ECG Interpretation:

June 3, 2024
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Management of patients with myocardial infarction complicated with cardiac asthma and pulmonary edema.

Resuscitation of patients with cardiac arrest and further management.

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Complications of acute myocardial infarction (MI) include ischemic, mechanical, arrhythmic, embolic, and inflammatory (pericarditis) disturbances. Nevertheless, circulatory failure from either severe left ventricular (LV) dysfunction or one of the mechanical complications of MI accounts for most fatalities.

 

heart attack

ISCHEMIC COMPLICATIONS

PREVALENCE

Infarct Extension
Infarct extension is a progressive increase in myocardial necrosis within the infarct zone of the original MI. This may present as an infarction that extends and involves the adjacent myocardium or as a subendocardial infarction that becomes transmural.

Reocclusion of infarct-related arteries (IRAs) occurs in 5% to 30% of patients after fibrinolytic therapy. These patients tend to have a poorer outcome.1 Reinfarction is more common in patients with diabetes mellitus or prior MI.

Recurrent Infarction
Infarction in a separate territory (recurrent infarction) may be difficult to diagnose in the first 24 to 48 hours after the initial event. Multivessel coronary artery disease is common in patients presenting with acute MI. In fact, angiographic evidence of complex or ulcerated plaques ion-IRAs is present in up to 40% of patients with acute MI.

Postinfarction Angina
Angina that occurs within a few hours to 30 days after acute MI is defined as postinfarction angina. The incidence of postinfarction angina is greatest in patients with non-ST-segment elevation MI (approximately 25%) and in those treated with fibrinolytics, compared with mechanical revascularization.

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PATHOPHYSIOLOGY

Reinfarction occurs more frequently when an IRA reoccludes than when it remains patent; however, reocclusion of an IRA does not always cause reinfarction because collateral circulation may be abundant. After fibrinolytic therapy, reocclusion is found on 5% to 30% of angiograms and is associated with worse outcome.

The pathophysiologic mechanism of postinfarction angina is similar to that of unstable angina and should be managed as such. Patients with postinfarction angina have a worse prognosis (sudden death, reinfarction, and acute cardiac events).

 

SIGNS AND SYMPTOMS

Patients with infarct extension or postinfarction angina usually have continuous or recurrent chest pain, with protracted elevation in creatine kinase (CK) and occasional new ECG changes.

 

DIAGNOSTIC TESTING

The diagnosis of infarct expansion, reinfarction, or postinfarction ischemia can be made with echocardiography or nuclear imaging. A new wall motion abnormality, larger infarct size, new area of infarction, or persistent reversible ischemic changes help to substantiate the diagnosis. CK-MB, the myocardial component of CK, is a more useful marker for tracking ongoing infarction than troponins, given their shorter half-life. Rising and falling CK-MB levels suggest infarct expansion or recurrent infarction. Elevations of CK-MB greater than or equal to 50% more than a previous nadir are diagnostic for reinfarction.

THERAPY

Medical therapy with aspirin, heparin, nitrates, and beta-adrenergic blockers is indicated for patients who had an MI and have ongoing ischemic symptoms. An intra-aortic balloon pump (IABP) should be inserted in patients with hemodynamic instability or severe LV systolic dysfunction. Coronary angiography should be preformed in patients who are stabilized with medical therapy. Emergency angiography should be undertaken in unstable patients. Revascularization, either percutaneous or surgical, is associated with improved prognosis.

MECHANICAL COMPLICATIONS

 

Mechanical complications of acute MI include ventricular septal rupture (VSR), papillary muscle rupture or dysfunction (causing mitral regurgitation), cardiac free wall rupture, pseudoaneurysm, LV failure with cardiogenic shock, right ventricular (RV) failure, ventricular aneurysm, and dynamic LV outflow tract (LVOT) obstruction.

 

VENTRICULAR SEPTAL RUPTURE

When ventricular septal rupture complicates acute myocardial infarction, the mortality is high. Reperfusion therapy has reduced the incidence of septal rupture. However, rapid diagnosis, aggressive medical management, and surgical intervention are required to optimize recovery and survival. This review summarizes information on septal rupture in both the era before thrombolytic therapy and after the advent of reperfusion therapy.

PREVALENCE

VSR occurred among 1% to 2% of patients after acute MI in the prethrombolytic era.2 The incidence has dramatically decreased with reperfusion therapy. The GUSTO 1 trial demonstrated a VSR incidence of approximately 0.2%.3 VSR is more likely to occur in patients who are older, female, hypertensive, nonsmokers, and who have anterior infarction, increased heart rate, and worse Killip class at admission. VSR may develop as early as 24 hours after MI; it was commonly seen 3 to 7 days after MI in the prefibrinolytic era and currently is seen 2 to 5 days after MI.2 Fibrinolytic therapy is not associated with increased risk of VSR.4

Pathogenesis

The septum adjacent to the rupture is often thin and necrotic. Without reperfusion, coagulatioecrosis develops within the first three to five days after infarction, with numerous neutrophils entering the necrotic zone. The neutrophils undergo apoptosis and release lytic enzymes, hastening the disintegration of necrotic myocardium.

The pathogenic process of the rupture changes over time. During the first 24 hours, coagulatioecrosis is just beginning and there are relatively few neutrophils within the infarcted tissue. Early ruptures occur in infarcts with large intramural hematomas that dissect into tissue and rupture. If patients survive for several weeks, the septum becomes fibrotic.

Becker and van Mantgem classified the morphology of free-wall rupture into three types, which are also relevant to ventricular septal rupture: type I ruptures have an abrupt tear in the wall without thinning; in type II, the infarcted myocardium erodes before rupture occurs and is covered by a thrombus; and type III has marked thinning of the myocardium, secondary formation of an aneurysm, and perforation in the central portion of the aneurysm.

The size of septal rupture ranges from millimeters to several centimeters. Morphologically, septal rupture is categorized as simple or complex. Figure 1 shows a simple septal rupture with a discrete defect and a direct through-and-through communication across the septum. The perforation is at the same level on both sides of the septum. Extensive hemorrhage with irregular, serpiginous tracts withiecrotic tissue characterizes complex septal rupture. Septal ruptures in patients with anterior myocardial infarction are generally apical and simple. Conversely, in patients with inferior myocardial infarction, septal ruptures involve the basal inferoposterior septum and are often complex (Figure 2 and Figure 4; also see the video clips in the Supplementary Appendix. Occasionally, muscles of the ventricular free wall or papillary muscles may tear, especially in the case of complex septal ruptures. Ventricular septal ruptures associated with an inferior or anterior myocardial infarction generally involve right ventricular infarction.

Figure. Findings at Autopsy in a Patient with a Simple Ventricular Septal Rupture.

There is a discrete defect with a direct through-and-through communication across the septum. The perforation is at the same level on both sides of the septum: the left ventricular aspect of the interventricular septum (LVS), and the right ventricular aspect of the interventricular septum (RVS). MV denotes mitral valve.

Figure Gross Findings in a Patient with a Posterior Ventricular Septal Rupture.

There is an infarction involving the basal inferior septum, the basal posteroinferior wall, and the right ventricle (RV). The ventricular septal rupture (arrow) is complex, with an irregular, serpiginous tract at the junction of the inferior wall and the interventricular septum (IVS). LV denotes left ventricle.

Figure Transthoracic Two-Dimensional Apical Four-Chamber Views in a Patient with Ventricular Septal Rupture Complicating an Anterior Acute Myocardial Infarction.

In Panel A, the ventricular septal rupture is apical and simple (arrow). RV denotes right ventricle, and LV left ventricle. The sites of both the right and the left ventricular perforation are at the same level. In Panel B, color Doppler ultrasonography shows turbulent flow (bright blue mosaic) from the left ventricle to the right ventricle through the interventricular septal defect.

 

 

Figure. Transesophageal Four-Chamber Views in a Patient with a Ventricular Septal Rupture Complicating an Acute Posterior Myocardial Infarction.

In Panel A, the ventricular septal rupture (arrow) is basal and at the junction between the basal inferior septum and the inferoposterior wall. In Panel B, a color Doppler image shows the shunt across the ventricular septal rupture. LA denotes left atrium, LV left ventricle, and RV right ventricle.

 

 

PATHOPHYSIOLOGY

With anterior MI, this defect usually occurs at the border of preserved and infarcted myocardium in the apical septum; with inferior MI, it affects the basal posterior septum. VSR almost always occurs in the setting of a transmural MI and is more frequently seen in anterolateral MIs. The defect may not always be a single large defect; it can be a meshwork of channels in 30% to 40% of patients.

SIGNS AND SYMPTOMS

 

Early in the disease process, patients with VSR may appear relatively comfortable, with no clinically significant cardiopulmonary symptoms. Rapid recurrence of angina, hypotension, shock, or pulmonary edema may develop later in the course.

Symptoms of septal rupture include chest pain, shortness of breath, and those associated with low cardiac output and shock. Acute septal rupture produces a harsh, loud holosystolic murmur along the left sternal border, radiating toward the base, apex, and right parasternal area, and a palpable parasternal thrill in half of patients. With cardiogenic shock and a low-output state complicating septal rupture, there is rarely a thrill, and the murmur is difficult to identify because turbulent flow across the defect is reduced. Right and left ventricular S3 gallops are common. The pulmonic component of the second heart sound is accentuated by pulmonary hypertension. Tricuspid regurgitation may also be present. Biventricular failure generally ensues within hours or days.

