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300  P R I N C I P L E S   A N D   P R A C T I C E   O F   C R I T I C A L   C A R E

         factors  such  as  preoperative  medications,  anaemia  or   including  full  blood  examination,  clotting  profile  and
         coagulopathies. Contributing factors include:        measures of fibrinolytic activity.
         ●  cardiopulmonary bypass influences:
            ●  heparinisation,  haemodilution,  platelet  damage   Heparin reversal
               and altered function                           Cardiopulmonary  bypass  requires  full  heparinisation
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            ●  disseminated  intravascular  coagulation  (DIC)   (initially 300 IU/kg), which is reversed at end-operation.
               following activation of the systemic inflammatory   The  specific  antidote,  protamine  sulphate,  is  adminis-
               response syndrome post-CPB                     tered as bypass is ceased, at a dose of 1 mg per 100 units
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         ●  preoperative  anticoagulant/antiplatelet  medications   heparin used (i.e. 3 mg/kg).  If reversal is less than com-
            commonly encountered                              plete,  as  evidenced  by  a  prolonged  ACT,  further  prot-
            ●  aspirin, coumadin, clopidogrel                 amine sulphate (at doses of 25–50 mg over 5–10 minutes)
         ●  preoperative  anaemia  due  to  aortic  valve  disease,   may be necessary.
            autologous  blood  donation  or  the  various  chronic
            anaemias                                          Management of bleeding
         ●  clotting factor deficiency                        Treatment approaches to bleeding once the patient is in
         ●  hypothermia                                       intensive care include further protamine administration
         ●  coexisting coagulopathies                         if the ACT remains prolonged, blood and blood product
         ●  increased fibrinolytic activity                   administration  (platelets,  clotting  factors,  fresh  frozen
         ●  surgical defects such as failure of access site closure, or   plasma), procoagulants (desmopressin acetate) and anti-
            vascular anastomosis defects.                     fibrinolytic  agents  (see  Table  12.2  for  more  details).
                                                              Other  general  measures  such  as  rewarming  the  patient
                                                              and  preventing  or  treating  hypertension  should  be
         Bedside assessment of bleeding                       undertaken.
         The activated clotting time (ACT) is the most commonly
         used  assessment  of  coagulation  and  heparin  activity   Autotransfusion
         during cardiac surgery and subsequently in intensive care.   Chest drain systems used in cardiothoracic surgery can be
         It measures the time to onset of fibrin formation (initial   configured  for  retransfusion  of  collected  blood  during
         clot development). The ACT has been valuable because it   rapid blood loss. If losses are fresh, and are collected with
         can  be  inexpensively  and  efficiently  performed  at  the   reliable  sterility,  they  can  be  transfused  back  into  the
         bedside,  providing  prompt  results  and  requiring  only   patient. Blood that has been collected and left standing
         modest personnel training. Bleeding patients with a pro-  in  the  drain  receptacle  rapidly  becomes  unsuitable  for
         longed ACT come under consideration for administration   retransfusion, and so autotransfusion is generally limited
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         of protamine or other agents.  Treatable levels vary from   to blood that has collected over 1–2 hours, rarely longer.
         greater than 120 sec to greater than 150 sec among dif-  Blood filters should always be used for protection against
         ferent centres.                                      clots that may have developed in the drain receptacle.
         A limitation of ACT measurements is that they provide   Assessment and Management of
         no  information  about  clotting  processes  beyond  initial
         fibrin formation, so clotting deficits such as impaired clot   Pericardial Tamponade
         strength or the presence of significant fibrinolysis as con-  Postoperative  pericardial  tamponade  results  from  the
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         tributors  to  bleeding  are  not  revealed  by  this  test.   By   accumulation of blood or effusion fluid within the peri-
         contrast,  the  thromboelastograph  (TEG)  measures  the   cardium.  An  increasing  volume  within  the  pericardial
                                             33
         clotting process as it proceeds over time.  TEG monitor-  space eventually compresses cardiac chambers, impeding
         ing not only reveals abnormalities early in the clot process   venous return and therefore causing low cardiac output
         (time to fibrin formation, as would be demonstrated by   and hypotension. Pericardial tamponade is an emergency,
         the  ACT)  but  also  the  subsequent  development  of  clot   and varies in severity from shock to pulseless electrical
         strength,  clot  retraction,  and  finally  fibrinolytic  activity   activity.
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         for each of their contributions in the bleeding patient.    Described as one of the extra-cardiac obstructive shocks,
         TEG monitoring, although considerably more expensive   pericardial  tamponade  often  resembles  cardiogenic
         than the ACT, is now available as a bedside or operating   shock. The low cardiac output and hypotension result in
         room technology and offers better insight into bleeding   oliguria,  altered  mentation,  peripheral  hypoperfusion
         causes.  In  addition,  because  TEG  monitoring  identifies   and  development  of  lactic  acidosis.  Compensation
         deficiencies at the various stages of clot formation, devel-  includes tachycardia and marked vasoconstriction, elevat-
         opment  of  clot  strength  and  the  presence  of  undue     ing  the  systemic  vascular  resistance.  As  in  cardiogenic
         fibrinolytic  activity,  it  may  permit  better  matching  of    shock, there is usually elevation of the filling pressures
         procoagulant, blood product or antifibrinolytic therapy   (right atrial, pulmonary artery and pulmonary capillary
         to needs. 33
                                                              wedge pressures), sometimes with a particularly sugges-
         No matter which of the above technologies is used at the   tive merging of the pulmonary artery diastolic, right atrial
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         bedside, the patient with significant bleeding should be   and pulmonary artery wedge pressures.  Additional fea-
         evaluated more fully as soon as bleeding develops. Blood   tures that may be present include muffled heart sounds,
         should  be  drawn  and  sent  for  laboratory  assessment,   decreased  QRS  voltage,  electrical  alternans,  narrowing
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