ch 49 and 50, shock, burns in adults and kids

Anaphylactic shock (type of reaction, caused by, CM, tx)

-widespread hypersensitivity to an allergen that triggers a reaction known as anaphylaxis ØAllergen causes an extensive immune and inflammatory response. •Massive vasodilation follows with a fluid shift into the interstitium. ØClinical manifestations •Anxiety, difficulty breathing, gastrointestinal (GI) cramps, edema, hives (urticaria), sensations of burning or itching of the skin, fever, and hemolysis. ØTreatment •Begins with the removal of the antigen, if possible. •Epinephrine: Decreases mast cell and basophil degranulation, causing vasoconstriction; reverses airway constriction. •Intravenous (IV) volume expanders (lactated Ringer solution): Reverses relative hypovolemia. •Antihistamines and steroids: Stops inflammatory reaction.

4 stages of septic shock progression

1. Systemic inflammatory response syndrome (SIRS) 2. Sepsis 3. Severe sepsis 4. Septic shock

hypovolemic shock sequences starting with decrease intravascular volume & decreased CO

1. catecholamine release --> increased SVR (syst vascular resistance) and increased HR/contractility 2. shift of interstitial fluid, aldosterone, ADH, splenic discharge --> increased volume increased cardiac output= more volume loss, decreased CO --> decreased systemic and pulmonary pressures decreased tissue perfusion and impaired cell metabolism

Endothelial cell dysfunction and mediator release in multiple organ dysfunction syndrome (MODS) produces 1.a net procoagulant state. 2.vasoconstriction. 3.a reduction in oxygen free radicals. 4.decreased proteases.

1.a net procoagulant state.

burns: 1st, 2nd, 3rd degree (

1st ØPartial-thickness injury (first degree) •Involves only the epidermis without injury to the underlying dermal or subcutaneous tissue. 2nd ØSuperficial partial-thickness injury (second degree) •Thin-walled, fluid-filled blisters develop within a few minutes after injury. ØDeep partial-thickness injury (second degree) •Involves the entire dermis, sparing skin appendages such as hair follicles and sweat glands. 3rd ØFull-thickness injury (third degree) •Entire epidermis, dermis, and often the underlying subcutaneous tissue are destroyed. •Escharotomy (cutting through burned skin): Is performed to release underlying pressure. •Injury is painless because nerve endings have been destroyed.

A nurse is assigned to care for a person with a 40% deep partial-thickness injury. Which parameter will the nurse closely monitor to best assess adequate fluid resuscitation? 1.Hematocrit level 2.Urine output 3.Heart rate 4.Blood pressure

2.Urine output

A person develops cardiogenic shock after an acute MI. The nurse understands this will produce a(an) 1.inhibition of the sympathetic nervous system. 2.stimulation of the renin-angiotensin system. 3.decreased activation of the complement system. 4.lowered production of catecholamine system.

2.stimulation of the renin-angiotensin system.

A person arrives at the emergency department with a burn injury. The burn area is covered with thin-walled, fluid-filled blisters and is very painful. The nurse suspects this is a 1.first-degree injury. 2.superficial partial-thickness injury. 3.deep partial-thickness injury. 4.full-thickness injury.

2.superficial partial-thickness injury.

major burn = what % of TBSA in adults and CM

20% Are associated with massive evaporative water losses and flux of large amounts of fluid and electrolytes. •Generalized edema •Circulatory hypovolemia

Which laboratory result should the nurse check for a person with suspected septic shock? 1. Hetastarches 2. Immunoglobulin E (IgE) 3. Lactate 4. Antigen titer

3. Lactate Elevated lactate levels indicate tissue hypoperfusion and patients should be entered in early goal directed therapy or resuscitation within 6 hours, regardless of blood pressure level.

Which parameter will the nurse monitor to best determine the systemic perfusion in a child? 1.Urinary output 2.Partial pressure of arterial oxygen (Pao2) 3.Serum lactate 4.Systolic hypotension

3.Serum lactate

In a child 3 years old, which information is correct regarding a burn injury? 1.Decreased intraabdominal pressure can impair hemodynamics and renal function. 2.Pulmonary edema is the main cause of morbidity and mortality. 3.Mucosal hypertrophy and diarrhea are common after major burns. 4.Intraosseous cannulation can be effective for fluid replacement.

