Shock

Effects of Shock on Body Systems : Neurologic system

-An early sign of shock is a change in LOC. Late signs of shock include mental status changes, hypotension, and marked tachycardia •Cerebral hypoxia produces altered LOCs, beginning with apathy and lethargy and progressing to coma •Common early symptom of cerebral hypoxia is restlessness •Brain cells eventually causes swelling, resulting in cerebral edema, neurotransmitter failure, and irreversible brain damage •As cerebral ischemia worsens, the sympathetic activity and vasomotor centers are depressed •This leads to a loss of sympathetic tone, causing systemic vasodilation and pooling of blood in the periphery

Implementation : Relieve anxiety

-Assess causes, manipulate environment to provide periods of rest, reduce stimuli -Administer pain medication. Pain precipitates and/or aggravates anxiety -Increase comfort, reduce restlessness ■Clean environment as unfamiliar sounds, sights, and odors can increase anxiety ■Skin, oral care. Damp skin or a dry mouth increases discomfort. ■Monitor the effectiveness of ventilation or oxygen therapy. Inadequate gas exchange with a decrease in oxygen or an increase in carbon dioxide in the blood may cause the patient to experience a "feeling of doom." ■Eliminate nonessential activities ■Remain with patient during procedures. Listening and touch provide support in an environment in which the patient often feels alone and abandoned ■Speak slowly, calmly, using short sentences, touch as appropriate -Provide patient, family support -Provide information about current setting to patient and family ■Provide time, space, privacy for family members ■Encourage the patient to express feelings and concerns. ■Allow family members access to patient when feasible

Implementation : Promote tissue perfusion

-Monitor skin color, temperature, turgor, moisture - Decreased tissue perfusion is evidenced by the skin becoming pale, cool, and moist; as hemoglobin concentrations decrease, cyanosis occurs. -Monitor cardiopulmonary functioning by regularly assessing BP - Baseline vital signs are necessary to determine trends in subsequent findings -Monitor body temperature - elevated body temperature increases metabolic demands, depleting energy reserves -Monitor urinary output -per indwelling urinary catheter hourly, using a urometer. Urine output is a reliable indicator of renal perfusion -Assess mental status, LOC - appropriateness of the patient's behavior and responses reflects the adequacy of cerebral circulation. Altered LOCs are the result of both cerebral hypoxia and the effects of acidosis on brain cells

Distributive (Vasogenic) Shock : Several types of shock resulting from widespread vasodilation, decreased PVR

-Septic shock (septicemia) - most often the result of gram negative bacterial infections (e.g., Pseudomonas, Escherichia coli, Klebsiella) but may also follow gram positive infections from Staphylococcus and Streptococcus bacteria -Neurogenic shock - result of an imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle ■parasympathetic overstimulation or sympathetic understimulation persists, sustained vasodilation occurs, and blood pools in the venous and capillary beds ■SVR decreases, pressure in the blood vessels becomes too low to drive nutrients across capillary membranes, and cellular metabolism is impaired ■Bradycardia occurs early in neurogenic shock, but tachycardia begins as compensatory mechanisms ■In early stages, the extremities are warm and pink (from the pooling of blood), but as shock progresses, the skin becomes pale and cool •Parasympathetic overstimulation → sustained vasodilation •Dramatic reduction in systemic PVR •Causes •Head injury or trauma to spinal cord •Insulin reactions, CNS drugs, anesthesia •Severe pain •Exposure to heat -Anaphylactic shock (our main focus) ■Allergens that can cause anaphylactic shock -Medications -Blood administration -Latex -Foods -Snake venom, insect stings

Hypovolemic Shock

Decreased blood volume → decreased venous return → decreased stroke volume → decreased CO and BP → Decreased tissue perfusion ■Decrease in circulating blood volume resulting from -External: fluid losses ■Trauma ■Surgery ■Vomiting ■Diarrhea ■Continuous nasogastric suctioning ■Diuresis ■Diabetes insipidus -Internal fluid shifts: ■Hemorrhage ■Burns ■Ascites ■Peritonitis ■Dehydration ■Intestinal obstruction •Is caused by a decrease in intravascular volume of 15% or more •Hypovolemic shock is the most common type of shock, and it often occurs simultaneously with other forms of shock •Its effects vary depending on the patient's age, the patient's general state of health, the extent of injury or severity of illness, the length of time before treatment is provided, and the rate of volume loss •The loss of circulating blood volume reduces CO by decreasing venous return to the heart •BP drops, and the body induces the sympathetic compensatory responses •If the fluid loss is less than 500 mL in adults, the sympathetic response is generally adequate to restore CO and BP to near normal, although the heart rate may remain elevated •Heart rate and vasoconstriction increase, and blood flow to the skin, skeletal muscles, kidneys, and abdominal organs decreases •Several renal mechanisms and a decline in capillary pressure help conserve blood volume •Atherosclerosis affects many vital organs' sensitivity to even the slightest reduction in blood flow •Patients who take beta-blockers may not present with tachycardia as an early indicator of shock will require early invasive monitoring in order to avoid excessive or inadequate volume restoration

