Which of the following statement(s) is/are true concerning the diagnosis and management of hypovolemic shock?
A. A fall in hematocrit or hemoglobin always accompanies hemorrhagic shock B. The treatment of shock is generic regardless of the etiology C. Pharmacologic intervention to increase myocardial contractility in hypovolemic shock is an important part the early management D. Complications are less frequent after treatment of hemorrhagic shock than septic or traumatic shock
Hypovolemic shock is an emergent issue in which critical blood or fluid loss makes the heart incapable of pushing enough blood through the body. This type of shock may cause many organs to stop working. Blood loss can occur due to bleeding from cuts or bleeding from other injuries, and internal bleeding, such as perforation of the gastrointestinal tract.
The severe fluid loss makes it impossible for the heart to pump a sufficient amount of blood to your body. Hypovolemic shock can lead to organ failure. The blood pressure falls rapidly, which can be life-threatening.
Complications are less frequent after treatment of hemorrhagic shock than septic or traumatic shock-hypovolemic shock is readily diagnosed when there is an obvious source of volume loss and overt signs of hemodynamic instability and increased adrenergic output are present. after acute hemorrhage, hemoglobin and hematocrit values do not change until compensatory fluid shifts have occurred or exogenous fluid is administered. these values decrease once transcapillary refill, osmotic-induced shifts, or non-rbc volume resuscitation expands the blood volume. it is imperative that the distinction be made between hypovolemic and cardiogenic forms of shock, because appropriate therapy differs dramatically. restoration of perfusion in hypovolemic shock requires reexpansion of circulating blood volume in conjunction with necessary interventions to control ongoing volume loss. continued hemodynamic instability after fluid resuscitation implies that shock has not been reversed or that there is ongoing blood or volume loss. in severe, prolonged hypovolemia, ventricular contractile function may itself become depressed and require inotropic support to maintain ventricular performance, but in general, pharmacologic interventions directed toward increased contractility in situations of inadequate preload are ineffective, further complicate metabolic derangements, and are not indicated until adequate volume replacement has been completed. complications are less frequent after treatment of hemorrhagic shock than in situations of septic or traumatic shock. in the later circumstances, the massive activation of inflammatory mediator response systems and consequences of their disseminated, indiscriminate cellular injury can be quite profound.