Ebook Ebook Herzog’s CCU book: Part 2

(BQ) Part 2 book “Herzog’s CCU book” has contents: Acute aortic syndrome, pathway for the management of pericardial disease, infective endocarditis, percutaneous therapy for valvular heart disease, contemporary surgical approach to valvular disease, mechanical ventilation in the cardiac care unit,… and other contents.

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Acute Aortic Syndrome

INTRODUCTION

Acute aortic syndrome (AAS) represents a spectrum of life-threateningconditions with similar clinical presentation and the need for urgentmanagement It includes classic acute aortic dissection (CAAD),intramural hematoma (IMH), and penetrating aortic ulcer (PAU) Althoughnot included in the original definition of AAS, traumatic aortic rupture(TAR) and aortic aneurysm rupture have also been considered to be part ofthe AAS spectrum

AAS is characterized by disruption of the media layer of the aorta andtypically presents with acute chest pain The term “acute aortic syndrome”was first coined in 2001 by the Spanish cardiologists Vilacosta and SanRomán, who described AAS as a spectrum of interlinked lesions1 with theintent to increase awareness and to speed up diagnosis and appropriate

treatment (Figure 32.1).

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FIGURE 32.1 Acute aortic syndrome The acute aortic syndrome triad first

described by Vilacosta and San Román Arrows signify possible progression of aortic lesions (penetrating aortic ulcer to IMH, penetrating aortic ulcer to classic dissection, IMH to classic dissection) IMH, intramural hematoma.

Although the incidence of AAS is lower than that of acute coronarysyndrome (ACS), AAS carries a higher mortality, and is therefore a criticalcomponent of the differential diagnosis of chest pain in the Cardiac CareUnit (CCU) Overall incidence of AASs is 2 to 4 cases per 100,000individuals Because AAS is rare, the International Registry of AcuteAortic Dissection (IRAD) was created in 1996 as a way to combine dataacquired from multiple top institutions in Europe, North America, andAsia.2 The 2010 intersocietal guidelines for the diagnosis and management

of patients with thoracic aortic disease proposed a standard approach to thediagnosis and treatment of AAS.3

Although clinical history and physical examination are important,imaging is essential in the diagnosis of AAS Transesophagealechocardiography (TEE), computed tomography (CT), and magneticresonance imaging (MRI) are the preferred imaging modalities andangiography is rarely needed

CLASSIFICATION OF ACUTE AORTIC SYNDROMES

Historically, CAAD was the first recognized form of AAS The

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classification schemes used for the classic aortic dissection weresubsequently extended to include IMH and PAU.

AASs are classified on the basis of the location and extent ofinvolvement of the aorta Two systems have been proposed, the DeBakey

and the Stanford systems (Figure 32.2) The DeBakey system, which was

proposed in 1965 by the Lebanese-American surgeon Michael EllisDeBakey, divided aortic dissection into three types based on the anatomiclocation Type I originates in the ascending aorta and propagates beyondthe aortic arch, type II is limited to the ascending aorta only, and type III islimited to the descending aorta.4

FIGURE 32.2 DeBakey and Stanford classifications Left: DeBakey classification

of aortic dissection Type I includes the ascending and descending aorta, type II includes the ascending aorta only, and type III includes the descending thoracic aorta only (DeBakey ME, Henly WS, Cooley DA, et al Surgical management of

dissecting aneurysms of the aorta J Thorac Cardiovasc Surg 1965;49:130-149.)

Right: Stanford classification Type A aortic dissection involves the ascending thoracic aorta, and type B involves the descending thoracic aorta only All three AAS conditions; CAAD, IMH, and PAU use the Stanford classification CAAD, classic acute aortic dissection; IMH, intramural hematoma; PAU, penetrating aortic ulcer (Daily PO, Trueblood HW, Stinson EB, et al Management of acute aortic

dissections Ann Thorac Surg 1970;10[3]:237-247.)

The Stanford system, which was created by researchers at StanfordUniversity in 1970, divides aortic dissections into two types Type Aincludes any dissection that involves the ascending aorta, whereas type Bdissections are limited to the descending thoracic aorta.5 The Stanfordclassification appears to have wider acceptance and is now used for all

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three AAS types: CAAD, IMH, and PAU.

INTRAMURAL HEMATOMA

IMH is defined by crescentic or circumferential thickening of the medialayer of the aortic wall IMH is likely due to a ruptured vasa vasorumresulting in intramural bleeding but without a detectable intimal tear Itwas first described in 1920 by the German pathologist Ernst Kruckenberg,who is also well known for his description of the so-called Kruckenbergtumors (transperitoneal ovarian metastases from stomach and coloncancers) On TEE, CT, or MRI, IMH is typically visualized as a crescentic

or concentric thickening of the aortic wall > 5 mm (Figure 32.3) The

natural history of IMH often includes progression to CAAD, whichaccounts for its high morbidity and mortality

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FIGURE 32.3 Intramural hematoma: CT CT of the chest shows the descending

thoracic aorta The crescentic-shaped lesion on the patient’s left signifies an IMH (dashed arrows) CT, computed tomography; IMH, intramural hematoma.

Etiology and Pathophysiology

IMH may account for up to 6% to 30% of all AAS, with a higher reportedprevalence among the Korean and Japanese populations as compared withWestern subjects.6 It is unclear whether this is a true discrepancy inprevalence versus a reflection of differing classification, evaluation, ortreatment practices Often, IMH is diagnosed as such even though verysmall intimal tears indicative of limited aortic dissection may be presentbut missed by modern imaging modalities This may overestimate the true

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prevalence of IMH as opposed to CAAD.