Cardiogenic Shock

Occurs when heart's pumping ability cannot maintain CO, perfusion ■Causes -MI (most common cause) -Cardiac tamponade -Restrictive pericarditis -Cardiac arrest -Dysrhythmias -Pathologic changes in valves, cardiomyopathies -Complications of cardiac surgery -Electrolyte imbalances especially changes in normal potassium and calcium levels -Drugs affecting cardiac muscle contractility -Head injuries causing damage to cardioregulatory center

Distributive (Vasogenic) Shock

•1. Precipitating event •2. Vasodilation •3. Activation of inflammatory response •4. Maldistribution of blood volume •5. Decreased venous return •6. Decreased CO •7. Decreased tissue perfusion

Assessment : Anaphylactic shock

•Allergies •Drug reactions •noting these allergies clearly on all documents •placing a special armband on the patient •Careful and frequent assessments during blood administration may prevent serious reactions to blood or blood products

Implementation : Preserve cardiac output

•Assess, monitor cardiovascular function •BP •Heart rate and rhythm •Pulse oximetry •Peripheral pulses •Hemodynamic monitoring •Conduct baseline assessment to establish stage of shock •Measure, record I&O hourly •Monitor bowel sounds, abdominal distention, abdominal pain •Monitor for sudden sharp chest pain, dyspnea, cyanosis, anxiety, restlessness •Monitor for dyspnea •Maintain bedrest, provide a calm, quiet environment

Class II: Compensatory Shock

•Begins after MAP falls 10-15 mmHg below normal or Circulating blood volume reduced 15-30% •The body shunts blood to vital organs and maintain BP •Away from skin, kidneys, GI tract •MAP can be maintained for only short time •During this period, perfusion and oxygenation of the heart and brain are adequate. •RR increases due to acidosis, may cause compensatory respiratory acidosis •If effective treatment provided, process stops with no permanent damage •Unless underlying cause is reversed, compensatory mechanisms become harmful, perpetuating shock •Monitor: •VS •Skin color and temperature •Body temperature •Pulses (may be rapid, weak, and thready) •LOC •MAP: The definition of mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole. MAP is influenced by cardiac output and systemic vascular resistance, each of which is under the influence of several variables •Stimulation of the SNS results in the release of epinephrine from the adrenal medulla and the release of norepinephrine from the adrenal medulla and the sympathetic fiber •Stimulated alphaadrenergic fibers cause vasoconstriction in the blood vessels that supply the skin and most of the abdominal viscera so perfusion of these areas decreases •Stimulated betaadrenergic fibers cause vasodilation in vessels supplying the heart and skeletal muscles (beta1 response) and increase the heart rate and force of cardiac contraction (beta2 response) •Furthermore, blood vessels in the respiratory system dilate, and the respiratory rate increases (beta2 response). Thus, stimulation of the SNS results in increased CO and oxygenation of these tissues •The reninangiotensin response occurs as blood flow to the kidneys decreases. Renin released from the kidneys converts a plasma protein to angiotensin II, which causes vasoconstriction and stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reabsorb water and sodium and to lose potassium. The absorption of water maintains circulating blood volume while increased vasoconstriction increases SVR, maintaining central vascular volume and raising BP. •The hypothalamus releases adrenocorticotropic hormone, causing the adrenal glands to secrete aldosterone. Aldosterone promotes the reabsorption of water and sodium by the kidneys, preserving blood volume and pressure •The posterior pituitary gland releases ADH, which increases renal reabsorption of water to increase intravascular volume. The combined effects of hormones released by the hypothalamus and posterior pituitary glands work to conserve central vascular volume •As MAP falls in the compensatory stage of shock, decreased capillary hydrostatic pressure causes a fluid shift from the interstitial space into the capillaries. The net gain of fluid raises the blood volume •Blood loss 750-1500 mL •% of blood volume loss 15-30% •Heart rate 100-120 •Blood pressure Normal •Pulse pressure Decreased •Capillary refill Mildly Increased •Respiratory rate Mildly Increased •Urine output 20-30 mL/hr •Mental status Mildly anxious to agitated

Diagnostic Tests

•Blood hemoglobin and hematocrit - Changes in hemoglobin and hematocrit concentrations usually occur in hypovolemic shock. Hypovolemic shock resulting from hemorrhage, hemoglobin and hematocrit concentrations are lower than normal. Hypovolemic shock resulting from intravascular fluid loss, hemoglobin and hematocrit concentrations are higher than normal •Arterial blood gases (ABGs) - effects of shock and of the body's compensatory mechanisms often cause a decrease in pH, a decrease in PaO2 and total oxygen saturation, and an increase in PaCO2 •Serum electrolytes - determine the severity and progression of shock. As shock progresses, glucose and sodium levels decrease, and potassium levels increase •Blood urea nitrogen (BUN), serum creatinine levels, urine specific gravity, and osmolality - As perfusion of the kidneys is decreased and renal function is reduced, BUN and creatinine levels increase, as does urine specific gravity and osmolality •Blood cultures - In cases of septic shock, blood cultures are critical to identifying the causative organism and choosing appropriate antibiotic therapy •White blood cell (WBC) count and differential - measurements are important for patients with septic or anaphylactic shock. total WBC count is increased in septic shock. Elevated neutrophils indicate acute infection, increased monocytes indicate a bacterial infection, and increased eosinophils indicate an allergic response •Serum cardiac enzymes - Levels of several enzymes are elevated in cardiogenic shock: lactate dehydrogenase, creatine kinase, and serum glutamicoxaloacetictransaminase •Central venous catheterization - can aid in the differential diagnosis of shock and provide information about the heart's preload. A pulmonary artery catheter may be inserted to monitor cardiac dynamics, fluid balance, and the effects of vasoconstrictors and vasopressors

