Olcay Aksoy and E. Murat Tuzcu
Despite advances in technology and therapeutics, in-hospital mortality following acute myocardial infarction (AMI) remains high. The leading cause of death in these patients is cardiogenic shock (CGS), with an incidence of approximately 7%.1 CGS in the AMI setting can result from severe left ventricular (LV) or right ventricular (RV) systolic dysfunction, dynamic left ventricular outflow tract (LVOT) obstruction, or mechanical complications. These mechanical complications include acute mitral regurgitation (MR) from papillary muscle rupture, tamponade from cardiac free wall rupture, and left-to-right shunting from a ventricular septal defect (VSD). Arrhythmias and inflammatory sequelae are most often less deleterious unless they occur in an unmonitored setting or in a patient who is already in shock or hemodynamically tenuous.
LEFT VENTRICULAR DYSFUNCTION COMPLICATED BY CARDIOGENIC SHOCK
Isolated LV failure accounts for the majority of shock cases following AMI. In the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) Trial and concurrent SHOCK Trial registry, predominant LV failure was the cause of CGS in 78.5% of the patients, and in-hospital mortality was 59.2%.2 Autopsy studies have shown that those patients who develop LV failure have lost approximately 40% of their myocardial mass to necrosis.3 This generally occurs after a large transmural myocardial infarction (MI) or following a relatively small, nontransmural event in a patient with prior ischemic damage. In the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) Trial that examined outcomes associated with thrombolytic therapy in 41,021 patients with acute ST-elevation myocardial infarction (STEMI), risk factors for the development of shock were advanced age, female gender, prior infarction, anterior infarction location, and diabetes mellitus.4
Symptoms and Signs
Upon presentation, subjective symptoms usually do not clarify the diagnosis; however, early recognition of symptoms of malperfusion can be critical. The physical examination can be helpful. One of the most popular systems to categorize these patients is the Killip classification (Table 42.1). Shock is present if there are signs of inadequate tissue perfusion with or without hypotension, which is defined as a systolic blood pressure <90 mm Hg. Signs of inadequate tissue perfusion include altered mental status, oliguria, and chemical evidence of end-organ damage such as a rise in serum creatinine, lactate, and/or liver transaminases. Patients are often tachycardic, hypothermic, and have cool extremities. Neck vein distention can be seen, and an S3 gallop is sometimes heard on physical examination. Peripheral edema and displacement of the point of maximal impulse is less likely unless it existed prior to the AMI.
TABLE
42.1 Killip Classification
Diagnosis
In addition to the symptoms and physical findings mentioned above, the electrocardiogram (ECG) is critical in diagnosis. Anterior STEMI is the most common cause of shock in the AMI setting.2,4 Chest x-ray (CXR) can demonstrate an enlarged cardiac silhouette, although this is rare in the acute phase if prior myocardial damage has not occurred. Varying degrees of pulmonary venous congestion and edema can be seen. Transthoracic echocardiography (TTE), though not necessary for diagnosis, should be performed urgently in patients with shock or signs of congestive heart failure (CHF) to assess the extent of LV and/or RV dysfunction and exclude mechanical complications. Right heart catheterization can also be used to confirm the diagnosis and monitor therapy. In CGS, the cardiac index is typically <2.2 L/min/m2; the mixed venous oxygen saturation is low, typically <65%; and the pulmonary capillary wedge pressure (PCWP) is elevated, typically >18 mm Hg.
Treatment
Treatment involves a combination of revascularization, medication, and mechanical therapy. It is important to remember that mechanical complications other than isolated LV dysfunction must be ruled out in the initial phases of management. Although this can be done with TTE, transport to the catheterization laboratory and implementation of aggressive supportive measures such as placement of an intra-aortic balloon pump (IABP) should not be delayed for this purpose. It is an American College of Cardiology/American Heart Association (ACC/AHA) Class I recommendation that intra-arterial blood pressure monitoring and a Class IIa recommendation that right heart catheterization should be used to monitor patients in CGS.5
REVASCULARIZATION
Thrombolytic therapy has a limited effect on the high mortality rate associated with AMI complicated by CGS.2,4 Data to support this come from the Italian Group for the Study of Streptokinase in Myocardial Infarction (GISSI), which randomized >11,000 patients with AMI to thrombolytic therapy versus no thrombolytic therapy. In both groups, the subset of patients with CGS had a 70% mortality rate.6Fortunately, with the advent of more aggressive and invasive strategies for the management of AMI, survival of patients with AMI complicated by CGS has improved. Although the SHOCK Trial did not show a significant reduction in 30-day mortality between patients undergoing early revascularization and those receiving initial medical stabilization, 6-month and 1-year survival were both significantly improved in those who underwent early revascularization, defined as within 18 hours of the diagnosis of shock.2,7 Only one subgroup in this study, those 75 years of age or older, did not benefit from early revascularization at 6 months and 1 year. It is therefore an ACC/AHA Class I recommendation that patients younger than 75 years of age with an acute STEMI (including new-onset left bundle branch block) complicated by CGS undergo early revascularization with either percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).5 This recommendation applies only to patients who present within 36 hours of MI onset and who can be revascularized within 18 hours of shock development. This recommendation is Class IIa for selected patients who are 75 years of age or older if they have good functional status. Therefore, treatment must be individualized in this group of patients. Whether shock is present upon arrival or manifests during the course of hospitalization, clinicians are charged with developing protocols to transfer patients to STEMI-referral centers in the event of CGS (Class I recommendation per ACC/AHA).8
Although the use of thrombolytic therapy has limited efficacy on the high mortality rate associated with this condition, it is acceptable in two circumstances. The first is when the patient is not a candidate for either surgical intervention or PCI. The second is when PCI or CABG is expected to be delayed. For specific recommendations regarding thrombolytic, interventional, and surgical strategies following AMI.
MEDICAL AND MECHANICAL THERAPIES
Although prompt cardiac catheterization and percutaneous or surgical revascularization are the primary goals in patients with AMI complicated by CGS, measures to stabilize the blood pressure and achieve adequate tissue perfusion must begin immediately. If the patient does not possess signs of volume overload, therapy can begin with rapid volume expansion. If this is not corrective, or the patient has volume overload, vasopressor therapy becomes necessary. Dopamine is the drug of first choice if systolic blood pressure is more than 70 mm Hg and <100 mm Hg, and norepinephrine should be added if the patient remains hypotensive or has signs of inadequate tissue perfusion on maximum doses. It is acceptable to start with norepinephrine if the patient’s blood pressure is <70 mm Hg, with an attempt to transition to dopamine once the patient’s systolic blood pressure improves.5 Epinephrine and phenylephrine are not first choices in CGS because of their significant α-agonist activity, which can lead to an increase in afterload and subsequent decrease in cardiac output. They may become necessary, however, if dopamine and norepinephrine fail to stabilize the patient. Dobutamine can also be used in patients with acute pulmonary edema with systolic blood pressure >70 mm Hg and <100 mm Hg.
Short-Term Circulatory-Assist Devices
In the reperfusion era, a large randomized trial and two large registries have shown benefit of IABP use in patients with AMI complicated by CGS. In GUSTO-I, early insertion of an IABP in conjunction with thrombolytic therapy demonstrated a trend toward lower 30-day and 1-year mortality, though the bleeding risk was higher.9 This trial also demonstrated that patients who received no or late IABP therapy had a much higher mortality within the first 8 hours of hospitalization than those receiving IABP therapy early In the SHOCK Trial Registry and the second National Registry of Myocardial Infarction, patients who received both IABP therapy and thrombolytic therapy had a significant mortality benefit over patients who received thrombolytic therapy alone.10,11 In addition, those who received early IABP and thrombolytic therapy in the SHOCK Trial Registry had a higher likelihood of receiving revascularization. Early IABP therapy, therefore, appears to have a mortality benefit in patients with CGS complicating AMI. This is why insertion under these circumstances remains an ACC/AHA Class I recommendation, provided no contraindications exist. These contraindications are aortic dissection, more than moderate aortic regurgitation, sepsis, bleeding diathesis, iliac or aortic atherosclerosis that impairs lower extremity blood flow, patent ductus arteriosus, and an anatomic abnormality of the femoral artery, iliac artery, or aorta that prevents insertion.12 IABP insertion should be performed concomitant with the early stabilization efforts discussed previously. Once in place, it may allow for weaning of both vasopressor and inotropic agents, which increase myocardial workload and are therefore not ideal in the AMI setting.
