Ebook Surgical review an integrated basic and clinical science study: Part 2

(BQ) Part 2 book Surgical review an integrated basic and clinical science study presents the following contents: Cardiovascular and respiratory systems, trauma, surgical subspecialties.

Porrett_ch19.qxd 6/2/09 6:38 PM Page 263 SECTION IV Cardiovascular and Respiratory Systems Porrett_ch19.qxd 6/2/09 6:38 PM Page 264 Porrett_ch19.qxd 6/2/09 6:38 PM Page 265 CHAPTER 19 Cardiovascular Disease and Cardiac Surgery PAVAN ATLURI AND Y JOSEPH WOO KEY POINTS • On taking initial breaths the neonatal pulmonary vascular resistance drops, pressure in the left atria exceeds that in the right atria, and spontaneous closure of the foramen ovale occurs • The anterior leaflet of the mitral valve is in proximity to the aortic valve • The coronary arteries are the first branches of the aorta • Cardiac cells can maintain prolonged action potentials, conduct from cell to cell via gap junctions, and self-generate roper function of the cardiovascular system is essential to normal homeostasis Alterations in the cardiovascular system’s ability to supply oxygen- and nutrient-rich blood result in multiple organ dysfunction The heart is a complex pump with many intricate components A thorough understanding of normal cardiovascular physiology allows for an intricate understanding of cardiovascular disease processes Normal cardiovascular physiology as well as disease processes will be discussed in detail P CARDIOVASCULAR PHYSIOLOGY Fetal Circulation Oxygenated blood from the placenta is brought to the fetus via the umbilical vein Roughly half of the blood from the placenta passes through hepatic sinusoids, while the remainder bypasses hepatic circulation flowing directly into the inferior vena cava (IVC) via the ductus venosus In the IVC, oxygenated placental blood mixes with deoxygenated venous blood from the lower extremities before entering the right atrium Once in the right atrium, the majority of blood passes directly to the left atrium via the foramen ovale, thereby bypassing the pulmonary circulation Left atrial blood mixes with the small amount of deoxygenated blood in the fetal pulmonary circulation before entering the left ventricle and ultimately the ascending aorta A small portion of right atrial blood mixes with superior vena caval (SVC) blood from the head and upper extremities as well as coronary sinus blood and passes into the right ventricle (5% to 10% of total cardiac output) Since there is very high pulmonary vascular resistance (PVR) in the fetus, the majority of right ventricular blood enters the pulmonary artery (PA) and is shunted to the descending aorta via a patent ductus arteriosus (PDA) Roughly • Coronary perfusion occurs during diastole • The major resistance to blood flow occurs at the level of penetrating arteries • Myocardial oxygen demand is dependent on myocardial oxygen tension • VSD is the most common congenital heart defect • New onset murmur following a myocardial infarction may signify either a postinfarction VSD or papillary muscle rupture • Type A dissections require emergent operation, while type B dissections are managed conservatively half of the descending aortic blood passes into paired umbilical arteries and is returned to the placenta These two fetal shunts, a patent foramen ovale (PFO) and PDA, allow many neonates born with cyanotic congenital heart disease to survive Figure 19.1 illustrates the fetal circulation At birth, as the placental circulation is no longer present and the neonatal lungs are expanded, the PVR is greatly reduced This allows increased pulmonary blood flow With increased pulmonary blood flow, left atrial pressure is greater than right atrial pressure This allows closure of the foramen ovale by the septum primum pressed against the septum secundum During the first days of life, this closure is reversible When an infant cries, an increase in pulmonary pressure with a right to left shunt through the foramen ovale may be present This is manifested as cyanosis in newborns Closure of the ductus arteriosus results from the release of bradykinin, which mediates contraction of the muscular ductus wall Functional closure of the ductus typically occurs within the first 15 hours after birth, and anatomic closure occurs by day 12 of parturition Prior to birth, locally produced prostaglandins maintain patency of the ductus The fibrotic, atrophied remnant of the ductus arteriosus is referred to as the ligamentum arteriosum Anatomy The human cardiovascular system is composed of the systemic circulatory system, pulmonary circulation, and heart at the center of the circulatory system The heart is situated obliquely within the pericardial sac, with one third situated to the right of the median plane and two thirds to the left The right ventricle abuts the sternocostal surface