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CPB Troubleshooting

TSRA Primer - Adult Cardiac

TSRA Content:


Author: Benjamin Kramer, DO, MS

This is a revision and update from the previous edition of the TSRA Primer in Cardiothoracic Surgery written by John Lazar, MD.

"It's not usually the complication that kills your patient but whether or not you recognize and treat it right the first time." – John Lazar, MD

Cardiopulmonary bypass (CPB) is the backbone of safe and effective cardiac surgery. Despite best efforts to use this technology safely, prompt recognition of complications related to CPB can be lifesaving. CPB components can be broken down to the pump, the reservoir, the oxygenator, tubing, and the arterial and venous cannulas. Each component serves a particular purpose but has the potential to result in a complication. While maintaining appropriate oxygenation and perfusion is the fundamental purpose of CPB, the complex interaction of this circuit with the patient introduces opportunity for complications.

Problems can happen at any time while using the CPB circuit, from pump set-up to weaning to re-establishing spontaneous circulation. Careful attention to detail is critical and prompt recognition of problems is fundamental to safe surgical practice.

Pre-CPB Initiation

Heparinization is the first and most critical step in initiating CPB. Heparin binds to the enzyme antithrombin III (AT III), causing a conformational change that results in inhibition of thrombin formation and inactivation of the coagulation cascade. This allows for supported circulation with very little risk of thrombotic events. Appropriate dosing of heparin for the initiation of CPB is 100 units/kg aiming for a goal activated clotting time (ACT) > 480.

Heparin Reactions:
Although the incidence is rare (~0.2-5%), acute allergic reactions to heparin do occur. While the most common heparin reaction is heparin-induced thrombocytopenia (HIT), traditional anaphylactic reactions have also been documented. The most common symptoms of an acute allergic reaction to heparin include sudden significant hypotension and pulmonary edema, and a few cases of disseminated intravascular coagulation (DIC) have also been documented. Prompt recognition, supportive care, and reversal of heparin are necessary. If unable to use heparin for CPB, currently recommended alternatives are direct thrombin inhibitors such as bivalirudin or argatroban.

Heparin Resistance:
Heparin resistance is the persistent measurement of a low ACT despite initial and/or repeated dosing of heparin. This is usually the result of AT III deficiency. This deficiency, and subsequent heparin resistance, is most often encountered in patients bridged preoperatively on heparin therapy, intravenous nitroglycerin, or those with thrombocytosis. For patients who fail to respond following an additional dose of 1-2mg/kg of heparin, appropriate anticoagulation may be reached by the addition of AT III via the transfusion of fresh frozen plasma (FFP) or commercially available AT III products (Thrombate III).

Cannulation Sites

Cannulation presents the next technical challenge that often requires attention during CPB troubleshooting. Any site where the CPB circuit engages a patient’s anatomy provides a risk of a complication. Special attention should be paid to these sites as complications at these locations can have particularly devastating sequelae.

Aortic Dissection:
Latrogenic aortic dissection may be inadvertently caused by intramural aortic cannula placement, unrecognized intimal injury, or suboptimal cannula positioning. Aortic dissection may result in systemic malperfusion or further aortic damage and is associated with significant comorbidity and increased operative difficulty. Immediate recognition of possible iatrogenic dissection is critical. The first and most common signs of aortic dissection at the time of cannulation and initiation of CPB are:

  • Sudden increase in arterial line pressure with low flow
  • Profound drop in systemic pressure
  • Decrease in venous return to CPB
  • Tissue color changes (darkening, enlargement)

Appropriate steps at this point include:

  • Recognition of dissection
  • Immediate cessation of CPB
  • Rule out kinked or obstructed arterial line
  • Clamp arterial and venous lines
  • Confirm diagnosis (visual/TEE evidence): flaccid aorta, expanding hematoma, dissection flap
  • Move arterial cannula to an alternate site (femoral)
  • Initiate cooling for deep hypothermic circulatory arrest (DHCA) and open aortic repair/replacement