The characteristic feature of IMH is its location in the portion of themedia closer to the adventitia, as opposed to CAAD which is typicallylocated in the media closer to the intima Although the most citedhypothesis of the pathophysiologic mechanism of IMH is rupture of thevasa vasorum, there is very little corroborating clinical or experimentalevidence Owing to the low incidence of IMH and the close associationwith CAAD, a definitive etiology still remains unclear.7

Diagnosis

As with all types of AAS, rapid diagnosis is paramount in IMH TEE, CT,and MRI are the preferred diagnostic tools CT is often chosen because ofwidespread availability, rapid acquisition, and its ability to diagnose othercauses of acute chest pain such as trauma and pulmonary embolism

Classically, absence of an intimal flap or tear differentiates IMH fromCAAD Often, IMH can be identified even on non–contrast-enhanced CT

On contrast CT scans, a crescentic or circular area of high attenuation thatdoes not enhance with contrast is present Similar findings are seen onMRI, which has the advantage of not requiring iodinated contrast

On TEE, IMH is diagnosed if there is regional thickening of the aorticwall > 5 mm in a crescentic or circumferential pattern without an intimal

flap or tear (Figure 32.4A, B) Limitations of TEE in diagnosing IMH

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arise from the TEE’s inability to visualize all portions of the aortaincluding the area around the origin of the brachiocephalic artery and allbut the most proximal portions of the abdominal aorta TEE is very useful

in diagnosing complications of IMH, such as pericardial effusion or aorticregurgitation

FIGURE 32.4 Intramural hematoma: TEE Two-dimensional (2D) TEE of the

ascending thoracic aorta in the long-axis (A) and short-axis (B) views Yellow arrows point to a crescentic thickening of the anterior portion of the ascending thoracic aortic wall, consistent with a type A IMH IMH, intramural hematoma; TEE, transesophageal echocardiography.

Small intimal tears may be missed by any modern imaging technique,challenging the diagnosis of classic IMH

Management and Prognosis

The prognosis of IMH is somewhat better than that of CAAD As in allAAS, the main determinant of prognosis is its aortic location According tothe IRAD registry, the mortality of type A IMH is approximately 27%,compared with 4% in type B IMH Invasively managed patients with type

A IMH typically fare better than medically managed patients Invasiveoptions include open surgical repair and percutaneous thoracicendovascular aortic repair Medical management typically consists of heartrate (HR), blood pressure, and pain control Surgical mortality for IMH issimilar to that for other forms of AAS

Type B IMH is often managed medically Approximately 50% of type Bpatients may improve with medical management alone, 15% will remain

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stable, and 35% may progress to aneurysm formation, CAAD, or focalaortic rupture (pseudoaneurysm).10

Intramural Hematoma in Pregnancy

Although there are no specific guidelines in pregnancy for patients withIMH, pregnancy is considered a risk factor for the development of aorticpathology, especially in Marfan syndrome As with other forms of AAS,expedited delivery via caesarian section is considered reasonable forpregnant patients with acute IMH, if possible

CLASSIC ACUTE AORTIC DISSECTION

CAAD is the most common form of AAS.2 It occurs in approximately66% to 75% of all AAS The overall incidence of CAAD is low, estimated

at 0.5 to 4.0 cases per 100,000 per year, and is thought to affect men morethan women in a 2:1 ratio

Risk factors for CAAD include connective tissue disorders such as

Marfan (fibrillin gene), Loeys–Dietz (transforming growth factor β

receptor 1 and 2 genes), Ehlers–Danlos type 4 (collagen gene), and Turnersyndrome (X monosomy), as well as the aortopathy associated with

bicuspid aortic valve (NOTCH1 gene) In addition, hypertension is a

significant risk factor and is more prevalent among older patients Last,aortic instrumentation or surgery, as well as cardiac catheterization, arerare but reported causes of aortic dissection

CAAD was first described in 1555 by Andreas Vesalius (1514–1564)who reported traumatic abdominal aortic aneurysm in a man who fell off ahorse.11 Intimal tear, the hallmark of CAAD, was first described by DanielSennert (1572–1637), a German anatomist and published in 1650posthumously.12 A very famous description of CAAD was by the Britishroyal physician Frank Nichols (1699–1778) who provided the firstunmistakable account of CAAD (deemed a “Transverse fissure of theaortic trunk”) in his autopsy of King George II, who died in 1760 whilestraining in the lavatory Successful surgical repair of descending aorticdissection was not reported until 1955, by Michael Debakey (1908–2008)and his colleagues, and ascending dissection until 1962 by Frank Spencerand Hu Blake.13,14

Etiology and Pathophysiology

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CAAD is characterized by an intimal tear, which leads to abnormal blood

flow from the aortic lumen into the media (Figure 32.5) Consequently,

there is a longitudinal separation of the media layers by the blood flow,which tears an intimomedial flap from the remainder of the aortic wall

(Figure 32.6A–C) This flap separates the abnormal false lumen from the

true aortic lumen Intimal tears typically occur at the locations within theaorta with the highest shear stress These are at the right side of theascending aorta immediately distal to the ostium of the right coronaryartery (type A dissections) and immediately distal to the ostium of thesubclavian artery adjacent to the insertion of the ligamentum arteriosus(type B dissections)

FIGURE 32.5 Classic acute aortic dissection: entry point on TEE

Two-dimensional (2D) TEE with color Doppler of the aortic arch in the upper esophageal view Yellow arrow points to the entry point of flow from the true lumen to the false lumen, characteristic of CAAD CAAD, classic acute aortic dissection; FL, false lumen; TEE, transesophageal echocardiography; TL, true lumen.

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FIGURE 32.6 Classic acute aortic dissection: CT Multidetector row CT with

intravenous iodinated contrast in the axial view (A), sagittal view (B), and the coronal view (C) Yellow arrows point to dissection flap at the junction of the aortic arch and descending thoracic aorta, consistent with CAAD CAAD, classic acute aortic dissection; CT, computed tomography.