As compared with acute mitral regurgitation, septal rupture has a loud murmur, a thrill, and right ventricular failure but is less often characterized by severe pulmonary edema. In patients with a low cardiac output, distinguishing between these two entities can be difficult. In addition, severe mitral regurgitation may occur in 20 percent of patients with septal rupture.

 

 

DIAGNOSIS

 

Rupture of the ventricular septum is often accompanied by a new harsh holosystolic murmur best heard at the left lower sternal border. The murmur is accompanied by a thrill in 50% of cases. This sign generally is accompanied by a worsening hemodynamic profile and biventricular failure. Therefore, it is important that all patients with MI have a well-documented cardiac examination at presentation.

An ECG may show atrioventricular (AV) nodal or infranodal conduction delay abnormalities in approximately 40% of patients. Echocardiography with color-flow imaging is the test of choice for diagnosis of VSR (Figure 1). Echocardiography can define LV and RV function (important determinants of mortality) as well as the size of the defect and degree of left-to-right shunt by assessing flow through the pulmonary and aortic valves. In some cases, it may be necessary to use transesophageal echocardiography to assess the ventricular septal defect.

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Figure 1. Ventricular septal rupture

Figure 2. Pathology specimen showing an acute posterior interventricular septal rupture

VSR also can be diagnosed by demonstrating a step-up in oxygen saturation in the right ventricle and pulmonary artery (PA) on PA catheterization. The location of the step-up is important, as there have been rare case reports of peripheral PA step-ups due to acute mitral regurgitation (MR). Diagnosis involves fluoroscopically guided measurement of oxygen saturation in the superior and inferior vena cava, right atrium, right ventricle, and pulmonary artery. A step-up in oxygen saturation of greater than 8% occurs in VSR between the right atrium and the PA with a left-to-right shunt across the ventricular septum. A shunt fraction can be calculated as follows:

Qp/Qs = Sao2-Mvo2/Pvo2-Pao2

Where Qp = pulmonary flow, Qs = systemic flow, Sao2 = arterial oxygen saturation, Mvo2 = mixed venous oxygen saturation, Pvo2 = pulmonary venous oxygen saturation, and Pao2 = pulmonary arterial oxygen saturation, Qp/Qs greater than or equal to 2 suggests a considerable shunt, which is likely to be poorly tolerated by the patient.

Pump failure in patients with myocardial infarction may be related to the major mechanical complications, such as ventricular septal rupture, papillary-muscle rupture, or free-wall rupture. Alternatively, it results from the infarction or ischemia of a large area, ischemic mitral regurgitation, right ventricular dysfunction, or hypovolemia. Doppler echocardiography is generally diagnostic (also see the video 1, video 2). Doppler techniques can be used to define the site and size of septal rupture, left and right ventricular function, estimated right ventricular systolic pressure, and the left-to-right shunt. The sensitivity and specificity of color Doppler echocardiography have been reported to be as high as 100 percent. In severely ill patients who are receiving assisted ventilation, the image quality of transthoracic echocardiography may not be sufficient for diagnosis, and transesophageal echocardiography is more sensitive.

 

Hemodynamics

Septal rupture results in a left-to-right shunt, with right ventricular volume overload, increased pulmonary blood flow, and secondary volume overload of the left atrium and ventricle. As left ventricular systolic function deteriorates and forward flow declines, compensatory vasoconstriction leads to increasing systemic vascular resistance, which, in turn, increases the magnitude of the left-to-right shunt. The degree of shunting is determined by the size of the septal rupture, the level of pulmonary vascular resistance and systemic vascular resistance and the ratio of the two, and left ventricular and right ventricular function. As the left ventricle fails and the systolic pressure declines, left-to-right shunting decreases and the fraction of the shunt diminishes.

Angiographic Findings

See Video

Some studies have found that septal rupture is associated with multivessel coronary artery disease. However, others found a high prevalence (54 percent) of single-vessel disease among patients with ventricular septal rupture.8,19 Ventricular septal rupture is likely to be associated with total occlusion of the infarct-related artery.3,6,8 In the GUSTO-I study, total occlusion of the infarct-related artery was documented in 57 percent of patients with ventricular septal rupture, as compared with 18 percent of those without ventricular septal rupture.6 Collaterals are less often evident in patients with ventricular septal rupture, supporting the hypothesis that collateral circulation reduces the risk of rupture of the cardiac free wall as well as septal rupture.

Time Course

Without reperfusion, septal rupture generally occurs within the first week after infarction. As explained above, there is a bimodal distribution of septal rupture, with a high incidence on the first day and on days 3 through 5 and rarely more than two weeks after infarction. The median time from the onset of symptoms of acute myocardial infarction to rupture is generally 24 hours or less in patients who are receiving thrombolysis.21 The median time from the onset of infarction to septal rupture was 1 day (range, 0 to 47; 94 percent of cases were diagnosed within 1 week) in the GUSTO-I trial6 and 16 hours in the Should We Emergently Revascularize Occluded Coronaries in Cardiogenic Shock (SHOCK) trial. Although thrombolytic therapy reduces the size of the infarct, it may in some cases promote hemorrhagic dissection in the myocardium, accelerating the onset of septal rupture.

Pulmonary-artery catheterization can be helpful. In patients with a septal rupture, the increase in oxygen saturation occurs within the right ventricle and not only in the pulmonary artery. Severe mitral regurgitation may result in an increase in oxygen saturation in the peripheral pulmonary arteries. The presence of large V waves in the pulmonary-capillary wedge tracing is a nonspecific finding that also occurs with mitral regurgitation and with poor left ventricular compliance.

Left ventriculography can also be used to diagnose septal rupture. Coronary angiography is useful for assessing the coronary anatomy if concomitant revascularization is being considered. Radionuclide scintigraphy is an alternative noninvasive technique for diagnosing septal rupture, assessing ventricular function, and calculating the size of the intracardiac shunt.

THERAPY

Early surgical closure is the treatment of choice, even if the patient’s condition is stable. Initial reports suggested that delaying surgery was likely to result in improved surgical mortality. These benefits were likely the result of selection bias,5 as the mortality rate among patients with VSD treated medically is 24% at 72 hours and 75% at 3 weeks.6 Therefore, patients should be considered for urgent surgical repair.

 

Cardiogenic shock and multisystem failure from VSR are associated with high mortality. This further supports early surgical intervention before complications develop.7 Mortality is highest in patients with basal septal rupture associated with inferior MI (70% compared with 30% in patients with anterior infarcts). The mortality rate is higher due to increased technical difficulty and frequently the need for mitral valve repair or replacement in the patients with MR.8 Regardless of the infarct location and hemodynamic condition of the patient, surgery should always be considered as it is associated with a lower mortality rate than conservative management.9

Intensive medical management should be started to support the patient before surgery. Unless there is significant aortic regurgitation, an IABP should be inserted emergently as a bridge to a surgical procedure. The IABP will decrease systemic vascular resistance and shunt fraction while increasing coronary perfusion and maintaining blood pressure. After insertion of an IABP, vasodilators can be used with close hemodynamic monitoring. Vasodilators also reduce left-to-right shunting and increase systemic flow by reducing systemic vascular resistance. The vasodilator of choice is intravenous (IV) nitroprusside, which is started at 0.5 µg/kg/min to 1.0 µg/kg/min and titrated to an MAP of 60 mm Hg to 75 mm Hg.

PAPILLARY MUSCLE RUPTURE
(ACUTE MITRAL REGURGITATION)

PREVALENCE

Acute MR after acute MI predicts poor prognosis. Nevertheless, MR of mild to moderate severity is found in 13% to 45% of patients after acute MI.10,11 Although most MR is transient and asymptomatic, MR caused by papillary muscle rupture is a life-threatening complication. Fibrinolytic agents decrease the incidence of rupture, however, rupture may occur earlier in the post-MI period. In the prefibrinolytic era, papillary muscle rupture had been reported to occur between day 2 and day 7; however, the SHOCK Trial Registry demonstrated a median time to papillary muscle rupture of 13 hours.12 Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to 5% of the mortality after acute MI.13

PATHOPHYSIOLOGY

MR can occur as a result of multiple mechanisms including:

1.     mitral annular dilatation secondary to LV dilatation,

2.     papillary muscle dysfunction with associated ischemic regional wall motion abnormality in close proximity to the insertion of the posterior papillary muscle, and

3.     partial or complete rupture of the papillary muscle as a result of papillary muscle infarction.14

 

Figure 3. Papillary muscle rupture. Pathology specimen showing a ruptured papillary muscle.

Papillary muscle rupture is most common with an inferior MI. The posteromedial papillary muscle is most frequently involved because of its single blood supply through the posterior descending coronary artery.15 The anterolateral papillary muscle has a dual blood supply, being perfused by the left anterior descending and left circumflex coronary arteries. In 50% of patients, the infarct is relatively small.

