Elsevier

Cardiology Clinics

Volume 30, Issue 2, May 2012, Pages 233-241
Cardiology Clinics

Right Ventricular Responses to Massive and Submassive Pulmonary Embolism

https://doi.org/10.1016/j.ccl.2012.03.003Get rights and content

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Clinical case

A 67-year-old man with a history of hypertension presented to the emergency room with 3 days of dyspnea. He denied leg swelling or pain, chest pain, palpitations, hemoptysis, lightheadedness, or syncope. He also denied any known risk factors for venous thromboembolism (VTE), except for his age. Physical examination revealed an anxious man who easily became dyspneic with minimal exertion. He was afebrile; his heart rate was 88 beats/min, blood pressure 130/92 mm Hg, and respiratory rate 21

Epidemiology

Every year, there are as many as 300,000 deaths in the United States from acute PE.1, 2 Unfortunately, the diagnosis is often not made until autopsy.3, 4 The case fatality rate for PE in the first 3 months after diagnosis has been reported to be about 15% to 18%, exceeding the mortality rate for acute myocardial infarction.5, 6 In fact, a prior study of PE demonstrated that sudden death was the initial clinical manifestation in nearly 25% of patients.7 Acute PE survivors may have sequelae that

Risk factors

Certain risk factors increase the likelihood of VTE, including a previous history of VTE. Trauma, major surgery (particularly hip and knee replacement and hip fracture), cancer, and hospitalization for acute medical illnesses (such as pneumonia and congestive heart failure)8 confer significant risks for thromboembolism. Immobility or markedly reduced mobility also imparts an increased risk. Prolonged air9 or ground travel appears to increase the risk for VTE, as do advanced age, obesity, and

Classifications of acute PE

Small to moderate PE commonly occur and are characterized by normotensive patients with preserved RV function.5 These patients appear clinically well and have an excellent prognosis with therapeutic anticoagulation alone.5

Massive PE is a life-threatening condition. The criteria that define massive PE include cardiogenic shock and systemic arterial hypotension. Shock leads to tissue hypoperfusion, hypoxia, and ultimately, multi-organ failure.10 The emboli are usually bilateral and widespread,

Hemodynamics

The RV response to massive and submassive acute PE is dependent on a few factors: the extent of the emboli, the patient's underlying cardiopulmonary status, and the release of vasoactive and bronchoactive agents such as serotonin from platelets.12, 13, 14 The extent of pulmonary arterial obstruction to blood flow plays a critical role in compromising physiology and predicting the degree of RV dysfunction.12, 15, 16 In addition to physical obstruction, there is an increase in pulmonary vascular

Experimental PE and the RV response

Murine experimental models have been used extensively to study the pathophysiology of RV dysfunction in acute PE. Sullivan and colleagues20 published a study in 2001 looking at biventricular dysfunction in the ex vivo perfused hearts of rats induced with acute massive PE via thrombus infusion. Their data (through examination of Starling curves) support the idea that the intrinsic mechanical function of both ventricles can become depressed in response to an acute massive PE (reduced RV systolic

Clinical Manifestations

It is critically important to prevent diagnostic and management delays when it comes to acute PE, particularly when the emboli are submassive or massive. Thus, having a clinical suspicion of PE is crucial in guiding diagnostic testing. Dyspnea, tachypnea, and tachycardia are the most common symptoms and signs of PE. In massive PE, severe dyspnea, syncope, and cyanosis can accompany hypotension, portending a poor prognosis.5, 13 Interestingly, significant pleuritic chest pain often signifies the

Massive PE

Given its poor prognostic implications, it is imperative to act quickly whenever massive PE is suspected. Intravenous unfractionated heparin (weight-based protocol) should be bolused immediately, followed by continuous infusion of unfractionated heparin targeting an activated partial thromboplastin time (aPTT) of at least 80 seconds.5, 10, 26 Although low-molecular-weight heparin can be used, the shorter half life of standard heparin may be advantageous if thrombolytic therapy, with its

Summary

It is critically important to quickly recognize and treat acute PE. Submassive and massive PE are associated with RV dysfunction and may culminate in RV failure, cardiac arrest, and death. The normally thin-walled right ventricle is a conduit that acutely cannot hold up to the abrupt increase in RV afterload following an extensive PE, and the resultant high RV pressure overload is crucial in appreciating the clinicopathologic progression of this disease. Ultimately, a rapid and coordinated

Clinical case (continued)

Several hours after admission to the hospital ward, the patient became hypotensive (BP 82/46). This hypotension did not respond to a normal saline bolus (1000 mL). His clinical deterioration further progressed and oxygen requirements increased; he ultimately required a 100% non-rebreather mask to maintain his oxygen saturation above 90%. Pressors were initiated, and the medical team agreed to treat with thrombolytic therapy. Recombinant t-PA was infused for 2 hours, and during this time his

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  • Cited by (0)

    Dr Castillo has nothing to disclose. Dr Tapson has consulted with companies active in the field of venous thromboembolism, including sanofi Aventis, Bayer, Johnson & Johnson, EKOS, Pfizer, and Boehringer Ingelheim.

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