Complications such as aortic regurgitation and pericardial tamponadecan occur; and, over time, chronic changes such as false lumen thrombosisand aneurysm are common

Clinical Manifestations

The typical symptom of acute aortic dissection is “aortic pain” similar toother forms of AAS Acute, severe, tearing chest pain is the hallmark

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symptom of CAAD Pain limited to the chest is typical of type A CAAD,and pain in the back is more often the symptom of type B CAAD Onestudy found older patients are less likely to abrupt onset of pain ascompared with younger patients.15

Pulse deficit, present in up to 33% of patients according to the IRADstudy, reflects impaired or absent blood flow to peripheral vessels This ismanifested by weak carotid, brachial, or femoral pulses on physicalexamination

Other physical examination findings of CAAD include diastolic murmur

or aortic regurgitation, hypotension related to either tamponade or aorticrupture, focal neurologic deficits reflecting propagation of the dissectiontoward involvement of carotid or cerebral arteries, and syncope

Electrocardiogram (ECG) may be useful in distinguishing the chest pain

of AAS from ACSs; unlike ACS, uncomplicated CAAD does not presentwith ischemic ECG changes However, if the aortic dissection leads tocoronary ischemia through involvement of coronary ostia (type A), theECG will be less helpful with differentiation of symptoms

Chest X-ray (CXR) imaging occasionally shows widening of themediastinum, a nonspecific finding seen with other syndromes such asmediastinal hematoma Other CXR findings are double aortic knob (40%

of patients), tracheal displacement to the right, and enlargement of thecardiac silhouette

Serum biomarkers such as D-dimer are often elevated in CAAD, but this

is a nonspecific finding In contrast, a normal D-dimer level may helpexclude the diagnosis of CAAD Investigational biomarkers such as elastindegradation products, calponin, fibrinogen, fibrillin, and smooth musclemyosin heavy chain are currently being evaluated

CT with intravenous iodinated contrast is often the diagnostic modality

of choice for CAAD because of its superb spatial resolution, rapidacquisition times, widespread availability, and its ability to diagnose othercauses of acute chest pain such as trauma and pulmonary embolism The

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reported sensitivity of CT for CAAD is 87% to 94% and specificity is 92%

to 100% CT features of CAAD are intimal tear, dissection flap with a trueand false lumen, dilatation of the aorta, and pericardial effusion

TEE is especially useful in the diagnosis of CAAD when a CT withcontrast cannot be performed, such as in hemodynamically unstablepatients or in patients in whom the risk of iodinated intravenous contrast ishigh such as renal insufficiency or severe allergy The reported sensitivity

of TEE is 98% and specificity is 63% to 93% Findings on TEE are adissection flap separating the true and false lumen, site of intimal tearrepresented by flow from the true lumen into the false lumen on color

Doppler (Figure 32.7) Spectral Doppler may help corroborate the

diagnosis by demonstrating “to and fro” flow into and out of the falselumen

FIGURE 32.7 Classic acute aortic dissection: dissection flap on TEE

Two-dimensional (2D) TEE of the ascending thoracic aorta in short axis (A) and long axis (B) demonstrating CAAD In this case, the dissection flap is circumferential with a 360° separation of the true and false lumens CAAD, classic acute aortic dissection; FL, false lumen; TEE, transesophageal echocardiography; TL, true lumen.

The true lumen is identified by its expansion with systole andcontraction in diastole The true lumen is often smaller than the falselumen In early stages, the false lumen may be echo free or may containspontaneous echo contrast (also known as “smoke”) due to stasis of bloodflow In later, more chronic stages, the false lumen may be partly orcompletely obliterated by thrombus formation

Complications of CAAD may be seen on echocardiography such asaortic regurgitation, pericardial effusion/tamponade, and wall motion

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abnormalities indicative of ischemia if there is coronary ostialinvolvement.

It is important not to confuse the intimomedial flap of CAAD witheither artifacts or surrounding vascular structures Linear reverberationartifacts in the ascending aorta should not be mistaken for type A aorticdissection Typically, reverberation artifacts are located twice as deep asthe anterior aortic wall In addition, a dilated azygos vein adjacent to thedescending thoracic aorta may give an illusion of a type B dissection.Color or spectral Doppler imaging in both instances may help distinguish

true aortic dissection from its masqueraders (Figure 32.8).

FIGURE 32.8 Reverberation artifact masquerading as type A dissection on TEE.

Two-dimensional (2D) TEE of the ascending thoracic aorta in a long-axis view (A) and a short-axis view (B) Red arrows point to linear reverberation artifact Note that the reverberation artifact is located twice as deep (2×) as the anterior aortic wall, characteristic of reverberation artifacts TEE, transesophageal echocardiography.

Although on transthoracic echocardiography (TTE) aortic dissection canoccasionally be seen, TTE should only be used as a screening tool owing

to lack of sufficient sensitivity and specificity

MRI and aortography also may reveal aortic dissection; however, theyare reserved for specific situations MRI may be used when the patientcannot receive iodinated contrast for CT nor undergo TEE Aortography is

of limited use and is typically performed during invasive endovasculartherapeutic procedures

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Management and Prognosis

Type A CAAD is a true medical emergency, requiring immediate surgicalrepair because the mortality increases by the hour Approximately 90% ofmedically managed patients with type A CAAD die within 3 months ofpresentation On the other hand, the prognosis is more favorable forpatients with type B CAAD in whom medical management is oftenpreferred over surgical repair because surgically managed patients havebeen shown to have higher mortality compared with those on medicaltherapy alone Medical therapy generally consists of tight blood pressure

control and β-blockade Surgical management of type A CAAD typically

consists of excision of the intimal tear if possible and obliteration of entryinto the false lumen, as well as implantation of a graft to replace theascending aorta.16 Surgical therapy for type B is more complicatedbecause of the presence of many spinal artery branches, and therefore has

a risk of paraplegia Nevertheless, surgical therapy of type B dissection isoften necessary when there is aortic branch ischemia and end-organdamage Endovascular graft therapy to treat type B CAAD has shown

promise (Figure 32.9).17

FIGURE 32.9 Endovascular graft repair: 3D CT Three-dimensional (3D)

reconstruction of contrast-enhanced chest CT in a sagittal view (A) and coronal view with surrounding structures removed (B) demonstrating an endovascular stent graft located between the junction of the aortic arch and descending thoracic aorta, extending to the distal descending thoracic aorta CT, computed tomography.

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It is important to identify risk factors for higher mortality in type ACAAD such as advanced age, prior cardiac surgery, hypotension or shock,pulse deficit, cardiac tamponade, and ischemic ECG changes.

