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Common Congenital Heart Lesions - page 74 / 126

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ETIOLOGY

  • Any acute pericarditis can progress to tamponade, but most commonly it’s from neoplastic, postviral and uremic pericarditis.

  • Acute hemorrhage into pericardium can also cause tamponade

    • o

      Blunt or penetrating chest trauma (a good reason not to get stabbed in the chest)

      • o

        Rupture of LV free wall after an MI

      • o

        Complication of a dissecting aortic aneurysm

PATHOPHYS

  • B/c of surrounding tense pericardial fluid, heart is compressed and diastolic pressure w/in each chamber becomes elevated and equal to the pericardial pressure.

  • Thus, normal venous return can’t be accommodated in heart so both systemic and pulmonic pressure rise (giving R-sided heart failure symptoms i.e. systemic venous congestion… and L-sided heart failure symptoms i.e. pulmonary congestion symptoms )

  • That’s not all… reduced filling of ventricles during diastole decreases SV and CO declines

  • This then triggers dangerous compensatory mechs to try to keep tissues perfused (initially thru Symp NS activation), but eventually you can’t keep up and you go into shock and… die (unless you treat it).

PRESENTATION

  • Suspect tamponade in anyone w/ known pericarditis, pericardial effusion, or chest trauma who develop signs/symptoms of vascular congestion and decr CO.

  • If tamponade happens suddenly, profound hypotension symptoms are prevalent (e.g. confusion, agitation)… if gradual, then fatigue (from low CO) and peripheral edema (from R-sided failure) may be presenting complaints

PHYSICAL EXAM

  • Key findings:

    • o

      JVD

      • o

        Systemic hypotension

      • o

        “small quiet heart” -- quiet precordium upon palpation b/c of insulation

  • other signs

      • o

        sinus tachycardia (reflex to hypotension)

      • o

        pulsus paradoxus Æ important sign in tamponade… it’s the cyclical decrease of systolic blood pressure (more than 10 mmHg) during normal inspiration. (this is actually just an exaggeration of normal cardiac physiology… when we inspire, systemic venous return is facilitated and the RV fills which pushes on the interventricular septum and causes a transient decr in LV size… thus, the SV and systolic BP is transiently reduced right after inspiration)… also see pulsus paradoxus in obstructive airway diseases and severe asthma…

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