If an IABP is felt to be insufficient in producing adequate cardiac support, there are several options for patients who present with CGS with LV dysfunction and severe MR (similar to indications for IABP). Impella—a device with the inlet end in the LV and output in the aorta with its body through the aortic valve—has been developed where the blood is pumped directly from the LV into the aorta with the use of a microaxial pump in the Impella catheter that’s controlled by an external console. Currently, two types of Impella are available: 2.5 and 5.0 corresponding to the maximum cardiac output produced by the device. The advantage of this device is its ability to be placed in the catheterization laboratory much like an IABP with higher cardiac output produced. A major disadvantage is the size of the sheath necessary to place the catheter, which is larger than those used for IABP placement. Preliminary studies have shown that the Impella device can be placed safely and might lead to improved aortic and coronary pressures with decreased coronary microvascular resistance.13,14 A small randomized trial comparing the 2.5 device with IABP in the setting of CGS post-MI has shown improved hemodynamics at 30 minutes; however, it has failed to show better survival compared to IABP.15 The Impella 5.0 device can provide larger cardiac outputs in patients when necessary; however, data are not yet available regarding outcomes. As such, no recommendations for the use of these devices are yet in the guidelines.
The Tandem Heart—a device where inflow cannula is placed in the left atrium via transseptal puncture using a venous access site and outflow cannula in the femoral artery—allows bypassing of the left ventricle with the use of a centrifugal pump. This device can provide up to 5.0 L/min of cardiac output in tandem with the heart when used percutaneously. While the Tandem Heart provides higher outputs produced than those by IABP and the Impella 2.5, the transseptal approach requires more advanced operator training which can be a limiting factor. In a small randomized study of patients with CGS in the setting of MI, use of the Tandem Heart was associated with improved hemodynamics compared to the IABP; however, mortality at 30 days was no different. Such improved hemodynamics come with a cost of increased bleeding and limb ischemia, however.16
There are no studies comparing the Tandem Heart with the Impella device, but the above studies have shown that when a higher level of support is necessary; both devices perform better than the IABP hemodynamically, and may be more beneficial in the critically ill when a higher level of cardiac support is necessary. Potentially higher vascular complication rates necessitate that experienced operators perform these procedures.
Longer-Term Circulatory-Assist Devices
Decisions regarding placement of circulatory-assist devices in the AMI setting, other than the short-term devices noted above, should involve collaboration with a cardiothoracic surgeon skilled in their placement and follow-up. In addition, the medical and surgical cardiac transplantation teams should be consulted. Decisions regarding their placement are complex and involve multiple considerations in addition to the hemodynamic status of the patient. Mechanical cardiac support devices in AMI complicated by isolated LV dysfunction should be considered when patients remain hemodynamically unstable and have evidence of end-organ hypoperfusion despite IABP therapy and maximal inotropic support. In addition, surgically correctable, mechanical complications of MI must be ruled out. Other issues such as transplant candidacy, potential reversibility of cardiac dysfunction, bleeding risks, expected duration of support, and the absence or presence of biventricular dysfunction are also important. In addition, the patient’s age, body habitus, and comorbid conditions must be considered.
There are a number of different circulatory-assist devices, grouped best into two categories. Extracorporeal membrane oxygenation (ECMO) is a device where the patient’s circulatory and respiratory system is fully supported by way of providing cardiac support and oxygenation of the blood externally. ECMO allows for temporizing the acute hemodynamic and respiratory decline while further decisions can be made as the patient is evaluated. If a patient is subsequently refused for transplantation, he or she can be weaned from the device and removal can occur without reinstitution of cardiopulmonary bypass. These devices are useful because they allow for observation of myocardial recovery after a period of rest and provide decision time concerning transplant candidacy. The second category of devices consists of ventricular assist devices that are suitable for long-term support. These devices are inserted via cannulation of the LV which then delivers blood to the aorta for perfusion. If a patient is deemed a transplant candidate in the acute setting, some centers will immediately place this type of device. If a short-term device was used initially, switching to a long-term device can be done as well. These devices are then explanted at the time of transplant or can be used as bridge-to-decision or destination therapies.
Vasodilators
Vasodilator therapy is ideal in patients with a low cardiac output who are not hypotensive. The two drugs most frequently used in the intensive care unit (ICU) setting are nitroprusside and nitroglycerin. Nitroprusside is a direct intravenous vasodilator that produces a balanced effect on both arteries and veins. It is initiated at low doses and titrated to a mean arterial blood pressure (MAP) of 65 to 70 mm Hg. Thiocyanate and cyanide toxicity have been reported but are uncommon unless patients receive a prolonged infusion. Patients with renal dysfunction are more prone to the former, and those with liver dysfunction, the latter. Thus, nitroprusside must be used cautiously in patients with these comorbidities. Intravenous nitroglycerin is the drug of first choice in the setting of AMI and CHF. In addition to its vasodilatory effect, it has anti-ischemic properties, plus, when compared to nitroprusside, is unlikely to cause coronary steal. If a nitroprusside infusion is initiated in a patient with low cardiac output in the setting of coronary instability, nitroglycerin should also be added to negate the potential coronary steal that can be associated with nitroprusside. Both of these drugs should be avoided in hypotensive patients.
Beta-Blockers
Intravenous beta-blockers should be avoided in patients with AMI complicated by CGS (ACC/AHA Class III recommendation).17 Once the patient is hemodynamically stable and has been weaned from inotrope and IABP support, it is safe to institute low doses of oral beta-blockers.
Diuretics
Intravenous diuretics are frequently necessary in the setting of AMI complicated by CGS for the treatment of pulmonary edema and volume overload. These can cause hypotension and therefore measures to stabilize the blood pressure should be instituted before diuretics are administered to a hypotensive patient. If the patient is in extremis from a respiratory standpoint, intubation should be considered.
Aldosterone Antagonists
Long-term administration of aldosterone antagonist— eplerenone—should be considered as its use has been associated with improved survival in the post-MI setting in patients who develop heart failure.18
Angiotensin-Converting Enzyme Inhibitors and Angiotensin-II Receptor Blockers
Multiple trials studying the administration of oral angiotensin-converting enzyme inhibitors (ACE-I) during the first few days following AMI complicated by CHF have shown a decrease in both mortality and adverse cardiovascular events.19–21 Angiotensin-II receptor blockers (ARBs) have also been shown to lower mortality and adverse cardiovascular events when instituted early in patients with AMI complicated by CHF.22,23 Importantly, these trials did not include patients in CGS. These medications are contraindicated in patients with hypotension in the setting of AMI. Once shock has resolved, ACE-I and/or ARBs can be initiated at low doses, provided no contraindications to these drugs exist.
MECHANICAL COMPLICATIONS
Ventricular Septal Defect
VSD is a serious complication of AMI that increases the risk of mortality substantially, even in patients who have undergone urgent surgical correction. In the prethrombolytic era, its occurrence was between 1% and 2%, and it accounted for approximately 5% of AMI-related deaths. The incidence has decreased with the use of thrombolytic agents, as demonstrated in the GUSTO-I Trial, where this was 0.2%.24Also noteworthy, in GUSTO-I the most important predictors of VSD were advanced age, female sex, anterior infarct location, and no current smoking.24 In addition, a history of hypertension was common among patients. Angiographically, >50% of the patients had two- and three-vessel coronary disease, and those patients with a VSD were more likely to have had total occlusion of the infarct-related artery.24
VSD typically presents in the first week after MI and usually within 3 to 5 days of symptom onset. It was noted to occur earlier in the GUSTO-I and SHOCK trials, with a median time of 1 day and 16 hours from MI symptom onset, respectively.24,25 Many of the patients in both of these trials received thrombolytic therapy, which has led investigators to hypothesize that timely administration of thrombolytic therapy restores patency of the infarct-related artery, thereby preventing or limiting the extensive transmural necrosis required for ventricular septal rupture. If VSD occurs with lytics, the presentation of the VSD is earlier as the use of lytics might exacerbate the myocardial hemorrhage associated with MI.24
VSD occurs with equal frequency in anterior, inferior, or posterior MIs. When it occurs in the setting of a right coronary artery (RCA) or dominant left circumflex artery (LCx) occlusion, the location of the defect is typically in the posterobasal region of the septum as opposed to the apical–septal region, seen with anterior infarctions. Posterobasal ruptures are often complex, with serpiginous courses containing multiple small defects. This differs from the direct, through-and-through communication sometimes seen with apical–septal defects. Further, posterobasal VSDs are in close proximity to the mitral and tricuspid valves. These anatomic issues make surgical and percutaneous closure of posterobasal ruptures more difficult. Additionally, patients with inferior or posterobasal infarctions often present with varying degrees of RV infarction, which adds to management complexity.