Classic Acute Aortic Dissection in Pregnancy

The 2010 intersocietal guidelines for the diagnosis and management ofpatients with thoracic aortic disease recommends expedited fetal deliveryvia caesarian section for patients with CAAD during pregnancy given thehigh mortality of the disease (class IIa recommendation) The diagnosticimaging modality of choice is MRI without gadolinium to avoid exposingthe mother and fetus to ionizing radiation.18 TEE is an option and isconsidered safe in pregnancy; however, caution must be used whenproviding procedural sedation because the medications typicallyadministered (midazolam and fentanyl) may be teratogenic, especially inthe first trimester In these cases, topical anesthesia with viscous lidocaine

is crucial There have been reports recommending monitoring fetal HR anduterine tone during TEE.19

PENETRATING AORTIC ULCER

PAU represents the process by which an atherosclerotic plaque erodes andpenetrates through the elastic lamina into the media layer of the aorta,

causing ulceration (Figure 32.10) PAU may further erode through the

adventitia leading to either focal (pseudoaneurysm) or complete aortic

rupture (Figure 32.11) Thrombus occasionally forms within PAU In

addition, PAU may lead to either IMH or aortic dissection, which is whyPAU is characterized as an AAS

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FIGURE 32.10 Penetrating aortic ulcer: TEE Two-dimensional (2D) TEE of the

descending thoracic aorta in the midesophageal short-axis view (A) and long-axis view (B) Yellow arrows point to demonstrating severe atherosclerotic plaque and PAU; yellow dashed arrows point to an area with developing IMH IMH, intramural hematoma; PAU, penetrating aortic ulcer; TEE, transesophageal echocardiography.

FIGURE 32.11 Penetrating aortic ulcer with rupture/pseudoaneurysm visualized

by contrast-enchanced 2D (A) and 3D CT (B) Arrows point to PAU with aortic rupture and pseudoaneurysm of anterior portion of the proximal descending thoracic aorta CT, computed tomography; PsA, pseudoaneurysm.

Etiology and Pathophysiology

PAU accounts for 2% to 11% of all AASs.20,21 It was first described in

1986 by Anthony Stanson and colleagues.22 Patients with PAU typicallyare older (>70 years old) and have risk factors for atherosclerosis includinghypertension, smoking, and hyperlipidemia

The natural history of PAU is not well described PAU may causeremodeling of the aortic wall and aneurysm formation, contained rupturethrough the aortic wall and attendant pseudoaneurysm formation, completeaortic rupture with mediastinal or pleural hemorrhage, or progression toIMH and CAAD

Clinical Manifestations

Symptoms of PAU are similar to that of other AASs The pain associated

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with PAU is variable, and dependent on the location of the ulceration.Type A PAU typically presents with chest pain and type B PAU is morelikely to present with back pain Unlike IMH or CAAD, there have beenreports of PAU as an incidental finding in asymptomatic patients.

Diagnosis

The diagnosis of PAU is primarily made by CT, TEE, and MRI.Aortography is not typically used for PAU because of lack of directvisualization of the aortic wall All three techniques are able to imageatherosclerotic changes, ulceration, and complications such aspseudoaneurysm, rupture, and mediastinal and pleural hemorrhage.Identification of an ulcer crater distinguishes PAU from IMH PAU lesionsare typically focal as opposed to those of CAAD and IMH, which are moreextensive

Management and Prognosis

The natural history of PAU is poorly understood On one hand, PAU isconsidered to be a surgical emergency with risk similar to or worse thanother forms of AAS On the other, reports have described the progression

of PAU as slow, with a low prevalence of life-threatening complications.23There is therefore equipoise regarding the optimal medical versus surgicaltreatment strategies Nevertheless, surgical management of PAU withaortic grafting is considered appropriate in the presence of aortic rupture,persistent or recurrent pain, hemodynamic instability, or rapidly expandingaortic diameter

Penetrating Aortic Ulcer in Pregnancy

Because PAU is a disease that primarily affects older people (>70 years ofage), it is highly unlikely that it will occur during pregnancy There istherefore no available guideline to direct optimal management

TRAUMATIC AORTIC RUPTURE

Although TAR is not considered to be a part of the original AAS triad, it is

a life-threatening aortic emergency with only a 15% to 20% survival.24TAR is typically caused by deceleration injuries sustained in motor vehicleaccidents (MVAs) and falls greater than 3 m.25 It is the second leadingcause of death after blunt trauma, occurring in approximately 1.5% to

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1.9% cases.26

Etiology and Pathophysiology

The most common site of injury in TAR is at the aortic isthmus,immediately distal to the left subclavian artery at the site of the ductusarteriosus This location is considered to be the most vulnerable totorsional and shear forces because it is thought to be a transition zonebetween the semi-mobile aortic arch and the fixed descending thoracicaorta Other possible sites of injury are the transverse arch, ascendingaorta, and descending aorta proximal to the diaphragm.27 Typically, theintima and medial layers rupture first, followed by rupture of the adventitiaafter an unpredictable interval of time.28 Multiple tears may occur

Clinical Manifestations

There is no specific symptom associated with TAR Chest pain in thepatient with trauma should, however, raise suspicion, especially in thepresence of the “seat belt sign” (seat belt imprint on the surface of theskin) Pulse deficit and murmur of aortic regurgitation may be present.CXR may show a widened mediastinum, obscured aortic knob, and lefthemothorax

Diagnosis

TAR is best diagnosed using either contrast-enhanced CT or TEE because

both modalities have high diagnostic sensitivity and specificity (Figure

32.12) Findings seen on CT include intimal flap, periaortic hematoma,

luminal filling defects, pseudoaneurysm, or active extravasation of contrastfrom the aorta It is important to distinguish TAR from a ductus arteriosusdiverticulum, which is helped by the improved special and temporalresolution of modern multidetector row CT scanners However, TEE may

be more specific in differentiating ductus arteriosus diverticula from TAR.Another very useful advantage of TEE is its portability, with the ability to

be performed at the bedside of hemodynamically unstable patients, acommon scenario in TAR The main limitation of TEE is an apparent

“blind spot” at the distal ascending aorta and proximal aortic arch caused

by bronchial shadowing Aortography, the former gold standard, may beperformed; however, it is invasive and can result in worsening of the aorticrupture in as many as 10% of patients and is therefore not the preferred

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diagnostic modality.

FIGURE 32.12 Traumatic aortic rupture CT of the chest with iodinated contrast,

coronal view (A), and TEE upper esophageal view (B) of the aortic arch Arrows point to traumatic aortic rupture Note that the TEE image was rotated to align with the CT image CT, computed tomography; TAR, traumatic aortic rupture; TEE, transesophageal echocardiography.

