The heart is a four-chambered mass of muscle that pulsates rhythmically and pumps blood into the circulatory system. The chambers of the heart are the atria and the ventricles. The atria, which are pathways for blood into the ventricles, are thin-walled, have myocardial muscle, and are divided into the right and left atria by a partition (Fig. 11.1). During each cardiac cycle, approximately 70% of the blood flows from the great veins through the atria and into the ventricles before the atria contract. The other 30% is pumped into the ventricles when the atria contract. On contraction of the right atrium, the pressure in the heart is 4 to 6 mm Hg. The contraction of the left atrium produces a pressure of 6 to 8 mm Hg.^1,2

Heart structure shows labels (clockwise) as follows: Head and upper extremity, aorta, pulmonary artery, lungs, pulmonary veins, left atrium, mitral valve, aortic valve, left ventricle, trunk and lower extremity, inferior vena cava, right ventricle, tricuspid valve, pulmonary valve, right atrium, and superior vena cava. Cross-section of bottom part of heart shows layers labeled (top to bottom) as follows: Endocardium, myocardium, pericardium (epicardium, pericardial space, parietal pericardium, fibrous pericardium).

Three pressure elevations are produced by the atria as depicted on the atrial pressure curve. They are termed the a, c, and v waves (Fig. 11.2). The a wave is a result of atrial contraction. The c wave is produced by both the bulging of atrioventricular (AV) valves and the pulling of the atrial muscle when the ventricles contract. The v wave occurs near the end of the ventricular contraction as the amount of blood in the atria slowly increases and the AV valves close.^1–3

Combined graph for phonocardiogram, electrocardiogram, ventricular volume, ventricular pressure, atrial pressure, and aortic pressure is depicted. The vertical axis shows volume in milliliters ranging from 50 through 130, in increments of 40. Pressure in millimeters of mercury ranges from 0 through 120, in increments of 20. The regions of graph from left to right are as follows: Aortic valve opens, isovolumic contraction, ejection, isovolumic relaxation, rapid inflow, diastasis, and atrial systole. • Phonocardiogram: The curve shows fluctuations at irregular intervals. • Electrocardiogram: The curve shows a small P peak labeled, followed by Q R S complex, and small T peak. • Ventricular volume: The curve shows two troughs below 50 milliliters. • Ventricular pressure: Two high U-shaped peaks are formed at 118 millimeters of mercury. • Atrial pressure: The dashed curve at 0 runs almost horizontally and marked A-V valve closes and A-V valve opens. • Aortic pressure: The dashed curve starting at 90, runs along the peaks. Aortic valve opens before the start of peak and aortic valve closes after the end of peak. All data are approximate.

The ventricles receive blood from the atria and then act as pumps to move blood through the circulatory system. During the initial third of diastole, the AV valves open and blood rushes into the ventricles. This phase is called the period of rapid filling of the ventricles. The middle third of diastole is referred to as diastasis during which a small amount of blood moves into the ventricles. During the final third of diastole, the atria contract and the other 30% of the ventricles fills. As the ventricles contract, the AV valves contract and then close, thereby preventing blood from flowing into the ventricles from the atria.^2–4

As the ventricles begin to contract during systole, the pressure inside the ventricles increases, but no emptying of the ventricles occurs. During this time, called the period of isometric contraction, the AV valves are closed. As the right ventricular pressure rises to more than 8 mm Hg and the left ventricular pressure exceeds 80 mm Hg, the valves open to allow the blood to leave the ventricles. This period, termed the period of ejection, consumes the first three quarters of systole. The remaining fourth quarter is referred to as protodiastole when almost no blood leaves the ventricles yet the ventricular muscle remains contracted. The ventricles then relax, and the pressure in the large arteries pushes blood back toward the ventricles, which forces the aortic and pulmonary valves to close. This phase is the period of isometric relaxation.

