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MedSurg I Shock

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olanjones's version from 2017-04-01 16:30

General Information

Question Answer
Definition Syndrome characterized by decreased tissue perfusion & impaired cellular metabolism
Caused by low blood flowCardiogenic; Hypovolemic
Caused by maldistribution of bloodSeptic; Anaphylactic; Neurogenic
Common ManisAnxiety/confusion/agitation - hypoperfusion!
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Low Blood Flow

Question Answer
Cardiogenic Shock Structural problemsSystolic dysfunction (ineffective forward movement of blood --> ↓SV &↓CO); Diastolic dysfunction (ineffective filling --> ↑pulmonary pressure --> pulmonary edema --> ↓Oxygenation)
Causes of systolic dysfunctionMI, Cardiomyopathy (also diastolic), Blunt cardiac injury, Severe systemic/pulmonary HTN
Causes of diastolic dysfunctionCardiomyopathy (also systolic), Cardiac tamponade
Cardiogenic Manis (this +common)Tachycardia, Narrowed pulse pressure, Decreased cap refill time, Pallor (cool, clammy skin), ↑pulmonary artery wedge pressure, decreased renal perfusion & UO
Wedge Pressurepressure measured in pulmonary artery after occlusion of that artery; provides an indirect measure of the left atrial pressure
Tx Goal for CardiogenicRestore blood flow to the myocardium by restoring the balance between O2 supply and demand (↑coronary blood supply, pick drugs based on action, may need circulatory assist device)
Hypovolemic Shock - Two typesAbsolute hypovolemia (actual loss of fluid); Relative hypovolemia (3rd spacing)
Causes of Absolute HypovolemicHemorrhage, GI loss, Fistula drainage, Diabetes insipidus, Hyperglycemia, Diuresis
Causes of Relative HypovolemicSepsis, Burns, Bowel Obstruction
Hypovolemic - Effects based on volume loss percentage15% ok; 15-30% compensation by SNS (↓EF & PAWP d/t decreased volume - may use volume expanders), >30% physiologic compensation begins to fail (need blood/blood products)
Tx Goal for HypovolemicPrimary Goal is to stop the loss of fluid and restore 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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Maldistribution of Blood

Question Answer
Neurogenic EtiologySNS is “turned off”; Results in massive vasodilation without SNS response leading to massive pooling of blood in arterial and venous vessels
Neurogenic Causesspinal cord injury at the fifth thoracic (T5) vertebra or above (can occur within 30 minutes & last up to 6 weeks); Spinal anesthesia; Some drugs (opioids, benzodiazepines)
Neurogenic Manis (this +common)Hypotension, Bradycardia, Temp dysregulation, Dry Skin, Hypothermia (poikilothermia = taking on temp of environment)
Tx Goal for NeurogenicTreat hypotension & bradycardia w/ vasopressors (maintain BP) & atropine (bradycardia); Solumedrol for swelling --> prevent secondary damage to spinal cord; Monitor for hypothermia
*If spinal injury FIRST stabilize the spine
Anaphylactic Etiologyallergic response which results in massive vasodilation (same outcome as neurogenic) & capillary permeability
Anaphylactic Manis (this +common)Sudden anaphylactic rxn --> Respiratory distress --> laryngeal edema/bronchospasm --> circulatory failure
S/S of Anaphylactic RxnSense of impeding doom, Chest pain, Incontinence, Swelling of lips & tongue/angioedema, Wheezing/stridor, Flushing/pruritus/urticaria
Tx Goal for AnaphylacticControl histamine response: Epinephrine (vasoconstriction, bronchodilation & opposes histamine), Benadryl (blocks histamine), Maintain airway (risk for laryngeal edema/bronchoconstriction)
May need intravenous corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive therapy
Septic EtiologyStronger than usual immune response coupled with endotoxins from organisms stimulating additional immune response
Septic Patho* Normal immune response to damage but then --> vasodilation & increased capillary permeability third spaces fluid --> aggregations & fibrin occlude fluid movement = fluid loss
* ↑cytokines lead to myocardial depression
* Hypermetabolic state --> initial hyperventilation but then failure to compensate and respiratory acidosis occurs
Vascular damage immune responseDamaged epithelium, vasodilation, ↑capillary permeability, neutrophil & platelet aggregation/adhesion to epithelium
Septic Manis (this +common)Tachypnea/hyperventilation, temp dysregulation, ↓UO, GI dysfunction, Resp failure
Septic Shock Fun FactsMortality rate as high as 50%; Common organisms: gram - & + bacteria; Respiratory failure occurs in 85% of sepsis patients (ARDS accounts for 40%)
Tx Goal for SepticInitially --> *Aggressive fluid replacement to restore perfusion (6-10 L of isotonic crystalloids & 2-4 L of colloids)
*May need to add vasopressor drugs, corticosteroids to ↑BP and inotropic agent to ↑ contractility
*Antibiotics admin after cultures obtained; Monitor glucose levels (keep <150)
Obstructive ShockOccurs when blood flow is restricted by decreased CO (Restricted diastolic filling = Tamponade, Pneumothorax, abdominal compartment syndrome; Outflow obstruction = RV thrombi, PE) Result is JVD & Pulsus paradoxus
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Stages of Shock (Remember - They are on a Continuum)