Management and Prognosis

Emergent surgical therapy is the standard of care for TAR As with AAS,medical therapy consists of very close blood pressure and HR control.Hemodynamically unstable patients should be operated on immediately.Surgical options comprise open repair with prosthetic grafts, andendovascularly delivered fabric-covered stents Endovascular repair hasbeen shown to have decreased overall mortality compared with surgicalrepair and is recommended when possible The overall survival of TAR isapproximately 10% to 18% Survival to emergency room care greatlyimproves the odds of long-term survival, and survival to surgical therapyimproves the odds even more, to approximately 70% to 90%.29

Traumatic Aortic Rupture in Pregnancy

Although there are no specific guidelines for the management of TAR inpregnancy, expedited delivery via caesarian section with emergent aorticsurgery is a reasonable therapeutic approach given the high mortality both

to the mother and fetus

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1 Vilacosta I, San Román JA Acute aortic syndrome Heart 2001;85:365-368.

2 Hagan PG, Nienaber CA, Isselbacher EM, et al The International Registry of

Acute Aortic Dissection (IRAD): new insights into an old disease JAMA.

2000;283:897-903.

ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease A Report

of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine.

J Am Coll Cardiol 2010;55:e27-e129.

4 DeBakey ME, Henly WS, Cooley DA, Morris GC Jr, Crawford ES, Beall AC

Jr Surgical management of dissecting aneurysms of the aorta J Thorac Cardiovasc Surg 1965;49:130-149.

5 Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE.

Management of acute aortic dissections Ann Thorac Surg

1970;10(3):237-247.

6 Harris KM, Braverman AC, Eagle KA, et al Acute aortic intramural

hematoma: an analysis from the International Registry of Acute Aortic

Dissection Circulation 2012;126:S91-S96.

7 Goldberg JB, Kim JB, Sundt TM Current understandings and approach to the

management of aortic intramural hematomas Semin Thorac Cardiovasc Surg.

2014;26:123-131.

8 Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K Clinical features and

long-term outcome of type A and type B intramural hematoma of the aorta J Thorac Cardiovasc Surg 2004;127:421-427.

9 Tittle SL, Lynch RJ, Cole PE, et al Midterm follow-up of penetrating ulcer

and intramural hematoma of the aorta J Thorac Cardiovasc Surg.

2002;123:1051-1059.

10 Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA.

Acute aortic dissection and intramural hematoma: a systematic review JAMA.

2016;316:754-763.

11 O’Malley CD Andreas Vesalius 1514–1564: In Memoriam Med Hist.

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12 Sennertus D Cap 42 Op Omn Lib 1650;5:306-315.

13 De Bakey ME, Cooley DA, Creech O Jr Surgical considerations of dissecting

aneurysm of the aorta Ann Surg 1955;142:586-610; discussion 611-612.

14 Spencer FC, Blake H A report of the successful surgical treatment of aortic

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regurgitation from a dissecting aortic aneurysm in a patient with the Marfan

syndrome J Thorac Cardiovasc Surg 1962;44:238-245.

15 Pape LA, Awais M, Woznicki EM, et al Presentation, diagnosis, and

outcomes of acute aortic dissection: 17-year trends from the International

Registry of Acute Aortic Dissection J Am Coll Cardiol 2015;66:350-358.

16 Braverman AC Acute aortic dissection: clinician update Circulation.

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17 Nienaber CA, Kische S, Rousseau H, et al Endovascular repair of type B

aortic dissection: long-term results of the randomized investigation of stent

grafts in aortic dissection trial Circ Cardiovasc Interv 2013;6:407-416.

ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: executive summary A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for

Vascular Medicine Catheter Cardiovasc Interv 2010;76:E43-E86.

19 Stoddard MF, Longaker RA, Vuocolo LM, Dawkins PR Transesophageal

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20 Hirst AE Jr, Johns VJ Jr, Kime SW Jr Dissecting aneurysm of the aorta: a

review of 505 cases Medicine 1958;37:217-279.

21 Eggebrecht H, Plicht B, Kahlert P, Erbel R Intramural hematoma and

penetrating ulcers: indications to endovascular treatment Eur J Vasc Endovasc Surg 2009;38:659-665.

22 Stanson AW, Kazmier FJ, Hollier LH, et al Penetrating atherosclerotic ulcers

of the thoracic aorta: natural history and clinicopathologic correlations Ann Vasc Surg 1986;1:15-23.

23 Hayashi H, Matsuoka Y, Sakamoto I, et al Penetrating atherosclerotic ulcer of

the aorta: imaging features and disease concept Radiographics

2000;20:995-1005.

24 Fabian TC, Richardson JD, Croce MA, et al Prospective study of blunt aortic

injury: multicenter trial of the American Association for the Surgery of

Trauma J Trauma 1997;42:374-380; discussion 380-383.

25 Sanchez-Ross M, Anis A, Walia J, et al Aortic rupture: comparison of three

imaging modalities Emerg Radiol 2006;13:31-33.

26 Dyer DS, Moore EE, Ilke DN, et al Thoracic aortic injury: how predictive is

mechanism and is chest computed tomography a reliable screening tool? A

prospective study of 1,561 patients J Trauma 2000;48:673-682; discussion

682-683.

27 Sevitt S The mechanisms of traumatic rupture of the thoracic aorta Br J Surg.

1977;64:166-173.

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28 Nikolic S, Atanasijevic T, Mihailovic Z, Babic D, Popovic-Loncar T.

Mechanisms of aortic blunt rupture in fatally injured front-seat passengers in

frontal car collisions: an autopsy study Am J Forensic Med Pathol.

2006;27:292-295.

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Patient and Family Information for:

ACUTE AORTIC SYNDROME

GENERAL CONCEPTS OF ACUTE AORTIC SYNDROME

WHAT IS THE ILLNESS?

AAS refers to four related diseases of the large vessel that leaves the heart,called the aorta These are CAAD, IMH, PAU, and TAR These conditionsinvolve damage to the wall of the aorta and require prompt care becausethey are associated with a high chance of dying unless treated rapidly

HOW WILL THE PATIENT BE TREATED?

