Hemodynamically stable?
Yes
Yes No
No
Initiation of β-blockers if normo/hypertensive
Diagnostic Imaging (see Table 21.3)
Type A dissection or complications (see Table 21.5)
Initiate urgent medical therapy (see Table 21.4)
• IV β-blockers for HR control
• IV antihypertensives
• Pain control
Hemodynamic goals met?
• MAP 60–75 or SBP 90–110
• HR 60–70 bpm Suspect Aortic Dissection
• Severe, abrupt chest/back pain
• Hypertension
• Pulse/pressure deficit
• Neurologic deficit
• Windened mediastinum on CXR
• Risk factors for dissection (see Table 21.1)
Stabilize Patient
• Emergent CT surgery consultation
• Bedside or intraoperative imaging To OR* if:
• Acute Type A dissection
• Aortic rupture
• Cardiac tamponade
• Emergent endovascular stent-grafting for Type B dissection with rupture.
To OR
CXR, chest x-ray; MAP, mean arterial pressure; SBP, systolic blood pressure; bpm, beats per minute;
IV, intravenous.
A
Figure 21.1. Types of acute aortic syndromes.A:Classic aortic dissection. (continued)
Cardiac Disorders rAortic Dissection 1 5 7
B
C
Figure 21.1. (Continued)B:Intramural hematoma (IMH) of the aorta. Black arrows indicate IMH in ascending aorta; white arrows denote crescentic IMH in descending aorta.C:Penetrating atherosclerotic ulcer (PAU) of the aorta (black arrow). White arrows point to associated contained hematoma. Modified from Braverman AC, Thompson RW, Sanchez LA. Diseases of the aorta. In:
Bonow RO, Mann DL, Zipes DP, Libby P, eds.Braunwald’s heart disease,9th ed. Philadelphia, PA: Elsevier, 2011:1309–1338.
is dependent on the location of the dissection. Broadly, dissections of the ascending aorta (types I, II, and A) require immediate surgical repair, while those involving the descending aorta (type III or B) are initially treated medically.
The clinical presentation of aortic dissection may be quite variable, and one must maintain a high index of suspicion for the diagnosis. In contrast to the crescendo discomfort of angina pectoris, the pain of acute dissection is maximal at its onset, usually sudden and severe, and often described as a sharp, tearing pain in the chest, neck, or interscapular areas. In addition to the dissection itself, presenting symptoms
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TABLE 21.1 Risk Factors for Aortic Dissection rHypertension
rThoracic rAortic rAneurysm rGenetic disordersa
◦ Marfan syndrome
◦ Loeys–Dietz syndrome
◦ Familial thoracic aortic aneurysm/
dissection syndrome
◦ Vascular Ehlers–Danlos syndrome
rCocaine/amphetamine use
rAtherosclerosis/penetrating aortic ulcer rTrauma—blunt or iatrogenic
◦ Catheter-induced
◦ Aortic valve surgery
◦ Coronary artery bypass grafting
◦ Deceleration injury (e.g., motor vehicle accident)
rInflammatory conditions
◦ Giant cell arteritis
◦ Takayasu’s arteritis
◦ Behcáet disease
◦ Syphilitic aortitis rCongenital conditions
◦ Bicuspid aortic valve
◦ Turner syndrome
◦ Aortic coarctation
◦ Supravalvular aortic stenosis
aFirst-degree relatives of patients with these conditions should be screened for aortic disease.
Figure 21.2. Classification systems for aortic dissection: Stanford and DeBakey. (Adapted from Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management. Part I:
from etiology to diagnostic strategies.Circulation.2003;108:628–635, with permission.)
Cardiac Disorders rAortic Dissection 1 5 9
TABLE 21.2 Complications of Aortic Dissection rAortic rupture
rMyocardial ischemia/infarction
rNeurologic deficits: stroke, coma, altered consciousness, syncope, paraplegia rMalperfusion: coronary, mesenteric, limb, spinal cord, renal, hepatic rHypotension
rHemothorax rCardiac tamponade
rAcute aortic regurgitation and congestive heart failure rSubsequent aneurysm formation
may also be related to malperfusion or complications involving various organ systems.
Physical examination should include a complete pulse exam and blood pressure in both arms and legs, as there may be pulse or pressure deficits. Cardiac auscultation may reveal an aortic regurgitation murmur. However, pulse differentials and an aortic regurgitation murmur are present in a minority of patients, and physical examination alone is not sufficient to rule out aortic dissection.
