Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Mechanical support in cardiogenic shock
Heart disease remains the leading cause of death in both men and women among African Americans, Hispanics, and Caucasians in the United States, accounting for nearly 650,000 deaths annually. Significant progress has been made over the past few decades in defining and recognizing cardiogenic shock (CS), and although there are many potential causes of this condition, acute myocardial infarction (AMI) with a large loss of functioning myocardium is the most frequent. , Despite advances in early reperfusion and mechanical support treatment approaches, CS remains the most common cause of in-hospital mortality after AMI, with rates exceeding 50%.
In 1912 James Herrick was the first to link observations of patients with AMI with autopsy findings of patients who had died from CS. His contention at the time, which was initially rejected by the medical community, was that AMI was not always immediately fatal and that efforts were needed to diagnose and treat the condition while the patient was still alive. It was not until the mid-to-late 20th century when selective coronary angiography became available in humans that DeWood and others reported evidence of coronary occlusion in patients suffering AMIs. These findings laid the foundational basis for developing interventional and medical treatments for AMI to intervene and support patients who were diagnosed with CS. A standard definition of CS was proposed by Binder and colleagues in 1955, which included factors such as a systolic blood pressure less than 80 mm Hg and tachycardia to greater than 100 bpm with signs of peripheral vascular collapse. At the time this definition was developed, the mortality associated with CS after AMI was still close to 100%.
Over the past several decades, the general definition of CS has evolved into a severe impairment of myocardial performance that results in diminished cardiac output (CO), end-organ perfusion, and hypoxia. Despite an updated definition, a level of uncertainty in the outcomes of CS persists, with some contemporary clinical trials lacking uniformity in their definitions for identifying CS. For instance, although the SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) and Intra-Aortic Balloon Pump (IABP)-SHOCK II trials used systolic blood pressure ≤90 mm Hg for ≥30 minutes, their exact parameters for confirming end-organ hypoperfusion were diverse ( Table 82.1 ). , Clinically CS is recognized to be on a continuum, but the presence of hypotension refractory to volume resuscitation and features of end-organ hypoperfusion requiring pharmacologic or mechanical support are the crux of this diagnosis. AMI remains the instigator of 81% of CS events. Furthermore, the incidence of CS in myocardial infarction has remained relatively constant in recent decades (,7%) and remains the leading cause of death in patients with AMI.
TABLE 82.1
Available Definitions of Cardiogenic Shock
From van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: A scientific statement from the American Heart Association. Circulation . 2017;136(16):e232–e268.
| Clinical Definition | SHOCK Trial | IABP-SHOCK II | ESC HF Guidelines |
|---|---|---|---|
| Cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion |
|
|
|
CI, confidence interval; PCWP, pulmonary capillary wedge pressure; SBP, systolic blood pressure.
History of mechanical circulatory support
The evolution of mechanical circulatory support (MCS) dates to the early 1950s when Gibbon developed the prototype cardiopulmonary bypass (CPB) apparatus. In the years that followed, Lillehei, Kirklin, and others applied the heart-lung machine to facilitate open heart surgery; their pioneering work and early observations led directly to the development of modern MCS systems. Their initial publications introduced the concept that left ventricular (LV) decompression and myocardial rest could afford enhanced cardiac recovery after the insult of open heart surgery. Clinical use of extracorporeal CPB for heart surgery became widespread in the early 1960s. Simultaneously, several groups of investigators were testing means of MCS for use outside the operating room to support patients in CS. The current modes of MCS are derivations of those originally developed.
The decision on the type of MCS used is based on the acuity of the patient’s presentation, level of flow or adjunctive CO, and the overall goals of therapy. This decision often changes as the patient’s clinical picture evolves. MCS devices include the intraaortic balloon pump (IABP), continuous flow pumps with or without an oxygenator, percutaneous devices, and durable continuous flow pumps. Temporary MCS devices are used in CS as a bridge to recovery (BTR), bridge-to-bridge with a long-term implantable MCS device, bridge to transplant (BTT), or bridge to decision. Some temporary MCS devices can be inserted percutaneously, whereas others require surgical implantation. Long-term MCS devices are used as a BTR, a BTT, or the definitive means of treatment for the patient’s remaining lifespan—that is, destination therapy (DT). These devices have been employed for a variety of causes of CS, including AMI, inability to wean from CPB (postcardiotomy CS), acute decompensation of chronic heart failure (HF), acute myocarditis, peripartum cardiomyopathy, HF secondary to acute or chronic valvular heart disease, and congenital heart defects.
