focus on shock

Focus on Shock

(Relates to Chapter 67, “Nursing Management: Shock and Multiple Organ Dysfunction Syndrome,” in the textbook)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

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Shock


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Shock

Classification of shock

Cardiogenic HypovolemicDistributiveObstructive


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Low Blood FlowCardiogenic Shock Definition:

Systolic or diastolic dysfunction Compromised cardiac output (CO)

Precipitating causes: MI Cardiomyopathy Blunt cardiac injury Severe systemic or pulmonary hypertension Cardiac Tamponade Myocardial depression from metabolic

problems Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Pathophysiology of Cardiogenic Shock

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 5

Fig. 67-1. Relationship of shock, systemic inflammatory response syndrome, and multiple

organ dysfunction syndrome. CNS, Central nervous system.

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Low Blood FlowCardiogenic Shock

Early manifestations TachycardiaHypotensionNarrowed pulse pressure ↑ myocardial O2 consumption


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Low Blood FlowCardiogenic Shock

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

↑ in pulmonary artery wedge pressure Decreased renal perfusion and UO


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Low Blood FlowHypovolemic Shock

Absolute hypovolemia: Loss of intravascular fluid volume

HemorrhageGI loss (e.g., vomiting, diarrhea) Fistula drainageDiabetes insipidusHyperglycemiaDiuresis


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Relative hypovolemia 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. The pathophysiology of hypovolemic shock.

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Body response to acute volume loss depends on :

Extent of injury or insultAgeGeneral state of health


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Distributive ShockNeurogenic 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


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Can occur in response to spinal anesthesia Results in massive vasodilation,

leading to pooling of blood in vessels


Pathophysiology of Neurogenic Shock


Fig. 67-4. The pathophysiology of neurogenic shock. BP, Blood pressure.

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Clinical manifestations HypotensionBradycardia Temperature dysregulation (resulting

in heat loss)Dry skin Poikilothermia (taking on the

temperature of the environment)


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Distributive ShockAnaphylactic Shock

Acute, life-threatening hypersensitivity reactionMassive vasodilationRelease of mediators ↑ capillary permeability


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Clinical manifestationsAnxiety, confusion, dizziness Sense of impending doom Chest pain Incontinence


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Clinical manifestations Swelling of the lips and tongue,

angioedemaWheezing, stridor Flushing, pruritus, urticariaRespiratory distress and circulatory

failure


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Distributive ShockSeptic Shock

Sepsis: systemic inflammatory response to documented or suspected infection

Severe sepsis = Sepsis + Organ dysfunction


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Septic shock = Presence of sepsis with hypotension

despite fluid resuscitation Presence of tissue perfusion

abnormalities


Pathophysiology of Septic Shock


Fig. 67-5. The pathophysiology of septic shock. CNS, Central nervous system.

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Clinical manifestations ↑ coagulation and inflammation ↓ fibrinolysis

Formation of microthrombi Obstruction of microvasculature

Hyperdynamic state: increased CO and decreased SVR


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Clinical manifestations (cont’d) Tachypnea/hyperventilation Temperature dysregulation ↓ urine outputAltered neurologic statusGI dysfunctionRespiratory failure is common.


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Obstructive Shock

Develops when physical obstruction to blood flow occurs with decreased CO From restriction to diastolic filling of

the right ventricle due to compressionAbdominal compartment syndrome


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Obstructive Shock

Patient will experienceDecreased CO Increased afterloadVariable left ventricular filling

pressures

Rapid assessment and immediate treatment are important.


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Stages of Shock1. Initial Stage

Usually not clinically apparentMetabolism changes from aerobic to

anaerobic. Lactic acid accumulates and must be

removed by blood and broken down by liver.

Process requires unavailable O2.


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Stages of Shock2. Compensatory Stage

Clinically apparent NeuralHormonalBiochemical compensatory

mechanisms

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


Compensatory Stage of Shock


Fig. 67-7. Compensatory stage: reversible stage during which compensatory mechanisms are

effective and homeostasis is maintained.

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Baroreceptors in carotid and aortic bodies activate SNS in response to ↓BP.Vasoconstriction while blood to vital

organs maintained

↓ blood to kidneys activates renin–angiotensin system ↑ venous return to heart, CO, BP


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Impaired GI motilityRisk for paralytic ileus

Cool, clammy skin from blood Except septic patient who is warm and

flushed


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Shunting blood from lungs increases physiologic dead space.

↓ arterial O2 levels Increase in rate/depth of respirations V/Q mismatch

SNS stimulation increases myocardial O2 demands.


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If perfusion deficit corrected, patient recovers with no residual sequelae

If deficit not corrected, patient enters progressive stage


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Stages of Shock3. Progressive Stage

Begins when compensatory mechanisms fail

Aggressive interventions to prevent multiple organ dysfunction syndrome


Progressive Stage of Shock


Fig. 67-8. Progressive stage: compensatory mechanisms are becoming ineffective and

fail to maintain perfusion to vital organs.

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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


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Movement of fluid from pulmonary vasculature to interstitium

Pulmonary edema Bronchoconstriction ↓ residual capacity


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Fluid moves into alveoli Edema Decreased surfactant Worsening V/Q mismatch Tachypnea Crackles Increased work of breathing


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CO begins to fall Decreased peripheral perfusion Hypotension Weak peripheral pulses Ischemia of distal extremities


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Myocardial dysfunction results in Dysrhythmias Ischemia Myocardial infarction End result: complete deterioration of

cardiovascular system


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Mucosal barrier of GI system becomes ischemic

Ulcers Bleeding Risk of translocation of bacteria Decreased ability to absorb nutrients


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Liver fails to metabolize drugs and waste.