Significant morbidity and mortality from dissection is attributed to end-organ damage and aortic rupture (Table 21.2). Organ systems may be compromised by com- pression of branch vessels by an expanding false lumen, or direct extension of a dissec- tion into the vessel. Cardiovascular and neurologic manifestations are two particularly devastating complications of aortic dissection. When the ascending aorta is involved, acute aortic regurgitation may lead to heart failure. Cardiac tamponade, aortic rupture, or myocardial infarction from coronary artery involvement may lead rapidly to hemo- dynamic shock and death. Dissection complicated by acute hemopericardium may lead to cardiac tamponade. Poor outcomes have been reported from pericardiocentesis secondary to further bleeding and acute decompensation. Therefore, pericardiocen- tesis should generally be avoided in favor of emergent surgery. Neurologic sequelae may result from acute dissection involving the carotid or vertebral arteries, as cere- bral hypoperfusion may lead to syncope, altered mental status, and stroke. Transverse myelitis, myelopathy, paraplegia, or quadriplegia may result from spinal malperfu- sion. Mesenteric ischemia may occur, which may be difficult to diagnose and can be fatal.
Standard laboratory tests are of limited utility in evaluating aortic dissection, though the chest x-ray and thed-dimer may be useful. The chest radiograph may demonstrate a widened mediastinum or abnormal aortic contour. Pleural effusion may represent hemothorax, and displaced calcium at the aortic arch may also be present in dissection. Regardless, up to 10% to 20% of aortic dissections are associated with a normal chest radiograph. Thed-dimer is another test that may be of assistance in the diagnosis; it is usually elevated in acute aortic dissection, and when normal, has been shown to have a high negative predictive value in the first 24 hours from symptom onset. Importantly, in IMH, thed-dimer may not be elevated, and in the setting of a high clinical index of suspicion, a negatived-dimer does not rule out an acute aortic syndrome. A clear role for thed-dimer in evaluation of aortic dissection has not been established.
Given the critical nature of aortic dissections, immediate diagnostic confirma- tion and definition of the extent of the dissection is imperative once it is suspected.
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TABLE 21.3 Comparison of Diagnostic Imaging Modalities Sensitivity Specificity
Test (%) (%) Advantages Disadvantages
TEE 98–99 94–97 Excellent evaluation of aortic root and descending thoracic aorta, aortic valve, and pericardium
Requires esophageal intubation; limited to thoracic aorta
CT 96–100 96–100 Widely and rapidly available; superior imaging of entire aorta, heart, branch vessels, and complications such as rupture and hemopericardium
Limited identification of the intimal tear/site of entry; nephrotoxic iodinated contrast required
MRI >98 >98 Superior accuracy, sensitivity, and specificity for all types of dissection
Limited availability, time-consuming procedure, less monitoring during scan
The choice of imaging should be made on the basis of sensitivity, specificity, clinical stability, and operator availability and experience (Table 21.3). If the patient presents with hemodynamic instability or hypotension, rapid evaluation by transesophageal echocardiogram or computed tomography (CT) scan should be performed to assess for complications of dissection, including pericardial effusion, aortic regurgitation, or aortic rupture. CT is widely and rapidly available. Though CT scans require intra- venous contrast dye, they offer superior imaging of the entire aorta, aortic arch, and branch vessels. Transesophageal echocardiogram requires an experienced operator and esophageal intubation to perform the procedure; however, it can be performed at the bedside, and visualizes the aortic valve, aortic root, and pericardium well. Because of the time delay and difficulties with hemodynamic monitoring, MRI is usually not the first test of choice.
When aortic dissection is suspected, immediate initiation ofβ-blocker therapy to reduce shear forces is paramount while pursuing confirmation of the diagnosis (Table 21.4). Blood pressure should be reduced to as low a level as possible without compro- mising organ perfusion.β-Blocker therapy is recommended to achieve a target heart
rate<70 beats per minute. Nondihydropyridine calcium channel blockers (diltiazem,
verapamil) may be considered ifβ-blocker therapy is contraindicated. Care should be taken to avoid vasodilators, such as sodium nitroprusside, in the absence of negative chronotropic medications, as they may induce reflex tachycardia, thereby increasing dP/dt, which may extend the dissection.
Emergent surgery is indicated with ascending aortic dissection because medical therapy alone is associated with a high risk of morbidity and mortality (Figure 21.3).
Cardiac Disorders rAortic Dissection 1 6 1
TABLE 21.4 Selected Pharmacologic Therapya 1. Intravenousβ-blocker (preferred negative inotrope)b
rEsmolol: Give 500μg/kg IV bolus, then continuous IV infusion at 50–200μg/kg/min, titrated to effect. Short half-life allows rapid titration.
rLabetalol: Give 20 mg IV over 2 min, then 40–80 mg IV every 15 min until adequate response (maximum 300 mg), then continuous IV infusion at 2–10 mg/min IV, titrated to effect.
