Cardiac Cycle and Pressure-Volume Relationship

The cardiac cycle encompasses the electrical, pressure, volume, flow, and valve motion events that occur during one complete cardiac systole and diastole. The temporal relationships of these events are demonstrated by plotting each independently versus time (Figure 106-5). During each cardiac cycle, the heart accomplishes two fundamental kinds of external work. It generates pressure (i.e., potential energy), and it ejects volume (i.e., kinetic energy). The relationship of these two events is illustrated by plotting instantaneous ventricular pressure and volume against each other to generate a ventricular pressure-volume plot (Figure 106-6). Pressure-volume plots form the basis of current understanding of cardiac physiology. Each loop of a pressure-volume plot represents one complete cardiac cycle and consists of two filling phases, an isovolumetric contraction phase, an ejection phase, and an isovolumetric relaxation phase. Under normal physiologic conditions, cardiac filling is divided into rapid diastolic filling (passive) and atrial filling (atrial systole). The principle pressure endpoints are end-diastolic pressure (EDP) and peak systolic pressure (P_sys). The principle volume endpoints are end-diastolic volume (EDV) and end-systolic volume (ESV). The difference between EDV and ESV is the stroke volume (SV). The area inside a pressure-volume loop represents the external work done by the heart in one cardiac cycle. The ejection fraction is the SV divided by EDV.

Stroke Volume (Preload, Afterload, Contractility)

SV is a major determinant of cardiac output (i.e., cardiac flow). SV, in turn, is determined by three important independent variables: preload, afterload, and contractility. Preload encompasses the Frank-Starling principle of the heart. On a cellular basis, preload is determined by the amount of diastolic strain on each cardiomyocyte. Within limits, the greater the diastolic strain, the more forceful the cardiac contraction. On a whole heart basis, preload is reflected by the EDV and EDP (Figure 106-7). On a beat-to-beat basis, the greater the EDV and EDP, the greater the preload and SV. Factors that determine the beat-to-beat EDV and EDP, and therefore preload, are the mean filling pressure of the circulation and vascular resistance. Mean filling pressure of the circulation is determined by the blood volume and venous vascular tone and has a direct relationship with preload. Vascular resistance has an inverse relationship with preload. Thus, the determinants of preload reside within the circulation and not in the heart. Cardiac remodeling can also change the EDV. Chronic changes in EDV attributable to remodeling do not represent changes in cardiac preload.

Afterload is the amount of systolic wall stress (SWS) the ventricle must overcome before it can eject volume. The determinants of systolic wall stress, and therefore cardiac afterload, are predicted by the LaPlace relationship according to:

Thus, on a beat-to-beat basis, afterload is determined by P_sys. On a chronic basis, cardiac remodeling (e.g., ventricular dilatation) also affects afterload. Thus, afterload is affected by events outside (i.e., P_sys) and inside (i.e., cardiac remodeling) the heart. Afterload has an inverse relationship with SV. The greater the cardiac afterload (e.g., P_sys), the less the SV (see Figure 106-7).

Contractility, also known as inotropic state, represents the intrinsic contractile state of the heart independent of preload and afterload. On a beat-to-beat basis, contractility is largely a function of the amount of sympathetic (β) influence on the heart. Contractility is also influenced by the diseases of the myocardium and cardiac drugs. Changes in cardiac mass (e.g., cardiac hypertrophy) also have a direct effect on the global contractility of the heart. Contractility has a direct relationship with SV. The greater the contractility or inotropic state, the greater the SV. On a pressure-volume loop, contractility is reflected by changes in the slope of the end-systolic pressure-volume relationship (ESPVR) (see Figure 106-7).