Massive Air Embolism:
Air entry into the arterial system is another emergency that requires urgent action. This presents a threat to cerebral circulation and the risk of irreversible neurologic sequelae. Air may enter the arterial system during CPB set-up and line checks, or secondary to poorly positioned/secured cannulas, loose stopcocks/connections, or permitting the venous reservoir to run low/empty. Unfortunately, the clinical signs of an air embolism are often subtle and clinically delayed resulting in significant morbidity. The most common signs of a massive air embolism are unfortunately based on clinician observation:

  • Visualization of air in the arterial line
  • Visualization of air in the aorta on TEE
  • Sudden change in bispectral index (BIS) / Pupillary dilation

Appropriate steps at this point include:

  • Recognition of potential air embolism
  • Stop CPB
  • Place patient in steep head-down position to prevent air from going to the brain
  • Remove aortic cannula from ascending aorta
  • Purge ascending aorta of air and refill arterial line
  • Begin retrograde cerebral perfusion (20°C at 1-2L/min for 2-3min) until the air is cleared
  • Return cannula to the aorta for systemic cooling and optional pharmacologic brain protection
  • Post-op Hyperbaric O2 therapy, maintenance of cerebral perfusion, and therapeutic hyperventilation may be beneficial

Venous Air Lock:
Defined as the entrapment of air within the venous system and is typically identified when de-airing the patient following CPB completion. This can also happen when initiating CPB, and can prevent venous return to the pump. Although less lethal than arterial air embolism it still presents potential for significant morbidity. Venous air lock may be a sign of venous cannulation site injury. The most common sites of injury are the vena cavae or the coronary sinus. The coronary sinus is thin walled and prone to injury by the retrograde cardioplegia catheter. Careful attention to retrograde cardioplegia line pressures and tactile/echo confirmation of catheter placement is critical. Once venous air lock is identified one must address the venous injury, elevate the venous lines to remove the air, and consider replacement and/or relocation of the cannula.

In the setting of significant caval injury the appropriate steps include:

  • Recognition of venous air lock
  • Advance venous cannula beyond tear and secure with supplemental purse string
  • Place patient in steep head-down position
  • Cool patient to 18°C for DHCA
  • Repair with direct suture repair of bovine pericardial patch
  • Purge system of air and monitor air burden on TEE

Managing Drainage during CBP

Drainage complications typically represent a venous line issue that needs to be addressed. The CBP circuit requires both inflow and outflow to maintain appropriate support. Ensuring adequate drainage maintains the necessary venous pressure gradients and aids in limiting cardiac filling and unwanted distension.

Inadequate Venous Drainage:
Inadequate drainage typically presents as right ventricular distention in the surgical field. Perfusion team members may note low reservoir levels or poor reservoir filling rate. Increased CVP may also be an observed warning sign of poor venous drainage. The most common causes of inadequate drainage are:

  • Kinked venous drainage lines
  • Venous air lock
  • Inadvertent venous clamping
  • Malposition of the venous cannula (IVC > SVC)

Careful evaluation of the venous tubing, cannula position, and open communication with the perfusion and anesthesia teams often are sufficient actions to address these issues. Perfusion can add vacuum to their venous drainage to promote more return to the pump. The surgeon will often have to reposition the cannula tubing to improve drainage.

Ventricular Distension:
Ventricular distention (either right or left) is typically a sign of poor venous drainage. This may be due to technical errors, semilunar valve insufficiency, or tremendous collateral flow. The use of venting, LV or PA venting, may be necessary to improve drainage, reduce myocardial injury, and reduce PA pressures. Do not forget that congenital abnormalities such as patent foramen ovale or persistent left superior vena cava may be responsible for poor drainage and increased ventricular distension. LV venting typically is performed by placing the vent in the right superior pulmonary vein and advancing the vent through the mitral valve.

Managing Circulation during CBP

Ensuring appropriate circulation and pressure support during CBP helps reduce non-cardiac complications in patients. Recommended mean pressures are at least 50-60mmHg. A general rule is that MAP should be roughly equal to the patient’s age to ensure appropriate organ perfusion.

