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SHOCK Shock is an acute, widespread process of impaired tissue perfusion that results in cellular, metabolic, and hemodynamic alterations.

Ineffective tissue perfusio n occurs when an imbalance develops between cellular oxygen supply and cellular oxygen demand Shock syndrome:- shock is a complex pathophysiologic process that often results in multiple organ dysfunction syndrome(MODS) and death. All types of shock even tually result in ineffective tissue perfusion and the development of acute circu latory failure. The shock syndrome is a pathway involving a variety of pathologi c process that may be categorized into four stages; Initial stage Compensatory stage Progressive stage Refractory stage Types of Shock:Hypovolemic shock:- it can result from rather absolute or relative hypovolemia. Absolute hypovolemic occurs when there is a loss of fluid from the intravascular spaces. This can result from an external loss of fluid from the body or when t here is an internal shifting of fluid from the intravascular spaces to the extra vascular spaces. Fluid shifts can result from loss in intravascular integrity, i ncreased capillary membrane permeability or decreased colloidal osmotic pressure . Relative hypovolemia occurs when vasodilation produces an increase in vascular capacitance to circulating volume. Etiology:1. Loss of whole blood 2. Trauma or surgery 3. Gastrointestinal bleeding 4. Loss of plasma by thermal injuries, large lesions 5. Loss of other body fluids such as; Severe vomiting or diarrhea , and Mas sive dieresis 6. Loss of intracascular integrity; Ruptured spleen, Long bone or pelvis fr actures, Hemorrhagic pancreatitis, Hemothorax or hemoperitoneum and Arterial dis section or rupture. 7. Relative:- Vasodilation, Sepsis, Anaphylaxis, Loss of sympathetic stimul ation, increased capillary membrane permeability, decreased colloidal osmatic pr essure, Severe Sodium depletion , Hypopituitarism, Cirrhosis, Intestinal obstruc tion.

PATHOPHYSIOLOGY:Relative Hypovolemia Decreased circulating volume Decreased venous return Decreased Stroke volume Decreased Cardiac output Absolute Hypovolemia

Decreased cellular oxygen supply Ineffective tissue perfusion Impaired cellular Metabolism Assessment and Diagnosis:The clinical manifestations of Hypovolemic shock vary, depending on the severity of fluid loss and the patients ability to compensate for it. The class have described the level of severity of Hypovolemic shock. Class I :- its indicate a fluid volume loss up to 15% or an actual volume loss up to 750 ml. Compensatory mechanism maintain CO, and the patient appears free of symptoms other than slight anxiety. Class II :- Hypovolemic shock occurs with a fluid volume loss of 10%-30% or an actual volume loss of 750-1500ml. Falling CO activates more intense compensatory responses. The HR increases to over 100bpm in response to increased SNS stimula tion. The pulse pressure (pp) narrows as the diastolic blood pressure increases because of vasoconstriction. Respiratory rate (RR) increase to 20-30breath per m inutes and respiratory depth increases in an attempt to improve oxygenation. ABC specimens drawn during this phase reveal respiratory alkalosis and hypoxemia, a s a evidenced by a low partial pressure of carbon dioxide (PaCO2) and a low part ial pressure of oxygen (PaO2), respectively. Urine output (UO) starts to decline to 20-30 ml per minutes as renal perfusion decreases. Urine sodium decrease, wh ereas urine osmolality and specific gravity increase as the kidney start t conse rve sodium and water. The patients skin becomes pale and cool, with delayed capil lary refill because of peripheral vasoconstriction , jugular vein appear flat as a result of decreased venous return. Class III :- it occurs with a fluid volume loss of 30%to40% or an actual volume loss of 1500-2000ml. This level of severity produces the progressive stage of s hock as compensatory mechanisms become overwhelmed and ineffective tissue perfus ion develops. Systolic BP decreases. The Heart rate increase to over120bpm and d ysrthmias develop as myocardial ischemia ensues. Respiratory distress occurs as the pulmonary system deteriorates. ABG values during this phase reveal respirati on and metabolic acidosis and hypoxemiam as evidenced by a high Paco2, low bicar bonate (HCO3-), AND LOW Pao2 respectively. Decreased renal perfusion results in the development of Oliguria. Blood urea nitrogen(BUN) and serum creatinine leve l start to rise as the kidney begin to fail. The patients skin becomes ashen, col d, and clammy, with marked delayed capillary refill. The patient appears confuse d as cerebral perfusion decreased and level of consciousness (LOC) deteriorates. Class IV :- hypovolemic shock is usually refractory in nature. It occurs with a fluid volume loss of greater than 40%or an actual volume loss of more than 2000 ml. The compensatory mechanisms of the body completely deteriorate, and organ fa ilure occurs. Severe tachycardia and hypotension ensue. Peripheral pulses are ab sent, and because of marked peripheral vasoconstriction, capillary refill does n ot occur. The skin appears cyanotic, mottled, and extremely diaphoretic. Urine o utput ceases. The patient becomes lethargic and unresponsive, and a variety of c linical manifestation associated with failure of the different body systems deve lop. Assessment of the hemodynamic parameters of a patient in hypovolemic shock varie s by stage, but commonly reveals a decreased CO and cardiac index (CI). Loss of circulating volume leads to a decrease in venous preload of the right and left ventrecles. This is evidenced by a decline in the right atrial pressure (RAP) an d pulmonary artery occlusion pressure (PAOP). Vasoconstriction of the artery sys tem results in an increase in the afterload of the heart as avidenced by a incr ease in the SVR. This vasoconstriction may produce a falsely elevated systolic B P when measured by arterial catheter. Mean arterial pressure (MAP) is more accur ate in this low flow state. MEDICAL MANAGEMENT:-