Symptoms and Signs
VSD results in a left-to-right shunt that leads to RV volume overload, increased pulmonary blood flow with reduced systemic blood flow. These hemodynamic alterations often lead to shock. Patients demonstrate signs of biventricular failure that include elevated neck veins and pulmonary edema. Peripheral edema is uncommon in the acute setting, as is displacement of the point of maximal impulse. There is often a loud, holosystolic, precordial murmur that has widespread radiation. A palpable, precordial thrill is present in >50% of these patients.26
Diagnosis
The physical examination is diagnostic in most patients with a VSD. The test of first choice to confirm its presence is TTE with color Doppler imaging. A basal VSD can be visualized in multiple views, including the parasternal long-axis view with medial angulation, the apical long-axis view, the subcostal long-axis view, and the parasternal short-axis view (Fig. 42.1). An apical VSD is best visualized in the apical four-chamber view, although it too can be appreciated in multiple views.
FIGURE 42.1 A: Subcostal short-axis view demonstrating an inferobasal VSD (arrow). B: Same view with Doppler across the defect, demonstrating a left-to-right shunt. RV, right ventricle; LV, left ventricle.
Diagnosis can be confirmed by right heart catheterization with a saturation run. This is performed by sequentially sampling blood from the pulmonary artery (PA), RV, right atrium (RA), superior vena cava (SVC), and inferior vena cava (IVC). At least a 7% step-up in the oxygen saturation from RA to PA is required to diagnose a LV to RV level. Subsequently, by using the O2 saturation values, one can calculate the degree of shunting, which is expressed as the ratio of pulmonary to systemic blood flow (Qp:Qs) (Fig. 42.2).
FIGURE 42.2 Calculation of left-to-right intracardiac shunts. When no shunt exists, MvO2 = pulmonary artery saturation. When a left-to-right shunt is present, MvO2 = the saturation in the chamber prior to the oxygen step-up. If there is no right-to-left shunt, and PvO2 is not collected, it is assumed to be 95%.
Lastly, VSD can be diagnosed by ventriculography. Typically, the best view for this is the LAO view with cranial projection, such as LAO 60 degrees with 20 degrees of cranial angulation. This image nicely demonstrates the full length of the septum and, with contrast injection, passage of the contrast material will be seen crossing into the RV (Fig. 42.3).
FIGURE 42.3 A: RAO 20-degree projection demonstrating filling of the left ventricle (LV). B: Same view demonstrating filling of the right ventricle (RV) from the LV through an inferoapical VSD (arrow). C: LAO 40-degree, cranial 25-degree projection demonstrating filling of the LV. D: Same view demonstrating filling of the RV from the LV through an inferoapical VSD (arrow).
Treatment
Emergency cardiac surgery with concomitant CABG is recommended for patients who present with VSD following AMI. This applies to both stable and unstable patients because stability can change rapidly if the necrotic edges of the defect expand abruptly. While surgical consultation is being obtained, patients should be placed in the ICU for invasive hemodynamic monitoring, initial treatment of shock, and consideration of IABP insertion. If the patient is not hypotensive, a short-acting vasodilator such as nitroprusside can be used to optimize hemodynamics.4 Percutaneous closure for a VSD complicating AMI has been reported in small case series.27 It remains investigational, as patient numbers were small, follow-up was short, different devices were used, and some patients underwent closure several weeks following the acute event. This technique however might be used as a last resort in patients who are poor surgical candidates because complete closure is typically not achieved with percutaneous devices.
Even in patients who undergo emergency surgical repair, mortality at 30 days in the thrombolytic era is estimated to be approximately 50%. This is in comparison to a >90% 30-day mortality in patients managed medically.24,25 This underscores the importance of prompt recognition, early placement of an IABP, and expeditious triage to the operating room for surgical repair.
Acute Mitral Regurgitation from Papillary Muscle Rupture or Functional Mitral Regurgitation
MR in the setting of AMI can occur for various reasons. It can result from papillary muscle rupture, which complicates 1% of AMIs and results in approximately 5% of AMI-related deaths. It can also result from abnormal coaptation of the mitral valve leaflets during systole due to dyssynchronous contraction of the LV walls. The latter may be seen in the acute setting when segmental LV wall dysfunction leads to restricted motion of the leaflet leading to MR. In the absence of early revascularization with scar formation, this type of MR might become chronic over time.
Although any degree of MR following AMI has been associated with an increase in mortality, papillary muscle rupture carries the gravest prognosis. In patients who develop severe MR, due to restrictive leaflet motion, the infarct is often extensive. In contrast, papillary muscle rupture is more often the result of a small infarction affecting the papillary muscle itself and typically occurs between the second and seventh days following AMI.26 Rupture of the posteromedial papillary muscle in the setting of an inferior infarction is more common because it has a single vessel blood supply from the posterior descending branch of the dominant coronary artery. The anterolateral papillary muscle receives a dual blood supply from the left anterior descending (LAD) and LCx arteries, making it more resistant to necrosis.
Symptoms and Signs
Severe MR caused by papillary muscle rupture or a restrictive leaflet manifests as sudden shortness of breath followed by rapid hemodynamic deterioration. The median time to its development in the SHOCK Trial registry was 12.8 hours.28 Also noteworthy in the SHOCK Trial Registry was that ST elevation was less frequent in those patients with CGS and severe MR in comparison to patients with CGS caused by severe LV dysfunction without MR.28 This important observation shows that an ECG with a relatively benign appearance in the setting of abrupt and severe hemodynamic deterioration should raise the suspicion of acute MR. Signs of shock are typically present with pulmonary rales. A precordial, systolic murmur may be heard, and its quality varies significantly from patient to patient. In some cases there is no appreciable murmur due to the rapid equilibration of pressures between the left ventricle and left atrium.
Diagnosis
Although physical examination is quite helpful, accurate diagnosis can be made by TTE or transesophageal echocardiography (TEE) with color Doppler imaging. The left ventricular ejection fraction (LVEF) may be normal or even supranormal in the case of papillary muscle rupture, as the infarcts occurring in this setting are often less extensive and the MR possesses an unloading effect on the left ventricle. If rupture has occurred, one will see the head of the papillary muscle attached to a flail mitral leaflet (Fig. 42.4).
FIGURE 42.4 TEE at 124 degrees at the midesophageal level demonstrating papillary muscle rupture and a flail posterior mitral leaflet. LV, left ventricle; LA, left atrium; PML, posterior mitral leaflet; AML, anterior mitral leaflet; PPM, posterior papillary muscle.
Right heart catheterization (RHC), though important for hemodynamic monitoring and therapy in MR complicating AMI, should not be used as a diagnostic modality. It can, however, help to confirm the diagnosis. In addition to an elevated PCWP, there will often be giant V waves in the PCWP tracing (Fig. 42.5). It should be noted however that large V waves are also seen in patients with acute VSD. Left ventriculography can also confirm the diagnosis, but it is often unnecessary because echocardiography is sufficient to make both diagnostic and treatment decisions.
FIGURE 42.5 A: PCWP tracing representing normal waveforms during the cardiac cycle. B: PCWP tracing representing severe MR in a patient in atrial fibrillation. Note the giant V wave that represents regurgitant volume into the left atrium during ventricular systole.
Treatment
Stabilization efforts for papillary muscle rupture and severe restrictive leaflet-related MR are the same as those discussed for patients with CGS related to isolated LV dysfunction. With regard to medical therapy, patients who are not hypotensive can be managed with an intravenous vasodilator such as sodium nitroprusside. This will reduce LV afterload, improve cardiac output, and subsequently reduce the degree of MR and pulmonary edema. An IABP should be placed if the patient is in shock or has overt pulmonary edema. In patients with papillary muscle rupture, even if these two signs are not present, IABP therapy should be considered because stability can change rapidly.5Stabilization efforts should begin immediately, but not prevent rapid transport to the catheterization laboratory. Patients should be cared for in the ICU, and there is general agreement that a RHC is warranted for short-term guidance of pharmacologic and/or mechanical management of severe MR complicating AMI.29 Diuretics should be used judiciously for relief of pulmonary edema.
Urgent cardiac surgery with concomitant CABG is indicated in all cases of AMI complicated by papillary muscle rupture (Class I ACC/AHA Recommendation).5 Stability can change rapidly, so stabilization and triage to the operating room must be swift. In-hospital mortality in surgically treated patients is approximately 40%, substantially lower than for those treated medically.28 In patients who survive to hospital discharge after surgery, short- and long-term survival remains excellent.