Cardiac Output, Blood Pressure, and Vascular Resistance

Cardiac output (Q) is the product of SV and heart rate. Mean arterial blood pressure (MAP) is a function of Q, vascular resistance (R), and atrial pressure (AP) according to the following:

Vascular resistance cannot be measured directly but can be calculated by knowing Q, MAP, and AP:

Vascular resistance is a function of the degree of vasoconstriction (i.e., vascular radius) in the resistance arteries and the viscosity of blood (i.e., hematocrit). The above relationships are applicable to the pulmonary and systemic circulations. On a chronic basis, R can be affected by vascular remodeling (e.g., hypoxic pulmonary hypertension).

The pulse pressure (P_p) is the difference between the systolic and diastolic blood pressures. It represents the pressure variation around the MAP but is independent of the MAP and R. The P_p is the principle determinant of the “strength” of a patient’s peripheral pulse on palpation. It is possible to have a high P_p and strong pulse but a low MAP and vice versa. The P_p is a direct function of the SV and inverse function of the compliance of the large elastic arteries (C_A):

The most likely reason for a diminished P_p and a “weak” pulse is a poor SV. Poor compliance or “stiffening” of the elastic conducting arteries can have the effect of elevating the P_p. Conditions that allow rapid diastolic “run off” of blood, such as patent ductus arteriosus or aortic insufficiency, can dramatically lower diastolic blood pressure and thereby elevate the P_p.

Electrophysiology

Cardiomyocytes are excitable cells with a negative resting membrane potential and the ability to generate an action potential. The predominant mechanisms supporting resting membrane potential are the electrochemical gradient for K⁺ across the sarcolemma established by the ATPase Na⁺–K⁺ pump and the presence of the inwardly rectifying K⁺ current. The cardiac action potential results from sequential activation of voltage-regulated Na⁺, Ca⁺⁺, and K⁺ currents. Entry of Ca⁺⁺ into the cell during the action potential initiates contraction of the cardiomyocyte (i.e., excitation–contraction coupling). Cardiomyocytes are electrically connected through gap junctions and thus have the ability to conduct their action potential to adjacent cells. Some cardiomyocytes have a slow diastolic depolarization that allows them to trigger their own action potential, a property known as automaticity.

The cardiac impulse is the wave of cardiac depolarization as it travels from cell to cell over the heart. Under physiologic conditions, the cardiac impulse arises from automatic (pacemaker) cells within the sinoatrial node. The impulse emerges from the sinoatrial node and travels leftward and ventrally as a uniform wave across the atrial muscle, initiating atrial systole. The impulse enters the atrioventricular node and is delayed by nodal cells that conduct slowly because of their lack of voltage-dependent Na⁺ channels and dependence on voltage-dependent Ca⁺⁺ channels. The impulse emerges from the atrioventricular node and is selectively conducted to the endocardial portion of the ventricular myocardium by the very fast conducting His-Purkinje conduction system. The cardiac impulse then travels as a uniform wave from the endocardial to the epicardial portions of the ventricular myocardium, initiating ventricular systole.

Beating Heart Surgery

Most cardiac surgeries in animals are performed on a beating, closed heart without circulatory or cardiac arrest. Procedures include surgery on structures outside of the heart, such as patent ductus arteriosus ligation or pulmonary artery banding; surgery performed by passing instruments through small portals controlled by suture tourniquets, such as closed valve dilatation; and surgery performed with the aid of tangential vascular clamps, such systemic-to-pulmonary shunts. A paramount principle of all cardiac surgery is control of bleeding. This is never truer than during beating heart surgery, in which there are few fallback options after significant hemorrhage occurs. It is important to have a plan and instrumentation available to control hemorrhage in the event that a cardiac structure is inadvertently opened. Mattress sutures should be buttressed with pledgets to keep them from cutting through cardiac tissues and redundant to ensure control of bleeding. Vascular clamps should be deeply placed to prevent slippage and to ensure adequate margins for closure of cardiac incisions. Advanced planning and a deliberate approach go a long way toward preventing crisis situations during cardiac surgery.