Classes of Shock

•Class I: Early Shock •Class II: Compensatory Shock •Class III: Decompensated Shock •Class IV: Refractory (irreversible) Shock

Pharmacologic Therapy

•Diuretics to increase urine output after fluid replacement has been initiated •Sodium bicarbonate to treat acidosis •Calcium to replace calcium lost as a result of blood transfusions •Antidysrhythmic agents to stabilize heart rhythm •Broadspectrum antibiotics to suppress organisms responsible for septic shock •Epinephrine, antihistamines, and inhaled beta2agonists to treat anaphylactic shock •Morphine to dilate veins and decrease anxiety

Pathophysiology : Shock

■One or more cardiovascular components malfunction → altered hemodynamic properties to sustain normal cellular metabolism → inadequate tissue perfusion → shock ■Manifestations result from body's attempts to maintain vital organs -Especially heart, brain -To preserve life following a drop in cellular perfusion -If the injury or condition triggering shock is severe enough or of long enough duration, then cellular hypoxia and cellular death occur ■Triggered by sustained drop in MAP -Decrease in cardiac output -Decrease in circulating blood volume -Increase in size of vascular bed from peripheral vasodilation ■Death if injury or condition severe enough, prolonged enough, physiologic events not stopped

Effects of Shock on Body Systems : Renal System

•During the progressive stage of shock, blood that normally perfuses the kidneys is shunted to the heart and brain, resulting in renal hypoperfusion •The drop in renal perfusion is reflected in a corresponding decrease in the glomerular filtration rate •Urine output is reduced, and the urine that is produced is highly concentrated •Oliguria of less than 20 mL/hr indicates progressive shock •Healthy kidneys can tolerate a drop in perfusion for only approximately 30 minutes; thereafter, acute tubular necrosis develops •As tubular necrosis occurs, epithelial cells slough off and block the tubules, disrupting nephron function •The accumulating loss of functional nephrons eventually causes renal failure •Without normal renal function, metabolic waste products are retained in the plasma •If treatment restores renal perfusion, the kidneys can regenerate the lost epithelial cells in the tubules, and renal function usually returns to normal •However, in patients who are older, chronically ill, or in sustained shock, loss of renal function may become permanent

Implementation

•ED, ICU often have guidelines for nursing actions in cases of hypovolemic shock •Assist in assessing, establishing IV access •Calculating correct amount of IV fluid, preparing it for administration •Employing IV push or pressure bag to ensure rapid fluid administration •Monitoring patient's physiologic response to fluid bolus •Preparing second and third fluid bolus •Use warmed fluids for resuscitation •Verify correct blood when administering packed RBCs •Change IV fluid to normal saline during blood administration •Carefully assess patient for transfusion reaction •Monitor patient's physiologic circulatory responses for improvement/deterioration •Notify physician immediately if any deterioration

Lifespan Considerations: Neonates and infants

•Even a small amount of blood loss can be devastating •Especially low-birthweight, very-low-birthweight neonates •Difficult to monitor BP in neonates •Although an accurate BP during shock is often obtained through invasive methods using an arterial catheter, this method may not be useful in preterm infants with very tiny arteries •Use of automated Doppler may be more useful in these infants •Prolonged very high or very low heart rate can compromise CO, contributing to shock •PDA, patent foramen ovale can disrupt blood flow → hypotension, cardiac failure •Hypotension usually indicates later stage of shock than in adults •Risk factors •Umbilical cord accident •Fetal or neonatal hemolysis or hemorrhage •Maternal infection or hypotension •Asphyxia, neonatal sepsis, other complications •Shock is a major cause of neonatal morbidity and mortality •Supportive measures include securing the airway, providing oxygen, achieving IV access, and infusing colloid or crystalloid solutions or whole blood as appropriate •Fluid bolus of 20 mL/kg should be given, with additional fluids being administered •Delayed treatment can lead to cerebral palsy, epilepsy, and mental retardation

Types of Shock

•For ALL types of shock •Identified according to underlying cause •Hypovolemic •Cardiogenic •Obstructive •Distributive •Neurogenic, anaphylactic, and septic shock

Effects of Shock on Body Systems : Skin, temperature, thirst

•In most types of shock, blood vessels supplying the skin are vasoconstricted, and the sweat glands are activated •As a result, changes in skin color occur: •The skin of Caucasian patients becomes pale •In individuals with darker skin (e.g., those of African, Hispanic, or Mediterranean descent), shock related skin color changes may be assessed as paleness of the lips, oral mucous membranes, nail beds, and conjunctive •The skin is usually cool and moist and, in the later stages of shock, often edematous

