**2. Pathophysiology during the early postoperative period**

#### **Arrival in the intensive care unit**

Upon arrival in the ICU, an efficient transfer of care from operation room staff to ICU staff is mandated, while at the same time vital signs are to be maintained stable.

The initial goals in postoperative cardiac recovery are sufficient analgesia, normothermia, adequate oxygenation and ventilation, control of bleeding, restoration of intravascular volume, optimization of blood pressure and cardiac output to maintain organ perfusion and metabolic stabilization.

#### **Hypothermia**

Hypothermic cardiopulmonary bypass is usually terminated after the patient has rewarmed to a core body temperature of at least 36 C. (1) However, patients usually arrive in the ICU with lower core temperatures. This drop in temperature from end of CPB until arrival in the ICU is due to the cool ambient temperatures in the operation room, poor peripheral perfusion and anesthesia-induced inhibition of normal themoregulation. Even patients operated under normothermic CPB, have a tendency to significantly cool down before conclusion of surgery.

Hypothermia has many potential adverse effects. (2) It increases the systemic vascular resistance (SVR) which increases myocardial afterload and myocardial oxygen demand. This compensatory mechanism to provide core warming may contribute to slow warming of peripheral tissues. Drugs that provide vasodilation may improve peripheral perfusion. To prevent hypotension, warmed infusions should be administered concomitantly. Peripheral vasodilation augments heat loss, and core hypothermia may therefore persist.

Hypothermia also precipitates shivering, thereby increasing CO2 production and oxygen consumption, and predisposes to ventricular arrhythmias and coagulation cascade impairments. (3,4)

Therefore, warming should be hastened by forced-air warming blankets, heated humidifiers in the ventilator circuit and warmed infusion fluids. The use of other types of warming blankets or radiant heading hoods can also be considered. (5)

After cardiac surgery, patients may rapidly rewarm and occasionally overwarm to higher temperatures. This phenomenon is attributed to the resetting of the central thermoregulation system.

#### **Blood loss after cardiac surgery**

Careful hemostasis in the operation room is the cornerstone in reducing postoperative blood loss. However, bleeding can also be medical and determing the cause of bleeding is often difficult. Although the clinical situation must be individualized for each patient, bleeding in general should not exceed 400 mL/hr during the first hour, 200 mL/hr for each of the first 2 hours, or 100 mL/hr over the first four hours. (6)

There are numerous medical causes for bleeding following cardiac surgery. Residual heparinization is common post cardiac surgery and usually occurs when insufficient protamine is used or heparined pump blood is transfused following CPB.

Platelet dysfunction is also common following cardiac surgery. The CPB circuit itself leads to contact activation and degranulation of platelets, resulting in their dysfunction. Fibrinolysis frequently occurs after CPB, caused by activation of inflammatory or coagulation pathways.

Coagulation factors may decrease from activation and dilution in the CPB circuit.

There has been a dramatic increase in the iatrogenic use of heparin and newer antiplatelet, antithrombotic and thrombolytic drugs during (interventional) treatment of acute cornary syndromes. If revascularization surgery is warranted immediately after these treatments, the anticoagulant effect of these drugs is notable in the postoperative period.

Conventional coagulation tests are helpful to identify the coagulation abnormality contributing to the bleeding. Common laboratory testing includes Hb, platelet count, aPTT, INR, and fibrinogen level. Thromboelastography is also commonly used and has been demonstrated to reduce transfusion requirements.

The most basis principles of the management of postoperative bleeding are:


operated under normothermic CPB, have a tendency to significantly cool down before

Hypothermia has many potential adverse effects. (2) It increases the systemic vascular resistance (SVR) which increases myocardial afterload and myocardial oxygen demand. This compensatory mechanism to provide core warming may contribute to slow warming of peripheral tissues. Drugs that provide vasodilation may improve peripheral perfusion. To prevent hypotension, warmed infusions should be administered concomitantly. Peripheral

Hypothermia also precipitates shivering, thereby increasing CO2 production and oxygen consumption, and predisposes to ventricular arrhythmias and coagulation cascade

Therefore, warming should be hastened by forced-air warming blankets, heated humidifiers in the ventilator circuit and warmed infusion fluids. The use of other types of warming