SIGNS AND SYMPTOMS

Complete transection of the papillary muscle is rare and usually results in immediate pulmonary edema, cardiogenic shock, and death. Physical examination demonstrates a new pansystolic murmur, which is audible at the cardiac apex and radiates to the axilla or the base of the heart. If a posterior papillary muscle rupture is present, the murmur radiates to the left sternal border and may be confused with the murmur of VSR or aortic stenosis. The intensity of the murmur does not always predict the severity of MR. In patients with severe failure, poor cardiac output, or elevated left atrial pressures, the murmur may be soft or absent.

DIAGNOSTIC TESTING

The ECG usually shows evidence of recent inferior or posterior MI. The chest radiograph reveals pulmonary edema. Focal pulmonary edema can occur in the right upper lobe when flow is directed at the right pulmonary veins.

The diagnostic test of choice is two-dimensional echocardiography with Doppler and color-flow imaging. In severe MR, the mitral valve leaflet is usually flail. Color-flow imaging can be useful in distinguishing papillary muscle rupture with severe MR from VSR. Transthoracic echocardiography may not fully appreciate the amount of MR in some patients with posteriorly directed jets. In these patients, transesophageal echocardiography may be particularly useful. Additionally, hemodynamic monitoring with a PA catheter may reveal large V waves (greater than 50 mm Hg) in the pulmonary capillary wedge pressure (PCWP).

THERAPY

Patients with papillary muscle rupture should be rapidly identified and should receive aggressive medical treatment while being considered for surgery. Medical therapy includes vasodilator therapy. Nitroprusside is useful in the treatment of acute MR because it decreases systemic vascular resistance, thereby reducing the regurgitant fraction and increasing the forward stroke volume and cardiac output. Nitroprusside can be started at 0.5 µg/kg/min to 1.0 µg/kg/min and titrated to an MAP of 60 mm Hg to 75 mm Hg. An IABP should be inserted to decrease LV afterload, improve coronary perfusion, and increase forward cardiac output. Patients with hypotension may tolerate vasodilators after insertion of an IABP.

Patients with papillary muscle rupture should be considered for emergency surgery because the prognosis is dismal among medically treated patients. Coronary angiography should be performed before surgical repair, as revascularization during mitral valve replacement (MVR) is associated with improved short-term and long-term mortality.16

Medical Therapy

Medical therapy consists of mechanical support with an intraaortic balloon pump, afterload reduction, diuretics, and usually, inotropic agents. Oxygenation should be maintained with the administration of oxygen by mask, continuous positive airway pressure, bilevel positive airway pressure, or intubation with mechanical ventilation. Nitroprusside may reduce left-to-right shunting and improve cardiac output, but it may also cause hypotension. Its use is contraindicated in patients with acute renal failure. Patients with hypotension ofteeed inotropic agents and vasopressors to maintain arterial blood pressure. However, an increase in left ventricular pressure increases left-to-right shunting. Attempts to stabilize the patient’s condition with medical therapy are only temporizing, because most patients have a rapid deterioration and die. Most patients require surgical intervention. Even patients whose condition appears to be clinically stable are at risk for abrupt hemodynamic deterioration, because the size of the septal rupture can increase without warning. The mortality rate among patients with septal rupture who are treated conservatively without mechanical closure is approximately 24 percent in the first 24 hours, 46 percent at one week, and 67 to 82 percent at two months. Lemery et al. reported a 30-day survival rate of 24 percent among medically treated patients, as compared with a rate of 47 percent among those treated surgically.

Mechanical Closure

It was long believed that shortly after an acute myocardial infarction, the myocardium was too fragile for the safe repair of the septal rupture. A waiting period of three to six weeks before surgery was standard to allow the margins of the infarcted muscle to develop a firm scar to facilitate the surgical repair. However, many patients died while awaiting surgery or underwent emergency surgery after sudden decompensation. A 1977 series of 43 patients reported an increased survival rate after early surgical repair, and these findings have since been confirmed by others.

Current guidelines of the American College of Cardiology–American Heart Association for the treatment of patients with acute myocardial infarction recommend immediate operative intervention in patients with septal rupture, regardless of their clinical status. Surgical management is based on six goals. Hypothermic cardiopulmonary bypass with optimal myocardial protection should be promptly established. The septal rupture should be approached through the infarct, and all necrotic and friable margins of the septum and ventricular walls should be excised to avoid postoperative hemorrhage, a residual septal defect, or both. Prosthetic material should be used to reconstruct the septum and the ventricular walls, and the geometric configuration of the ventricles and function of the heart should be preserved.35 The septal rupture should be closed by a method chosen according to its location — apical, anterior, or posterior. The mitral valve should undergo concomitant repair or replacement if indicated. Coronary-artery bypass grafting should be performed in patients with multivessel coronary artery disease, although there is no need to bypass the artery responsible for the infarcted septum. Newer surgical techniques, which avoid direct incision of the ventricles, can be used in selected patients. Exposure of the septum through the right atrium may reduce the risk associated with early surgery by averting additional damage to the left ventricle and decreasing the risk of postoperative bleeding.

In selected patients, percutaneous closure of septal rupture with catheter-based devices may be an alternative to surgical repair. Although only a few case reports have been described to date, several points should be stressed. As the site of the septal rupture in patients with myocardial infarction becomes surrounded by fragile necrotic tissue, attempts to pass the closure device through the site may increase the size of the rupture. The septal rupture in patients with anterior infarction is usually near the apex, whereas in patients with inferior infarction it is usually near the base of the right and left ventricular free wall. Thus, it may not be possible to open the wings of catheter-based closure devices such as the Amplatzer (AGA Medical) completely without distorting the right or left ventricle. Moreover, in patients with inferior infarction, the septal ruptures are usually basal and thus close to the tricuspid and mitral valves. Consequently, positioning and opening the sealing devices may markedly impinge on these valves and cause tricuspid or mitral regurgitation (or both).

Postoperative Care

Postoperative care is directed toward reversing cardiogenic shock and incipient multiorgan failure, particularly in elderly patients. The management of right ventricular failure is aimed at reducing afterload while maintaining systemic arterial pressure. Optimal management includes continuation of an intraaortic balloon pump, pharmacologic inotropic support, control of arrhythmias, optimization of volume status, correction of metabolic acidosis and coagulopathy, institution of dialysis for oliguric renal failure, reversal of the catabolic state with nasogastric-tube feeding, and slow weaning from ventilatory support once all hemodynamic and metabolic variables have been stabilized.

Echocardiography is essential to assess the completeness of the repair, to determine whether septal rupture has recurred as a result of dehiscence of the interventricular patch, and to evaluate right and left ventricular function, since such knowledge will be used to guide pharmacologic and mechanical support. Patients with severe and persistent hypoxemia and systemic organ desaturation should be evaluated for a patent foramen ovale.

Prognosis

In the prethrombolytic era, outcomes after septal rupture were extremely poor, with an in-hospital mortality rate of approximately 45 percent among surgically treated patients and 90 percent among those treated medically. In the SHOCK trial, the in-hospital mortality rate was significantly higher among patients in cardiogenic shock as a result of septal rupture than among patients with all other categories of shock (87.3 percent, as compared with 59.2 percent among those with pure left ventricular failure and 55.1 percent among those with acute mitral regurgitation). Surgical repair was performed in 31 patients with septal rupture (56 percent), 21 of whom underwent concomitant bypass surgery, and 6 of whom (19 percent) survived. Of the 24 patients who were treated medically, only 1 survived.22 Pretre et al. reported that among 54 patients who underwent surgical repair of a ventricular septal rupture, 28 underwent concomitant coronary-artery bypass surgery (52 percent), 14 died after surgery (26 percent), and 19 (35 percent) died during follow-up (mean follow-up, 42 months). The cumulative survival rate (including perioperative deaths) was 78 percent at 1 year, 65 percent at 5 years, and 40 percent at 10 years. Thus, the mortality rate among patients with ventricular septal rupture remains extremely high, even in the reperfusion era. In the GUSTO-I trial, the 34 patients who underwent surgical repair had a lower 30-day mortality rate than the 35 patients who were treated medically (47 percent vs. 94 percent, P<0.001) as well as a lower 1-year mortality rate (53 percent vs. 97 percent, P<0.001).6 However, selection bias may have accentuated the differences in the rates.

For patients who survive surgery, the long-term prognosis is relatively good. Crenshaw et al. reported a mortality rate of only 6 percent among patients who survived the first 30 days after surgery.6 Among 60 patients who survived surgical repair, the 5-year survival rate was 69 percent, the 10-year survival rate was 50 percent, and the 14-year survival rate was 37 percent. Eighty-two percent of these patients were in New York Heart Association class I or II at follow-up, and angina and other medical problems were not prevalent.

