Common misconceptions and mistakes
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Believing that the target of heparin is the already embolized clot (preventing its extension in the pulmonary vasculature)
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Missing the most common abnormal chest x-ray (CXR) finding in pulmonary embolism (PE) (subsegmental atelectasis and a small effusion)
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Assuming a VQ scan will be useless in an individual with underlying lung disease
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Failing to realize that thrombosis in the superficial femoral vein is a deep vein thrombosis ( DVT )
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Undertreating an upper extremity DVT occurring in the outpatient setting
Overview of Acute Venous Thromboembolic Disease
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Represents a spectrum from DVT to symptomatic PE
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Every acute DVT will have caused tiny, subclinical (asymptomatic and/or undetectable) pulmonary emboli based on the unstable nature of a newly formed clot in the deep veins
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Therefore , when DVT is found in the absence of pulmonary symptoms, presume asymptomatic PE
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Treat DVT and asymptomatic PE the same way
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No need to perform thoracic imaging to attempt to prove asymptomatic PE once DVT is diagnosed
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Every acute PE that is diagnosed is a “ heralding event”
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If survived, the individual’s intrinsic fibrinolytic system will lyse the embolized clot (often quickly)
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Therefore the already embolized clot is not the focus of acute management
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The primary goal of acute management is to prevent the next PE (ie, recurrent embolism) with anticoagulation
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Each recurrent embolism carries a mortality risk of approximately 25%
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Although the CXR is normal the majority of the time in acute PE:
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The most common abnormality seen by CXR is a small effusion with subsegmental atelectasis reflecting focal inflammatory mediator release (eg, histamine) and bronchoconstriction
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CT angiography (CTA) is useful in the initial diagnosis of PE, often providing an alternate explanation for symptoms when PE is not discovered
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A VQ scan is a reasonable alternative if the patient has a contraindication to IV contrast or an individual desire to minimize CT-related radiation exposure
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Once a symptomatic PE is diagnosed, patients should be risk stratified with an echocardiogram ECG, BNP, and troponin, looking for RV strain
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IV heparin is the anticoagulant of choice for individuals at risk of clinical deterioration, given its ability to be reversed and resumed quickly
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Urgent inferior vena cava (IVC) filter placement should be pursued in individuals who have a contraindication to anticoagulation
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Individuals with an unprovoked venous thromboembolism (VTE) (and a normal bleeding risk) should be offered indefinite anticoagulation
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Patients with VTE disease should be screened for persistent perfusion defects by VQ scan after 6 months of anticoagulation, or at the time anticoagulation is to be stopped (eg, 3 months for small provoked VTE)
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Individuals with persistent perfusion defects should be screened for chronic thromboembolic pulmonary hypertension (CTEPH) via an echocardiogram looking for an elevated pulmonary artery systolic pressure (PAS) and isolated right-sided heart failure
Pathophysiology of Pulmonary Embolism
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A DVT (typically in the leg or pelvis) has both of the following:
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A stable , organized edge that is attached to the vessel wall
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And an unstable leading edge, extending into the lumen of the vessel
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Fresh clot extends from this leading edge until shear forces cause it to break off and embolize to the lung
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This process repeats until death (from obstructive, right ventricular [RV]-mediated cardiogenic shock), anticoagulation, or IVC filter placement
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Symptomatic PE occurs when clot extension and breakage creates a large enough fragment to cause significant pulmonary artery (PA) occlusion
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Heparin (anticoagulation) stops this extension and embolism cycle, stabilizing the leading edge and dramatically reducing the risk of significant recurrent PE
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Contraindication to anticoagulation mandates urgent IVC filter placement to prevent death from recurrent PE
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PE symptoms and causes:
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Pleuritic chest pain is caused by either:
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Atelectasis causing pleural traction (common)
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Pulmonary infarct (less common)
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Pulmonary infarction occurs when PE is accompanied by shock (systemic hypotension)
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Compromising both the pulmonary artery and bronchial artery circulation
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A-a gradient and hypoxemia are caused by VQ mismatch related to:
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Atelectasis from local inflammatory mediator release (eg, histamine) and bronchoconstriction
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Alveolar edema occurring in the unobstructed regions of the lung from the increased blood flow
