Jumat, 08 April 2011
Kamis, 07 April 2011
Cardiopulmonary Bypass and Cardioplegia
P.A. Iaizzo (ed.), Handbook of Cardiac Anatomy, Physiology, and Devices, DOI 10.1007/978-1-60327-372-5_30,Springer ScienceþBusiness Media, LLC 2009
Cardiopulmonary Bypass
Extracorporeal circulation and cardiopulmonary bypass are synonymous terms denoting a method by which the blood that usually returns directly to the heart is temporarily drained from superior and inferior vena cavae. The blood is diverted into a reservoir where it is oxygenated and subsequently returned to the patient’s arterial circulation. This process effectually excludes the heart from the general circulation and leaves it empty so that it can accommodate surgical intervention.
The breakthrough technologies that first allowed this type of open-heart operation were developed by two separate centers in the United States in the early 1950s.
Importantly, Lillehei and Varco [1] at the University of Minnesota developed a cross-circulation technique. This technique utilized a human donor (usually the parent of a child undergoing cardiac surgery) who, in essence, functioned as an extracorporeal pump for the patient’s circulatory system. This type of extracorporeal circulation also allowed the blood to be drained from the child’s vena cava so that the surgical procedure could be performed within the empty heart. The subsequent development of the heart–lung machine by Gibbon [2] was considered revolutionary in that it eliminated the need for a support donor (a second patient). Gibbon’s system has been improved since the mid-1950s and has gradually evolved into the standardized, but very complex and sophisticated,
machine it is today.
The basic components of an extracorporeal circuit include: (1) a reservoir into which the patient’s blood is diverted; (2) an oxygenator that replaces the function of the lungs; and (3) a pump that propels the oxygenated blood back into the patient’s arterial circulation. In this manner, the machine bypasses both the heart and the lungs while maintaining the functions of other organs during surgical interventions within the heart.
Venous Drainage
The venous blood that is normally delivered to the right atrium is commonly iverted to the heart–lung machine,either by cannulating the veins themselves or by cannulating the right atrial chamber. Surgery performed in or through the right atrial chamber requires that both the right atrium and right ventricle be empty. To do so, cannulas are placed directly into the superior and inferior venae cavae. Constricting tourniquets are then placed around the vein over the cannulas, and blood is diverted into the heart–lung machine. These proceduresconstitute total cardiopulmonary bypass. Venous cannulation is normally performed in one of two ways: (1) by placing a purse string suture either directly in the superior vena cava or in the right atrium or (2) by advancing the cannula into the superior vena
cava. It should be noted that direct cannulation of the superior vena cava generally provides more room for any work that may need to be done inside the right atrium.
A modification of this type of bypass can be used when the cardiac chambers are not surgically entered, such as in coronary bypass operations involving procedures on the surface of the heart. In such cases, a single cannula is placed in the right atrium, or a double-staged cannula is placed with the tip of the cannula in the inferior vena cava and the side drainage holes positioned at the level of the
right atrium. Coronary bypass surgery does not involve direct vision of the inside of the cardiac chambers, so there is no need to constrict the superior or inferior
venae cavae. When coronary bypass operations are undertaken simultaneously with cardiac valve repairs or replacements, total cardiopulmonary bypass is typically
implemented.
Arterial Return
Once the blood has been oxygenated in the heart–lung machine, it is returned to the patient’s general circulation via cannulas placed directly in the arterial system
(Fig. 30.1). The most common method involves the placement of a cannula in the highest portion of the ascending aorta below the origin of the innominate artery. Depending on the type of surgery, other sites are also used, including cannulation of the femoral artery in the groin and infusion of the arterial system in a retrograde manner. The ascending aorta is cross-clamped at this point, so
no systemic blood enters the coronary artery circulation. The heart is, therefore, totally excluded from the circulation. Thus the heart needs to be protected by using one of a number of methods to infuse cardioplegic solutions . Any blood remaining in the operative field is removed via cardiotomy suction lines
which are used to aspirate it back to the heart–lung machine, where it reenters the bypass circulation with the rest of the removed blood. In some operations involving the descending thoracic aorta, total cardiopulmonary bypass is not necessary. If
the portion of the aorta that needs to be isolated lies between the left carotid artery and the diaphragm, only part of the total blood volume needs to be removed, and partial bypass can be implemented. The blood is removed by the heart–lung machine via a cannula inserted into either the left atrium or left superior pulmonary vein. Then, the blood is infused back into the descending thoracic aorta beyond the level of distal aortic cross-clamping. Doing so allows the heart to continue to beat normally and helps maintain the viability of the proximal organs (head, neck, and arms), while the rest of the lower body is perfused and thus maintained by the pump. This technique is called left heart bypass, because it involves only removal of blood and decompression of the left side cardiac chambers.
after a descending thoracic aorta aneurysm operation is completed, the bypass is discontinued. The clamps which were placed to occlude the aorta in the arch and the descending portion are removed. The normal physiological perfusion of the body (which was interrupted during surgery without ever stopping the heartbeat)
is thus reestablished. In contrast, total cardiopulmonary bypass involves complete stoppage of the heart. After an operation applying total cardiopulmonary bypass and cardiac arrest,the aortic clamp is released allowing the general circulation
to reperfuse the coronary arteries and to rewarm the heart.
