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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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.
Linda S. Costanzo, Ph. Autonomic Nervous System 33 I. Sensory Systems 37 IIL. In order for action potentials to be conducted in myelinated nerves, there must be periodic breaks in the myelin sheath at the nodes of Ranvier. In myelinated nerves, these Na and K channels are not distributed along the entire axon membrane, but are concentrated at nodes of Ranvier. Thus, at the nodes, the ionic currents, necessary for the action potential, can low across the membrane.
Between nodes, membrane resistance is very high and current is forced to low rapidly down the nerve axon to the next node, where the next action potential can be generated. Myelinated axon. Action potentials can occur at nodes of Ranvier. Multiple sclerosis is the most common demyelinating disease of the central nervous system.
In other words, current decays more rapidly decreased length constant as it lows down the axon and, because of this decay, may be insuficient to generate an action potential when it reaches the next node of Ranvier. Neuromuscular Transmission Wendy Chu is a year-old photographer for a busy local newspaper. She had severe eyestrain when she read for longer than 15 min. She became tired when she chewed her food, brushed her teeth, or dried her hair; and she had extreme fatigue on the job.
Wendy is not a complainer, but she began to worry about these vague symptoms. She was evaluated by her physician, who suspected myasthenia gravis.
While awaiting the results of a serum antibody test, the physician initiated a trial of pyridostigmine, an acetylcholinesterase inhibitor. Wendy immediately felt better while taking the drug; her strength returned to almost nor- mal. Meanwhile, the results of the antibody test were positive, conirming the diagnosis of myasthe- nia gravis. What steps are involved in neuromuscular transmission? Against what protein is this antibody directed?
Using your description of neuromuscular transmission, explain why severe muscle weakness e. Why does pyridostigmine, an acetylcholinesterase inhibitor, improve muscle strength in myas- thenia gravis?
Consider the following drugs that act at various steps in neuromuscular transmission. What is the action of each drug, and which drugs are contraindicated in myasthenia gravis? Botulinus toxin Curare Neostigmine Hemicholinium 6. Lambert—Eaton syndrome is another neuromuscular disease that has symptoms of progressive muscle weakness and fatigue. The antibodies bind to the channels and prevent Ca entry into motoneuron ter- minals, thus preventing depolarization and release of acetylcholine.
In experimental models of myasthenia gravis and Lambert—Eaton syndrome, one can repetitively stimulate the motoneu- rons and observe the action potentials produced in the skeletal muscle ibers that they innervate. Based on the pathophysiology of the two diseases, what effect on skeletal muscle action potentials would you expect with repetitive motoneuron stimulation?
Given the difference that you predict, what role might repetitive nerve stimulation play in the treatment of the two diseases? Neuromuscular transmission is the process whereby an action potential in a motoneuron produces an action potential in the muscle ibers that it innervates. The steps in neuromuscular transmis- sion, shown in Figure 1—12, are as follows: As a result, depolarization occurs. Through this elaborate sequence of events, an action potential in the motoneuron causes an action potential in the muscle ibers that it innervates.
Steps in neuromuscular transmission. The numbers correspond to the steps discussed in the text. Accordingly, the antibody is called AChR-ab. In myasthenia gravis, abnormal antibodies to AChR AChR-ab are produced, circulate in the blood, and bind to nicotinic receptors on the muscle end plates.
When antibodies are bound to AChR, the receptors are not available to be activated by the ACh that is released physiologically from moto- neurons. Thus, while normal action potentials occur in the motoneurons and ACh is released normally, the ACh cannot cause depolarization of muscle end plates. Without depolarization of muscle end plates, there can be no action potentials or contraction in the muscle. After ACh binds to and activates AChR on the muscle end plate, it is degraded by acetylcholinesterase, an enzyme that is also present on the muscle end plate.
This degradative step, whose byproducts are choline and acetate, terminates the action of ACh on the muscle iber. Choline is taken up into the motoneuron terminal and recycled into the synthesis of more ACh. Pyridostigmine is an acetylcholinesterase inhibitor that binds to acetylcholinesterase and thereby reduces binding and degradation of ACh at the muscle end plate. In the treatment of myasthenia gravis, pyridostigmine prevents the degradation of ACh, increasing its synaptic concentration and prolonging its action.
The longer the muscle end plate is exposed to high concentrations of ACh, the greater the likelihood that action potentials and contraction in the muscle will occur. Chapter 1 Cellular and Autonomic Physiology 35 5. In principle, any drug that interferes with any step in neuromuscular transmission is contraindi- cated in myasthenia gravis.