History of aortic counterpulsation
The concept of arterial counterpulsation was introduced in 1961 by Clauss and coworkers. It involved use of an external “ventricular” chamber that filled with blood from a catheter in the iliac artery and was subsequently compressed by a piston. Compression of the “ventricle” was synchronized to either the QRS complex of an electrocardiogram (ECG) or the impulse of a pacemaker so that a counterpulse of blood was delivered into the arterial system during diastole. It was demonstrated in dogs that cardiac stroke work and LV end-systolic pressures were substantially reduced with the use of a counterpulsation into the aorta. The following year, Moulopoulus and associates adapted the model to create an IABP that could provide a similar counterpulsation without the need for blood reservoirs. The investigators used a balloon that was rapidly inflated and deflated with carbon dioxide during native diastole. The IABP was subsequently adapted and described for clinical use by Kantrowitz and colleagues in 1968. There is little difference in the modern IABP and that originally described, other than the availability of different-sized balloons (30- to 50-mL balloons), the use of helium instead of carbon dioxide, and subtle differences in the materials used to make the catheters.
History of mechanical assist devices
The need for effective MCS devices with more options for greater cardiac flow support became apparent in the 1950s during the development of CPB for open heart surgery. The first attempt at isolated extracorporeal LV support was with a simple roller pump in 1962. Initial attempts with prolonged postoperative CPB demonstrated that the bypass circuit was damaging to both end-organ function and blood constituents after several hours of use. Subsequently, femoral venous–to–femoral arterial CPB was successfully used by Spencer and colleagues in four patients with postcardiotomy cardiac failure. Simultaneous to Spencer and colleagues’ work with extracorporeal systems, DeBakey designed the first intracorporeal LV assist device (LVAD), the DeBakey blood pump. A remodeled extracorporeal version was subsequently used for postcardiotomy failure in a 37-year-old woman after aortic and mitral valve replacements. The device was needed for 10 days, and the patient survived.
By 1972 investigators at the Texas Heart Institute had developed a pneumatically driven LVAD designed to be implanted in the abdomen. This device had a blood chamber compressed by pulses of air delivered into the pump by a percutaneous driveline. Modern devices have chamber compression that is electrically powered via percutaneous drivelines. Paracorporeal, pneumatically driven devices were a parallel development. Paramount to the evolution of these devices was the sponsorship of the Artificial Heart Program of the National Heart, Lung, and Blood Institute, which was chartered in 1964.
By the 1960s continuous flow pumps, as compared with pulsatile pumps, were under development. , Over the subsequent 15 years, continuous flow centrifugal pumps were perfected and introduced into clinical use. These pumps work on the principle of a forced, constrained vortex devised from three magnetic cones. , They have been shown to be useful in a variety of clinical settings where short-term MCS is needed and an IABP is inadequate. Several types of small, axial-flow, or rotary pumps have also been developed, including some that allow for percutaneous deployment. These pumps generally contain a magnetically suspended impeller that rotates at fast rates between 25,000 and 35,000 rpm. The latest generation of rotary pump technology comprises continuous flow devices that use fully magnetically levitated rotors that eliminate the need for seals or bearings. This technology reduces the risk of damage to blood elements and has been shown to lead to lower rates of thromboembolism.
Initial management of cardiogenic shock
The initial focus in the treatment of CS is to prevent end-organ failure through stabilization of CO and the establishment of hemodynamic stability while simultaneously diagnosing and treating the reversible causes of CS. Fig. 82.1 illustrates an algorithm for the management strategies in CS. Identification of the primary cause of CS can allow for the appropriate pharmacologic or mechanical therapies to be applied. The American Heart Association recommends that patients undergo noninvasive testing with chest x-ray, resting 12-lead ECG, and echocardiography. Suggested laboratory tests include complete blood count, electrolytes, hepatic function tests, serum creatinine, mixed venous oxygen saturation, natriuretic peptides, serial troponin levels, arterial blood gas, and lactate. The mainstay of evidence supports timely reperfusion in patients presenting with CS caused by AMI. The potential revascularization strategies can be noninvasive, with tissue fibrinogen activator or streptokinase, or invasive, with percutaneous coronary interventions (PCI) or coronary artery bypass grafting (CAGB). , , Vasoactive medications are often required for support in patients with CS, and the decision for which medication to initiate in CS remains challenging. The SOAP II trial (Sepsis Occurrence in Acutely Ill Patients) evaluated vasopressor selection in a subgroup of patients with CS and found that dopamine was associated with a higher rate of arrhythmias in addition to increased mortality, which may be the result of a tachycardia-induced ischemic propogation. This has led to assertion of using norepinephrine as a first-line agent. Unfortunately, the methodology and clinical definitions of CS used within the SOAP II trial caused major concerns regarding the generalizability and applicability of the findings. Additional studies have suggested that epinephrine should also not be used in the initial management of CS because of its effect in increasing lactate levels, increasing oxygen consumption, lowered arrhythmogenicity thresholds, and association with higher mortality. , Additionally, in a recent randomized clinical trial (RCT), norepinephrine was found to be superior to epinephrine in achieving hemodynamic stability without increasing lactate levels in patients in CS after AMI. Escalating doses of vasopressors and inotropes in patients with CS are associated with increased mortality. In the setting of refractory CS and impending or worsening end-organ failure, MCS should be discussed with the multidisciplinary heart team and initiated in appropriate candidates.