and forms the anterior surface of the heart The right side of the heart receives deoxygenated systemic blood via the 265 Porrett_ch19.qxd 266 6/2/09 6:38 PM Page 266 Section IV • Cardiovascular and Respiratory Systems FIGURE 19.1 Diagram of the human circulation before birth Arrows indicate the direction of blood flow Note where oxygenated blood mixed with deoxygenated blood: in the liver (I), in the inferior vena cava (II), in the right atrium (III), in the left atrium (IV), and at the entrance of the ductus arteriosus into the descending aorta (V) (From Sadler TW Langman’s Medical Embryology 7th ed Baltimore: Williams & Wilkins; 1995:225, with permission.) superior and IVC as well as deoxygenated blood from the coronary circulation via the coronary sinus The right heart then pumps this blood through the low-pressure, high-flow pulmonary arteries Once the blood has circulated through the pulmonary circulation, it is returned to the left atrium via four posteriorly situated pulmonary veins (two superior and two inferior pulmonary veins) Blood from the left heart is ejected from the left ventricle into the systemic circulation via the aorta Valvular Anatomy The mammalian heart is composed of four one-way valves Two atrioventicular valves (mitral and tricuspid) provide unidirectional diastolic flow from the atria to the ventricles and allow a systolic pressure gradient between the atria and ventricles The semilunar valves (aortic and pulmonary) allow systolic flow and maintain a diastolic pressure gradient between the ventricles and outflow circulations The tricuspid and mitral valves are fibrous endocardium–lined valves The tricuspid valve separates the right atrium from the right ventricle and consists of a large anterior leaflet attached to the anterior wall of the heart, a posterior leaflet at the right margin, and a septal leaflet attached to the septum Three chordae tendinae are attached to the free surface of the leaflets and to the papillary muscles at the right ventricular base This apparatus prevents prolapse of the tricuspid valve leaflets into the right atrium during systole The mitral valve, located at the orifice of the left ventricle, consists of a large anterior leaflet in continuity with the posterior wall of the aorta and a smaller posterior leaflet The anterior leaflet of the mitral valve is anatomically in proximity to the aortic valve Chordae tendineae (Fig 19.2) secure the leaflets to the anterior and posterior papillary muscles and ensure coaptation of the valve leaflets during systole The aortic and pulmonic valves are situated at the outflow of the left and right ventricles, respectively The aortic valve is a trileaflet valve These leaflets are named according to the origin of the coronary arteries, namely the right coronary, left coronary, and noncoronary leaflets (Fig 19.3) Similarly, the pulmonic valve is a trileaflet valve with a right, left, and noncoronary leaflet Coronary Anatomy The coronary circulation (Fig 19.4) supplies oxygen-rich blood to the myocardium and epicardium The endocardium is in continuous contact with intracardiac blood and does not require additional blood flow The right and left coronary arteries of the heart arise just superior to the aortic valve in the coronary sinuses and are the first branches of the aorta The right coronary artery arises from the anterior (right) sinus of Valsalva in the aorta and runs along the atrioventricular (AV) Porrett_ch19.qxd 6/2/09 6:38 PM Page 267 Chapter 19 • Cardiovascular Disease and Cardiac Surgery 267 coronary arteries supply the posterior descending artery, branches to the septum, and AV node (Fig 19.5) The left coronary artery arises from the left sinus of Valsalva and passes between the left auricle (atrial appendage) and pulmonary trunk toward the anterior AV groove In 40% of the patients, the SA branch arises from the left coronary artery The left coronary artery divides at the AV groove to give off the left anterior descending artery (LAD) and circumflex coronary artery (Fig 19.5) The LAD passes anteriorly along the interventricular groove to the apex and provides septal branches that supply the anterior two thirds of the interventricular septum and diagonals that supply the anterior-lateral wall of the left ventricle The circumflex coronary artery follows the AV groove around the left border of the heart to the posterior surface of the heart and provides marginal branches (i.e., obtuse marginal) that supply the posterior left ventricle In 10% of the population, the circumflex coronary artery ends in the posterior descending artery, providing blood flow to the posterior one third of the interventricular septum and AV node, defining a left-side dominant circulation The venous drainage of the heart is via veins that drain into the coronary sinus as well as into smaller venae cordis