Cardiac motion is an intrinsic aspect of beating heart surgery and adds to its psychologic and technical challenges. Gentle compression on the surface of the heart is useful to intermittently control cardiac motion during suture placement. Placement of fingers within the ring handles of a needle holder, as opposed to “palming” the instrument, provides much greater instrument control that facilitates suturing on the beating heart. As a general rule, pharmacologic manipulation of the heart rate during beating heart surgery is not necessary or warranted and should be avoided, given its inherent risks. As surgeons become familiar with operating on the beating heart, they soon realize that it is not fundamentally different from surgery on other tissues or organs.

Inflow Occlusion

Inflow occlusion is a strategy for performing brief open cardiac repairs. It involves interruption of venous blood returning to the heart and a brief period of complete circulatory arrest. The principal advantages are its simplicity; lack of need for specialized equipment; and associated minimal cardiopulmonary, metabolic, and hematologic derangement after surgery.⁴⁹ The main disadvantages of inflow occlusion are limited time provided to perform the cardiac procedure, motion of the surgical field, and unavailability of a fallback or rescue strategy if something delays completion of surgery. As a result, cardiac surgery performed during inflow occlusion must be meticulously planned and executed.

Circulatory arrest duration in a normothermic patient should ideally be 2 minutes or less to minimize the risk of cerebral injury and ventricular fibrillation. If necessary, inflow occlusion can be repeated to allow completion of a cardiac surgery. Adequate time for complete recovery of the myocardium must be allowed between inflow occlusions if more than one occlusion is used. Circulatory arrest time can be extended up to 4 minutes with mild whole-body hypothermia (32° to 34° C); however, the risk of cardiac arrest increases as circulatory arrest time increases, regardless of whether or not the patient is hypothermic. Body temperature should not be allowed to fall below 32° C; as the risk of ventricular fibrillation increases significantly below this temperature. After surgery, surface warming with water blankets or beds is used to return the animal to a normal temperature.

Inflow occlusion can be accomplished from a left or right thoracotomy or median sternotomy, depending on the procedure to be performed. Tourniquets are placed on the venae cavae and azygous vein to accomplish inflow occlusion. Care should be taken to exclude the right phrenic nerve during placement of tourniquets on the venae cavae to avoid injury during occlusion. Direct access to the venae cavae and azygous vein for inflow occlusion is obtained readily from a right thoracotomy (Figure 106-8) or median sternotomy. Access for inflow occlusion is more difficult from a left thoracotomy, particularly when the heart is enlarged. With the left approach, the venae cavae and azygous vein are accessed by dissecting through the mediastinum (Figure 106-9).

Ventilation should be discontinued during inflow occlusion to prevent pulmonary blood from being pushed into the surgical field during inspiration. Drugs and equipment for full cardiac resuscitation should be immediately available after inflow occlusion. Gentle cardiac massage may be necessary after inflow occlusion to reestablish cardiac function. Digital occlusion of the descending aorta during this period helps direct available cardiac output to the heart and brain. If ventricular fibrillation occurs, the heart should be defibrillated by direct electrical shock as soon as inflow occlusion is discontinued. Generally, cardiac incisions are initially closed with vascular clamps to keep circulatory arrest times as short as possible. After discontinuation of inflow occlusion and restoration of cardiac function, cardiac incisions are closed with suture.

Cardiopulmonary Bypass

Cardiopulmonary bypass is a procedure whereby an extracorporal system provides flow of oxygenated blood to the patient. Cardiopulmonary bypass provides for a motionless and bloodless operative field and time to perform more complex cardiac repairs. Cardiopulmonary bypass has been used to treat a variety of cardiac conditions in dogs. Successful cardiopulmonary bypass requires a team approach. The primary bypass team consists of a surgeon, perfusionist, anesthesiologist, and scrub nurse. Initiation, maintenance, and discontinuation of cardiopulmonary bypass require a coordinated and practiced effort among these individuals. There must be clear communication between team members. The surgeon is ultimately responsible for the overall conduct of cardiopulmonary bypass.