Lifespan Considerations: Neonates, Infants, and Children

•Infants and young children differ from adults in that their cardiac output depends on their heart rate, not their stroke volume. •Hypotension is a late sign in children, and it is correlated with a poor prognosis •Early use of PALS decreases risk of mortality •Children are at risk of the same types of shock as adults •gastroenteritis, burns, diabetes insipidus, heat stroke, trauma, surgery, and intestinal obstruction •Children with gastroenteritis can lose up to 20% of their circulating volume within 1-2 hours, and clinical deterioration may be rapid if rehydration efforts are hindered by continued vomiting. •Nursing Interventions: •Perform quick Health History and Assessment •Manage the Child's ABCs •Obtain Vascular Access •Restore Fluid Volume even in the absence of hypotension •Administer Medications •For septic shock, early treatment with antibiotics also reduces mortality in children •Signs and symptoms of shock in children include altered mental status, tachypnea, tachycardia, reduced urine output, delayed capillary refill (less than 2 sec), temperature instability, and metabolic acidosis

Assessment : Cardiogenic shock

•Left anterior wall MI •maintaining or improving myocardial oxygen supply •immediate pain relief •maintaining rest

Class III: Decompensated Shock

•Occurs after sustained decrease in MAP of 20 mmHg or more below normal, blood volume loss of 30-40% •Compensatory mechanisms still active but cannot maintain MAP at sufficient level for perfusion of vital organs •Vasoconstriction limits blood flow → cells become oxygen deficient, all organs/tissues/cells damaged •To remain alive, the affected cells switch from aerobic to anaerobic metabolism. •Heart rate and vasoconstriction increase but perfusion of the skin, skeletal muscles, kidneys, and gastrointestinal organs is greatly diminished •The lactic acid formed as a by product of anaerobic metabolism contributes to an acidotic state at the cellular level •As a result, production of ATP, the source of cellular energy, is inefficient. Lacking energy, the sodium-potassium pump fails •Cells in heart, brain become hypoxic - mental status further deteriorates •Body cells and tissues become ischemic and anoxic •Unless treated rapidly, patient has poor chance of survival • •Clinical Manifestations: •Systolic < 90 mmHg; MAP < 65 mmHG (requires fluid resuscitation) •Rapid, shallow RR; crackles •PAO2 < 80 mmHG •PACO2 >45 mmHG •Mottled skin; petechiae •Urinary output < 0.5 ml/kg/hr •Lethargy •Metabolic Acidosis and hyperkalemia •Potassium moves out of the cell, while sodium and water move inward. As this process continues, the cell swells, cell membrane integrity is lost, and cell organelles are damaged •Lysosomes within the cell spill out their digestive enzymes, which disintegrate any remaining organelles. Some enzymes spread to adjacent cells, where they erode and rupture cell membranes •The acid byproducts of anaerobic metabolism dilate the precapillary arterioles and constrict the postcapillary venules. •This causes increased hydrostatic pressure within the capillary, and fluid shifts back into the interstitial space. •The capillaries also become increasingly permeable, allowing serum proteins to shift from the vascular space into the interstitium. •The buildup of plasma proteins increases the osmotic pressure in the interstitium, further accelerating the fluid shift out of the capillaries. •Blood Loss 1500-2000 mL •% of blood loss volume 30-40% •Heart Rate 120-140 •Blood Pressure Decreased •Pulse Pressure Decreased •Capillary Refill Usually delayed •Respiratory Output Moderate tachypnea •Urine Output 5-15 mL/hr •Mental Status Anxious to confused

Nursing Process

■Rapid assessment ■Reaction to subtle symptoms to prevent downward cascade of events ■Anticipating potential for shock can promote rapid intervention

Lifespan Considerations: Older Adults

•Older clients are at an increased risk for developing shock and MODS •With aging comes a relative decrease in sympathetic activity in relation to the cardiovascular system •Older adults who have a heart attack, especially those with a history of heart failure, diabetes, or hypertension, have an increased risk of cardiogenic shock •In addition, many older adults experience secondary volume depletion because of chronic diuretic use or malnutrition •Recovery is possible if it is detected & treated aggressively early •Important things to note in the assessment of the older client: •The use of beta-blockers may mask tachycardia •The older client may not be febrile •May report fatigue & malaise instead •Dysrhythmias occur in response to hypoxemic states •Older clients have a decreased respiratory reserve & decompensate quickly •Changes in mentation are often misinterpreted as dementia •Older adults have a lower tolerance for hypovolemia than younger adults, so they should be aggressively treated with fluids during hypovolemic shock •Assess the older adult with shock for preshock functional status, including identifying any difficulties with ADLs and instrumental ADLs •A sudden decrease in the ability to per form ADLs may be an older adult's only sign of sepsis •Aggressive fluid administration can cause problems in older adults with diastolic dysfunction, which is common in this age group should carefully monitor the older patient for signs of fluid overload •Common treatments such as dobutamine administration may have a lesser effect on an older patient or cause a dysrhythmia, especially if the patient has a history of CAD •Initial bolus dose and aggressive dosing should still be maintained, because inadequate antibiotic therapy is associated with poor outcomes in the older adult population •Mechanical ventilation of older adults during shock is associated with increased mortality. a low tidal volume is preferred over traditional tidal volume

