Free Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine by Marc Sabatine Page B

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 (AV 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 ↑