Ch 61- Shock

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SHOCK
--Has been described as the "rude unhinging" of the machinery of life
--Not a disease, but a clinical manifestation of the body's inability to perfuse tissues adequately
--Regardless of the cause, systemic response is detrimental
>Can lead to multiple organ dysfunction syndrome (MODS) and death

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SHOCK
--Understanding the causes can prevent life threatening complications
--There are multiple etiologies that may place the patient at risk for developing shock
--Most common classification is by the cause of the shock syndrome
>Ex: Sepsis from infection-septic shock
--Other classification system related to amount of circulating volume in the body
>Ex: low volume shock-absolute hypovolemia-major loss of blood or circulating

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ANAPHYLACTIC SHOCK
--Results from an antigen-antibody reaction
>Body becomes hypersensitive to a specific agent
>Vasodilation of blood vessels occurs, causing pooling blood in the periphery
>Perfusion to tissues is markedly diminished or absent
>Other body systems react to toxins
>Pulmonary system responds with vasoconstriction, causing respiratory distress and potential respiratory arrest
>Causes insect bites, medication allergies, food allergies, latex allergies, idiopathic reactions

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CARDIOGENIC SHOCK
--Develops when the heart is unable to pump effectively
--Myocardial infarction is one of the most common causes of damage to the heart
--Other causes: myocardial contusion, ruptured vessels, ruptured papillary muscles, cardiomyopathy
--Mortality rate remains high despite advances in technological care

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HYPOVOLEMIC SHOCK
--Most common type of shock seen with multiple system traumas
--Results from significant fluid loss that alters the amount of circulating volume in the body
--Hemorrhagic
>Blood, plasma, or other body fluids
>Upper/Lower GI bleeding
>Ruptured aortic aneurysm
>Hemorrhagic pancreatitis
>Long-Bone fractures
--Nonhemorrhagic
>Diarrhea, vomitting
>Inadequate fluid repletion after loss-heat stroke, burn wounds, leaking of plasma into the interstitial or "third spacing"
--Causes inadequate blood volume returning to the heart
--Blood loss=oxygen carrying capacity also lost

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HYPOVOLEMIC SHOCK
--In patient with major trauma-may have in addition to neurogenic or spinal shock; important to differentiate
--Hypotension and tachycardia
--Cool pale skin due to vasoconstriction
--Treatment: Fluids, plasma expanders, blood

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NEUROGENIC SHOCK
--Due to imbalance between sympathetic and parasympathetic stimulation of vascular smooth muscle which results in vasodilation
--Injury or medications that affect the spinal cord or medulla can cause an imbalance
--Because of this imbalance, clinical symptoms usually associated with shock are different- the patient may be hypotensive, but not tachycardic
--Causes: spinal cord or medulla trauma, anesthetic agents, severe emotional distress, severe pain

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NEUROGENIC SHOCK
--Most commonly seen with SCI at T6 or above
--Disruption of the sympathetic nervous system- originates in thoracolumbar region of spinal cord
--Brainstem impulses that help control heart rate and BP are disrupted, sympathetic impulses are blocked and parasympathetic is dominant-vagal tone unopposed
--Hypotension and Bradycardia; decreased cardiac output
--Warm reddened skin due to vasodilation
--Treatment: Atropine and vasopressors
--Orthostatic hypotension significant problem- loss of sympathetic tone-pooling of blood in abdomen and lower extremities
--Pooling of blood, flaccid extremities and immobility- high risk of DVT
--Change position slowly, lower head if dizzy, TEDs or ace wraps

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SEPTIC SHOCK
--Sepsis that is refractory to fluid resuscitation
--Results in hypotension and perfusion abnormalities
--Occurs when an infectious agent or infection induced mediator causes systemic decompensation
--Decreased systemic vascular resistance and maldistribution of the blood into the microcirculation cause compromised tissue perfusion and cellular dysfunction

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IMPAIRED OXYGENATION
--Shock results from inadequate tissue perfusion
--Causes alterations in circulating volume, cardiac pump function, or alterations in peripheral vascular resistance
--These changes lead to impairment of cellular metabolism
--This results in impaired oxygen and glucose use
--When the patient has an injury or illness that causes alteration in the blood flow an oxygen debt will occur