Once the diagnosis of AAS is established by CT, TEE, or MRI, the disease

is typically treated with mediations that lower blood pressure and HR Thedoctor will determine the type of AAS (type A or type B) based on thelocation of involvement in the aorta A cardiothoracic surgeon may beconsulted, who will assess the need for surgery Surgery is often needed assoon as possible

WHAT IF THE PATIENT IS PREGNANT OR THINKING OF

INTRAMURAL HEMATOMA

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WHAT IS THE ILLNESS?

IMH is described as bleeding into the wall of the aorta due to breakage ofthe internal blood vessels of the aorta Symptoms of IMH are suddensevere chest or back pain IMH is best diagnosed by imaging the aortausing CT, TEE, or MRI On experiencing symptoms suggestive of IMH,the patient or a family member should seek medical care immediatelybecause the risk of dying from this condition increases by the hour

HOW WILL THE PATIENT BE TREATED?

Once the diagnosis of IMH is established, medications will be given toreduce the blood pressure and HR A cardiothoracic surgeon may beconsulted, who will assess the need for surgery Surgery will often involveeither replacement of the diseased portions of the aorta or placement ofspecial type of stent within the aorta that will help contain the bleeding andprevent the aorta from bursting

WHAT IF THE PATIENT IS PREGNANT OR THINKING OF

BECOMING PREGNANT?

IMH carries a high risk of mortality, and often requires emergencysurgery The doctor will tailor the medications for IMH to include onlythose with minimal risk to the baby If the pregnant patient or familymember requires emergency surgery, expedited delivery is prudent Rapidconsultation with an obstetrician is crucial If the person has a conditionthat puts her at risk for IMH such as Marfan syndrome or other geneticdisorders of the aorta, consult the doctor to assess the risk if thinking aboutbecoming pregnant

CLASSIC ACUTE AORTIC DISSECTION

WHAT IS THE ILLNESS?

CAAD is the most common type of AAS It is caused by a tear of the innerlayer of the aorta, called the intima This tear can then propagate, leading

to separation of the layers of the aorta There are hereditary disorders such

as Marfan syndrome and bicuspid aortic valve that may put the person or afamily member at risk of CAAD because of weakening of the aortic wall.Symptoms typically experienced are severe “tearing” chest or back pain

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that occurs at rest If the person or a family member experiences suchsymptoms, seek medical care immediately.

CAAD will be diagnosed using CT, TEE, or MRI, which are widelyavailable and can be performed and interpreted rapidly

HOW WILL THE PATIENT BE TREATED?

As with other types of AAS, the doctor will prescribe medications thatlower blood pressure and HR A cardiothoracic surgeon may be consultedimmediately, who will assess the need for surgery The location of thedissection is a crucial component in deciding what the best treatment is.Surgical options are open heart surgery or placement of a tube called stent.The cardiothoracic surgeon will assess which procedure is the mostappropriate

WHAT IF THE PATIENT IS PREGNANT OR THINKING OF

BECOMING PREGNANT?

As with other types of AAS, CAAD is often a surgical emergency Assuch, consultation with an obstetrician and expedited delivery may berecommended If the patient or a family member has a disorder thatinvolves the aorta, consult the obstetrician before deciding to conceive

PENATRATING AORTIC ULCER

WHAT IS THE ILLNESS?

Atherosclerosis or hardening of the arteries is a disease in whichcholesterol and fat build up within the walls of the blood vessels calledarteries PAU is caused when a very severe plaque breaks through theaorta, causing a hole, or ulceration Risk factors for PAU include advancedage, high blood pressure, high cholesterol, and smoking Symptomsinclude chest and back pain, although some patients may have nosymptoms

Along with other forms of AAS, PAU is diagnosed by CT, TEE, orMRI

HOW WILL THE PATIENT BE TREATED?

The doctor may recommend close monitoring with imaging studies,

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TRAUMATIC AORTIC RUPTURE

WHAT IS THE ILLNESS?

TAR describes tearing of the aorta after a chest injury It most commonlyoccurs after MVAs and bad falls

TAR is a very dangerous condition and requires prompt medicalattention A mark across the skin of the chest due to a seat belt often ispresent when TAR is caused by an MVA TAR is diagnosed using CT andTEE

HOW WILL THE PATIENT BE TREATED?

Emergency surgery is the standard of care for TAR The doctor mayprescribe medications to lower HR and blood pressure if necessary;however, a cardiothoracic surgeon may be consulted as soon as possible.Treatment typically requires open heart surgery

WHAT IF THE PATIENT IS PREGNANT OR THINKING OF

Pericardial Effusion and

Tamponade

INTRODUCTION

Pericardial effusion is a relatively common finding in high-risk patientsevaluated in the acute setting.1 It should be considered in differentialdiagnosis for a variety of clinical presentations including chest pain,shortness of breath, and hypotension.1 Pericardial effusion can be directlycausal for patients’ complaints (like in patients with pericardialtamponade) or be an incidental finding still carrying a prognosticsignificance (like in patients with pulmonary hypertension) The generalapproach to pericardial effusion once it is recognized includes establishingthe cause of pericardial disease and assessing its hemodynamicsignificance

RECOGNIZING THE PRESENCE OF PERICARDIAL

EFFUSION

Pericardial effusion can be recognized on the basis of clinical suspicion or

it can be an incidental finding on chest or cardiac imaging.2 The followingclinical settings may indicate the need to specifically evaluate for the

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presence of pericardial effusion3:

1 Cardiac arrest with pulseless electrical activity or asystole

2 Chest discomfort and/or any signs of hemodynamic instability in chest

trauma, recent cardiac surgery, or percutaneous cardiac intervention

3 Any of the following when otherwise unexplained: chest pain, fever,

dyspnea, and elevated cardiac biomarkers

4 Physical and electrocardiographic findings attributable to pericardial

disease; the latter includes tachycardia, low voltage, and electrical

alternans (Figure 33.1)

5 Enlarged cardiac silhouette or pleural effusions on chest X-ray

6 Any patient with ascending aortic dissection, severe pulmonary

hypertension, renal failure, use of some medications, rheumaticdiseases, malignancy, or other systemic conditions when pericardialeffusion is thought to contribute to presentation or have prognosticsignificance3

FIGURE 33.1 Electrocardiogram in a patient with large pericardial effusion.

