Shock and Shock Syndrome PDF

Shock Intended Learning Objectives (ILOs): 1- Knowledge and Understanding: ▪ List the classification of shock ▪ Identify the pathophysiological changes that may occur in shock. ▪ Identify vasoactive medications used in treating shock. 2- Intellectual Skills: Compare etiology and clinical manif...

Shock Intended Learning Objectives (ILOs): 1- Knowledge and Understanding: ▪ List the classification of shock ▪ Identify the pathophysiological changes that may occur in shock. ▪ Identify vasoactive medications used in treating shock. 2- Intellectual Skills: Compare etiology and clinical manifestations of different types of shock Evaluate management modalities of various types of shock. 3- Professional and Practical Skills:- a) Use the nursing processes as a framework for care of critically ill patients with different types of shock  Out lines: Description of shock Stages of shock syndrome Classification of shock Pathophysiology of shock Assessment and Diagnosis Medical Management  Shock Definition: is an acute, widespread process of impaired tissue perfusion that results in cellular, metabolic, and hemodynamic alterations.  Classification of Shock Hypovolemic shock: results from a loss of circulating or intravascular volume. Cardiogenic shock: results from the impaired ability of the heart to pump. Distributive shock: results from maldistribution of circulating blood volume and can be further classified as septic, anaphylactic, or neurogenic..  Classification of Shock Septic shock: is the result of microorganisms entering the body. Anaphylactic shock: is the result of a severe antibody-antigen reaction. Neurogenic shock: is the result of the loss of sympathetic tone  Shock syndrome: is a generalized systemic response to inadequate tissue perfusion which consists of four different stages: Initial stage Compensatory stage Progressive stage Refractory stage Pathophysiology of Initial Stage of Shock: Decreased cardiac output and impaired tissue perfusion causes the cells to switch from Aerobic to Anaerobic metabolism as a source of energy Pathophysiology of Initial Stage of Shock: Anaerobic metabolism produces small amounts of energy but large amounts of lactic acid Lactic acidemia causes cellular damage Pathophysiology of Compensatory Stage The compensatory mechanisms are mediated by the sympathetic nervous system (SNS) and consist of : Neural response Hormonal response Chemical response  Neural Response Increase in HR and contractility Arterial & venous vasoconstriction Shunting of blood to the vital organs  Hormonal Compensation Hormonal compensation includes: Activation of the renin response Stimulation of the anterior pituitary Stimulation adrenal medulla. Hormonal Compensation 1) Activation of the renin response results in the production of angiotensin II, which causes vasoconstriction and the release of aldosterone and antidiuretic hormone (ADH), leading to sodium and water retention  Hormonal Compensation 2) Stimulation of the anterior pituitary results in the secretion of adrenocorticotropic hormone (ACTH), which in turn stimulates the adrenal cortex to produce glucocorticoids. Glucocorticoids increases blood glucose level by increasing the conversion of glycogen to glucose  Hormonal Compensation 3) Stimulation of the adrenal medulla causes the release of epinephrine and norepinephrine, which further enhance the compensatory mechanisms  Chemical Compensation Chemical compensation includes hyperventilation. As the patient hyperventilates, carbon dioxide is excreted causing respiratory alkalosis Pathophysiology Progressive Stage Cardiovascular System Cardiac dysfunction develops as a result Myocardial hypoperfusion The release of myocardial depressant cytokines. Ventricular failure occurs, Pathophysiology Progressive Stage Central nervous system: (CNS) dysfunction develops as a result of Cerebral hypoperfusion, leading to failure of the SNS, Cardiac and respiratory depression, Thermoregulatory failure. Pathophysiology Progressive Stage Pulmonary dysfunction occurs as a result of Increased pulmonary capillary membrane permeability, Pulmonary micro-emboli, Pulmonary vasoconstriction. Ventilatory failure and acute Lung Injury (ALI) develop. Pathophysiology Of Progressive Stage Renal dysfunction develops as a result of Renal vasoconstriction Renal hypoperfusion Leading to acute kidney injury (AKI). Pathophysiology of Progressive Stage Gastrointestinal dysfunction: Splanchnic vasoconstriction and hypoperfusion and leads to failure of the gut organs. Disruption of the intestinal epithelium releases gram-negative bacteria into the system, increases the entire shock syndrome  Refractory Stage: During the refractory stage, shock becomes unresponsive to therapy and is considered irreversible. As the individual organ systems die. MODS—defined as failure of two or more body systems—occurs. Death is the final outcome.  