Class IV: Refractory (irreversible) Shock

•Organ and tissue damage is so severe no treatment can reverse damage •Even if MAP is temporarily restored, too much cellular damage to maintain life •Cell death followed by tissue death → death of organs → death of body •Death of vital organs contributes to subsequent death of the body •Judgement that shock is irreversible is only made in retrospect •Clinical Manifestations: •BP requires mechanical or pharmacologic support (vasopressors) •Heart rate is erratic; asystole •Requires intubation •Jaundice •Anuric (requires dialysis) •Unconscious •Profound acidosis •Blood loss > 2000 mL •% of blood volume loss > 40% •Heart rate > 140 •Blood pressure Decreased •Pulse pressure Decreased •Capillary refill Delayed •Respiratory rate Marked tachypnea •Urine output Anuria •Mental status Lethargic to obtunded

Effects of Shock on Body Systems : Respiratory system

•Oxygen delivery to cells may be impaired by a drop in circulating blood volume or, in the case of blood loss, by an insufficient number of RBCs that carry oxygen •The number of alveoli that are perfused decreases, and gas exchange is impaired •As a result, blood oxygen levels decrease, and carbon dioxide levels increase •As perfusion of the lungs diminishes, carbon dioxide is retained, and respiratory acidosis occurs •A complication of decreased perfusion of the lungs is ARDS, or "shock lung" •The pulmonary capillaries become increasingly permeable to proteins and water, resulting in noncardiogenic pulmonary edema •Production of surfactant, which controls surface tension within alveoli, is impaired, and the alveoli collapse or fill with fluid •This potentially lethal form of respiratory failure may result from any condition that causes hypoperfusion of the lungs, but it is most common in shock caused by hemorrhage, severe allergic responses, trauma, and infection

Effects of Shock on Body Systems : Cardiovascular system

•Perfusion and oxygenation of the heart are adequate in the early stages of shock •As shock progresses, myocardial cells become hypoxic, and myocardial muscle function diminishes •The BP may be normal or even slightly elevated and the heart rate may increase only slightly •Sympathetic stimulation increases the heart rate (a sinus tachycardia of 120 bpm is common) in an effort to increase CO. As a result of vasoconstriction and decreased blood volume, the palpated pulse is rapid, weak, and thready; as shock progresses, peripheral pulses are usually not palpable •Tachycardia reduces the time available for left ventricular filling and coronary artery perfusion, further reducing CO. •With progressive shock, altered acid-base balance, hypoxia, and hyperkalemia damage the heart's electrical systems and contractility

Assessment : Hypovolemic shock

•Recent surgery •Multiple traumatic injuries •Serious burns •Monitoring fluid status is essential •daily assessments of weight •fluid intake by all routes •measurable fluid loss

Distributive (vasogenic) Shock: Anaphylactic shock

•Severe allergic reaction result of a widespread hypersensitivity reaction (called anaphylaxis) •Acute onset •Pathophysiology in this type of shock includes vasodilation, pooling of blood in the periphery, and hypovolemia with altered cellular metabolism •Presence of two or more systems with multi-system involvement •Medical management: •IM/SubQ epinephrine (vasoconstriction) ***NOT IV*** •IV diphenhydramine (reverse histamine effects) •H2 blocker (famotidine) •Nebulized albuterol (reverses histamine induced bronchospasms) Clinical Manifestations •BP: Hypotension •Pulse: Increased, dysrhythmias •Respirations: Dyspnea, stridor, wheezes, laryngospasm, bronchospasm, pulmonary edema •Skin: Warm, edematous (lips, eyelids, tongue, hands, feet, genitals) •Mental status: Restless, anxious, lethargic to comatose •Urine output: Oliguria to anuria •Other: Paresthesias, pruritus, abdominal cramps, vomiting, diarrhea

Assessment : Neurogenic shock

•Spinal cord injuries •Spinal anesthesia •maintaining immobility of the patient with spinal cord trauma •elevating the head of the bed 15-20 degrees following spinal anesthesia

Effects of Shock on Body Systems : Gastrointestinal System

•The gastrointestinal organs normally receive 25% of the CO through the splanchnic circulation •Shock constricts the splanchnic arterioles and redirects arterial blood flow to the heart and brain •Gastrointestinal organs consequently become ischemic and may be irreversibly damaged •Lesions of the gastric and duodenal mucosa (stress ulcers) can develop within hours of severe trauma, sepsis, or burns •Gastrointestinal ulcers may hemorrhage within 2-10 days following the original cause of shock •The permeability of damaged mucosa increases, allowing enteric bacteria or their toxins to enter the abdominal cavity and then progress to the circulation, resulting in sepsis •Gastric and intestinal motility is impaired during shock, and paralytic ileus may result •If the episode of shock is pro longed, necrosis of the bowel may occur •Shock also alters the metabolic functions of the liver •Gluconeogenesis (the process of forming glucose from noncarbohydrate sources) and glycogenolysis (the breakdown of glycogen into glucose) initially increase •This process allows blood glucose levels to increase as the body attempts to respond to the stressor; however, as shock progresses, liver function becomes impaired, and hypoglycemia develops •Metabolism of fats and protein is impaired, and the liver can no longer effectively remove lactic acid, contributing to the development of metabolic acidosis Bacteria may proliferate within the circulatory system, causing over whelming bacterial infection and toxicity