Treatment of the patient in hypovolemic shock requires an aggressive approach. T he major goals of therapy are to correct the cause of the hypovolemia and to res tore tissue perfusion. This approach includes indentifying and stopping the sour ce of fluid loss and vigorously administering fluid to replace circulating volum e. Fluid administration can be accomplished with use of either a crystalloid or a colloid solution used usually depends on the type of fluid lost, the degree of hypovolemia, and the severity of hypoperfusion. CARDIOGENIC SHOCK:Cardiogenic shock is the result of failure of the heart to effectively pump blo od forward. If can occur with dysfunction of either the right or the left ventri cle, or both the lack of adequate pumping function leads to decreased tissue per fusion and circulatory failure. It occurs in approximately 6%-10% f the patients with an acute myocardial infarction (MI) and is the leading cause of death in patients hospitalized with MI. The mortality rate for cardiogenic shock has dec reased with the advent of early revascularization therapy and is currently aroun d 50%to 60%. ETIOLOGY:Primary vascular Ischemia; Acute myocardial Infarction, Cardiopulmonary arrest, Open heart surgery Structural Problems; Septal rupture, Free wall rupture, Papillary muscles ruptur e, Ventricular Aneurysm, Cardiomyopathies, Congestive, Hypertrophic, Restrictive , Intracardiac Tumor, Pulmonary Embolus, Atrial myocarditis, Cardiac Tamponade, Myocardial contusion. Dysrhythemias; Bradydysrhythemia, tachydysrhythmias. PATHOPHYSIOLOGY:Cardiogenic shock results from the impaired ability of the ventricle to pump blo od forward, which leads to a decrease in SV and an increase in the blood left in the ventricle at the end of systole. The decrease in SV results in a decrease i n CO, which leads to decreased cellular oxygen supply and ineffective tissue per fusion. Typically myocardial performance spirals downward as compensatory vasoco nstriction increases myocardial afterload and low blood pressure worsens myocard ial ischemia. Evidence of a systemic inflammatory response has been noted in a number of patie nts with Cardiganic Shock (recent research suggest). Activation of inflammatory cytokines may induce systemic vasodilation, normalization of the CO2, and defect ive cellular oxygen use. It is unknown whether this process contributes to the g enesis or the outcome of cardiogenic shock. As left ventricular contractility fa lls, an increase in end systolic volume results in the back up of blood into the pulmonary system and the subsequent development of pulmonary edema. Pulmonary e dema causes inpaired gas exchange and decreased oxygenation of the arterial bloo d, which further impair tissue perfusion. Death due to cardiogenic shock may res ult from multiple organ failure or cardiopulmonary collapse. Clinical manifestation of Cardiogenic Shock: Systolic blood pressure less than 90 mmHg Heart rate more than 100 beats per minute Weak, thread pulse Diminished Heart Sound Change in Sensorium Cool, Pale, and moist Skin Urine output less than 30 ml/hr Chest pain Dysrhythmias Tachypnea Crackles Decreased cardiac output Cardiac Index less than 2.2/min/m2 Increased pulmonary artery occlusion pressure Increased right atrial pressure Increased systemic vascular resistance

ABG values at this time indicate respiratory alkalosis as evidenced by a decreas e in Paco2 Urinalysis finding demonstrate a decrease in Sodium and an increase in urine osm alality and specific gravity as the kidney start to conserve sodium and water Cradkles and Rhonchi , indicating the development of pulmonary Edema Jugular vein distention is evident with right sided failure Increased filling pressures are necessary to rule out hypovolemia as the causes of circulatory failure. Pathophysiology of cardiologic shock