The immediate preoperative hemodynamic status is a major determinant of the postoperative outcome, rather than the ejection fraction or the size of the intracardiac shunt. In the GUSTO-I trial, all 8 patients with septal rupture who were in Killip class III or IV at presentation died, as compared with 53 of 74 patients (72 percent) who were in Killip class I or II at presentation. Among patients who are undergoing surgical repair, the prognosis is associated with the preoperative systolic blood pressure and right atrial pressure and the duration of cardiopulmonary bypass. Patients whose systemic arterial blood pressure remained high had the best prognosis. The combination of an elevated right atrial pressure with a low systemic blood pressure was associated with an extremely poor prognosis.2,52 Right ventricular function is also a predictor of survival.5 Others report that renal failure and diabetes mellitus are strong negative predictors of survival after surgery. Patients with septal rupture complicating inferior rather than anterior myocardial infarction have the poorest outcome. No correlation has been demonstrated between the risk of early death and age or sex. Blanche et al. found that preoperative use of an intraaortic balloon pump reduced immediate postoperative mortality, but it was not associated with an improved long-term prognosis.

The development of a residual or recurrent septal defect is reported in up to 28 percent of patients who survive repair and is associated with high mortality. In asymptomatic patients who have a small residual left-to-right shunt, conservative therapy may be warranted. In patients who have clinical heart failure or a pulmonary–systemic shunt fraction of more than 2.0, repeated surgical intervention is clearly indicated to improve the outcome.

FREE WALL RUPTURE

PREVALENCE

Free wall rupture (Figure 4) occurs in 3% of MI patients and accounts for approximately 10% of mortality after MI. Cardiac rupture occurs within 5 days of MI in 50% of patients and within 2 weeks of MI in 90%.

free wall rupture fig 2

Figure 4. Left ventricular free wall rupture

Free wall rupture occurs only among patients with transmural MI. Risk factors include advanced age, female sex, hypertension, first MI, and poor coronary collateral vessels.

PATHOPHYSIOLOGY

Although free wall rupture accounts for part of the early (first 24 hours) mortality risk among patients treated with fibrinolytic agents, the overall incidence of free wall rupture is not greater in patients treated with fibrinolytics.17 Any wall can be involved, but cardiac rupture most commonly occurs in the lateral wall.

Free wall rupture occurs at three distinct intervals with three distinct pathologic subsets:

  • Type I increases with the use of fibrinolytics. It occurs early (within the first 24 hours) and is a full-thickness rupture.
  • Type II occurs 1 to 3 days post-MI and is a result of erosion of the myocardium at the site of infarction.
  • Type III rupture occurs late (days 5-10) and is located at the border zone of the infarction and normal myocardium. The reduction in Type III ruptures due to fibrinolytic therapy results io change in the overall free wall rupture rate. It has been postulated that Type III ruptures can occur as a result of dynamic LVOT obstruction, which leads to increased wall stress.18

SIGNS AND SYMPTOMS

Sudden onset of chest pain with straining or coughing may herald the onset of myocardial rupture. Acute rupture patients often develop electromechanical dissociation, shock, and sudden death. Other patients may have a more subacute course as a result of a contained rupture (pseudoaneurysm). They may complain of pain consistent with pericarditis, nausea, and develop hypotension. In a study evaluating 1,457 patients with acute MI, 6.2% of patients had free wall rupture. Approximately one third of these patients presented with a subacute course.19

Jugular venous distention, pulsus paradoxus, diminished heart sounds, and a pericardial rub suggest subacute rupture. New to-and-fro murmurs may be heard in patients with subacute rupture or pseudoaneurysm. A junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T waves may be evident on ECG. Additionally, a large number of patients develop transient bradycardia just before rupture.

DIAGNOSTIC TESTING

Although there is often insufficient time for diagnostic testing in the management of patients with acute rupture, echocardiography is the test of choice. Echocardiography may demonstrate a pericardial effusion with findings of cardiac tamponade. These findings include right atrium and RV diastolic collapse, dilated inferior vena cava, and marked respiratory variation in mitral and tricuspid inflow. Additionally, a PA catheter may reveal hemodynamic signs of tamponade, with equalization of the right atrium, RV diastolic pressure, and PCWP.

THERAPY

The goal of therapy is to diagnose the problem quickly and perform early emergency cardiac surgery to correct the rupture. Emergency pericardiocentesis may be performed on patients with tamponade and severe hemodynamic compromise while arrangements are being made for transport to the operating room. Pericardiocentesis may be dangerous due to reopening of the communication with the pericardium as the intrapericardial pressure is relieved. Medical management has no role in the treatment of these patients except for vasopressors to maintain blood pressure as the patient is transported to the operating room.

Acute Cardiac Tamponade

Cardiac tamponade is life-threatening, slow or rapid compression of the heart due to the pericardial accumulation of fluid, pus, blood, clots, or gas, as a result of effusion, trauma, or rupture of the heart. Because the causes of pericardial disease1 and thus of tamponade are diverse, clinicians must choose the most probable diagnosis, always anticipating surprises. Thus, traumatic tamponade is most apt to follow cardiac surgery, and tuberculous tamponade is relatively common in Africa but rare in the United States.

Understanding the physiological changes produced by tamponade is essential to diagnosis and treatment. The primary abnormality is rapid or slow compression of all cardiac chambers as a result of increasing intrapericardial pressure. The pericardial contents first reach the limit of the pericardial reserve volume the volume that would just distend the pericardium — and the rate of expansion then increases, soon exceeding that of pericardial stretch. Although the pericardium stretches normally over time, at any instant it is inextensible, making the heart compete with the increased pericardial contents for the fixed intrapericardial volume. As the chambers become progressively smaller and myocardial diastolic compliance is reduced, cardiac inflow becomes limited, ultimately equalizing mean diastolic pericardial and chamber pressures.1,2,3 Key elements are the rate of fluid accumulation relative to pericardial stretch and the effectiveness of compensatory mechanisms. Thus, intrapericardial hemorrhage from wounds or cardiac rupture occurs in the context of a relatively stiff, unyielding pericardium and quickly overwhelms the pericardial capacity to stretch before most compensatory mechanisms can be activated, whereas in the case of a slow increase in pericardial volume as a result of inflammation, 2 liters or more may accumulate before critical, life-threatening tamponade occurs.13

The stiffness of the pericardium determines fluid increments precipitating tamponade, as illustrated by characteristic pericardial pressure–volume (strain–stress) curves (Figure 1): there is an initial slow ascent, followed by an almost vertical rise. This steep rise makes tamponade a “last-drop” phenomenon: the final increment produces critical cardiac compression, and the first decrement during drainage produces the largest relative decompression.

Figure  Cardiac Tamponade.

Pericardial pressure–volume (or strain–stress) curves are shown in which the volume increases slowly or rapidly over time. In the left-hand panel, rapidly increasing pericardial fluid first reaches the limit of the pericardial reserve volume (the initial flat segment) and then quickly exceeds the limit of parietal pericardial stretch, causing a steep rise in pressure, which becomes even steeper as smaller increments in fluid cause a disproportionate increase in the pericardial pressure. In the right-hand panel, a slower rate of pericardial filling takes longer to exceed the limit of pericardial stretch, because there is more time for the pericardium to stretch and for compensatory mechanisms to become activated.

 

The true filling pressure is the myocardial transmural pressure, which is intracardiac minus pericardial pressure.14 Rising pericardial pressure reduces and ultimately offsets this transmural pressure, first for the right heart and ultimately for all chambers. On average, during inspiration and expiration, the right heart increases its filling at the expense of the left, so that its transmural pressure transiently improves and then reverts during expiration. In florid tamponade such a mechanism cannot compensate for reduced stroke volumes, since these volumes depend on the elements that protect cardiac output and arterial pressures, principally beta-adrenergically increased heart rate, peripheral resistance and ejection fractions, and given sufficient time, expansion of the blood volume. Additional compensation provided by neurohormonal stimulation is similar to that occurring in heart failure, except that the levels of atrial natriuretic peptide do not increase because the compressed myocardium cannot stretch.

Acute tamponade thus reflects decompensation as patients reach the steep portion of the pressure–volume curve. Moreover, intercurrent factors can cause the decompensation of any effusion — for example, the influx of blood, effusion-expanding osmotic effects of fragmenting intrapericardial clots, or inflammatory stiffening of the pericardium. Finally, although coronary blood flow is reduced in tamponade, there is no ischemic component because coronary flow remains proportional to the reduced work and operational requirements of the heart.

Clinical Findings

Critical tamponade is a form of cardiogenic shock, and the differential diagnosis may initially be elusive. Since most symptoms are nonspecific, tamponade must be suspected in many contexts — for example, in patients who have wounds of the chest or upper abdomen and hypotension or in those who have hypotension preceded by symptoms of an inciting pericardial disease, such as chest discomfort and pleuritic pain. Tachypnea and dyspnea on exertion that progresses to air hunger at rest are the key symptoms, but it may not be possible to obtain such information from patients who are unconscious or obtunded or who have convulsions at presentation. Most patients are weak and faint at presentation and can have vague symptoms such as anorexia, dysphagia, and cough. The initial symptom may also be one of the complications of tamponade, such as renal failure.

Most physical findings are equally nonspecific. Tachycardia (a heart rate of more than 90 beats per minute) is the rule. Exceptions include patients with bradycardia during uremia and patients with hypothyroidism. Contrary to common belief, a pericardial rub is a frequent finding in patients with inflammatory effusions.20 Heart sounds may be attenuated owing to the insulating effects of the pericardial fluid and to reduced cardiac function. Although the precordium may seem quiet, an apical beat is frequently palpable, and patients with preexisting cardiomegaly or anterior and apical pericardial adhesions may have active pulsations.