The lethality of CS and limited availability of donor hearts for patients with chronic HF has been the impetus for the ongoing search for an ideal form of MCS over the past 60 years. The complexity and heterogeneity of this patient population have led to the development of a vast array of devices, none of which has proven optimal for support in all patients across the spectrum. The decision for which type of MCS device to use is based on the amount of supplemental flow required or CO that the patient requires, the duration of support required, and the patient’s candidacy for cardiac transplantation ( Figs. 82.2 and 82.3 ). The biologic barriers to MCS present a constant challenge to clinicians, and the types of MCS devices available are continually evolving. Nonetheless, MCS remains an important adjunct in the treatment of CS and HF, with many devices demonstrating significant improvement in survival and quality of life. Accordingly, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines recommend nondurable MCS as a reasonable “bridge to recovery” or “bridge to decision” for patients with acute profound heart failure and a durable MCS for carefully selected patients with stage D heart failure and reduced ejection fraction (class IIa; level B). The current indications, benefits, and limitations of MCS devices are outlined in this chapter.
Current use of mechanical circulatory support devices
Temporary mechanical circulatory support
Percutaneous insertion
Intraaortic balloon pump.
The physiologic rationale for the efficacy of the IABP is that balloon deflation provides a rapid, synchronized reduction in impedance (afterload) during isovolemic LV contraction. This is followed by a rapid, synchronized increase in aortic pressure during isovolemic LV relaxation (diastolic augmentation) caused by balloon inflation. In combination, these events achieve two important goals. First, LV systolic unloading directly reduces stroke work, which in turn reduces myocardial oxygen consumption during the cardiac cycle. Second, diastolic augmentation raises arterial blood pressure and provides better coronary arterial perfusion during diastole, yielding increased oxygen delivery to the myocardium. The IABP does not directly move or redistribute blood flow; however, peak diastolic coronary flow velocity can be increased as much as 87% with IABP augmentation and peak diastolic flow velocity by as much as 117%. Since its introduction into clinical use in 1968, the IABP has remained an important adjunct to supporting patients in CS. Myocardial recovery is promoted by the reduction of cardiac work and the simultaneous increase in myocardial oxygen supply. However, therapeutic success is dependent on the patient having a minimum degree of LV function that, in combination with IABP support, facilitates an adequate CO to sustain end-organ function. When this minimal CO is not met, alternative MCS must be considered.
The absolute indications for IABP placement include CS, uncontrolled angina pectoris, acute postinfarction ventricular septal defect (VSD), postinfarction mitral regurgitation (MR) secondary to papillary muscle rupture, and postcardiotomy left-sided HF with low CO. In these settings, IABP should be considered as a primary therapy that should not be delayed. It is important to recognize that blood pressure alone is not an adequate indication of hemodynamic or cardiac stability. Limb perfusion, renal function, mental status, and even gastrointestinal function need to be considered in the assessment of adequate resuscitation and homeostasis. Additional measurable indices include arterial (SaO 2 ) and mixed venous oxygen saturation, acid-base status, urine output, and body temperature. A multivariate analysis of data accrued from 391 postcardiotomy patients requiring an IABP demonstrated that epinephrine requirements greater than 0.5 μg/kg/min, a left atrial pressure greater than 15 mm Hg, urine output less than 100 mL/hr, and mixed venous oxygen saturation less than 60% correlated with mortality. These criteria were used to help predict mortality and the need for subsequent MCS.
