Hemorrhagic Shock Is a Condition of Inadequate

Hemorrhagic Shock

Shock is a condition of inadequate tissue perfusion, which results in decreased amount of oxygen in the vital tissues and organs (Metrng 2010, Klabunde 2010, Sarathy 2010, Spaniel et al. 2007). It reduces the rate of elimination of waste products of metabolism. Causes are heart attack, severe or sudden blood loss from injury or severe illness, blood poisoning from major infections, large decrease of body fluids, and exposure to extreme heat or cold for long duration. The American College of Surgeons classified shock into four, namely distributive, obstructive, cardiogenic, and hemorrhagic (Metrng, Klabunde, Sarathy & Spaniel et al.).

Hemorrhagic shock is a serious and life-threatening condition, which affects all body systems (Sarathy 2010). Cardiac output is reduced and depriving tissue of adequate oxygen. Hemorrhagic shock is further classified into four, according to the amount of blood lost. In Class I hemorrhage, there is a 15% or less blood loss with no other signs. In Class II hemorrhage, blood loss is 15-30% with definite tachycardia and tachypnea and decreased pulse pressure. It is Class III hemorrhage when the blood loss is 30-40% and all typical signs and symptoms of shock are evident. More than 40% blood loss is Class IV (Sarathy).

The clinical signs of hemorrhagic shock differ according to the volume of blood loss or Class (Medtrng 2010). In Class 1 or less than 15% blood loss, there are only slightly increased heart rate, local swelling and bleeding. In Class 2, the heart rate and diastolic blood pressure both increase and there is prolonged capillary refill. In Class 3, All these signs are present and, in addition, there are hypotension, confusion, acidosis, and decreased urine output. And the clinical signs of Class 4 are refractory hypotension, refractory acidosis and death. Other common signs are a continuing decrease in systolic and diastolic blood pressure; skin coldness and paleness; cyanosis; fast but weak and thready pulse rate; shallow and fast breathing, accompanied by a grunt; subnormal temperature; oliguria or reduced renal blood flow caused by vasoconstriction on account of reduced cardiac output; and uneasiness, stupor and unconsciousness (Metrng).

Increased Heart Rate vs. Decreased Blood Pressure

Hemorrhagic shock usually develops from a traumatic event, which leads to an acute loss of blood from the intravascular space (Spaniel et al. 2007). The condition severely affects the body's ability to provide sufficient tissue perfusion and oxygenation after the loss of blood. The reduction of circulating blood volume diminishes the return of blood from the veins to the heart and the end-diastolic volume or preload. The reduction in turn lessens myocardial muscle fiber length, contractility of the heart and its output. This decrease in cardiac output results in inadequate cellular oxygen supply and impaired tissue perfusion (Spaniol et al.). This result is hypovolemia.

This acute blood loss also results in compensatory responses, which affect all the body's organ systems. The initial response of the body to hypovolemia is to reduce the circulation of less vital organs, like the kidneys, the gut and the skin. This is an innate mechanism meant to preserve circulation to priority organs, such as the heart, brain, lungs, and skeletal muscle. This occurs with a decrease in cardiac output and the pulse pressure. This mechanism is perceived by baro-receptors within the aortic arch and atrium. Neural reflexes trigger a sympathetic outflow to the heart and other organs. These organs, in turn, respond by increasing heart rate and vasoconstriction. A hormonal response occurs. The rennin system is activated and leads to vasoconstriction. Sodium and water are retained. The body stimulates the anterior pituitary and adrenal medulla to release adrenocorticotropic hormone, epinephrine, and no-repinephrine, which enhance the compensatory mechanisms. At the cellular level, decreased perfusion leads the cells to turn from aerobic to anaerobic metabolism. The body produces lactic acid, which causes metabolic acidosis. With continued loss of blood, these compensatory mechanisms will fail and induce further damage throughout the body. Myocardial hypoperfusion and lactic acidosis can produce cardiac dysfunction. Cerebral hypoperfusion produces cardiac and respiratory depression as well as failure of the sympathetic nervous system. Failure of the systemic nervous system causes vasodilation, which leads to venous pooling and greater capillary permeability. Disseminated intravascular coagulation also develops from hematologic dysfunction. This dysfunction includes hypotension, hypoxemia, acidosis, and termination of capillary blood flow. Respiratory distress may also develop from increased pulmonary capillary membrane permeability, formation of micro-emboli, and pulmonary vasoconstriction. Renal vasoconstriction and hypoperfusion may further cause acute tubular necrosis and even renal failure. Gastrointestinal organs may also break down because of hypoperfusion and vasoconstriction. Irreversible damage at the cellular level may begin when the cell membrane loses its integrity. This is largely due to the presence of free radicals, especially those of the reactive oxygen and reactive nitrogen species. Both have unpaired electron, which causes the oxidation of DNA molecules, fatty acids, and amino acids. These advance cell degradation. The electrical gradient is lost, leading to the swelling of the cell. This damages the endoplasmic reticulum and mitochondria and leads to the dysfunctional use of oxygen. Enzymes from ruptured lysosomes take up other cellular structure. These events lead to cell death (Spanion et al.).#