Lifespan Considerations: Pregnant Women : Causes

•Trauma •Postpartum hemorrhage e.g., related to placenta previa, placental abruption, or uterine rupture •Septic abortion •Chorioamniotic and postpartum infection •Valvular disease •Amniotic fluid embolism •Different from shock other adults because of the normal physio logic changes that take place during pregnancy and the concern during treatment for both the mother and fetus •Can affect normal changes of pregnancy: increased blood volume, heart rate, SV, CO; decreased peripheral resistance, BP •Fetal perfusion, oxygenation depend on mother's circulation, putting fetus at risk if mother's circulation fails •Shock can affect all of these measures, and because fetal perfusion and oxygenation depend on the mother's circulation, the fetus is also at risk for circulatory failure if the mother's circulation fails during shock •Pregnant women in shock should be ventilated to maintain their oxygenation status; respiratory alkalosis should be avoided because it decreases uterine blood flow •If CPR is needed, the pregnant woman should be placed in a left lateral tilt position to avoid pressure on the vena cava •The firstline vasoactive drug for pregnant women in shock is ephedrine •If the cause of shock is postpartum hemorrhage, oxytocin should be administered •If the cause of shock is sepsis, the nurse should monitor the patient for complications

Lifespan Considerations: Pregnant Women

•Treatment of fetus •While mother is being treated for shock, fetus should undergo continuous heart rate monitoring •Fetal bradycardia may indicate hypoxia •Ultrasound to assess fetal movement, reactivity, amniotic fluid volume •Fetal distress may necessitate delivery •Therefore, emergency equipment should be available for cesarean section and neonatal care

Colloid Solutions (Plasma Expanders)

■Albumin 5% (Albuminar-5, Buminate 5%) Albumin 25% (Albuminar-25, Buminate 25%) Dextran 40 (Gentran 40) Dextran 70 (Gentran 70, Macrodex) Dextran 75 (Gentran 75) Hetastarch (Hespan [HES]) Plasma protein fraction (Plasmanate, Plasma-Plex, Plasmatein, Protenate) -MECHANISMS OF ACTION -These solutions are blood volume expanders and are used to treat hypovolemic shock caused by surgery, hemorrhage, burns, or other trauma -Albumin and plasma protein fraction are prepared from healthy blood donors -Dextran and hetastarch are synthetically prepared large molecules -The solutions promote circulatory volume and tissue perfusion by rapidly expanding plasma volume. Dextran solutions are used infrequently NURSING CONSIDERATIONS •Before infusion begins, establish a baseline of vital signs, lung sounds, heart sounds, and (if possible) CVP and pulmonary artery wedge pressure •Start administration of ordered IV fluids, using a large-gauge (18-or 19-gauge) infusion needle •Take and record vital signs as required by institutional policy (usually every 15-60 minutes) and patient status •Take and record intake and output every 1-2 hours •Monitor the patient for manifestations of CHF or pulmonary edema (dyspnea, cyanosis, cough, crackles, or wheezes). If these manifestations appear, stop the fluids, and notify the physician immediately •Monitor the patient for bleeding from new sites; an increase in BP may cause bleeding in severed vessels that did not bleed with decreased BP •Monitor the patient for manifestations of dehydration (dry lips; scant, dark-colored urine; loss of skin turgor). Increased IV fluids are usually ordered if the patient becomes dehydrated •Monitor the patient for manifestations of circulatory overload (JVD, increase in CVP, or increase in pulmonary artery wedge pressure). If these manifestations occur, slow the rate of infusion, and notify the physician •Monitor PT, partial thromboplastin time, and platelet counts • If administering dextran or plasma protein fraction, have epinephrine and antihistamines readily available for any manifestations of a hypersensitivity reaction (fever, chills, rash, headache, wheezing, or flushing) •Maintain the patient on bedrest with side rails elevated •Health Education for the Patient and Family •The solutions are given to replace lost serum protein, which helps maintain the volume of blood •Vital signs are taken frequently to ensure the patient's safety

Class I: Early Shock

■Begins when baroreceptors in aortic arch, carotid sinus detect sustained drop in MAP of <10 mmHg from normal ■The circulating blood volume may decrease (usually to less than 500 mL), but not enough to cause serious effects in an adult patient ■Causing the SNS to increase the heart rate and force of cardiac contraction, thus increasing CO. Sympathetic stimulation also causes peripheral vasoconstriction, resulting in increased SVR and a rise in arterial pressure. This aids in maintaining BP, and cardiac output (CO) ■These physiologic responses aid in maintaining perfusion ■Symptoms almost imperceptible -Pulse slightly elevated -If the injury is minor or of short duration, arterial pressure is usually maintained, and no further symptoms occur •Blood loss < 750 mL •% of blood volume loss < 15% • Heart rate < 100 •Blood pressure Normal •Pulse pressure Normal •Capillary refill Normal •Respiratory rate Normal •Urine output >30mL/hr •Mental status Normal to slightly anxious

Obstructive Shock

■Caused by obstruction in heart, great vessels -Impedes venous return or prevents effective cardiac pumping -Causes ■Impaired diastolic filling (e.g., pericardial tamponade, pneumothorax) ■Increased right ventricular afterload (e.g., pulmonary emboli) ■Increased left ventricular afterload (e.g., aortic stenosis, abdominal distention) -Manifestations result from decreased CO and BP → reduced tissue perfusion, cellular metabolism