Jaundice Elevated enzymes Loss of immune function Risk for DIC and significant bleeding


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Stages of Shock4. Irreversible Stage

Exacerbation of anaerobic metabolism Accumulation of lactic acid ↑ capillary permeability


Irreversible Stage of Shock


Fig. 67-9. Irreversible or refractory stage: compensatory mechanisms are not functioning or are

totally ineffective, leading to multiple organ dysfunction syndrome.

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Stages of Shock4. Irreversible Stage

Profound hypotension and hypoxemia Tachycardia worsens. Failure of one organ system affects

others. Recovery unlikely


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Diagnostic Studies

Thorough history and physical examination No single study to determine shock

Blood studies Elevation of lactate Base deficit

12-lead ECG Chest x-rayHemodynamic monitoring


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Collaborative Care

Identify patients at risk Integration of the patient’s history, physical

examination, and clinical findings to establish a diagnosis

Interventions to control or eliminate the cause of decreased perfusion

Protection of target and distal organs from dysfunction

Provision of multisystem supportive care


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Collaborative Care

General strategies Ensure patent airway.Maximize oxygen delivery.

Cornerstone 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 Care

Volume expansion If the patient does not respond to 2 to

3 L of crystalloids, then blood administration and central venous monitoring may be instituted.

Complications of fluid resuscitation Hypothermia

Coagulopathy


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Collaborative Care

Primary goal of drug therapy = Correction of decreased tissue perfusion Vasopressor drugs (e.g., norepinephrine)

Achieve/maintain MAP >60 to 65 mm Hg. Reserved for patients unresponsive to fluid

resuscitation

Vasodilator therapy (e.g., nitroglycerin, nitroprusside) Achieve/maintain MAP >65 mm Hg.


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Collaborative Care

Nutrition: vital to decreasing morbidity

from shock.

Initiate enteral nutrition within the first 24 hours.

Initiate parenteral nutrition if enteral feedings contraindicated or fail to meet at least 80% of 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 O2supply & demand.

Thrombolytic therapy Angioplasty with stenting Emergency revascularization Valve replacement


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Collaborative CareCardiogenic Shock

Hemodynamic monitoring Drug therapy (e.g., diuretics to

reduce preload) Circulatory assist devices (e.g.,

intraaortic balloon pump, ventricular assist device)


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Collaborative CareHypovolemic Shock

Management focuses on stoppingthe 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 CareSeptic Shock

Fluid replacement to restore perfusion Hemodynamic monitoring

Vasopressor drug therapy

Vasopressin for patients refractory to vasopressor therapy

IV corticosteroids if failed vasopressor therapy & fluid resuscitation, to maintain adequate BP


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Collaborative Care Septic Shock

Antibiotics after cultures are obtained (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/dL Stress 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 CareNeurogenic Shock

In spinal cord injury: spinal stability

Tx hypotension and bradycardia with vasopressors and atropine

Fluids cautiouslyMonitor for hypothermia.


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Collaborative CareAnaphylactic Shock

Epinephrine, diphenhydramine Maintaining a patent airway

Nebulized bronchodilators Endotracheal intubation or

cricothyroidotomy may be necessary Aggressive fluid replacement Intravenous corticosteroids if significant

hypotension persists after 1 to 2 hours of aggressive therapy

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Collaborative CareObstructive Shock

Early recognition and treatment is primary strategy.Mechanical decompression Radiation or removal of mass Decompressive laparotomy


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Nursing Assessment

ABCs: airway, breathing, and circulation

Focused assessment of tissue perfusion Vital signs Peripheral pulses Level of consciousness Capillary refill Skin (e.g., temperature, color, moisture) Urine output


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Nursing Assessment

Brief history Events leading to shockOnset and duration of symptoms

Details of care received before hospitalization Allergies Vaccinations


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Nursing Diagnoses

Ineffective tissue perfusion: renal, cerebral, cardiopulmonary, gastrointestinal, hepatic, and peripheral Fear Potential complication: organ

ischemia/dysfunction


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Planning

Goals for patientAssurance 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 Implementation

Health promotion Identify patients at risk.

Elderly patients Those with debilitating illness Those who are immunocompromised Surgical or accidental trauma patients


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Health promotion (cont’d)

Planning to prevent shock Monitoring fluid balance to prevent

hypovolemic shock Maintenance of hand washing to prevent

spread of infection


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Neurologic status: orientation and level of consciousness Cardiac status

Continuous ECG VS, capillary refillHemodynamic parameters: central

venous pressure, PA pressures, CO, PAWP

Heart sounds: murmurs, S3, S4


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Respiratory status Respiratory rate and rhythmBreath sounds Continuous pulse oximetry Arterial blood gases Most patients will be intubated and

mechanically ventilated.


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Urine output Tympanic or pulmonary arterial

temperature Skin: temperature, pallor, flushing,

cyanosis, diaphoresis, piloerection Bowel sounds


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Nasogastric drainage/stools for occult blood I&O, fluid and electrolyte balance Oral care/hygiene based on O2

requirements Passive/active range of motion


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Assess level of anxiety and fear.Medication PRN Talk to patientVisit from clergy Family involvement Comfort measures Privacy Call light within reach


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Evaluation

Normal or baseline, ECG, BP, CVP, and PAWP Normal temperatureWarm, dry skin Urinary output >0.5 mL/kg/hr Normal RR and SaO2 ≥90% Verbalization of fears, anxiety


focus on shock

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