It is important to recognize that outcome of patients with even moderate MR after AMI is much worse than that without MR. Although a patient with severe MR with restrictive leaflet may ultimately require CABG and mitral valve repair or replacement, emergency surgery may not be not necessary for the MR alone. This is because the degree of regurgitation often improves with revascularization and aggressive medical and/or mechanical therapies. If the patient’s coronary anatomy is felt to require surgical revascularization, the degree of MR should be reassessed and valve repair or replacement considered.5
Cardiac Free Wall Rupture
Cardiac free wall rupture, though an infrequent complication of AMI, is the second leading cause of in-hospital mortality in AMI patients. Approximately half of cardiac ruptures occur within the first 5 days of AMI, and approximately 90% within the first 2 weeks. It can present in an acute or subacute fashion. The acute presentation is typically associated with hemodynamic collapse. There may not be time for life-saving emergency treatment. Subacute rupture presents more subtly, and if diagnosis is made early, prognosis with surgery is favorable.
Rupture most commonly involves the LV, but on occasion may involve the RV Although the incidence of cardiac rupture has decreased recently, there has been an increase in the incidence of in-hospital mortality following rupture. This is particularly more common in the first 2 days following AMI, in those patients who have received thrombolytic therapy.30,31 Risk factors associated with free wall rupture have been variable across studies, but those commonly seen include: age >70 years, female gender, no history of prior MI or angina, transmural myocardial involvement, poor coronary collateral blood flow, and hypertension.32–35
Signs and Symptoms
The acute presentation of free wall rupture is typically one of cardiovascular collapse and electromechanical dissociation. This is commonly associated with transmural, through-and-through tears that cause abrupt tamponade. The subacute presentation is less severe, and patients slowly begin to manifest signs of CGS (see above) from tamponade. This is due to the slow egress of blood into the pericardial space from gradual or incomplete rupture of the infarcted myocardium. It can also occur when thrombus or pericardium incompletely seals off the rupture site, also known as a pseudoaneurysm, or contained rupture. Patients may experience persistent or recurrent chest pain with ST- and T-wave abnormalities. Additionally, they may experience episodes of transient hypotension, nausea, a feeling of doom, and/or have a fleeting pericardial friction rub prior to decompensation. Signs of tamponade, such as hypotension, tachycardia, and neck vein distention, may be present.
Diagnosis
In addition to the above symptoms and signs, the ECG often demonstrates persistent ST elevation and evidence of infarct extension or expansion.35 Hemodynamics by RHC will demonstrate elevation of intracardiac pressures, along with equalization of diastolic filling pressures and a reduced cardiac output. Pulsus paradoxus can be appreciated on the intra-arterial waveform, along with blunting of the Y decent on the right atrial and pulmonary arterial pressure waveforms (Fig. 42.6). TTE will demonstrate a large pericardial effusion and signs of tamponade, including right atrial collapse during ventricular systole (Fig. 42.7), RV collapse during ventricular diastole (Fig. 42.8), respiratory variation of the tricuspid and mitral valve inflow velocities, and a plethoric IVC (see Fig. 42.7) that fails to collapse by 50% of its diameter with inspiration. It is important to note that pericardial effusion is a common finding following uncomplicated MI. Its presence should heighten one’s suspicion for the possibility of subacute rupture. Serial echocardiography and close clinical observation can then be performed in order to exclude further accumulation of pericardial fluid.
FIGURE 42.6 Hemodynamic findings in tamponade. Note that the aortic pressure tracing demonstrates hypotension and pulsus paradoxus (drop in systolic blood pressure by >10 mm Hg upon inspiration). In addition, the right atrial pressure is elevated and the y-descent is extremely blunted (arrow). a, atrial contraction; x, atrial relaxation; v, atrial filling (ventricular systole); y, atrial emptying (ventricular diastole). (Modified from Wu LA, Nishimura RA. Pulsus paradoxus. N Engl J Med. 2003;349(7):666.)
FIGURE 42.7 A: Subcostal long-axis view demonstrating a large pericardial effusion adjacent to the RA. B: Same view demonstrating right atrial wall inversion (arrow) during systole. Note that IVC plethora is present in both images. HV, hepatic vein; PE, pericardial effusion; RA, right atrium.
FIGURE 42.8 A: Parasternal short-axis view demonstrating that the right ventricle, while small and underfilled, remains open during systole (arrow). B: Same view demonstrating RV diastolic collapse (smaller arrow). LV, left ventricle; PE, pericardial effusion.
Treatment
Patients with acute or subacute rupture should be supported with intravenous fluids and, if hypotensive, with vasopressors while emergency cardiothoracic surgical consultation is obtained. Pericardiocentesis should be performed only in the operating room, as decompression of the pericardial space will result in further bleeding. If a patient is hemodynamically unstable despite treatment with fluids and vasopressors, pericardiocentesis can be performed as a last resort because decompression may be the only chance for survival.
Pseudoaneurysm
Although it is an infrequent complication of AMI, it is important to recognize a pseudoaneurysm because it is prone to rupture. It occurs when pericardial adhesions and thrombus seal off an area of myocardial rupture. Although this can happen at any location, a recent review found that the posterior wall was the most common area of involvement. This was followed by the lateral, apical, and finally inferior regions of the myocardium.36 In comparison to a true aneurysm, there is no myocardium between the LV cavity and the pericardial space (Fig. 42.9). Risk factors for the development of postinfarction pseudoaneurysm are similar to those for myocardial free wall rupture.
FIGURE 42.9 Pseudoaneurysm versus aneurysm. (Modified from Cercek B, Shah PK. Complicated acute myocardial infarction: heart failure, shock, mechanical complications. Cardiolo Clin. 1991;9(4):569-593.)
Symptoms and Signs
Pseudoaneurysms are often silent and are discovered on follow-up imaging or postmortem. Gradual enlargement of the aneurysmal cavity can lead to progressive heart failure symptoms, although this is rare. Some patients present with ventricular arrhythmias. Others develop arterial embolization after expulsion of thrombus from the aneurysmal cavity. The physical examination can be normal or consistent with CHF. Some patients will have a new murmur on auscultation, although 30% will have no murmur.28 Rarely, a patient will present in CGS.
Diagnosis
The ECG may show persistent ST elevation or regional pericarditis, although it most often demonstrates nonspecific ST changes.36 CXR can demonstrate an abnormal bulge around the site of involved myocardium but more frequently shows cardiomegaly. There are several imaging modalities available for diagnosis, including contrast ventriculography, TTE, TEE, magnetic resonance imaging (MRI), and computed tomography (CT). None of these tests has been 100% accurate, and no adequate comparisons between modalities have been made. Contrast ventriculography is the “ gold standard” and has been associated with a high degree of diagnostic accuracy. One will see a narrow orifice leading to a saccular cavity. If concomitant coronary arteriography is performed, there will be a lack of vessels at the site of the pseudoaneurysm. Because this is an invasive modality, TTE with color Doppler is a reasonable test to perform first, although its diagnostic accuracy was found to be 26% for this condition36 (Fig. 42.10). Although TEE and MRI have shown a higher degree of diagnostic accuracy, only small numbers have been studied and a definitive conclusion regarding superiority cannot be made. If MRI is used, cine runs will increase diagnostic sensitivity with its ability to highlight abnormal blood flow patterns and turbulence in and around the cavity of a pseudoaneurysm. In addition, it will often demonstrate loss of epicardial fat at the site of rupture.
FIGURE 42.10 A: Apical long-axis view demonstrating a pseudoaneurysm of the posterior LV wall. B: Same view with Doppler demonstrating the rupture site (arrow) with turbulence of blood flow in and surrounding the cavity. LA, left atrium; AML, anterior mitral leaflet; PML, posterior mitral leaflet; Pan, pseudoaneurysm; Ao, aorta.
Treatment
Once a pseudoaneurysm is diagnosed, urgent surgery is indicated because of a 30% to 45% risk of rupture.36 If the pseudoaneurysm is incidentally diagnosed or the patient is asymptomatic, the patient should be monitored until surgical evaluation has occurred. Successful percutaneous closure of pseudoaneurysms has been recently reported.
Left Ventricular Aneurysm
A true ventricular aneurysm differs anatomically from a pseudoaneurysm in that myocardium is present in its wall and there is no communication between the ventricular cavity and pericardial space (see Fig. 42.9). Its incidence following AMI has been reported as high as 38%. With the advent of reperfusion therapy, its frequency has decreased to between 8% and 15%.26,37 Ventricular aneurysms most commonly complicate transmural anterior wall MIs and are thought to be the result of infarct expansion. In contrast to post-MI pseudoaneurysms, true ventricular aneurysms rarely rupture because the walls become fibrotic and calcified with time. True aneurysms have a wide base and are frequently associated with mural thrombus.26
Signs and Symptoms
Aneurysms place the entire ventricle, including the noninfarcted portion, at a mechanical disadvantage. Contractile energy is expended during passive outward expansion of the aneurysmal wall, and cardiac output decreases. This functional decline is more significant with acute aneurysms because the aneurysmal wall is more compliant and therefore expands to a greater degree during systole. Additionally, the distorted geometry can lead to misalignment of the mitral valve apparatus and result in MR.
