Article Contents ::
- 1 Details Descriptions About :: Shock
- 2 Shock is a clinical syndrome that leads to reduced perfusion of tissues and organs and organ failure. Shock can be classified into three categories: distributive (neurogenic, septic, and anaphylactic), cardiogenic, and hypovolemic.
- 3 Causes for Shock
- 4 Pathophysiology Shock
- 5 Signs and symptoms Shock
- 6 Diagnostic Lab Test results
- 7 Treatment for Shock
- 8 Disclaimer ::
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Details Descriptions About :: Shock
Shock is a clinical syndrome that leads to reduced perfusion of tissues and organs and organ failure. Shock can be classified into three categories: distributive (neurogenic, septic, and anaphylactic), cardiogenic, and hypovolemic.
Causes for Shock
Causes Neurogenic shock Spinal cord injury, spinal anesthesia Vasomotor center depression Severe pain Medications Hypoglycemia Septic shock Gram-negative bacteria, gram-positive bacteria Viruses, fungi, rickettsiae, parasites, yeast, protozoa, mycobacteria Anaphylactic shock Medications, vaccines, contrast media Foods ABO-incompatible blood Cardiogenic shock Myocardial infarction (MI), most common cause Heart failure, cardiomyopathy Pericardial tamponade Pulmonary embolism Hypovolemic shock Blood loss (most common cause) GI fluid loss, renal loss, fluid shifts Burns
Pathophysiology Each type of shock has three stages. Compensatory stage: When arterial pressure and tissue perfusion fall, compensatory mechanisms are activated to maintain cardiac output and perfusion to the heart and brain. As the baroreceptors in the carotid sinus and aortic arch sense a drop in blood pressure, epinephrine and norepinephrine are secreted to increase peripheral resistance, blood pressure, and myocardial contractility. Reduced blood flow to the kidney activates the renin-angiotensin-aldosterone system, causing vasoconstriction and sodium and water retention. Progressive stage: When compensatory mechanisms can’t maintain cardiac output, tissues become hypoxic. Cells switch to anaerobic metabolism and lactic acid accumulates, producing metabolic acidosis. Tissue hypoxia promotes the release of endothelial mediators, leading to venous pooling and increased capillary permeability. Sluggish blood flow increases the risk of disseminated intravascular coagulation (DIC). Irreversible (refractory) stage: Inadequate perfusion damages cell membranes, lysosomal enzymes are released, and energy stores are depleted, leading to cell death. Lactic acid continues to accumulate, increasing capillary permeability and the movement of fluid out of the vascular space, further contributing to hypotension. Perfusion to the coronary arteries is reduced, causing myocardial depression and a further reduction in cardiac output. Circulatory and respiratory failure occur.
Signs and symptoms Shock
Signs and symptoms Compensatory stage Tachycardia and bounding pulse Tachypnea Reduced urinary output Cool, pale skin (or warm, dry skin in septic shock) Progressive stage Hypotension Narrowed pulse pressure; weak, rapid, thready pulse Shallow respirations Cold, clammy skin; cyanosis Irreversible stage Unconsciousness and absent reflexes Rapidly falling blood pressure; weak pulse Slow, shallow or Cheyne-Stokes respirations
Diagnostic Lab Test results
Diagnostic test results Hematocrit is reduced in hemorrhage or elevated in other types of shock caused by hypovolemia. Blood, urine, and sputum cultures identify the organism responsible for septic shock. Coagulation studies may detect coagulopathy from DIC. Complete blood count reveals increased white blood cell count and erythrocyte sedimentation rate. Blood chemistry reveals elevated blood urea nitrogen and creatinine levels; and elevated serum glucose (in early stages). Serum lactate is increased secondary to anaerobic metabolism. Elevated cardiac enzymes and proteins indicate MI as a cause of cardiogenic shock. Arterial blood gas analysis reveals respiratory alkalosis. Urine specific gravity will be elevated in response to the effects of antidiuretic hormone. Chest X-rays will be normal in early stages; pulmonary congestion may be seen in later stages. Electrocardiography may show arrhythmias, ischemic changes, and an MI. Echocardiography reveals valvular abnormalities.
Treatment for Shock
Treatment Identification and treatment of the underlying cause Maintaining a patent airway, oxygen and mechanical ventilation, and continuous cardiac monitoring I.V. fluids, crystalloids, colloids, or blood products Neurogenic shock Vasopressor drugs Septic shock Treatment with drotrecogin alfa (Xigris) antibiotics, and inotropic and vasopressor drugs Cardiogenic shock Inotropic drugs, vasodilators, diuretics Intra-aortic balloon pump therapy Thrombolytic therapy or coronary artery revascularization Ventricular assist device Heart transplantation Hypovolemic shock Pneumatic antishock garment