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Selective Aortic Arch Perfusion
Introduction
Selective aortic arch perfusion (SAAP) is an emerging endovascular resuscitation technique that provides temporary extracorporeal perfusion to the heart and brain during cardiac arrest. The aim of SAAP is to reverse the cardiac arrest, resulting in restoration of intrinsic cardiac output with a palpable pulse (a return of spontaneous circulation [ROSC]), with a good neurological outcome. SAAP was developed specifically as a cardiac arrest therapy and is applicable to both medical cardiac arrest (sudden cardiac death) and hemorrhage-induced (including traumatic) cardiac arrest. The series of SAAP interventions (SAAP modalities) provides a stepwise escalation of aortic balloon occlusion and extracorporeal perfusion that generates higher blood flow than that achieved by closed-chest cardiopulmonary resuscitation (CPR). The sequence of SAAP modalities are used to achieve a ROSC, or to provide bridging heart and brain perfusion support until cannulation for prolonged venoarterial extracorporeal life support (VA-ECLS) if required. The ability to escalate sequentially through these SAAP modalities has potential utility to better inform the complex risk:benefit decision-making of resuscitation interventions in states of severe hemorrhagic shock and cardiac arrest. This chapter will include a description of SAAP and its sequential escalating interventions, the rationale for SAAP in clinical practice, a summary of large-animal laboratory data, an explanation of how SAAP complements other endovascular resuscitation techniques, and the implications for trauma and vascular surgery.
A Description of SAAP
SAAP uses a large-lumen, balloon occlusion catheter inserted into a femoral artery and advanced to the level of the descending thoracic aorta with an insertion length based on body surface measurement (femoral insertion site-to-umbilicus-to-xyphisternal junction). This method positions the SAAP catheter balloon in the aorta between the diaphragm and the left subclavian artery ( Fig. 13.1 ). This leeway in balloon position within the descending thoracic aorta allows for insertion and initiation of resuscitative perfusion without the need for imaging technology to verify balloon location ( Fig. 13.2A,B ). When the SAAP catheter balloon is inflated, the aortic arch vessels, including the coronary, carotid, and vertebral arteries, are relatively isolated for perfusion with an oxygenated perfusate via the central infusion lumen of the SAAP catheter.
After the SAAP catheter balloon is inflated, an initial rapid bolus of perfusate (50 mL/2–3 seconds) into the aortic arch is used to close the aortic valve, followed immediately by a steady infusion of perfusate to maintain aortic valve closure ( Fig. 13.3 ). This step is important, as failure to close the aortic valve can lead to regurgitation of the perfusate into the left ventricle, left atrium, and pulmonary venous system limiting the beneficial effects of SAAP therapy in cardiac arrest. After the initial bolus, the infusion rate required to maintain closure of the aortic valve can be lower: 10 mL/kg/min has been used in most of the laboratory research studies to date. The key to maintaining competent aortic valve closure is that the subsequent infusion must begin immediately after the bolus, thereby not allowing the aortic pressure to drop and the aortic valve to open.
The initial perfusate is preferably an exogenous oxygen carrier, such as stored (allogeneic) whole blood or packed red blood cells, or a non-blood product, such as a hemoglobin-based oxygen carrier (HBOC) or a perfluorocarbon (PFC) emulsion. The perfusate is passed through an oxygenator and infused using a pump system. Centrifugal pumps, roller-wheel pumps, and peristaltic pumps have all been used successfully to perform SAAP in laboratory models. Limited experiments to date have also shown that rapid serial boluses performed manually are also effective, but the overall perfusion rate is lower than mechanical pump continuous infusion and the time required to achieve ROSC is generally longer. Nonetheless, in austere environments—such as military theaters and some prehospital settings—manual infusion for SAAP may prove to be most practical.
The Rationale for SAAP
Cardiac Arrest Survival
Cardiac arrest is a major public health problem in the United States and throughout the world. According to a 2015 Institute of Medicine Report, there are an estimated 600,000 cardiac arrests each year in the United States alone. This includes cardiac arrest due to primary cardiac causes as well as trauma, poisonings, and other etiologies. Of these, approximately 395,000 occur outside of a hospital setting and the survival rate overall for this population is less than 8%. There are an estimated 200,000 in-hospital cardiac arrests each year with a survival rate of about 24%. The major limiting factors in achieving a ROSC in medical cardiac arrest are the inadequate myocardial blood flow produced by closed-chest CPR, delays in initiation of bystander CPR, and lack of early defibrillation.
