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(Relates to Chapter 67, “Nursing Management: Shock, SIRS,
and Multiple Organ Dysfunction Syndrome,”
in the textbook)
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ShockSyndrome characterized by decreased tissue
perfusion and impaired cellular metabolism
Imbalance between the supply and demand for O2 and nutrients
shock
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ShockClassification of shock
Low blood flow Cardiogenic Hypovolemic
Maldistribution of blood flow Septic Anaphylactic Neurogenic
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Low Blood Flow Cardiogenic Shock
Definition
Systolic or diastolic dysfunction
Compromised cardiac output (CO)
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Low Blood Flow Cardiogenic Shock
Precipitating causesMyocardial infarction CardiomyopathyBlunt cardiac injurySevere systemic or pulmonary
hypertensionCardiac tamponadeMyocardial depression from metabolic
problems
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Pathophysiology of Cardiogenic Shock
Fig. 67-2
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Low Blood Flow Cardiogenic Shock
Early manifestationsTachycardiaHypotensionNarrowed pulse pressure ↑ Myocardial O2 consumption
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Low Blood Flow Cardiogenic Shock
Physical examination Tachypnea, pulmonary congestionPallor; cool, clammy skinDecreased capillary refill timeAnxiety, confusion, agitation
↑ in pulmonary artery wedge pressure
Decreased renal perfusion and UO
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Low Blood Flow Hypovolemic Shock
Absolute hypovolemia: Loss of intravascular fluid volume HemorrhageGI loss (e.g., vomiting, diarrhea)Fistula drainageDiabetes insipidusHyperglycemiaDiuresis
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Low Blood Flow Hypovolemic Shock
Relative hypovolemiaResults when fluid volume moves out of the
vascular space into extravascular space (e.g., interstitial or intracavitary space)
Termed third spacing
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Pathophysiology of Hypovolemic Shock
Fig. 67-3
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Low Blood Flow Hypovolemic Shock
Response to acute volume loss depends on Extent of injury or insultAgeGeneral state of health
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Low Blood Flow Hypovolemic Shock
Clinical manifestationsAnxietyTachypneaIncrease in CO, heart rateDecrease in stroke volume, PAWP, UO
If loss is >30%, blood volume is replaced
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Maldistribution of Blood Flow Neurogenic Shock
Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks
Can be in response to spinal anesthesiaResults in massive vasodilation leading to
pooling of blood in vessels
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Pathophysiology of Neurogenic Shock
Fig. 67-4
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Maldistribution of Blood Flow Neurogenic Shock
Clinical manifestations HypotensionBradycardiaTemperature dysregulation
(resulting in heat loss)Dry skinPoikilothermia (taking on the
temperature of the environment)
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Maldistribution of Blood Flow Anaphylactic Shock
Acute, life-threatening hypersensitivity reaction
Massive vasodilationRelease of mediators↑ Capillary permeability
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Maldistribution of Blood Flow Anaphylactic Shock
Clinical manifestationsAnxiety, confusion, dizzinessSense of impeding doomChest painIncontinence
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Maldistribution of Blood Flow Anaphylactic Shock
Clinical manifestationsSwelling of the lips and tongue, angioedemaWheezing, stridorFlushing, pruritus, urticariaRespiratory distress and circulatory failure
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Maldistribution of Blood Flow Septic Shock
Sepsis: Systemic inflammatory response to documented or suspected infection
Severe sepsis = Sepsis + Organ dysfunction
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Maldistribution of Blood Flow Septic Shock
Septic shock = Presence of sepsis with hypotension despite fluid resuscitation + Presence of tissue perfusion abnormalities
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Maldistribution of Blood Flow Septic Shock
Mortality rates as high as 50%Primary causative organisms
Gram-negative and gram-positive bacteriaEndotoxin stimulates inflammatory response
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Pathophysiology of Septic Shock
Fig. 67-5
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Maldistribution of Blood Flow Septic Shock
Clinical manifestations
↑ Coagulation and inflammation
↓ FibrinolysisFormation of microthrombiObstruction of microvasculature
Hyperdynamic state: Increased CO and decreased SVR
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Maldistribution of Blood Flow Septic Shock
Clinical manifestationsTachypnea/hyperventilationTemperature dysregulation↓ Urine outputAltered neurologic statusGI dysfunctionRespiratory failure is common
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Stages of Shock Initial Stage
Usually not clinically apparentMetabolism changes from aerobic to
anaerobic Lactic acid accumulates and must be removed
by blood and broken down by liverProcess requires unavailable O2
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Stages of Shock Compensatory Stage
Clinically apparent NeuralHormonalBiochemical compensatory mechanisms
Attempts are aimed at overcoming consequences of anaerobic metabolism and maintaining homeostasis
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Compensatory Stage of Shock
Fig. 67-6
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Stages of Shock Compensatory Stage
Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BPVasoconstriction while blood to vital organs
maintained
↓ Blood to kidneys activates renin–angiotensin system↑ Venous return to heart, CO, BP
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Stages of Shock Compensatory Stage
Impaired GI motilityRisk for paralytic ileus
Cool, clammy skin from bloodExcept septic patient who is warm and flushed
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Stages of Shock Compensatory Stage
Shunting blood from lungs increases physiologic dead space
↓ Arterial O2 levelsIncrease in rate/depth of respirations
V/Q mismatchSNS stimulation increases myocardium O2
demands
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Stages of Shock Compensatory Stage
If perfusion deficit corrected, patient recovers with no residual sequelae
If deficit not corrected, patient enters progressive stage
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Stages of Shock Progressive Stage
Begins when compensatory mechanisms fail
Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS)
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Progressive Stage of Shock
Fig. 67-7
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Stages of Shock Progressive Stage
Hallmarks of ↓ cellular perfusion and altered capillary permeability:
Leakage of protein into interstitial space
↑ Systemic interstitial edema
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Stages of Shock Progressive Stage
Anasarca Fluid leakage affects solid organs and peripheral tissues
↓ Blood flow to pulmonary capillaries
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Stages of Shock Progressive Stage
Movement of fluid from pulmonary vasculature to interstitium
Pulmonary edemaBronchoconstriction↓ Residual capacity
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Stages of Shock Progressive Stage
Fluid moves into alveoliEdemaDecreased surfactantWorsening V/Q mismatchTachypneaCracklesIncreased work of breathing
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Stages of Shock Progressive Stage
CO begins to fallDecreased peripheral perfusionHypotensionWeak peripheral pulsesIschemia of distal extremities
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Stages of Shock Progressive Stage
Myocardial dysfunction results inDysrhythmias IschemiaMyocardial infarctionEnd result: Complete deterioration of cardiovascular system
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Stages of Shock Progressive Stage
Mucosal barrier of GI system becomes ischemic
Ulcers BleedingRisk of translocation of bacteriaDecreased ability to absorb nutrients
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Stages of Shock Progressive Stage
Liver fails to metabolize drugs and wastesJaundice Elevated enzymesLoss of immune functionRisk for DIC and significant bleeding
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Stages of Shock Progressive Stage
Acute tubular necrosis/acute renal failure
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Stages of Shock Refractory Stage
Exacerbation of anaerobic metabolismAccumulation of lactic acid↑ Capillary permeability
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Refractory Stage of Shock
Fig. 67-8
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Stages of Shock Refractory Stage
Profound hypotension and hypoxemiaTachycardia worsensDecreased coronary blood flowCerebral ischemia
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Stages of Shock Refractory Stage
Failure of one organ system affects others
Recovery unlikely
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Diagnostic StudiesThorough history and physical
examinationNo single study to determine shock
Blood studies Elevation of lactateBase deficit
12-lead ECGChest x-rayHemodynamic monitoring
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Collaborative CareSuccessful management includes
Identification of patients at risk for shockIntegration of the patient’s history, physical
examination, and clinical findings to establish a diagnosis
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Collaborative CareSuccessful management includes
Interventions to control or eliminate the cause of the decreased perfusion
Protection of target and distal organs from dysfunction
Provision of multisystem supportive care
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Collaborative CareGeneral management strategies
Ensure patent airwayMaximize oxygen delivery
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Collaborative CareCornerstone of therapy for septic,
hypovolemic, and anaphylactic shock = volume expansion Isotonic crystalloids (e.g., normal saline) for
initial resuscitation of shock
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Collaborative CareVolume expansion
If the patient does not respond to 2 to 3 L of crystalloids, blood administration and central venous monitoring may be instituted
Complications of fluid resuscitationHypothermia Coagulopathy
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Collaborative CarePrimary goal of drug therapy = correction of
decreased tissue perfusionVasopressor drugs (e.g., epinephrine)
Achieve/maintain MAP >60 to 65 mm Hg
Reserved for patients unresponsive to other therapies
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Collaborative Care
Primary goal of drug therapy = correction of decreased tissue perfusionVasodilator therapy (e.g., nitroglycerin
[cardiogenic shock], nitroprusside [noncardiogenic shock])
Achieve/maintain MAP >60 to 65 mm Hg
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Collaborative CareNutrition is vital to decreasing morbidity
from shockInitiate enteral nutrition within the first
24 hoursInitiate parenteral nutrition if enteral
feedings contraindicated or fail to meet at least 80% of the caloric requirements
Monitor protein, nitrogen balance, BUN, glucose, electrolytes