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IMPAIRED OXYGENATION
--Oxygen delivery- the amount of oxygen available for tissue consumption per unit of time
--Body generally has an oxygen reserve to respond to stress, but if person has a preexisting illness or injury this will decrease or eliminate the oxygen reserve
--Oxygen Consumption- the amount of oxygen extracted from the tissues for metabolism
>Calculated by determining the difference between the amounts of oxygen returned to the right side of the heart
>Dependent on the person's cardiac output, hemoglobin concentration, and arterial and venous oxygen saturation

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CELLULAR RESPONSES TO OXYGEN DEBT
--Sodium moves from outside the cell to increase water in the cell
--Potassium exits the cell, altering nervous, cardiovascular, and muscular cell function and impairing these systems
--To compensate for water drawn into cells
--Water drawn from vascular space further reducing circulating blood volume

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CELLULAR RESPONSES TO OXYGEN DEBT
--Shift from aerobic to anaerobic metabolism to compensate or oxygen loss
--Metabolic acidosis results which effects enzyme activities and cellular functions such as repair and division
--Cellular damage causes enzymes to be released, which destroys non injured cells
--Glucose metabolism impaired in a manner similar to that of oxygen metabolism, resulting in insulin resistance
>Insulin resistance and glucose toxicity impair cellular growth metabolic responses
>Insulin Restistance has been associated with multiple organ failure, nosocomial infections, and renal failure

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GENERAL EFFECT OF SEPSIS
--General effect on all body systems
--Illustrated in Figure 61-1 p1959
--Inadequate tissue perfusion
>Anaerobic metabolism to produce energy
--Alterations in cellular metabolism
>Alteration in ATP production
>Failure of the sodium potassium pump
>Redistribution of cellular ions
>Interstitial fluid shifts

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SEPSIS
--General effect on all body systems
>Cell rupture releases enzymes
-Further damage to other cells
>Other pathophysiological pathways initiated
-Release toxins and affect all body systems
>If not stopped, toxins cause multiple organ failure, death

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RESPONSE TO INFLAMMATION
--Cascading evens in response to inflammation
>Immune system activates complement cascade system that macrophages to respond
>Macrophages cause release of platelet aggregators
>Causes clots to form, which can plug the vessels and cause vasodilation
>End result: more tissue damage due to inadequate perfusion

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OXYGEN AND GLUCOSE DEPRIVATION
--Septic effects on "the machinery of life"
>When the brain does not achieve adequate oxygen or glucose, changes occur to cerebral perfusion, resulting in altered mental status and possible coma or death
>Decline in cardiac output alteration in both preload and after load
>Specific toxins such as myocardial depressant factor are released from damaged cardiac cells and a hypoperfused pancreas, causing further myocardial dysfunction and hypoxia and then cardiac dysrhythmia
>Acute lung injury=acute respiratory distress

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OXYGEN AND GLUCOSE DEPRIVATION
--Specific effects on "the machinery of life"
>Urinary output is decreased b/c shift of sodium which pulls water back in cell to conserve fluid
>Anaerobic metabolism produces toxins
>Impaired kidneys less able to detoxify
>Inadequate blood flow to GI tract activates neutrophils that provoke multiple organ failure
>Effects on the integumentary system-blood diverted from skin placing patient at risk for hypothermia

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OXYGEN AND GLUCOSE DEPRIVATION
--Specific effects on "the machinery of life"
>Change in blood flow to vital organs
>Triggers baroreceptors to trigger release of catecholamines
>Increases heart rate and cardiac output
>Skeletal muscle breaks down releasing amino acids
>Muscle weakness and eventual wasting

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CONT
--The "unhinging" continues until irreversible changes and eventually death occurs
--Unfortunately many of the interventions used for the treatment of shock, contribute to the development of further complications such as third spacing, ischemia reperfusion injury- major trigger of MOD, VAP, etc.

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SHOCK
--Primary treatment for shock syndromes is prevention, early recognition of factors that may place the patient at risk for developing shock, and appropriate interventions
--Be aware of specific risk factors that may cause particular shock syndromes
>Ex: Patient with indwelling catheter at risk for becoming septic predisposing them to septic shock

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GENERAL RISK FACTORS
--Significant Injuries
--Catastrophic Illness
--Allergies
--Age

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AGE RELATED RISK FACTORS
--Shared by the very young and aged
>Compromised immune systems
>Fluid shifts
>An integumentary system that may not afford needed protection

