Aortic Dissection

Definitions (Grc 2003:108:628)

• Classic dissection: intimal tear extravasation of blood into and along aortic media

• Intramural hematoma (IMH):vasa vasorum rupture — medial hemorrhage.

• Penetrating ulcer ulceration of plaque penetrating intima medial hemorrhage Classification

• Proximal: involves ascending Ao. regardless of origin ( Stanford A. DeBakey I & II)

• Distal: involves descending Ao only, distal to subclavian art. ( Stanford B. DeBakey III)

Risk factors (predispose to medial micro apoplexy or "cystic medial necrosis")

• Hypertension (h/o HTN in >70% of dissections)

• Connective tissue disease

Marfan (fibrillin-1 gene): arachnodactyly. joint disloc.. pectus, ectopia lentis, MVP Ehlers-Danlos type IV (type III procollagen): translucent skin: bowel or uterine rupture Annuloaortic ectasia, familial aortic dissection, adult PCKD

• Congenital aortic anomaly: bicuspid aortic valve or coarctation (eg. in Turners)

• Aortitis:Takayasu's. giant cell arteritis. Behcet's, syphilis

• Pregnancy: typically in 3rd trimester: can also see spont. coronary artery dissections

• Trauma: blunt. IABP. cardiac or aortic surgery, cardiac catheterization

Clinical Manifestations and Physical Examination

Feature

Proximal

Distal

Pain {often abrupt, severe, persistent.

»4%

98%

tearing)

(chest, back)

(back, chest, abd)

Syncope (often tamponade)

13%

4%

CHF (usually Al)

9%

3%

CVA

6%

2%

Hypertension

35%

70%

Hypotension/shock (camp..AI. rupt.)

25%

4%

Pulse deficit

19%

9%

Al murmur

44%

12%

(IRAD jama 2000:283:897)

(IRAD jama 2000:283:897)

Diagnostic studies (Grc 2005:112:3802)

• CXR: abnormal in 60-90% (' mediastinum, effusion), but cannot be used to r/o dissection

• CT: quick, noninvasive, good Se (80% for proximal; 90-95% for distal); multidetector CT

may improve Se: however, if 0 & high din. suspicion — additional studies

• TEE: Se >95% for proximal. 80% for distal; can assess coronaries. pericardium. Al

• MRI: Se & Sp >98%. but time-consuming & not readily available

• Aortography: Se 90%. time-consuming, cannot detect IMH; can assess coronaries Treatment (Grc 2003:10*772)

• Medical:. dP/dt targeting SBP 110 and HR 60

first with IV ^-blockers (eg. propranolol, esmolol. labetalol) to blunt reflex T HR &

inotropy that will occur in response to vasodilators then . SBP with IV vasodilators (eg, nitroprusside) control pain with MSO« prn

• Surgery proximal (root replacement): all acute; chronic if c/b progression. Al or aneurysm distal: if c/b progression, signif. branch artery involvement, uncontrolled HTN. aneurysm

• Endovascular stenting r fenestration is an evolving treatment (nejm 1999:340.1539.1546) Complications

• Rupture: pericardial sac -» tamponade; pleural space; mediastinum; retroperitoneum

• Obstruction of branch artery coronary - AMI (usually RCA — IMI)

innominate/carotid — CVA Horner; intercostal/lumbar — spinal cord ischemia/paraplegia innominate/subciavian — upper extremity ischemia; iliac — lower extremity ischemia celiac/mesenteric — bowel ischemia; renal acute renal failure

• Al: due to annular dilatation or disruption or displacement of leaflet by false lumen

Prognosis

• Acute proximal dissection: mortality 1 -2%/h • 48 h

• Acute distal dissection: mortality 10% at 30 d

ARRHYTHMIAS

Id Bradycardias, AV Block, and AV Dissociation

I Sinus bradycardia (SB) (NifM 2000 342 703)

O • Etiologies: medications (ßB. CCB, amiodarone. Li. dig), t vagal tone (ind. IMI), || metabolic (severe hypoxia, sepsis, myxedema, hypothermia), t ICP E3 • Treatment: usually none required; atropine or pacing if symptomatic E3 Sick sinus syndrome (SSS)

hi • Features may include: periods of unprovoked SB. SA arrest, paroxysms of SB and atrial tachyarrhythmias ("tachy-brady" syndrome) • Treatment: meds alone (? ßB w/ intrinsic sympathomimetic activity) usually fail (adeq. control tachy — unacceptable brady); usually need combination of meds (ßB. CCB. dig) for tachy & PPM for brady

AV Block

Type

Features

Prolonged PR (>200 ms),all impulses conducted.

2° Mobitz 1 (Wenckebach)

Progressive i PR until impulse not conducted (-♦ "grouped beating"). Abnl AV node due to ischemia (IMI). inflammation (myocarditis), high vagal tone (athletes). MV surgery, drug-induced. Classically ( 50%). absolute t in PR decreases over time (-♦ i RR intervals, duration of pause <2 x preceding RR interval). AVB usually worsens w/ carotid sinus massage, improves w/ atropine. Often paroxysmal / asymptomatic, no Rx required.