After the air is expelled from the cardiac chambers, the heart usually elicits ventricular fibrillation. Such fibrillation normally requires cardioversion with an electric shock administered directly to the heart by employing paddles that deliver currents that vary from 20 to 30 watts/sec. The patient is then ventilated using the endotracheal tube connected to the anesthesia machine, which reinflates the
lungs. After the normal sinus rhythm of the heart is reestablished, the patient is gradually weaned off the extracorporeal circulation until the heart takes over full function. At this point the heart–lung machine is stopped, and all cannulas are removed and access areas closed. In some complex surgical cases involving the aortic
arch, separate independent perfusion of the arch vessels may require implementation, that is, in addition to the perfusion of the lower part of the body through the cannula inserted in the femoral artery. This situation places a
great demand on the perfusionist operating the heart– lung machine. The perfusionist must monitor two separate infusions to regulate pressures and make certain that a balance and sufficient perfusion is achieved in both
the upper and the lower areas of the patient’s body. Another specialized bypass method that needs description is the deep hypothermia and total circulatory arrest
technique. This type of total cardiopulmonary bypass employs a decreasing body temperature to very low levels (15–208C); this is typically accomplished using heat
exchangers installed in the heart–lung machine circuits. Circulation is stopped altogether when the proper temperature is reached, and the heart is emptied for several minutes with the entire volume of the patient’s blood remaining in the reservoir of the heart–lung machine. The pump is then stopped and the arterial perfusion ceases. The venous return line, however, is left open to continue emptying the patient’s blood volume completely into the reservoir of the heart–lung machine. This technique is used in special cases to allow repair of
very complicated conditions. The period of total circulatory arrest induced during deep hypothermia is usually less than 45 min [3, 4]. This time restriction is to insure that the patient does not suffer neurological deterioration or central
nervous system damage during such global ischemia. As soon as the repair is completed, normal cardiopulmonary bypass is reestablished. The patient is gradually
rewarmed to a normal core temperature of 378C prior to removal from extracorporeal circulation. The use of such deep hypothermia always requires careful evaluation by
the surgical team. In such clinical cases, the danger of inducing neurological damage must be weighed against the benefits of correcting a major cardiac anomaly.
Anticoagulation
To prevent the formation of clots during cardiopulmonary procedures, both within the body and in the extracorporeal heart–lung machine, it is necessary to anticoagulate the patient. The most common agent used for such anticoagulation is heparin. It is commonly administered intravenously before cannulation at a dose of 300 units/kg. There are two types of heparin: (1) the lung beef type which is extracted from a bovine source and (2) the porcine mucosal type which is from a swine source. Since the mid-1980s, the porcine mucosal heparin has been
preferred because it is less likely to lead to thrombocytopenia and production of heparin antibodies in the patient, a condition known as HIT syndrome [5].
The effectiveness of anticoagulation therapy requires testing, usually by measuring the activated clotting time of the patient’s blood. The result is expressed in seconds, with normal values ranging between 100 and 120 s.
Heparinization is deemed adequate when the activated clotting time runs above 300 s. At any time after such values are achieved, it is considered that the patient can
undergo cannulation and be placed on extracorporeal circulation. Typically, the anticoagulant effects induced during such surgeries must be reversed postoperatively. Protamine sulfate is the drug of choice to neutralize the
effects of the heparin and allow the patient to elicit normal clotting values. Yet, this drug is a macromolecule compound that may produce pulmonary vasoconstriction
and severe hypotension [6, 7], particularly in diabetic patients. Nevertheless, such side effects are rare and, in most patients, this drug can be used safely, as it neutralizes the effects of heparin. Naturally, the amount of protamine necessary to achieve neutralization depends on the amount and timing of heparin administered. Initially, a test dose is given; if no reaction occurs, protamine is then administered in the appropriate amounts. Its effects are monitored by measuring activated clotting times until they return to a normal range. It should be
noted that if any reaction or side effect occurs, additional treatments are commonly employed, such as the administration of epinephrine, calcium, steroids, or fluids [7].
Occasionally patients cannot be given heparin because they have developed heparin antibodies from previous exposure. Other anticoagulant agents are studied and
occasionally used in such cases, including hirudin (Lepirudin) [8], a potent anticoagulant that is extracted from leaches and lampreys. Other drugs include the heparinoids [9] like Orgaran (Org10172, Organon Company,West Orange, NJ), for which a different monitoring protocol is implemented. Unfortunately, to date, no drug has
been identified that can reverse the effects of Orgaran, thus it must be metabolized by the human body. For such patients bleeding is a constant, and often very difficult, postoperative complication.
If the cardiopulmonary bypass takes an extended time, coagulopathies often pose complications. In such cases, the body, primarily the liver, is unable to produce the appropriate clotting factors to reverse the anticoagulation status.Other factors that can contribute to coagulopathies include ischemia of the abdominal organs, particularly if necrosis occurs in the liver cells and/or in the intestine. Bleeding, therefore, can be a very serious and difficult complication to treat; administration of multiple coagulation factors, platelets, and cryoprecipitates may be required.
Temperatures of Perfusion
Since their inception, cardiopulmonary bypass and extracorporeal circulation have been implemented using some degree of hypothermia. Lowering core body temperature
decreases the overall oxygen demands of body tissues, and a more desirable protective state during pulseless circulation is provided by the heart–lung machine.
Several degrees of hypothermia are commonly identifiable relative to extracorporeal circulation interventions. Normothermia indicates that core body temperature is
between 35.5 and 378C [10], mild hypothermia is between 32 and 358C, and moderate hypothermia is between 24 and 328C. An important distinction must be made between
mild and moderate hypothermia. If the heart is perfused at mild levels (above 318C), the heart will continue to beat although at a slower rate. This mild level of hypothermia allows surgical correction of some congenital anomalies
without arresting the heart. An addition level of hypothermia used occasionally is deep or profound hypothermia, which was previously mentioned, and usually brings the body temperature below 208C. Currently, most open cardiac operative procedures are conducted under conditions somewhere between moderate and mild hypothermia. Some centers routinely use moderate hypothermia, while others employ normothermia
[11, 12]. One reason to maintain normothermic perfusion is to avoid coagulopathies that may develop when body temperature is lowered to the moderate levels, and
thus allow for normal function of the body’s enzyme systems. Normothermic temperatures also enable the kidneys to respond better to diuretics.