Patients can present early or several weeks following AMI. They can be asymptomatic, or develop CHF, CGS, or recurrent ventricular arrhythmias. The index event is less often systemic embolization. The physical examination may demonstrate signs of CHF and/or CGS. In addition, patients may have a diffuse, dyskinetic apical impulse that is shifted leftward. Auscultation may reveal a murmur suggestive of MR or a third heart sound.
Diagnosis
In addition to the above physical findings, as with pseudoaneurysms, the CXR may demonstrate cardiomegaly and a bulge representing the aneurysmal area. The ECG will often show evidence of a transmural anterior MI and persistent ST-segment elevation. TTE is the diagnostic test of choice and will show thinning of the myocardium and dyskinetic wall motion at the site of infarction. Thrombus should always be excluded, as it is found in more than half of the surgical and autopsy cases that have been studied. If there is inability to exclude thrombus with a standard surface echocardiogram, contrast can be given simultaneously to improve distinction between the ventricular cavity and endocardial lining. Other imaging modalities such as cardiac MRI or CT scanning can be useful in this regard.
Treatment
Diagnosis of a ventricular aneurysm in itself does not change the treatment algorithm for a post-MI patient with comparable degrees of heart failure and/or CGS (see above). It is important to note that administration of an ACE-I within 24 hours of infarction is especially crucial in this situation, because of the drug’s inhibitory effect on infarct expansion and beneficial effect on ventricular remodeling. If a patient is stable off mechanical and vasopressor support, an ACE-I should be started.
Surgery, which should include an LV aneurysmectomy and concomitant CABG, may be indicated when there are symptoms and signs related to the aneurysm.5 However, careful evaluation and patient selection are necessary as there was no improvement in long-term outcome when aneurysmectomy was added to CABG alone in a recent RCT.38 Patients with small or moderate-sized, asymptomatic aneurysms should not undergo surgery. They do require medical management for heart failure when it is present. Management of large, asymptomatic aneurysms remains controversial, and decisions to proceed with surgery are often individualized as above.
Anticoagulation with warfarin for at least 3 months is indicated for all post-STEMI patients who develop a mural thrombus in the acute setting. This applies to diagnoses made within 1 month of the event. Anticoagulation is indicated because systemic embolization can occur in as many as 10% with documented mural thrombi, and the risk of late thromboembolism appears to be decreased with oral anticoagulant therapy.39,40 Although the risk of embolization decreases dramatically in the subsequent months following the infarction, therapy should be continued indefinitely for those patients who are not at an increased risk of bleeding.5 Anticoagulation in these patients consists of the early administration of intravenous, unfractionated heparin or subcutaneous low-molecular-weight heparin, along with Coumadin therapy until the international normalized ratio is between two and three. Once this has been achieved, heparin may be discontinued. Patients who develop an LV aneurysm but no identifiable thrombus in the acute setting can similarly be anticoagulated because the incidence of thrombus in these patients, postmortem and intraoperatively, is at least 50%.39 There is limited evidence to support long-term anticoagulation in these patients, and practice patterns often differ.
ADDITIONAL COMPLICATIONS
Right Ventricular Infarction with Hemodynamic Compromise
RV infarction rarely happens in isolation and more commonly occurs during an inferior or inferoposterior LV MI. Patients present with various degrees of RV dysfunction, but only 10% to 15% develop hemodynamically significant RV impairment. This typically occurs when there is an ostial or proximal RCA occlusion prior to takeoff of the RV marginal branches.
Symptoms and Signs
If one understands the hemodynamic relationship between the LV, RV, and pericardium, the symptoms and signs of RV infarction become clear. It is important to realize that many of the hemodynamic changes overlap with tamponade, constrictive pericarditis, and restrictive cardiomyopathy. This makes clinical context and echocardiographic examination very important.
When RV infarction occurs, the RV filling pressure becomes elevated due to systolic and diastolic dysfunction, which in turn causes elevation of right atrial filling pressures. Simultaneously, a decrease in RV output leads to a reduced LV end diastolic volume and the PCWP will be low. This is not always the case when there is concomitant LV dysfunction from a previous infarction or the current event. LV preload becomes further reduced when intrapericardial pressure is increased by abrupt dilation of the RV. Similar to tamponade, the LV and RV become interdependent.41 This combination of events leads to the triad of hypotension, elevated neck veins, and clear lung fields.42 Neck vein distention may not be seen if the patient is hypovolemic but may become apparent following aggressive fluid resuscitation, one of the key aspects of treatment.
Diagnosis
This diagnosis should be considered in any patient who presents with inferior ST-segment elevation on ECG. In fact, it is an ACC/AHA Class I indication to obtain a tracing of lead V4R and a TTE to look for RV infarction in patients with inferior STEMI and hemodynamic compromise.5 RV infarction should also be considered in patients with ST depression in leads V1 and V2, as this may represent acute infarction of the posterior myocardium as opposed to septal, subendocardial ischemia. Again, TTE can confirm the diagnosis by demonstrating hypokinesis and dilatation of the RV. Right heart catheterization can help confirm the diagnosis, but findings are nonspecific and may overlap with those of tamponade, constriction, and restriction. One will see elevated RV filling pressures that are equal to or greater than LV filling pressures, normal or low pulmonary arterial and PCWP, and a reduced cardiac index. Another clue to significant RV involvement in patients with inferior or posterior MI is hypotension following the administration of preload reducing agents such as diuretics and nitrates.
Treatment
Similar to patients with AMI and CGS secondary to LV dysfunction, patients with AMI complicated by severe RV dysfunction should undergo emergency diagnostic angiography and revascularization. If CABG is indicated, it is reasonable (Class IIa ACC/AHA Recommendation) to delay it in patients with clinically significant RV dysfunction as the RV function frequently improves following several weeks of medical therapy.5
Patients should be monitored in the ICU with both intra-arterial blood pressure monitoring and a RHC. If shock is present, the first line of therapy is aggressive fluid resuscitation. This is done with isotonic saline until the PCWP is between 15 and 18 mm Hg. If shock remains after this is achieved, an inotropic agent should be added. Dobutamine is the preferred drug in this situation because it causes less hypotension. If vasopressors are required, a pure α-agonist should be avoided, as it will lead to pulmonary arterial vasoconstriction and further decrease forward flow into the left ventricle. If severe LV dysfunction and an elevated PCWP exist, unlike the situation of isolated LV systolic dysfunction complicating AMI, sodium nitroprusside should be avoided as a reduction in preload might cause further deterioration of hemodynamics. These patients should be considered for IABP counterpulsation. It is important to avoid factors that increase RV afterload, such as hypoxemia, α-agonists, and elevations in PCWP, which include positive end-expiratory pressure (PEEP). In addition, one should avoid agents that decrease RV preload. This includes medications such as nitrates, morphine, and diuretics; but also dysrhythmias that lead to disruption of atrioventricular (AV) synchrony, such as atrial fibrillation and high-degree AV block.
Atrial fibrillation must be dealt with emergently in the hemodynamically unstable patient following RV infarction, with immediate direct-current cardioversion (DCCV). If the patient is not hemodynamically compromised, a trial of antiarrhythmic therapy can be attempted; however, if sinus rhythm is not restored promptly, DCCV should be performed.
Bradyarrhythmias, a frequent complication of inferior myocardial infarction (IMI) with RV involvement, can be quite dangerous even when the atrium and ventricle contract synchronously. This is because the dilated right ventricle has a relatively fixed stroke volume and depends largely on heart rate to increase its output. Management of bradycardia in AMI is discussed in a subsequent section. It is important to know that if a patient with RV infarction requires temporary pacing; both atrial and ventricular leads should be placed, in order to maintain AV synchrony.
Dynamic Left Ventricular Outflow Tract Obstruction
Although development of dynamic LVOT obstruction is a rare complication of MI, it is important to recognize because many of the traditional therapies used in the treatment of AMI complicated by CGS should be avoided. These include nitrates, afterload reduction, diuretics, IABPs, and inotropic agents.
Dynamic LVOT obstruction most often occurs in the setting of an anteroapical MI with compensatory basal hyperkinesis. This combination of segmental wall motion abnormalities causes a decrease in the cross-sectional area of the LVOT and acceleration of blood flow across this region. The acceleration of blood flow decreases pressure above the mitral valve, causing systolic anterior motion (SAM) of the anterior mitral leaflet against the interventricular septum, which worsens the LVOT obstruction.43 These patients often have a single, significant stenosis in the LAD coronary artery, in addition to mild concentric LV hypertrophy or asymmetric septal hypertrophy.