2° Mobitz II

Occasional or repetitive blocked impulses w/ consistent PR interval. Abnl His-Purkinje system due to ischemia (AMI), degeneration of conduction system, infiltrative disease, inflammation. AV surgery. AVB usually improves w/ carotid sinus massage, worsens w/ atropine. Often progresses to 3° AVB. Pacing wire or PPM often required.

3° (complete)

No AV conduction. Must disting. from other forms of AV dissociation.

"High-grode~AVB uwoUy refers to bbck of 2 or mort UKCCiitvt impulses

AV dissociation (not a primary diagnosis, rather a manifestation of I of 3 processes)

• Default: slowing of SA node allows subsidiary pacemaker (eg.AV junction) to take over

• Usurpation: acceleration of subsidiary pacemaker (eg.AV jxnal tachycardia.VT)

• AV block: normal pacemaker unable to capture ventricles, subsidiary pacemaker emerges

Supraventricular Tachycardias (SVTs)

Arise above the ventricles, narrow QRS unless aberrant conduction or preexcitation.

Etiologies ofSVT

SVT

Comments

Sinus tachycardia (ST)

Caused by pain, fever, hypovolemia, hypoxia.

SA node reentrant tachycardia (SANRT)

anemia, anxiety, P-agonists. etc.

Rare. Reentrant loop w/in SA node, discern from ST by rapid onset & termination.

Atrial

Atrial tachycardia (ATAC)

Originate at site in atria other than SA node Seen w/ CAD, COPD. Î catechols. EtOH. dig

Multifocal atrial tachycardia (MAT)

Î automaticity at multiple sites in the atria

Atrial flutter (AFL)

Macroreentry usually within the right atrium

Atrial fibrillation (AF)

Wavelets irregularly passing down AVN. often originate from the pulmonary veins

AV nodal reentrant tachycardia (AVNRT)

Reentrant circuit using dual pathways w/in AVN

c x >

Atrioventricular reciprocating tachycardia (AVRT)

Reentrant circuit using AVN and accessory pathway

3

Nonparoxysmal junctional tachycardia (NPJT)

T automaticity at AV junction

May see retrograde P waves or AV dissociation

Seen in myo/endocarditis. card, surg, IMI. dig

(NEJM 1995:332:162: NEJM 2006:354:1039)

Diagnosis of SVT

Onset

Abrupt onset/offset suggests reentrant (AVNRT. AVRT. SANRT) "Warm up" period suggests ST or ATAC

Rate

Not diagnostic as most SVTs can range from 140-250 bpm. but: ST usually <150 bpm

AFl often conducts with 2:1 AVB to yield ventricular rate of 150 bpm AVNRT & AVRT are usually -150 bpm

Rhythm

Irregular AF. AFL w/ variable block, or MAT

P wave morphology

Upright before QRS - ST. ATAC (P different from sinus). MAT ( -3

different P waves morphologies) Retrograde after QRS & inverted in inf. leads — atrial activation via jxn AVNRT: buried in or distort terminal portion of QRS (pseudo RSR' in V,) AVRT: slightly after but usually distinct from QRS Usually short RP interval (c/w PR), but can be long RP FibnUation or no P waves -* AF

Saw-toothed "F' waves (best seen in inferior leads & Vi) — AFL

Response to vagal stim. or adenosine

t automaticity rhythms (ST. ATAC. MAT) -» slow rate or * AV block AVN reentry (AVNRT. AVRT) - abruptly terminate (classically with a P

wave after last QRS) or no response AFL t AV block — unmasking of "F" waves

(NEJM 2006,354 1039) Figure M Approach to SVT

(NEJM 2006,354 1039) Figure M Approach to SVT

Regular

*P wave morphology j~Irregular ]

SP wave morphology

r

1

upright

» sinus

I

ST

ATAC

SANRT

AVRT NPJT

Treatment of SVT

Rhythm

Acute treatment

Long-term treatment

Unstable

Cardioversion perACLS

n/a

ST

Treat underlying stressor(s)

n/a

ATAC

3-blockers or CCB

3-blockers or CCB, • antiarrhythmics ! Radiofrequency ablation

AVNRT or AVRT

Vagal maneuvers Adenosine (caution in AVRT) CCB or 3-blockers

For AVNRT (see next section for AVRT): Radiofrequency ablation CCB or ß-blockers (chronic or pm) i Class IC AAD (ifnl heart)

NPJT

CCB, 3-blockers, amiodarone

Rx underlying disease (eg, ischemia, dig)

AF AFL

3-blockers, CCB, digoxin, AAD 3-blockers, CCB, digoxin, AAD

See "Atrial Fibrillation" Radiofrequency ablation 3-blockers or CCB • antiarrhythmics

MAT

CCB or ^-blockers if tolerated

Treat underlying disease process i AVN ablation • PPM

Avoid adenosine & nodal agents in AVRT w/ pre-cxcitcd tachycardia (Le.. wide-complex tachycardia due to anterograde conduction down accessory pathway). (JACC 2003:42:1493)

Avoid adenosine & nodal agents in AVRT w/ pre-cxcitcd tachycardia (Le.. wide-complex tachycardia due to anterograde conduction down accessory pathway). (JACC 2003:42:1493)

• Radiofrequency ablation has high overall success rate (AFL/AVNRT 95%. AF 80%). Complications include stroke. Ml. bleeding, cardiac perforation, and conduction block.