Other relative indications for IABP use include (1) high-risk, catheter-based interventional procedures such as left main coronary artery angioplasty, (2) after unsuccessful attempts at catheter-based intervention in patients with poorly controlled ventricular arrhythmias and concomitant poor LV function, and (3) in settings of persistent stunned, ischemic myocardium. These are circumstances in which reduction of LV systolic wall tension and oxygen consumption by the IABP might enhance myocardial recovery after intervention. The Benchmark Counterpulsation Outcomes Registry of IABP use in 22,663 patients from 250 hospitals worldwide demonstrated that CS and high-risk angioplasty were the most common indications for use of the device.
The optimal site of insertion of an IABP is a common femoral artery that can be accessed either percutaneously with the Seldinger technique or by surgical cutdown. Modern intraaortic balloon catheters are available for adults and children, according to the appropriate size and length for a given height and weight of the patient. Adult intraaortic balloons have a range in volume filled between 30 and 50 mL, with a standard balloon size holding 40 mL of helium. IABP catheters placed through the femoral artery are positioned so that the tip is just distal to the takeoff of the left subclavian artery in the proximal descending thoracic aorta. Optimally, the tip of the catheter should be positioned with transesophageal echocardiographic or fluoroscopic guidance. To reduce the diameter of femoral cannulation, the sheathless IABP technique can be used and is our preferred method.
Inflation of the balloon should be timed with closure of the aortic valve (at the dicrotic notch of the aortic pressure tracing) and should be inflated to nearly occlude the descending thoracic aorta. Timing can be synchronized in one of three ways: (1) using an arterial (preferably aortic) pressure tracing in synchrony with the dicrotic notch, (2) using the descent of the R wave on a rhythm tracing, or (3) timed after a ventricular pacing spike when a pacemaker is in use. The optimal physiologic benefit of the IABP is significantly improved by proper timing of inflation and deflation, which can be difficult when there is an accelerated heart rate, cardiac rhythm disturbances, atrioventricular dyssynchrony, or low mean arterial pressure. Timing should be adjusted to maximize diastolic augmentation; hence, deflation should be as late as possible but just before opening of the aortic valve. If this cannot be gauged by pressure tracing, it can be timed to the onset of the R wave on ECG tracing or with the use of M-mode echocardiography.
When femoral arterial cannulation is not desirable because of aortoiliac occlusive disease or extensive peripheral vascular disease (PVD), the subclavian artery or the ascending aorta can be used. With either technique, the IABP catheter is advanced antegrade down the descending thoracic aorta so that the balloon tip sits above the level of the diaphragmatic hiatus, and the most proximal end of the balloon is distal to the takeoff of the left subclavian artery. These antegrade balloons should always be placed with either fluoroscopic or echocardiographic guidance. They should be removed with open arterial repair in all cases.
IABP catheters should not be left in place after weaning because of the risk of thrombus formation and embolization. An IABP should be weaned stepwise from a rate that is equivalent to heart rate (1:1) down to a ratio of 1:4 just before removal. Balloon catheters placed via the open surgical technique should also be removed surgically. Percutaneous removal of catheters placed in the iliac artery above the inguinal ligament (most common in obese individuals) can result in significant retroperitoneal bleeding. Consideration of operative removal is warranted.
Relative contraindications to IABP use include severe atheromatous disease of the descending thoracic aorta, descending aortic dissection or aneurysm, recent descending thoracic aortic surgery, and mild to moderate aortic insufficiency. Severe aortic insufficiency is an absolute contraindication to use because diastolic augmentation cannot be accomplished, and LV end-diastolic volume and pressure are actually increased rather than decreased.
The overall complication rate of IABP use is between 5% and 10%. Major complications occur at a rate of about 3% and include severe bleeding, major limb ischemia or amputation, infection, visceral or spinal cord ischemia, and attributable IABP mortality. , In the Benchmark registry, rates of complications were quite low; the most common complications were access site bleeding (4.3%) and limb ischemia (2.3%). The rates of amputation, stroke, visceral or spinal cord ischemia, and IABP-related mortality were all 0.1% or less. Intraaortic balloon entrapment is a rare complication. The incidence of major vascular complications according to the STS National Database (1996–1997) and the Benchmark Registry (1997–1999) was 5.4% and 1.4%, respectively. , Ipsilateral limb ischemia should be immediately addressed after its recognition. This usually requires removal of the IABP with replacement at another location if it is still indicated. The ischemic limb may require thrombectomy with or without revascularization and fasciotomy.