minimae and anterior cardiac veins that drain into the right atrium The coronary sinus is a large vein that receives coronary venous blood from the left (great cardiac, left marginal, and left posterior ventricular veins) and right (middle and small cardiac veins) side veins It runs in the posterior AV groove FIGURE 19.2 Chordae tendineae tether the leaflets of the mitral and tricuspid valves, allowing precise coaptation during systole (From Chitwood WR Jr Mitral valve repair: ischemic In: Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery Philadelphia: Lippincott–Raven Publishers; 1998:312, with permission.) (coronary) groove In about 60% of the population, the right coronary artery gives off a sinoatrial (SA) branch near its origin to supply the SA node It traverses posteriorly toward the apex of the heart and gives off a right marginal artery, which supplies the right ventricle After giving off this branch it continues in the posterior interventricular groove In roughly 85% of patients, the posterior descending artery arises from the right coronary artery and defines a right-side dominant circulation In approximately 5% of patients, a balanced pattern exists in which the right coronary and circumflex Left coronary cusp Electrophysiology As with any striated muscle, cardiac muscle contraction is initiated by action potentials (rapid voltage changes of the cell membrane) Certain cells within the cardiac muscle are capable of acting as the pacemaker and spontaneously initiate action potentials The action potentials of cardiac muscle are special in that they can self-generate, conduct from cell to cell via gap junctions, and are long in duration Action potentials of the myocardium can be classified as either fast action potentials or slow action potentials Fast action potentials occur in normal myocardium of atria, ventricle, bundle of His, and Purkinje fibers Slow action potentials are seen in the pacemaker cells of the SA and AV nodes As seen in Figure 19.6 (solid line), fast action potentials are characterized by a rapid depolarization (phase Left coronary artery Anterior mitral leaflet Right coronary cusp Right coronary artery Noncoronary cusp Bundle of His FIGURE 19.3 Normal aortic valve from a surgeon’s point of view (From Damiano RJ Aortic valve replacement: prosthesis In: Kaiser LR, Kron IL, Spray TL, eds Mastery of Cardiothoracic Surgery Philadelphia: Lippincott–Raven Publishers; 1998:362, with permission.) Porrett_ch19.qxd 268 6/4/09 3:24 PM Page 268 Section IV • Cardiovascular and Respiratory Systems FIGURE 19.4 Anatomy of the coronary arteries and cardiac veins A Anterior view The origin of the left main coronary artery is left lateral and somewhat posterior with respect to the aorta; it courses behind the pulmonary artery and then divides into the left anterior descending and circumflex coronary arteries The origin of the right coronary artery is almost directly anterior, and it runs in the atrioventricular groove B Posterior view The great, middle, and small cardiac veins come together at the level of the coronary sinus, which lies in the left inferior atrioventricular groove and empties into the right atrium (From Greenfield LJ, Mulholland MW, Oldham KT, et al Surgery: Scientific Principles and Practice 3rd ed Philadelphia: Lippincott Williams & Wilkins; 2001:1487, with permission.) A B Right 0—transient increase in Naϩ conductance), partial repolarization (phase 1—outward movement of Kϩ), a plateau (phase 2—inward Ca2ϩ), membrane repolarization (phase 3—decreased Ca2ϩ conductance and increased Kϩ conductance), and a resting membrane potential (phase 4—equal inward and outward currents) In contrast, slow action potentials demonstrate a slower depolarization phase (phase 0), and shorter plateau and repolarization (phase 3) to an unstable slow depolarization resting phase (phase 4) The alterations in the membrane potential are a factor of a cell membrane’s permeability to particular ions (Naϩ, Kϩ, Ca2ϩ) and the resulting gradients that exists During an action potential, cardiac myocytes are in an effective refractory period (ERP) and cannot be stimulated by another action potential This occurs during phases and 2, and at the beginning of phase Shortly after this period is a relative refractory period (RRP, late phase 3), during which a supranormal action potential is needed for excitation Immediately after the action potential, before return to a normal resting state (phase 4), is the supranormal period during which the cells are hyperexcitable and require a lower than normal action potential for stimulation Once an action potential arises, it is conducted across the cell membrane to adjacent cells via gap junctions The speed of transmission of the action potential is determined by a combination of cell size and rate of depolarization The smaller cells