Electrical alternans is evident in multiple leads including V1and V5 ECG, electrocardiogram.

Echocardiography is the most commonly used modality to diagnosepericardial effusion: owing to its accuracy and portably, it can be easilyused in any health care setting including bedside in an acutely ill patient

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Other modalities (such as computed tomography [CT] scan or cardiacmagnetic resonance) can be occasionally used to diagnose pericardialeffusion, especially when echocardiographic examination is limited ornondiagnostic.4

ESTABLISHING THE CAUSE OF PERICARDIAL

EFFUSION

There is a long list of possible causes for pericardial effusion (Table 33.1),

but a limited number of etiologies account for the majority of diagnoses.5

A structured approach helps establish the cause of pericardial effusion inmost cases.6 A very aggressive approach, as is used in some studies, has ahigh diagnostic yield but low clinical relevance, especially for smalleffusions.7,8 Routine sampling of pericardial fluid for diagnostic purposes

is unnecessary.3 History and physical examination often provide clues tothe etiology of pericardial effusion For example, the pericardium can beinvolved in patients with active systemic malignancy, and malignanteffusion should be strongly considered in these patients Active or recentinfection, radiation therapy, rheumatic disease, and recent acute coronarysyndrome, cardiac surgery, or percutaneous cardiac procedure, all providerelevant clues to etiology A typical clinical presentation, physicalfindings, and electrocardiographic changes commonly confirm thediagnosis of acute idiopathic pericarditis.9 In one study, the presence of

“inflammatory” signs (characteristic chest pain, pericardial friction rub,fever, and/or diffuse ST-segment elevation) in patients with pericardialeffusion was strongly associated with acute idiopathic pericarditis.10

TABLE 33.1 Causes of Pericardial Effusion

Neoplastic (typically secondary)

Perimyocardial infarction and postcardiotomy syndrome

Pulmonary hypertension and right-sided heart failure

Radiation

Renal failure

Rheumatic/autoimmune diseases

Traumatic (chest injury, procedure, surgery)

We use a parsimonious stepwise approach to laboratory testing and

imaging in patients with pericardial effusion at our institution (Figure

33.2).6 Transthoracic echocardiography is the standard test in establishingthe presence of pericardial effusion, quantifying the size of the effusionand assessing its hemodynamic impact The initial tier of testing includescomplete blood count, complete metabolic panel, coagulation studies,inflammatory markers (erythrocyte sedimentation rate, C-reactive protein),cardiac biomarkers, thyroid stimulating hormone level, and chest X-ray Inappropriate clinical settings, human immunodeficiency virus (HIV)testing, autoantibodies, and blood cultures are obtained Advanced chestimaging (CT scan, positron emission tomography, and magnetic resonanceimaging) can be helpful in certain clinical situations, especially whenmalignancy is suspected Besides, CT scan and cardiac magneticresonance can be used as adjunct imaging modalities for assessingpericardial effusion in some patients.4 They offer precise effusionlocalization, quantification, and tissue characterization, which areespecially important for loculated and complex effusions Tuberculosistesting should also be considered in the right epidemiologic and clinicalsettings Viral cultures have little clinical significance and should not beroutinely obtained, but they may be useful in some patients (eg,cytomegalovirus infection in transplant patients).3 Transesophagealechocardiography can diagnose loculated effusion when transthoracicechocardiography is limited (eg, postoperative patients) and regionaltamponade is considered Our structured approach has yielded diagnosis

by noninvasive targeted testing in 68% of patients, based on aretrospective review.6

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FIGURE 33.2 Parsimonious stepwise approach to laboratory testing and imaging

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in patients with pericardial effusion This systematic approach allows establishing diagnosis noninvasively in the majority of patients with moderate-to-large pericardial effusion Question mark indicates optional and controversial.

Simple clinical assessment has also been shown to assist in establishingthe diagnosis: large effusion without “inflammatory” signs or clinical signs

of tamponade (jugular venous distension, hypotension, and/or pulsusparadoxus) commonly signifies chronic idiopathic pericardial effusion

(likelihood ratio = 20, P < 001), whereas large effusions with clinical

signs of tamponade and without “inflammatory” signs should raise the

suspicion for malignancy (likelihood ratio = 2.9, P < 001).10

Pericardial effusion sampling for diagnostic purposes and occasionallyfor pericardial biopsy should be considered in the following settings:

1 Concern for purulent and tuberculous pericarditis

2 Clinical suspicion of neoplastic pericardial effusion

3 Moderate-to-large pericardial effusion in patients with advanced HIV

and/or immune suppression

4 Moderate-to-large or progressive pericardial effusion in patients who

are not responding to initial therapy or when the tiered workup isinconclusive

Pericardial fluid analysis can include Gram and acid-fast bacilli stainsand cultures, polymerase chain reaction, tuberculosis-specific testing (eg,adenosine deaminase, lysozyme, and gamma-interferon), tumor markers,and cytology.3 Contrary to common practice and unlike pleural effusionworkup, cell count, lactate dehydrogenase, and protein and glucose levelshave not been shown to be particularly useful in differential diagnosis andmanagement of patients with pericardial effusion.11 Pericardioscopyallows a targeted pericardial biopsy and it can potentially increase thediagnostic accuracy of sampling (eg, neoplastic pericardial effusion)

ASSESSING HEMODYNAMIC SIGNIFICANCE OF

PERICARDIAL EFFUSION

When evaluating the hemodynamic impact of pericardial effusion oneshould take into account the acuity of presentation Acute accumulation offluid (within minutes to hours) rapidly exceeds the pericardial stretch limit

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and commonly presents as cardiogenic shock.12 This dramatic presentation

is called acute or surgical tamponade and it requires immediateintervention Chamber perforation during a percutaneous procedure is agood example of acute tamponade Blunt chest trauma and ascendingaortic dissection resulting in blood accumulation within the pericardiumrequire prompt surgical intervention, and percutaneous pericardial effusiondrainage is relatively contraindicated When pericardial fluid accumulatesslowly (within days to weeks), a large amount of fluid can be presentwithout dramatic lowering of the cardiac output.12 This can lead tosubacute or medical tamponade, which requires careful assessment of bothclinical and imaging data to establish the need for pericardial effusiondrainage.13 The following discussion elaborates the assessment forsubacute (medical) tamponade