Cardiopulmonary bypass is accomplished with a heart–lung machine. Major components of a heart–lung machine include three to five pumps, a temperature-controlled circulating heater/cooler water bath, an oxygen blender, a gas flowmeter, and an anesthetic vaporizer. The primary bypass circuit consists of a reservoir, pump, membrane oxygenator, heat exchanger, and circulating heater/cooler water bath (Figure 106-10). A membrane-type oxygenator should be used to minimize injury to the blood. A pediatric-size oxygenator is preferred in dogs that weigh less than 40 kg to minimize volume necessary to prime the circuit. During cardiopulmonary bypass, blood is drawn away from the patient to the reservoir by gravity flow. Blood is then pumped through the oxygenator under pressure and returned to the patient by means of a roller or centrifugal pump. The heater/cooler water bath is used to control body temperature by means of a heat exchanger built into the primary circuit. Shed blood in the operative field is salvaged and returned to the reservoir by one or two suction lines driven by additional roller pumps.

Before surgery, a triple-lumen catheter is placed into a jugular vein to provide central venous access and monitor central venous pressure. An arterial catheter is placed to monitor direct arterial pressure and provide sampling access for arterial blood gas analysis. The electrocardiogram, arterial blood pressure, central venous pressure, end-tidal CO₂, and esophageal and rectal temperatures are monitored continuously during surgery. Arterial and venous blood gases, activated clotting time, hematocrit, total protein, and Na⁺, K⁺, ionized Ca⁺⁺, and lactate concentrations are measured periodically throughout the procedure.

Cannulation for cardiopulmonary bypass can be accomplished from a right or left thoracotomy or median sternotomy, depending on the cardiac procedure being performed. Oxygenated blood is returned to the patient through the arterial cannula and line. Arterial cannulation is performed before cardiac manipulations and other cannulation. If bleeding occurs before initiation of cardiopulmonary bypass, blood can be salvaged from the operative field and returned to the patient by the arterial cannula and line. Arterial cannulation of a femoral or carotid artery is preferred over direct aortic cannulation in dogs (Figure 106-11) and should be performed before the thoracic cavity is opened. If a thoracotomy approach is used, the femoral artery on the opposite side (down) limb is chosen for cannulation. A straight arterial cannula, ranging in size from 8 to 14 Fr, is used.

Blood is diverted from the right heart to the cardiopulmonary bypass circuit by means of one or two venous cannula(s) and a venous line. Venous cannulation can be accomplished by several configurations, depending on the cardiac surgery undertaken. Bicaval venous cannulation is required for surgeries performed through a right atrial cardiac approach (e.g., septal defect repairs and tricuspid valve surgery) (Figure 106-12). Alternatively, venous cannulation can be accomplished by introducing a single, two-stage, cavoatrial cannula through the right auricle (Figure 106-13). Cavoatrial cannulation is the only option for venous cannulation for cardiopulmonary bypass from a left thoracotomy.

Hemodilution is desirable during cardiopulmonary bypass to counter effects of increased blood viscosity during hypothermia.⁴³ The goal is to decrease the hematocrit to approximately 25% to 28%. Hemodilution is accomplished by priming the bypass circuit with a calculated volume of crystalloid solution. The hematocrit decreases when the patient’s blood mixes with the circuit prime. A balanced, pH-adjusted (7.4) crystalloid solution should be used to prime the circuit (Box 106-1). Whole blood can be added to the prime solution if the volume of crystalloid prime is insufficient to adequately prime the circuit without causing excessive hemodilution. Other additives to crystalloid prime include NaHCO₃ and heparin.