At the end of diastole, each ventricle usually contains approximately 120 mL of blood—the end-diastolic volume. During systole, each ventricle ejects 70 mL of blood, which is the stroke volume. The blood remaining in the ventricle at the end of systole is end-systolic volume and amounts to approximately 50 mL.^2–4

Cardiac Output

Cardiac output (CO) is the amount of blood ejected from the left or right ventricle in 1 minute. In the normal adult with a heart rate of 70 bpm, the CO is approximately 5000 to 6000 mL/minute. This estimate can be derived by taking the rate of 70 bpm times the stroke volume of 70 mL. CO is a surrogate of oxygen delivery and important as part of hemodynamic monitoring in critically ill surgical patients.5 User-friendly sophisticated equipment is available to monitor a patient’s CO in the PACU. The information derived from serial measurements of the CO can be helpful in assessing the general status of the cardiovascular system and determining the appropriate amount and type of fluid therapy for the patient.^5,6

The CO is measured via a variety of techniques. Methods of calculation of the CO include the Fick and Stewart-Hamilton techniques. The Fick technique involves calculations of the amount of blood needed to carry oxygen taken up from the alveoli per unit of time. This technique is said to be accurate within a 10% margin of error. In the Stewart technique, a known quantity of dye is injected, and its concentration is measured after the dye is dispersed per unit of time.^5,6 These methods are difficult to use in practice, so other methods of use are more common.⁷

The thermodilution method, which uses a pulmonary artery catheter, is the clinical method of choice and gold standard for calculating CO.^7,8 For a higher degree of reproducibility, technique of standardization in which the injectate temperature and volume and the speed of injection are carefully controlled and duplicated is recommended. The most reproducible results have been obtained with injections of 10 mL of cold (1° C to 2° C) 5% dextrose in water. It is important to remember that the thermodilution technique measures right-sided COs; therefore, measurements of CO with the thermodilution technique are usually unreliable for patients with intracardiac shunts.^3,6–8 Recently, transpulmonary thermodilution has been used to attempt to decrease the complications associated with pulmonary artery thermodilution.^7,8 An arterial cannula with a thermistor is placed in the femoral, axillary, or brachial artery. Cold saline is injected into a central venous catheter. Transpulmonary thermodilution measures left heart CO. A high degree of correlation has been established between the two forms of thermodilution.^7,8 The esophageal Doppler method is a minimally invasive method of measuring CO. The device measures blood flow in the descending aorta. There is much evidence that supports its use and guidelines advocate its use.^7,8 Transthoracic echocardiography is also a Doppler option that has also been shown to be accurate.⁵

CO can be influenced by venous return. If the heart receives an extra amount of blood from the veins (↑ preload), the cardiac muscle becomes stretched and the stretched muscle contracts with an increased force to pump the extra blood out of the heart. If the heart receives less blood than normal (↓ preload), according to the Frank-Starling law of the heart, it contracts with less force. This concept is important to the perianesthesia nurse. For example, if a patient is undergoing mechanical ventilation and too much positive end-expiratory pressure is overinflating the lungs, the increased pressure on the inferior vena cava impedes the venous return to the heart, thereby decreasing blood pressure. The blood pressure is derived from the following interacting factors: the force of the heart, the peripheral resistance, the volume of blood, the viscosity of blood, and the elasticity of the arteries. Thus, CO can be seen to play a major role in the maintenance of a normal blood pressure.^1–4,9

Arterial Blood Pressure

The arterial blood pressure consists of the systolic and diastolic arterial pressures. The systolic blood pressure is the highest pressure that occurs within an artery during each contraction of the heart. The diastolic blood pressure is the lowest pressure that occurs within an artery during each contraction of the heart. The mean arterial pressure is the average pressure that pushes blood through the systemic circulatory system. Methods of assessing and monitoring the arterial blood pressure in the PACU are discussed in Chapter 27.

Some factors that affect the arterial blood pressure are the vasomotor center, the renal system, vascular resistance, the endocrine system, and chemical regulation. The vasomotor center, located in the pons and the medulla, has the greatest control over the circulation. This center picks up impulses from all over the body and transmits them down the spinal cord and through vasoconstrictor fibers to most vessels of the body. These impulses can be excitatory or inhibitory. One type of pressoreceptor that sends impulses to the vasomotor center is the baroreceptor. The baroreceptors are located in the walls of the major thoracic and neck arteries, in particular the arch of the aorta. When these vessels are stretched by an increased blood pressure, they send inhibitory impulses to the vasomotor center, which lowers the blood pressure. The aortic and carotid bodies located in the bifurcation of the carotid arteries and along the aortic arch can increase systemic pressure when stimulated by a low partial pressure of oxygen in arterial blood (PaO₂).^10,11 The renal regulation of arterial pressure occurs through the renin-angiotensin-aldosterone mechanism (see Chapter 13).