Several reports have indicated the relative safety of normothermic perfusion [10–16], but an equal number have suggested complications with this modality [17, 18]. As a result, the spontaneous drifting to mild hypothermic levels is generally preferred. Deep or profound hypothermia is associated with the implementation of total circulatory arrest as mentioned before. With this level of hypothermia, body temperature is lowered to between 15 and 188C. Such operations are thus usually prolonged given the time it takes to cool the body to those levels before surgery and also by the required time to rewarm it afterwards.
Perfusion Pressures
Under normal physiological conditions, the heart provides a pulsatile pressure and flow. The systolic pressure depends on the ventricular function. The diastolic pressure in normal states is primarily regulated by the blood volume and the vascular tonus. During cardiopulmonary bypass, the heart–lung machine facilitates pulseless perfusion; there is no systolic or diastolic pressure, but rather
one steady mean pressure throughout the arterial circulatory system. Therefore, this pressure should be high enough to provide adequate blood oxygen to all
organs of the body, particularly the brain and kidneys.
Since the patient is typically hypothermic, the oxygen requirements are lower; the perfusion pressure is usually maintained around 70 mmHg. Occasionally, specifically
in patients with severe obstructive carotid disease, a higher perfusion pressure is recommended to ensure proper perfusion of the brain. Nevertheless, this recommendation is somewhat debated because the brain is known to have its own regulatory system to maintain low resistance near obstructed areas [12, 14].
During cardiopulmonary bypass, if the patient shows decreased vascular tonus (despite adequate volume of fluid), vasoconstrictors are routinely used; a typical therapy is a bolus or drips of neosynephrine [10]. A decreased vascular tonus is common in septic patients with bacterial endocarditis, for whom an emergency operation sometimes is necessary to replace the affected valve and reverse
the profound heart failure. In general, a mean perfusion pressure of around 70 mmHg during cardiopulmonary bypass should be maintained.
Hemodilution
Up to a certain level, hemodilution can be a desirable side effect of cardiopulmonary bypass. Lowering the hematocrit prevents ‘‘clumping’’ of the red cells or ‘‘sludging,’’ thereby providing better circulation at the capillary level;
viscosity of the circulating blood is decreased, on the other hand, to also ensure that oxygen is adequately delivered to the body’s tissues during cardiopulmonary bypass. Hematocrit levels are monitored and maintained at a minimum between 22 and 26%. Toward the end of the bypass operation,typically the perfusionist deliberately removes some of the fluid from the patient’s circulation to hemoconcentrate
the blood toward more normal hematocrit levels [19,20]; this rises to above 30% by the time the patient is removed from cardiopulmonary bypass. Subsequent diuresis
and/or removal of red blood cells will further aid in reestablishing the hematocrit to normal levels. Pulseless perfusion, as provided by the heart–lung
machine, and hemodilution will both invariably lead to a transfer of fluid across the capillary walls into the third space (interstitial). Therefore, all patients develop, to some degree, peripheral third spacing or edema, which is particularly seen in children and usually requires several days to clinically resolve completely. In an attempt to avoid this condition, plasma expanders (such as albumin, hetastarch, dextran, and mannitol) are usually added to
the priming solution of the heart–lung machine. 30.1.7 Heart–Lung Machine Basics
The basic components of the heart–lung machine include an oxygenator, a reservoir for the perfusion solution, a perfusion pump, line filters, two heat exchangers, and
monitoring devices. Although the bubble oxygenator has been used for many years, it has been largely supplanted by the membrane oxygenator. The membrane
oxygenator is associated with less trauma to red blood cells and is less likely to produce micro-bubbles that might pass into the patient’s arterial system and cause air embolism. In addition, the newer centrifugal pumps like the Bio-Medicus (Medtronic, Inc., Minneapolis, MN) and the Performer1 CPB (Medtronic, Inc.), offer
a distinct advantage over the older roller-type pumps such as the standard DeBakey type. More specifically, the roller pumps use occlusive pressure to propel the blood
within the tubing, and can cause damage to the red blood cells and dislodge debris from the tubing material. In contrast, the newer centrifugal pumps minimize trauma
to the red blood cells, because the motion required to move the blood does not constrict the tubing
Cardiopulmonary Bypass
Extracorporeal circulation and cardiopulmonary bypass are synonymous terms denoting a method by which the blood that usually returns directly to the heart is temporarily drained from superior and inferior vena cavae. The blood is diverted into a reservoir where it is oxygenated and subsequently returned to the patient’s arterial circulation. This process effectually excludes the heart from the general circulation and leaves it empty so that it can accommodate surgical intervention.
The breakthrough technologies that first allowed this type of open-heart operation were developed by two separate centers in the United States in the early 1950s.
Importantly, Lillehei and Varco [1] at the University of Minnesota developed a cross-circulation technique. This technique utilized a human donor (usually the parent of a child undergoing cardiac surgery) who, in essence, functioned as an extracorporeal pump for the patient’s circulatory system. This type of extracorporeal circulation also allowed the blood to be drained from the child’s vena cava so that the surgical procedure could be performed within the empty heart. The subsequent development of the heart–lung machine by Gibbon [2] was considered revolutionary in that it eliminated the need for a support donor (a second patient). Gibbon’s system has been improved since the mid-1950s and has gradually evolved into the standardized, but very complex and sophisticated,
machine it is today.
The basic components of an extracorporeal circuit include: (1) a reservoir into which the patient’s blood is diverted; (2) an oxygenator that replaces the function of the lungs; and (3) a pump that propels the oxygenated blood back into the patient’s arterial circulation. In this manner, the machine bypasses both the heart and the lungs while maintaining the functions of other organs during surgical interventions within the heart.