4.Intraosseous cannulation can be effective for fluid replacement.

cariogenic shock patho: -cardiac output -compensatory responses

As cardiac output decreases, compensatory adaptive responses are activated: Renin-angiotensin, neurohormonal, and sympathetic nervous system •Compensatory responses: Fluid retention, systemic vasoconstriction, and tachycardia. •Activates inflammatory response.

1.Neurogenic shock is a form of hypovolemic and A.cardiogenic shock. B.vasogenic shock. C.multiple organ dysfunction syndrome. D.reperfusion injury.

B.vasogenic shock. It is caused by a loss of vasomotor tone after severe head injury or spinal cord injury. Massive vasodilation and loss of sympathomimetic tone result in a relative hypovolemia and hypotension.

CM of shock: -BP -Labs

Blood pressure ØShock may be present, despite a systolic blood pressure within the normal range for the age of the child. ØSystolic hypotension develops, or the mean arterial pressure falls. •Indicates hypotensive shock. •Urgent treatment is needed. LABS: elevated liver enzymes, metabolic acidosis, serum lactate above 4 (los perfusion),

2.In all types of shock, cells do not receive adequate amounts of oxygen because of decreased delivery or increased cellular consumption. Decreased oxygen and nutrient delivery to cells impairs the cells' ability to compensate and maintain normal function. Organ failure is caused by the depletion of A.fat. B.glycogen. C.protein. D.calcium.

C.protein. As proteins are broken down anaerobically, ammonia and urea are produced. Ammonia is toxic to living cells. Uremia develops and uric acid further disrupts cellular metabolism

vesicants cause ___ on epithelium

Can cause blistering of the epithelial surfaces.

causes for different types of shock: cardiogenic neurogenic/vasogenic anaphylactic septic hypovolemic

Cardiogenic Heart failure Neurogenic or vasogenic Alterations in smooth muscle tone Anaphylactic Hypersensitivity Septic Infection Hypovolemic Insufficient intravascular fluid

kids burns: Ebb vs Catabolic/FLow phase

Ebb Phase •Initial: Occurring during the immediate postburn period; continuing for 3-5 days •Reduced oxygen consumption, impaired circulation, and cellular shock Catabolic (Flow) Phase •After the resolution of the shock and the restoration of circulating volume •Hypermetabolism with increased oxygen consumption and elevation of catecholamines, glucocorticoids, and glucagon

septic shock Gram + vs Gram - and pro/anti inflammation cytokines

Gram +: -release exotoxin: pepitoglycans, super antigens, Gram - -release of endotoxin: LPS lipopolysaccharide containing toxic lipid A pro inflammatory cytokines (TNF, IL 1 and 6) complement, coagulation, kinin, neutrophil/monocyte/macrophage release of anti inflammatory: - LPS protein, IL 1 antagonist, IL 10, NO

is the rule of 9s TBSA accurate for children? (modified rule of 9s, %s)

NO arms and trunk the same as adult trunk/ back : 18% each 1 arm = 9% front and back head and neck = 18% each leg = 4% ØModified Rule of nines •Modification deducts 1% from the head and adds 0.5% to each leg for each year of life after 2 years of age.

newborns show what instead of fever and tachycardia in septic shock

Often develop hypothermia rather than fever; may develop bradycardia instead of tachycardia

most accurate parameter or adequate fluid resuscitation

Urine output: •Urine output of 1 mL/kg/hour in children weighing less than 30 kg: Suggested endpoints

shock peds urine output levels

Urine volume decreases, despite adequate fluid intake •Less than 2 mL/kg/hour in infants •Less than 1 mL/kg/hour in children •Less than 0.5 mL/kg/hour in adolescents

anaphylactic shock sequence starting with antigen (capillary, peripheral, smooth muscle, serotonin/leukotriene, heparin)

