Lukas was a year-old homemaker and mother of three children, 15, 14, and 12 years of age.

Keeping house and driv- ing the children to activities kept her very busy. To stay in shape, she took aerobics classes at the local community center. The irst sign that Celia was ill was vague: However, within 6 months, Celia was short of breath dyspnea , both at rest and when she exercised, and she had swell- ing in her legs and feet.

She made an appointment to see her physician. A fourth heart sound was audible over her right ventricle. The physician was very concerned and immediately scheduled Celia for a chest x-ray, an ECG, and a cardiac catheterization. The chest x-ray showed enlargement of the right ventricle and prominent pulmonary arteries. The ECG indings were consistent with right ventricular hypertrophy.

The results of cardiac catheterization are shown in Table 2—4. These abnormalities lead to increased pulmonary vascular resistance and pulmo- nary hypertension, which causes right ventricular failure cor pulmonale.

Celia was treated with vaso- dilator drugs, but they were not effective. Her name was added to a list of patients awaiting a heart—lung transplant. However, she died of right heart failure before a transplant could be performed. Why did increased pulmonary vascular resistance cause an increase in pulmonary artery pressure pulmonary hypertension?

What values are needed to calculate pulmonary vascular resistance? What is the afterload of the left ventricle? What is the afterload of the right ventricle? What is the effect of increased afterload on stroke volume, cardiac output, ejection fraction, and end-systolic volume?

Why does right ventricular failure cause right ventricular hypertrophy? Use the law of Laplace to answer this question. Chapter 2 Cardiovascular Physiology 87 6. Increased systemic venous pressure and jugular vein distension are the sine qua non deining characteristics of right ventricular failure. During what portion of the cardiac cycle is the fourth heart sound heard? What is the meaning of an audible fourth heart sound? Why did right ventricular failure lead to edema on the systemic side of the circulation e.

Discuss the Starling forces involved. Would you expect pulmonary edema to be present in right ventricular failure? Celia very much wanted to attend a family reunion in Denver. Why is ascent to high altitude so dangerous in a person with pulmonary hypertension? Knowledge of pulmonary physiology is necessary to answer this question. To explain why increased pulmonary vascular resistance caused by intrinsic pathology of the small pulmonary arteries led to increased pulmonary artery pressure, it is necessary to think about the relationship between pressure, low, and resistance.

Recall this relationship from Case Increased blood volume in the pulmo- nary arteries caused increased pressure. Pulmonary vascular resistance is calculated by rearranging the equation for the pressure, low, resis- tance relationship.

Pulmonary blood low is equal to the cardiac output of the right ventricle, which, in the steady state, is equal to the cardiac output of the left ventricle. Thus, the values needed to calculate pulmonary vascular resistance are pulmo- nary artery pressure, pulmonary vein pressure or left atrial pressure , and cardiac output.

Afterload of the ventricles is the pressure against which the ventricles must eject blood. Afterload of the right ventricle is pulmonary artery pressure. For blood to be ejected during systole, left ventricular pressure must increase above aortic pressure and right ventricular pressure must increase above pulmonary artery pressure.

Much more work was required to develop the pressure required to open the pul- monic valve and eject blood into the pulmonary artery. As a result, right ventricular stroke vol- ume, cardiac output, and ejection fraction were decreased. Right ventricular end-systolic volume was increased, as blood that should have been ejected into the pulmonary artery remained in the right ventricle.

Celia had cor pulmonale, or right ventricular failure secondary to pulmonary hypertension. Right ventricular pressure increased because more blood than usual remained in the ventricle after systolic ejection. As right ventricular pressure increased, it was more dificult for blood to move from the right atrium to the right ventricle; as a result, right atrial volume and pressure also increased.

Pulmonary capillary wedge pressure left atrial pressure was normal, suggesting that there was no failure on the left side of the heart. The right ventricular wall thickens hypertrophies as an adaptive mechanism for performing more work.

This adaptive response is explained by the law of Laplace for a sphere a sphere being the approximate shape of the heart: The thicker the ventricular wall, the greater the pressure that can be devel- oped at a given tension.

A fourth heart sound is not normally audible in adults. However, it may occur in ventricular hypertrophy, where ventricular compliance is decreased. During illing of a less compliant ventricle, blood low produces noise the fourth heart sound. Thus, when it is present, the fourth heart sound is heard during atrial systole. As already explained, right ventricular failure caused blood to back up into the systemic veins, which increased systemic venous pressure.

The Starling forces that determine luid movement across capillary walls can be used to explain why edema would form on the systemic side of the circulation e. Starling pressures across the capillary wall. There are four Starling pressures or forces across the capillary wall: In most capillary beds, the Starling pressures are such that there is a small net iltration of luid that is returned to the circulation by the lymphatics.

The answer lies in her increased systemic venous pressure, which caused an increase in capillary hydrostatic pressure Pc. Increases in Pc favor iltration. Pulmonary edema would not be expected to occur in right ventricular failure.

Pulmonary edema occurs in left ventricular failure, where blood backs up behind the left ventricle into the left atrium and pulmonary veins. An increase in pulmonary venous pressure then leads to increased pulmo- nary capillary hydrostatic pressure and increased iltration of luid into the pulmonary intersti- tium.

At high altitude, barometric pressure is decreased, resulting in decreased partial pressure of atmo- spheric gases, such as O2.

If Celia had traveled to Denver, she would have breathed air with a lower PO2 than the air at sea level. Such alveolar hypoxia produces vasoconstriction in the pulmonary cir- culation normally a protective mechanism in the lungs that diverts blood low away from hypoxic areas. The so-called hypoxic vasoconstriction at high altitude would have further increased her pulmonary vascular resistance and pulmonary arterial pressure, and further increased the afterload on her right ventricle.

Incidentally, hypoxic vasoconstriction is unique to the lungs.

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