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Collaborative CareCardiogenic Shock
Restore blood flow to the myocardium by restoring the balance between O2 supply and demand
Thrombolytic therapyAngioplasty with stentingEmergency revascularizationValve replacement
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Collaborative Care Cardiogenic Shock
Hemodynamic monitoringDrug therapy (e.g., diuretics to reduce
preload)Circulatory assist devices (e.g., intra-aortic
balloon pump, ventricular assist device)
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Collaborative Care Hypovolemic Shock
Management focuses on stopping the loss of fluid and restoring the circulating volume
Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)
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Collaborative Care Septic Shock
Fluid replacement (e.g., 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids) to restore perfusion
Hemodynamic monitoring Vasopressor drug therapy; vasopressin for
patients refractory to vasopressor therapy
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Collaborative Care Septic Shock
Intravenous corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP
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Collaborative Care Septic Shock
Antibiotics after obtaining cultures (e.g., blood, wound exudate, urine, stool, sputum)
Drotrecogin alfa (Xigris)Major side effect: Bleeding
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Collaborative Care Septic Shock
Glucose levels <150 mg/dlStress ulcer prophylaxis with histamine
(H2)-receptor blockers Deep vein thrombosis prophylaxis with low-
dose unfractionated heparin or low-molecular-weight heparin
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Collaborative Care Neurogenic Shock
In spinal cord injury: Spinal stabilityTreatment of the hypotension
and bradycardia with vasopressors and atropine
Fluids used cautiously as hypotension is generally not related to fluid loss
Monitor for hypothermia
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Collaborative CareAnaphylactic Shock
Epinephrine, diphenhydramine Maintaining a patent airway
Nebulized bronchodilators Endotracheal intubation or cricothyroidotomy may be necessary
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Collaborative CareAnaphylactic Shock
Aggressive fluid replacement Intravenous corticosteroids if significant
hypotension persists after 1 to 2 hours of aggressive therapy
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Nursing Assessment
ABCs: Airway, breathing, and circulation
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Nursing Assessment
Focused assessment of tissue perfusionVital signsPeripheral pulsesLevel of consciousnessCapillary refillSkin (e.g., temperature, color, moisture)Urine output
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Nursing AssessmentBrief history
Events leading to shockOnset and duration of symptoms
Details of care received before hospitalization AllergiesVaccinations
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Nursing DiagnosesIneffective tissue perfusion: Renal, cerebral,
cardiopulmonary, gastrointestinal, hepatic, and peripheral
Fear Potential complication: Organ
ischemia/dysfunction
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PlanningGoals for patient
Assurance of adequate tissue perfusionRestoration of normal or baseline BPReturn/recovery of organ functionAvoidance of complications from prolonged
states of hypoperfusion
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Nursing ImplementationHealth Promotion
Identify patients at risk (e.g., elderly patients, those with debilitating illnesses or who are immunocompromised, surgical or accidental trauma patients)
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Nursing ImplementationHealth Promotion
Planning to prevent shock (e.g., monitoring fluid balance to prevent hypovolemic shock, maintenance of handwashing to prevent spread of infection)
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Nursing ImplementationAcute Interventions
Monitor the patient’s ongoing physical and emotional status to detect subtle changes in the patient’s condition
Plan and implement nursing interventions and therapy
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Nursing ImplementationAcute Interventions
Evaluate the patient’s response to therapy
Provide emotional support to the patient and family
Collaborate with other members of the health team when warranted
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Nursing ImplementationNeurologic status: Orientation and
level of consciousnessCardiac status
Continuous ECG VS, capillary refillHemodynamic parameters: central venous
pressure, PA pressures, CO, PAWP
Heart sounds: Murmurs, S3, S4
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Nursing ImplementationRespiratory status
Respiratory rate and rhythmBreath soundsContinuous pulse oximetry Arterial blood gases Most patients will be intubated and
mechanically ventilated
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Nursing ImplementationUrine outputTympanic or pulmonary arterial temperature Skin: Temperature, pallor, flushing, cyanosis,
diaphoresis, piloerection Bowel sounds
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Nursing Implementation Nasogastric drainage/stools for occult bloodI&O, fluid and electrolyte balanceOral care/hygiene based on O2 requirementsPassive/active range of motion
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Nursing ImplementationAssess level of anxiety and fear
Medication PRNTalk to patientVisit from clergyFamily involvementComfort measuresPrivacyCall light within reach
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EvaluationNormal or baseline, ECG, BP, CVP,
and PAWPNormal temperatureWarm, dry skinUrinary output >0.5 ml/kg/hrNormal RR and SaO2 ≥90%Verbalization of fears, anxiety