History

• 1953: cardiopulmonary bypass was first successfully performed (using a screen oxygenator) for atrial septal defect closure by Dr. John H. Gibbon at Jefferson University Hospital (Philadelphia, PA)

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Differences Between Cardiopulmonary Bypass and Extracorporeal Membrane Oxygenation (ECMO) (see Extracorporeal Membrane Oxygenation, [[Extracorporeal Membrane Oxygenation]])

• Cardiopulmonary Bypass is Equipped with Reservoir Into Which Blood in the Heart is Drained: allows a bloodless surgical field for valve and aortic operations
  • In contrast, the ECMO circuit does not contain a reservoir, so blood flow needs to be continuous
    continuous
• Cardiopulmonary Bypass Can Be Utilized in Conjunction with Air Vent Tubing, Cardioplegia Line for Myocardial Preservation, or Cell Salvage Tubing
• Requirement for Systemic Heparin Anticoagulation is Less Intense for ECMO Because Blood Flow is Continuous and There is No Blood-Air Interface in the Reservoir
  • However, continuous anticoagulation is necessary to prevent thrombus formation on the synthetic thrombogenic surfaces of both CPB and ECMO

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Indications

• Cardiac Assist Device for Use in Acute Cardiogenic Shock (see Cardiac Assist Devices, [[Cardiac Assist Devices]])

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Technical Aspects

Cannulation of Vessels

• Right Atrium (RA): venous limb
• Aorta: arterial limb

Anticoagulation

• Heparin (see Heparin, [[Heparin]]): standardly used during cardiopulmonary bypass
• Argatroban (see Argatroban, [[Argatroban]]): alternative agent
• Bivalirudin (see Bivalirudin, [[Bivalirudin]]): alternative agent

Intraoperative Cell Salvage (Cell-Saver)

• Used to Wash Collected Blood of Fat/Cell Debris/Fibrin Clot/Cytokines/Complement: washed blood is returned to the patient intraoperatively
  • However, platelets/coagulation factors/inhibitors are progressively lost during the cell-save washing process

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Adverse Effects

Cardiovascular Adverse Effects

Myocardial Ischemia-Reperfusion Injury

• Physiology: due to fact that the blood supply to the myocardium is interrupted to achieve a bloodless surgical field
• Preventative Strategies to Minimize Myocardial Ischemia-Reperfusion Injury
  • Aggressive Treatment of Ventricular Fibrillation During Reperfusion
  • Avoidance of Ventricular Distension
  • Controlled Aortic Reperfusion with Mean Arterial Pressure <70 mm Hg
  • Extensive Deairing Circuit to Prevent Coronary Emboli
  • Warming of Hyperkalemic Cardioplegia at Reperfusion (“Hot Shot”)

Vasoplegic Syndrome (Post-Cardiac Surgery Vasodilation) (see Vasoplegic Syndrome, [[Vasoplegic Syndrome]])

• Epidemiology
• Physiology: vasodilation
• Clinical
  • Hypotension (see Hypotension, [[Hypotension]])

Endocrinologic Adverse Effects

Hyperglycemia (see Hyperglycemia, [[Hyperglycemia]])

• Physiology: all are common mechanisms during hypothermic non-pulsatile cardiopulmonary bypass
  • Elevated Epinephrine Levels
  • Hypoinsulinemia
  • Insulin Resistance

Hematologic Adverse Effects

General Comments-Post-Cardiopulmonary Bypass Coagulopathy/Hemorrhage

• Epidemiology
  • Coagulopathy is common with prolonged pump times (>2 hrs)
  • Approximately 33% of cases will require allogeneic packed red blood cell transfusion due to cardiopulmonary bypass
  • Excessive hemorrhage is observed in approximately 10% of cardiopulmonary bypass cases
  • Chest tube output of >3 mL/kg in the first 6 hrs post-op is considered excessive (95th percentile: 475 mL at 6 hrs): high outputs are associated with an approximate 3x-fold increase in mortality, as compared to those who do not bleed excessively [MEDLINE]
• Physiology: post-cardiopulmonary bypass coagulopathy is usually multifactorial (due to multiple factors, as detailed noted below)
• Treatment
  • Specific Treatments for Entities Below
  • Recombinant Factor VIIa (NovoSeven RT) (see Factor VIIa, [[Factor VIIa]])
    • May be given as a last resort (due to high cost and unclear clinical benefit)
    • However, prospective trials suggest that factor VIIa manifests a non-statistically-significant trend toward increased mortality rate when used in this setting [MEDLINE]

Depletion of Coagulation Factors

• Epidemiology: may occur
• Physiology : depletion of coaogulation factors (especially factors V and VIII)
• Diagnosis
  • INR: prolonged
  • PTT: prolonged
• Treatment: fresh frozen plasma (FFP) (see Fresh Frozen Plasma, [[Fresh Frozen Plasma]])