Accessory Pathways (Wolff-Parkinson-White)

Definitions

• Accessory pathway (bypass tract) of conducting myocardium connecting atria to ventricles, allowing impulses to bypass normal AVN conduction delay

• Preexcitation (WPW) pattern: 1 PR interval. 1 QRS width w/ 8 wave (slurred onset, can be subtle). ST & Tw abnormalities (can mimic old IMI); only seen w/ pathways that conduct antegrade (if pathway only conducts retrograde then ECG normal during SR "concealed" bypass tract)

• WPW syndrome: accessory pathway • paroxysmal tachycardia

Tachycardias

• Orthodromic AVRT: narrow-complex SVT. conducting J AVN & f accessory pathway;

requires retrograde conduction and .. can occur w/ concealed bypass tracts

• Antidromic AVRT: wide<omplex SVT. conducting i accessory pathway & T AVN;

requires antegrade conduction and . should see WPW pattern during SR

• AF with rapid conduction down accessory pathway, wide-complex irregular SVT:

requires antegrade conduction and . should see WPW pattern during SR Treatment

• AVRT: vagal maneuvers. (i-blockers. ? CCB; caution w/ adenosine as can precip.AF (see below); always have defibrillator ready

• AF/AFL w/ conduction down accessory pathway: need to Rx arrhythmia and I pathway refractoriness; use ibutilidc. flecainide. procainamide or cardiovert: avoid CCB & pB (ineffecL) and dig/adenosine (can i refractoriness of pathway -»1 vent, rate ~»VF)

• Long term: Rx tachycardias wI radiofrequency ablation or antiarrhythmics (IA. IC)

consider prophylactic ablation if asx but AVRT or AF inducible on EPS (Nejm 2003.34*1803) risk of SCD related to how short R-R interval is in AF and if SVT inducible w/ exercise

Wide-Complex Tachycardias (WCTs)

Etiologies

• Ventricular tachycardia (VT)

• SVT conducted with aberrancy (either fixed BBB, rate-dependent BBB. or an accessory pathway). Rate-dependent aberrancy usually p/w RBBB morphology.

Ventricular tachycardia

• Monomorphic (predominantly upward in Vi RBBB-type vs. downward LBBB-type)

Structurally abnormal heart: prior Ml. CMP. arrhythmogenic RV dysplasia (ARVD. incomplete RBBB. R-sided TWI.»: wave terminal notch in QRS in right precordial leads on resting ECG. LBBB-type VT. dx wI MRI) Structurally normal heart RVOT VT (normal resting ECG. LBBB-type VT w/ inf. axis), idiopathic LV VT (responds to verapamil)

• Polymorphic: ischemia. CMP. torsades de pointes ( polymorphic VT + T QT).

Brugada syndrome: pseudo-RBBB w/ STE in Vvj (provoked w/ IA or IC) on resting ECG

Diagnostic clues that favor VT

• Assume all WCT is VT until proven otherwise

• Prior Ml. CHF. or LV dysfunction best predictors that WCT is VT (Amy Med 1998:84.53)

• Hemodynamics and rate do not reliably distinguish VT from SVT

• Monomorphic VT is regular, but initially it may be slightly irregular, mimicking AF with aberrancy; grossly irregularly irregular rhythm suggests AF with aberrancy

• ECG features that favor VT (Ore 1991.83:1649)

AV dissociation (independent P waves, capture or fusion beats) proves VT very wide QRS (140 msec in RBBB-type or 160 msec in LBBB-type) extreme axis deviation QRS morphology atypical for BBB RBBB-type: absence of tall R' (or presence of monophasic R) in Vi. r/S ratio 1 in VA LBBB-type: onset to nadir >60-100 msec in Vi. q wave in V6 concordance (QRS in all precordial leads w/ same pattern/direction)

Long-term management (jacc 2006:48 1064)

• Workup: echo to ✓ LV fxn. cath or stress test to r/o ischemia. ? MRI and/or RV bx to look for infiltrative CMP or ARVD. i EP study to assess for inducibility

• I CD: 2° prevention after documented VT/VF (unless due to acute ischemia)

1° prevention if EF 30-35% (see "Heart Failure"). ? ARVD. ? Brugada.! certain long QT

• Medications: {J-blockers, antiarrhythmics (eg. amiodarone) to suppress recurrent VT

triggering ICD firing or if not ICD candidate

• Radiofrequency ablation if isolated VT focus or if recurrent VT triggering ICD firing

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