of the pacemaker cells demonstrate a slower conduction velocity than the larger Purkinje cells Similarly, the slow response of the pacemaker cells mediates a slower conduction velocity when compared with the fast response of ventricular myocardial cells SA nodal cells demonstrate the most rapid spontaneous depolarization and hence act as the pacemaker under routine conditions This tissue lies within the wall of the right atrium at the junction of the right atrium and SVC Once the action potential is initiated in the SA node, it is propagated via the atria to the AV node The AV node is located in the interatrial septum above the tricuspid valve near the coronary sinus In pathologic conditions with SA nodal discontinuity, the AV node can act as a pacemaker The AV node protects the ventricle from excess stimulation in the case of increased atrial rates, allowing the ventricle adequate diastolic filling From the AV node, the action potential is sent to the ventricle via the bundle of His The bundle of His splits into Porrett_ch19.qxd 6/2/09 6:38 PM Page 269 Chapter 19 • Cardiovascular Disease and Cardiac Surgery 269 FIGURE 19.5 Coronary anatomy: RCA, right coronary artery; PDA, posterior descending artery; LAD, left anterior descending artery; OM, obtuse marginal artery (From P Atluri, YJ Woo The cardiovascular system In: A Atluri, GC Karakousic, PM Porrett et al., eds The Surgical Review 2nd ed Philadelphia: Lippincott Williams & Wilkins; 2005, with permission.) +25 Transmembrane potential (mV) −25 gm −50 ERP RRP SNP −75 −100 Na+ influx Ca2+ influx K+ efflux Na+ efflux right and left bundle branches and ultimately into Purkinje fibers, which conduct to the subendocardial surfaces (Fig 19.7) The autonomic nervous system (sympathetic and parasympathetic nervous systems) innervates the SA node and controls heart rate by modifying SA nodal activity The sympathetic nervous system increases heart rate by increasing the rate of depolarization In contrast, the parasympathetic nervous system increases potassium K+ influx FIGURE 19.6 Schematic fast action potential of human ventricular myocardium (solid) with electrolyte movements, refractory periods (see text) and force generated (dashed line) The five phases of fast cardiac action potential are indicated as numbers Phase 4: the resting membrane potential Potassium conductance is high and sodium conductance is low Phase 0: Upstroke of the action potential due to membrane depolarization An increase in sodium conductance due to the opening of voltage dependent fast sodium channels causes depolarization There is a simultaneous decrease in potassium conductance Phase 1: Period of partial repolarization due to a dramatic decrease in sodium conductance and a brief increase in chloride conductance Phase 2: Plateau phase during which changes in potassium efflux (conductance decrease and then plateaus) is matched by calcium influx (conductance increases and then plateaus) Phase 3: Membrane repolarization phase due to an increase in potassium efflux (increase potassium conductance) and a decrease in calcium influx (decreased calcium conductance) (From P Atluri, YJ Woo The cardiovascular system In: A Atluri, GC Karakousic, PM Porrett et al., eds The Surgical Review 2nd ed Philadelphia: Lippincott Williams & Wilkins; 2005, with permission.) conductance, increases the magnitude of hyperpolarization, slows down the rate of spontaneous depolarization, decreases the rate of closure of potassium channels, and slows down the heart rate In addition to increasing heart rate (positive chronotropic effect), the sympathetic nervous system increases the rate of conduction of action potentials through the conduction system The parasympathetic nervous system, in contrast, acts to slow down conduction Porrett_ch19.qxd 270 6/2/09 6:38 PM Page 270 Section IV • Cardiovascular and Respiratory Systems FIGURE 19.7 Structure of conduction system of the heart (From Johnson LR Essential Medical Physiology 2nd ed Philadelphia: Lippincott–Raven; 1998:166, with permission.) Superior vena cava SA node Right atrium AV node Left atrium Tricuspid valve Bundle of His Left bundle branch Right ventricle Septum Right bundle branch Left ventricle Purkinje fibers The electrical activity of the heart can be interpreted utilizing an electrocardiogram (ECG) The normal ECG demonstrates P waves and QRS complexes, which represent atrial and ventricular depolarization, respectively Ventricular repolarization is demonstrated by the T wave Circulatory Physiology As previously stated, the cardiovascular system is composed of the pulmonary circulation to provide perfusion to the lung parenchyma and the systemic circulation to provide systemic perfusion (and a very small degree of pulmonary circulation via the bronchial vessels) The pulmonary circuit is a low-pressure (mean PA pressure of 15 