Venous Drainage
The venous blood that is normally delivered to the right atrium is commonly iverted to the heart–lung machine,either by cannulating the veins themselves or by cannulating the right atrial chamber. Surgery performed in or through the right atrial chamber requires that both the right atrium and right ventricle be empty. To do so, cannulas are placed directly into the superior and inferior venae cavae. Constricting tourniquets are then placed around the vein over the cannulas, and blood is diverted into the heart–lung machine. These proceduresconstitute total cardiopulmonary bypass. Venous cannulation is normally performed in one of two ways: (1) by placing a purse string suture either directly in the superior vena cava or in the right atrium or (2) by advancing the cannula into the superior vena
cava. It should be noted that direct cannulation of the superior vena cava generally provides more room for any work that may need to be done inside the right atrium.
A modification of this type of bypass can be used when the cardiac chambers are not surgically entered, such as in coronary bypass operations involving procedures on the surface of the heart. In such cases, a single cannula is placed in the right atrium, or a double-staged cannula is placed with the tip of the cannula in the inferior vena cava and the side drainage holes positioned at the level of the
right atrium. Coronary bypass surgery does not involve direct vision of the inside of the cardiac chambers, so there is no need to constrict the superior or inferior
venae cavae. When coronary bypass operations are undertaken simultaneously with cardiac valve repairs or replacements, total cardiopulmonary bypass is typically
implemented.
Arterial Return
Once the blood has been oxygenated in the heart–lung machine, it is returned to the patient’s general circulation via cannulas placed directly in the arterial system
(Fig. 30.1). The most common method involves the placement of a cannula in the highest portion of the ascending aorta below the origin of the innominate artery. Depending on the type of surgery, other sites are also used, including cannulation of the femoral artery in the groin and infusion of the arterial system in a retrograde manner. The ascending aorta is cross-clamped at this point, so
no systemic blood enters the coronary artery circulation. The heart is, therefore, totally excluded from the circulation. Thus the heart needs to be protected by using one of a number of methods to infuse cardioplegic solutions . Any blood remaining in the operative field is removed via cardiotomy suction lines
which are used to aspirate it back to the heart–lung machine, where it reenters the bypass circulation with the rest of the removed blood. In some operations involving the descending thoracic aorta, total cardiopulmonary bypass is not necessary. If
the portion of the aorta that needs to be isolated lies between the left carotid artery and the diaphragm, only part of the total blood volume needs to be removed, and partial bypass can be implemented. The blood is removed by the heart–lung machine via a cannula inserted into either the left atrium or left superior pulmonary vein. Then, the blood is infused back into the descending thoracic aorta beyond the level of distal aortic cross-clamping. Doing so allows the heart to continue to beat normally and helps maintain the viability of the proximal organs (head, neck, and arms), while the rest of the lower body is perfused and thus maintained by the pump. This technique is called left heart bypass, because it involves only removal of blood and decompression of the left side cardiac chambers.
after a descending thoracic aorta aneurysm operation is completed, the bypass is discontinued. The clamps which were placed to occlude the aorta in the arch and the descending portion are removed. The normal physiological perfusion of the body (which was interrupted during surgery without ever stopping the heartbeat)
is thus reestablished. In contrast, total cardiopulmonary bypass involves complete stoppage of the heart. After an operation applying total cardiopulmonary bypass and cardiac arrest,the aortic clamp is released allowing the general circulation
to reperfuse the coronary arteries and to rewarm the heart.
After the air is expelled from the cardiac chambers, the heart usually elicits ventricular fibrillation. Such fibrillation normally requires cardioversion with an electric shock administered directly to the heart by employing paddles that deliver currents that vary from 20 to 30 watts/sec. The patient is then ventilated using the endotracheal tube connected to the anesthesia machine, which reinflates the
lungs. After the normal sinus rhythm of the heart is reestablished, the patient is gradually weaned off the extracorporeal circulation until the heart takes over full function. At this point the heart–lung machine is stopped, and all cannulas are removed and access areas closed. In some complex surgical cases involving the aortic
arch, separate independent perfusion of the arch vessels may require implementation, that is, in addition to the perfusion of the lower part of the body through the cannula inserted in the femoral artery. This situation places a
great demand on the perfusionist operating the heart– lung machine. The perfusionist must monitor two separate infusions to regulate pressures and make certain that a balance and sufficient perfusion is achieved in both
the upper and the lower areas of the patient’s body. Another specialized bypass method that needs description is the deep hypothermia and total circulatory arrest
technique. This type of total cardiopulmonary bypass employs a decreasing body temperature to very low levels (15–208C); this is typically accomplished using heat
exchangers installed in the heart–lung machine circuits. Circulation is stopped altogether when the proper temperature is reached, and the heart is emptied for several minutes with the entire volume of the patient’s blood remaining in the reservoir of the heart–lung machine. The pump is then stopped and the arterial perfusion ceases. The venous return line, however, is left open to continue emptying the patient’s blood volume completely into the reservoir of the heart–lung machine. This technique is used in special cases to allow repair of
very complicated conditions. The period of total circulatory arrest induced during deep hypothermia is usually less than 45 min [3, 4]. This time restriction is to insure that the patient does not suffer neurological deterioration or central
nervous system damage during such global ischemia. As soon as the repair is completed, normal cardiopulmonary bypass is reestablished. The patient is gradually
rewarmed to a normal core temperature of 378C prior to removal from extracorporeal circulation. The use of such deep hypothermia always requires careful evaluation by
the surgical team. In such clinical cases, the danger of inducing neurological damage must be weighed against the benefits of correcting a major cardiac anomaly.
