Myocardial Rupture

Myocardial rupture occurs in the setting of acute myocardial infarction (AMI),11 blunt and penetrating cardiac trauma, primary cardiac infection, primary and secondary cardiac tumors, infiltrative diseases of the heart, and aortic dissection. Myocardial rupture (or perforation) may also occur iatrogenically during percutaneous cardiac procedures (including device implantation) or open heart surgery (particularly valve replacement). Myocardial rupture has also been reported in the setting of stress cardiomyopathy (Takotsubo[1, 2] or regional ventricular ballooning syndrome). The clinical presentation of myocardial rupture depends on the mechanism and site of injury and the hemodynamic effects of the rupture. Mortality is extremely high unless early diagnosis is made and urgent surgical intervention is provided.

Ischemic myocardial rupture after acute myocardial infarction (AMI) may involve left ventricular (LV) and right ventricular (RV) free walls, ventricular septum, and LV papillary muscle, in decreasing order of frequency. It rarely involves the left or right atrial walls.

The consequences of myocardial rupture in the setting of AMI can include the following:

• Pericardial tamponade

• Ventricular septal defect (VSD) with left-to-right shunt

• Acute mitral regurgitation (MR)

• Formation of a pseudoaneurysm

In most instances, the catastrophic clinical presentation occurs within 3-5 days of a rather small AMI. Both hemodynamic factors (increased intracavitary pressure) and regional myocardial structural weakness (myocyte necrosis, collagen matrix resolution, and intense inflammation) can make important contributions to myocardial rupture in the setting of AMI.

In rare instances, patients simultaneously experience LV free-wall rupture and ventricular septal or papillary muscle rupture (double rupture) after AMI. Rupture of both papillary muscles after AMI has been reported.

In the case of a papillary muscle rupture, the posteromedial papillary muscle is twice as likely to rupture as the anterolateral papillary muscle is. This is because the anteromedial papillary muscle is more often supplied by 2 arterial systems (the left anterior descending and left circumflex coronary arteries), whereas the posteromedial papillary muscle is frequently supplied by only 1 coronary artery (usually the right).

In some patients who survive LV free-wall rupture following AMI, the rupture can be sealed by the epicardium (visceral pericardium) or by a hematoma on the epicardial surface of the heart. This entity has been referred to as LV diverticulum (or contained myocardial rupture[3] ) and represents a subacute pathologic condition between free rupture into the pericardial cavity and formation of a pseudoaneurysm.

A pseudoaneurysm is formed if the area of rupture is contained locally by the adjacent parietal pericardium and represents the chronic stage of LV free-wall rupture. The most common etiology of LV pseudoaneurysm is AMI. (LV pseudoaneurysm is twice as common with inferior AMI as it is with anterior AMI.) LV pseudoaneurysms may also develop after surgical interventions, especially after mitral valve replacement.

Blunt cardiac trauma, most commonly occurring in the setting of an automobile accident, may cause myocardial rupture as a result of cardiac compression between the sternum and the spine, direct impact on the heart (sternal trauma), or deceleration injury. It may result in rupture of the papillary muscles, the cardiac free wall, or the ventricular septum.

The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, the left ventricle, the right atrium, and the left atrium. However, among patients who reach the hospital alive, the right atrium is most commonly involved. In as many as 30% of cases, the rupture involves more than 1 chamber. Delayed myocardial rupture has been reported as a result of cardiac contusion. Acute mitral or tricuspid regurgitation, VSD, or pericardial tamponade may result from myocardial rupture secondary to blunt cardiac trauma.

Penetrating myocardial injury occurs most commonly as a result of stab or gunshot wounds (see the image below). The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, the left ventricle, the right atrium, and the left atrium.

Unlike blunt trauma, penetrating cardiac injury always involves the pericardium. Consequently, ventricular free-wall rupture in this setting may result in either pericardial tamponade (if the pericardial wound is obliterated) or intrathoracic hemorrhage. Pericardial tamponade is more common with stab wounds, whereas hypovolemic shock is more frequently associated with gunshot wounds.

Myocardial abscesses accompanying infective endocarditis may rupture transmurally, resulting in VSD or pericardial tamponade (pyohemopericardium). Such abscesses are observed most commonly in the setting of Staphylococcus aureus endocarditis involving prosthetic valves in the aortic position. Rarely, myocardial necrosis due to acute myocarditis, tuberculosis, or sarcoidosis may result in myocardial rupture.