Inadequate Systemic Pressure:
Whether low-flow or high-flow CBP is optimal for organ system protection remains a point of debate. However, a MAP of at least 50 mmHg is generally recommended. Ensuring appropriate perfusion pressure is critical, especially in patients with known severe carotid disease and/or diabetic nephropathy. Low perfusion pressure is typically secondary to cannula malposition or autonomic dysfunction due to vasoplegia. Vasoplegia results in decreased vascular tone limiting both arterial pressure and venous return. Medications such as vasopressin, and in rare occasions methylene blue, may be helpful in addition to traditional norepinephrine for vascular support. Patients on ACE inhibitors or ARBs typically have increased incidence of vasoplegia during and after CPB, so it is prudent to stop these medications several days prior to surgery.

High Arterial Cannula Pressure:
High arterial line pressure is an urgent matter that requires immediate attention. Elevated arterial line pressure is most often due to poor cannula position and accidental kinking or clamping of arterial tubing. Cannula malposition against the aortic wall induces increased shear stress increasing risk for intimal injury and dissection. Elevated line pressures may also be early signs of aortic dissection and in that setting are usually accompanied by decreased systemic pressure readings. High arterial cannula pressure is an ominous sign that requires immediate evaluation.

Managing Oxygenation during CBP

Inadequate Systemic Oxygenation: The goals of CPB are delivery of oxygen rich blood at appropriate pressures to maintain systemic perfusion. While decreased oxygenation may be the result of oxygenator failure within the CBP circuit, this is very rare. Other complications that may present as decreased oxygenation include aortic dissection or malperfusion syndrome. Additionally, make sure that when weaning from CBP you remember to re-inflate the lungs and begin respirations prior to ending perfusion support. Signs of decreased oxygenation on CBP include:

  • Decreased cerebral oximetry
  • Decreased pulse oximetry
  • Decreased systemic venous oxygen saturation

Weaning CBP

Weaning CBP is a delicate task that requires balancing perfusion support with the return to spontaneous circulation. Once off CBP, and bleeding is controlled, reversal of heparin agents is completed with the use of protamine. Originally derived from the sperm of salmon, protamine is a cationic protein used to neutralize and deactivate heparin in a 1:1 ratio. Prior to full administration, a test dose of protamine is administered slowly to assess for protamine reactions.

Protamine Reactions:

Type I: Most common is hypotension, mediated by histamine release, result of quick infusion:
a. Low pulmonary arterial pressure
b. Low systolic blood pressure
c. Right ventricular underfilling.

The effect is transient, and the treatment is vasoconstrictor support.

Type II: Anaphylactic reaction, type-I hypersensitivity reaction:
a. Low pulmonary arterial pressure
b. Low systolic blood pressure
c. Right ventricular underfilling.

The treatment is inotropes, vasoconstrictors, and stopping the protamine. Wait for the ACT to normalize naturally.

Type III: Acute pulmonary vasoconstriction: mediated by complement activation and thromboxane-A2
a. Increased pulmonary arterial pressure
b. RV distension/failure
c. Pulmonary Edema

Treatment is with 100% FiO2, steroids, antihistamines, bronchodilators, a pulmonary arterial dilator (flolan), IV fluids, vasoconstrictors, and inotropes. Resume CPB if severe pulmonary edema prevents adequate oxygenation. Wait for the ACT to normalize naturally.

Simplifying the process of troubleshooting CPB issues permits quick correction of errors and improves patient care. Most complications fall into one of four categories and can be remembered by the acronym D.A.D.D.

  • Drugs: Complications secondary to pharmacologically active agents. This may include allergic reactions, insensitivity, or refer to the need for pharmacologic support to manage patient perfusion.
  • Air: Air in the arterial or venous system can be a catastrophic event and require immediate correction. Identification, timely cessation of CBP, deairing, and cerebral or coronary protection are necessary. Air in the tubing may also be due to cannulation site injury or venous/sinus tearing, and ruling out inadvertent injuries is important.
  • Drainage: Drainage complications are typically secondary to tubing kinking or cannula positioning. Venting strategies may be necessary to decompress and relieve ventricular distension.
  • Drive: Drive complications are secondary to inadequate perfusion or the identification of unsafe excess line pressurization. These complications typically require correcting technical tubing errors and ruling out iatrogenic aortic dissection.

In summary, troubleshooting CBP issues is a skill that is learned through experience. Timely recognition, diagnosis, and treatment of any CBP issue is critical to safe and effective cardiac surgery.