The vascular resistance of the systemic vascular system can alter systemic pressure. As the total cross-sectional area of an artery decreases, the systemic vascular resistance increases. Therefore, as the blood flows out of the aorta, a decrease in the arterial pressure in each portion of the systemic circulation is directly proportional to the amount of vascular resistance. This principle is the reason the arterial pressure in the aorta is much higher than the pressure in the arterioles, which have a small cross-sectional area.

The nervous system, when stimulated with exercise or stress, elevates the arterial pressure via sympathetic vasoconstrictor fibers throughout the body.

Historically, when the radial artery was to be cannulated for direct monitoring of blood pressure and sampling of arterial blood gases in the PACU, a modified Allen test was performed. This test was used for assessing the risk of hand ischemia if occlusion of the cannulated vessel occurred. The modified Allen test is performed with the patient making a tight fist, which partially exsanguinates the hand. The nurse then occludes both the radial and the ulnar arteries with digital pressure. The patient is asked to open the hand, and the compressed radial artery is then released. Blushing of the palm (postischemic hyperemia) should be observed. After approximately 1 minute, the test should be repeated on the same hand with the nurse now releasing the ulnar artery while continuing to compress the radial artery. If the release of pressure over the ulnar artery does not lead to postischemic hyperemia, the contralateral artery should be similarly evaluated. The results of the modified Allen test should be reported as “refill time” for each artery. The modified Allen test is subjective at most and rarely used in clinical practice.¹²

Valves of the Heart

The semilunar valves are the aortic and pulmonary valves. They consist of three symmetric valve cusps, which can open to the full diameter of the ring yet provide a perfect seal when closed. During diastole, they prevent backflow from the aorta and pulmonary arteries into the ventricles (see Fig. 11.1)

The AV valves are the tricuspid and mitral valves. These valves prevent blood from flowing back into the atria from the ventricles during systole.

Attached to the valves are the chordae tendineae, which are attached to the papillary muscles, which in turn are attached to the endocardium of the ventricles. When the ventricles contract, so do the papillary muscles, thus pulling the valves toward the ventricles to prevent bulging of the valves into the atria (Fig. 11.3).^1,2

Heart Muscle

The cardiac muscle fibers are arranged in a latticework; they divide and then rejoin. The constriction of the cardiac muscle fibers facilitates action potential transmission. The muscle is striated, and the myofibrils contain myosin and actin filaments. Cardiac muscle cells are separated by intercalated disks, which are actually the cardiac cell membranes that separate the cardiac muscle cells from one another. The intercalated disks do not hinder conductivity or ionic transport between cardiac muscle cells to any great extent. When the cardiac muscle is stimulated, the action potential spreads to excite all the muscles, which is called a functional syncytium (Fig. 11.4). This functional syncytium can be divided into atrial and ventricular syncytia, which are separated by fibrous tissue. However, an impulse can be transmitted throughout the atrial syncytium and then via the AV bundle to the ventricular syncytium. The “all-or-none” principle is in effect; when one atrial muscle fiber is stimulated, all the atrial muscle fibers react if the action potential is met. This principle applies to the entire ventricular syncytium as well.^1,2

The main properties of cardiac muscle are excitability (bathmotropism), contractility (inotropism), rhythmicity and rate (chronotropism), and conductivity (dromotropism). When cardiac muscle is excited, its action potential is reached and the muscle contracts. Certain chemical factors alter the excitability and contractility of cardiac muscle (Box 11.1).

Conduction of Impulses

The heart has a special system for generating rhythmic impulses. This system for providing rhythmicity and conductivity consists of the sinoatrial (SA) node, the AV node, the AV bundle, and the Purkinje fibers (Fig. 11.5). The SA node is situated at the posterior wall of the right atrium just below the opening of the superior vena cava. The SA node generates impulses with self-excitation and is the fastest pacemaker of the heart. It is produced by the interaction of sodium and potassium ions. The SA node provides a rhythmic excitation approximately 72 times per minute in an adult at rest. The action potential then spreads throughout the atria to the AV node via several tracts and has been implicated in abnormal atrial rhythms such as atrial flutter and fibrillation.^1,2

The AV node is located at the base of the wall between the atria. Its primary function is to delay the transmission of the impulses to the ventricles, which allows time for the atria to empty before the ventricles contract. The impulses then travel through the AV bundle, sometimes called the bundle of His. The AV node is able to discharge impulses 40 to 60 times per minute if not stimulated by an outside source.

