**3. Contemporary management: diagnosis and prognostication**

**Figure 3.** Vena Cava Filter.

398 Principles and Practice of Cardiothoracic Surgery

**Figure 4.** Nitinol OptionTM Vena Cava Filter (Argon Medical Devices, Plano, TX). Features of contemporary filters in‐

clude retrievability, MRI compatibility, and percutaneous insertion.

Classification of PE was historically based on the angiographic burden, using the Miller In‐ dex [22]. Current classification by American Heart Association differentiates between mas‐ sive PE (sustained hypotension for at least 15 minutes or requiring inotropic support, pulselessness, or persistent profound bradycardia) from submassive (acute PE without sys‐ temic hypotension but with either RV dysfunction or myocardial necrosis) (Table 1) [23]. Early identification and risk stratification is mandatory at the time of diagnosis in order to coordinate multimodality treatment strategies. Prompt diagnosis and initiation of treatment can reverse RV failure and reduce mortality. Current tools for prognostication include clini‐ cal parameters, radiographic findings, and laboratory markers.


**Table 1.** American Heart Association Classification of Pulmonary Embolism [23].

Clinical signs consistent with major PE include transient syncope, cyanosis, elevated jugular venous pressure, tachypnea, unilateral restriction of chest wall movement, fever, and signs of RV dysfunction (Table 2).

**Revised Geneva Score Points**

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Age > 65 years 1 Previous DVT or PE 3 Surgery under general anesthesia or lower limb fracture within 1 month 2 Active malignant condition (solid or hematologic, currently active or considered cured < 1 year) 2 Unilateral lower limb pain 3 Hemoptysis 2 Heart rate 75-94 beats/min 3 Heart rate > 94 beats/min 5 Pain on lower limb deep venous palpation and unilateral edema 4

Biomarkers assessing the degree of right ventricular dysfunction associated with massive PE that have been studied include troponin and beta-natriuretic peptide (BNP). Right ventricu‐ lar strain results in elevated troponin levels through acute shear stress causing microinjury and microinfarction, as well as increased oxygen demand and diminished perfusion from an acutely dilated and overloaded RV. Troponin levels have been found to correlate with the presence of RV dysfunction [27,28], and cutoff values for troponin prognostication in PE are identical to those in acute MI [29] while cutoff values for BNP are lower than those in con‐ gestive heart failure. Negative predictive value for both troponin and BNP are 97-100%; however the positive predictive values are low, with a wide range of sensitivities and low

While most patients with suspected PE will have computed tomography angiography of the chest, on occasion concerns for acute renal injury will prompt workup with ventilation-per‐ fusion scans. RV enlargement, defined as RV to LV dimension ratio > 0.9 on a reconstructed CT 4-chamber view, has been found to correlate with echocardiographic findings of RV dys‐ function [30]. Subsequently, a study of 431 consecutive patients with acute PE found that RV enlargement predicted 30-day mortality (15.6% vs 7.7%, hazard ratio 5.17) as well as the composite end-point of death and in-hospital complications [31]. Dynamic CT assessment of right ventricular response to reperfusion therapy or surgical embolectomy found that al‐ though RV enlargement persisted in 43%, significant reductions in mean RV dimension and RV/LV ratio and significant increases in mean LV occurred with therapy, and did so equally in patients treated with thrombolysis versus embolectomy. Patients presenting with cardio‐ genic shock had a greater degree of initial RV enlargement and a greater reduction post-

Clinical Probability Low: 0 - 3 points

High: >10 points

Intermediate: 4-10 points

**Table 4.** Revised Geneva Score [26]

specificity for adverse events.


**Table 2.** Clinical and Electrocardiographic Signs of RV dysfunction [24]

Several scoring systems including the Pulmonary Embolism Severity Index [25] and Revised Geneva Score [26] have been developed based primarily on clinical signs and history (Tables 3 & 4). They have been shown to have prognostic value [23] and do not require diagnostic studies, making them a valuable tool for early prognostication.


**Table 3.** Pulmonary Embolism Severity Index [25]


**Table 4.** Revised Geneva Score [26]

Clinical signs consistent with major PE include transient syncope, cyanosis, elevated jugular venous pressure, tachypnea, unilateral restriction of chest wall movement, fever, and signs

> Left parasternal heave Accentuated P2

Distended neck veins

Right axis deviation T-wave in V1-V4 Qr pattern in V1

RBBB

Several scoring systems including the Pulmonary Embolism Severity Index [25] and Revised Geneva Score [26] have been developed based primarily on clinical signs and history (Tables 3 & 4). They have been shown to have prognostic value [23] and do not require diagnostic

Murmur of tricuspid regurgitation

Unilateral restriction of chest wall

**Class Mortality Risk**

**Score**

of RV dysfunction (Table 2).

