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516                     Cardio Diabetes Medicine 2017







                                             Inotropes And Heart :

                                When to Use and When Not to Use






                                         Dr. J. Cecily Mary Majella, DM (Cardio).,
                                     Asst. Prof .Cardiology, Madras Medical College ,Chennai.
                                      Dr.  S. Anneprincy, Post Graduate in Cardiology





              INTRODUCTION:                                      tricles and  reduced ejection fraction  who  present
               Systolic heart failure is a systemic disease due to re-  with low SBP (<90 mm Hg) or low measured cardiac
              duced cardiac contractility. Although it is logical that   output in  the presence  of  signs  of  congestion and
              this condition can be treated by employing therapeu-  organ  hypoperfusion  such as  decreased  mentation
              tic strategies to directly improve contractility, inotro-  and reduced urine output. Its benefit are mainly due
              pic  agents in failure  patients  have universally  failed   to direct increase in cardiac output and reduction in
              to live up to their expectations. Paradoxically, favor-  neurohumoral activation.
              able outcomes  can  be achieved  by administering   The conventional agents include adrenergic inotropes
              drugs  that  acutely decrease  contractility  and block   such as dopamine, dobutamine, and norepinephrine,
              neurohormonal  stimulation.  The proven success of   non adrenergic inotropes like milrinone, enoximone,
              this latter  approach, especially  in combination  with   levosimendan and digoxin.  The newer  and emerg-
              implantable cardioverter-defibrillator  and cardiac re-  ing agents includes omecamtiv mecarbil, istaroxime,
              synchronization  therapy  (ICD-CRT),  has drawn our   SERCA2a gene therapy. (Table 1)
              attention  away from addressing  the  root cause  of
              the  problem:  reduced contractility.  In this update,   Inotropic agents are mainly used for AHF and should
              we will discuss current options for inotropic therapy   be used with  close hemodynamic  monitoring and
              in HF, when  it might  be appropriate  to employ  ino-  should be stopped as soon as adequate organ perfu-
              tropes  in HF  patients, and what  steps  can  be  tak-  sion is restored. This is because all of these agents in-
              en  to mitigate  their  risks  while  maximizing benefit.   crease conduction through the atrioventricular node,
                These  inotropic  agents  acts  via cyclic adenosine   causing a rapid ventricular response in patients pre-
              monophosphate (cAMP)-mediated inotropy  increas-   senting with atrial fibrillation. Other conditions where
              es the cardiac output and through vasodilatation re-  inotropes  prove  useful is  in cardiogenic shock as a
              duce  PCWP. Although these drugs can  successfully   temporary therapy to prevent hemodynamic collapse
              increase cardiac output, their use has been proved to   or as a life-sustaining bridge to more definitive thera-
              have excessive mortality due to increased tachycar-  py for those patients awaiting mechanical circulatory
              dia and  myocardial oxygen  consumption  leading to   support,  ventricular assist  devices,  or  cardiac trans-
              arrhythmia and myocardial ischemia.  Even the short   plantation.
              term use (hours to few days) of intravenous inotro-  CONVENTIONAL INOTROPES
              pes  is associated with  significant  side  effects such
              as hypotension, atrial or ventricular arrhythmias, and   ADRENERGIC AGENTS
              an increase in long-term mortality. Thus the need for   Dopamine
              new inotropic agents that are devoid of these harmful   Initiation of dopamine therapy causes a rapid release
              effects i.e improve systolic performance without nec-  of norepinephrine  that  can precipitate  tachycardia,
              essarily increasing the myocardial oxygen consump-  atrial and ventricular arrhythmias.  Dopamine has
              tion.Inotropes  have beneficial hemodynamic  effects   complex effects that vary significantly with dose.
              especially in patients with heart failure with reduced
              ejection fraction (HFrEF; also known as systolic HF)   Low-dose  dopamine  (≤2  μg/kg/min)  has  been  pro-
              and should be limited to patients with  dilated ven-  posed to cause selective dilation of renal, splanchnic,


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