Anticoagulation
To prevent the formation of clots during cardiopulmonary procedures, both within the body and in the extracorporeal heart–lung machine, it is necessary to anticoagulate the patient. The most common agent used for such anticoagulation is heparin. It is commonly administered intravenously before cannulation at a dose of 300 units/kg. There are two types of heparin: (1) the lung beef type which is extracted from a bovine source and (2) the porcine mucosal type which is from a swine source. Since the mid-1980s, the porcine mucosal heparin has been
preferred because it is less likely to lead to thrombocytopenia and production of heparin antibodies in the patient, a condition known as HIT syndrome [5].
The effectiveness of anticoagulation therapy requires testing, usually by measuring the activated clotting time of the patient’s blood. The result is expressed in seconds, with normal values ranging between 100 and 120 s.
Heparinization is deemed adequate when the activated clotting time runs above 300 s. At any time after such values are achieved, it is considered that the patient can
undergo cannulation and be placed on extracorporeal circulation. Typically, the anticoagulant effects induced during such surgeries must be reversed postoperatively. Protamine sulfate is the drug of choice to neutralize the
effects of the heparin and allow the patient to elicit normal clotting values. Yet, this drug is a macromolecule compound that may produce pulmonary vasoconstriction
and severe hypotension [6, 7], particularly in diabetic patients. Nevertheless, such side effects are rare and, in most patients, this drug can be used safely, as it neutralizes the effects of heparin. Naturally, the amount of protamine necessary to achieve neutralization depends on the amount and timing of heparin administered. Initially, a test dose is given; if no reaction occurs, protamine is then administered in the appropriate amounts. Its effects are monitored by measuring activated clotting times until they return to a normal range. It should be
noted that if any reaction or side effect occurs, additional treatments are commonly employed, such as the administration of epinephrine, calcium, steroids, or fluids [7].
Occasionally patients cannot be given heparin because they have developed heparin antibodies from previous exposure. Other anticoagulant agents are studied and
occasionally used in such cases, including hirudin (Lepirudin) [8], a potent anticoagulant that is extracted from leaches and lampreys. Other drugs include the heparinoids [9] like Orgaran (Org10172, Organon Company,West Orange, NJ), for which a different monitoring protocol is implemented. Unfortunately, to date, no drug has
been identified that can reverse the effects of Orgaran, thus it must be metabolized by the human body. For such patients bleeding is a constant, and often very difficult, postoperative complication.
If the cardiopulmonary bypass takes an extended time, coagulopathies often pose complications. In such cases, the body, primarily the liver, is unable to produce the appropriate clotting factors to reverse the anticoagulation status.Other factors that can contribute to coagulopathies include ischemia of the abdominal organs, particularly if necrosis occurs in the liver cells and/or in the intestine. Bleeding, therefore, can be a very serious and difficult complication to treat; administration of multiple coagulation factors, platelets, and cryoprecipitates may be required.
Temperatures of Perfusion
Since their inception, cardiopulmonary bypass and extracorporeal circulation have been implemented using some degree of hypothermia. Lowering core body temperature
decreases the overall oxygen demands of body tissues, and a more desirable protective state during pulseless circulation is provided by the heart–lung machine.
Several degrees of hypothermia are commonly identifiable relative to extracorporeal circulation interventions. Normothermia indicates that core body temperature is
between 35.5 and 378C [10], mild hypothermia is between 32 and 358C, and moderate hypothermia is between 24 and 328C. An important distinction must be made between
mild and moderate hypothermia. If the heart is perfused at mild levels (above 318C), the heart will continue to beat although at a slower rate. This mild level of hypothermia allows surgical correction of some congenital anomalies
without arresting the heart. An addition level of hypothermia used occasionally is deep or profound hypothermia, which was previously mentioned, and usually brings the body temperature below 208C. Currently, most open cardiac operative procedures are conducted under conditions somewhere between moderate and mild hypothermia. Some centers routinely use moderate hypothermia, while others employ normothermia
[11, 12]. One reason to maintain normothermic perfusion is to avoid coagulopathies that may develop when body temperature is lowered to the moderate levels, and
thus allow for normal function of the body’s enzyme systems. Normothermic temperatures also enable the kidneys to respond better to diuretics.
Several reports have indicated the relative safety of normothermic perfusion [10–16], but an equal number have suggested complications with this modality [17, 18]. As a result, the spontaneous drifting to mild hypothermic levels is generally preferred. Deep or profound hypothermia is associated with the implementation of total circulatory arrest as mentioned before. With this level of hypothermia, body temperature is lowered to between 15 and 188C. Such operations are thus usually prolonged given the time it takes to cool the body to those levels before surgery and also by the required time to rewarm it afterwards.
Perfusion Pressures
Under normal physiological conditions, the heart provides a pulsatile pressure and flow. The systolic pressure depends on the ventricular function. The diastolic pressure in normal states is primarily regulated by the blood volume and the vascular tonus. During cardiopulmonary bypass, the heart–lung machine facilitates pulseless perfusion; there is no systolic or diastolic pressure, but rather
one steady mean pressure throughout the arterial circulatory system. Therefore, this pressure should be high enough to provide adequate blood oxygen to all
organs of the body, particularly the brain and kidneys.
Since the patient is typically hypothermic, the oxygen requirements are lower; the perfusion pressure is usually maintained around 70 mmHg. Occasionally, specifically
in patients with severe obstructive carotid disease, a higher perfusion pressure is recommended to ensure proper perfusion of the brain. Nevertheless, this recommendation is somewhat debated because the brain is known to have its own regulatory system to maintain low resistance near obstructed areas [12, 14].
During cardiopulmonary bypass, if the patient shows decreased vascular tonus (despite adequate volume of fluid), vasoconstrictors are routinely used; a typical therapy is a bolus or drips of neosynephrine [10]. A decreased vascular tonus is common in septic patients with bacterial endocarditis, for whom an emergency operation sometimes is necessary to replace the affected valve and reverse
the profound heart failure. In general, a mean perfusion pressure of around 70 mmHg during cardiopulmonary bypass should be maintained.