Disseminated Intravascular Coagulation (DIC) (see Disseminated Intravascular Coagulation, [[Disseminated Intravascular Coagulation]])

• Epidemiology : uncommon following cardiopulmonary bypass
• Diagnosis: the diagnosis of DIC post-cardiopulmonary bypass is difficult (since the identification of microthrombi is difficult and hemolysis and consumption of coagulation factors may be commonly seen following cardiopulmonary bypass)

Hemodilution

• Epidemiology: common
• Physiology: due to the fact that the extracorporeal circuit is filled (primed) with a balanced electrolyte solution to avoid air embolism before it is connected to the patient
  • Priming volume is approximately 30% of the adult blood volume

Heparin-Induced Thrombocytopenia (HIT) (see Heparin-Induced Thrombocytopenia, [[Heparin-Induced Thrombocytopenia]])

• Epidemiology: HIT occurs in 1% of cardiopulmonary bypass cases [MEDLINE]

Hyperfibrinolytic State (see Hyperfibrinolytic States, [[Hyperfibrinolytic States]])

• Epidemiology: commonly described in the literature related to post-operative coagulopathy following open heart surgery in the 1950’s-1960’s
  • The routine use of lysine analogues (epsion aminocaproic acid and tranexamic acid) have presumably decreased the incidence in the modern era
• Physiology
  • Contact Activation Involving Factor XII and Kallikrein
  • Elevated Tissue Plasminogen Activator (tPA) Levels Due to Surgical Stress and Cardiopulmonary Bypass: peaks at 30-60 min during cardiopulmonary bypass
• Diagnosis
  • Elevated D-Dimer (see D-Dimer, [[D-Dimer]]): peaks toward the end of cardiopulmonary bypass (in cases where no anti-fibrinolytic agent is administered)
  • Elevated Fibrin Degradation Products
  • Thromboelastography (TEG) (see Thromboelastography, [[Thromboelastography]]): clot lysis
• Treatment
  • ε-Aminocaproic Acid (Amicar) (see Epsilon Aminocaproic Acid, [[Epsilon Aminocaproic Acid]])
  • Tranexamic Acid (see Tranexamic Acid, [[Tranexamic Acid]])

Hypofibrinogenemia (see Hypofibrinogenemia, [[Hypofibrinogenemia]])

• Diagnosis: fibrinogen <100 mg/dL
• Treatment: cryoprecipitate (see Cryoprecipitate, [[Cryoprecipitate]])

Hypothermia-Induced Coagulopathy (see Hypothermia, [[Hypothermia]])

• Physiology: may occur with body temperature <35 degrees C

Incomplete Reversal of Heparin by Protamine (see Protamine, [[Protamine]])

• Physiology: so-called “reheparinization” (“heparin rebound”) may occur after a prior apparent pharmacologic reversal of heparin
  • Possible Mechanims
    • Redistribution of Peripherally Bound Heparin to the Central Compartment
    • Short Blood Half-Life of Protamine
• Diagnosis: activated clotting time (ACT) performed with/without heparinase will reveal residual effect of heparin -> if persistent heparin is present, ACT with/without heparinase will be different and will be equalized in the presence of heparinase
• Treatment: repeat protamine dosing (see Protamine, [[Protamine]])

Inflammatory Response

• Complement Activation: occurs in almost all surgical procedures, but magnitude is higher in cardiopulmonary bypass
• Neutrophil Activation: due to anaphylatoxins and kallikreins
• Release of Pro-Inflammatory Cytokines: due to tissue injury and endotoxin
  • Interleukin-1
  • Interleukin-6
  • Interleukin-8
  • Tumor Necrosis Factor

Platelet Dysfunction (see [Coagulopathy, [[Coagulopathy]])

• Epidemiology: common complication of cardiopulmonary bypass
• Treatment
  • Desmopressin (DDAVP, 1-Deamino-8-d-Arginine Vasopressin) (see Desmopressin, [[Desmopressin]])
  • Platelet Transfusion (see Platelet Transfusion, [[Platelet Transfusion]])

Thrombocytopenia (see Thrombocytopenia, [[Thrombocytopenia]])

• Epidemiology : common
• Treatment
  • Platelet Transfusion (see Platelet Transfusion, [[Platelet Transfusion]])

Neurologic Adverse Effects

Ischemic Cerebrovascular Accident (CVA) (see Ischemic Cerebrovascular Accident, [[Ischemic Cerebrovascular Accident]])

