الفهرس 
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Abstract
Hemodynamically unstable patients include A wide variety of patients in ICU. They include polytruma patients, septic patients, burn patients and shocked patients. Instability of hemodynamics makes these patients in high risk of complications otherthan patients of stable hemodynamics. There are many patterns of resuscitation in hemodynamically unstable patients using different types of fluids including crystalloids and colloids.
The cornerstone of resuscitation of haemodynamically unstable patients is often considered to be fluid loading. However, only roughly half of haemodynamically unstable patients respond to a fluid challenge, defined as an increase in stroke volume or cardiac output upon fluid loading. Although rapid optimisation of volume status has shown to improve outcome, extended fluid loading is associated with increased morbidity and mortality. Little evidence is available for the type and exact dosing of fluid administration.
Establishing volume status is complex, making accurate prediction of an increase in stroke volume upon fluid loading, so-called fluid responsiveness, difficult. Static cardiac filling pressures such as central venous pressure have shown to be incapable of predicting fluid responsiveness accurately. Dynamic parameters on the other hand, using mechanical ventilation-induced changes in preload to track subsequent changes in stroke volume, have shown promise and have been the subject of extensive research in critically ill patients. New methods have been conceived that can easily be used at the bedside in a large variety of patients.
Evaluation and management of intravascular volume are a central challenge in caring for the critically ill. Patients with hypotension are commonly resuscitated with intravenous crystalloid fluid, in keeping with recommendations for treatment of many shock states.
The therapeutic goal of fluid administration is to increase preload, or the stressed venous volume, leading to an increased stroke volume and cardiac output. However, studies of patients with acute illness or hypotensive patients in the operating room consistently demonstrate that approximately 50% of fluid boluses fail to achieve the intended effect of increasing cardiac output.
Moreover, there is increasing data to demonstrate that excess fluid administration may be harmful, and is associated with increased mortality. Large volume resuscitation promotes endothelial injury, fluid extravasation, and tissue edema. In turn, increasing interstitial fluid and extravascular lung water are associated with progressive organ dysfunction and death.
Giving fluid is a familiar response to hypotension or tachycardia, and the alternatives to crystalloid resuscitation, such as initiating vasopressors, colloids, or blood product transfusion, have attendant risks and resource utilization. The tensions between giving intravenous fluid and using a resource-intensive alternative increase the challenge of using fluid judiciously highlight the importance of accurate techniques to predict a patient’s response to fluid administration.
Clinicians have traditionally relied on physical examination and physiologic variables such as blood pressure and heart rate to decide whether to provide fluid therapy, but clinical examination alone has consistently proven unreliable in guiding the decision to give intravenous fluid.
In conclusion, fundamentally, one may ask just three questions regarding the cardiovascular system during resuscitation: will blood flow to the body increase with fluid resuscitation? Is arterial hypotension due to inadequate blood flow or loss of vasomotor tone, or both; and is the heart capable of maintaining effective blood flow without going into failure? If the answer to the first question is ‘yes’, then treatment must include volume expansion. However, if the patient is also hypotensive and has reduced vasomotor tone, then vasopressor therapy may be started simultaneously because arterial pressure will not increase with volume expansion alone, even though cardiac output will increase. If the patient is not preload responsive but has reduced vasomotor tone associated with hypotension, then a vasopressor alone is indicated. If the patient is neither preload responsive nor exhibiting reduced vasomotor tone nor hypotension, then the problem is the heart, and both diagnostic and therapeutic actions must be taken to address these specific problems (e.g. echocardiography, dobutamine). Protocolized cardiovascular management based on functional hemodynamic monitoring has the added advantages of being intuitively obvious (facilitating buy-in by stakeholders), pleuripotential (many different monitoring devices can all drive the same protocol) and scalable (alter intensity of resuscitation), and lends itself to automation.