2. Intravenous vasodilator (after initiation ofβ-blockade)
rSodium nitroprusside: Start continuous infusion with no bolus at 20μg/min, titrate 0.5–5μg/kg/min with a maximum of 800μg/min.Use only in presence ofβ-blockers.
rCaution: thiocyanate toxicity may occur in patients with renal impairment or prolonged infusions.
rEnalaprilat: Give 0.625–1.25 mg IV, then increase by 0.625–1.25 mg every 6 hr to a maximum of 5 mg every 6 hr, titrated to effect.
aGoal of therapy is HR less than 70 beats per minute and blood pressure as low as possible without compromising organ perfusion.
bIf contraindication toβ-blockers, use diltiazem: 0.25 mg/kg IV over 2 min, then continuous IV infusion at 5–15 mg/hr, titrated to effect.
Surgery or endovascular repair in descending aortic dissection is reserved for complica- tions such as end-organ ischemia, refractory pain, uncontrolled hypertension, rupture, or a rapidly expanding aortic diameter (Table 21.5). There is growing experience man- aging complications of descending aortic dissections with percutaneous interventional therapy using stent grafting to exclude intimal tears, and balloon fenestration of the
60 50 40 30 20 10 0
<24hr 1 2 3 4 5
Days Following Presentation 14-Day Mortality by Type and Management
Cumulative Mortality, %
6 7 8 9 10 11 12 13
Type A:
Medical
Type B:
Medical Type B:
Surgical Type A:
Surgical
14
All patients (n = 645) A/Med (n = 95) A/Surg (n = 320) B/Med (n = 166) B/Surg (n = 41)
Figure 21.3.IRAD graph of outcomes after medical/surgical treatments for type A and B dissec- tions. (Adapted from 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, with permission.)
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TABLE 21.5 Indications for Surgerya rType I, II, or A dissection
rType III or B with
◦ Rupture
◦ Branch vessel compromise/organ ischemia
◦ Refractory hypertension
◦ Aneurysmal dilation
◦ Refractory pain
aOr endovascular intervention for appropriate patients.
false lumen to relieve ischemia of a compromised branch vessel. These techniques and others continue to evolve the management of complex aortic dissections.
S U G G E S T E D R E A D I N G S
Braverman AC. Acute aortic dissection: clinician update.Circulation.2010;122:184–188.
Current review of diagnosis and management of acute aortic dissection.
Braverman AC, Thompson RW, Sanchez LA. Diseases of the aorta. In: Bonow RO, Mann DL, Zipes DP, Libby P, eds. Braunwald’s heart disease, 9th ed. Philadelphia, PA: Elsevier, 2011:1309–1338.
Comprehensive overview of entire spectrum of aortic disease.
Estrera A, Miller C, Lee T, et al. Acute type A intramural hematoma: analysis of current man- agement strategy.Circulation.2009;120:S287–S291.
Nice review of management of Type A IMH.
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.
The largest database of acute aortic dissection with emphasis on clinical presentation.
Mehta RH, Suzuki T, Hagan PG, et al. Predicting death in patients with acute type A aortic dissection.Circulation.2002;105:200–206.
IRAD study of 547 patients which develops a risk prediction tool in patients with acute type A aortic dissection.
Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management. Part I:
from etiology to diagnostic strategies.Circulation.2003;108:628–635.
A broad review of aortic dissection with emphasis on etiology and diagnostic methods of detecting aortic dissection.
Nienaber CA, von Kodolitsch Y, Petersen B, et al. Intramural hematoma of the thoracic aorta:
diagnostic and therapeutic implications.Circulation.1995;92:1465–1472.
Describes clinical features and prognosis of a series of patients with aortic intramural hematoma.
Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes.Circulation.2005;112:3802–3813 Outstanding review of the three different acute aortic syndromes, and key points for diagnosis,
imaging, and management.
Tsai TT, Trimarchi S, Nienaber CA. Acute aortic dissection: perspectives from the International Registry of Acute Aortic Dissection (IRAD).Eur J Vasc Endovasc Surg.2009;37(2):149–159.
Update of IRAD database.
Von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection.
Arch Intern Med.2000;160:2977–2982.
Proposes independent predictors of acute aortic dissection and creates a prediction model for facilitated estimation of the individual risk of dissection.
22 Acute Decompensated Heart Failure
Shane J. LaRue and Gregory A. Ewald
The combination of an increasing elderly population and successful reperfusion strate- gies for acute myocardial infarction (MI) has led to an epidemic growth in the number of patients with left ventricular dysfunction and heart failure (HF). It is estimated that there are 5 million Americans living with HF, with 500,000 new cases occurring each year. In fact, HF is the leading cause of hospitalization for patients age 65 or more years and costs nearly 40 billion dollars per year in the United States and is an estimated 1% to 2% of the entire health-care budget in Europe. The 1-year mortality from this condition approaches 50% for patients with advanced HF, corresponding to 300,000 deaths annually in the United States.