Symptoms and Signs
Patients with dynamic LVOT obstruction usually have chest pain and evidence of an anterior or anteroapical STEMI. This complication has also been seen in non–ST-elevation myocardial infarction (NSTEMI), but much less frequently. Symptoms and signs of CHF and CGS are often present (see above). Patients can have a holosystolic murmur at the left lateral sternal border that radiates to the apex and represents MR in addition to a harsh crescendo–decrescendo systolic murmur in the left second intercostal space, representing LVOT obstruction.
Diagnosis
The possibility of LVOT obstruction should be considered in patients who have progressive hemodynamic deterioration in the setting of standard medical and mechanical therapies used to treat patients with AMI and CGS. The diagnosis is made by TTE. LVEF may be normal or depressed. Apical hypo or akinesis along with hyperkinesis of the basal segments of the heart will be seen, in addition to SAM and regurgitation of the mitral valve. The LVOT, best interrogated with continuous-wave Doppler in the apical five- and three-chamber views, will demonstrate a gradient >30 mm Hg.
Treatment
Standard revascularization and anticoagulant therapy for AMI must be instituted in these patients. What is different are the supportive measures used during the periinfarction period. This consists of beta-blockers and fluids. If shock is present, an α-agonist should be used. All of these therapies decrease the degree of LVOT obstruction. Phenylephrine, the most commonly used α-agonist, is started at 20 to 40 μg/min and titrated upward, until there is clinical improvement or the maximum dose has been reached.
Pericarditis
There are two forms of pericarditis that occur in the setting of MI. The first, typically occurring within 24 to 96 hours of transmural MI, is a form of localized inflammation in the pericardial region above the necrotic myocardium, which tends to run a benign course. The second, a form of post–cardiac injury syndrome also referred to as Dressler syndrome, can manifest 1 to 8 weeks following MI. Although the exact mechanism is unclear, it is felt to be the result of an autoimmune reaction involving myocardial antigen and antibody complexes. This form of pericarditis tends to be a more systemic inflammatory process, is often refractory to first-line therapies, and frequently recurs.
Symptoms and Signs
Patients with pericarditis often develop positional chest pain. This tends to be sharp, pleuritic, exacerbated by recumbency, and commonly radiates to the trapezius ridge. If the patient has Dressler syndrome, he or she may also complain of arthralgias and myalgias. Dressler syndrome can also be associated with pleuritis and pleural effusions. Although these effusions are typically small, they may enlarge and cause dyspnea. Patients may be febrile in both forms of pericarditis, and those with Dressler syndrome can run fevers as high as 40°C. All patients with pericarditis may have leukocytosis and elevation of inflammatory markers such as the erythrocyte sedimentation rate and C-reactive protein. Physical examination may demonstrate a pericardial friction rub.
Diagnosis
Symptoms and the presence of a pericardial friction rub are quite specific for pericarditis. ECG can be helpful but is less sensitive, especially in the acute situation, as the evolutionary changes seen following MI can mask the typical ECG features of pericarditis (Table 42.2). Although TTE is not diagnostic in situations of post-MI pericarditis, it must be obtained to rule out a significant pericardial effusion, seen more commonly in patients with Dressler syndrome. It is important to realize that the presence of an effusion is not diagnostic, as it is commonly seen following uncomplicated AMIs. Likewise, absence of a pericardial effusion does not exclude the diagnosis.
TABLE
42.2 ECG Changes in Pericarditis versus STEMI
aIn pericarditis, the evolution of repolarization abnormalities does not always occur simultaneously as they typically do in MI. In addition, the distribution of repolarization abnormalities in myocardial infarction remains constant, whereas in pericarditis, multiple areas on the ECG can demonstrate different repolarization patterns.
bIf ST-segment elevation does not resolve by 6 weeks, consider the possibility of ventricular aneurysm or a large area of dyskinetic myocardium.
Treatment
There are two issues to consider and balance when treating patients with post-MI pericarditis. One is the need for antiinflammatory agents and the need to avoid anticoagulation. In terms of anti-inflammatory agents, aspirin is the first line of therapy. If patients are refractory to standard doses, as much as 650 mg every 4 to 6 hours may be used. When high doses are needed, it is advisable to place the patient on an acid-suppressive regimen. Some patients will be refractory to or unable to take high-dose aspirin therapy. In these patients, 0.6 mg of colchicine every 12 hours and/or 650 mg of acetaminophen every 4 to 6 hours can be tried. Nonsteroidal anti-inflammatory drugs (NSAIDs) other than aspirin and corticosteroids should be avoided unless used as a last resort. Corticosteroids and NSAIDs adversely affect myocardial scar formation, which can lead to thinning of the scar and, in some circumstances, infarct expansion. There are reports suggesting that both drug classes put the patient at increased risk for myocardial rupture following AMI. Per ACC/AHA, the use of NSAIDs (except for aspirin) at the time of infarction are contraindicated, and these agents should be discontinued when patients present with MI (Class I ACC/AHA recommendation).17 There are no clear recommendations for patients who present with pericarditis after recovery from their AMI; however, given overall association of NSAIDs with progression of CAD, it is advisable not to use these agents in patients with established disease.
Clinical judgment is necessary if anticoagulation is required for a patient with post-MI pericarditis. It is an ACC/AHA Class I indication to discontinue anticoagulant therapy if an effusion develops or enlarges. This decision must be individualized and based on the risk-to-benefit ratio. If a decision is made to continue anticoagulation, the patient must be observed diligently for effusion enlargement and impending tamponade.
ARRHYTHMIC COMPLICATIONS
Bradyarrhythmias
In the setting of AMI, management of bradyarrhythmias is complex because decisions regarding temporary and permanent pacing must be made and require multiple considerations. In the acute setting, if a patient is hemodynamically stable despite a bradyarrhythmia, a decision must be made regarding the need for prophylactic, backup pacing. This requires one to predict which patients are likely to progress to a life-threatening rhythm abnormality such as third-degree AV block. The route by which pacing is performed must involve considerations regarding patient stability, the need for AV synchrony, and the bleeding risks associated with the use of thrombolytic and postinterventional therapies.
Sinus bradycardia occurs in approximately 30% to 40% of AMIs, most commonly with inferior MI and reperfusion of the RCA.5 Although multiple mechanisms can be responsible, the most common is hyperactivity of para-sympathetics due to stimulation of vagal afferents. This is termed the Bezold–Jarisch reflex and causes both bradycardia and hypotension. When patients become symptomatic from sinus bradycardia or from sinus pauses >3 seconds in duration, intravenous atropine is the first line of therapy.5 This should be administered in doses of 0.5 to 1 mg every 3 minutes until the patient is no longer symptomatic or a total dose of 0.4 mg/kg has been reached. If symptomatic bradycardia persists, transcutaneous or transvenous pacing must be initiated.
The development of atrioventricular conduction block (AVB), intraventricular conduction delay (IVCD), and/or bundle branch block (BBB) in the setting of AMI is associated with an increased risk of in-hospital mortality. Decisions regarding prophylactic or therapeutic temporary pacing depend on the infarction location, the type of block and its presumed relationship to the AV node, the extent of preexisting conduction system disease, and the presence or absence of symptoms.
When dealing with any form of heart block, its relationship to the AV node is an important factor to consider. This is significant because blocks proximal to or within the AV node, often referred to as intranodal block, are generally benign, with prophylactic and eventual permanent pacing typically not required. This is in contradiction to infranodal blocks, which tend to be more dangerous, often require prophylactic and therapeutic temporary pacing, and frequently result in permanent pacemaker insertion prior to hospital discharge.5,44 Typical intranodal blocks are first-degree and second-degree, Mobitz type I AVB. These are usually seen in inferior or inferoposterior AMIs, and the RCA is usually the culprit artery, although the LCx can be involved. If third-degree AVB develops in the intranodal region, the QRS width is typically <0.12 seconds, the escape rate tends to be between 45 to 60 beats per minute (bpm), and asystole is uncommon. Common infranodal blocks are second-degree, Mobitz type II AVB and third-degree AVB. When infranodal blocks are present, the LAD is typically the culprit lesion. When third-degree AVB of the infranodal variety is present, the QRS width tends to be wider than 0.12 seconds, escape rates are often <30 bpm, and asystole is common. Hence, the majority of these patients require either prophylactic or therapeutic temporary pacing during the AMI setting. It is important to remember that whereas atropine is commonly the first line of treatment in patients with symptomatic, presumed intranodal AVB and sinus bradycardia, it can be dangerous in the presence of infranodal AVB. This is due to an increase in the sinus rate without an increase in the escape rate, leading to a decrease in the effective ratio of conduction and a decrease in ventricular rate.5 Atropine is administered in intravenous doses of 0.5 to 1 mg and repeated if no response, to a total dose of 0.04 mg/kg. If the patient is hemodynamically unstable and not responsive to atropine, temporary pacing is indicated. For a summary of the Class I recommendations regarding prophylactic, temporary pacing in AMI complicated by AV and intraventricular conduction abnormalities, see Table 42.3. Third-degree AVB in the AMI setting should be treated with transvenous temporary pacing. Ventricular asystole should be treated as per the Advanced Cardiac Life Support guidelines.