The Purkinje fibers originate at the AV node, form the AV bundle, divide into the right and left bundle branches, and spread downward around the ventricles. The Purkinje fibers can transmit the action potential rapidly, thus allowing immediate transmission of the cardiac impulse throughout the ventricles. The Purkinje fibers are able to discharge impulses between 15 and 40 times per minute if not stimulated by an outside source. The Purkinje fibers have been implicated in right and left bundle branch conduction delays, which can lead to slower blood supply to the ventricles.

The parasympathetic nerve endings are distributed mostly at the SA and AV nodes, over the atria, and to a lesser extent over the ventricles. If stimulated, they produce a decrease in the rate of rhythm of the SA node and slow the excitability at the AV node. The sympathetic nerves are distributed at the SA and AV nodes and all over the heart, especially the ventricles. Sympathetic stimulation increases the SA node rate of discharge, increases cardiac excitability, and increases the force of contraction.^1,2

Coronary Circulation

The regulation of coronary blood flow is determined primarily with the oxygen tension of the cardiac tissues. The most powerful vasodilator of the coronary circulation is hypoxemia. Other factors that can affect coronary blood flow are carbon dioxide, lactate, pyruvate, and potassium, all of which are released from the cardiac muscle. Coronary artery steal occurs when collateral perfusion of the myocardium is significantly reduced by an increase in blood flow to a portion of the myocardium that is normally perfused. More specifically, drug-induced vasodilatation of normal coronary arterioles can then divert or steal blood flow from potentially ischemic areas of the myocardium perfused by the vessels that have increased resistance (atherosclerotic vessels). Coronary artery steal can occur when arteriolar-vasodilating drugs such as nitroprusside are administered. This situation is especially likely to occur in people who are “stealprone”; they constitute approximately 23% of the patients with coronary artery disease, especially patients who have significant stenosis and occlusions to one or more coronary arteries.^1,2

Stimulation of the parasympathetic nervous system causes an indirect decrease in coronary blood flow. Direct stimulation is slight because of the sparse amount of parasympathetic nerve fibers to the coronary arteries. The sympathetic nervous system serves to increase coronary blood flow both directly (as a result of the action of acetylcholine and norepinephrine) and indirectly (caused by a change in the activity level of the heart). The coronary arteries have both alpha and beta receptors in their walls see the section on Adrenergic and Cholinergic Receptors later in this chapter.^1,2

Because so much cardiac disease involves the coronary arteries, the anesthetic risk rate increases in patients with cardiac disease. A functional classification of cardiac cases is based on the ability to perform physical activities (Box 11.2). Patients in classes III and IV have a significant risk for surgery and anesthesia and should undergo complete monitoring when they receive care in the PACU.¹³

Effect of Anesthesia on the Heart

Cardiac dysrhythmias are observed in over half of all patients who undergo anesthesia.^14,15 The inhalation anesthetics, such as isoflurane, sevoflurane, and desflurane, can evoke junctional rhythms or increase ventricular automaticity or both. These anesthetics also slow the rate of SA node discharge and prolong the bundle of His-Purkinje and ventricular conduction times. Along with these changes in rhythm, alterations in the balance of the autonomic nervous system between the parasympathetic and sympathetic systems caused by drugs such as anticholinergics and catecholamines or by light anesthesia can initiate cardiac dysrhythmias. QT intervals may be elongated by drugs including but not limited to ondansetron and droperidol with the potential of predisposing patients to torsade de pointes.¹⁶ Therefore, in the immediate postoperative period, cardiac dysrhythmias are likely because of light anesthesia during emergence, patient factors such as preexisting comorbidities, and because of the administration of drugs that alter sympathetic activity and fluid shifts intraoperatively, which can cause electrolyte imbalances. Consequently, continuous monitoring of cardiac rate and rhythm is mandated in the PACU.^15,17 With the increased use of regional anesthesia for procedures in the perioperative setting, signs and symptoms of anesthesia toxicity must be monitored. Regional blocks using epinephrine in conjunction with sedation medications may have an adverse effect on the cardiovascular system. Symptoms initially present as hypertension and tachycardia, which untreated can lead to progressive hypertension and dysrhythmias. Depending on the medications administered, side effects involving the cardiovascular system can by masked by sedation medication.¹⁸