Myocardial rupture is rarely caused by primary tumors (eg, hemangiopericytoma, angiosarcoma, or lymphoma) or secondary (metastatic) cardiac tumors. Lymphomas and acute myeloblastic leukemia also have been associated with myocardial rupture.

Risk factors for myocardial rupture after acute myocardial infarction (AMI) include the following:

• Relatively small first AMI

• Female sex

• Age older than 60 years

• Hypertension

• Use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of AMI (interference with the healing process)

• Late thrombolysis (>11 hours)[4]

• Postinfarction angina

• Elevated peak serum C-reactive protein levels

Protective factors include the following:

• LV hypertrophy

• History of previous infarcts

• Congestive heart failure (CHF)

• History of chronic ischemic heart disease (well-developed coronary collateral circulation)

• Early use of beta blockers after AMI or early in the course of stress cardiomyopathy[5]

• Successful (and timely) primary percutaneous coronary intervention (PCI)

Trauma may be blunt or penetrating. It also may be iatrogenic in nature, resulting from any of the following:

• Diagnostic catheterization, including transseptal puncture and endomyocardial biopsy

• Balloon valvuloplasty

• Transcatheter aortic valve implantation (replacement), particularly from the transapical approach[6]

• Pericardiocentesis

• Placement of temporary or permanent pacing catheters

• Cardiac surgery, especially mitral valve replacement

Rupture of a myocardial abscess or AMI secondary to coronary embolism of the vegetative material may occur in patients with infective endocarditis. Other infections may include tuberculosis, echinococcal cysts, and myocarditis.

Aortic dissection may also be a cause. This occurs in the setting of an ascending aortic dissection with the rupture of the false lumen into the pericardial space, causing hemorrhagic cardiac tamponade or retrograde dissection into the left ventricular myocardium (myocardial hematoma).

Primary or secondary (metastatic) tumors of the myocardium (including lymphoma and acute myeloblastic leukemia) may result in myocardial rupture involving any of the cardiac chambers.

Sarcoidosis is a rare cause of myocardial rupture through transmural noncaseating granulomas. The highest risk of myocardial rupture in this setting is observed during aggressive anti-inflammatory (commonly steroid) therapy that may lead to rapid dissolution of granulomas.

Myocardial rupture complicates up to 10% of acute myocardial infarctions (AMIs), with myocardial free-wall rupture occurring in 2-4% of AMIs.[7] Approximately 6-10% of penetrating chest wounds and 15-75% of blunt chest injuries are associated with cardiac trauma. Myocardial rupture occurs in 10-15% of fatal motor vehicle accidents. The incidence of cardiac rupture after blunt trauma is 0.5-2% among hospital trauma admissions. Myocardial rupture after AMI is more common in patients aged 60 years or older. Traumatic myocardial rupture is observed more commonly in those aged 15-63 years (mean, 34 years).[8] Myocardial rupture after AMI is reported more commonly in women than in men (1.4:1). The incidence of traumatic myocardial rupture is higher in males (up to 85% in some series) than in females.

A Japanese study found a decrease in the incidence of and mortality rate from cardiac rupture over a period of more than 3 decades (1977-2011) in patients with AMI. The study involved 5699 patients, including 144 with cardiac rupture, with the patients divided into three 10- to 12-year cohorts; ie, 1977-1989, 1990-2000, and 2001-2011. The mortality rate associated with cardiac rupture declined from 90% in the earliest group to 56% in the 1990-2000 group and 50% in the 2001-2011 group. The incidence of cardiac rupture also went through successive declines, from 3.3% to 2.8% to 1.7%, respectively.[9]

The prognosis depends on the type, size, hemodynamic effects, and cause of the myocardial rupture. Accordingly, making a quick diagnosis and initiating prompt surgical intervention are crucial.

Myocardial rupture is responsible for nearly 15% of all in-hospital deaths among patients with AMI. After pump failure, it is the second most common cause of in-hospital mortality among patients with AMI.

Approximately 50% of patients with cardiac rupture after AMI die within 5 days, and 82% die within 2 weeks of the index infarction. Aggressive early diagnosis and surgery may confer a survival rate as high as 75%.

The overall mortality from myocardial rupture after blunt trauma is 76-93%. However, among those who reach the hospital alive, the mortality is 29-50%. The mortality from myocardial rupture resulting from penetrating trauma ranges from 62-89% in the field to 2-83% in the hospital. Mortality after the patient arrives at the hospital largely depends on the type of injury, the rapidity of the transfer to a hospital, and the patient’s vital signs and condition on arrival.