After cardiac surgery, patients may rapidly rewarm and occasionally overwarm to higher temperatures. This phenomenon is attributed to the resetting of the central

Careful hemostasis in the operation room is the cornerstone in reducing postoperative blood loss. However, bleeding can also be medical and determing the cause of bleeding is often difficult. Although the clinical situation must be individualized for each patient, bleeding in general should not exceed 400 mL/hr during the first hour, 200 mL/hr for each of the first 2

There are numerous medical causes for bleeding following cardiac surgery. Residual heparinization is common post cardiac surgery and usually occurs when insufficient

Platelet dysfunction is also common following cardiac surgery. The CPB circuit itself leads to contact activation and degranulation of platelets, resulting in their dysfunction. Fibrinolysis frequently occurs after CPB, caused by activation of inflammatory or

There has been a dramatic increase in the iatrogenic use of heparin and newer antiplatelet, antithrombotic and thrombolytic drugs during (interventional) treatment of acute cornary syndromes. If revascularization surgery is warranted immediately after these treatments,

Conventional coagulation tests are helpful to identify the coagulation abnormality contributing to the bleeding. Common laboratory testing includes Hb, platelet count, aPTT, INR, and fibrinogen level. Thromboelastography is also commonly used and has been

3. Restore clotting parameters to normal by means of medications , transfusion of blood

protamine is used or heparined pump blood is transfused following CPB.

Coagulation factors may decrease from activation and dilution in the CPB circuit.

the anticoagulant effect of these drugs is notable in the postoperative period.

The most basis principles of the management of postoperative bleeding are:

vasodilation augments heat loss, and core hypothermia may therefore persist.

blankets or radiant heading hoods can also be considered. (5)

conclusion of surgery.

impairments. (3,4)

thermoregulation system.

coagulation pathways.

**Blood loss after cardiac surgery** 

hours, or 100 mL/hr over the first four hours. (6)

demonstrated to reduce transfusion requirements.

4. Monitor for stability of clotting parameters.

2. Rule out surgical bleeding;

1. Diagnose underlying medical cause by coagulation tests;

products or clotting factors, and restore normothermia;

Most cardiac surgical centers use the antifibrinolytic lysine analogues, tranexaminic acid and aminocaproic acid, to reduce intraoperative bleeding. These drugs significantly reduce allogeneic blood transfusion after cardiac surgery.

Although rescue therapy with recombinant factor VII can be life-saving in massive bleeding after cardiac surgery, its safety has been questioned. A recent meta-analysis (N = 4468 from 35 studies) demonstrated that this therapy significantly increased the rate of arterial but not venous thromboembolic events. Given its cost and arterial thrombotic risk, it is likely that this hemostatic intervention will continue to be reserved for life-saving therapy of massive coagulopathy after cardiac surgery.(7)

#### **Blood transfusion management**

Although there are guidelines for blood transfusion in cardiac surgery, considerable variability has persisted in clinical practice. This variability also exists in anticoagulation and coagulation management.

A recent randomized controlled trial has already demonstrated that restrictive perioperative transfusion does not result in inferior clinical outcome after cardiac surgery. (8) Transfusion burden may in the future be interpreted as a quality indicator in cardiac surgery that must balance risks and benefits to achieve cost-effective optimal clinical outcomes. (9,10)

Perioperative transfusion algorithms for the administration of blood products, coagulation factors and pro-coagulant drugs should assist in preserving resources with improvement in patient safety. (11)

#### **Fluid resuscitation**

Cardiac surgery and CPB elicit a systemic inflammatory response which produces a capillary leak. Therefore, fluid resuscitation with cristalloids and/or colloids is necessary to offset the hemodynamic consequences of the capillary leak and the vasodilation that occurs from rewarming and vasodilating drugs. However, the maintenance of intravascular volume in the leakage phase occurs at the expense of expansion of the interstitial space. (12,13)

After the capillairy leak has ceased and hemodynamics have stabilized, diuretics are often used to eliminate the excessive salt and water administered during surgey and the early postoperative phase. This forced diuresis may beneficially affect pulmonary function and early successful extubation.