Assessment and Diagnosis MAP less than 60 mm Hg and Systolic blood pressure less than 90 mm Hg Accompanied by either tachycardia or bradycardia Altered mental status is considered to be a shock state Serum lactate, arterial base deficit, serum bicarbonate, and central or mixed venous oxygen saturation levels  Medical Management Improvement and preservation of tissue perfusion. Adequate tissue perfusion depends on an adequate supply of oxygen being transported to the tissues and the cell's ability to use it. Oxygen transport is influenced by pulmonary gas exchange, CO, and hemoglobin level, Improve Pulmonary Gas Exchange Establishing and maintaining an adequate airway are the first steps in ensuring adequate oxygenation. After the airway is patent, emphasis is placed on improving ventilation and oxygenation by administration of supplemental oxygen and mechanical ventilator/ support.  Improve Pulmonary Gas Exchange An adequate CO and hemoglobin level are crucial to oxygen transport. CO depends on heart rate, preload, after-load, and contractility. The types of fluids used include crystalloids and colloids. The medications used as vasoconstrictors, vasodilators, positive inotropes, and anti- dysrhythmics Hypovolemic Shock Hypovolemic shock occurs from inadequate volume in the intravascular space The lack of adequate circulating volume leads to decreased tissue perfusion and causing the general shock syndrome Types of Hypovolemic Shock 1- Absolute hypovolemia: Loss of fluid from the intravascular space. External loss of fluid from the body including whole blood, plasma, or any other body fluid. 2- Relative hypovolemia: Vasodilation produce vascular capacitance relative to circulating volume. Vasodilation, decrease osmotic pressure Pathophysiology of Hypovolemic Shock Hypovolemia results in: Loss of circulating fluid volume Decrease in venous return, which in turn, results in a decrease in preload Decrease in CO Inadequate cellular oxygen supply and ineffective tissue perfusion  Clinical Manifestations ⚫The initial stage: ⚫fluid volume loss up to 15% or 750 ml. Compensatory mechanisms maintain CO, and the patient appears symptoms- free ⚫ The compensatory stage: ⚫ Fluid volume loss of (15% to 30%) 750 to 1500 mL.CO falls resulting in a variety of compensatory responses: ⚫ The HR increases more than 100 B/M in response to increased SNS stimulation ⚫ Respiratory rate 20 to 30 b/ m and depth increase in an attempt to improve oxygenation ⚫ ABG reveals respiratory alkalosis and hypoxemia, as evidenced by low PaCo2 and low PaO2 The compensatory stage: Urine output start to decline to 20 to 30 mL/h as renal perfusion decreases The patient’s skin becomes pale and cool, with delayed capillary refill because of peripheral vasoconstriction Jugular veins appear flat as a result of decreased venous return The progressive stage: ⚫ Fluid volume loss of (30 to 40%) 1500 to 2000mL ⚫ The compensatory mechanisms become overwhelmed and ineffective tissue perfusion develops 1) The HR continues to increase more than 120 b/m and dysrhythmias develop as myocardial ischemia occurs 2) Respiratory distress occurs as the pulmonary system deteriorates The progressive stage: ⚫ ABG values during this phase reveal respiratory and metabolic acidosis and hypoxemia, as evidenced by a high PaCo2, low bicarbonate and low PaO2 ⚫ Decreased renal perfusion results in the development of oliguria. The progressive stage: ⚫ BUN and serum creatinine levels start to rise as the kidneys begin to fail ⚫ The patient’s skin becomes ashen, cold, and clammy, with marked delayed capillary refill ⚫ Patient appears lethergic as cerebral perfusion decreases and level of conscious continues to deteriorate ⚫ The refractory stage: ⚫ Fluid loss of greater than (40%) 2000 ml. ⚫ The compensatory mechanisms of the body completely deteriorate and organ failure occurs ⚫ Severe tachycardia and hypotension occur ⚫ Peripheral pulses are absent, absent of capillary refill because of marked peripheral vasoconstriction, ⚫ The skin appears cyanotic and extremely diaphoretic ⚫ The patient becomes unresponsiveness, and a variety of clinical manifestations associated with failure of the different body systems develop Hemodynamic Parameters in Hypovolemic Shock ⚫ Decrease CO and CI ⚫ Decrease preload (decline in the CVP- RAP-PAOP) ⚫ Increase in the after-load (increase in the systemic vascular resistance SVR) ⚫ Decrease MAP Management of Hypovolemic Shock ⚫ correct the causes of the hypovolemia and to restore tissue perfusion ⚫ stopping the source of fluid loss and administering fluid to replace circulating volume. ⚫ Fluid administration can be accomplished with use of a crystalloid solution, a colloid solution, blood products, or a combination of fluids. ⚫ 1) Vigorous fluid administration to replace the circulating volume ⚫ 2) Measures to enhance volume replacement ⚫ 3) Monitoring the patient for clinical manifestations of fluid overload  yo u a nk Th