Before cannulation and initiation of cardiopulmonary bypass, the animal must undergo complete anticoagulation by administration of heparin (see Box 106-1). The activated clotting time is monitored every 30 minutes during bypass and kept above 480 seconds. Perfusion flow rates during bypass depend on several factors, including patient size, temperature, and hematocrit (see Box 106-1). Standard cardiopulmonary bypass perfusion strategies with mild to moderate hypothermia can be used for dogs weighing more than 10 kg.⁵³ For small dogs (<10 kg), deep hypothermic (15° to 18° C) low-flow (20 mL/kg/min) cardiopulmonary bypass may be a more appropriate strategy to decrease the adverse effects associated with bypass.⁵⁷ Ultimately, perfusion flow should be kept at the lowest level that meets the needs of the patient, with a goal of maintaining a venous oxygen saturation of 70% or greater and normal lactate concentrations. MAP, which should be 50 to 70 mm Hg during bypass, usually decreases dramatically for several minutes after bypass initiation because of sudden hemodilution. Phenylephrine is administered as necessary to increase vascular resistance and maintain adequate MAP.

Esophageal and rectal temperatures are monitored continuously during cardiopulmonary bypass. Dogs are cooled to between 25° and 28° C during the cardiac surgery using the heater/cooler water bath and heat exchanger in the pump circuit. Requirement for inhalation and other anesthetic drugs decreases during hypothermia. During cardiopulmonary bypass, the oxygenator receives continuous flow of a mixture of oxygen and nitrogen from an oxygen blender. The fraction of inspired oxygen (FIO₂) should be adjusted to keep PaO₂ above 120 mm Hg during cardiopulmonary bypass. PaCO₂ is adjusted during cardiopulmonary bypass by varying total gas flow (L/min) to the oxygenator by means of the flowmeter. Blood gases should be measured every 30 minutes during cardiopulmonary bypass. An α-stat strategy (temperature uncorrected blood gas measurements) for acid–base management, which permits relative alkalosis as the patient cools, is most appropriate for patients on cardiopulmonary bypass.⁴³ Metabolic acidosis during cardiopulmonary bypass should be corrected by administration of NaHCO₃.

Complete cardiopulmonary bypass is accomplished by cross-clamping the ascending aorta (Figure 106-14). Protection of myocardium from ischemic injury during aortic cross-clamping is accomplished by immediate cessation of electromechanical activity and rapid myocardial cooling. This is achieved by administration of cold cardioplegia solution into the coronary circulation just after the aortic cross-clamp has been placed. The solution contains a high concentration of K⁺ that arrests the electrical and mechanical activities of the myocardium, thereby greatly reducing its metabolic requirement. Cooling myocardium to approximately 4° to 8° C further decreases its metabolic requirement. Sanguineous crystalloid cardioplegia solutions are superior to pure crystalloid cardioplegia solutions.⁵ A sanguineous crystalloid cardioplegia solution is made by blending a crystalloid cardioplegia solution (see Box 106-1) with heparinized blood from the bypass circuit. Cardioplegia solution is delivered by a cannula placed in the ascending aorta before aortic cross-clamping. All electrical activity on the electrocardiogram should cease after cardioplegia administration. Cardioplegia is repeated every 20 minutes while the aorta is cross-clamped. Ideally, aortic cross-clamp time should not exceed 90 minutes.

The heart must be de-aired before discontinuing bypass. This is accomplished by diverting venous blood back to the heart and allowing the cardiac incisions to bleed before closure. The anesthesiologist assists this process by applying continuous positive pressure to the lungs to push pulmonary blood back toward the heart. After the aortic cross-clamp is removed, continuous suction is applied to the cardioplegia cannula to savage any small air bubbles ejected from the left heart. The left ventricle, left atrium, and left auricle should be manipulated to release any trapped air before reestablishing left ventricular ejection.

After closure of cardiac incisions, the aortic cross-clamp is removed, and coronary circulation is reestablished. If ventricular fibrillation occurs, the heart should be electrically defibrillated with direct current and internal paddles. If initial attempts at defibrillation are unsuccessful, then defibrillation should be repeated every few minutes as the patient is rewarmed until a normal rhythm is restored. Rewarming should begin as the cardiac surgery is being completed, usually while cardiac incisions are being closed. After the patient is rewarmed to 37° C and an effective cardiac rhythm established, a gradual process of weaning from cardiopulmonary bypass is begun. During this period, calcium chloride and inotropic drugs are usually required to support cardiovascular function (see Box 106-1). After the animal has been fully weaned from cardiopulmonary bypass and is hemodynamically stable, cannulae are removed in reverse of the order in which they were introduced. Protamine sulfate (see Box 106-1) is administered to reverse the heparin anticoagulation. Protamine has a very potent hypotensive effect in dogs and must be administered slowly. The activated clotting time should return to less than 150 seconds. Administration of fresh whole blood is indicated after cardiopulmonary bypass.