mm Hg), high-flow system As compared to the systemic circulation, the pulmonary vessels contain very little smooth muscle and are much shorter This results in highly compliant (compliance [mL/mm Hg] ϭ volume [mL]/pressure [mm Hg]; inversely proportional to elastance), low-resistance vessels It should be remembered that the pulmonary circulation must be capable of handling the same volume as the systemic circulation, as right heart output is equal to left heart output The pulmonary circulation is capable of handling increased cardiac output as seen with exercise by both recruiting additional pulmonary capillaries that are not normally utilized as well as distending the pulmonary vessels PVR is able to decrease with increasing cardiac output because of these two mechanisms This drop in resistance maintains low PA pressures, thereby preventing pulmonary edema and decreasing right heart cardiac work Other regulators of pulmonary blood flow are lung volume, hypoxia (which causes pulmonary vasoconstriction), and hypercapnea (which results in pulmonary vasodilation) In contrast to the pulmonary circuit, the systemic circulation operates at a high pressure, with high resistance to blood flow The flow of blood is from the left heart (left ventricle) to the aorta From the aorta, blood flows down a pressure gradient through various branches to arterioles and capillary beds The large and small arteries are thick-walled vessels with extensive elastic tissue and smooth muscle They are under high pressure but offer little resistance to blood flow Resistance can be calculated using the following equation derived from the work of Jean Leonard Marie Poiseuille on flow mechanics: Resistance ϭ 8(viscosity of blood) (length of vessel) ⌸(radius of blood vessel)4 Aortic and arterial elasticity maintains perfusion during the diastolic/filling phase of left ventricular cycling Arterioles, the short, terminal branches of the arteries, are the principal resistance vessels of the systemic circulation They comprise a large percentage of vascular smooth muscle innervated by the autonomic nervous system within the vessel wall that can constrict and impede the flow of blood Arterioles provide the largest pressure drop in the circulation Arteriolar resistance is regulated by the autonomic nervous system As arterial structures progressively branch from the aorta ultimately to the capillary bed, the cross-sectional area of the vascular bed continues to increase On the outflow side of the capillary bed, the cross-sectional area decreases as capillaries drain into venules that merge into small veins, large veins, and ultimately the vena cava The velocity of blood flow is directly proportional to volume of blood flow and inversely proportional to cross-sectional area Velocity of blood flow (cm/sec) ϭ Flow (cm3/sec)/cross-sectional area (cm2) As illustrated in Figure 19.8, there is a decrease in the velocity of blood flow as the cross-sectional area of the vascular bed increases This is ideal at the capillary level (high surface area, low velocity), where a high contact surface area and low velocity provide for optimal exchange of metabolic products at a cellular level Cardiac Mechanics The heart is a biomechanical pump The mechanical force generated by the heart is utilized to eject blood from the heart to either the pulmonary or systemic circulations providing perfusion to end organs There must be synchrony of the cardiac myocytes, valves, Porrett_ch19.qxd 6/2/09 6:38 PM Page 271 Chapter 19 • Cardiovascular Disease and Cardiac Surgery 125 Area 100 y cit 55 5,000 45 4,000 FIGURE 19.8 Pressure, area, and velocity relationship across the systemic circulation (From Kreisel D, Krupnick AS, Kaiser LR, eds The Surgical Review 1st ed Philadelphia: Lippincott Williams & Wilkins; 2001:308, with permission.) 25 3,000 2,000 Area (cm2) 50 re ssu Velocity (cm/s) 35 P re Pressure (mm Hg) lo Ve 75 271 25 15 0 Vena cava Large veins Small veins Venules Capillaries Aorta, large arteries, small arteries Arterioles 1,000 and four chambers of the heart for maximum efficiency The heart is in a constant state of flux to ensure that adequate end organ perfusion is achieved The primary variables that alter cardiac function are preload, afterload, and autonomic nervous system stimulation A proper understanding of these forces is a prerequisite to an adequate understanding of cardiac mechanics The left and right ventricles function in a cyclical manner Contraction and ejection of blood occurs during systole Myocardial perfusion as well as filling of the ventricles occurs during the relaxation phase known as diastole To simplify the discussion all references to ventricular function will focus on left ventricular mechanics The left ventricular intracavitary volume and pressure at end diastole (immediately prior to contraction) determine