11 The cardiovascular system
The cardiovascular system has a significant impact on the patient recovering from anesthesia. Fortunately, there are many ways available to monitor its status. The cardiovascular system also reflects the status of the patient in the postanesthesia care unit (PACU). More specifically, a return to normal values by the cardiovascular system is a good indicator of the progression of emergence of the patient from anesthesia.1
In addition, many drugs used for anesthesia depend on the cardiovascular system to produce their effects. Many of the same drugs also have effects on the cardiovascular system. As a result, the perianesthesia nurse must understand the physiologic principles that relate to the cardiovascular status of the patient in the PACU who has received an anesthetic.
The basic anatomy of certain structures of the cardiovascular system is not covered completely in this chapter because basic nursing texts provide ample material on this subject. However, the clinical correlation between the physiology of the cardiovascular system and perianesthesia nursing care is provided throughout the chapter.2
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. 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
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. 11-1). 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
FIG. 11-1 Events of cardiac cycle, showing changes in left atrial pressure, left ventricular pressure, aortic pressure, ventricular volume, electrocardiogram, and phonocardiogram. A-V, Atrioventricular.
(From Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)
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.3,4
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 that remains in the ventricle at the end of systole is end-systolic volume and amounts to approximately 50 mL.3,4
Cardiac output 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 cardiac output is approximately 4900 mL. This estimate can be derived with taking the rate of 70 times the stroke volume of 70 mL. User-friendly sophisticated equipment is available to monitor a patient’s cardiac output in the PACU. The information derived from serial measurements of the cardiac output 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.6
The cardiac output is measured with a variety of techniques. Kaplan suggests that the thermodilution method, which uses a pulmonary artery catheter, is the clinical method of choice. For a higher degree of reproducibility, Kaplan recommends a technique of standardization in which the injectate temperature and volume, and the speed of injection, are carefully controlled and duplicated. The most reproducible results have been obtained with injections of 10 mL of cold (1° to 2° C) 5% dextrose in water. It is important to remember that the thermodilution technique measures right-sided cardiac outputs; therefore measurements of cardiac output with the thermodilution technique are usually unreliable for patients with intracardiac shunts.6,7
Other methods of calculation of the cardiac output are the Fick and Stewart 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.7
Cardiac output 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, cardiac output can be seen to play a major role in the maintenance of a normal blood pressure.6–8
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).9,10
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 that the arterial pressure in the aorta is much higher than the pressure in the arterioles, which have a small cross-sectional area.
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 should occur. 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 at most, is subjective, especially when hand blushing is slow and is rarely done in clinical practice.11
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.
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. 11-2).1,2
The heart muscle comprises three major muscle types: atrial muscle, ventricular muscle, and excitatory and conductive muscle fibers. The atrial and ventricular muscles act much like skeletal muscles. The excitatory and conductive muscles function primarily as an excitatory system for the heart and a transmission system for conducting impulses throughout the heart.
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. 11-3). 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
FIG. 11-3 Syncytial nature of cardiac muscle.
(From Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)
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).
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. 11-4). The SA node is situated at the posterior wall of the right atrium and just below the opening of the superior vena cava. The SA node generates impulses with self excitation, which 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.1,2
(From Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)
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 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
The coronary arteries furnish the heart with its blood supply. The main coronary arteries are on the surface of the heart, but smaller arteries penetrate the heart muscle to provide it with nutrients. The inner surface of the heart derives its nutrition directly from the blood in its chambers.
The coronary arteries originate at two orifices just above the aortic valve. The right coronary artery descends by the right atrium and ventricle and usually terminates as the posterior descending coronary artery. The left coronary artery is usually approximately 1 cm in length and divides into the anterior descending and circumflex arteries. The anterior descending artery usually terminates at the apex of the heart and anastomoses with the posterior descending artery. The anterior descending artery supplies part of the left ventricle, the apex of the heart, and most of the interventricular septum.
The left circumflex artery descends posteriorly and inferiorly down to and terminates in the left marginal artery or communicates with the posterior descending coronary artery. Venous drainage is with superficial and deep circuits. The superficial veins empty into either the coronary sinus or the anterior cardiac veins, both of which drain into the right atrium. The deep veins drain into the thebesian or sinusoidal channels.
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 and isoflurane (Forane), 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).12
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
Class IV: Inability to carry on any physical activity without discomfort. Symptoms of congestive failure or angina are present even at rest. With any physical activity, increased discomfort is experienced.
Modified from Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2010, Saunders.
Cardiac dysrhythmias are observed in approximately 60% 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. Therefore, in the immediate postoperative period, cardiac dysrhythmias are likely because of light anesthesia during emergence or because of the administration of drugs that alter sympathetic activity. Consequently, continuous monitoring of cardiac rate and rhythm is mandated in the PACU.14,15
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 degree of coronary obstruction and 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.15,16 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 on the basis of 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.16
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, paradoxic second heart sound, friction rub, and abnormal precordial pulsations.16
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.
Necrosis of myocardial tissue causes disruption of sarcolemma, so that the intracellular macromolecules leak into the bloodstream. Detection of such molecules in the serum, particularly cardiac-specific troponin and creatine kinase MB isoenzyme, serves important diagnostic and prognostic roles.8–11
Troponin is a cardiac specific regulatory protein in muscle cells that controls interactions between myosin and actin. Although found in both skeletal and cardiac muscles, the cardiac forms of troponin I and troponin T are structurally unique, and highly specific assays for their detection in the serum have been developed. Cardiac troponin serum levels begin to rise 3 to 4 hours after the onset of chest discomfort, peak between 18 and 36 hours, and then decline slowly, allowing for detection for up to 10 to 14 days after a large infarction.8–11
In the absence of trauma, the elevation of CK-MB is highly suggestive of myocardial injury. To facilitate the diagnosis of infarction using this marker, it is common to calculate the ratio of CK-MB to total CK. The ratio is usually greater than 2.5% in the setting of myocardial injury and less than that when CK-MB is from another source. The serum level of CK-MB starts to rise 3 to 8 hours after infarction, peaks at 24 hours, and returns to normal within 48 to 72 hours.8–11
Research studies have shown that patients who have had a myocardial infarction within 6 months before surgery have a recurrence rate of 54.5% for a myocardial infarction that could occur during or after the surgical procedure. If the myocardial infarction occurred between 6 months and 2 years before surgery, the rate of recurrence of infarction is between 20% and 25%. Between the second and third years, the incidence rate of reinfarction is approximately 5%. Most studies indicate that 3 years after the original myocardial infarction, the recurrence rate is approximately 1%, which equals the normal rate of myocardial infarction in the general population. Therefore the chance of a patient having an acute myocardial infarction in the PACU can be considered significant. This chance is especially true for patients in the PACU who have had a myocardial infarction within the last 3 years, who have a documented myocardial infarction risk factor (e.g., angina, hypertension, diabetes), or who have some combination of the previous factors.16–17