antibody IgE triggers complement, histamine, kinins, prostaglandins 1. increased cap permeability, extravasation of intravascular fluids, edema, relative hypovolemia 2. peripheral vasodilation, decreased SVR, relative hypovolemia 3. constriction of extravascular smooth muscle [bronchoconstriction, laryngospasm, GI cramps] 4. increased serotonin and leukotrienes = swelling = relative hypovolemia 5. increased heaping, (potential hemorrhage/DIC ** relative hypovolemia, decreased CO, decreased tissue perfusion, impaired cell metabolism

peds shock breathing, skin color CM

breathing CM •Extremely rapid respiratory rate: Tachypnea •Increased depth of respirations: Hyperpnea •Evidence of increased respiratory effort: Retractions, grunting •Apnea or inadequate respiratory rate or effort Indicates deterioration. Needs immediate support of airway, oxygenation, and ventilation. skin CM ØMottling: Marbleized or blotchy appearance to the skin •May not be shock if mottling comes from a cold environment, those who have undergone hypothermic surgery or a procedure in a cold room ØPallor •Poor perfusion ØFlushed, bright red skin •Sepsis VS/capr refill: ØCapillary refill •Compromise in systemic perfusion: Prolonged capillary refill time (>2 seconds) •Subjective interpretation; therefore not reliable ØVital signs •Not always indicative or appropriate in the child who is seriously ill or injured

what indicated the end of burn shock

capillary seal immediate/acute phase of burn shock

shock (common pathways

cardiovascular system fails to perfuse the tissues adequately; causes general and widespread impairment of cellular metabolism. •decreased delivery of oxygen and nutrients - increased demand and consumption of oxygen and nutrients •Decreased removal of cellular waste products

cardiogenic shock

caused by: Øcardiovascular surgery or with inflammatory heart diseases ØClinical manifestations •Cool extremities, delayed capillary refill, despite a warm, ambient temperature; mottled skin ØTreatment •Fluid titration: To optimize cardiac preload •Vasoactive drugs: To improve myocardial function •Vasodilators or vasoconstrictors: To support systemic perfusion

Septic shock (6 common infection sites, inflammatory process fx,

infection (6 common sites, lungs, bloodstream, intravascular catheter, intraabdominal, urinary tract, and a surgical wound.) inflammatory process (complement, coagulation, kinin) •Initiates and promotes widespread vasodilation. ØClinical manifestations •Persistent low arterial pressure, low tissue perfusion, low SVR from vasodilation, and an alteration in oxygen extraction by all cells. ØTreatment •Check lactate level; obtain blood cultures; start antibiotic and vasopressor medications; implement fluid challenge; and achieve goals for blood pressure, central venous pressure, and central venous oxygen saturation. •Norepinephrine: Is the initial vasopressor of choice.

Failure to administer fluid resuscitation in burns results in

irreversible hypovolemic shock and death.

cariogenic shock sequence starting with decreased cardiac output

low CO 1. compensatory renin-aldosterone, ADH = increased blood volume 2. catecholamine compensation = increased SVR preload, SV, HR increase --> systemic & pulmonary edema (dyspnea --> increased O2 requirements, dec CO, dec EF, dec perfusion, dec BP, ischemia, impaired ell metabolism, myocardial dysfunction

burns in kids: high or low- CO, SVR, intraabdominal pressure

low CO immediately SVR high at first increased intraabdominal pressure

Neurogenic (vasogenic) shock: sequence starting with imbalance between SNS and PNS

massive vasodilation vascular tone decreases decreased SVR low CO dec tissue perfusion impaired cell metabolism

burn edema complications

mechanical airway obstruction, necessitating tracheal intubation, and increased severity of the interstitial pulmonary edema associated with inhalation injury.

