Page 449 - Clinical Small Animal Internal Medicine
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42  Cardiogenic Shock  417

               pericardial effusion and will likely correctly identify tam-  As with all forms of shock, oxygen administration
  VetBooks.ir  ponade if present. Additionally, with a small amount of   should be started immediately upon recognition of the
                                                                  shock state in an effort to maximize arterial oxygen con-
               focused training, the emergency clinician can recognize
               acute systolic failure (e.g., dilated cardiomyopathy).
                                                                  ety of methods. The use of flow‐by oxygen with a mask
               Evaluation of ventricular function and filling pressures in   tent as far as possible. Oxygen can be provided by a vari-
               patients with chronic valvular disease requires more train-  is easy to perform but requires constant restraint of the
               ing and is complicated by the fact that ventricular systolic   patient. This method of oxygen supplementation is rela-
               and diastolic function changes with age and  disease sever-  tively inefficient unless a tight‐fitting mask is used.
               ity in dogs. The recognition of chordae tendinae rupture,   Unfortunately, animals in shock are often intolerant of
               mild to moderate valvular insufficiency, caval syndrome   having a mask held over their muzzles and they may
               or pulmonary hypertension will likely require evaluation   struggle or resist. Holding a tube attached to an oxygen
               by a veterinary cardiologist. Echocardiography can also   source in front of an animal’s face is an extremely inef-
               be used to identify rare causes of cardiogenic shock such   ficient method of providing oxygen but, recalling that
               as intracardiac tumors.                            perfect is the enemy of good, is probably better than not
                 The use of biomarkers in veterinary medicine is an   providing any supplemental oxygen. Occasionally, ani-
               area of active investigation. While many biomarkers have   mals will tolerate placement of nasal prongs similar to
               been studied and show promise for distinguishing car-  those used in human medicine. Due to the large size
               diac disease from respiratory disease or for stratifying   of  the prongs, this is most feasible in large‐breed,
               severity of cardiac disease (NT‐proBNP, troponin‐I),   no‐brachycephalic dogs.
               most are not available as point‐of‐care (POC) tests, lim-  A less labor‐intensive way of providing oxygen is
               iting the clinical usefulness of these assays for evaluation   through the use of an oxygen chamber or cage. Purpose‐
               of the patient in cardiogenic shock. The exception to this   built oxygen cages are available but require a significant
               is troponin‐I, which is available as a POC test (iStat by   financial investment and utilize large amounts of oxygen.
               IDEXX) and has been shown in several veterinary stud-  A less expensive alternative is a plexiglass door with a
               ies to correlate with myocardial injury. A high troponin‐I   gasket attached to a standard cage that allows introduc-
               level in a patient presenting for shock should prompt the   tion of oxygen through a port. While this method is less
               clinician to further explore the possibility of an underly-  expensive than installing purpose‐made cages, the clini-
               ing cardiac cause. It should be noted, however, that tro-  cian has little control of the oxygen content and limited
               ponin‐I levels have been shown to increase in dogs with   ability to reduce carbon dioxide accumulation within the
               gastric dilation and volvulus and may be elevated in any   cage. The amount of oxygen used in these cages is usu-
               patient that has cardiovascular instability. The degree of   ally higher than in purpose‐made oxygen cages due to
               troponin‐I elevation is likely greater in dogs with myo-  leakage through imperfect seals.
               cardial injury than in those with shock of noncardiac ori-  When providing supplemental oxygen in the acute set-
               gin. Therefore, the true utility of troponin‐I may be in its   ting, the highest achievable F i O 2  should be used. Once
               ability to rule out myocardial injury in the acute setting.  the patient begins to stabilize, the F i O 2  can be reduced to
                 Determination of cardiac output would provide strong   below 60% to decrease the likelihood of oxygen toxicity
               support for a diagnosis of cardiogenic shock, especially in   developing.
               the absence of other possible causes of shock. While car-  Animals with confirmed or suspected pulmonary
               diac output monitoring technology exists in veterinary   edema and cardiogenic shock should be given loop diu-
               medicine, its clinical use remains limited at this time.  retics upon presentation. Loop diuretics are rapidly act-
                                                                  ing, effective diuretics that can quickly improve the
                                                                  clinical condition of  patients  with pulmonary edema.
                 Therapy                                          Furosemide (2 mg/kg) should be administered intramus-
                                                                  cularly and repeated every 30–60 minutes as needed
               Cardiogenic shock is a unique form of shock that is not   until clinical signs improve. Attempts at IV catheter
               generally responsive to traditional treatments for other   placement or IV administration of diuretics can be con-
               types of shock, (i.e., volume expansion and vasopres-  sidered but patient safety must always be kept in mind.
               sor  support). In fact, intravascular volume expansion   Sometimes  it  becomes  apparent  that  without  more
               and  vasopressor therapy can be detrimental or even   aggressive intervention (i.e., IV administration of medica-
               fatal when administered to a patient with cardiogenic   tions), the patient’s condition will continue to deteriorate.
               shock. Rather, cardiogenic shock must be treated pri-  If, in the clinician’s mind, the patient is progressing irre-
               marily by improving cardiac performance and second-  versibly toward cardiopulmonary arrest unless such inter-
               arily by altering vasomotor tone (usually reduction of   vention is undertaken, all  attempts  should be made  to
               vasomotor tone).                                   minimize the stress and duration of restraint by carefully
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