Several intraoperative measures that have been implemented throughout the years caused a reduction in the inflammatory response and may have contributed to the faster recovery times currently observed after cardiac surgery. The measures include the use of membrane oxygenation, centrifugal pumps, anti-fibrinolytic drugs and steroids, leukocyte filters and coated CPB tubings. (14,15)

#### **Perioperative cardiovascular dysfunction**

Adequacy of organ perfusion and tissue oxygenation is the primary goal of hemodynamic management in the postoperative cardiac surgical patient. Preload, afterload and contractility should therefore be maintained at their optimal level. This commonly requires atrial or atrioventricular pacing.

Approximately 20 % of cardiac surgical patients develop cardiovascular dysfunction in the perioperative period, resulting in an inability to pump sufficient blood at normal end-diastolic pressures. There are three distinct clinical scenarios of cardiac impairment in the perioperative period of cardiac surgery - precardiotomy, failure to wean and postcardiotomy – differing from each other substantially concerning diagnosis, monitoring and management.

#### *Precardiotomy heart failure*

Myocardial ischaemia is one of the most frequent causes of precardiotomy low output syndrome. The dysfunctional myocardium may not be irreversibly damaged and possibly only 'stunned'or 'hibernating'. Revascularization of the reversibly injured heart areas may result in improved cardiac performance. The first priority should therefore be prompt surgery avoiding further alterations in myocardial contractility, possibly by introducing an IABP preoperatively. However, inadequate myocardial protection during cardiac surgery may exacerbate ischaemic injury in some patients. Patients with longer standing previous poor preoperative cardiac function or with recently irreversibly injured ischaemic heart areas, will of course continue to have poor ventricular performance postoperatively.

#### *Failure to wean*

For the successful therapeutic approach of failure to wean, a correct diagnosis of the underlying cause is necessary. The heart failure may be procedure related or patient specific and includes inadequate myocardial protection, reperfusion injury, ischaemia, infarction, incomplete revascularization, metabolic, uncorrected pathology, mechanical issues, conduction issues, pulmonary hypertension and right ventricular failure.

#### *Postcardiotomy heart failure*

The priority is to preserve end organ function. Preload and heart rhytm should be optimized, and positive inotropic and/or vasopressor drugs are often used to maintain adequate cardiac output and blood pressure. Although this strategy will restore haemodynamics in most patients, mechanical circulatory support may be indicated.

#### *Monitoring and assessing volume status*

Heart failure cannot be ascertained unless the volume status is optimal. However, it is difficult to ascertain volume loading using single haemodynamic measures. Pressure estimates such as pulmonary capillary wedge pressure and central venous pressure are generally unreliable indicators of LV and RV preload. Uncoupling between PCWP and LVEDP frequently occurs as a consequence of elevated pulmonary vascular resistance, pulmonary venoconstriction, mitral stenosis and reduction in transmural cardiac compliance.

Volumetric estimates by echocardiography or transpulmonary thermal dilution techniques are more predictive of preload. In predicting fluid responsiveness in ICU patients, it is preferable to use more reliable dynamic indicators reflecting hypovolaemia, such as stroke volume variation, than static parameters. (16) Several devices are now being used to assess cardiac function based on pulse contour analysis of an arterial waveform. (17)

Echocardiography is of great value in the perioperative cardiac surgical setting. It not only is helpfull in assessing the optimal volume status, but may also immediately identify causes of cardiovascular failure, including valvular problems, cardiac tamponade, systolic anterior motion of the anterior mitral valve leaflet and pulmonary embolism. Echocardiography may differentiate between acute right, left and global heart failure as well as between systolic and diastolic dysfunction.

If there are echocardiographic signs of RV failure, a pulmonary artery catheter (PAC) preferably with continuous SvO2 measurement should be introduced. PACs can differentiate between pulmonary hypertension and RV ischaemia, which necessitates a reduction of RV afterload. PAC and TEE are complementary to each other for diagnosis and treatment of the cardiac surgical patient. Indications for the use of a PAC are, high risk and/or complex cardiac surgery, hemodynamic instability, low cardiac output syndrome, pulmonary hypertension, differentiating between severe right and left ventriclular dysfunction, vasodilation/vasoconstriction, hypovolemia. SvO2 in combination with lactate concentration was used postoperative as a goal-oriented hemodynamic therapy to improve outcome.(18,19)
