Shock

Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

(Relates to Chapter 67, “Nursing Management: Shock, SIRS,

and Multiple Organ Dysfunction Syndrome,”

in the textbook)

Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

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


Low Blood Flow Cardiogenic Shock

Definition

Systolic or diastolic dysfunction

Compromised cardiac output (CO)



Precipitating causesMyocardial infarction CardiomyopathyBlunt cardiac injurySevere systemic or pulmonary

hypertensionCardiac tamponadeMyocardial depression from metabolic

problems

Pathophysiology of Cardiogenic Shock

Fig. 67-2




Early manifestationsTachycardiaHypotensionNarrowed pulse pressure ↑ Myocardial O2 consumption



Physical examination Tachypnea, pulmonary congestionPallor; cool, clammy skinDecreased capillary refill timeAnxiety, confusion, agitation

↑ in pulmonary artery wedge pressure

Decreased renal perfusion and UO


Low Blood Flow Hypovolemic Shock

Absolute hypovolemia: Loss of intravascular fluid volume HemorrhageGI loss (e.g., vomiting, diarrhea)Fistula drainageDiabetes insipidusHyperglycemiaDiuresis



Relative hypovolemiaResults when fluid volume moves out of the

vascular space into extravascular space (e.g., interstitial or intracavitary space)

Termed third spacing

Pathophysiology of Hypovolemic Shock

Fig. 67-3




Response to acute volume loss depends on Extent of injury or insultAgeGeneral state of health



Clinical manifestationsAnxietyTachypneaIncrease in CO, heart rateDecrease in stroke volume, PAWP, UO

If loss is >30%, blood volume is replaced


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

Pathophysiology of Neurogenic Shock

Fig. 67-4



Maldistribution of Blood Flow Neurogenic Shock

Clinical manifestations HypotensionBradycardiaTemperature dysregulation

(resulting in heat loss)Dry skinPoikilothermia (taking on the

temperature of the environment)


Maldistribution of Blood Flow Anaphylactic Shock

Acute, life-threatening hypersensitivity reaction

Massive vasodilationRelease of mediators↑ Capillary permeability



Clinical manifestationsAnxiety, confusion, dizzinessSense of impeding doomChest painIncontinence



Clinical manifestationsSwelling of the lips and tongue, angioedemaWheezing, stridorFlushing, pruritus, urticariaRespiratory distress and circulatory failure


Maldistribution of Blood Flow Septic Shock

Sepsis: Systemic inflammatory response to documented or suspected infection

Severe sepsis = Sepsis + Organ dysfunction



Septic shock = Presence of sepsis with hypotension despite fluid resuscitation + Presence of tissue perfusion abnormalities



Mortality rates as high as 50%Primary causative organisms

Gram-negative and gram-positive bacteriaEndotoxin stimulates inflammatory response

Pathophysiology of Septic Shock

Fig. 67-5




Clinical manifestations

↑ Coagulation and inflammation

↓ FibrinolysisFormation of microthrombiObstruction of microvasculature

Hyperdynamic state: Increased CO and decreased SVR



Clinical manifestationsTachypnea/hyperventilationTemperature dysregulation↓ Urine outputAltered neurologic statusGI dysfunctionRespiratory failure is common


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


Stages of Shock Compensatory Stage

Clinically apparent NeuralHormonalBiochemical compensatory mechanisms

Attempts are aimed at overcoming consequences of anaerobic metabolism and maintaining homeostasis

Compensatory Stage of Shock

Fig. 67-6




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



Impaired GI motilityRisk for paralytic ileus

Cool, clammy skin from bloodExcept septic patient who is warm and flushed



Shunting blood from lungs increases physiologic dead space

↓ Arterial O2 levelsIncrease in rate/depth of respirations

V/Q mismatchSNS stimulation increases myocardium O2

demands



If perfusion deficit corrected, patient recovers with no residual sequelae

If deficit not corrected, patient enters progressive stage


Stages of Shock Progressive Stage

Begins when compensatory mechanisms fail

Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS)

Progressive Stage of Shock

Fig. 67-7




Hallmarks of ↓ cellular perfusion and altered capillary permeability:

Leakage of protein into interstitial space

↑ Systemic interstitial edema



Anasarca Fluid leakage affects solid organs and peripheral tissues

↓ Blood flow to pulmonary capillaries



Movement of fluid from pulmonary vasculature to interstitium

Pulmonary edemaBronchoconstriction↓ Residual capacity



Fluid moves into alveoliEdemaDecreased surfactantWorsening V/Q mismatchTachypneaCracklesIncreased work of breathing



CO begins to fallDecreased peripheral perfusionHypotensionWeak peripheral pulsesIschemia of distal extremities



Myocardial dysfunction results inDysrhythmias IschemiaMyocardial infarctionEnd result: Complete deterioration of cardiovascular system



Mucosal barrier of GI system becomes ischemic

Ulcers BleedingRisk of translocation of bacteriaDecreased ability to absorb nutrients



Liver fails to metabolize drugs and wastesJaundice Elevated enzymesLoss of immune functionRisk for DIC and significant bleeding



Acute tubular necrosis/acute renal failure


Stages of Shock Refractory Stage

Exacerbation of anaerobic metabolismAccumulation of lactic acid↑ Capillary permeability

Refractory Stage of Shock

Fig. 67-8




Profound hypotension and hypoxemiaTachycardia worsensDecreased coronary blood flowCerebral ischemia



Failure of one organ system affects others

Recovery unlikely


Diagnostic StudiesThorough history and physical

examinationNo single study to determine shock

Blood studies Elevation of lactateBase deficit

12-lead ECGChest x-rayHemodynamic monitoring


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


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


Collaborative CareGeneral management strategies

Ensure patent airwayMaximize oxygen delivery


Collaborative CareCornerstone of therapy for septic,

hypovolemic, and anaphylactic shock = volume expansion Isotonic crystalloids (e.g., normal saline) for

initial resuscitation of shock


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


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


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


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


Collaborative CareCardiogenic Shock

Restore blood flow to the myocardium by restoring the balance between O2 supply and demand

Thrombolytic therapyAngioplasty with stentingEmergency revascularizationValve replacement


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)


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)


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



Intravenous corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP



Antibiotics after obtaining cultures (e.g., blood, wound exudate, urine, stool, sputum)

Drotrecogin alfa (Xigris)Major side effect: Bleeding



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


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


Collaborative CareAnaphylactic Shock

Epinephrine, diphenhydramine Maintaining a patent airway

Nebulized bronchodilators Endotracheal intubation or cricothyroidotomy may be necessary


Collaborative CareAnaphylactic Shock

Aggressive fluid replacement Intravenous corticosteroids if significant

hypotension persists after 1 to 2 hours of aggressive therapy


Nursing Assessment

ABCs: Airway, breathing, and circulation


Nursing Assessment

Focused assessment of tissue perfusionVital signsPeripheral pulsesLevel of consciousnessCapillary refillSkin (e.g., temperature, color, moisture)Urine output


Nursing AssessmentBrief history

Events leading to shockOnset and duration of symptoms

Details of care received before hospitalization AllergiesVaccinations


Nursing DiagnosesIneffective tissue perfusion: Renal, cerebral,

cardiopulmonary, gastrointestinal, hepatic, and peripheral

Fear Potential complication: Organ

ischemia/dysfunction


PlanningGoals for patient

Assurance of adequate tissue perfusionRestoration of normal or baseline BPReturn/recovery of organ functionAvoidance of complications from prolonged

states of hypoperfusion


Nursing ImplementationHealth Promotion

Identify patients at risk (e.g., elderly patients, those with debilitating illnesses or who are immunocompromised, surgical or accidental trauma patients)


Nursing ImplementationHealth Promotion

Planning to prevent shock (e.g., monitoring fluid balance to prevent hypovolemic shock, maintenance of handwashing to prevent spread of infection)


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


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


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


Nursing ImplementationRespiratory status

Respiratory rate and rhythmBreath soundsContinuous pulse oximetry Arterial blood gases Most patients will be intubated and

mechanically ventilated


Nursing ImplementationUrine outputTympanic or pulmonary arterial temperature Skin: Temperature, pallor, flushing, cyanosis,

diaphoresis, piloerection Bowel sounds


Nursing Implementation Nasogastric drainage/stools for occult bloodI&O, fluid and electrolyte balanceOral care/hygiene based on O2 requirementsPassive/active range of motion


Nursing ImplementationAssess level of anxiety and fear

Medication PRNTalk to patientVisit from clergyFamily involvementComfort measuresPrivacyCall light within reach


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

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Shock