For myocardial rupture resulting from penetrating cardiac trauma, hospital mortality is higher in patients presenting with hypovolemia than in those presenting with pericardial tamponade (22% vs 8%). In-hospital mortality is lowest for patients with RV rupture.

Complications of myocardial rupture include the following:

• Tamponade

• Hemothorax

• Sudden death

Myocardial rupture after acute myocardial infarction (AMI) may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction.

In most patients, myocardial rupture manifests as a catastrophic event (acute pulmonary edema, cardiogenic shock, or circulatory collapse) within days of a first, small, uncomplicated AMI. Older women, especially those with recurrent postinfarction angina, and patients with systemic hypertension more commonly experience myocardial rupture after AMI.[10]

Acute onset of shortness of breath, chest pain, shock, diaphoresis, unexplained emesis, cool and clammy skin, and syncope may herald the onset of ventricular septal rupture after AMI (see the image below).

Sudden death due to left ventricular (LV) free-wall rupture may be the first manifestation of coronary artery disease (CAD) in a small percentage of patients with AMI.

Immediate, early, or delayed acute pulmonary edema (associated with papillary muscle rupture), congestive heart failure (CHF; associated with ventricular septal rupture), and hypotension (associated with free-wall rupture) are the cardinal manifestations of myocardial rupture following blunt chest trauma. Concomitant rupture of the myocardium, pericardium, and diaphragm may result in the accumulation of blood in the abdominal cavity.

In patients with traumatic myocardial rupture, manifestations depend on the site, mode, and extent of cardiac injury. Sudden death occurs shortly after the injury in most patients with traumatic myocardial rupture and is due to pericardial tamponade or exsanguination. Cardiogenic or hypovolemic shock is the predominant manifestation of traumatic myocardial rupture in patients who reach a hospital. Patients with pericardial tamponade may present with dyspnea, chest pain, hypotension, cold peripheries, and mental status changes.

A small percentage of patients with significant penetrating cardiac trauma have few or no symptoms upon presentation to a hospital.

Pseudoaneurysms may manifest as cerebral or systemic embolic events or as sudden death (rupture). Hemoptysis may occur as a consequence of the formation of ventriculopulmonary fistulas. Approximately 10% of patients with a pseudoaneurysm are asymptomatic.

Of those patients who sustain cardiac trauma from stab wounds, 18-35% remain without clinical signs of myocardial injury.

Acute pulmonary edema from partial or complete papillary muscle rupture (see the image below) manifests as tachypnea, tachycardia, hypotension, respiratory distress, diffuse pulmonary rales, and signs of mitral regurgitation (MR).

The MR murmur may be absent or atypical (soft and not holosystolic) as a result of rapid equalization of pressures between the left ventricle and the left atrium. This equalization is due to the noncompliance of the acutely volume-overloaded left atrium (ie, the left atrial pressure increases sharply in response to sudden rise in volume). Sudden unexplained hypotension or pulmonary edema in patients experiencing their first inferior AMI should raise the possibility of papillary muscle rupture, even in the absence of a murmur.

Post-AMI pericarditis manifested as pleuritic chest pain and friction rub may be present in some patients before the onset of LV free-wall rupture and generally indicates transmural extension of the infarct (see the image below). Cardiogenic shock due to pericardial tamponade manifests as sudden onset of bradycardia, clear lung fields, distended neck veins, Kussmaul sign (ie, paradoxical inspiratory increase in jugular venous pressure), muffled heart sounds, and pulsus paradoxus (ie, an inspiratory drop in systolic blood pressure of more than 10 mm Hg).

Hypovolemic shock may occur due to direct communication with the thoracic or abdominal cavity through a pericardial tear. This manifests as hypotension, tachycardia, cool and clammy extremities, pallor, and diaphoresis.

In ventricular septal rupture, hypotension may be present. Patients may have acute pulmonary edema. A loud holosystolic murmur may be heard at the lower left sternal border or diffusely over the precordium and is often associated with a thrill. Ventricular arrhythmias may be present.

In pseudoaneurysm, a friction rub may be heard. Pseudoaneurysms frequently rupture, resulting in cardiogenic or hypovolemic shock. Some patients may have a systolic murmur due to the turbulent flow across the narrow neck of the pseudoaneurysm. Systemic embolism that originates from the pseudoaneurysm may result in various cerebrovascular or systemic ischemic symptoms. Arrhythmia may be present, especially ventricular tachycardia and fibrillation.