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Unobstructed pulmonary arteries receive the entire cardiac output
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Tachypnea and dyspnea occur with:
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Respiratory alkalosis (low P co 2 ) , which may be caused by pain, anxiety, and/or hypoxemic mediated hyperventilation
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Normal or high P co 2 from the increased dead space created by the obstructed regions of the lung
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Tachycardia and hypotension represent the spectrum of right-sided cardiogenic shock
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Tachycardia is compensatory, attempting to maintain cardiac output (CO) in the face of a falling stroke volume
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Hypotension reflects the failure to maintain CO (despite compensatory tachycardia and increased systemic vascular resistance [SVR])
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Acute respiratory failure from PE:
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PE is an uncommon cause of respiratory failure in individuals without underlying lung disease
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Patients with obstructive lung disease and PE are prone to hypercapnic failure from an inability to compensate for the increased dead space caused by the PA obstruction
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Hypoxemia (from VQ mismatch) is typically easy to support with ≤ 6 L of O 2 by NC
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Shunt physiology (ie, marginal oxygenation despite a 100% Fi o 2 ) is uncommon but may be seen with:
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Right-to-left shunting through an intracardiac shunt (eg, patent foramen ovale [PFO])
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Increased PA and right-sided intracardiac pressure occur with low left-sided intracardiac pressure, promoting right-to-left shunting
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Screen for this with a contrast echocardiogram (ie, immediate left-sided bubbles with IV agitated saline infusion)
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PE with refractory hypoxemia from shunting though a PFO is a reason to consider thrombolysis (in hopes of rapidly dropping right-sided pressure)
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Massive saddle emboli that fragment diffusely may cause shunt physiology ( Fig. 15.1 ) from the combination of:
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Atelectasis, adjacent to obstructed segments, via local inflammatory mediator release with bronchoconstriction
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Alveolar edema occurring in the unobstructed segments, as they receive the entire cardiac output
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This causes mechanical pulmonary capillary injury and alveolar edema, clinically similar to cardiogenic edema (ie, pink, frothy fluid that responds quickly to PEEP)
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Fig. 15.1
Encapsulated case of a saddle pulmonary embolism causing an obstructive cardiac arrest with return of spontaneous circulation (ROSC) occurring after CPR dislodged and fragmented the clot, followed by a second cardiac arrest from hypoxemia, with ROSC occurring after improved oxygenation with increased positive end-expiratory pressure (PEEP). (A) Initial prearrest presentation demonstrates the classic features of PE, namely the patient’s sense of impending doom, tachycardia, tachypnea, and arterial blood gas (ABG) showing a respiratory alkalosis with a significant A-a gradient. The respiratory alkalosis threatens to mask an underlying metabolic acidosis by normalizing the pH. This is easy to spot, acknowledging that a P co 2 of 29 mm Hg (< 35 mm Hg) is low and thus the pH should be high (> 7.45). Instead, the acidemic pH reveals the underlying metabolic acidosis, which was secondary to lactate from developing cardiogenic shock (not something to be missed). The prearrest chest x-ray shows bilateral oligemia or Westermark’s sign (solid arrows) and main pulmonary artery “sausage-like” dilation with rapid tapering or Palla’s signs (dashed arrows). The patient’s repeat ABG shows both shunt physiology and the development of a (relative) respiratory acidosis, as evidenced by a P co 2 of 35 mm Hg (despite the fact that the value is in the normal range). Appropriate compensation for a metabolic acidosis yielding a pH of 7.22 is a P co 2 of 22 mm Hg. Because the patient was tachypneic, attempting but unable to ventilate maximally impending hypercapnic respiratory failure should be anticipated. Shunt physiology is suggested by the PaO 2 of 66 mm Hg on 100% Fi o 2 . (B) Development of lung failure occurring after ROSC, as evidenced by extreme dead space physiology with a P co 2 > 90 mm Hg despite a minute ventilation > 17.5 L/min and critical shunt physiology with a PaO 2 of 38 mm Hg despite mechanical ventilation with a Fi o 2 of 100% and a PEEP of 10 cm H 2 O. (C) Initial management of the shunt physiology, (which was) attributed to pulmonary edema and atelectasis involved increasing PEEP. Though the high PEEP decreased venous return (evidenced by an increased HR and decreased BP), a priority was placed on maintaining the patient’s PaO 2 > 60 mm Hg, given his prolonged cardiac arrest (for both CNS and RV protection). The shunt physiology resolved approximately 10 hours after its onset, as evidenced by a PaO 2 > 200 mm Hg. (D) CTA showing multiple subsegmental pulmonary emboli evident in all lobes (globally L > R) with atelectasis and ground glass opacities diffusely (R > L). The absence of a saddle embolus, or obstructing thrombus in either main PA, suggests that the saddle emboli seen on the prearrest chest x-ray was fragmented and mechanically dislodged during CPR. Although this saved the patient’s life, it lead almost immediately to near fatal lung failure, which resolved in hours with supportive care, as intrinsic thrombolysis occurred and VQ matching improved. (E) Detailed highlight of the mechanisms of extreme VQ mismatch and dead space. The obstructed segments receive the majority of the ventilation but no perfusion (ie, they become physiologic dead space), whereas the unobstructed segments receive all of the perfusion but no ventilation (because they are prone to flow-related edema and inflammatory atelectasis).