Myocardial Infarction

Acute myocardial infarction is a commonly encountered medical emergency that can occur in the PACU. More than 90% of myocardial infarctions result from disruption of an atherosclerotic plaque with subsequent platelet aggregation and formation of an intracoronary thrombus. The form of myocardial infarction that results depends on the location and the degree of coronary obstruction as well as associated ischemia. A partially occlusive thrombus is the typical cause of non–ST-elevation myocardial infarction. At the other end of the spectrum, if the thrombus completely obstructs the coronary artery, the results are more severe ischemia and a larger amount of necrosis, manifesting as an ST-elevation myocardial infarction.19 The objectives in the management of a patient with an acute myocardial infarction are pain relief, control of complications, salvage of ischemic myocardium, and a return to a productive life. The diagnosis of myocardial infarction is made based on clinical findings, and therapy should be instituted immediately when suspected. (Cardiopulmonary resuscitation is discussed in Chapter 57.) An electrocardiogram performed in the PACU may reveal an injury pattern, but normal electrocardiographic results certainly do not exclude a diagnosis of myocardial infarction.¹⁹

Physical assessment for a suspected myocardial infarction can include the following subjective findings: (1) pain or pressure, which is usually substernal but may be manifested in the neck, shoulder, jaws, arms, or other areas; (2) nausea; (3) vomiting; (4) diaphoresis; (5) dyspnea; and (6) syncope. The onset of pain can occur with activity but can also occur at rest. The duration may be prolonged, from 30 minutes to several hours. Objective findings can include hypotension, pallor, and anxiety. The blood pressure, pulse, and heart sounds may be normal with an acute myocardial infarction. On auscultation of the chest, the abnormal cardiac findings may include atrial gallop, ventricular gallop, paradoxical second heart sound, friction rub, and abnormal precordial pulsations.¹⁹

The electrocardiographic pattern can vary by the location and extent of the infarction, but myocardial damage can occur without changes in the electrocardiogram. Some typical features of a transmural infarction are acute ST-segment elevation in leads that reflects the area of injury, abnormal Q waves, and T wave inversion.

Perianesthesia Nursing Care

The perianesthesia nurse should be constantly alert for complications such as anxiety, arrhythmias, shock, left ventricular failure, and pulmonary and systemic embolisms. Pain and apprehension can be relieved with treatment with morphine sulfate, fentanyl, or hydromorphone (Dilaudid). Oxygen should be administered with nasal prongs because a face mask may increase the patient’s apprehension. Continuous cardiac monitoring should be instituted, and the patient should be kept in a quiet area. Drugs such as atropine, lidocaine, digitalis, quinidine, sodium nitroprusside (SNP), phentolamine, and nitroglycerin should be available. A machine for countershock also should be immediately available. Fluid therapy and urine output should be monitored completely for prevention of fluid overload. A pulmonary artery catheter or central venous pressure (CVP) monitor may be used for determining fluid replacement in patients with reduced intravascular volume and hypotension (see the discussion of CVP catheters in the following section). A benign myocardial infarction does not exist; all patients with a diagnosed myocardial infarction need constant competent perianesthesia care.^9,19

RBCs are produced by the bone marrow. The normal rate of production is sufficient to form approximately 1250 mL of new blood per month. This rate is also the normal rate of destruction. The average life span of an RBC is 120 days. The hematocrit value is the percentage of RBCs in the blood. The optimal hematocrit range in adults is between 30% and 42%. When the hematocrit level is reduced to less than 30%, the oxygen-carrying capacity declines steeply. Moreover, when the hematocrit level rises to greater than 55%, the oxygen-carrying capacity declines because the increase in blood viscosity causes increased work for the heart and decreased CO. The normal amount of hemoglobin in the RBC ranges from 10 g to 13.5 g. In fact, the amount and type of hemoglobin determine the oxygen-carrying capacity. Recent evidence indicates that the cutoff value for risk of reduced oxygen-carrying capacity and blood volume is a hemoglobin level of 11 g, a hematocrit of 27%, or both. Transfusion with blood or blood products to raise the level of hemoglobin should be strongly considered for any patient with values lower than the cutoff values.2