TABLE
42.3 Class I Recommendations for Prophylactic, Temporary Pacing in AMI
The actions listed—transcutaneous (TC) pacing, transvenous (TV) pacing, or observation—are based on the patient’s AV and intraventricular conduction patterns as well as the location of the MI. TC pacing refers to having pacing pads on the patient while monitoring closely. If in fact patient requires persistent TC pacing, TV pacing should be strongly considered. To determine the Class I indication, follow the row containing the patient’s intraventricular conduction pattern to the column containing the patient’s AV conduction pattern and MI location. Class I recommendations are those for which there is evidence and/or general agreement that the treatment is beneficial, useful, and effective. Class IIa recommendations are those for which there is conflicting evidence and/or a divergence of opinion regarding the usefulness/effectiveness of the treatment; however, the weight of evidence or opinion is in favor of usefulness/efficacy. Class IIa is included only when a Class I recommendation does not exist. AVB, atrioventricular block; BBB, bundle branch block; RBBB, right bundle branch block.
Modified from Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary. J Am Coll Cardiol. 2004:44(3):671–719.
Tachyarrhythmias
Tachyarrhythmias are common in the setting of AMI. The most deadly, primary ventricular fibrillation (VF), occurs in 3% to 5% of patients within the first few hours of STEMI. This high frequency and early occurrence underscores the importance of early hospitalization and rapid triage to an area where continuous monitoring and rapid defibrillation can occur.
In the setting of AMI, especially when complicated by CGS, tachyarrhythmias must be dealt with emergently. They increase myocardial oxygen consumption, exacerbate ischemia, and can lead to or worsen CHF and CGS. Betablockers and calcium channel blockers must be avoided if shock or significant heart failure is present, as they can contribute to hemodynamic decompensation. Often cardioversion becomes the treatment of first choice. Heightened vigilance is appropriate when sinus tachycardia is present in the AMI setting, as this may be compensatory for a severely depressed myocardium. Although betablocker administration has been proven beneficial in the AMI setting, it can be deadly if used to treat sinus tachycardia that is compensatory for a severely depressed myocardium. Finally, accelerated idioventricular rhythm occurs in approximately 30% of AMI patients, often in those with involvement of the inferior wall and following reperfusion therapy.41 It is characterized by a wide complex QRS with regular rates between 60 and 120 bpm, AV dissociation with the V-rate surpassing the A-rate, with fusion and capture beats. It occurs because an ectopic ventricular focus assumes the role of the predominant pacemaker. Accelerating the sinus rhythm or atrial pacing can cause suppression of this rhythm if treatment becomes necessary. Treatment is indicated only when there is hemodynamic compromise, symptoms as a result of the rhythm, or the R wave consistently falls on the T wave, predisposing to more serious ventricular arrhythmias.
SUMMARY
Although short- and long-term mortality following AMI has improved with the use of thrombolytic therapy and early coronary reperfusion strategies, both remain high.
The greatest fraction of deaths comes from CGS, which results from isolated LV systolic dysfunction or mechanical disruption of the myocardium.
It is imperative that these patients be identified early for the institution of appropriate therapeutic measures in a prompt manner. These include immediate efforts to achieve hemodynamic stability, rapid transport to the cardiac catheterization laboratory, and emergency PCI or surgical consultation when indicated.
These patients should be monitored closely in an ICU setting, where arrhythmias and other potentially catastrophic complications can be dealt with expediently.
ACKNOWLEDGMENT
We would like to thank Dr. Amy L. Seidel for her work on the previous version of this chapter.
SUGGESTED READINGS
Abu-Omar Y, Tsui SS. Mechanical circulatory support for AMI and cardiogenic shock. J Card Surg. 2010;25(4):434–441.
Bonow RO. Braunwald’s Heart Disease—A Textbook of Cardiovascular Medicine. 9th ed. Part VII Atherosclerotic Cardiovascular Disease. Philadelphia: Elsevier.
Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. 1999;341(9):625–634.
Kushner FG, Hand M, Smith SC Jr, et al. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update) a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2009;54:2205–2241.
REFERENCES
1. Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. 1999;340:1162–1168.
2. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction—etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000;36:1063–1070.
3. Domanski MJ, Topol EJ. Cardiogenic shock: current understandings and future research directions. Am J Cardiol. 1994;74:724–726.
4. Holmes DR Jr, Bates ER, Kleiman NS, et al. Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol. 1995;26:668–674.
5. Antman EM, Anbe DT, Armstrong PW et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004;44:671–719.
6. Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986;1:397–402.
7. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. 1999;341:625–634.
8. Kushner FG, Hand M, Smith SC Jr, et al. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update) a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2009;54:2205–2241.
9. Anderson RD, Ohman EM, Holmes DR Jr, et al. Use of intraaortic balloon counterpulsation in patients presenting with cardiogenic shock: observations from the GUSTO-I Study. Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries. J Am Coll Cardiol.1997;30:708–715.
10. Sanborn TA, Sleeper LA, Bates ER, et al. Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000;36:1123–1129.
11. Barron HV Every NR, Parsons LS, et al. The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction: data from the National Registry of Myocardial Infarction 2. Am Heart J. 2001;141:933–939.
12. Kern MJ. The Cardiac Catheterization Handbook. 3rd ed. St. Louis: Mosby; 1999.
13. Henriques JP, Remmelink M, Baan J Jr, et al. Safety and feasibility of elective high-risk percutaneous coronary intervention procedures with left ventricular support of the Impella Recover LP 2.5. Am J Cardiol. 2006;97:990–992.
14. Remmelink M, Sjauw KD, Henriques JP, et al. Effects of left ventricular unloading by Impella recover LP2.5 on coronary hemodynamics. Catheter Cardiovasc Interv. 2007;70:532–537.
15. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol.2008;52:1584–1588.
16. Thiele H, Sick P, Boudriot E, et al. Randomized comparison of intra-aortic balloon support with a percutaneous left ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock. Eur Heart J. 2005;26:1276–1283.
17. Antman EM, Hand M, Armstrong PW et al. 2007 focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol.2008;51:210–247.
18. Pitt B, Remme W Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003;348:1309–1321.
19. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med. 1992;327:669–677.
20. Kober L, Torp-Pedersen C, Carlsen JE, et al. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group. N Engl J Med.1995;333:1670–1676.
21. Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Lancet. 1993;342:821–828.
22. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003;349:1893–1906.
23. Dickstein K, Kjekshus J. Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the OPTIMAAL randomised trial. Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan. Lancet.2002;360:752–760.
24. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTOI (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation.2000;101:27–32.
25. Menon V, Webb JG, Hillis LD, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol. 2000;36:1110–1116.
26. Cercek B, Shah PK. Complicated acute myocardial infarction. Heart failure, shock, mechanical complications. Cardiol Clin. 1991;9:569–593.
27. Maltais S, Ibrahim R, Basmadjian AJ, et al. Postinfarction ventricular septal defects: towards a new treatment algorithm? Ann Thorac Surg. 2009;87:687–692.
28. Thompson CR, Buller CE, Sleeper LA, et al. Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we use emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol.2000;36:1104–1109.
29. Mueller HS, Chatterjee K, Davis KB, et al. ACC expert consensus document. Present use of bedside right heart catheterization in patients with cardiac disease. American College of Cardiology. J Am Coll Cardiol. 1998;32:840–864.
30. Becker RC, Hochman JS, Cannon CP, et al. Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study. J Am Coll Cardiol.1999;33:479–487.
31. Becker RC, Gore JM, Lambrew C, et al. A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol. 1996;27:1321–1326.
32. Fuster V Hurst’s the Heart. 12th ed. New York: McGraw-Hill, Medical Pub. Division; 2008.
33. Moreno R, Lopez-Sendon J, Garcia E, et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction. J Am Coll Cardiol. 2002;39:598–603.
34. Pohjola-Sintonen S, Muller JE, Stone PH, et al. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J. 1989;117:809–818.
35. Figueras J, Cortadellas J, Soler-Soler J. Left ventricular free wall rupture: clinical presentation and management. Heart. 2000;83:499–504.