Clinically significant tamponade usually produces absolute or relative hypotension; in rapid tamponade, patients are often in shock, with cool arms and legs, nose, and ears and sometimes peripheral cyanosis. Jugular venous distention is the rule, with peripheral venous distention in the forehead, scalp, and ocular fundi unless the patient has hypovolemia. Thus, rapid tamponade, especially acute hemopericardium, may produce exaggerated jugular pulsations without distention, because there is insufficient time for blood volume to increase. Venous waves usually lack the normal early diastolic y descent. In compressive pericardial disease (tamponade and constriction), venous waves are not outward pulsations; rather, x and y collapse from a high standing pressure level.1

A key diagnostic finding, pulsus paradoxus — conventionally defined as an inspiratory systolic fall in arterial pressure of 10 mm Hg or more during normal breathing — is often palpable in muscular arteries. With very low cardiac output, however, a catheter is needed to identify pulsus paradoxus. Other conditions causing pulsus paradoxus include massive pulmonary embolism, profound hemorrhagic shock, other forms of severe hypotension, and obstructive lung disease. Moreover, certain conditions can impede the identification of tamponade by making pulsus paradoxus undetectable.

Laboratory Investigations

Cardiac catheterization will show equilibration of average diastolic pressure and characteristic respiratory reciprocation of cardiac pressures: an inspiratory increase on the right and a concomitant decrease on the left — the proximate cause of pulsus paradoxus. Except in low-pressure tamponade, diastolic pressures throughout the heart are usually 15 to 30 mm Hg. These are similar to pressures present in heart failure, but for unknown reasons, tamponade does not cause alveolar pulmonary edema. Although any type of large cardiac silhouette in a patient with clear lung fields should suggest the presence of pericardial effusion, chest films may not be helpful initially, since at least 200 ml of fluid must accumulate before the cardiac silhouette is affected. In the lateral film, definite pericardial-fat lines are uncommon but are highly specific for large effusions.

An electrocardiogram may show signs of pericarditis, but the only quasispecific sign of tamponade is electrical alternation, which may affect any or all23 electrocardiographic waves or only the QRS. If the QRS complex is affected, every other QRS complex is of smaller voltage, often with reversed polarity. Combined P and QRS alternation is virtually specific for tamponade.1 In rare cases, very large effusions, even without tamponade, cause QRS alternation. Echocardiography reveals its mechanism: swinging of the heart (Figure ) The volume of most nonhemorrhagic effusions that cause tamponade is moderate to large (300 to 600 ml).

Figure Swinging of the Heart with a Large Pericardial Effusion (PE), Causing Electrical Alternation and Consequent Tamponade.

Apical four-chamber two-dimensional echocardiograms show the extremes of oscillation and the resultant effect on the QRS complex. In Panel A, the heart swings to the right, and lead II shows a small QRS complex. In Panel B, the heart swings to the left, and the QRS complex is larger. P denotes pericardium, and LV left ventricle.

Doppler echocardiography is the principal tool for diagnosing pericardial effusion and cardiac tamponade (see video). Computed tomography (CT) and magnetic resonance imaging are often less readily available and are generally unneeded unless Doppler echocardiography is not feasible. In the absence of myocardial disease or injury, echocardiography demonstrates the usually circumferential fluid layer and compressed chambers with high ventricular ejection fractions. Doppler study discloses marked respiratory variations in transvalvular flows. One mechanism of pulsus paradoxus is visible: on inspiration, both the ventricular and atrial septa move sharply leftward, reversing on expiration; in other words, each side of the heart fills at the expense of the other, owing to the fixed intrapericardial volume. The inferior vena cava is dilated, with little or no change on respiration.

Among echocardiographic signs, the most characteristic, although they are not entirely specific, are chamber collapses, which are nearly always of the right atrium and ventricle. During early diastole, the right ventricular free wall invaginates, and at end diastole, the right atrial wall invaginates.25 Right ventricular collapse is a less sensitive but more specific finding for tamponade, whereas right atrial collapse is more specific if inward movement lasts for at least 30 percent of the cardiac cycle. Right atrial collapse may be seen in patients with hypovolemia who do not have tamponade. In about 25 percent of patients, the left atrium also collapses, and this finding is highly specific for tamponade. Left ventricular collapse usually occurs under special conditions such as localized postsurgical tamponade. These wall changes occur when respective chamber pressures temporarily fall below the pericardial pressure.

Variant Forms of Cardiac Tamponade

Low-pressure tamponade occurs at diastolic pressures of 6 to 12 mm Hg and is virtually confined to patients with hypovolemia and severe systemic diseases, hemorrhage, or cancer, or in patients with hypovolemia after diuresis.19 Patients are weak and generally normotensive, with dyspnea on exertion and no diagnostic pulsus paradoxus, but with characteristic respiratory fluctuations in transvalvular diastolic Doppler flows. The low-pressure effusion equilibrates only with right-sided diastolic pressures and does so at first only during inspiration (“inspiratory tracking”). A fluid challenge with a liter of warm saline can evoke tamponade dynamics.26

Hypertensive cardiac tamponade with all the classic features of tamponade, occurs at high and very high arterial blood pressures (even over 200 mm Hg) and is ascribed to excessive beta-adrenergic drive. Affected patients typically have had antecedent hypertension.

Regional cardiac tamponade occurs when any cardiac zone is compressed by loculated effusions, which are usually accompanied by localized pericardial adhesions, especially after cardiac surgery. Sometimes the typical hemodynamic abnormalities are found only in the compressed chambers or zones. However, loculation can also produce classic tamponade, presumably by tightening the uninvolved pericardium; for example, loculated effusions after cardiac surgery may include hematomas over the right atrium and atrioventricular groove. Localized right atrial tamponade may also cause right-to-left shunting through a patent foramen ovale or an atrial septal defect.

After right ventricular infarction, loculated effusion can cause selective right-heart tamponade in which right atrial pressure is higher than left atrial pressure. The absence of pulsus paradoxus makes this form difficult to recognize. Effusive–constrictive pericarditis is characterized by mixed clinical, imaging, and hemodynamic signs, because a constrictive epicarditis underlies the pericardial effusion. In some patients with scarred, rigid parietal and visceral pericardium, tamponade can occur with relatively little accumulation of fluid. Effusive–constrictive pericarditis is revealed in these patients when drainage of pericardial fluid does not cause intracardiac pressures to return to normal.

Special Problems

Postoperative tamponade, which is more frequent after valve surgery than after coronary-artery bypass surgery and is more frequent with postoperative anticoagulant therapy, is due to trauma-induced pericardial effusion and bleeding. Since some degree of pericarditis occurs after every cardiac operation,28 and most patients have a small, seemingly benign effusion postoperatively, it is not surprising that tamponade eventually occurs in some. Postoperative myocardial stiffness, variable fluid–electrolyte abnormalities, and hemorrhage tend to preclude the appearance of classic signs such as pulsus paradoxus; thus, when tamponade is suspected postoperatively, prompt imaging — particularly Doppler echocardiography — is necessary. Late tamponade, occurring more than five days postoperatively, must be suspected in any patient in whom hypotension develops. Primary care physicians may not be familiar with tamponade, and if it occurs very late (two weeks or more) after surgery, they may not suspect it. Some episodes of late hemorrhage may be delayed because the rates of bleeding are relatively slow and intrapericardial clotting complicates diagnosis and management.

Management of Acute Cardiac Tamponade

The treatment of cardiac tamponade is drainage of the pericardial contents, preferably by needle paracentesis with the use of echocardiographic or another type of imaging, such as fluoroscopy or CT. The needle tip is evident on imaging, and imaging can thus safely be used to identify the optimal point at which to penetrate the pericardium. Drainage may be performed in the catheterization laboratory when the diagnosis is uncertain or effusive constrictive pericarditis is possible. However, sudden circulatory collapse warrants the use of pericardiocentesis without imaging, since further decompensation may occur without warning. If the heart cannot be reached by a needle or catheter, surgical drainage is required, usually through a subcostal incision. Surgical drainage is desirable in patients with intrapericardial bleeding and in those with clotted hemopericardium or thoracic conditions that make needle drainage difficult or ineffective. Subcritical uremic tamponade often responds to intensified renal dialysis, but if this approach is unsuccessful, drainage is required.

Figure. Most Common Sites of Blind and Image-Guided Insertion of the Needle for Pericardiocentesis.

In the paraxiphoid approach, the needle should be aimed toward the left shoulder. In the apical approach, the needle is aimed internally.

Recurrences, especially in patients with malignant tamponade, may require balloon pericardiotomy through the use of special catheters that create “windows” between the pericardium and the absorbing surface of the pleura or peritoneum. Death in patients with tamponade is usually heralded by pulseless electrical activity: the electrocardiogram continues to register complexes in the absence of blood flow or pressure.