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PATIENT CARE IN EMERGENCY PERIOD OVERALL
--Identify and correct the cause of shock
--Maintain oxygen perfusion
--Control active bleeding
--Support the patient's circulatory status
--Maintain body temperature
--Manage pain
--Provide emotional support

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FROM PREHOSPITAL CARE TO ER
--"Load and Go"-Transport as quickly as possible to the nearest hospital
--Critical interventions to save a life only before transport
--Additional interventions during transport
>Obtain IV access
>Immobilization and stabilization measures
>Warm the patient
>Perform a secondary assessment
--No additional delays in getting to appropriate and life saving care

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EMERGENCY DEPARTMENT CARE
--Collaborative approach
--Primary Assessment
--Initiate critical interventions to support circulation, airway, and breathing
--Evaluate prehospital interventions
>Ex: How was fluid administered? Meds?
--Secondary assessment
>Attempt to identify source of shock-obvious injuries or illness

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EMERGENCY DEPARTMENT CARE
--Primary goal of shock management
>Identify the cause
>Prevent results of ischemic and anoxic cell injury
--Assess for source-obvious illness or injury
--Possible sources: hemorrhage, sepsis, hypovolemia
--Page 1961 Risk Factors for the development and source of shock
>Hemorrhage-active bleeding anywhere, abdominal bruising, long bone deformities etc
>Sepsis-purpura, rashes, decubitits, gangrene, indwelling catheter, etc
>Hypovolemia- burns, dehydration

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IDENTIFYING UNDERLYING CAUSE
--When no obvious indication, other pieces of the patient history and risk factors must be considered
>Age of patient-elderly and young at risk
>Medications- immunosuppressives, antibiotic and antiviral therapies
>Source of blood or other fluid loss

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MANAGEMENT-ABC
--A=AIRWAY, B=BREATHING, C=CIRCULATION
--Airway and Breathing
>Hypoxic patient requires airway and ventilatory support
--Circulation
>Circulatory status needs to be assessed
>Determine perfusion: peripheral and central pulses
>Skin is pale, cold, clammy
-Blood is diverted to enhance oxygenation of vital organs
>Keep patient warm
-Increase room temperature, cover with blankets, use warming device

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DIAGNOSTIC TEST
--Page 1962 "Diagnostic Test for Shock"
--CBC, CMP, PT, PTT, Blood cultures, urinalysis, type and crossmatch, cardiac enzymes
--ECG
--CT, MRI

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OXYGEN AND CIRCULATORY MANAGEMENT
--Primary purposes of circulatory resuscitation:
>Restore oxygen transport, cellular uptake
>Mitigate against oxygen debt accumulation
>Decrease anaerobic metabolism
>Restore pre-resuscitation oxygen deficit
>Prevent metabolic derangements that can lead to Multiple Organ Dysfunction Syndrome (MODS), Multiple Organ System Failure (MOSF)

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OXYGEN AND CIRCULATORY MANAGEMENT
--Circulatory resuscitation
>To maintain adequate end organ perfusion
>Both volume resuscitation and vasoactive meds
--Fluid Resuscitation
>Research challenges common methods
-For Ex, hypotension may act as a protective mechanism, increasing BP may multiply clots, dilute circulating volume, and increase clotting time
-Complications of massive fluid resuscitation Chart 61-5
>Fluids used commonly LR and NS; amount ranges from 2-3 liters if cause of shock unknown
>Blood loss patients will need blood products
>Closely monitor for complications
-Urinary catheter to monitor output, monitor vitals, peripheral pulses, LOC, bowel sounds

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PHARMACOLOGICAL INTERVENTIONS
--Different medications may be used for different shock states
>Medications typically used in selected shock states:
-Antibiotics-broad spectrum used initially
-Recombinant human-activated protein C- used for antithrombotic, anti-inflammatory, and profibrinolytic action
-Corticosteroids- used to treat adrenal insufficiency in septic shock and inflammatory response related to spinal cord injury
-Vasopressors- used to reverse vasodilation and reduce systemic vascular resistance
-Insulin therapy- induct euglycemia, also has anti-inflammatory effect
-Recombinant activated coagulation factor VII promotes coagulation
--CHART P1981-1982

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PAIN SEDATION AND MANAGEMENT
--Pain management in shock is often neglected
--Major reason: can cause hypotension and respiratory depression, furthering complications
--Poor pain management can also cause problems
>Increased vascular resistance
>Increased consumption of myocardial oxygen
>Increased metabolic rate
>Increased levels of circulating stress hormones
>Hyper-coagulability
>Decreased gastric motility
>Hopelessness