burn metabolic and cellular response

metabolic: body's catabolism accelerated cellular: intracellular high Na, H2O; low Mg and PO -during shock: K, H2O, Na, Ablumin OUT of capillary; NA into cell K out -after burn: H2O and Na in capillary, K into cell, Na out of cell immune response: -immunosuppression (sepsis fatal) -release cytokines, free radicals, chemotactic factors, eicosanoids

burns: rule of 9s

trunk/ back : 18% each head 9% total 1 arm = 9% front and back 1 leg = 18% front and back

peds burns: how long does it take for a scar to mature

up to 2 years

Multiple Organ DysfunctionSyndrome: CM timeline (24 hrs, 24-72, 7-10 days, 14-21 days, later)

ØAt approximately 24 hours •Low-grade fever, tachycardia, tachypnea, dyspnea, altered mental status, general hyperdynamic and hypermetabolic state ØAt 24-72 hours •Beginning of lung failure; possible appearance of ARDS ØBetween days 7 and 10 •Development of hepatic, intestinal, and renal failure ØDuring days 14-21 •Increased severity of renal failure and liver failure; also possible occurrence of death ØLater: Hematologic failure and myocardial failure

Shock Cm and tx

ØClinical manifestations •Weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath, and generally "feeling sick" •Decreased blood pressure, cardiac output, and urinary output •Increased respiratory rate ØTreatment •Oxygenation: Absolute necessity in all shock states •Correct or remove underlying cause •Provide supportive therapy

pro and anti inflammatory effects of cytokines in children's burns

ØCytokines increase inflammation by enhancing catabolism and hypermetabolism. •Proinflammatory function of cytokines enhances protection from sepsis, whereas the antiinflammatory function supports anabolism (tissue repair).

impaired cell metabolism in shock: -impaired O2 use (Na, Cl, K, coagulation, enzyme) -impaired glucose delivery and use (gluconeogenesis and proteins, acid/base)

ØImpaired oxygen use, regardless of cause •Shift from aerobic to anaerobic metabolism •Loss of the ability to maintain electrochemical gradient •Accumulation of sodium and chloride in the cell Water follows, thus reducing the extracellular volume. •Exiting of potassium from the cell •Activation of coagulation pathway •Release of lysosomal enzyme ØImpaired glucose delivery and use •Cells shifting to glycogenolysis, gluconeogenesis, lipolysis •Gluconeogenesis causes proteins to be used for fuel (no longer available for maintaining cellular structure, function, repair, and replication) Toxic ammonia and urea production •Metabolic acidosis Compensatory mechanism initiated: Enables cardiac and skeletal muscles to use lactic acid as a fuel source but only for a limited time •Glycogenolysis and lipolysis contribute to cellular failure.

CM of types of burns partial thickness, superficial partial, deep partial, full thicnkess

ØPartial-thickness injury •Local pain is felt; erythema develops. •No blisters form until approximately 24 hours after injury. ØSuperficial partial-thickness injury •Is painful; thin-walled and fluid-filled blisters develop within a few minutes after injury. ØDeep partial-thickness injury •Waxy white skin is surrounded by margins of the superficial partial-thickness injury; the skin may peel off in sheets. Is indistinguishable from a full-thickness injury until 7-10 days, at which time skin buds and hair appear ØFull-thickness injury •Burn color is white, cherry red, or black. •Delineation between normal and burned skin is not accompanied by a significant color change. •Blisters are rare. •Wound is dry and leathery.

peds septic shock CM: SIRS criteria, severe sepsis, septic shock, vascular/CO

ØSystemic inflammatory response syndrome (SIRS) = 2+ of the following changes: •Temperature: Fever higher than 38.5°C (101.3°F) or hypothermia: Body temperature lower than 36°C (96.8°F) •Heart rate: Tachypnea or bradycardia (in infants) •Respiratory rate: Requiring mechanical ventilation •White blood cell (WBC) count: Leukocytes, leukopenia, or an increase in the percentage of immature or band forms of WBCs •Severe sepsis: Evidence of sepsis (SIRS with suspected infection) •Septic shock: Development of cardiovascular dysfunction •Severe peripheral vasoconstriction, high systemic vascular resistance, and low cardiac output

Anaphylactic shock leads to (3 things; blood volume level, vessel constricted or dilated, peripheral blood flow)

Øvasodilation, peripheral pooling, and relative hypovolemia.