Physicians should have a high index of suspicion for myocardial rupture after acute myocardial infarction (AMI). Especially during the first week, it is critical to make the diagnosis and perform emergency life-saving interventions as expeditiously as possible. Failure to diagnose or act quickly could expose physicians to legal liability.

The possibility of cardiac injury should be considered in all patients with high-velocity deceleration blunt injuries. Failure to diagnose myocardial rupture or early discharge of stable patients from the emergency department could result in serious legal consequences.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include true ventricular aneurysm and cardiac contusion.

Chest radiographs may show cardiomegaly with clear lung fields in patients with free-wall rupture or pseudoaneurysm (see the image below). Pulmonary edema with a normal cardiothoracic ratio may be present after papillary muscle or ventricular septal rupture. Mediastinal widening with or without pleural effusion (hemothorax) may be present in those with aortic dissection. Hemothorax also may be observed in patients who have free-wall rupture with an associated pericardial tear.

Emergency bedside transthoracic echocardiography (TTE) is the diagnostic modality of choice in all types of myocardial rupture. The following points should be noted:

• A regional left ventricular (LV) or right ventricular (RV) wall motion abnormality due to acute myocardial infarction (AMI) or traumatic myocardial injury may be apparent

• Evidence of cardiac tamponade may manifest as diffuse or loculated pericardial effusion, atrial collapse, diastolic RV collapse, and marked inspiratory decrease in transmitral Doppler flow velocities

• Sampling pulmonary venous and hepatic blood flow with pulse-wave Doppler may help reveal the hemodynamic significance of pericardial effusion

• Ruptured papillary muscle may appear as a mobile echo density prolapsing into the left atrium during systole or as a flail mitral leaflet; occasionally, a tear may be evident in one of the papillary muscle heads

• Color-flow Doppler studies can determine the severity and mechanism of MR and differentiate papillary muscle rupture from a ventricular septal defect (VSD); acute severe MR may be difficult to identify with color Doppler because of the patient’s general condition (acute pulmonary edema that results in tachypnea and tachycardia) and a low pressure difference between left ventricle and atrium during systole

• The size, location, and type of VSD are demonstrated in more than two thirds of patients; color-flow Doppler is especially useful for detection of the high-velocity turbulent flow through the defect in almost all patients and can be used to estimate the severity of the shunt; continuous-wave Doppler can be used to estimate RV systolic pressure with the use of the Bernoulli equation and systemic systolic blood pressure

• Pseudoaneurysm appears as an echo-free space that enlarges during systole and communicates with the ventricular cavity by a narrow neck; it may be partially or completely filled with thrombus; Doppler studies may show flow through the narrow neck

• No abnormalities are observed in as many as 20% of patients who have sustained penetrating or blunt cardiac injury

In a case study of an 82-year-old woman with an anterolateral ST segment elevation myocardial infarction treated with thrombolysis, investigators performed echocardiography and used contrast to improve visualization.[12] They found a small- to moderate-sized circumferential pericardial effusion without frank tamponade. In addition, they found significant intramyocardial tracking of the contrast into the epicardial space, consistent with rupture or disruption of the wall segment.[12]

Transesophageal echocardiography (TEE) is valuable in unstable intubated patients if TTE findings are suboptimal or negative despite a high index of suspicion for aortic dissection or papillary muscle rupture.

Alternatives to echocardiography

Computed tomography (CT) and magnetic resonance imaging (MRI) are useful imaging techniques when echocardiography produces suboptimal images in stable patients, such as those with pseudoaneurysm.

Electrocardiographic (ECG) evidence of transmural (ST elevation) AMI is present in most patients with ischemic myocardial rupture before the event. Persistent ST-segment elevation after AMI is associated with a higher incidence of myocardial rupture. In the setting of an anterior AMI, ST elevation or development of Q waves in inferior leads (as a result of occlusion of a large wraparound left anterior descending coronary artery) is associated with an increased risk of VSD.[13]

After traumatic cardiac injury, ECG changes usually are nonspecific.

Free-wall rupture is often associated with the sudden onset of bradycardia and electromechanical dissociation (pulseless electrical activity).

In pericardial tamponade, ECG may show low-voltage QRS complexes, especially in the precordial leads. Electrical alternans, commonly seen with large, slowly accumulating effusions, is often absent in the setting of acute hemorrhagic pericardial tamponade.

Right bundle-branch block is frequently observed in patients with VSD. Less frequently, patients may have complete heart block.

Patients with pseudoaneurysm may demonstrate ST-segment elevation, nonspecific ST changes, or pathologic Q waves on ECG.

