2. Introduction
– Acute aortic syndromes include
– Classic aortic dissection
– Aortic intramuralhematoma (IMH)
– Penetrating atherosclerotic ulcer (PAU)
– In approximately 90% of acute aortic syndromes, classic
aortic dissection is present, with intimal disruption leading to
a dissection plane in the aortic wall that may propagate
anterogradely (orless commonly, retrogradely) throughout
the length of the aorta.
3. Incidence
– Population studies in the United States have
estimated the incidence of aortic dissection to
range from 2 to 3.5 cases per 100,000
personyears.
– 14 Aortic dissection occurs at least twice as
often in males as in females
4. – There are two main hypotheses for acute aortic dissection
– (1) a primary tear in the aortic intima with blood from the
aortic lumen penetrating into the diseased media and leading
to dissection and creation of the true and false lumina
– (2) primary rupture of the vasa vasorum leading to
hemorrhage in the aortic wall, with subsequent intimal
disruption creating the intimal tear and aortic dissection
– The pressure of the pulsatile blood within the aortic wall
after dissection leads to extension of the dissection.
7. Predisposing Factors
• Men/Female Ratio 2:1 to 5:1
• Chronic Systemic HTN (62-78%)
• Proximal Dissection:
• Peak age 50-55 years
• MC on initial presentation to have HTN 70%
• Distal Dissection:
• Peak Age 60-70 years
• Direct Iatrogenic Trauma: 5% of cases
• Indirect Trauma (eg sudden
deceleration)
9. Predisposing Factors
• Females in 3rd Trimester Pregnancy or
1stStage of Labor
• Case Reports of:
– Cocaine (
(Eber et• Abrupt Discontinuation of Beta Blockers
• Probably Secondary to rapid rise in first derivative of
pressure (dp/dt) on aortic wall.
10. Cystic Medial Degeneration
• Medial Degeneration predisposes dissection
by decreasing cohesiveness of layers of
aortic wall
• More extensive in patients with:
• HTN
• Marfan Syndrome
• Bicuspid Aortic Valves
• But, even in other causes of dissection, medial
degeneration is much greater than expected
with normal aging.
11. Pathogenesis
• Intimal tears occur in regions of aorta
subjected to greatest dp/dt and pressure
fluctuations.
• MC sites for initiation of intimal tear:
• Ascending Aorta
• 1st Portion Descending Aorta
13. Natural History
• Hydrodynamic forces propagate the dissection until
rupture occurs either:
• Back into the lumen of the aorta
• Through the adventitia (causing death)
• Mortality Rates if untreated:
• 1-3% per hour
• 90% within 3 months
• Death usually caused by:
• Acute aortic regurgitation
• Major branch vessel obstruction
• Aortic Rupture ( into pericardium, L pleural cavity, or mediastinum)
14. Proximal Dissection
• Substernal chest pain
• Neck, jaw, throat or face pain
• Aortic Insufficiency
• Decreased pulse or blood pressure in R arm
• Decreased R carotid pulse
• Pulse abnormalities are seen in 50% of
proximal dissections
• Ischemic EKG changes
• AMI – Inferior (5%)
• Marfans Syndrome
• Hypotension
• Syncope – 12%
• CVA – 5-10%
15. Aortic Regurgitation
• AR in 18-50% cases
• Diastolic murmur reported in 25% pts.
• Acute Severe AR – 2nd MC cause of death
AD.
• Murmur can wax and wane and intensity
will vary with BP
• 3 possible mechanisms for acute AR
in dissection
Hagan et al. IRAD. JAMA 2000;283:897-903.
17. Hypotension with Proximal
Dissection
• Cardiac tamponade
• Severe acute Aortic regurgitation with
cardiogenic shock
• Myocardial Infarction with resultant LV systo
dysfunction – usually RCA.
• Acute Aortic Rupture.
• Pseudohypotension by involving
brachiocephalic artery
18. • Interscapular pain
• HTN less commonly associated about 35%
• Left Pleural effusion
• Pulse defecits are less frequent about 15%
• Usually involve femoral or left subclavian
• Spinal Cord Ischemia (10%)
• Transverse Myelitis
• Paraplegia
• Quadriplegia
Distal Dissection
19. Laboratory Findings
• The chest radiograph may be the first clue to the diagnosis of aortic dissection
• The most common abnormality seen on a chest radiograph in a patient with
aortic dissection is an abnormal aortic contour or widening of the aortic
silhouette, which appears in 80% to 90% of cases
• Nonspecific widening of the superior mediastinum may be present.