36. Frances C, Romero A, Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol. 1998;32:557–561.
37. Cohn LH, Edmunds LH. Cardiac Surgery in the Adult. 2nd ed. New York: McGraw-Hill, Medical Pub. Division; 2003.
38. Jones RH, Velazquez EJ, Michler RE, et al. Coronary bypass surgery with or without surgical ventricular reconstruction. N Engl J Med. 2009;360:1705–1717.
39. Keeley EC, Hillis LD. Left ventricular mural thrombus after acute myocardial infarction. Clin Cardiol. 1996;19:83–86.
40. Sherman DG, Dyken ML, Fisher M, et al. Antithrombotic therapy for cerebrovascular disorders. Chest. 1989;95:140S–155S.
41. Lavie CJ, Gersh BJ. Mechanical and electrical complications of acute myocardial infarction. Mayo Clin Proc. 1990;65:709–730.
42. Reeder GS. Identification and treatment of complications of myocardial infarction. Mayo Clin Proc. 1995;70:880–884.
43. Haley JH, Sinak LJ, Tajik AJ, et al. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock. Mayo Clin Proc. 1999;74:901–906.
44. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation. 2008;117:e350–e408.
QUESTIONS AND ANSWERS
Questions
1. All of the following should raise suspicion of subacute free wall rupture, except:
a. Intermittent chest pain, hypotension, and electromechanical dissociation
b. Agitation and apprehension
c. Intermittent, nonspecific, ST–T-wave abnormalities
d. Pericardial effusion and echodensities in the pericardium
e. Nonsustained ventricular tachycardia
2. Which of the following statements regarding ventricular septal rupture complicating acute myocardial infarction (AMI) is true?
a. It is usually seen in elderly, hypertensive patients with a history of multiple prior infarctions.
b. It is more common in anterior than inferior infarctions.
c. A 4/6 holosystolic murmur indicates a large defect.
d. Either echocardiography or right heart catheterization can be used as the initial diagnostic tool.
e. Surgery should be delayed several weeks until infarct healing occurs.
3. Which of the following statements regarding papillary muscle rupture complicating AMI is true?
a. Papillary muscle rupture is most frequently seen in large, anterolateral infarctions.
b. Patients should be referred for emergency catheterization and percutaneous intervention.
c. A harsh holosystolic murmur and systolic thrill are very common.
d. Despite pulmonary edema or shock, overall left ventricular (LV) systolic function may be normal.
e. Right heart catheterization is the diagnostic modality of choice.
4. Case: A 75-year-old woman with a history of hypertension and hyperlipidemia presents to the emergency department (ED) with dyspnea and fatigue. Thirty-six hours prior to presentation, she experienced substernal chest pressure that was severe, sudden in onset, and persisted for “ a few hours.” She provides a history of exertional chest discomfort for the past 2 months.
Exam: Blood pressure 95/60, heart rate 110, respiratory rate 28, pulse oximetry 88%, room air temperature 37°C
Neck: Elevated neck veins
Lungs: Bibasilar inspiratory crackles halfway up posterior thorax
Heart: Point of maximal impact displaced laterally, palpable thrill over the left, fourth intercostal space, tachycardic, regular, S1 and S2 normal, 3/6 holosystolic murmur heard best at left, lateral sternal border
Extremities: Trace edema, somewhat cool, 2+ distal pulses throughout
Electrocardiogram (ECG): sinus tachycardia, Q waves and T-wave inversion in leads V1–V5.
Chest x-ray (CXR): Cardiomegaly, pulmonary edema
Labs: CK 500 U/L, CKMB 50 ng/mL, troponin-T 12 ng/mL, creatinine 1.5 mg/dL
In addition to ordering oxygen therapy, Lasix, aspirin, and nitroglycerin, what should be performed next?
a. Arterial blood gas
b. Left heart catheterization
c. Transthoracic echocardiogram
d. Placement of a right heart catheter
e. Cardiac computed tomography (CT) scan
5. The above study demonstrated that the patient had an apical ventricular septal defect (VSD), an akinetic anterior wall, and right ventricular (RV) dilation. What should be the next step?
a. Cardiothoracic surgery consultation
b. Left heart catheterization
c. Placement of an intra-aortic balloon pump (IABP)
d. Placement of a right heart catheter
6. Case: A 68-year-old male with history of hypertension, hyperlipidemia, and diabetes mellitus presents to the ED with an episode of chest pain and syncope.
Exam: Blood pressure 92/50, heart rate 128, respiratory rate 28, pulse oximetry 94%, room air temperature 37°C
Neck: Elevated neck veins
Lungs: Clear to auscultation
Heart: Irregularly irregular rhythm with S1 and S2 normal, 3/6 holosystolic murmur heard best at left, lateral sternal border which increases with respiration
Extremities: Trace edema, somewhat cool, 1 + distal pulses throughout
ECG: Atrial fibrillation, ST elevations in II, III, and AVF (highest in lead III).
CXR: Cardiomegaly, clear lungs
Labs: CK 750 U/L, CKMB 80 ng/mL, troponin-T 12 ng/mL, creatinine 1.2 mg/dL
You have access to a catheterization laboratory in the next 90 minutes. Aside from activating the catheterization team, all of the following approaches are reasonable except:
a. Obtaining an EKG with right-sided leads
b. IV fluid administration
c. Direct current cardioversion (DCCV) for treatment of atrial fibrillation
d. IV NTG administration for relief of chest pain
e. A-V synchronous pacing in the event of bradycardia
Answers
1. Answer E: A high index of suspicion is needed to diagnose subacute free wall rupture. Accurate and timely diagnosis provides valuable time for surgical treatment before acute rupture and pericardial tamponade lead to death. Intermittent chest pain, nausea, electromechanical dissociation, and hypotension along with dynamic ST-T-wave changes and agitation can all be present in cases of subacute rupture.
2. Answer D: In most series, the frequency of ventricular septal rupture was equal in anterior and inferior myocardial infarctions (IMIs). Although it is usually seen in elderly hypertensive patients, many times it occurs in the setting of a first myocardial infarction (MI). The intensity of the murmur is usually inversely proportional to the size of the defect. Both echocardiography and right heart catheterization can be used as initial diagnostic modalities. Surgery should be performed emergently.
3. Answer D: Many times a relatively small MI may be the culprit in papillary muscle rupture. Hyperdynamic LV function in the setting of a relatively small MI may appear puzzling in a patient with severe pulmonary edema and cardiogenic shock (CGS). Papillary muscle rupture is most frequently seen in inferior and posterior MIs because of the single blood supply of the posteromedial papillary muscle. Although coronary angiography may be needed before surgery, definitive treatment requires emergency surgery, not percutaneous intervention. In many patients a systolic murmur may be audible, but the absence of a murmur does not rule out presence of papillary muscle rupture. A systolic thrill is very uncommon in papillary muscle rupture, as opposed to ventricular septal rupture. The diagnostic modality of choice is echocardiography.
4. Answer C: The clinical picture is consistent with an anterior MI that occurred more than 24 hours ago and the patient now presents in Killip Class III heart failure. Although the congestive heart failure (CHF) may very well be secondary to a large anterior MI, her exam creates concern of a mechanical complication. In addition to oxygen therapy and initial measures to treat her pulmonary edema, she should have an emergency transthoracic echocardiography (TTE). An arterial blood gas is not essential in this situation because the clinical picture is clear and CO2 retention is not a concern at the moment. One can follow her oxygenation status by pulse oximetry. Although urgent left heart catheterization is indicated in patients with AMI complicated by CHF and CGS, this patient is several hours out of her acute event and the route of revascularization will be dictated by the presence or absence of a mechanical complication. A ventriculogram can diagnose a VSD as well, but there is time to obtain a transthoracic echocardiogram in the present situation. A right heart catheterization is also indicated in this situation, but this can be performed in the catheterization laboratory or the coronary intensive care unit (ICU) and does not need to be done immediately. A cardiac CT has no place in this situation.
5. Answer A: The next step should be a consultation to cardiothoracic surgery. Make the page, and while you are waiting for a response, make arrangements for the patient to go to the catheterization laboratory and subsequently the coronary ICU until surgery can be performed. In the catheterization laboratory, in addition to obtaining the coronary anatomy, an IABP and RHC can be placed. Further medical management can occur in the coronary care unit while plans for surgery are being made.
6. Answer D: The patient is presenting with IMI with RV involvement. This is suggested in a scenario of MI with clear lung fields, elevated jugular venous pressure, and suggestive EKG changes. In this scenario, EKG with rightsided leads might show ST elevations in leads V4r and V5r. These patients might present with syncope due to the preload dependence of the RV. As such, fluid administration and maintenance of sinus rhythm with AV synchrony help stabilize the hemodynamics. Administration of nitroglycerin should be avoided as this might lead to diminished preload further worsening the hemodynamic picture.