Botulinus toxin blocks the release of ACh from motoneuron terminals and therefore causes total blockade of neuromuscular transmission; it is contraindicated in myas- thenia gravis. Curare, a competitive inhibitor of ACh for the AChR on the muscle end plate, pre- vents depolarization of the muscle iber; it is contraindicated. Neostigmine is an acetylcholinester- ase inhibitor that is related to pyridostigmine and is used to treat myasthenia gravis by preventing ACh degradation.
Hemicholinium blocks the reuptake of choline into motoneuron terminals, thereby depleting stores of ACh; it is contraindicated. In myasthenia gravis, the defect lies in the AChRs on the muscle end plate, wherein antibodies to the receptors prevent ACh from binding to the end plate and depolarization; without depolariza- tion of the end plate, there can be no action potentials or contraction in the skeletal muscle.
Thus, in an experimental model of myasthenia gravis, repetitive stimulation of motoneurons will not increase the amplitude of the end plate potentials or the action potential iring in skeletal muscle. Thus, repetitive nerve stimulation would have no therapeutic value in myasthenia gravis, whereas it could increase muscle strength in Lambert—Eaton syndrome. Effects of Catecholamines Helen Ames is a year-old homemaker who experienced what she thought were severe meno- pausal symptoms. Her heart raced and pound- ed; she had a throbbing headache and visual disturbances; she felt hot, but her hands and feet were cold; and she was nauseated, sometimes to the point of vomiting.
Ames called her physician, who agreed that the symptoms were probably menopausal and prescribed hormone replacement therapy over the phone. Ames took the hormones a combination of estrogen and progester- one , but they did not relieve her symptoms. The attacks were occurring almost daily. She made an appointment with her physician. To rule out a pheochromocytoma a rare tumor of the adrenal medulla , the physician ordered a hour urine measurement of vanillylmandelic acid VMA. To his surprise, the results of the hour urinary VMA test were positive, a inding that pro- vided nearly conclusive evidence of a pheochromocytoma.
A computed tomographic scan con- irmed that Mrs. Ames had a 3-cm mass on her right adrenal gland. What is the relationship of the adrenal medulla to the autonomic nervous system?
What hormones are secreted by a pheochromocytoma? Why does an elevated urinary level of VMA a metabolite of epinephrine and norepinephrine suggest the presence of a pheochromocytoma? Why is it necessary to do a hour measurement of VMA, rather than a spot-urine test? In view of the pathophysiology of pheochromocytoma, explain Mrs. What receptors are involved in each of these symptoms? Why are two values reported for arterial pressure, and what is the signiicance of each value?
Why were both the systolic and diastolic blood pressures elevated? Is there a plausible explanation for the fact that Mrs. Ames felt hot, even though her hands and feet were cold? How did phenoxybenzamine lower Mrs. After the dosage of phenoxybenzamine was established, what was the goal of adding a low dose of propranolol?
What might have happened if Mrs. Ames had been given propranolol alone? The adrenal medulla is a specialized ganglion of the sympathetic division of the autonomic nervous system. The preganglionic neurons have their cell bodies in the thoracic spinal cord. Axons of these preganglionic neurons travel in the greater splanchnic nerve to the adrenal medulla, where they synapse on chromafin cells and release the neurotransmitter acetylcholine.
When stimulated, chromafin cells the postsynaptic unit secrete catecholamines epinephrine and norepineph- rine into the circulation Fig. Organization of the autonomic nervous system. The somatic nervous system is included for reference only. CNS, central nervous system. A pheochromocytoma is a tumor of the adrenal medulla gland that secretes large quantities of epi- nephrine and norepinephrine.
Thus, when a pheochromocytoma produces large quantities of epinephrine and norepinephrine, urinary excretion of VMA is increased. All of Mrs. In the heart, catecholamines have three major effects, each mediated by a b1 receptor: In Mrs. Ames, excess amounts of catecholamines caused the sensation that her heart was racing increased heart rate and pounding increased contractility.
In blood vessels, primarily arterioles, catecholamines cause vasoconstriction in most vascular beds e. Vasoconstriction of cutaneous blood vessels leads to decreased cutaneous blood low and cold skin, especially in the feet and hands.
In blood vessels of skeletal muscle, however, catechol- amines cause the opposite effect vasodilation through b2 receptors.
The effects on vision are explained by sympathetic effects on the eye muscles. The coordinated actions on the muscle wall and sphincters slow the motility of chyme through the gastrointestinal tract and may lead to nausea and even vomiting.
The two numbers refer, respectively, to systolic arterial pressure and diastolic arterial pressure. Arterial pressure is not expressed as a single value because systemic arterial pressure changes over the course of the cardiac cycle. Systolic pressure is the highest value for arterial pressure and is mea- sured just after blood is ejected from the left ventricle into the large arteries i.