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NUTRITIONAL MANAGEMENT
--Important intervention in the acute care period
--Comprehensive plan for nutrition aids in:
>Healing
> Regaining Strength
>Preventing additional complications
--Focus is to provide exogenous energy and protein
--Hypermetabolic state requires support to prevent malnutrition

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SKIN CARE
--Pale, fragile skin increases risk for hypothermia
--Handle and move patient as gently as possible
--Skin breakdown and immobility can increase risk of sepsis
--Prevention
>Range of motion exercise
>Turning
>Meticulous skin care

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NURSING MANAGEMENT
--In depth assessment- ID current and past medical history that may place patient at risk for developing
--Frequent monitoring- trends in vitals, neuro, tissue perfusion, signs of hypoxia, urinary output
--ROM exercises
--Skin Care
--Medication management
--Emotional Support

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DEFINITIONS
--SIRS: nonspecific; organized immune response triggered by infectious or noninfectious clinical insults including burns, pancreatitis, acute respiratory distress syndrome, surgery, and trauma.
--Has 2 or more of the following variables
>Fever of more than 38 C (100.4 F) or less than 36 C (96.8 F)
>Heart rate more than 90 beats per minute
>Respiratory rate of more than 20 breaths per minute or arterial carson dioxide tension (PACO2) of less than 32 mmhg
>Abnormal WBC count (>12,000/uL or < 4,000/uL or >10% immature [band] forms)

--Sepsis: SIRS associated with confirmed infectious process

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DEFINITIONS
--Septic shock is a state of acute circulatory failure characterized by persistent hypotension unexplained by other causes (for Ex: despite adequate fluids being administered)
--Severe Sepsis: sepsis with single or multiple organ failure. The patient is hypotensive, which causes hypoperfusion abnormalities, such as arterial hypoxemia, acute oliguria, and coagulation abnormalities

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SIRS, SEPSIS, SEVERE SEPSIS
--Progression from SIRS to sepsis and severe sepsis
>3 principal actions occur within the body with sepsis
-Inflammation is a complex systemic response to mechanical, ischemic, chemical, or microbial triggers that activate an immediate inflammatory and immune response
-Purpose is to protect the body from further injury and promote rapid healing
-When infections occur, endotoxins and exotoxins are produced that initiate a cellular response that results in inflammation and cellular injury
-Inflammation normally localizes an infections and kills the invading organism, but when inflammation is extreme- vascular congestion, endothelial injury and dysfunction, and overstimulation of the coagulation system

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SIRS, SEPSIS, SEVERE SEPSIS
--Progression from SIRS to sepsis and severe sepsis
>3 principal actions with sepsis
-The coagulation cascade is activated by the endothelial injury leading to clot formation
-The cytokines activate tumor necrosis factor and the endothelial injury activates Factor XII, resulting in the activation of clotting factors that cause thrombin generation
-Normally this cascade is helpful in the healing process because it helps repair damaged blood vessels and mediators are released to keep it controlled to the affected area
-Fibrinolysis: spreads beyond the isolated area of infection

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SIRS, SEPSIS, SEVER SEPSIS
--Progression from SIRS to sepsis and severe sepsis
>3 principal actions with sepsis
--Fibrinolysis
>Normally with infection, the body suppresses fibrinolysis (clot breakdown) to allow time to destroy the antigen
>In sepsis, coagulation produces thrombi that become emboli, which ultimately block microvasculature throughout the body, causing cellular death and organ dysfunction
>Another reason for increased formation of thrombi with sepsis is the decrease in circulating activated protein C (normal component of anticoagulation; achieves homeostasis by decreasing inflammation, coagulation, and increase fibrinolysis)
>A low serum level of activated protein C is associated with sepsis, coagulopathy, multiple organ dysfunction, and increased mortality

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SIRS, SEPSIS, SEVERE SEPSIS
--When sepsis occurs, the regulatory mechanisms have failed, and uncontrolled inflammation overwhelms the body's normal protective responses
--Excess coagulation, exaggerated inflammation, and abnormal fibrinolysis spread beyond the isolated area of infection
--This leads to systemic vasodilation, hypotension, and a generalized increase in vascular permeability, extravascular sequestration and increased cellular aggregation with microvascular obstruction and greatly accelerated coagulation
--This cascade of events ultimately may lead to multiple organ failure and death