Cardiogenic Shock : Patho

■Decrease in CO leads to decrease in MAP ■Heart rate may increase due to compensatory mechanisms. However, tachycardia increases myocardial oxygen consumption and decreases coronary perfusion ■Myocardium becomes progressively deleted of oxygen → further myocardial ischemia, necrosis ■Typical sequence of shock unchanged ■Cyanosis more common because stagnating blood increases extraction of oxygen from the hemoglobin at the capillary beds ■Pulmonary edema may occur left ventricular end diastolic pressure increases ■Also, retention of blood in the right side of the heart increases right atrial pressure, which leads to JVD as a result of back flow through the vena cava

Vasodilators

■Drug example: Nitroglycerin (Nitrostat) Nitroprusside (Niprid) -MECHANISMS OF ACTION -Drugs that cause vasodilation act directly on smooth muscle, affecting both arterioles and veins -Peripheral resistance, CO, and pulmonary wedge pressure are all reduced as a result of the vasodilation -These effects decrease both the heart's oxygen need and pulmonary congestion -Vasodilators are used primarily in the treatment of cardiogenic shock and may be combined with a sympathomimetic (e.g., dopamine) NURSING CONSIDERATIONS •Protect these drugs from light by wrapping the IV bag in the package that is provided •Mix only with 5% dextrose in water •Infuse with an infusion pump, and use within 4 hours of reconstitution •Do not add other medications to the solution •Assess mental status, BP, and pulse before initiating medication. Thereafter, assess BP and pulse according to institutional policy (usually every 5 minutes initially, then every 15 minutes until stable, and then every hour) •Monitor the patient for confusion, dizziness, tachycardia, dysrhythmias, hypotension, and adventitious breath sounds. If they occur, report them immediately, and slow the infusion to a keep-open rate •Monitor the patient receiving nitroprusside for signs of thiocyanate poisoning (nausea, disorientation, muscle spasms, and decreased or absent reflexes) if infusion lasts longer than 72 hours •Keep the patient in bed with side rails up •Health education for the patient and family: • It is important to stay in bed and change positions slowly to avoid dizziness •BP and pulse are taken frequently to assist in adjusting the dose of medication •Headache is a common side effect

Sympathomimetics Vasoconstrictors (drugs causing vasoconstriction)

■Drug examples: Norepinephrine (Levophed) Phenylephrine (Neo-Synephrine) Epinephrine ■Inotropes (also called cardiotonics) Drug examples: Dopamine (Intropin) (receptors are dose dependent) Dobutamine (Dobutrex) Isoproterenol (Isuprel) -MECHANISMS OF ACTION -Sympathomimetics mimic the fight-or-flight response of the SNS, selectively stimulating alpha-adrenergic and beta-adrenergic receptors -These drugs have both vasopressor (vaso-constricting) effects and positive inotro-pic effects - Stimulation of alpha-adrenergic receptors results in vasoconstriction and increased systemic BP -Stimulation of beta-adrenergic receptors increases the force and rate of myocardial contraction -The physiologic effects of these drugs include improved perfusion and oxygenation of the heart, with increased SV and heart rate, and increased CO -In turn, increased CO increases tissue perfusion and oxygenation -The major disadvantage is that increases in SV and heart rate also increase the oxygen requirements of the myocardium. -These drugs may be used during the early stages of shock, especially in types of shock characterized by vasodilation -Note that epinephrine is used primarily to treat anaphylactic shock •Carefully monitor responses in the older adult, who may be especially sensitive to sympathomimetics and require lower doses. •Use the IV route only with continuous-infusion pumps •Carefully adjust the dose to accommodate the patient's cardiovascular status (as ordered by the physician or by written protocol). •Document lung sounds, vital signs, and hemodynamic parameters before starting the medication and then according to institutional policy (usually every 5-15 minutes). •Monitor for signs of dysrhythmias and hypertension •Record and monitor urine output. Report output of less than 30 mL/hr. •Be aware that the sympathomimetics are incompatible with sodium bicarbonate or alkaline solutions •When administering drugs that cause vasoconstriction, such as norepinephrine (Levophed), monitor the IV insertion site for infiltration •If infiltration does occur, stop the infusion, and notify the physician immediately. (Infiltration may cause ischemia and necrosis of tissue.) •Health education for the patient and family: • Because these drugs mimic a physiologic reaction to stress, they may cause feelings of anxiety •Close monitoring to adjust the dose will be carried out by qualified nurses using written protocols •Report heart palpitations or chest pain immediately •These drugs increase venous return through vasoconstriction of peripheral vessels; they also improve the heart's pumping ability by facilitating myocardial contractility and by dilating coronary arteries to increase perfusion of the myocardium

Oxygen Therapy and Fluid Replacement Therapy

■Establishing and maintaining a patent airway and ensuring adequate oxygenation are critical nursing interventions in reversing shock ■All patients in shock (even those with adequate respirations) should receive oxygen therapy (usually by mask or nasal cannula) to maintain the PaO2 at greater than 80 mmHg during the first 4-6 hours of care ■The most effective treatment for the patient with hypovolemic shock is to administer IV fluids or blood ■are also used to treat septic, neurogenic, and anaphylactic shock ■Patients with cardiogenic shock may require either fluid replacement or restriction, depending on pulmonary artery pressure -Whole blood or blood products increase the oxygen carrying capacity of the blood and thus increase oxygenation of cell -Fluid replacements, such as crystalloid and colloid solutions, increase circulating blood volume and tissue perfusion