Multiple Organ DysfunctionSyndrome (def, caused by, RF, CM, prevent, Tx)

• progressive dysfunction of two or more organ systems from an uncontrolled inflammatory response to a severe illness or injury. 2 common causes: shock and sepsis [•Trauma, burns, acute respiratory disorder (ARDS), major surgery, circulatory shock, necrotic tissue, disseminated intravascular coagulation (DIC), acute renal failure, acute pancreatitis] RF: old, preexisting tissue injury CM: •Encephalopathy, characterized by mental status changes ranging from confusion to deep coma, can occur at any time. •Sequence can rapidly evolve, or it can evolve over weeks. Prevention: •Is essential. •Eliminate or control the initial source of stress. •Avoid second insults. •Remove any potential site of infection. Tx: •Provide oxygen and nutrition •Administer antibiotics. •Restore intravascular volume. ØRespiratory system: Mechanical ventilation •Low tidal volumes, high oxygen concentrations, and positive end-expiratory pressures (PEEP) ØGI system: Enteral feedings or hyperalimentation •Tight glucose control: 140-180 mg/dL •Calories for hypermetabolic state ØRenal system •Dialysis or continuous hemofiltration for fluid and electrolyte balance ØCardiovascular system •Inotropic drugs or vasopressors •Steroids: Controversial

kid burns: lung CM

• pulmonary edema, and respiratory failure to aspiration and pneumonia. •Fatigue, related to the increased work of breathing, results in more rapid desaturation than in adults. •Soft cartilage of the pediatric airway is prone to collapse in the presence of partial obstruction.

burns in children: -renal: how long after injury does edema mobilize -GI

•Approximately 36 hours after injury, edema fluid begins to mobilize and output increases. GI: •Mucosal atrophy occurs, digestive absorption changes, and intestinal permeability increases. •Depending on the burn size, atrophy of the gastrointestinal tract mucosa can occur, immediately leading to increased bacterial translocation and ultimately to sepsis. •Paralytic ileus often occurs after a major burn injury.

Neurogenic (vasogenic) shock: what is the blood volume level? SVR?

•Blood volume is unchanged, but the amount of space containing the blood has increased; therefore the SVR decreases drastically. •Pressure in the vessels is inadequate to drive nutrients across capillary membranes; nutrient delivery to cells is impaired.

Burns: Ebb phase (time, blood away from..)

•Cardiac contractility: Is diminished during the initial 24-hour resuscitation period with shunting of blood away from the liver, kidney, and gut.

•Catecholamines ___ contractility and heart rate.

•Catecholamines increase contractility and heart rate.

peds shock LOC/responsiveness, HR

•Extremely irritable •Lethargy: Severe deterioration of consciousness •Decreased response to painful stimulation Is an abnormal response. Usually indicates severe cardiorespiratory or neurologic compromise. HR: ØTachycardia •Primary vs. secondary to stress •If extremely rapid or present with decreased myocardial function: Possible cause rather than a symptom of shock •Ventricular rate exceeding 200-220 beats/minute (bpm) in an infant or 160-180 bpm in a child Ventricular diastolic filling time and coronary artery perfusion time are significantly reduced, and stroke volume falls. ØBradycardia •Abnormally low heart rate: Possible cause or a symptom of deterioration •Most common cause: Hypoxia •Often indicates impending cardiovascular collapse •Most common terminal cardiac rhythm observed in children

burn Tx

•First-degree burns: Usually no treatment ØAdequate fluids •Massive amounts of IV fluid are needed. •Fluid resuscitation, with lactated Ringer solution, involves the infusion of fluids at a rate faster than the loss of circulating volume. •Urine output is the most reliable criterion for adequate fluid resuscitation.