HISTORY AND PHYSICAL EXAMINATION

Although many refer to pericardial tamponade as a “clinical diagnosis,”the existing evidence suggests that subacute tamponade is a difficultdiagnosis to make on mere clinical grounds.13 Dyspnea is the cardinalsymptom of subacute pericardial tamponade, but it is nonspecific Othersymptoms such as fever, cough, and chest pain can occur and typicallyreflect the underlying cause (ie, pericarditis) rather than pericardial fluidaccumulation Clinical findings of pericardial tamponade includetachycardia, jugular venous distension, pulsus paradoxus, and diminishedheart sounds; and all lack both sensitivity and specificity.14 Tachycardia iscommon in hospitalized patients for many reasons and it could be blunted

by medications such as β-blockers In a systematic review, the jugularvenous distension had a pooled sensitivity of 76% for pericardialtamponade.14 Assessment of jugular venous distension is limited by theexperience of the observer; it can be difficult in some patients, even forexperienced clinicians Besides, jugular venous distension is associatedwith other conditions causing shortness of breath such as pulmonaryhypertension and congestive heart failure Although patients with acute(surgical) tamponade rapidly progress to cardiogenic shock, hypotension israther uncommon in patients with subacute tamponade who accumulatepericardial effusion within days to weeks On the contrary, many patientsare hypertensive because of the high levels of circulating catecholamines

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in response to hemodynamic stress In studies of pericardial tamponade,the mean systolic blood pressure ranged from 127 to 144 mm Hg.15According to a recent review, hypertensive tamponade is seen in 27% to43% of patients.15 Systolic blood pressure commonly decreases in thesepatients after pericardial effusion drainage, and treating the hypertensiveresponse without draining the effusion can be dangerous.

PULSUS PARADOXUS

Pulsus paradoxus is considered the cornerstone of the clinical diagnosis ofpericardial tamponade.12 Under normal conditions, the decrease in bloodpressure is <10 mm Hg, and it is explained by phasic variation in thefilling of the right- and left-sided cardiac chambers related to intrathoracicpressure changes with respiration With tamponade, the accumulatingpericardial effusion restricts cardiac filling and makes the respiratoryvariation in the right and left ventricular filling more pronounced andinterdependent.12 Pulsus paradoxus is measured by manualsphygmomanometer as the difference between intermittent and persistentKorotkoff sounds during normal respiration, not with deep breathing

(Figure 33.3).14 A wide variation in the incidence of pulsus paradoxus hasbeen reported in patients with pericardial tamponade, ranging from 12% to75%.16 In patients with “low-pressure” tamponade, the incidence of pulsusparadoxus was reported as only 7%.17 Besides limited sensitivity forpericardial tamponade, pulsus paradoxus is not very specific A myriad ofconditions have been reported to be associated with pulsus paradoxus; ashort list includes asthma, right ventricular infarction, severe hypovolemia,constrictive pericarditis, restrictive cardiomyopathy, pneumothorax,chronic obstructive lung disease, and pulmonary embolism.13 Some ofthese conditions can also cause jugular venous distension and tachycardia,common associated findings of pericardial tamponade

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FIGURE 33.3 Assessing for pulsus paradoxus Pulsus paradoxus is measured by

manual sphygmomanometer as the difference between intermittent and persistent Korotkoff sounds during normal respiration.

INVASIVE AND IMAGING DATA

Before the widespread use of echocardiography, invasive data usingcardiac catheterization were commonly obtained to confirm the diagnosis

of tamponade Cardiac catheterization in tamponade demonstratesequilibration of diastolic intracardiac pressures and respiratory variation in

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right- and left-sided cardiac pressures corresponding to pulsus paradoxus.Echocardiography is currently the cornerstone of hemodynamicevaluation of pericardial effusion.4 Pericardial effusion is easilyrecognized during ultrasound examination as an echo-free space around

the heart (Figure 33.4) Normally, intrapericardial pressure is lower than

the central venous pressure As pericardial fluid accumulates, theintrapericardial pressure equilibrates first with the right-sided fillingpressures and then left-sided filling pressures.14 During tamponade,intrapericardial pressure temporarily exceeds intracavitary pressure invarious chambers during the cardiac cycle and results in chamber collapse

(Figure 33.5).4 Certain pitfalls should be kept in mind when interpretingechocardiographic findings Transient buckling of the right atrium iscommonly seen in patients with pericardial effusion and it is not specific

A more sustained collapse of the right atrium lasting at least one-third ofthe cardiac cycle appears to be more specific for pericardial tamponade.18Right ventricular early diastolic collapse is a less sensitive finding but has

a high specificity Left-sided chamber collapse is much less sensitive buthighly specific for tamponade Importantly, a study by Merce et al showedthat 34% of patients with pericardial effusion but without clinical features

of pericardial tamponade had at least one chamber collapse onechocardiography.19 Therefore, in patients with pericardial effusion whohave chamber collapse, one should carefully document respiratory flow

variation across valves as a sign of ventricular interdependence (Figure

33.6) and interrogate the inferior vena cava size and collapsibility as a sign

of elevated right-sided filling pressures.20 The presence of respiratoryvariation in the inflow velocities is defined by consensus as >30% acrossthe mitral valve and >60% for the tricuspid valve.4 Theseechocardiographic signs, when present, increase the specificity ofdiagnosis Finally, the size of the pericardial effusion seems to be animportant but frequently underappreciated part of the echocardiographicassessment In one study of hospitalized patients with pericardial effusion,the size of the effusion was the only independent predictor of adverse in-hospital outcomes in a multivariate model, but not chamber collapse orinferior vena cava plethora.21

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FIGURE 33.4 Pericardial effusion as seen with the ultrasound examination.

Pericardial effusion (Pef) is easily recognized during ultrasound examination as an

echo-free space around the heart.

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FIGURE 33.5 Chamber collapse with pericardial tamponade as seen with the

ultrasound examination There is evidence of right atrial collapse (arrowhead) as well as right ventricular compression by pericardial fluid (arrow).

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