Diastolic pressure is the lowest value for arterial pressure and is measured when the ventricle is relaxed and blood is lowing from the arteries to the veins and back to the heart i. These elevations are explained by the effects of excess catecholamines on the heart and blood vessels that have already been discussed.
Catecholamines increase both heart rate and contractility. These two effects combine to produce an increase in cardiac output the volume of blood ejected from the ventricle per minute. An increase in cardiac output means that, during systole, a greater blood volume is ejected into the arteries. This increase in arterial volume is relected in a higher systolic pressure.
In addition, catecholamines cause constriction of arterioles in many vascular beds. The preceding explanation of the effects of catecholamines on the heart and blood vessels may be somewhat misleading because it suggests that these effects are entirely independent. They are not independent, but interact as follows.
As described earlier, the vasoconstrictor effect of cate- cholamines in several vascular beds causes an increase in total peripheral resistance TPR , which increases systemic arterial pressure.
Systemic arterial pressure is the afterload of the left ventricle i. An increase in systemic arte- rial pressure, or afterload, means that the left ventricle must work harder to eject blood.
As a result, the effects of catecholamines to increase cardiac output are partially, or even completely, offset by the increase in afterload. As already discussed, Mrs. However, why would she feel hot?
The answer lies in the role of the cutaneous circulation in dissipating the heat generated by metabolism. Normally, heat is removed from the body through responses directed by the hypothalamus. These responses include decreased sympathetic outlow to the cutaneous blood vessels, resulting in vasodilation. Warm blood from the body core is shunted to the skin surface, where heat is then dissipated by convection and radiation.
When a pheochromocytoma is present, the large quanti- ties of circulating catecholamines cancel or override this cutaneous vasodilatory response. As a result, the body retains heat from metabolism that should have been dissipated.
These effects include vasoconstriction of cutaneous and splanchnic blood vessels; contraction of the sphincters of the gastrointestinal tract; and contraction of the radial muscle of the iris. As discussed earlier, one of the major reasons that Mrs.
The drugs were intentionally given in this sequence because of the effects of high levels of catecholamines on the heart and blood vessels. Recall that constriction of arterioles by catecholamines increases arterial pressure afterload. One effect of this increased afterload is that it is more dificult for the left ventricle to eject blood. Thus, increased afterload offsets the other effects of catecholamines to increase cardiac output. Once Mrs. At this point, the effects of excess catecholamines to increase cardiac output through increased heart rate and contractility would have become evident.
In other words, Mrs.
Chapter 1 Cellular and Autonomic Physiology 41 9. It would have been dangerous to give Mrs. As we have already discussed, excess circulat- ing catecholamines caused vasoconstriction of her arterioles and increased her arterial pressure afterload. Increased afterload made it more dificult for the ventricles to eject blood.
If Mrs. Central Autonomic Failure Ben Garcia was a year-old executive with a large, thriving investment company. He was well regarded among his clients as the consummate professional. He and his wife of 32 years had two children, both of whom were college graduates.
Life was great until Mr. Garcia found, to his embar- rassment, that he was occasionally impotent. Garcia was experiencing urinary problems. He felt enormous urgency to urinate, but had dificulty producing a urinary stream. His embarrassment because of the nature of his symptoms , combined with his busy schedule, kept him from seeking medical attention.
By the time he saw his physician, he had been feeling dizzy every morning for a month and had an array of symptoms that convinced him that something was terribly wrong. In addition to impotence, urinary dificulties, and dizziness when he stood up, he had double vision, indigestion, diarrhea, and heat intolerance. Garcia was referred to a neurologist who, based on the global nature of his symptoms and the results of a speciic ocular test, diagnosed him as having Shy—Drager syndrome, a rare, progressive disease of the central autonomic nervous system.
Shy—Drager syndrome is associated with degen- eration of preganglionic neurons of the intermediolateral cell column of the spinal cord, autonomic ganglia in the periphery, and autonomic centers in the hypothalamus. As a result, both the sympa- thetic and parasympathetic divisions of the autonomic nervous system are profoundly impaired.
As part of his treatment, Mr. Garcia was instructed to elevate his head during sleep and to wear support stockings to prevent blood from pooling in his veins.
He also took an aldosterone analogue to increase his blood volume.
Each of these measures was an attempt to ameliorate the dizziness and fainting that he experienced when he stood up.
Garcia and his family understood that the treat- ments were palliative and that there was no cure for his degenerative disease. He died at home at 58 years of age, 4 years after the onset of his symptoms. Which organ systems or bodily functions would you expect to be adversely affected by degenera- tion of the central autonomic nervous system? As experienced by Mr. Garcia, often the earliest symptom of Shy—Drager syndrome is impotence.