All patients with significant thoracic blunt trauma should undergo ECG and cardiac monitoring. The ECG may show ST elevation or nonspecific ST-T changes. Normal ECG findings do not exclude myocardial injury following blunt trauma.

Heart

In patients with AMI complicated by myocardial rupture, emergency cardiac catheterization, coronary angiography, and ventriculography may be necessary in a relatively stable patient before surgical intervention. The aim of the study under these circumstances is to assess the distribution and severity of coronary artery disease (CAD). Timely surgical intervention, however, is essential in the treatment of these patients and should not be delayed.

Coronary and LV angiography may be also useful for diagnosis of pseudoaneurysm, MR, and VSD in rare instances.

Pulmonary artery

The presence of large V waves on pulmonary artery wedge tracing can help diagnose acute MR. However, a large acute VSD may also produce large V waves.

Swan-Ganz catheterization can be useful for hemodynamic monitoring and guiding initial medical management of a VSD. An oxygen saturation step-up of more than 10% from the right atrium to the right ventricle is highly suggestive of the presence of a large VSD.

In case of pericardial effusion, elevation (generally >15 mm Hg) and equalization (within 5 mm Hg) of diastolic pressures (LV, pulmonary capillary wedge, RV and right atrial) indicate tamponade.

After AMI, myocytes exhibit cytoplasmic hypereosinophilia and nuclear pyknosis, and they develop a typical wavy appearance. Approximately 8 hours post infarction, interstitial edema and neutrophilic infiltration can be observed. After 24 hours, cross-striations are lost, and focal hyalinization appears.

Removal of necrotic fibers starts within 96 hours of AMI. An increase in collagenase activity appears by day 2 and peaks at day 7, leading to collagen degradation. New collagen fibers (type III early and type I later) are evident by day 14. After 4-6 weeks, removal of necrotic myocardium is complete, and the removed myocardial tissue is replaced by scar tissue.

Ischemic myocardial rupture commonly occurs between the time of collagen degradation and the laying down of new fibrous tissue (days 2-14 post infarction). Intense inflammatory response (evidenced by the number of leukocytes), expression of matrix metalloproteinases (collagenases), and presence of intramyocardial hemorrhage (often intensified by thrombolysis, especially if administered late) are pathologic findings that favor myocardial rupture after AMI.

Early surgical intervention is essential for the treatment of myocardial rupture; medical therapy plays a supporting role in some instances. Immediate consultation with a cardiothoracic surgeon is indicated in all cases of myocardial rupture. Pericardiocentesis and surgical drainage of hemopericardium may be indicated.

All patients with cardiac rupture should be transferred to the operating room (OR) immediately and admitted to the medical intensive care unit (ICU) or the surgical intensive care unit after operative management. Transfer should be considered only for patients who are in a center without a cardiothoracic surgery unit. The outcome in this setting is quite poor.

Intra-aortic balloon counterpulsation can be used to temporarily stabilize patients with ventricular septal defect or papillary muscle rupture. Although advocated by some, intra-aortic balloon pumps are not generally used in the treatment of patients with left ventricular (LV) free-wall rupture.

Patients should receive nothing by mouth (nil per os; NPO). Complete bed rest is indicated.

Medical therapy may be used in some cases to stabilize the patient during the time needed to assemble the surgical team.

In less severe cases of papillary muscle rupture, vasodilators should be started to decrease afterload in an attempt to stabilize patients before surgery. This is often accomplished with intravenous (IV) nitroprusside. In severe cases, insertion of an intra-aortic balloon pump may be necessary.

In ventricular septal defect, intravenous inotropic agents, vasodilators, and diuretics can be used to increase cardiac output and decrease afterload. Insertion of an intra-aortic balloon pump is helpful.

Rapid fluid administration to increase preload and inotropic drugs to improve cardiac output can be useful in cases of free-wall rupture while patients are being transferred to the operating room.

In most patients, immediate surgery is necessary and should not be delayed by attempts to stabilize the patient medically.

Papillary muscle rupture is generally treated with mitral valve replacement.

