2012年2月14日 星期二

Cardiogenic shock


Systemic hypoperfusion:
–      cardiac index [<2.2 (L/min)/m2]
–      sustained systolic arterial hypotension (<90 mmHg),
–      elevated filling pressure [pulmonary capillary wedge pressure (PCWP) > 18 mmHg].
    


It is associated with in-hospital mortality rates >50%
•       Major causes 
–      Acute myocardial infarction (MI): most common
•       Most often due to massive MI (5-10%)
–      dead myocardium does not contract
–      40% loss of muscle mass or greater
–      Cardiomyopathy or myocarditis or cardiac tamponade: less frequent


昨天看到的病人是hereditary and preipartum-

associated DCM 造成的heart 


failure 兩側下肢水腫 端坐呼吸 今天作心導管和心臟切片 準備換心


•       Leading cause of death of patients hospitalized with MI.
•       Early reperfusion therapy for acute MI decreases the incidence of CS.
•       The rate of CS complicating acute MI fell from 20% in the 1960s but has plateaued at ~8% for >20 years.
•       Shock is typically associated with ST elevation MI (STEMI) and is less common with non-ST elevation MI
•       LV failure accounts for ~80% of the cases of CS complicating acute MI.
•       Acute severe mitral regurgitation (MR), ventricular septal rupture (VSR), predominant right ventricular (RV) failure, and free wall rupture or tamponade account for the remainder.
•       Shock is present on admission in only ¼ of patients who develop CS complicating MI; ¼ develop it rapidly thereafter, within 6 h of MI onset. Another ¼ develop shock later on the first day.
•       Subsequent onset of CS may be due to reinfarction, marked infarct expansion, or a mechanical complication.
•       Initial damage/event
•       Cascade of inflammatory and other mediators- histamine, LTs, PAF, lactic acid, myocardial depressant factor
•       Increased oxygen demand, worsened coronary perfusion
•       Damage begets more damage
•        
•        
•        
Presentation•       Acute MI typical presentation
Tachycardia, cool clammy skin, hypotension, poor peripheral pulses, decreased urine output, MS changes
•       Jugular vein distension, pulmonary congestion
•       Rule out surgically corrected causes-
–      valves, papillary rupture, tamponade
•       Lab studies specific for underlying cause
–      cardiac enzyme, Complete blood count (CBC), electrolytes, coagulation factors, arterial blood gas, etc..
–      X-ray, echocardiography, Electrocardiography, etc
•       ABCs: airway, breathing,circulation
–      Oxygen
–      Ventilation
–      Vasopressors (volume expansion?)
•       Central line placement
•       Address cause
–      revascularization, PCI (percutaneous coronary intervention), stent, thrombolytics
•       Nitrates, morphine
–      reduce pain
–      hypotension dangerous
•       Dopamine, dobutamine
•       Amrinone, milrinone
•       Beta blockers when able
–      BP, HR limitations
•       Misc: diuretics, antiplatelet, LMWHs (low molecular weight heparin), etc
Outcome

•       Very very poor
–      70% with medical management
–      perhaps 30-50% with surgical/cath lab intervention
•       Prevention
•       Early identification

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