The incidence of cardiac arrest secondary to trauma is estimated to be 60,000 cases/year in the United States. Reported survival in traumatic cardiac arrest (TCA) is improving but may be even lower than medical cardiac arrest—many of the potentially survivable deaths are due to exsanguination. The major limiting factors in achieving a ROSC in hemorrhage-induced TCA (HiTCA) are the diminished effectiveness of closed-chest CPR in the setting of hypovolemia, the deleterious effects of CPR chest compressions in the presence of chest trauma, the lack of hemorrhage control, and the lack of high-volume fluid resuscitation required to revive the nonbeating, or inadequately beating, heart.
Severe uncontrolled hemorrhage rapidly leads to a state of profound hypovolemia and shock that, if left untreated, can result in cardiovascular collapse and death within minutes. Trauma is the leading cause of severe uncontrolled hemorrhage that is responsible for much of the morbidity and mortality in both military and civilian trauma populations. Uncontrolled hemorrhage due to noncompressible torso hemorrhage (NCTH) is the leading cause of reported preventable death in military combatants and civilian trauma patients with otherwise survivable injuries (predominantly the lack of devastating traumatic brain injury). Survival from HiTCA is currently extremely low, estimated to be between 1% and 5%.
Limitations of CPR and Standard Resuscitation
Cardiac arrest is the abrupt, or rapidly progressive, loss of cardiac function needed to sustain survival. Sudden cardiac death can be due to a lethal dysrhythmia (i.e., ventricular fibrillation) resulting in abrupt loss of blood flow, often without any preceding global hypoperfusion or global ischemic deficit. Other etiologies of medical (nontraumatic) cardiac arrest involve an acute insult with rapid decompensation, for example: hypoxemia (airway obstruction), heart failure (myocardial infarction), circulatory obstruction (massive pulmonary embolus), or hypovolemia (nontraumatic hemorrhage). Traumatic cardiac arrest can also occur rapidly and is often due to uncontrolled severe hemorrhage, but other etiologies include pericardial tamponade, tension pneumothorax, and hypoxemia related to airway, brain, or cervical spinal cord injury.
Standard cardiac arrest therapy, developed over the past 60 years, has primarily included closed-chest CPR, electrical therapies (defibrillation and cardiac pacing, when appropriate), and intravenous administration of drugs (including epinephrine and antiarrhythmics). Although identification and treatment of a specific cause is emphasized in cardiac arrest algorithms, the reality is that in most cases of cardiac arrest a rapidly reversible etiology is not found and resuscitation interventions follow an algorithmic approach (e.g., American Heart Association guidelines for Advanced Cardiac Life Support) with little or no tailoring of interventions to the individual patient. A major limitation in this regard is the lack of physiological parameters to guide resuscitation interventions (pulse quality and pupillary response are inadequate guides). Continuous end-tidal carbon dioxide measurement is the most promising noninvasive measure readily available, but even this is at best a semi-quantitative guide to therapy.
Closed-chest CPR has been widely taught since its landmark description in 1960 and has helped save many lives by creating a coronary perfusion pressure (CPP) gradient (defined as aortic pressure minus right atrial pressure during the relaxation or diastolic phase of CPR chest compressions) high enough to perfuse the myocardium. CPR performed with good technique and without time delay can generate up to 25% to 33% of normal physiological cardiac output. Although this can be sufficient to result in ROSC, survival data over the decades have been relatively dismal. Important factors that influence survival outcome are: (1) decline in CPR blood flow over time (even with good CPR technique) and (2) time delay to initiation of CPR which leads to lower CPP and lower CPR blood flow due to peripheral arterial vasodilation. In HiTCA, the problems of CPR are magnified. In states of severe hypovolemia, CPR has been shown to generate lower aortic diastolic pressure and therefore CPP, starving the myocardium of oxygenated perfusate. In the setting of thoracic trauma, the mechanics of CPR may be less effective and chest compressions may even cause further injury. Furthermore, in all causes of traumatic cardiac arrest, it is likely that CPR will hamper other interventions aimed at reversing the arrest etiology, for example, endotracheal intubation for hypoxia, thoracostomy for pneumothorax, and vascular access for volume replacement in hypovolemia; the risk to providers of inadvertent needle-stick injury is significant.
Another major limitation of standard cardiac arrest therapy is that the intravenous administration of resuscitation drugs is usually ineffective. Epinephrine is most commonly used, given for its peripheral arterial vasoconstrictor effects. Epinephrine increases aortic pressure and CPP to improve CPR blood flow. Both laboratory and clinical studies have shown that the higher the CPP, the greater the myocardial blood flow and higher the rate of ROSC. However, during the low blood flow state of CPR, the circulation of epinephrine from a peripheral venous injection site to the peripheral arterial system is highly variable. Paradoxically, cardiac arrest victims with very low CPR blood flow, who most need the vasoconstrictor effect, are the very patients in whom epinephrine is most ineffectively circulated from the peripheral vein to the peripheral arterial effector sites. This leads to excessive doses of intravenous epinephrine that have been associated with lower survival rates.