White Blood Cells

White blood cells (WBCs), or leukocytes, are the body’s major defense against infection. The two primary types of circulating leukocytes are polymorphonuclear leukocytes (PMNs) and lymphocytes. The role of the PMNs in combating infection is to migrate to the infectious site in large numbers and phagocytize the invading microbe. The role of the lymphocytes is to mediate immunoglobulin production and act in the delayed hypersensitivity in the type IV reaction (see Chapter 18). Evaluations of the WBC count should focus on the number of PMNs. When the PMN level is less than 1000 per mm³, the incidence rate of infections is increased. Postanesthesia patients with a PMN level of 500 to 100 per mm³ are at great risk of infection.²

Some of the major clinical situations that cause a reduction in PMN levels (leukopenia) are viral infections including human immunodeficiency virus and cancer chemotherapy.

Blood Platelets

Normal hemostasis requires a proper interaction among blood vessels, platelets, and coagulation proteins. Any dysfunction in any one of the three components has a profound effect on hemostasis. When a tissue injury occurs, the vessel wall undergoes vasoconstriction and activates the extrinsic pathway for coagulation proteins. Platelet adhesion and aggregation occur along with the activation of the intrinsic and extrinsic pathways for the coagulation proteins. The result of this interaction is a hemostatic plug.2

Clinical evaluation for proper coagulation focuses on the following four tests: bleeding time (BT), platelet count (PC), prothrombin time (PT), and partial thromboplastin time (PTT). The BT and PC are tests for evaluation of platelet function, and the PT and PTT are tests for evaluation of the coagulation system.

A prolongation of the BT and surgically related hemorrhage seem to be correlated. The normal BT is between 2 and 11 minutes. The test results are considered abnormal when the BT is longer than 12 minutes. The template procedure should be used when the BT is performed because it is more sensitive than older methods. The normal PC is between 200,000 and 450,000 per mm³. More specifically, the patient usually tolerates surgery and the postanesthesia phase well in regard to hemostasis with a PC of 100,000 per mm³ or higher. Patients with a PC of 50,000 to 100,000 per mm³ may have ecchymoses from tissue trauma. If the PC is less than 50,000 per mm³, many alterations in bleeding may occur. These patients need constant evaluation and therapy in the postoperative period.^4,11

The PTT is a test for evaluation of the intrinsic and common coagulation pathways of the coagulation system and is most commonly used for monitoring heparin therapy. Normal results are 33 to 45 seconds, depending on the reagent.¹¹ The PT is used to examine the extrinsic coagulation system for evaluation of oral anticoagulant therapy. Normal results are based on laboratory control for interpretation. Usually, the control is normal in patients with an appropriately functioning extrinsic coagulation system. When the value is more than 3 seconds greater than the control, the test results are considered as abnormal. The international normalized ratio (INR) evaluates the extrinsic and common pathway independently of various reagents used in different laboratory settings and in different areas of the world. The normal INR is 0.9 to 1.3.² Many institutions report both the PT and INR values.⁹ Postoperative bleeding can occur when the patient’s preoperative or intraoperative coagulation study results are abnormal. Bleeding tendencies are enhanced by the presence of postoperative hypertension. In addition, when hemostasis is lacking at the suture line or extensive surgical tissue trauma exists, the likelihood of postoperative bleeding is increased. Finally, the use of antibiotics during and after surgery can also increase bleeding tendencies. Therefore, the perianesthesia nurse should evaluate the patient’s preoperative and intraoperative coagulation study results and examine the surgical incision for bleeding during initial assessment. Certainly, the postoperative trauma patient who has undergone extensive surgical trauma should be constantly monitored for bleeding tendencies, especially if intraoperative antibiotics were administered. If the patient is undergoing anticoagulant therapy, continued monitoring of the anticoagulant activity is mandated. Finally, in the patient with a demonstrated bleeding tendency, maintenance of a normal arterial blood pressure must be ensured.²¹ For a complete review of the fluid and electrolyte administration, see Chapter 14.