Medical treatment of acute cardiac tamponade, including inotropic support with or without vasodilators, is relatively controversial and is aimed at supporting compensatory mechanisms to reduce the elevated vascular resistance. Thus, dobutamine, administered to reverse the hypotension, is theoretically ideal. During tamponade, however, endogenous inotropic stimulation of the heart is often already maximal.

The approach to medical therapy has been based on studies in animals. However, these results are the subject of controversy, since in short-term surgical experiments in anesthetized animals, the presence of myocardial depression causes almost any measure to improve function. Studies in intact, unanesthetized animals with indwelling instruments and euvolemia have yielded different results that have cast doubt on the value of various approaches, especially volume infusion. Indeed, increasing the volume may help only in patients with hypovolemia, since in patients with normovolemia and hypervolemia, volume infusion may increase intracardiac pressures as well as heart size, which in turn increases pericardial pressure, further reducing or eliminating the low transmural myocardial pressures supporting the circulation. Moreover, intravenous administration of resuscitative fluid can precipitate tamponade.

An opioid mechanism contributes to the hypotension of cardiac tamponade; experiments in animals show that naloxone counteracts the hypotension, but this approach has not been used clinically.

Mechanical ventilation with positive airway pressure should be avoided in patients with tamponade, because this further decreases cardiac output.19 In patients with cardiac arrest and a large amount of pericardial fluid, external cardiac compression has little or no value, because there is little room for additional filling and because even if systolic pressure rises, diastolic pressure falls and, in doing so, reduces coronary perfusion pressure.

Pericardiocentesis                                                                    

Needle drainage of pericardial fluid, whether or not it is done on an emergency basis (e.g., in a patient in rapidly worsening hemodynamic condition), requires the clinician to select a point on the patient’s chest or epigastrium to insert the needle. This is best done with imaging, as already discussed, to determine which anterior landmarks, usually paraxiphoid or apical, are closest to the fluid. The paraxiphoid approach is also most often used for pericardiocentesis that is performed without imaging.1 Common points of access are illustrated in Figure 3. The needle is usually inserted between the xiphoid process and the left costal margin; in patients with tough skin, a small nick may be made first with a scalpel. The needle is inserted at a 15-degree angle to bypass the costal margin, and then its hub is depressed so that the point is aimed toward the left shoulder. The needle is then advanced slowly, until the pericardium is pierced and fluid is aspirated. Electrocardiography should not be used to monitor the patient’s condition, since attaching an electrode to the needle may provide misleading results.1 The use of a 16-gauge to 18-gauge polytetrafluoroethylene-sheathed needle facilitates the process, since its steel core can be withdrawn once the pericardium has been breached, leaving only the sheath in the pericardial space. For prolonged drainage, a guide wire passed through the sheath will facilitate the introduction of a pigtail angiographic catheter. Thereafter, patients should be followed with the use of Doppler echocardiography to ensure that the pericardial space has been adequately drained and to avert a recurrence. When the amount of fluid drained is less than 50 ml a day, the catheter may be withdrawn; the patient should continue to be observed.

http://content.nejm.org/content/vol347/issue18/images/large/08t1.jpeg

PSEUDOANEURYSM

PATHOPHYSIOLOGY

Pseudoaneurysm is caused by a contained rupture of the LV free wall. The aneurysm may remain small or undergo progressive enlargement. The outer walls are formed by the pericardium and mural thrombus. The pseudoaneurysm communicates with the body of the left ventricle through a narrow neck, the diameter of which is less than 50% of the diameter of the fundus.

SIGNS AND SYMPTOMS

Pseudoaneurysms may remain clinically silent and be discovered during routine investigations; however, some patients may have recurrent tachyarrhythmia and heart failure. Some patients may have systolic, diastolic, or to-and-fro murmurs related to blood flow across the narrow neck of the pseudoaneurysm during systole and diastole.

A chest radiograph may show cardiomegaly with an abnormal bulge on the cardiac border. There may by persistent ST-segment elevation on ECG. The diagnosis can be confirmed by echocardiography, magnetic resonance imaging, or computed tomography.

THERAPY

Spontaneous rupture may occur without warning in approximately one third of patients with a pseudoaneurysm. Therefore, surgical intervention is recommended to prevent sudden death for all patients, regardless of symptoms or the size of the aneurysm.

LEFT VENTRICULAR FAILURE
AND CARDIOGENIC SHOCK

 

PREVALENCE

Some degree of LV dysfunction is expected after an acute MI. The degree of dysfunction correlates with the extent and location of myocardial injury. Patients with small and more distal infarctions may have discrete regional wall motion abnormalities with preserved overall LV function due to hyperkinesis of unaffected segments. Risk factors for development of cardiogenic shock include prior MI, older age, female sex, diabetes, and anterior infarction.

Killip and Kimball20 developed a classification scheme to predict a patient’s prognosis based on their hemodynamic profile. Patients were classified into four hemodynamic subsets-from no evidence of congestive heart failure to cardiogenic shock (Table 1). They reported an 81% mortality rate in the patients presenting with cardiogenic shock.

Table 1:

Killip Classification System

Killip Class

Characteristics

Patients (%)

I

No evidence of congestive heart failure

85

II

Rales, ↑ JVD, or S3 gallop

13

III

Pulmonary edema

1

IV

Cardiogenic Shock

 

They reported an 81% mortality rate in the patients presenting with cardiogenic shock.

 

Forrester et al21 classified patients by their hemodynamic profile with a PA catheter. The parameters used included PCWP and cardiac index. They reported a 50% mortality rate in the most compromised subset (PCWP greater than 18 mm Hg, cardiac index less than 2.2 L/min/m2). GUSTO I reported that 0.8% of patients clinically developed cardiogenic shock. In those receiving fibrinolytics, the mortality rate remained high at 58%.22

 

PATHOPHYSIOLOGY

Patients may develop cardiogenic shock in association with an acute MI from multiple etiologies, including large LV infarction, severe RV infarction, VSR, free wall rupture, acute MR, and pharmacologic depression of LV function (alpha blockers in proximal left anterior descending MI). Patients with cardiogenic shock as a result of acute MI typically have severe multivessel disease with involvement of the left anterior descending arteries.23 Generally, at least 40% of the LV mass is affected in patients who present in cardiogenic shock as a result of a first MI.24 In patients with prior MIs and depressed LV function, a smaller acute insult may result in cardiogenic shock.

SIGNS AND SYMPTOMS

Patients who present in Killip class 3 often have respiratory distress, diaphoresis, and cool clammy extremities in addition to the typical signs and symptoms of acute MI. Patients in Killip class 4 (cardiogenic shock) may have severe orthopnea, dyspnea, oliguria, and altered mental status as well as multisystem organ failure from hypoperfusion.

It may be possible to palpate an area of dyskinesia on the precordium. Additionally, an S3 gallop is a common physical finding in association with pulmonary rales and elevated jugular venous pressures.

DIAGNOSTIC TESTING

Patients with cardiogenic shock due to acute MI generally have extensive ECG changes, demonstrating a large infarct, diffuse ischemia, or multiple prior infarcts. If these changes are not present, then another cause of shock should be considered. Chest radiograph can reveal pulmonary edema, and laboratory tests often demonstrate lactic acidosis, renal failure, and arterial hypoxemia.

The patient in cardiogenic shock should be monitored with a PA catheter and an arterial line. These help distinguish between primary LV failure and other mechanical causes of cardiogenic shock. Echocardiography determines the extent of dysfunctional myocardium and helps identify mechanical complications.

THERAPY

 

A patient in cardiogenic shock should immediately have an IABP placed to reduce afterload, improve cardiac output, and improve coronary perfusion.

Medical therapy with vasodilators (nitroglycerin, nitroprusside, and angiotensin-converting enzyme [ACE] inhibitors) and diuretics should be used as tolerated. IV nitroglycerin is the drug of choice among vasodilators because it is anti-ischemic and less likely to produce coronary steal thaitroprusside. The starting dose is 10 µg/min to 20 µg/min; the dose may be increased by 10 µg/min every 2 to 3 minutes to a goal MAP of 70 mm Hg. IV nitroprusside can be added if further reduction in afterload is necessary. Nitroprusside is started at 0.5 µg/kg/min to 1.0 µg/kg/min and is also titrated to an MAP of approximately 70 mm Hg. Patients with low blood pressures (MAP less than 70 mm Hg) may not tolerate vasodilators.

ACE inhibitors improve LV performance and decrease myocardial oxygen consumption by reducing the cardiac preload and afterload of patients with heart failure and acute MI. ACE inhibitors can reduce infarct expansion if started within the first 12 hours of an MI if the patient is not already in cardiogenic shock.25,26 It is recommended that captopril be started early at 6.25 mg every 8 hours, with each dose subsequently doubled as tolerated to a maximal dose of 50 mg every 8 hours. Patients in cardiogenic shock should be treated with short-acting IV medications until they are stabilized.

Patients with mild pulmonary edema MI can be treated with diuretics such as furosemide administered intravenously and adjusted for creatinine and history of diuretic usage. Beta-adrenergic agonists such as dobutamine or dopamine may be needed for patients with severe heart failure and hypotension. Nevertheless, this therapy should generally be reserved for patients who do not respond to IABP and maximal medical therapy, or those with RV infarct.