Hemodilution
Up to a certain level, hemodilution can be a desirable side effect of cardiopulmonary bypass. Lowering the hematocrit prevents ‘‘clumping’’ of the red cells or ‘‘sludging,’’ thereby providing better circulation at the capillary level;
viscosity of the circulating blood is decreased, on the other hand, to also ensure that oxygen is adequately delivered to the body’s tissues during cardiopulmonary bypass. Hematocrit levels are monitored and maintained at a minimum between 22 and 26%. Toward the end of the bypass operation,typically the perfusionist deliberately removes some of the fluid from the patient’s circulation to hemoconcentrate
the blood toward more normal hematocrit levels [19,20]; this rises to above 30% by the time the patient is removed from cardiopulmonary bypass. Subsequent diuresis
and/or removal of red blood cells will further aid in reestablishing the hematocrit to normal levels. Pulseless perfusion, as provided by the heart–lung
machine, and hemodilution will both invariably lead to a transfer of fluid across the capillary walls into the third space (interstitial). Therefore, all patients develop, to some degree, peripheral third spacing or edema, which is particularly seen in children and usually requires several days to clinically resolve completely. In an attempt to avoid this condition, plasma expanders (such as albumin, hetastarch, dextran, and mannitol) are usually added to
the priming solution of the heart–lung machine. 30.1.7 Heart–Lung Machine Basics
The basic components of the heart–lung machine include an oxygenator, a reservoir for the perfusion solution, a perfusion pump, line filters, two heat exchangers, and
monitoring devices. Although the bubble oxygenator has been used for many years, it has been largely supplanted by the membrane oxygenator. The membrane
oxygenator is associated with less trauma to red blood cells and is less likely to produce micro-bubbles that might pass into the patient’s arterial system and cause air embolism. In addition, the newer centrifugal pumps like the Bio-Medicus (Medtronic, Inc., Minneapolis, MN) and the Performer1 CPB (Medtronic, Inc.), offer
a distinct advantage over the older roller-type pumps such as the standard DeBakey type. More specifically, the roller pumps use occlusive pressure to propel the blood
within the tubing, and can cause damage to the red blood cells and dislodge debris from the tubing material. In contrast, the newer centrifugal pumps minimize trauma
to the red blood cells, because the motion required to move the blood does not constrict the tubing
Senin, 07 Februari 2011
GAGAL JANTUNG
DEFINISI
Gagal jantung adalah suatu sindroma klinis yang disebabkan oleh disfungsi jantung dengan akibat berkurangnya aliran darah dan suplai oksigen ke jaringan sehingga jantung tidak dapat lagi memenuhi kebutuhan metabolik tubuh.
Gagal jantung adalah suatu keadaan ketidakmampuan jantung untuk memompakan darah ke seluruh tubuh sesuai dengan kebutuhan metabolisme.
Gagal jantung adalah keadaan dimana jantung tidak mampu memompakan cukup darah guna memenuhi kebutuhan oksigen untuk metabolism tubuh serta kebutuhan nutrisi sehingga menyebabkan ketidakseimbangan suplai dan deman oksigen miokard. Fungsi utama jantung adalah memompakan darah yang masuk ke venrikel dari system vena yang bertekanan rendah melawan system arterial yang bertekanan tinggi. Gangguan kemampuan pompa ini mengakibatkan ketidak adekuatan pengosongan vena dan ketidak adekuatan hantaran darah ke sirkulasi pulmonal dan sistemik.
B. ETIOLOGI
1. Penyebab gagal jantung secara menyeluruh menurut Hurts JW, et al (eds): The Heart, vol 1, ed 7, New York
a. Gangguan mekanis
1) Peningkatan beban tekanan
a) Central (stenosis aorta)
b) Periphrela (hipertensi sistemik)
2) Peningkatan beban volume
a) Regurgitasi katup
b) Pirau (shunt)
c) Meningkatnya preload
3) Hambatan pengisian ventrikel
§ Stenosis mitral atau trikuspid
4) Kontriksi pericard, tamponade
5) Retriksi endokard atau miocard
6) Aneurisma ventricular
7) Dis-sinergi ventrikel
b. Kelainan miokardial
1) Primer
a) Kardiomiopati
b) Gangguan neuromuscular
c) Miokarditis
d) Metabolic (DM)
e) Keracunan (alcohol, kobalt dst)
f) Presbikardia
2) Sekunder
a) Ischemia (penyakit jantung koroner/ketidakseimbangan suplai dan deman koroner)
b) Gangguan metabolic
c) Inflamasi
d) Penyakit infiltrative (restrictive cardiomiophaty)
e) Penyakit sistemik
f) Penyakit paru obstruktif kronis
g) Obat-obatan yang mendepresi miokard
3) Gangguan irama jantung
a) Henti jantung
b) Fibrilasi
c) Takhikardia atau bradikardia yang ekstrim
d) Gangguan konduksi
c. Pencetus gagal jantung
1) Hipertensi
2) Infark miokard
3) Aritmia
4) Anemia
5) Febris
6) Emboli paru
7) Stress
8) infeksi
C. PATOFISIOLOGI
Fungsi jantung sebagai sebuah pompa di indikasikan oleh kemampuannya untuk memenuhi suplai darah yang adekuat ke seluruh tubuh, baik dalam keadaan istirahat maupun saat mengalami stress fifiologis. Mekanisme fisiologis dasar jantung seperti stroke volume (isi sekuncup), cardiac output (curah jantung), heart rate (laju jantung), pre load (beban awal), dan after load (beban akhir) serta kontraktilitas sangat berpengaruh dalam mekanisme terjadinya gagal jantung.