Evaluation

■Expected outcomes may include -Patient maintains adequate airway, oxygenation -Patient maintains adequate urinary output -Patient does not progress to uncompensated shock -Family copes adequately with stress of patient's condition -If evaluation indicates that the patient's condition has worsened, the nurse will need to review the care plan and implement additional nursing interventions to ensure that the patient maintains adequate oxygenation and perfusion

General Management Strategies

■Fluid replacement (two large bore IVs or central line) -Crystalloid - contain dextrose or electrolytes dis solved in water; they are hypertonic, isotonic, or hypotonic ■Hypertonic solutions include 3% saline. Isotonic solutions include normal saline (0.9%), lactated Ringer's solution, and Ringer's solution. Hypotonic solutions include one half nor mal saline (0.45%) and 5% dextrose in water. Fluid volume is only minimally expanded by infusion of crystalloid solutions, and the potential for peripheral edema is increased when they are used. LR's solution (an electrolyte solution) and 0.9% saline are the fluids of choice in treating hypovolemic shock, especially during the emergency phase of care while blood is being typed and crossmatched -Colloid Solutions ■tend to remain in the vascular system and increase the osmotic pressure of the serum, causing fluid to move into the vascular compartment from the interstitial space ■Colloid solutions used to treat shock include 5% albumin, 25% albumin, hetastarch, plasma protein fraction, and dextran. ■Reduce platelet adhesiveness and have been associated with reductions in blood coagulation. There fore, the patient's PT, INR, platelet count, and aPTT should be monitored when these solutions are administered -Blood components ■If hypovolemic shock is caused by hemorrhage ■keep the hematocrit at 30-35% and the hemoglobin level between 12.5 and 14.5 g/100 mL for adults -Complications of fluid administration ■Vasoactive medication therapy ■Oxygen therapy ■Nutritional support •Advancing cardiac disease increases the risk for cardiogenic shock (prevention of cardiogenic shock involves taking the same steps as for preventing heart disease controlling BP to avoid hypertension, not smoking, exercising regularly, maintaining a healthy weight, and reducing the intake of cholesterol and saturated fats) •Individuals who practice high risk behaviors, are at increased risk for trauma and shock that results from bleeding or multisystem injury •Patients with diseases that slow the body's ability to clot (e.g., hemophilia) are at increased risk for hemorrhagic shock •Shock often results from trauma or infection, safety measures aimed at preventing trauma, such as use of helmets, seatbelts, and other protective gear, and preventing infection, such as good hand hygiene and infection control measures, should be used consistently •Often, packed RBCs are given to provide hemoglobin concentration and are supplemented with crystalloids to maintain an adequate circulatory volume

Planning

■Goals may include that the patient will -Maintain airway, breathing, circulation -Maintain perfusion -Understand all procedures -Verbalize feelings to reduce anxiety -Reduce cardiac workload

Overview : Shock

■Life-threatening condition in which tissue perfusion is inadequate to deliver oxygen and nutrients to support cellular function ■A clinical syndrome characterized by a decrease in blood flow to body organs and tissues, resulting in inadequate oxygenation and life-threatening cellular dysfunction ■Affects all body systems ■To maintain cellular metabolism, the cells of all body organs and tissues require a regular and consistent supply of oxygen and removal of metabolic wastes ■May develop rapidly or slowly ■Any patient with any disease state may be at risk for developing shock ■Regardless of the initial cause of shock, certain physiologic responses are common to all types of shock: -hypoperfusion of tissues -hypermetabolism -activation of the inflammatory response

Class III: Decompensated Shock (2)

■Lungs begin to fail, decreased pulmonary blood flow causes further hypoxemia, carbon dioxide levels increase, alveoli collapse, pulmonary edema occurs ■Inadequate perfusion of heart leads to dysrhythmias, ischemia ■As MAP falls below 70, GFR cannot be maintained ■Acute kidney injury may occur ■Liver function, GI function, hematologic function are all affected ■Disseminated intravascular coagulation (DIC) may occur as cause or complication of shock

Hypovolemic Shock: Management

■Medical Management -Treat underlying cause -Fluid, blood replacement ■Rapid bolus for hemorrhage or severely dehydrated (may use rapid infuser) -Redistribution of fluid -Pharmacologic therapy ■Nursing management: -Administering fluids/blood safely -Implementing other measures

Diagnosis

■Nursing diagnoses may include -Decreased Cardiac Output -Ineffective Tissue Perfusion -Anxiety

Clinical Manifestations

■The onset of shock may be rapid or slow, depending on its cause and severity ■Signs of early shock may be nonspecific ■As the body compensates for hypotension or hypovolemia, signs of shock include tachycardia, increased respiratory effort, and decreased urine output ■The patient may also be diaphoretic (perspire excessively) ■If treatment is not begun in the early stages of shock, the condition may progress until the patient can no longer compensate ■At that time, the systolic BP drops, and the pulse pressure narrows ■Reduced cerebral blood flow ultimately results in a decreased LOC ■If shock is not reversed, it progresses to cardiopulmonary failure and death

Collaboration

■Treat underlying cause ■Increase arterial oxygenation ■Improve tissue perfusion ■Nutritional status ■Emergency care (first course) -Oxygen therapy -Fluid replacement -Medications