• Epidemiology: occurs in 1.3–4.3% of coronary artery bypass grafting cases
• Risk Factors
  • Chronic Obstructive Pulmonary Disease (COPD) (see Chronic Obstructive Pulmonary Disease, [[Chronic Obstructive Pulmonary Disease]])
  • Diabetes Mellitus (see Diabetes Mellitus, [[Diabetes Mellitus]])
  • History of Cerebrovascular Disease
  • Hypertension (see Hypertension, [[Hypertension]])
  • Increased Number of Aortic Anastomoses
  • Peripheral Vascular Disease (see Peripheral Vascular Disease, [[Peripheral Vascular Disease]])

Intracerebral Hemorrhage (see Intracerebral Hemorrhage, [[Intracerebral Hemorrhage]])

• Epidemiology: may occur

Nonspecific Neurocognitive Decline

• Epidemiology: frequently observed after cardiopulmonary bypass

Pulmonary Adverse Effects

Acute Lung Injury-ARDS (Post-Pump Syndrome) (see Acute Lung Injury-ARDS, [[Acute Lung Injury-ARDS]])

• Epidemiology
• Physiology
• Treatment

Renal Adverse Effects

• Acute Kidney Injury (AKI) (see Acute Kidney Injury, [[Acute Kidney Injury]])

Other Adverse Effects

• Air Embolism (see Air Embolism, [[Air Embolism]])
• xxx
• xxx
• xxx
• xxx
• xxx

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References

• Ann Thorac Surg 1999;67:978–85
• Impact of the patient population on the risk for heparin-induced thrombocytopenia. Blood 2000; 96:1703 [MEDLINE]
• Cardiac surgery and inflammation: the inflammatory response and strategies to reduce the systemic inflammatory response syndrome. Curr Card Rev 2007;3:91-98
• A review of transfusion risks and optimal management of perioperative bleeding with cardiac surgery. Transfusion 2008; 48(1 Suppl): S2–S30 [MEDLINE]
• The inflammatory response to cardiopulmonary bypass. J Cardiothoracic Vasc Anes 2009;23:223- 231
• Safety and efficacy of recombinant activated factor VII: a randomized placebo-controlled trial in the setting of bleeding after cardiac surgery. Circulation. 2009 Jul 7;120(1):21-7. doi: 10.1161/CIRCULATIONAHA.108.834275. Epub 2009 Jun 22 [MEDLINE]
• The coagulopathy of cardiopulmonary bypass. Crit Rev Clin Lab Sci. 2010 Dec;47(5-6):197-212. doi: 10.3109/10408363.2010.549291 [MEDLINE]
• Perioperatively acquired disorders of coagulation. Curr Opin Anaesthesiol. 2015 Apr;28(2):113-22. doi: 10.1097/ACO.0000000000000176 [MEDLINE]
• Acute kidney injury and prognosis after cardiopulmonary bypass: a meta-analysis of cohort studies. Am J Kidney Dis. 2015 Feb;65(2):283-93. doi: 10.1053/j.ajkd.2014.09.008. Epub 2014 Nov 5 [MEDLINE]

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Post-Pump Syndrome

Epidemiology

• Fulminant adult respiratory distress syndrome (ARDS) develops in 1.3% of CPB patients with a mortality of 53% [1]. The adult respiratory distress syndrome (ARDS) following CPB is known as post-perfusion or post-pump syndrome. Since nearly 400,000 people are placed on CPB each year in the United States post-pump syndrome remains a significant clinical problem [2].

Physiology

• The etiology of post-pump syndrome is not well understood. Post-pump syndrome may be caused by a single, massive insult such as protracted bypass time [1], although clinically it is more likely caused by multiple, relatively minor, sequential insults. In our proposed paradigm CPB initiates the systemic inflammatory re- sponse syndrome (SIRS) that constitutes the first insult. This response is most likely caused by contact between blood and the artificial surfaces of the perfusion circuit [3–7]. A subsequent insult (eg hypoxia, ischemia, endotoxemia) that, by itself, would not be of clinical significance results in an overwhelming inflammatory response leading to vascular injury, ARDS, and MOF.

• The inflammatory response elicited by bypass involves activation of complement, leukocytes, and the coagulation cascade by the extracorporeal circuit. Ischemic reperfusion injury and endotoxin release also contribute to organ failure in the latter phases.

• The mechanism believed responsible for multiple insult ARDS is a priming of polymorphonuclear leukocytes (PMN) causing them to sequester in the lung without lung injury. Priming is defined as the enhancement or amplification of a PMN response to a given stimulus following prior exposure to a different agonist [8]. If a second insult occurs, the primed PMNs are activated and release large amounts of toxic oxygen metabolites and proteases causing tissue injury that eventually precipi- tates ARDS [9–16]. We hypothesize that post-pump syn- drome can also occur by the same mechanism with CPB acting as the primary or initial insult.

Clinical

• Fever
• Leukocytosis
• Thombocytopenia
• Organ Dysfunction