Stroke volume (SV) adalah jumlah darah yang dipompakan oleh ventrikel setiap kali kontraksi. Cardiac output (CO) adalahjumlah darah yang dipompakan oleh ventrikel setiap menit. Ada
1. Pre load
Pre load menggambarkan tekanan miokardium pada fase akhir diastolic atau sesaat sebelum kontraksi ventrilkel. Secara klinik diambarkan sebagai “ventricle filling”. Menurut hokum Frank Strarling : makin besar isi jantung saat diastolic, semakin besar juga jumlah darah yan dipompakan ke aorta.
2. After load
After load menggambarkan tekanan aortic total (impedance) yang menahan ejeksi ventrikel. Apabila tekanan sistemik arterial meningkat maka kerja jantung akan meningkat pula.
3. Kontraktilitas
Adalah kemampuan intrinsic serabut-serabut miokard untuk menguncup. Peningkatan stroke volume menggambarkan peningkatan kontraktilitas dan sebaliknya, penurunan stroke volume menggambarkan penurunan kontraktilitas.
Sebagai respon terhadap gagal jantung, ada tiga mekanisme primer yang dapat dilihat : meningkatnya aktivitas adrenergic simpatik, meningkatnya beban awal akibat aktivasi system rennin-angiotensin-aldosteron, hipertropi ventrikel. Ketiga repon kompensatorik ini mencerminkan usaha untuk mempertahankan curah jantung. Mekanisme-mekanisme ini mungkin memadai untuk mempertahankan curah jantung pada tingkat normal atau hamper normal pada gagal jantung dini, dan pada keadaan istirahat. Tetapi, kelainan pada kerja ventrikel dan menurunnya curah jantung biasanya tampak pada keadaan beraktivitas. Dengan berlanjutnya gagal jantung, maka kompensasi akan menjadi semakin kurang efektif.
Sebagai akibat gagal jantung , maka terjadilah mekanisme kompensasi tubuh yang meliputi :
1. Peningkatan aktifitas adrenergic simpatis
Meningkatnya aktifitas simpatik adrenergic akan merangsang pengeluaran katekolamin dari saraf-saraf agrenergik jantung dan medulla adrenal. Hal ini akan meningkatkan kontraktilitas dan denyut jantung, yang akan menjamin cardia output. Peningkatan kontraktilitas dan denyut nadi sangat bergantung pada respon simpatik tubuh. Akibat lain dari mekanisme ini otot akan berkontraksi, sehingga jantung harus memopa lebih kuat lagi karena tahanan perifer meningkat. Seperti yang diharapkan, kadar katekolamin yang beredar dalam akan meningkat pada gagal jantung, terutama selama latihan. Jantung akan semakin bergantung pada katekolamin yang beredar dalam sirkulasi untuk mempertahankan kerja ventrikel. Namun pada akhirnya respon moikardium terhadap rangsangan simpatik akan menurun, katekolamin akan berkurang pangaruhnya terhadap ventrikel. Perubahan ini paling tepat dikonseptualisasikan dengan melihat kurva fungsi ventrikel (gambar 1). Dalam keadaan normal katekolamin akan menimbulkan efek inotropik positif terhadap ventrikel, menggeser kurva ke atas dan ke kiri, dengan berkurangnya respon ventrikel yang gagal terhadap rangsangan katekolamin, maka derajat pergeseran sebagai respon terhadap perangsangan juga berkurang. Perubahan ini dapat dihubungkan dengan observasi yang menunjukan bahwa penyimpanan norepineprin pada miokardium menjadi berkurang pada gagal jantung kronik.
2. Peningkatan pre load
Aktivasi system RAA (Rennin Angiotensin Aldosteron) menyebabkan retensi garam natrium dan air oleh ginjal, meningkatnya volume ventrikel dan regangan serabut. Peningkatan beban awal ini akan menambah kontraktilitas miokardium sesuai hukum Starling. Mekanisme pasti yang mengakibatkan aktivasi system rennin-angiotensin-aldosteron pada gagal jantung masih belum jelas. Tetapi, seumlah faktor telah diperkirakan, antara lain perangsangan simpatik adrenergic pada reseptor beta di dalam apparatus juktaglomerulus, respon reseptror macula densa terhadap perubahan pelepasan natrium pada tubulus distal, dan respon baroreseptor terhadap perubahan volume dan tekanan darah yang bersirkulasi.
3. Hipertropi ventrikel
Penebalan dinding ventrikel tanpa disertai penambahan ukuran ruang jantung akan menyebabkan jantung bekerja lebih keras untuk mencukupi kebutuhan tubuh.
Ketiga respon kompensatorik ini menggambarkan usaha untuk mempertahankan curah jantung, namun bila gagal jantung berlanjut maka kompensasi ini menjadi semakin tidak efektif.
A. KLASIFIKASI GAGAL JANTUNG
Gagal jantung menurut NewYork Heart Association terbagi atas empat kelas fungsional, yaitu :
1. Timbul gejala sesak pada aktivitas fisik berat
2. Timbul gejala sesak pada aktivitas sedang
3. Timbul gejala sesak pada aktivitas ringan
4. Timbul gejala sesak pada aktivitas sangat ringan atau istirahat
B. MANIFESTASI KLINIK
Tanda dominan gagal jantung adalah meningkatnya volume intravascular. Kongesti jaringan terjadi akibat tekanan arteri dan vena yang meningkat akibat turunnya curah jantung pada kegagalan jantung. Peningkatan tekanan vena pulmonalis dapat menyebabkan cairan mengalir ke dari kapiler paru ke alveoli, akibat terjadi edema paru, yang dimanifestasikan dengan batuk dan napas pendek. Meningkatnya tekanan vena sistemik dapat mengakibatkan edema perifer umum dan penambahan berat badan.