The SHOCK trial showed that early revascularization in CS after AMI, often facilitated by IABP use (86%), yielded a lower 6-month mortality rate (50%) than that with medical therapy alone (63%). Additional studies have shown that in patients undergoing urgent or emergent revascularization after an AMI, those supported preoperatively with an IABP had a lower operative mortality than those in whom an IABP was not used (5.3%–8.8% vs. 11.8%–28.2%). These data seem to justify a strategy of aggressive IABP use to facilitate early revascularization in a postinfarction patient. The Second Angioplasty in Myocardial Infarction (PAMI-II) Trial data examined high-risk patients with AMI revascularized by PCI only and demonstrated a modest survival advantage at 6 months with the use of periprocedural IABP support. When evaluating hospital mortality rates among patients undergoing CABG and/or valve surgery who received preoperative IABP or required intraoperative/postoperative IABP support, the mortality rate was significantly lower among patients supported preoperatively, as depicted in Table 82.2 . , Hence, there appears to be a survival advantage to earlier IABP support for patients with CS after AMI who undergo revascularization. In the setting of an acute VSD or acute MR after an AMI, IABP support can offer a dramatic improvement in the hemodynamic response of the patient. It is clear that the mortality rate of patients in CS after AMI remain high. However, these studies suggest that IABP support, combined with revascularization, portends a better prognosis than adjunctive IABP use with medical therapy alone. This benefit is likely greatest in those who are revascularized and present with class 3 or 4 HF. A meta-analysis of 16 studies demonstrated a significant survival benefit for the use of IABP in CS after AMI (relative risk [RR]: 0.78; confidence interval [CI]: 0.60–0.86; P <0.0004). However, no benefit was seen in patients with high-risk AMI that was not complicated by CS.
TABLE 82.2
Hospital Mortality (Outcome Parameter) for Patients Undergoing Cardiac Surgery Who Either Received Preoperative IABP or Intra/Postoperative IABP Support
From Christenson JT, Cohen M, Ferguson JJ 3rd, et al. Trends in intraaortic balloon counterpulsation: Complications and outcomes in cardiac surgery. Ann Thorac Surg. 2002;74:1086–1090.
| Type of Therapy | Benchmark Registry 1997–1999 Mortality/Total Operations With IABP, N (%) | STS National Database 1996–1997 Mortality/Total Operations With IABP, N (%) | STS National Database 1996–1997 Mortality/Total Operations Without IABP, N (%) |
|---|---|---|---|
| Preoperative IABP | 8.8 (329/3721) | 9.5 (2487/26,077) | 2.9 (10,919/378,810) |
| Intraoperative/postoperative IABP | 28.2 (954/3380) | 23.6 (3528/14,933) | 2.5 (9878/389,954) |
Based on data from the Benchmark Counterpulsation Registry 1997–1999 and the STS National Database 1996–1997 compared with hospital mortality for patients who had neither preoperative nor intraoperative/postoperative IABP support.
Conversely, a Cochrane Database meta-analysis of six RCTs reviewed the use of IABP in CS after AMI in 190 patients and found no significant improvement in in-hospital, 30-day, or 6-month all-cause mortality. , A meta-analysis of cohort studies of IABP use in patients in CS after AMI by Sjauw and colleagues found an 18% decrease in 30-day mortality in patients treated with thrombolysis and IABP. However, in patients treated with PCI, they noted a 6% increase in mortality associated with the additional use of an IABP. In the prospective IABP-SHOCK II trial, 600 patients in CS after AMI were randomized with and without placement of IABP after undergoing revascularization, primarily with PCI (>95%). No difference in the primary endpoint of 30-day, all-cause mortality was seen (39.7% IABP, 41.3% control). However, a 10% crossover to the IABP arm was noted. Additionally, a meta-analysis of 12 RCTs found no improvement in 30-day mortality with the use of IABP in patients with AMI, regardless of whether or not the patients suffered from CS. From this compilation of results, it may be concluded that the use of IABP in CS after AMI has little benefit in any treatment strategy that does not employ the use of early revascularization. Furthermore, improvement in the patient’s hemodynamics often seen with the use of IABP does not suffice as a surrogate marker for survival in patients in CS after AMI. An IABP should be placed in the case of acute postinfarction VSD or acute MR without delay.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here