Question Answer
Initial Stage* Cellular metabolism changes from aerobic to anaerobic; Lactic acid accumulates requires unavailable O2 for removal = ↓ perfusion (not usually clinically apparent)
* Mean Arterial Pressure used to determine adequate perfusion (>60 organs are usually adequately perfused, below that may indicate ischemia)
Compensatory Stage: Body attempts to overcome consequences of anaerobic metabolism & tries to maintain homeostasis via SNS response, ADH release, RAAS activation
: Metabolic acidosis indicates compensatory --> progressive stage
S/S Compensatory Stage↓BP & ↓CO - 1st clinical signs
Progressive Stage* Proteins leak into interstitial space --> ↑ Systemic interstitial edema, May have anasarca (solid organs & peripheral tissue)
* VQ perfusion ratio worsens from restricted blood flow, ↑ capillary permeability moves fluid into alveoli
* Aggressive interventions needed to prevent MODS
S/S Progressive Stagetachypnea, crackles; Changes in LOC; Weak, thready pulses & peripheral ischemia, ↑ likelihood of dysrhythmias, ischemia, & MI; Renal failure; GI ischemia; ↑ liver dysfunction
Irreversible StageExacerbation of anaerobic metabolism & Accumulation of lactic acid, ↑ Capillary permeability, Profound hypotension and hypoxemia, Tachycardia worsens, Decreased coronary blood flow, Cerebral ischemia --> Organ failure
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Diagnosis and Treatment

Question Answer
There is no single study to determine shock, you must get ___ ___The Story! Thorough H&P, events leading up to condition
Blood studies may demonstrate↑lactate (byproduct of anaerobic metabolism); ↓base (bicarb depletion from compensation of acidosis)
12-lead ECG may demonstrateunderlying arrhythmia or MI
Chest X-ray may demonstratepulmonary edema
Hemodynamic monitoring (PAWP) may demonstrateArterial hypotension (SBP <90 mm Hg, MAP <70 mm Hg, or ↓SBP >40 mm Hg)
Goal for managementIdentify patients at risk (using H&P, clinical findings), Interventions to control/eliminate cause of decreased perfusion, Protect organs from dysfunction (MAP >60 to 65 mmHg), Provide multi-system supportive care
Oxygen & ventilationENSURE AIRWAY!, Increase supply (use hemodynamic monitor to adjust), Decrease demand (tx depends on cause) by grouping activities
Fluid resuscitation*Use isotonic crystalloids (NS) solution - Cornerstone of therapy for septic, hypovolemic, & anaphylactic shock is volume expansion (not neurogenic or cardiogenic)
*Monitor patient (if no response to 2-3L may need blood and central venous monitoring)
*If large amounts of fluid are needed may need to warm to avoid hypothermia
Drug TherapyVasodilators used to break the cycle of vasoconstriction (nitroglycerin for cardiogenic, nitroprusside for noncardiogenic); Vasopressor drugs (vasoconstrict periphery but ↑SVR so used as last resort)
Nutrition TherapyInitiate enteral nutrition within the first 24 hours (enhances GI tract perfusion); Initiate parenteral nutrition if enteral feedings contraindicated or fail to meet at least 80% of the caloric requirements
Physical AssessmentABCs, Focused assessment of tissue perfusion (VS, peripheral pulses, LOC, cap refill, Skin, UO)
Obtain HistoryEvents leading to shock, Onset & duration of symptoms, Details of care prior to hospitalization, Allergies, Vaccinations
Shock NDIneffective tissue perfusion: Renal, cerebral, cardiopulmonary, gastrointestinal, hepatic, and peripheral; Fear; Potential complication: Organ ischemia/dysfunction
Shock NI-Monitor Neurologic status: Orientation and level of consciousness
-Cardiac status: Continuous ECG, VS, cap refill, Hemodynamic parameters, Heart sounds (murmurs, S3, S4)
-Respiratory status: Rate & rhythm, breath sounds, continuous pulse ox, ABGs (most patient's will be intubated)
-Urine output & Bowel sounds
-Tympanic or pulmonary arterial temperature; Skin: (temp, pallor/flushing/cyanosis, diaphoresis, piloerection)
Important for the nurse to*Monitor the patient’s ongoing physical and emotional status to detect subtle changes in the patient’s condition
*Plan & implement nursing interventions and therapy
*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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