The management of chronic HF has improved substantially during the past decade. Successful approaches validated by clinical trials have become well established and are documented in numerous evidence-based guidelines. These approaches will not be detailed here but involve (a) modulation of neurohormonal activation, specif- ically the renin-angiotensin-aldosterone system (via angiotensin converting enzyme inhibitors [ACEIs], angiotensin receptor blockers [ARBs], and aldosterone antagonists) and sympathetic nervous system (via beta-blockers); (b) fluid management (via diuret- ics and sodium/water restriction); (c) reducing cardiac work and improving cardiac output (via hydralazine, nitrates, and digoxin); and (d) attempting to restore synchro- nized ventricular contraction and preventing sudden cardiac death (via implantation of biventricular pacemakers and cardiac defibrillators).
In contrast to chronic HF, the management of acute decompensated HF (ADHF) is not as well studied in randomized controlled trials, and evidence-based guidelines have only recently appeared. There are now three sets of guidelines that provide the clinician with recommendations for treating ADHF, with one from the European Society of Cardiology, one from the American College of Cardiology/American Heart Association, and another from the Heart Failure Society of America. Our approach to HF in the critical care setting is consistent with these guidelines and is summarized in this chapter.
Recognizing HF is an important first step, as previously existent HF may not have been diagnosed, or there may be acute HF in the setting of MI or acute cardiomy- opathy. Typical patients have a history of coronary artery disease, MI, or HF with subjective complaints of paroxysmal nocturnal dyspnea, orthopnea, and dyspnea on exertion. Physical findings that correlate with HF include a third heart sound (S3) and signs of volume overload, such as jugular venous distention, hepatojugular reflux, pul- monary rales, and lower extremity edema. Chest radiography may show cardiomegaly
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or pulmonary venous congestion. Electrocardiogram findings are not specific but may show atrial fibrillation, ventricular hypertrophy, or evidence of prior MI.
It is important to remember that although HF is a clinical diagnosis, echocardio- graphy, angiography, and invasive hemodynamic monitoring are useful to document systolic or diastolic dysfunction. The role of blood testing is limited in the diagnosis of HF, although B-type natriuretic peptide (BNP) levels can be helpful if the diagnosis is uncertain. In particular, patients with serum BNP<100 pg/mL are very unlikely to have decompensated HF, whereas values>500 pg/mL are consistent with the diag- nosis, with the exception of patients on hemodialysis or with an estimated glomerular filtration rate<60 mL/min. In these patients, the BNP should not be used for diag- nosis as it is typically elevated out of proportion to the degree of HF. Elevated serum creatinine and hepatic function tests may suggest poor end-organ perfusion secondary to reduced cardiac output.
It is critical to make an accurate assessment regarding the precipitating events for the patient’s decompensated state. Common precipitants include myocardial ischemia, acute MI, hypertensive crisis, arrhythmias, sepsis, anemia, and decompensation of pre-existing HF secondary to medical or dietary nonadherence. Less common pre- cipitating factors include acute myocarditis, peripartum cardiomyopathy, valvular heart disease (including infective endocarditis), cardiac tamponade, and thyrotoxicosis (Table 22.1).
Once the diagnosis of ADHF is confirmed, an initial algorithmic approach should focus on stabilizing the patient and performing noninvasive assessments of heart rhythm, oxygenation, hemodynamics, and volume status (Algorithm 22.1). This will guide therapies such as digoxin or amiodarone for atrial fibrillation with rapid ven- tricular response, vasodilators to reduce afterload and the work of the failing heart, or inotropes for the patient with inadequate end-organ perfusion.
Two classification schemes are frequently used for ADHF: the Killip and Forrester classifications, both of which were developed for ADHF in the setting of MI. The Forrester classification is useful with either noninvasive data (clinical perfusion status and evidence of pulmonary congestion) or invasive hemodynamic data (Algorithm 22.2). When an accurate clinical assessment of hemodynamic and volume status cannot be made, a pulmonary artery catheter (Swan-Ganz) can be useful to measure the cardiac index, pulmonary capillary wedge pressure (PCWP), and systemic vascular resistance (SVR), with the additional benefit of monitoring the response to therapy. However, this procedure is not without risks and thus should be reserved for selected cases and only performed by an experienced operator (see Chapter 76).
TABLE 22.1 Precipitants of Acute Decompensated Heart Failure
Common Less common
Medical/dietary noncompliance Peripartum cardiomyopathy Acute myocardial infarction Acute myocarditis
Hypertensive crisis Infective endocarditis
Arrhythmias Valvular heart disease
Sepsis Cardiac tamponade
Anemia Thyrotoxicosis
Cardiac Disorders rAcute Decompensated Heart Failure 1 6 5