400 Principles and Practice of Cardiothoracic Surgery

**Clinical Signs of RV dysfunction**

**Electrocardiogram Signs of Right Heart Strain**

RV = right ventricle

P2 = pulmonic second heart sound RBBB = right bundle branch block

**Table 2.** Clinical and Electrocardiographic Signs of RV dysfunction [24]

studies, making them a valuable tool for early prognostication.

**Pulmonary Embolism Severity Index**

Male Sex 10 History of Cancer 30 History of Heart Failure 10 History of Chronic Lung Disease 10 Pulse > 110 beats/min 20 Systolic Blood Pressure < 100 mm Hg 30 Respiratory Rate > breaths/min 20 Temperature < 35 ˚C 20 Altered Mental Status 60 Arterial oxyhemoglobin saturation level <90% 20

Class I - < 65 points 0 - 1.6% Class II - 65-85 points 1.7 - 3.5% Class III - 85-105 points 3.2 - 7.1% Class IV - 106-125 points 4.0 - 11.4% Class V - >125 points 10.0 - 24.5%

**Table 3.** Pulmonary Embolism Severity Index [25]

Age 1 point per year

Biomarkers assessing the degree of right ventricular dysfunction associated with massive PE that have been studied include troponin and beta-natriuretic peptide (BNP). Right ventricu‐ lar strain results in elevated troponin levels through acute shear stress causing microinjury and microinfarction, as well as increased oxygen demand and diminished perfusion from an acutely dilated and overloaded RV. Troponin levels have been found to correlate with the presence of RV dysfunction [27,28], and cutoff values for troponin prognostication in PE are identical to those in acute MI [29] while cutoff values for BNP are lower than those in con‐ gestive heart failure. Negative predictive value for both troponin and BNP are 97-100%; however the positive predictive values are low, with a wide range of sensitivities and low specificity for adverse events.

While most patients with suspected PE will have computed tomography angiography of the chest, on occasion concerns for acute renal injury will prompt workup with ventilation-per‐ fusion scans. RV enlargement, defined as RV to LV dimension ratio > 0.9 on a reconstructed CT 4-chamber view, has been found to correlate with echocardiographic findings of RV dys‐ function [30]. Subsequently, a study of 431 consecutive patients with acute PE found that RV enlargement predicted 30-day mortality (15.6% vs 7.7%, hazard ratio 5.17) as well as the composite end-point of death and in-hospital complications [31]. Dynamic CT assessment of right ventricular response to reperfusion therapy or surgical embolectomy found that al‐ though RV enlargement persisted in 43%, significant reductions in mean RV dimension and RV/LV ratio and significant increases in mean LV occurred with therapy, and did so equally in patients treated with thrombolysis versus embolectomy. Patients presenting with cardio‐ genic shock had a greater degree of initial RV enlargement and a greater reduction posttherapy [32]. Echocardiography may demonstrate the McConnell sign of acute pulmonary embolism, a characteristic pattern of akinesis of the mid free wall and normal motion of the apex [33]. Other signs include right ventricular hypokinesis, right ventricle dilation, and signs of pulmonary hypertension. In normotensive patients, RV dilation is present in 30-40% and predicts in-hospital mortality as well higher non-resolution and recurrence of pulmona‐ ry thrombus burden [34].

ment are optimization of RV preload and systolic function, reduction of pulmonary vascular resistance, and maintenance of right coronary perfusion pressure by adequate aortic root pressure [35]. Acute massive pulmonary embolism is initially a pressure overload problem of the RV. Higher filling pressures may be required; however an altered Frank-Starling curve in the setting of RV dysfunction may lead to volume overload as well. For patients with low cardiac output and normal blood pressure, modest fluid challenges may be benefi‐ cial, and the use of dobutamine and dopamine is a class IIa recommendation. Class I recom‐ mendations include correction of systemic hypotension and use of vasopressors, although the use of norepinephrine lacks clinical data, while the beneficial use of epinephrine in PE

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Acute RV Dysfunction

Pressure Load

Decreased RV Output

Ischemia

Increased RV Wall Stress

Increased RV Volume

Decreased LV Compliance

Hypotension, Reduction in CO

with shock has been reported [36].

Decreased Coronary Flow

**Figure 6.** Hemodynamic effects of acute massive PE

Increased RV Pressure