Describe the normal autonomic control of male sexual response and explain why it is impaired in patients who have central autonomic failure. Describe the autonomic control of micturition, including the functions of the detrusor muscle and the sphincters of the bladder. Why did Mr. Garcia experience urinary urgency, but was then unable to void normally? Why was Mr. Garcia heat intolerant? The ocular test involved instilling methacholine a cholinergic muscarinic agonist into the con- junctival sac.
In Mr. Garcia, methacholine caused exaggerated miosis constriction of the pupil caused by contraction of the circular muscle of the iris.
Is there a plausible explanation for why his response to methacholine was greater than that of a healthy person? Chapter 1 Cellular and Autonomic Physiology 43 6.
The hallmark of Shy—Drager syndrome is orthostatic hypotension a decrease in blood pressure that occurs when a person stands up. When a healthy person stands up, orthostatic hypotension does not occur because autonomic relexes operate to maintain a constant arterial pressure.
What are the relex responses that prevent orthostatic hypotension in healthy individuals, and why were these responses impaired in Mr. Support stockings prevent blood from pooling in the leg veins. How would these stockings have been helpful in alleviating Mr. Aldosterone and its analogues produce an increase in extracellular luid volume. How did the aldosterone analogue help to alleviate Mr.
Name three classes of drugs that would have been absolutely contraindicated in Mr.
The autonomic nervous system controls the function of virtually every organ system and every bodily function, usually as a result of an interplay between the sympathetic and parasympathetic divisions. See Table 1—5 in Case 8 to review autonomic control of organ system functions. Central failure of the autonomic nervous system, as seen in Shy—Drager syndrome, would be pre- dicted to adversely affect every organ system.
This failure affects control of arterial blood pressure; function of the bronchioles, which regulate the low of air into the lungs; motility, secretion, diges- tive, and absorptive functions of the gastrointestinal tract; illing and emptying of the bladder; male sexual response, including erection and ejaculation; function of the eye muscles that control near and far vision; activity of the sweat glands involved in thermoregulation; and metabolic func- tions of the liver and adipose tissue.
It is dificult to imagine a more comprehensive list of bodily functions, and it is easy to appreciate why Mr. Garcia was so sick. The male sexual response consists of erection and ejaculation. Erection is under parasympathetic control muscarinic receptors , which causes the venous sinuses of the corpus cavernosa to ill with blood and the penis to become erect.
The external sphincter is skeletal mus- cle, which is under trained voluntary control. Normal bladder function has two phases: When the bladder is illing with urine, sympathetic control dominates. When the bladder is full, mechanoreceptors in the wall sense the fullness and relay this information to the spinal cord and then to the brainstem, where the micturition relex is coordinated. During micturition, or emp- tying, parasympathetic control dominates.
The detrusor muscle contracts parasympathetic mus- carinic receptors , and the internal sphincter relaxes parasympathetic muscarinic receptors , allowing the bladder to empty. Garcia, both sympathetic control illing and parasympathetic control emptying of the bladder were impaired. Because of the loss of sympathetic control, his bladder did not ill normally, and he felt urinary urgency when his bladder contained a small amount of urine.
Because of the loss of parasympathetic control, his bladder could not contract forcefully enough to produce a normal urinary stream.
Thermoregulatory sweat glands are controlled by the sympathetic nervous system. This sympathetic innervation is unusual in that postganglionic neurons innervating the sweat glands release ace- tylcholine i. In contrast, most sympathetic postgan- glionic neurons release norepinephrine—i. In keeping with this unusual feature, the receptors on sweat glands are the cholinergic muscarinic type.
As the name suggests, thermoregulatory sweating is important for dissipation of the heat generated by metabolism, especially when the ambient temperature is high. Loss of sympathetic innerva- tion in Shy—Drager syndrome led to the impairment of thermoregulatory sweating and caused heat intolerance. The ocular test involved instilling a cholinergic muscarinic agonist into the eye. In healthy per- sons, the cholinergic agonist methacholine produces miosis constriction of the pupil by causing the circular muscle of the iris to contract.
Garcia, the miosis response was exaggerated.
Why would he have an exaggerated parasympathetic cholinergic response when his central para- sympathetic nervous system was impaired? 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. Part of the challenge in answering these questions will be in deciding which information you need in order to perform each calculation.
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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.
Physiology (Board Review Series)
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.
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.Because of the parallel arrangement of arteries off the aorta, renal blood low is only a fraction of the total systemic blood low.
Normal bladder function has two phases: CNS, central nervous system. 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. Meanwhile, the results of the antibody test were positive, conirming the diagnosis of myasthe- nia gravis.
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 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.
Internal K balance.