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CLINICAL MANIFESTATIONS
--Septic shock may initially manifest with different clinical manifestations from other forms of shock
>Febrile and chilling
>Flushed skin
>Bounding peripheral pulses
--The SSCM describes septic shock as sepsis with signs of hypoperfusion

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CLINICAL MANIFESTATIONS
--As the shock syndrome progresses, and hypoperfusion becomes more profound, the patient will become hypotensive and develop:
>Weak and thready pulse
>Cool and clammy skin
>Increased capillary refill
>Altered mental status
>Decreased or absent urinary output
>Hypoactive bowel sounds
>Rapid shallow respirations
--A patient who is suspected of being in septic shock who is hypothermic is in an advanced stage of sepsis and a a great risk of dying

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LAB AND DIAGNOSTIC PROCEDURES
--P1971
--CBC
--Cultures, sensitivity
--ABG's
--Serum lactate levels
--Coagulation studies

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MANAGEMENT
--The patients airway, breathing, and circulation need to be assessed and critical interventions needed
--The major focus during resuscitation of patients with septic shock is to prevent the consequences of tissue hypoperfusion and hypoxia
--The source of infection must be quickly determined and appropriately treated to stop the sepsis
--Antibiotic use should be reevaluated every 48-72 hours to ensure that the correct medications are being administered and that no toxic side effects are occurring

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MANAGEMENT
--See chart 61-8
--Fluid resuscitation, vasopressors, and in some cases blood transfusions for perfusion and oxygenation to compromised tissues
>Blood transfusions only when HGB less than 7; blood transfusions may worsen sepsis by initiating additional inflammation
--Appropriate cultures of blood or any other potential infection site should be obtained before antibiotic therapy

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MANAGEMENT
--Diagnostic studies should be performed promptly to identify the source of the infection or causative agent organism
--Sources such as abscesses need to be drained
--Antibiotic therapy based on patient history, underlying diseases, clinical syndrome, and susceptibility patterns in the patient's community and in health care facility

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MANAGEMENT
--Inotropic support to supplement low cardiac output
--IV corticosteroids for the patient in septic shock who does not respond to fluid replacement and vasopressor therapies
--Use of recombinant human activated C protein is recommended in patients with a high risk of death
--Mechanical ventilation should be closely monitored to prevent ventilator associated pneumonia, pulmonary injury, and adequate oxygenation
--Deep venous prophylaxis should be started to prevent the risk of emboli

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NURSE MANAGEMENT
--Key role in prevention and early recognition
--Be aware of potential sources- IV, Central line, foley catheter etc
--Meticulous aseptic technique, hand hygiene
--Education for patient's taking immunosuppressives or steroids on how to recognize Signs and symptoms of infections
--Assist medical management interventions

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ETIOLOGY OF MODS
--Multiple organ dysfunction syndrome (MODS) is a spectrum of organ dysfunction in a patient who has SIRS or septic complications- end result of severe sepsis
--Does not have to be an infectious agent to trigger
--One or more organ systems may be involved
--Triggers include
>Multiple injuries
>Burns
>Hemorrhagic or hypovolemic shock
> Acute pancreatitis
>Acute respiratory distress syndrome (ARDS)
>Acute renal failure

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RISK FOR MODS
--Chronic diseases
--advanced age
--Diabetes, cancer, pulmonary contusions, widespread necrosis
--Chronic infections treated with immunosuppressives

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PROGRESSION OF MODS
--MODS ranges from organ impairment to failure
--MODS is classified into primary or early MODS and secondary or late MODS
--In primary or early MODS, there is localized and generalized hypoperfusion, which triggers both the inflammatory and stress responses
--Secondary or late MODS results from an excessive inflammatory response after a latent period following the initial insult that is manifested in organs distant from the original site of injury
--Just as in sepsis, three primary mechanisms are activated: inflammatory response, coagulation, fibrinolysis- it is the body's own defense mechanisms that ultimately contribute to organ compromise and failure

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MODS PREVENTION STRATEGIES
--Primary focus: prevent MODS from occurring
--Nursing care for the patient with MODS includes:
>Early recognition of risk factors for MODS
>Close monitoring of invasive lines and catheters
>Meticulous skin care and aseptic technique
>Aseptic technique
>Frequent monitoring and assessment
>Focus on decreasing oxygen demand, including managing pain, anxiety, space activity
>Positioning to prevent complications of immobility

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