the preload of the heart There are several factors that affect preload Increasing venous return increases preload, while fibrotic, hypertrophied, and aging hearts become increasingly stiff and limit left ventricular filling and preload As described earlier, relaxation is an energy-dependent process (calcium-ATPase), which is augmented by adrenergic stimulation, but is impaired in ischemia, hypothyroidism, and congestive heart failure—all conditions that limit preload The afterload of a muscle is the pressure against which it must contract For the left ventricle, this is equivalent to the aortic pressure against which it must eject blood during systole Afterload for the right ventricle is equal to the PA pressure The greater the afterload, the greater the potential energy the heart must generate to provide adequate ejection into the aorta, and subsequently the greater the cardiac work (described in the following text) Maximal velocity of contraction is achieved when afterload is minimal Within normal physiologic ranges, the heart is able to accommodate a broad range of end-diastolic volume by altering contractility This dynamic activity is described by the Frank–Starling relationship, which describes the interplay between ventricular filling and contractility With increased ventricular filling the sarcomeres are stretched to an optimal length, thereby facilitating increased contractility Adrenergic stimulation can further increase contractility (inotropy) of the heart, thereby increasing the stroke volume (volume of blood ejected from the heart with each beat) Parasympathetic innervation decreases inotropy Additionally, right atrial stretch leads to an increase in heart rate with subsequent increase in cardiac output Cardiac output (l/min) ϭ stroke volume (l/beat) ϫ heart rate (beats/min) The cardiac cycle, as well as the interplay between preload and afterload on stroke volume, can best be described using pressure–volume loops (Fig 19.9) These pressure–volume loops are constructed by combining systolic and diastolic pressure curves The diastolic component (dotted line) is determined by diastolic filling (preload) The shape of the loop is determined by both contractility and the afterload against which the ventricle must contract The cardiac cycle begins at end diastole when the left ventricle is filled with left atrial blood and the cardiac muscle is relaxed On excitation the muscle begins to contract and generate force against closed valves (isovolumetric contraction) Once the pressure in the left ventricle exceeds aortic pressure, the blood is ejected into circulation during systole This volume ejected is the stroke volume (depicted by the width of the pressure–volume loop) The remaining volume at the end of contraction is the end-systolic volume At the end of contraction the ventricle begins to relax (isovolumetric relaxation) and the aortic valve closes as the pressure in the aorta exceeds that of the left ventricle With a drop in left ventricular pressure the mitral valve opens and left atrial blood begins to fill the left ventricle during diastole It should be noted that in the ideal system following passive flow of atrial blood, atrial contraction near the end of diastole optimizes filling of the left ventricle (atrial kick), thereby optimizing the Frank–Starling relationship Loss of this end-diastolic atrial contraction as in atrial fibrillation in a heart with ventricular hypertrophy can have adverse systemic hemodynamic consequences There are several factors that affect the pressure–volume loops Increased preload increases end-diastolic volume and stroke volume Increased afterload increases pressure that is required to be generated during isovolumetric contraction to eject blood and decreases the stroke volume Increased contractility, as with adrenergic stimulation, increases stroke volume and decreases end-systolic volume The ability of a hypertrophic heart to increase stroke volume is severely limited by its decreased diastolic compliance, limiting preload 272 6/2/09 6:38 PM Page 272 Section IV • Cardiovascular and Respiratory Systems FIGURE 19.9 Pressure–volume loop of one cardiac cycle (From Mohrman DE, Heller LJ Cardiovascular Physiology 3rd ed New York: McGraw-Hill; 1991:54, with permission.) 