The dilemma of present cardiac arrest resuscitation includes: (1) closed-chest CPR that provides only a fraction of normal cardiac output which diminishes with delay in CPR initiation and with increasing duration of CPR, (2) lack of a noninvasive method of effectively assessing blood flow during CPR so that resuscitation efforts can be individualized, (3) resuscitation medications are ineffectively circulated when given intravenously, and (4) the time frame allowing for ROSC is short, and therefore often exhausted prehospital.
Rationale for Endovascular Resuscitation
The limitations of standard cardiac arrest resuscitation attributable to inadequate CPR blood flow, ineffective drug delivery, and inadequate parameters to guide therapy are all addressed to varying degrees by emerging endovascular resuscitation interventions that allow for continuous or intermittent invasive pressure monitoring, extracorporeal perfusion support, and effective drug delivery during cardiac arrest. Endovascular interventions reported in the literature for cardiac arrest resuscitation are set out in Table 13.1 and include: (1) aortic catheterization for hemodynamic monitoring and intraaortic drug delivery, (2) resuscitative endovascular balloon occlusion of the aorta (REBOA), (3) SAAP, (4) extracorporeal perfusion support (ECLS/ECMO—these terms are interchangeable, and when used in the setting of cardiac arrest can also be referred to as extracorporeal-CPR [ECPR]), (5) Impella intravascular rotor-flow device, and (6) emergency preservation and resuscitation (EPR).
Table 13.1
Comparison of Characteristics of Endovascular Resuscitation Interventions
| Endovascular Resuscitation Intervention | Placement Without Imaging | Aortic Pressure Monitoring With Closed-Chest CPR | Aortic Pressure Support With Closed-Chest CPR | Arterial Drug Delivery | Distal/Caudal Hemorrhage Control | Extracorporeal Perfusion to Achieve ROSC | Post-ROSC Perfusion Support | Easily Withdrawn Post-ROSC |
|---|---|---|---|---|---|---|---|---|
| Aortic pressure catheter (±central venous catheter) | Yes | Yes AoP (±CPP) | No | Yes Epinephrine titration | No | No | No | Yes |
| REBOA catheter | Yes | Yes AoP | Potentially increased SVR with aortic occlusion | Yes | Yes Aortic balloon occlusion | No | No | Yes |
| SAAP catheter | Yes | Yes AoP (intermittent) | Yes Aortic arch perfusion (but CPR not needed) | Yes | Yes Aortic balloon occlusion | Yes Aortic arch perfusion | Limited, temporary or bridge to ECMO, if needed | Yes |
| Impella device | No | No | Yes Aortic perfusion (but CPR not needed) | No | No | Yes Whole body perfusion | Yes | Potentially |
| ECLS/ECMO/ECPR | Yes | Yes (arterial side of ECMO circuit) | Yes Aortic perfusion (but CPR not needed) | Yes via ECMO circuit | No | Yes Whole body perfusion | Yes | No
|
| EPR procedure | N/A Thoracotomy for aortic access | N/A No CPR | N/A No CPR |
|
N/A | N/A Induction of profound hypothermia | N/A | N/A |
AoP , Aortic pressure; CPP , coronary perfusion pressure; CPR , cardiopulmonary resuscitation; ECLS , extracorporeal life support; ECMO , extracorporeal membrane oxygenation; ECPR , extracorporeal-CPR; EPR , emergency preservation and resuscitation; REBOA , resuscitative endovascular balloon occlusion of the aorta; SAAP , selective aortic arch perfusion; SVR , systemic vascular resistance.
The endovascular interventions, other than SAAP, that can be used in resuscitation are briefly described later; REBOA, ECLS, and EPR are more thoroughly covered in other chapters.
Thoracic aortic catheterization can be used to continuously measure CPR-diastolic aortic pressure (or CPP, if a central venous pressure catheter is also inserted) and allow for adjustments in CPR mechanics to optimize aortic pressure and CPP. The aortic catheter can also be used to deliver resuscitation drugs, such as epinephrine, allowing for rapid titration to therapeutic effect while avoiding excessive doses that could prove deleterious.
REBOA has been shown to be effective in uncontrolled hemorrhage below the diaphragm (zone 1 REBOA, thoracic aortic occlusion) or isolated to the pelvic region (zone 3 REBOA, infrarenal aortic occlusion). Clinical reports show favorable survival in patients with severe hemorrhagic shock, particularly if initiated before cardiac arrest with loss of cardiac contractility has developed. However, the exact physiological state (i.e., the patient’s place on the spectrum of hemorrhage) at which the potential benefits of aortic balloon occlusion outweigh the potential risks of the procedure is not currently well understood. REBOA catheters allow for central aortic pressure monitoring, which is valuable in guiding intravenous fluid resuscitation and could potentially be used for intraaortic drug delivery. There is some evidence that REBOA may have utility in medical cardiac arrest.