Turunnya curah jantung pada gagal jantung dimanifestasikan secara luas karena darah tidak dapat mencapai jaringan dan organ (perfusi rendah) untuk menyampaikan oksigen yang dibutuhkan. Beberapa efek yang biasanya timbul akibat perfusi rendah adalah pusing, konfusi, kelelahan, tidak toleran terhadap latihan dan panas, ekstremitas dingin, dan haluaran urin berkurang (oliguri). Tekanan perfusi ginjal menurun, mengakibatkan pelepasan rennin dari ginjal, yang pada gilirannya akan menyebabkan sekresi aldosteron, retensi natrium dan cairan, serta peningkatan volume intravascular.
Ventrikel kanan dan kiri dapat mengalami kegagalan secara terpisah. Gagal ventrikel kiri paling sering mendahului gagal ventrikel kanan. Gagal ventrikel kiri murni sinonim dengan edema paru akut. Karena curah ventrikel berpasangan atau sinkron, maka kegagalan salah satu ventrikel dapat mengakibatkan penurunan perfusi jaringan. Tetapi manifestasi kongesti dapat berbeda tergantung pada kegagalan ventrikel mana yang terjadi.
Kegagalan pada ventrikel kiri umumnya menyebabkan kongesti paru, karena ventrikel kiri tidak mampu memompakan darah yang datang dari paru. Peningkatan tekanan dalam sirkulasi paru menyebabkan cairan terdorong ke jaringan paru. Manifestasi klinis yang terjadi meliputi dipsneu, batuk, mudah lelah, denyut jantung cepat (takikardia) dengan bunyi jantung S3, cemas dan gelisah. Dipsneu terjadi akibat penimbunan cairan dalam alveoli yang mengganggu pertukaran gas. Dipsneu bahkan dapat terjadi saat istirahat atau dicetuskan oleh gerakan yang minimal atau sedang. Dapat terjadi Ortopneu, kesulitan bernapas saat berbaring. Pasien yang mengalami ortopneu tidak akan mau berbaring, tetapi akn menggunakan bantal agar bias tegak di tempat tidur atau duduk dikursi, bahkan saat tidur. Bebarapa pasien hanya mengalami ortopneu pada malam hari, suatu kondisi yang dinamakan paroximal nocturnal dipsneu (PND). Hal ini terjadi bila pasien, yang sebelumnya duduk lama dengan posisi kaki dan tangan di bawah, pergi berbaring ke tempat tidur. Setelah beberapa jam cairan yang tetimbun di ekstremits yang sebelumnya berada di bawah mulai diabsorbsi, dan ventrikel kiri yang sudah terganggu, tidak mampu mengosongkan peningkatan volume dengan adekuat. Akibatnya, tekanan dalam sirkulasi paru meningkat dan lebih lanjut, cairan berpindah ke alveoli. Batuk biasanya berhubungan dengan kegagalan ventrikel kiri bias kering atau tidak produktif, tetapi yang tersering adalah batuk basah, yaitu batuk yang menghasilkan sputum berbusa dalam jumlah banyak, yang kadang disertai bercak darah. Mudah lelah terjadi akibat curah jantung yang kurang yang menghambat jaringan dan sirkulasi normal dan oksigen serta menurunnya pembuangan sisa hasil katabolisme, juga terjadi akibat meningkatnya energy yang digunakan untuk bernapas dan insomnia yang terjadi akibat distress pernapasan dan batuk. Kegelisanan dan kecemasan biasanya terjadi akibat gangguan oksigenasi jaringan, stes akibat kesulitan bernapas dan pengetahuan bahwa jantung tidak berfungsi dengan baik. Begitu terjadi kecemasan, terjadi juga dipsneu, yang pada gilirannya memperberat kecemasan.
Bila kegelalan terjadi pada ventrikel kanan, yang menonjol adalah kongesti visera dan jaringan perifer. Hal ini terjadi karena sisi kanan jantung tidak mampu mengosongkan volume darah dengan adekuat sehingga tidak dapat mengakomodasi semua darah yang secara normal kembali dari sirkulasi vena. Manifestasi klinis yang tampak meliputi edema ekstremitas bawah (edema dependen), yang biasanya merupakan pitting edema, pertambahan berat badan, hepatomegali, distensi vena leher, asites ( penimbunan cairan di dalam rongga peritoneum), anoreksia, mual, nokturia dan lemah. Edema dimulai pada kaki dan tumit (edema dependen) dan secara bertahap bertambah ke atas tungkai dan paha dan pada akhirnya ke genitalia eksterna dan tubuh bagian bawah. Edema sacral sering jarang terjadi pada pasien yang berbaring lama, karena daerah sacral menjadi daerah yang dependen. Pitting edema, adalah yang akan tetap cekung bahkan setelah penekanan ringan dengan ujung jari, baru jelas terlihat setelah terjadi retensi cairan paling tidak sebanyak 4.5 kg. Hepatomegali dan nyeri tekan pada kuadran kanan atas abdomen terjadi akibat pembesaran vena di hepar. Bila proses ini berkembang, maka tekanan dalam pembuluh portal meningkat sehingga cairan terdorong keluar rongga abdomen, suatu kondisi yang dinamakan asites. Pengumpulan cairan dalam rongga abdomen ini dapat menyebabkan tekanan pada diagfragma dan distress pernapasan. Anoreksia (hilangnya selera makan) dan mual terjadi akibat pembesaran vena dan statis vena di dalam rongga abdomen. Nokturia atau rasa ingin kencing pada malam hari, terjadi karena perfusi renal didukung oleh posisi penderita pada saat berbaring. Dieresis terjadi paling sering pada malam hari karena curah jantung akan mmbaik dengan istirahat. Lemah yang menyertai gagal jantung sisi kanan disebabkan karena menurunnya curah jantung, gangguan sirkulasi, dan pembuangan produk sampah katabolisme yang tidak adekuat dari jaringan.
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