Septic Shock kids (what mediators of infection are formed? blood vessels? blood flow? RF)

•Formation or activation of cytokines and other mediators from infection Vasodilation, increased capillary permeability, maldistribution of blood flow, and cardiovascular dysfunction RF: low birth wt neonates

peds shock glucose labs/levels

•Hypoglycemia (glucose ≤60 mg/dL) in infants who are seriously ill or injured: Possible cardiovascular or neurologic deterioration •Hyperglycemia (>150 mg/dL): Insulin-resistant state from catecholamines and hydrocortisone secretion; often observed in the first 12-18 hours, then falling to normal •Critical illness hyperglycemia (>180 mg/dL): Linked with poor survival in children who are critically ill

peds burn shock (fluid/electrolytes, TBSA to weight ratio, fluid resuscitation if burn greater than __%)

•Hypovolemia and extracellular sodium are depleted. •Child's relatively greater ratio of body surface area to weight results in increased evaporative water losses and proportionately more fluid during resuscitation. •Fluid resuscitation is generally required for children after thermal injuries in excess of 10% to 15% of their TBSA. Use modified Parkland formula.

Cardiogenic shock: caused by

•Inability of the heart to pump adequate blood to tissues and end organs from any cause •Causes: Myocardial ischemia, myocardial infarction (MI) •Persistent hypotension and tissue hypoperfusion caused by cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure •Decrease in cardiac output CM: •Chest pain, dyspnea, and faintness, along with feelings of impending doom •Classic hallmarks: Tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output Tx: •Intraaortic balloon counterpulsation (IABP) or percutaneous or ventricular assist devices (VADS) Implantable VADS, pacemakers, or internal defibrillator devices •Fibrinolytic therapies: To disintegrate coronary thrombus •Percutaneous interventions: Balloon angioplasty, stent placement, and thrombectomies •Surgery: Coronary artery bypass, ventriculoplasty, or heart transplantation •Cardiosupportive drug and fluid regimens •Continuous hemodynamic monitoring

Hypovolemic shock (caused by loss of...; compensation by, CM, tx)

•Insufficient intravascular fluid volume •Loss of whole blood, blood plasma, or interstitial fluid --Hemorrhage, burns, emesis, diuresis, diaphoresis, diabetes •Compensatory vasoconstriction, increased systemic vascular resistance (SVR), and afterload To improve blood pressure and perfusion to core organs CM: •Poor skin turgor, thirst, oliguria •Low systemic and pulmonary preloads •Rapid heart rates Tx: •Prompt control of hemorrhage •Fluid replacement

Multiple Organ DysfunctionSyndrome becomes 100% mortality rate with failure of ___ organ systems

•Mortality rate increases to 100% with the failure of five systems.

hypovolemic shock peds: common causes, relative hypovolemia

•Most common causes: Dehydration and trauma •Relative hypovolemia: Burns or sepsis or "third spacing"

age for scald vs flame injuries in children

•Scald injuries Most common in young children •Flame injuries Most common in older children

Neurogenic (vasogenic) shock (caused by, Cm, tx)

•Widespread vasodilation occurs from an imbalance between parasympathetic and sympathetic stimulation. •Causes include trauma, severe pain and stress, anesthesia, and depressant drugs. CM: •Very low SVR, bradycardia Tx: decrease pain level

Peds: Obstructive Shock (def; CM: ductal dependent pulmonary flow, ductal dependent systemic blood flow, tension pneumothorax, cardiac tamponade, pulmonary embolus)

•inadequate cardiac output caused by an impediment to blood flow to or from the heart into the pulmonary or systemic circulation. CM: ØDuctal-dependent pulmonary blood flow •Hypoxemia will become profound when the ductus arteriosus begins to constrict. ØDuctal-dependent systemic blood flow •Systemic pulses will become faint or absent; extremities will become cold and pale. •Signs of pulmonary venous congestion will develop when the ductus arteriosus begins to close. ØTension pneumothorax •Decreased breath sounds and chest expansion on the side of the pneumothorax •Shift of the mediastinum to the contralateral chest •Significant hypoxemia ØCardiac tamponade •Systemic or pulmonary edema, or both, with low cardiac output ØPulmonary embolus •Hypoxemia, severe respiratory distress (or shortness of breath), and signs of right ventricular failure