ECPR involves the implementation of femoro-femoral VA-ECLS during cardiac arrest to achieve a ROSC. ECPR has been reported both in-hospital and prehospital for the treatment of medical cardiac arrest deemed to have a good chance of neurological recovery. Clinical reports of ECPR show high survival rates with favorable neurological recovery in the patients meeting criteria for this intervention.
The Impella device is an endovascular rotational pump that is inserted across the aortic valve with an intake port at the distal tip situated in the left ventricle and an outlet port in the aorta. Impella was developed for the treatment of severe left ventricular failure. It has also been suggested as a potential intervention for perfusion support during cardiac arrest, but it is not well established. A potential limitation in cardiac arrest is the present need for imaging for insertion to verify proper placement in the left ventricle.
EPR is experimental and involves the rapid induction of profound hypothermia in trauma patients with extensive injuries who cannot be resuscitated prior to surgical intervention. The current method for performing EPR is thoracic aortic cannulation via a thoracotomy with the infusion of 4°C crystalloid until the target core temperature (about 10°C) is achieved. The right atrial appendage is incised to allow blood and fluid to drain during the induction of profound hypothermia.
One of the major challenges for endovascular resuscitation is obtaining vascular access in a time-critical manner, often under suboptimal circumstances. A 2018 report from the R Cowley Adams Shock Trauma Center, arguably the most experienced aortic balloon occlusion facility, demonstrated a significant difference in the median time to common femoral artery access in severe traumatic hemorrhage compared to traumatic cardiac arrest—141 seconds versus 300 seconds respectively, P < .001. Cardiac arrest complicates femoral arterial access due to arterial vasomotor contraction that is unopposed by normal distending pulsatile pressure. This is particularly true with hemorrhage-induced hypovolemia. Rapid and reliable cannulation of a contracted femoral artery is likely to be the most variable component of an endovascular resuscitation procedure, and ideally is secured in all at-risk patients prior to cardiac arrest. The increasing use of ultrasound-guided percutaneous vascular access and improvements in ultrasound technology are important advances, but there may still be circumstances in which surgical vascular access is needed to initiate time-critical endovascular resuscitation to promote survival. The optimal approaches for percutaneous, surgical cutdown, and hybrid vascular access techniques is an area of ongoing study and discussion. Proper procedural skills training and sustained proficiency with vascular access are central to the evolution of endovascular resuscitation.
The endovascular resuscitation era that is emerging offers a set of interventions that can be applied in both medical and traumatic cardiac arrest where standard noninvasive resuscitation therapies have either failed or are entirely inadequate to address the complex pathophysiology and injuries of the patient. These endovascular resuscitation interventions provide extracorporeal perfusion support, hemorrhage control, physiological monitoring, and drug delivery beyond the capabilities of present standard resuscitation. These interventions may be used alone, in series, or in combination depending upon the needs of the individual patient, allowing for more precisely tailored care to promote survival. Endovascular resuscitation requires a high level of skill and a significant commitment of resources. However, endovascular interventions offer the best hope for a substantial improvement in survival from medical cardiac arrest and HiTCA.
Sequential SAAP Interventions
SAAP was developed specifically for the treatment of cardiac arrest and is applicable to both medical cardiac arrest and HiTCA. In medical cardiac arrest, the balloon occlusion isolates the flow of perfusate to the aortic arch (to preferentially achieve optimal heart and brain perfusion) and theoretically increases cardiac afterload and CPP. SAAP with an exogenous oxygenated perfusate is a volume-loading intervention. However, SAAP with exogenous perfusate is time/volume-limited—excessive loading risks circulatory overload and pulmonary edema. In HiTCA, the volume loading by SAAP is beneficial as a means of rapidly restoring the intravascular volume loss associated with severe hemorrhage. If the major source of hemorrhage is subdiaphragmatic, the SAAP catheter balloon inflated in the thoracic aorta serves to limit further arterial hemorrhage caudal to the balloon in the same way as zone 1 (thoracic aortic) REBOA. However, the principal aim of SAAP with exogenous perfusate is to provide heart and brain perfusion to achieve ROSC just as in medical cardiac arrest. The immediate need to achieve ROSC in HiTCA means that SAAP is not contraindicated in the setting of intrathoracic hemorrhage even if it may lead to additional bleeding. The effectiveness of SAAP may be more limited with thoracic trauma, depending upon the vascular injuries and the rate of bleeding.
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