120 Intraventricular pressure (mm Hg) Porrett_ch19.qxd Ejection Reaches endsystolic volume Aortic valve opens 80 Systole Isovolumetric relaxation Isovolumetric contraction Diastolic filling Mitral valve opens 60 Reaches end-diastolic volume 130 Stroke volume Intraventricular volume (mL) Oxygen utilization by the heart is twofold A small amount of oxygen is utilized for cellular homeostasis and a large amount is utilized during contraction Changes in myocardial oxygen consumption are directly related to the work of the heart and changes in contractility Cardiac work can be quantified as stroke work, or work that the heart performs with each beat (stroke work ϭ aortic pressure ϫ stroke volume) The minute work of the heart is equal to the product of heart rate times the stroke volume multiplied by the aortic pressure (or cardiac output ϫ aortic pressure), so an increase in any of these three variables will increase cardiac work and ultimately increase myocardial oxygen consumption and demand The major determinant of oxygen demand is myocardial wall tension Tension in the wall of the ventricle is determined by both the pressure in the ventricle and the geometry of the ventricle The normal left ventricle is a pressurized irregularly shaped chamber If we were to consider the ventricle as a cylinder then the law of Laplace states that wall tension is proportional to internal pressure times the radius Increasing the wall thickness decreases the wall tension by distributing the internal pressure over a greater number of muscle fibers In other words, wall tension equals pressure times radius divided by wall thickness Altering the geometrical configuration of the ventricle (as with cardiomyopathy), increasing the radius, decreasing the wall thickness, and increasing ventricular pressure all increase wall tension and myocardial oxygen demand Changing the geometry of the ventricle requires extra energy consumption to realign the myocytes prior to each systolic contraction As stated previously, cardiac output is equal to the product of stroke volume multiplied by the heart rate A clinically feasible means of calculating cardiac output is to utilize the Fick equation: Cardiac output = Total body oxygen consumption 3O2] arterial blood - [O2] venous blood Dye dilution and thermal dilution of heat are other clinically utilized methods of calculating cardiac output Given the varying sizes of patients (varying body surface area), simply calculating a cardiac output may not provide enough information regarding cardiac function and adequate systemic perfusion The calculated parameter of cardiac index factors in patient size and expresses cardiac output per square meter of surface area, thereby eliminating the variable of patient size (cardiac index ϭ cardiac output/ body surface area) A cardiac index greater than L/min/m2 is accepted as adequate Figure 19.10 demonstrates the mechanical and electrical events during the various phases of the cardiac cycle (Table 19.1) Coronary Physiology Coronary blood flow follows the major vessels into smaller penetrating arteries, which provide the majority of the resistance to blood flow There is a dense capillary network by which the extensive metabolic demands of the heart can be provided At rest coronary blood flow is approximately mL/g of myocardium, but with demand this flow is capable of increasing nearly fourfold The increase in blood flow is accomplished with a combination of local vasodilatation of the penetrating arteries as well as recruitment of vessels that are collapsed at rest Since nearly 70% of the oxygen is derived from delivered coronary blood, there exists a very tight regulatory system to ensure adequate perfusion of the myocardium The myocardial tissue functions most optimally under aerobic conditions and is capable of sustaining only a few minutes of anaerobic activity Coronary perfusion is accomplished during the relaxing diastolic phase During systole the compressive forces within the myocardial wall are powerful enough to collapse the penetrating vessels and prevent myocardial perfusion Therefore, increasing heart rate will not only increase myocardial oxygen demand but also decrease myocardial perfusion Regulation of coronary blood flow is accomplished by a combination of the autonomic nervous system, metabolic vascular mediators, and vascular endothelium– mediated vasodilatation There are a combination of ␣- and ␤-receptors on the conductance vessels, which regulate nervous system–mediated vasoconstriction and vasodilatation, respectively Adenosine is produced by cardiac myocytes in response to ischemia and is the primary metabolic vascular mediator It acts locally on vascular smooth muscle to cause vasodilatation The vascular endothelium is capable of releasing both vasodilatory and vasoconstricting mediators ... Porrett_ch29.qxd 436 6 /2/ 09 6:59 PM Page 436 Section VI • Surgical Subspecialties malignancy of the parotid gland and the second most common malignancy of the submandibular and minor glands Of... regions of the head and neck (Fig 29 .9) Level I nodes are located in the submental and submandibular triangles and drain the oral cavity and submandibular gland Level II nodes are found from... with anastomoses performed between left and right atria, aorta, and PA (Fig 19 .23 ) Newer techniques utilize bicaval anastomosis (SVC and IVC, left atrium, aortic, and PA anastomosis) in an attempt