Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (20 page)

Complications

•
Rupture
: pericardial sac → tamponade (avoid pericardiocentesis unless PEA); blood in pleural space, mediast., retroperitoneum; ↑ in hematoma on imaging portends rupture.

•
Malperfusion
(obstruction of branch artery)

can be
static
(avulsed/thrombosed) or
dynamic
(Δs in pressure in true vs. false lumen)

coronary → MI (usually RCA → IMI, since dissection often along outer Ao curvature)

innominate/carotid → CVA, Horner; intercostal/lumbar → spinal cord ischemia/paraplegia

innominate/subclavian → upper extremity ischemia; iliac → lower extremity ischemia

celiac/mesenteric → bowel ischemia; renal → acute renal failure, refractory HTN

•
AI
: due to annular dilatation or disruption or displacement of leaflet by false lumen • Mortality: 1–2%/h × 48 h for acute proximal; 10% at 30 d for acute distal

ARRHYTHMIAS

BRADYCARDIAS, AV BLOCK AND AV DISSOCIATION

Sinus bradycardia (SB) (
NEJM
2000;342:703)

• Etiologies:
meds
(incl bB, CCB, amio, Li, dig), ↑
vagal tone
(incl. athletes, sleep, IMI),
metabolic
(hypoxia, sepsis, myxedema, hypothermia, ↓ glc), OSA, ↑ ICP

• Treatment: usually none required; atropine, b
₁
agonists or temp. pacing if symptomatic • Most common cause of sinus pause is
blocked premature atrial beat
Sick sinus syndrome (SSS)

• Features may include: periods of unprovoked SB, SA arrest, paroxysms of SB and atrial

tachyarrhythmias (“tachy-brady” syndrome), chronotropic incompetence w/ ETT

• Treatment: meds alone usually fail (adeq. control tachy → unacceptable brady); usually need
combination of meds
(bB, CCB, dig) for tachy &
PPM
for brady

AV dissociation

•
Default
: slowing of SA node allows subsidiary pacemaker (eg, AV junction) to take over •
Usurpation:
acceleration of subsidiary pacemaker (eg, AV junctional tach, VT) •
3
°
AV block:
atrial pacemaker unable to capture ventricles, subsidiary pacemaker emerges distinguish from
isorhythmic dissociation
(A
V rate, some P waves nonconducting)
Temporary pacing wires

• Consider w/ bradycardia with hemodyn instability or unstable escape rhythm when perm pacer not readily available. Risks: RV perf, VT, PTX, CHB if existing LBBB,
etc.

• Consider instead of PPM for sx bradycardia due to reversible cause (bB/CCB O/D, Lyme, myocarditis, SBE, s/p cardiac surgery/trauma), TdP, acute MI (sx brady, high grade AVB)

SUPRAVENTRICULAR TACHYCARDIAS (SVTS)

Arise above the ventricles
, ∴
narrow QRS
unless aberrant conduction or pre-excitation
.

Figure 1-4 
Approach to SVT (adapted from
NEJM
2012;367:1438)

•  
Catheter ablation
: high overall success rate (AFL/AVNRT ~95%, AVRT ~90%, AF ~80%)

Complications: stroke, MI, bleeding, perforation, conduction block (
JAMA
2007;290:2768)

ACCESSORY PATHWAYS (WOLFF-PARKINSON-WHITE)

Definitions

•
Accessory pathway
(bypass tract) of conducting myocardium connecting atria & ventricles, allowing impulses to bypass normal AVN delay •
Preexcitation (WPW) pattern
: ↓ PR interval, ↑ QRS width w/ Δ wave (slurred onset,
can be subtle
), ST & Tw abnl (can mimic old IMI);
only seen w/ pathways that conduct antegrade
(if pathway only conducts retrograde then

ECG will be normal during SR; “concealed” bypass tract)

PAC can exaggerate preexcitation if AV node conduction slowed

•
WPW syndrome
: accessory pathway + paroxysmal tachycardia

Classic tachycardias of WPW

•
Orthodromic AVRT
:
narrow-complex
SVT (typically), conducting ↓ AVN & ↑ accessory pathway; requires retrograde conduction and ∴ can occur w/ concealed bypass tracts •
Antidromic AVRT
(rare):
wide-complex
SVT, conducting ↓ accessory pathway & ↑ AVN;

requires antegrade conduction and ∴ should see WPW pattern during SR

•
AF
w/ rapid conduction down accessory pathway; ∴ wide-complex irregular SVT; requires antegrade conduction; ∴ should see WPW pattern in SR. Rarely can degenerate into VF.

Treatment

•
AVRT
: vagal, bB, ? CCB; caution w/ adenosine (can precip. AF);
have defibrillator ready
•
AF/AFL
w/ conduction down accessory pathway: need to Rx arrhythmia
and
↑ pathway

refractoriness; use
procainamide
,
ibutilide
, amio, flecainide or DCCV; avoid CCB & bB (ineffective), dig/adenosine (can ↓ refractoriness of pathway → ↑ vent. rate → VF)

•
Long term
: Rx sx tachycardias w/ RFA, antiarrhythmics (IA, IC) if not candidate for RFA;

consider RFA if asx but AVRT or AF inducible on EPS (
NEJM
2003;349:1803) of if rapid conduction possible (✓ w/ EPS if preexcitation persists despite exercise testing)

risk of SCD related to how short RR interval is in AF and if SVT inducible w/ exercise

WIDE-COMPLEX TACHYCARDIAS (WCTS)

Etiologies (
Lancet
2012;380:1520)

•
Ventricular tachycardia (VT)
•
SVT conducted with aberrancy
: either fixed BBB, rate-dependent BBB (usually RBBB), conduction via an accessory pathway or atrially triggered ventricular pacing
Monomorphic ventricular tachycardia (MMVT)