Approach to the patients with shock AA Khaleghi Emergency medicine specialist

PERSPECTIVE In philosophic terms, shock can be viewed as a transition between life and death. Whether shock results from hemorrhage, sepsis, or cardiac failure, mortality rates exceed 20%. In scientific lexicon, shock results from the widespread failure of the circulatory system to oxygenate and nourish the body adequately.

Classification For years, shock has been classified into four broad categories based on Blalock's 1934 description: hematological,neurologic, vasogenic, and cardiogenic

Epidemiology The epidemiology of shock in the emergency department remains speculative Patients presenting with traumatic, cardiogenic, or septic shock constitute about 1% of all emergency department visits

PATHOPHYSIOLOGY At the subcellular level, shock first affects the mitochondria. In the early stage of shock, the skeletal muscle and splanchnic organs are affected more by oxygen deprivation than by a lack of delivery of fuel substrate Regardless of etiology, elevated concentrations of lactate in the blood serve as a sentinel marker of widespread inadequate tissue perfusion and disappear when adequate resuscitation has been achieved.

At the whole-body level, shock from any etiology initiates a sequence of stress responses that are intended to preserve flow to vital organs and to signal cells to expend internal energy stores Although lactic acidosis is a unifying feature of shock, its exact source may depend on the cause of shock. Initiation of inflammatory events constitutes a third unifying feature of shock.

Specific Causes Hemorrhagic Shock In general, hemorrhage first increases pulse and cardiac contraction, then increases vasoconstriction. The first clinical manifestations of hemorrhage are tachycardia, then a slight increase in the diastolic BP, causing the pulse pressure (difference between systolic and diastolic BP) to narrow Arterial hypotension is generally and arbitrarily defined as a systolic arterial BP less than 90 mm Hg, but this threshold should be increased to 100 mm Hg in patients with known systemic hypertension and inpatients older than age 60 years The second phase of organ injury from hemorrhagic shock occurs during resuscitation.

Septic Shock Septic shock can be produced by infection with any microbe. gram-negative aerobic gram-positive In one third of cases of septic shock, no organism is identified. Septic shock causes three major effects that must be addressed during resuscitation: hypovolemia, cardiovascular depression, and induction of systemic inflammation.

Cardiogenic Shock Cardiogenic shock results when more than 40% of the myocardium becomes necrosed from ischemia, inflammation toxins, or immune destruction. Acute massive pulmonary embolism produces circulatory shock by obstruction of the pulmonary vasculature, which leads to right ventricular overload and impairs left ventricular filling

Anaphylactic Shock Anaphylactic shock results from an IgE- mediated systemic response to an allergen. IgE causes mast cells to release histamine, which results invascular smooth muscle relaxation, bronchial smooth muscle constriction, and capillary leak of plasma into interstitial spaces. Platelets also participate in anaphylaxis by secreting platelet-activating factor (PAF),

CLINICAL FEATURES

The HR-to-systolic BP ratio may provide a better marker of shock than either measurement alone; a normal ratio is less than 0.8," Measuring urine output requires at least 30 minutes, however, to determine accurately if output is normal (>1 mL/kg/hr), reduced (0.5 to 1 mL/kg/hr), or severely reduced«0.5 mL/kg/hr). An arterial lactate concentration greater than 4 mM/L or an arterial base deficit more negativethan -4 mEq/L predicts the presence of circulatory insufficiency

The physical examination should be performed on an undressed patient should begin with general inspection of the body for visual or tactile evidence of trauma odor of ethanol or other toxins presence of any indwelling devices evidence of soft tissue or bone infection, rashes, or extremity edema Dry mucous membranes distended jugular heart sounds pulmonary rales Wheezing Abdominal tenderness Rectal and pelvic examinations Recta] temperature

Laboratory, radiographic, and other ancillary data to assess tissue and vital organ perfusion to diagnose injury from trauma, find the source of infection with sepsis, or identify the cause of cardiac failure.

MANAGEMENT Monitoring Perfusion Status In all patients with shock, circulation must be monitored by continuous ECG and pulse oximetry BP should be measured by cuff sphygmomanometer every 2 to 5 minutes during resuscitation Urine output should be measured as an index of vital organ perfusion lactate concentration or the base deficit, method of achieving intravenous access

Goal-Directed Therapy refers to the practice of resuscitating patients to a defined physiologic endpoint indicating that systemic perfusion and vital organ function have been restored. lactate clearance Mixed venous oxygen saturation (SV02) central venous oxygen saturation (Scvo2] Gastric or rectal tonography

Ventilation Volume Replacement The goal in volume replacement is slightly elevated left ventricular end- diastolic volume