Phosphodiesterase inhibitors such as milrinone may be beneficial to some patients. Patients without adequate MAP may not tolerate milrinone. Some patients may need norepinephrine to maintain arterial pressure. Norepinephrine is started at 2 µg/min and titrated to 20 µg/min to maintain a MAP of about 70 mm Hg.

Percutaneous revascularization of IRA has been associated with an improved prognosis in patients with cardiogenic shock, reducing the mortality rate from 80% to 50%. Generally, intervention has been performed on only the IRA, although some report multivessel percutaneous revascularization with more complete revascularization for patients with refractory shock after IRA recanalization.27,28

Emergency surgical revascularization is indicated in patients with severe multivessel disease or substantial left main coronary artery stenosis. Other surgical modalities that may be considered include LV or biventricular assist devices or extracorporeal membrane oxygenation as a bridge to heart transplantation. Some patients may gradually be weaned from assist devices after recovery of the stunned portion of myocardium without need for cardiac transplantation.

RIGHT VENTRICULAR FAILURE

 

PREVALENCE

Mild RV dysfunction is common (approximately 40% of cases) after MI of the inferior or inferior-posterior wall; however, right heart failure occurs in only 10% of patients with inferior or inferior-posterior wall MI, normally only in infarcts involving the proximal right coronary artery

PATHOPHYSIOLOGY

The degree of RV dysfunction depends on the location of the right coronary artery occlusion. Only proximal occlusions (proximal to the acute marginal branch) of the right coronary artery result in marked dysfunction. The degree of RV involvement also depends on the amount of collateral flow from the left coronary artery. Because the right ventricle is thin walled and has a low oxygen demand, there is coronary perfusion during the entire cardiac cycle; therefore, widespread irreversible infarction is rare.29

SIGNS AND SYMPTOMS

The triad of hypotension, jugular venous distention with clear lungs, and absence of dyspnea has high specificity (but low sensitivity) for RV infarction.30 Patients with severe RV failure also may present with symptoms of low cardiac output, including diaphoresis, cool and clammy extremities, and altered mental status. Additionally, they often have oliguria and hypotension.

Physical examination reveals elevated jugular venous pressures, a right-sided S3 gallop, and normal lung exam. The presence of jugular venous pressure greater than 8 cm water and Kussmaul’s sign (an exaggerated increase in jugular venous distention with inspiration) is both highly sensitive and specific for severe RV failure. A rare but clinically important complication of an RV infarct is right-to-left shunting, which is manifested by RV infarction and hypoxemia when RA pressures exceed LA pressures in patients with a patent formen ovale.

Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in V4R. These findings have a positive predictive value of 80% for RV infarction.31 Chest radiograph results usually are normal.

DIAGNOSTIC TESTING

Echocardiography is the diagnostic study of choice for RV infarction. It can detect RV dilatation and dysfunction as well as LV inferior wall dysfunction. It is also helpful in excluding cardiac tamponade, which may hemodynamically mimic RV infarction. The hemodynamic profile of acute RV infarct is similar to an acute pulmonary embolism.

Hemodynamic monitoring with a PA catheter reveals high right atrial pressures with a low PCWP (unless severe LV dysfunction is present) because RV failure results in underfilling of the left ventricle and low cardiac output. In some patients, RV dilatation can cause decreased LV performance on the basis of flattening or bowing of the septum into the left ventricle and restriction of ventricular filling with elevation of PCWP. A right atrial pressure greater than 10 mm Hg and a right atrial pressure to PCWP ratio of 0.8 or more strongly suggest RV infarction.32,33

THERAPY

Volume loading to increase LV preload and cardiac output is the key to management of RV infarction. Some patients may require several liters in 1 hour to reach a target PCWP of 15 mm Hg. These patients should have hemodynamic monitoring with a PA catheter. The target central venous pressure for fluid administration is approximately 15 mm Hg. When volume loading is insufficient to improve cardiac output, treatment with inotropic agents is indicated. Administration of dobutamine increases the cardiac index and improves RV ejection fraction.34

Patients may benefit from reperfusion therapy because patients who undergo successful reperfusion of RV branches have enhanced RV function and lower 30-day mortality.35 Patients with RV infarction and bradyarrhythmias or loss of sinus rhythm may have significant improvement with AV sequential pacing. Optimal pacer settings tend to be longer AV delays (approximately 200 msec) and a heart rate of 80 to 90 beats per minute.

Although only case reports have shown that IABPs improve cardiac index in combination with dobutamine, an IABP may be useful even though it acts primarily on the left ventricle. Pericardiectomy may be considered for patients with refractory shock because it reverses the septal impingement on LV filling. Most patients with RV infarction spontaneously improve after 48 to 72 hours. An RV assist device is indicated for patients who remain in cardiogenic shock despite these measures.

VENTRICULAR ANEURYSM

PREVALENCE

Patients with apical transmural MIs are at greatest risk of aneurysmal formation; however, patients with posterior-basal infarcts may also develop aneurysms. Patients who do not receive reperfusion therapy are at greatest risk of developing this complication (10% to 30%).

PATHOPHYSIOLOGY

The early open artery hypothesis states that early reperfusion results in improved myocardial salvage with inhibition of infarct expansion. Even late reperfusion limits infarct expansion through multiple mechanisms, including immediate change in infarction characteristics, preservation of residual myofibrils and interstitial collagen, accelerated healing, the scaffold effect of a blood-filled vasculature, and elimination of ischemia in viable but dysfunctional myocardium. Infarct expansion and progressive LV dilatation are associated with persistent occlusion of an IRA. The aneurysm consists of a stretched portion of the myocardium, containing all three layers and connected with the ventricle by a wide neck.

SIGNS AND SYMPTOMS

Congestive heart failure and even cardiogenic shock can develop as a result of a large LV aneurysm. Because acute aneurysms expand during systole, contractile energy generated by normal myocardium is wasted and puts the entire ventricle at a mechanical disadvantage.

Chronic aneurysms persist for more than 6 weeks after the acute event, are less compliant than acute aneurysms, and are less likely to expand during systole. Patients with chronic aneurysms may have heart failure, ventricular arrhythmias, and systemic embolism, or may be asymptomatic.

Palpation of the precordium may reveal a dyskinetic segment of the ventricle. An S3 gallop may be heard in patients with poor ventricular function.

DIAGNOSTIC TESTING

Typical ECG findings include ST elevation, which persists despite reperfusion therapy, and Q waves (Figure 5). ST elevations that persist for more than 6 weeks suggest a chronic ventricular aneurysm.

figure3 LV aneur EKG

Figure 5. Left ventricular anterior aneurysm

A chest radiograph may reveal a localized bulge in the cardiac silhouette (Figure 6).

fif 4 x ray lv aneur

 

Figure 6. Left ventricular aneurysm

Echocardiography accurately depicts the aneurysmal segment and may also demonstrate the presence of a mural thrombus. Additionally, echocardiography is useful in differentiating true aneurysms from pseudoaneurysms. True aneurysms have a wide neck, whereas pseudoaneurysms have a narrow neck in relation to the fundus of the aneurysm. Magnetic resonance imaging may also be useful in delineating the aneurysm.

THERAPY

Congestive heart failure with acute aneurysms is managed with IV vasodilators. ACE inhibitors have been shown to reduce infarct expansion and unfavorable LV remodeling. ACE inhibitors are best started within 12 to 24 hours of the onset of acute MI, as infarct expansion starts early. Corticosteroids and nonsteroidal anti-inflammatory agents should be avoided in the acute setting because they have been demonstrated to induce infarct expansion and aneurysm formation in experimental models. Heart failure with chronic aneurysms can be managed with ACE inhibitors, digoxin, and diuretics.

Anticoagulation with warfarin sodium is indicated for patients with a mural thrombus. Patients should be initially treated with IV heparin with a target partial thromboplastin time of 50 to 70 seconds. Warfarin is started simultaneously. Patients should be treated with warfarin at a target international normalized ratio of 2-3 for 3 to 6 months. Whether patients with large aneurysms without thrombus should receive anticoagulants is controversial. Many clinicians prescribe anticoagulants for 6 to 12 weeks after the acute phase. Patients with LV aneurysms and a low global ejection fraction (less than 40%) have a higher stroke rate and should take anticoagulants for at least 3 months after the acute event. These patients may be subsequently observed with echocardiography. Anticoagulation may be reinitiated if a thrombus develops.

Refractory heart failure and refractory ventricular arrhythmias in patients with aneurysms is an indication for surgical resection. Surgical resection may be followed by either conventional closure or newer techniques to restore LV geometry. Revascularization is beneficial for patients with viable myocardium around the aneurysmal segment.

DYNAMIC LEFT VENTRICULAR
OUTFLOW OBSTRUCTION

 

PREVALENCE

Dynamic LVOT obstruction is an uncommon complication of acute anterior MI. It was first described in a case report by Bartunek et al.18

PATHOPHYSIOLOGY

This event is dependent on compensatory hyperkinesis of the basal and mid segments of the left ventricle. Predictors of enhanced regional wall motion ioninfarct zones are the absence of multivessel disease, female gender, and higher TIMI flow (Thrombolysis in Myocardial Infarction trial) in the infarct-related vessel. The increased contractile force of these regions decreases the cross-sectional area of the LVOT. The resulting increased velocity of blood through the outflow tract can produce decreased pressure below the mitral valve and result in the leaflet being drawn anteriorly toward the septum (Venturi effect). This leads to further outflow tract obstruction as well as mitral regurgitation.