• If calcification of the aortic knob occurs, one may detect separation of the
intimal calcification from the outer aortic soft tissue border by more than 0.5 to
1.0 cm—the “calcium sign”
• Pleural effusions occur in approximately 20% of dissections
22. Biomarkers
– Release of smooth muscle proteins, soluble elastin fragments, myosin heavy
chain and the BB isoform of creatine kinase, and TGF-β occurs after aortic
dissection.
– These markers have limited usefulness because of sensitivity, specificity, or
time delay and are not currently available for clinical use.
– Patients with acute aortic dissection have elevated D-dimer Levels
– A D-dimer level higher than 1600 ng/mL within the first 6 hours after
– The recent thoracic aortic disease guideline writing committee did not
recommend D-dimer screening for all patients being evaluated for aortic
dissection.
23. Aortography
• Sensitivity: 86-88%
• Specificity: 75-94%
• False negatives if intramural
hematoma or thrombosis of false
lumen
• Good at detecting branch vessel
involvement and Coronary
Artery invovlvement.
25. CT
• Sensitivity 83-94%
• Specificity of 100%
• Spiral CT increased sensitivity to 96%
• Non-invasive with rapid availability (MC initial
imaging modality in IRAD pts)
• Needs contrast to be effective
• Disadvantages:
• Cannot Detect AR
• Does not detect Site of Intimal Tear well
• Cannot detect Coronary Artery Involvement
27. TEE
• Non-Invasive, Performed Quickly at Bedside
• Sensitivity 98 – 99%
• Specificity: 94 – 95% (biplane or multiplane TEE)
• Good at detecting Coronary Artery
Involvement
• Disadvantage: does not evaluate distal ascending
aorta and proximal arch (because of the interposition of air filled trachea
and main stem bronchus)
29. MRI
• Gold Standard for Diagnosis
• Sensitivity and Specificity of 98-100%
• Disadvantages:
• Limited Availability
• Limit the presences of monitoring and support devices
• Relatively CI in unstable patients.
• CI:
• Pacemakers
• Certain types of vascular clips
• Older metallic heart valves
30.
31.
32. MANAGEMENT
• Therapy is targeted at halting the progression
of the dissection
• It is the course of the tear not the tear itself that
leads to compromise of vasculature or rupture
• Goal:
• Reduction of SBP (100-120)
• Dimunition of dp/dt (reflects force of LV ejection)
through use of a beta blocker.
33. Sodium Nitroprusside
• Sodium Nitroprusside for acute reduction starting
10 – 20 mcg/min and titrated upward
• Must initiate BB prior to instituion of Nipride due
to its effect on raising dP/dT when used alone
• Adding IV BB prior until desired effect such as HR
60 – 80s (propranolol 1 mg Q 3-5 minutes max 10
mg)
• Then Q 4-6 hrs at a dose of 2 – 6 mg
34. Labetolol
• Effectively lowers dP/dT as well as
reducing arterial pressure
• Initial dose is 20mg followed by 40 to 80
mg Q 10 – 15 minutes (max 300mg IV)
• Once BP controlled maintenance
by continuous infusion
• Infusion at 2mg/min titrating up to 5 –
10 mg/min
35. Esmolol
• Ultra short acting BB for those with labile
blood pressure or those that are surgical
candidates. (Long acting medications may affect intraoperative
bp management)
• Load with 500 mcg/kg bolus
• Infusion starts @ 50mcg/kg/min titrate to
200 mcg/kg/min for control
• Controls dP/dT as well as blood pressure
• Can be used in patients with uncertain risk
for bronchospasm
36. Contraindications to BB
• Patients with severe Brady or AV block or
bronchospasm BB may be CI
• Calcium channel blockers specifically Cardizem and
Diltiazem can be used if bronchospasm
• Provide negative Inotrope and Chronotropic effects
• If Dissection involves the renal arteries patients may
develop high renin HTN
• Treat with IV enalapril
37. Other Considerations
• Hypotension must ensure if its true or false
• May be secondary to compromise of artery by
dissection (pseudohypotension) so check both arms
• If true hypotension may indicate rupture or
tamponade
• Fluids first then use levophed (norepinephrine) or
phenylephrine (neosynephrine)
• Dopamine should be avoided since it can raise dP/dT
unless used at low doses for renal perfusion
38. Cardiac
Tamponade
• Increase in Intraaortic pressure after pericardiocentesis
causing a reopening of the closed communication
between the false lumen and pericardial space, leading to
lethal cardiac tamponade.
• Prudent to do Pericardiocentesis in AD only if in EMD or
marked hypotension, and aspirate only enough
pericardial fluid to raise bp.