Free-wall rupture is treated by resecting the infarcted area and closing the rupture zone with Teflon or Dacron patches or by using of biologic glues. Successful off-pump surgery (without the use of cardiopulmonary bypass) has been reported. A 2020 multicenter retrospective study (2001-2018) that reviewed surgical management of postinfarction left ventricular (LV) free-wall rupture and its early outcomes in 140 patients found a 36.4% operative mortality, with the main cause of death low cardiac output syndrome.[14]  Postoperative myocardial rerupture occurred in 10 patients (7.1%). Independent predictors for early operative mortality were preprocedure LV ejection fraction, cardiac arrest at presentation, female sex, and the need for preprocedure extracorporeal life support (including extracorporeal membrane oxygenation [ECMO]).[14]

Ventricular septal defects (VSDs) can be closed directly or by placing a patch, depending on the size of the defect and the timing of the surgery. The operative mortality after surgical repair is high,[15, 16, 17]  particularly in the setting of cardiogenic shock. A 2020 retrospective study (2015-2017) of data from eight patients who underwent delayed surgery following postinfarction ventricular septal rupture with cardiogenic shock found that a combination of preoperative mechanical circulatory support and delayed surgery potentially improved patient outcomes possibly by improving end-organ perfusion.[16]  All the patients received preoperative intra-aortic balloon pump support, and five also received ECMO support. No patient underwent emergency repair; it took a median time of 7.1 days from myocardial infarction onset to surgery and 1.9 days from rupture diagnosis to surgery. Operative mortality was 12.5%, there was a 12.5% complication rate associated with mechanical circulatory support, and survival was 62.5% at 2 years.[16]

In a 2020 systematic review and meta-analysis (1998-2020) that comprised data from 6361 patients from 41 studies who underwent surgical repair for postinfarction ventricular septal rupture, investigators found a 38.2% operative mortality[17]  Factors that raised the likelihood of operative mortality were need for pre-/perioperative intra-aortic balloon pump (IABP) support, right ventricular dysfunction at presentation, posterior defects, and emergency surgery.[17]

Pseudoaneurysms carry a high risk of rupture, even though long-term survivors have been reported. Therefore, surgical repair is recommended, even in asymptomatic patients. Surgical repair is similar to that of ventricular rupture.

Coronary artery bypass surgery is often needed as part of the treatment of patients with mechanical complications of AMI undergoing surgical correction (especially patients with VSD). A report from the Society of Thoracic Surgery National Cardiac Database indicated that patients undergoing coronary artery bypass surgery for cardiogenic shock after AMI have a 19% operative mortality; this increases to 31% for those also requiring mitral valve replacement and to 58% for those requiring repair of a ruptured ventricular septum.[18]

Coronary risk factor modification decreases the risk of acute myocardial infarction (AMI). Avoid nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids in the early phase of AMI. Control hypertension and use beta blockers early in patients with AMI. Early successful percutaneous coronary intervention (eg, balloon angioplasty and placement of a stent) reduces the risk of myocardial rupture after AMI.

A risk score to predict cardiac rupture after ST-elevation MI has been proposed; it uses seven predictors: female sex, advanced age, anterior MI, delayed admission, heart rate, leukocytosis, and anemia.[19]

Using seat belts can significantly reduce the rate of blunt thoracic trauma resulting from high-speed accidents.

Medications are useful to help stabilize patients who are waiting for emergency surgery. Agents used in patients who have sustained a myocardial rupture include inotropes, vasodilators, and diuretics.

Class Summary

Inotropes are used in patients with a ventricular septal defect (VSD) or free-wall rupture to increase myocardial contractility and cardiac output in the state of hypotension.

Dopamine

Dopamine stimulates alpha1-adrenergic, beta-adrenergic, and dopaminergic receptors, which are stimulated at lower dosages (< 2 µg/kg/min) and result in renal and mesenteric arterial vasodilation. Beta-adrenergic stimulation occurs at dosages of 2-10 µg/kg/min with positive inotropic effects. Alpha-adrenergic stimulation at dosages exceeding 10 µg/kg/min results in vasoconstriction and increase in blood pressure and afterload.

Dobutamine

Dobutamine is primarily a beta-receptor agonist with both inotropic and chronotropic effects.

Class Summary

Vasodilators may be used in patients with VSD or mitral regurgitation (MR) to decrease afterload and, subsequently, shunt severity.

Sodium nitroprusside (Nitropress)

Sodium nitroprusside reduces peripheral resistance by acting directly on arteriolar and venous smooth muscle.

Nitroglycerin IV (Nitro-Bid, Nitrostat, Nitro-Dur, Nitrolingual, NitroMist)

Nitroglycerin is primarily a venodilator that decreases both preload and afterload. It is preferred to sodium nitroprusside in patients with acute myocardial infarction (AMI).

Class Summary

Diuretics can be used in pulmonary edema caused by VSD or MR.

Furosemide (Lasix)

Furosemide is a loop diuretic that decreases preload through reduction of plasma volume and direct vasodilation.