It has been postulated that this complication can play a role in free wall rupture. LVOT obstruction leads to increased end-systolic intraventricular pressure. This in turn leads to increased wall stress of the weakened necrotic infarcted zone. This fatal complication occurs most frequently in women, patients older than 70 years of age, and in those without prior MI.

SIGNS AND SYMPTOMS

Patients may have respiratory distress, diaphoresis, and cool and clammy extremities in addition to the typical signs and symptoms of acute MI. Patients with severe obstruction may appear to be in cardiogenic shock, with severe orthopnea, dyspnea, and oliguria. They also may have altered mental status from cerebral hypoperfusion. Patients present with a new systolic ejection murmur heard best at the left upper sternal border with radiation to the neck. Additionally, a new holosystolic murmur can be heard at the apex with radiation to the axilla as a result of systolic anterior motion of the mitral leaflet. An S3 gallop, pulmonary rales, hypotension, and/or tachycardia can also be present.

DIAGNOSTIC TESTING

Echocardiography is the diagnostic test of choice. It accurately depicts the hyperkinetic segment and the LVOT obstruction as well as the systolic anterior motion of the mitral leaflet.

THERAPY

Treatment centers on decreasing myocardial contractility and heart rate while expanding intravascular volume and modestly increasing afterload. Beta-blockers should be added slowly with careful monitoring of heart rate, blood pressure, and Svo2. Patients can receive gentle IV hydration with several small (250 mL) aliquots of normal saline solution to increase preload and decrease LVOT obstruction and the systolic anterior motion of the mitral leaflet. The patient’s hemodynamic and respiratory status should be monitored closely during this therapeutic intervention with a Swan-Ganz catheter. Vasodilators, inotropic agents, and IABP should be avoided.

ARRHYTHMIC COMPLICATIONS

 

Dysrhythmia is the most common complication after acute MI. It is related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium. Premature ventricular contractions occur in approximately 90% of patients. The incidence of ventricular fibrillation is approximately 2% to 4%. Although lidocaine reduces the rate of primary ventricular fibrillation in patients with MI, there is no survival benefit, and there may be excess mortality. Therefore, lidocaine is not recommended as prophylactic therapy.36 Amiodarone may be used in patients with MI and frequent premature ventricular contractions, nonsustained ventricular tachycardia, or post-defibrillation for ventricular fibrillation. Amiodarone is administered as a bolus of 150 mg, then 1 mg/min IV for 6 hours followed by 0.5 mg/min. During cardiac arrest (ventricular fibrillation or pulseless ventricular tachycardia), the bolus should be increased to 300 mg (may repeat 150-mg boluses every 10 minutes to maximum dose of 24 grams). Ventricular arrhythmias not responsive to amiodarone may be treated with lidocaine (1 mg/kg bolus to a maximum of 100 mg followed by 1 mg/min to 4 mg/min drip)37 or procainamide. Polymorphic ventricular tachycardia is a rare complication of acute MI that can be treated with amiodarone, lidocaine, and/or procainamide as described for monomorphic ventricular tachycardia.

Recently, the risk of sudden cardiac death after MI has been evaluated. A significant correlation exists between significant systolic dysfunction and potential for sudden cardiac death. Implantable defibrillators have been shown to reduce mortality in patients with a prior MI and an ejection fraction of less than 30%, regardless of whether ventricular dysrhythmia is present.38

Supraventricular arrhythmias occur in less than 10% of patients with acute MI. Patients who develop these arrhythmias tend to have more severe ventricular dysfunction and worse outcome. Incipient heart failure should be suspected and treated in patients presenting with new atrial arrhythmias in the setting of an acute MI.

Bradyarrhythmias, including AV block and sinus bradycardia, occur most frequently with inferior MI. Complete AV block occurs in approximately 20% of patients with acute RV infarction. Infranodal conduction disturbances with wide complex ventricular escape rhythms occur most frequently in large anterior MIs and portend a very poor prognosis.

Transvenous pacing is indicated in patients who present with asystole, Mobitz type II, second-degree AV block, or with complete AV block. Consideration for transvenous pacing should be given in patients with new onset bifascicular and trifascicular block in the setting of acute MI. Pacing is not indicated for patients with sinus bradycardia or AV dissociation and a more rapid ventricular escape rhythm as long as the patient is maintaining adequate hemodynamics. Initial treatment for these rhythm disturbances is IV atropine at a dose of 0.5 mg to 1.0 mg. This may be repeated every 5 minutes to a maximum dose of 2 mg.

EMBOLIC COMPLICATIONS

 

PREVALENCE

The incidence of clinically evident systemic embolism after MI is less than 2%. This figure increases in patients with anterior wall MIs. The overall incidence of mural thrombus after MI is approximately 20%. Large anterior MI may be associated with mural thrombus in as many as 60% of patients.39

PATHOPHYSIOLOGY

Most emboli arise from the left ventricle as a result of wall motion abnormalities or aneurysms. Atrial fibrillation may also contribute to systemic embolic complications.

SIGNS AND SYMPTOMS

The most common clinical presentation of embolic complications is stroke, although patients may have limb ischemia, renal infarction, or intestinal ischemia. Most episodes of systemic emboli occur in the first 10 days after acute MI. Physical findings vary with the site of embolism. Focal neurologic deficits occur in patients with central nervous system emboli. Peripheral emboli cause limb ischemia, renal infarction, or mesenteric ischemia. Limb pain in a cold pulseless extremity is indicative of limb ischemia, and flank pain and hematuria are characteristic of renal infarction. Mesenteric ischemia causes severe abdominal pain, out of proportion to physical findings, and bloody diarrhea.

THERAPY

IV heparin should be started immediately with a target partial thromboplastin time of 50 seconds to 70 seconds and continued until the international normalized ratio is in the therapeutic range. Warfarin therapy should also be started immediately, with a goal international normalized ratio of 2-3 and continued for at least 3 to 6 months for patients with mural thrombi and those with large akinetic areas detected during echocardiography.

PERICARDITIS

 

PREVALENCE

 

The incidence of early pericarditis after acute MI is approximately 10%. The inflammation usually develops 24 to 96 hours after MI.40 Dressler’s syndrome, or late pericarditis, occurs in 1% to 3% of patients 1 to 8 weeks after MI.

 

PATHOPHYSIOLOGY

The pathogenesis of acute pericarditis is an inflammatory reaction in response to necrotic tissue. As such, acute pericarditis develops more often in patients with transmural MI. The pathogenesis of Dressler’s syndrome is not known, but an autoimmune mechanism has been suggested.

SIGNS AND SYMPTOMS

Most patients with early pericarditis report no symptoms. Patients with symptoms (from either early or late pericarditis) report progressive, severe chest pain that lasts for hours. The symptoms are postural (worse in the supine position) and can be alleviated when the patient sits up and leans forward. The pain tends to be pleuritic iature and, therefore, is exacerbated with deep inspiration, coughing, and swallowing. Radiation of pain to the trapezius ridge is nearly pathognomonic for acute pericarditis. The pain also may radiate to the neck and, less frequently, to the arm or back. A pericardial friction rub on exam is pathognomonic for acute pericarditis; however, it can be ephemeral. The rub is best heard at the left lower sternal edge with the diaphragm of the stethoscope. The rub has three components: atrial systole, ventricular systole, and ventricular diastole. In about 30% of patients, the rub is biphasic; in 10%, it is uniphasic. A pericardial effusion may cause fluctuation in the intensity of the rub.

Evolving MI ECG changes may mask the diagnosis of pericarditis. Pericarditis produces generalized ST-segment elevation, which appears on ECG tracings in a concave upward or saddle-shaped pattern. As pericarditis evolves, T waves become inverted after the ST segment becomes isoelectric. On the other hand, in acute MI, T waves may become inverted when the ST segment is still elevated. Four phases of ECG abnormality have been described in association with pericarditis (Table 2).41

Table 2:

ECG Changes of Pericarditis

Stage

Description

Stage 1

ST elevation, upright T waves

Stage 2

ST elevation resolves, upright to flat T waves

Stage 3

ST isoelectric, inverted T waves

Stage 4

ST isoelectric, upright T waves

  

A pericardial effusion on echocardiography is strongly suggestive of pericarditis; however, the lack of an effusion does not rule out pericarditis.

THERAPY

Aspirin is the therapy of choice for post-MI pericarditis in doses of 650 mg every 4 to 6 hours. Nonsteroidal anti-inflammatory drugs and corticosteroids should be avoided for 4 weeks after the acute event. These agents may interfere with myocardial healing and contribute to infarct expansion.42 In late pericarditis, nonsteroidal anti-inflammatory drugs and even corticosteroids may be indicated if severe symptoms persist beyond 4 weeks after MI. Colchicine may be beneficial in patients with recurrent pericarditis.

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