Blood Vessels

The circulatory system can be divided into the systemic and the pulmonary circulation. The systemic or peripheral circulation comprises arteries, arterioles, capillaries, venules, and veins. The walls of the blood vessels, except the capillaries, are composed of three distinct coats: the tunica adventitia, the tunica media, and the tunica intima. The outer layer, the tunica adventitia, consists of white fibrous connective tissue, which gives strength to and limits the distensibility of the vessel. The vasa vasorum, which supplies nourishment to the larger vessels, is in this layer. The middle layer, the tunica media, consists of mostly circularly arranged smooth muscle fibers and yellow elastic fibers. The innermost layer, the tunica intima, is a fine transparent lining that serves to reduce resistance to the flow of blood. The valves of the veins are formed by the foldings of this layer. The capillaries consist of a single layer of squamous epithelial cells, which is a continuation of the tunica intima.2

The arteries are characterized by elasticity and extensibility. The veins have a poorly developed tunica media and are therefore much less muscular and elastic than arteries.

Microcirculation

Microcirculation is the flow of blood in the finer vessels of the body. It involves the arterioles, capillaries, and venules. The arteries subdivide to the last segment of the arterial system, the arteriole. The arteriole consists of a single layer of smooth muscle in the shape of a tube for conducting blood to the capillaries. As the arterioles approach the capillaries, they lack the coating of smooth muscle and are termed metarterioles. At the point at which the capillaries originate from the metarterioles, a smooth muscle fiber (the precapillary sphincter) encircles the capillary. At the other end of the capillary is the venule, which is larger but has a much weaker muscular coat than the arteriole.2

The capillaries are usually no more than 4 to 9 mcg in diameter, which is barely large enough for corpuscles to pass through in single file. Blood moves through the capillaries in intermittent flow caused by the contraction and relaxation of the smooth muscle of the metarterioles and the precapillary sphincter. This motion is termed vasomotion. The metarterioles and precapillary sphincter open and close in response to oxygen concentration in the tissues—a form of local autoregulation.

The microcirculation serves three major functions: (1) transcapillary exchange of nutrients and fluids, (2) maintenance of blood pressure and volume flow, and (3) return of blood to the heart and regulation of active blood volume.²

Functional Anatomy: The Mediators

Cholinergic is a term used to describe the nerve endings that liberate acetylcholine. The cholinergic neurotransmitter, acetylcholine, is present in all preganglionic parasympathetic fibers, all preganglionic sympathetic fibers, all postganglionic parasympathetic fibers, and all somatic motor neurons. Two exceptions to the general rule are postganglionic sympathetic fibers to the sweat glands and the vasculature of skeletal muscle. These fibers are considered sympathetic anatomically but cholinergic in terms of their neurotransmitter (i.e., they release acetylcholine as their neurotransmitter).^22,23

The term adrenergic is used to describe nerves that release norepinephrine as their neurotransmitter. Epinephrine may be present in the adrenergic fibers in small quantities, usually representing less than 5% of the total amount of both epinephrine and norepinephrine. The adrenergic fibers are the postganglionic sympathetic fibers, with the exception of the postganglionic sympathetic fibers to the sweat glands and the efferent fibers to the skeletal muscle^22,23 (Fig. 11.6).

A) Sympathetic division: Preganglionic neuron (cholinergic) in C N S leads to A C h released. Cholinergic (nicotinic) receptors bind to axon in P N S, followed by postganglionic neuron (adrenergic) and release of N E. A cell to the right shows labels for adrenergic (alpha or beta) receptors and effector cell. B) Sympathetic division: Preganglionic neuron (cholinergic) in C N S leads to A C h released. Cholinergic (nicotinic) receptors bind to axon in P N S, followed by postganglionic neuron (cholinergic). Thereafter, A C h is released. Cholinergic (muscarinic) receptors bind to effector cell. C) Parasympathetic division: Preganglionic neuron (cholinergic) in C N S leads to A C h released. Cholinergic (nicotinic) receptors bind to axon in P N S, followed by postganglionic neuron (cholinergic). Cholinergic (muscarinic) receptors bind to effector cell.

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