Cardiopulmonary bypass initiates a systemic inflammatory response that has a profound effect on management after surgery.⁴³ The first 12 hours after cardiopulmonary bypass are most critical. Major problems that can occur during this period include hemorrhage, hypoxemia, circulatory collapse, cardiac arrhythmias, low urine output, and electrolyte and acid–base abnormalities. Hemorrhage is a major postoperative concern after cardiopulmonary bypass and can be surgical, biologic, or both. Surgical hemorrhage results from bleeding from cardiotomy sites and is best prevented by careful inspection of those sites before thoracotomy closure. Even with perfect closure of cardiotomy sites, significant bleeding can occur after cardiopulmonary bypass because of biologic effects of cardiopulmonary bypass. Dilutional and consumptive thrombocytopenia, acquired platelet dysfunction, consumptive and dilutional coagulopathy, and fibrinolysis all contribute to biologic bleeding after surgery. In most cases, hemorrhage after cardiopulmonary bypass is biologic and is best managed conservatively with supportive care. Administration of fresh whole blood is indicated to restore red blood cells, platelets, and clotting factors and should begin in the operating room. Additional stored blood or plasma may be necessary in the postoperative period. Shed blood can be collected, washed with a cell washer, and returned to the patient as necessary.

Some degree of hypoxemia is invariably present after cardiopulmonary bypass because of pulmonary injury and increased pulmonary vascular permeability.⁴³ This well-recognized condition is referred to as pump lung. Ventilatory support with PEEP (5 to 8 cm of water) for 4 to 12 hours after surgery is generally necessary. Circulatory support after cardiopulmonary bypass should include volume expansion to keep central venous pressure between 4 and 10 mm Hg, which should maintain adequate cardiac output without causing congestion. Because of the generalized increase in vascular permeability after cardiopulmonary bypass, volume deficits should be restored primarily with plasma or blood; hematocrit should be kept above 30%. Administration of high volumes of crystalloid fluids should be avoided after cardiopulmonary bypass. Inotropic support may be necessary after surgery to maintain adequate cardiac output and mean systemic blood pressure. Ventricular tachycardia often occurs after cardiopulmonary bypass and should be controlled with lidocaine. Urine output should be monitored for 12 hours after surgery to ensure adequate renal function. Hypokalemia and hypocalcemia are frequently encountered after surgery and should be corrected.

Patent Ductus Arteriosus

The ductus arteriosus is a fetal vessel that connects the main pulmonary artery to the descending aorta and directs venous blood away from the collapsed fetal lungs. The ductus arteriosus closes soon after birth during the transition from fetal to extrauterine life. Continued patency of the ductus arteriosus for more than a few days after birth results in patent ductus arteriosus.

Patent ductus arteriosus is the most common congenital heart defect seen in dogs, accounting for 25% to 30% of congenital malformations.18,30 The defect also occurs in cats but with a much lower prevalence.⁵⁰ Patent ductus arteriosus is seen more commonly in purebred dogs, with a predilection for females. Poodles, Keeshonds, Maltese, Bichon Frises, Yorkshire terriers, Cocker spaniels, Pekingese, collies, Shelties, Pomeranians, Welsh corgis, and other breeds have an established predisposition for patent ductus arteriosus.¹⁸ A heritable basis for patent ductus arteriosus has been established in poodles and Welsh corgis.^68,71 The heritable defect is hypoplasia and segmental asymmetry of the ductus muscle mass that results in failure of ductus contraction.^17,19

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