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VTE diagnosis and risk stratification ( Fig. 15.2 )
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Diagnostic approach hinges on presenting signs and symptoms
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DVT (extremity) signs and symptoms occurring alone should be evaluated by ultrasound
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Unilateral lower extremity edema should be evaluated with bilateral lower extremity ultrasound
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May identify undetected clot burden by identifying a contralateral DVT that was not appreciated during the physical examination
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Demonstration of a DVT ends the VTE workup
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Patients with a DVT and no cardiopulmonary signs or symptoms can be presumed to have suffered small, asymptomatic pulmonary emboli (based on the pathophysiology of VTE disease)
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Because of this, DVT and asymptomatic pulmonary embolism are treated the same
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PE (cardiopulmonary) signs and symptoms occurring alone should be evaluated by CTA (ie, 1.25-mm chest CT with contrast timed for PA opacification)
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CTA is the preferred mode for PE evaluation because of its ability to provide an alternate diagnosis for the cardiopulmonary symptoms (eg, tumor, pneumonia)
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Major limitations to CTA for the diagnosis of PE (timing and artifact):
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Poorly timed contrast, which inadequately opacifies the pulmonary arteries, can lead to a false negative study
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Motion artifact with volume averaging (especially at the bases) and streak artifact can decrease intraluminal contrast opacification, leading to a false positive study
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An equivocal CTA should be followed up with a VQ scan (to minimize the risk of radiation exposure from repeating the CTA)
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Normal perfusion in an area that was equivocally opacified during CTA is very reassuring
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In those in whom CTA is contraindicated, or “relatively” contraindicated (eg, poor renal function), the VQ scan is the second-line modality for PE diagnosis:
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Made by identifying regions of the lung that demonstrate ventilation without perfusion (ie, unmatched perfusion defect)
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This separates PE from parenchymal disease that affects both ventilation and perfusion (ie, matched perfusion defect) via hypoxemic vasoconstriction
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VQ scan interpretation:
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High probability = two or more unmatched segmental perfusion defects
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Intermediate probability = one unmatched segmental perfusion defect
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Low probability = one matched segmental perfusion defect
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Very low probability = no segmental perfusion defects
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When clinical suspicion for PE is high, a low- or very low–probability VQ scan is required to suggest an alternate diagnosis
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PE (cardiopulmonary) signs and symptoms occurring with an edematous extremity is very suggestive of VTE
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The initial step should be an ultrasound examination of the abnormal extremity that looks for DVT (as well as the contralateral side for good measure)
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If a DVT is found, symptomatic PE is presumed (on clinical grounds)
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Urgent CTA or VQ scan to confirm the diagnosis of PE in this setting is not indicated
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VQ should eventually be done, at hospital discharge and/or shortly after therapy has begun, to establish an early “postinitiation of therapy” perfusion baseline (see initial management section)
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If no DVT is found, a CTA (or VQ scan if CTA is contraindicated) should be performed
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When PE is diagnosed, risk stratification by looking for evidence of RV strain or injury is required to establish the appropriate therapy
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PE kills by causing isolated RV failure:
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Pulmonary obstruction increases RV afterload
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As the RV fails to maintain CO, it dilates, increasing wall tension
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As wall tension increases, subendocardial perfusion decreases, leading to catastrophic RV ischemia and failure, causing sudden cardiac death
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RV strain, injury, or dysfunction is screened for by:
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ECG looking for right axis deviation and/or RV strain pattern (Q1, S3, flipped T3)
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Cardiac markers looking for RV ischemia (eg, troponins) and RV/RA dilation (eg, BNP)
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Echocardiogram looking for evidence of increased right-sided pressure/decreased RV function
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Patients with PE and hypotension, or signs of systemic hypoperfusion (eg, lactate production, prerenal indices), are in cardiogenic shock from isolated right-sided heart failure and have a high mortality from either worsening RV failure or recurrent embolism
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Dopamine is the inotrope of choice for isolated RV failure (based on expert clinical observations of efficacy)
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Ultimately, patients with VTE are divided into four categories:
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Asymptomatic/subclinical PE
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Every patient with a DVT
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Symptomatic PE
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Patients with PE and symptoms not caused by RV strain or injury (eg, tachypnea, pleuritic chest pain)
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These symptoms are caused by increased dead space, parenchymal atelectasis, and/or pleural involvement
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Submassive PE
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Patients with PE and evidence of RV strain, dysfunction, or injury without cardiogenic shock
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Massive PE
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Patients with PE and evidence of RV strain, dysfunction, or injury with cardiogenic shock
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Patients with submassive or massive PE need a bilateral LE ultrasound (if not already done) to risk stratify by screening for a residual clot
