HYPOVOLEMIC SHOCK

 HYPOVOLEMIC SHOCK 

Hypovolemic shock occurs as a result of decreased circulating blood volume, mess volume depletion or fluid sequestration within the abdomen provides a commonly from acute hemorrhage. It may also result from heat-related intravasculas classification of hypovolemic shock based on the amount of whole blood volume lost. In general, the greater the loss of whole blood, the greater the resultant risk of mortality. However, it is important to note that other factors can influence the outcome of hypovolemic shock including age, underlying comorbidities (e.g., cardiovascular disease), and the rapidity and adequacy of the fluid resuscitation.

Lactic acidosis occurs during hypovolemic shock because of inadequate tissue perfusion. The magnitude of the serum lactate elevation is correlated with mortality in hypovolemic shock and may be an early indicator of tissue hypoperfusion, despite near-organ hypoperfusion. This is reflected in the equation for tissue oxygen delivery shown normal-appearing vital signs. The treatment of lactic acidosis depends on reversing determinant of cardiac output. Providing adequate intravascular volume will ensure here. Optimizing oxygen delivery to tissues requires a sufficient hemoglobin concentration to carry oxygen to tissues. In addition, ventricular preload is an important that stroke volume and cardiac output are optimized to meet tissue demands for oxygen and other nutrients. If. despite adequate preload, cardiac output is not sufficient for the demands of tissues, then dobutamine can be employed to further increase cardiac output and oxygen delivery.

Classification of Hypovolemic Shock

Category

Whole Blood Volume Loss (%)

Mild (compensated)

Peripheral vasoconstriction to preserve blood flow to critical organs (brain and heart)

<20%

Moderate

Pathophysiology

Decreased perfusion of organs such as the kidneys, intestine, and pancreas

20-40%

Severe (uncompensated)

Decreased perfusion to brain and heart

>40%

Management of hypovolemic shock

Clinical picture of shock SBP-90 mm Hg MAP <60 mm Hg Lactate 24 mmol/L

Control source of bleeding: compression of visible vascular injury, meticulous exposure and control of Injury to internal bleeding vessel or tissue, esophageal banding or tamponade of rapid variceal bleeding

Establish vascular access lan 8.5 French central vein catheter or two 14-gauge peripheral vein catheters) for rapid fluid/blood product adminstration

If yes Continue Intravenous resuscitation and exclude concomitant causes of shock including cardiac tamponade, pneumothorax spinal injury, pulmonary embolism, and myocardial Injury in the approprate clinical setting Control of bleeding source achieved?

If no Continue intravenous fluid resuscitation and consider alternative methods to control bleeding source (eg. vascular embolization

Measure Hb

If >9g/dL administer 0.9 NaCI/ lactated ringer solution

If <9g/dL RBC transfusion until Hb >9 g/dL and correct any Identified coagulation or platelet abnormalities

Measure CVP and MAP

If CVP <8 mm Hg Repeat fluid boluses of at least 20 ml/kg of 0.9 Nacl or lactated Ringer solution

Administer vasopressor NORAD or DOPAMINE

Resuscitation complete

If CVP >8 mm Hg and MAP <60 mm Hg

Adjunctive Therapies for Hypovolemic

Therapy

Airway control

Cardiac/hemodynamic monitoring

Platele fresh-frozen plasma administration

Rationale

To provide appropriate gas exchange in the lungs and to prevent aspiration

To identify dysrhythmias and inadequate fluid resuscitation

Required because of dilutional effects of crystalloid and blood administration as well as consumption from ongoing bleeding The prothrombin time and partial thrombocia tin time should be corrected and the pistele count should be kept > 50.000/mm wh ongoing bleeding

Therapy

Activated Factor VII

Calcium chloride, magnesium chloride

Rewarming techniques (eg, warm fluids, blankets. radiant lamps, head covers, warmed humidified air, heated body cavity lavage)

Rationale

Should be considered in the presence of diffuse or nonoperative ongoing hemorrhage when clotting abnormalities have been corrected

To reverse ionized hypocalcemia and hypomagnesemia resulting from the administration of citrate with transfused blond which binds ionized calcium and magnes

Hypothermia is a common consequence of massive blood transfusion that can contribute to cardiac dysfunction and coagulation abnormalities

Therapy

Monitor and treat for transfusion-related complications including transfusion-related acute lung injury (TRALI) and transfusion reactions

Corticosteroids

Antibiotics

Rationale

These are immunologically mediated, requirme appropriate use of mechanical ventilation with positive end-expiratory pressure for TRALI and bronchodilators and corticosteroids for severe bronchoconstriction, subglottic edema, and anaphylaxis

When open dirty or contaminated wounds are present to prevent and treat bacterial infection

For patients presumed to have adrenal injury and patients unable to mount an appropriate stress response

DO= CaO2 X CO

CaO (Hb x 1.34 x SaO2) + 0.0031 PaO2

CO-SV X HR

where DO2= oxygen delivery, CaO2= arterial oxygen content, CO = cardiac output

Hb= hemoglobin concentration, SaO2= arterial hemoglobin oxygen saruration,

PaO2= arterial oxygen tension, SV = stroke volume, and HR = heart rate.

The treatment goals in hypovolemic shock are to control the source of hemorrhage and to administer adequate intravascular volume replacement. Control of the source of hemorrhage may be as simple as placing a pressure dressing on an open bleeding wound. or it may require urgent operative exploration to identify and control the bleeding source from an intra-abdominal or intrathoracic injury. Angiographic embolization of a bleeding vessel may also be helpful for bleeding injuries that are not amenable to surgical intervention (e.g., multiple pelvic fractures with ongoing hemorrhage). Therefore, most episodes of hypovolemic shock are managed by managed by trauma specialists, usually in the emergency department setting. However, all clinicians caring for critically ill patients should be able to recognize the early clinical manifestations of hypovolemic shock and to initiate appropriate fluid management.

At least two large-bore (14 to 16 gauge or larger) peripheral vein catheters and/or an 8.5 French central vein catheter should be placed to allow rapid blood product and crystalloid administration. A mechanical rapid transfusion device should also be used to decrease the time required for each unit of blood or liter of crystalloid to be infused. In a patient with ongoing hemorrhage, blood transfusion should be given. The goal of blood transfusion therapy during ongoing hemorrhage is to maintain the hemoglobin value above 8 g/dL. In addition to the initial administration of crystalloid and red blood cells, other therapies will be required in patients with hypovolemic shock. It is important for patients requiring massive transfusions or those with ongoing blood loss.