Primary ventricular ischemia dysrthemias Ineffective forward motion of blood Decreased stroke volume emptying Decreased cardiac output ry pressure

structural problems

ineffective ventricular increased pulmona Pulmonary edema Decreased oxyge

nation Decreased cellular oxygen supply Ineffective tissue perfusion Impaired cellular metabolism MEDICAL MANAGEMEN:Treatment of the patient in cardiogenic shock requires an aggressive approach. The major goals of therapy are to treat the underlying cause, enhance the effect iveness of the pump, and improve tissue perfusion. Inotropic agents are used to increase contractility and maintain adequate BP and tissue perfusion. Diuretics are used for preload reduction. Once blood pressure has been stabilise d, vasodilating agent are used for preload and afrerload reduction. Antidysrhythmic agent should be used to suppress or control dysrhythmias that ca n affect CO. Intubation and mechanical ventilation may be necessary to support oxygenation. Intraaortic balloon pump (IABP) support should be instituted if drug therapy doe s not quickly reverse the shock state. Once the problem of pump failure has been identified, measures should be taken t o correct the problem if possible. If the problem is related to an acute MI , ea rly revascularization by coronary angioplasty or coronary artery bypass surgery provides significant survival benefit. Thrombolytic agent may be used in select patient. Therapies to decrease myocardial demand should include activity restr iction, analgesics and sedatives. When conventional therapies fail, extracorpore al membrane oxygenation (ECMO) and /or a ventricular assist device (VAD ) may b e used to support the patient in acute cardiogenic shock. NURSING MANAGEMENT:Prevention of cardiogenic shock is one of the primary responsibilities of the nu rse in the critical care area. Prevention measures include the identification of patients at risk and frequent assessment and management of the patients cardiopu

lmonary status. Measures to limit myocardial oxygen demand include administratin g analgesics, sedatives, and agent to control afterload and dysrhythmias; positi oning the patient for comfort; limit activities; providing a calm and quiet envi ronment and offering support to reduce anxiety; and teaching the patient about t he condition. Measures to enhance myocardial oxygen supply include administering supplement oxygen, monitoring the patients respiratory status, and administering prescribed medication. Effective nursing management of cardiogenic shock requires precise monitoring an d management of HR, preload afterload, and contractility. This is accomplished through accurate measurement of hemodynamic variables and controlled administrat ion of fluids and inotropic and vasoactive agents. Close assessment and manageme nt of respiratory function is also essential to maintain adequate oxygenation. Patients who require IABP therapy need to be observed frequently for complicatio n. Complication include emblolus formation, infection, rupture of the aorta, thr ombocytopenia, improper balloon placement, bleeding, improper timing of the ball oon, balloon rupture and circulatiory compromise of the cannulated extremity. ANAPHYLATIC SHOCK:Anaphylactic shock, a type of distributive shock, is the result of an immediate hypersensitivity reaction. It is a life threatening event that requires prompt i ntervention. The severe antibody-antigen response leads to decreased tissue perf usion and initiation of the general shock response. Etiolgy:Anaphylactic shock is caused by an antibody-antigen response. Almost any substan ce can cause a hypersensitivity reaction. These substance known as antigen, can be introduced by injection or ingestion or through the skin or respiratory tract . Anaphylactic reaction can be either IgE mediated or non IgE mediated response. T he first time an antigen enters the body, an antibody IgE, specific for the anti gen, is formed. The antigen specific IgE antibody is then stored by attachment t o mast cells and basophils. This initial contact with the antigen is known as a primary immune response. The next time the antigen enters the body, the performe d IgEantibody reacts with it and a secondary immune response occurs. This reacti on triggers the release of biochemical mediators from the mast cells and basophi ls and initiates the cascade of event that precipitates anaphylactic shock. Some anaphylactic reactions are non-IgE mediated responses in that they occur in the absence of activation of IgE antibodies. These responses occur as a result of direct mediators. Direct activation of mast cells can be triggered by humoral mediators, such as the complement system and the coagulation-fibrinolytic syste m. In addition, biochemical mediators can be released as a direct or indirect re sponse to many drugs. This types of reaction is known as anaphylactoid reactio n. Anaphylactoid reaction are produced in persons not previously sensitized and can occur with the first exposure to an antigen. Pathophysiology:The antibody-antigen response (immunologic stimulation) or the direct triggering ( non-immunologic activation) of the mast cells results in the release of bioch emical mediators. These mediators include histamine, eosinophil chemotactic fact or of anaphylaxis (ECF-A), neutrophil chemotactic factor of anaphylaxis (NCF-A), platelet activating factor (PAF), Proteinases, heparin, serotonin, leukotrienes , and prostaglandins. The activation of biochemical mediators causes vasodilati on, increased capillary permeability, bronchoconstriction, excessive mucus secre tion, coronary vasoconstriction, inflammation, cutaneous reactions, and constric tion of smooth muscle in the intestinal wall, the bladder, and the uterus.