NLE Emergency & Critical Care Nursing — Shock, Sepsis & Multi-Organ DysfunctionRevision Notes

Formulas

Exam tips

• NLE questions often test whether you know that a NORMAL blood pressure does NOT rule out shock — the key clue is rising RR and narrowing pulse pressure in early shock.
• When a question mentions elevated lactate with clinical deterioration, think sepsis or shock regardless of BP.
• MAP ≥ 65 mmHg and urine output ≥ 0.5 mL/kg/hr are the two most tested perfusion targets — memorize both.

Key points

• Shock = inadequate tissue perfusion where oxygen delivery (DO2) fails to meet oxygen consumption (VO2) at the cellular level.
• The fundamental result is anaerobic metabolism, producing lactic acid and leading to metabolic acidosis.
• Shock is a SYNDROME, not a single disease — many different causes converge on the same final pathway of failing perfusion.
• Serum lactate is the biochemical marker of anaerobic metabolism; elevated lactate (>2 mmol/L) signals impaired tissue oxygenation.
• The goal of all shock management is to restore adequate oxygen delivery to tissues before irreversible cellular death occurs.
• Three determinants of cardiac output (CO) are affected in shock: preload, afterload, and contractility — different classes of shock affect these differently.
• MAP (Mean Arterial Pressure) = (SBP + 2×DBP) / 3; target MAP ≥ 65 mmHg to maintain organ perfusion.
• Urine output is a bedside marker of renal perfusion; target ≥ 0.5 mL/kg/hr.

Definitions

Common mistakes

• Confusing blood pressure with perfusion — a normal BP does NOT rule out shock in the compensatory stage.
• Forgetting that lactate, not blood pressure, is the earliest biochemical marker of shock.
• Thinking 'shock = hypotension' — hypotension is a LATE sign that appears only in the progressive stage.
• Calculating MAP incorrectly — remember the formula uses 2×DBP because diastole lasts twice as long as systole.

Exam tips

• When the NLE gives you a patient with hypotension AND bradycardia AND a history of spinal cord injury, the answer is neurogenic shock.
• When the question mentions a patient who was stung by a bee or received penicillin and now has bronchospasm and hypotension, think anaphylaxis — give epinephrine FIRST.
• When the question says 'JVD + hypotension + muffled heart sounds' after a chest trauma, think cardiac tamponade (obstructive shock) — pericardiocentesis is the treatment.
• In NLE scenarios, if both hypovolemic and cardiogenic shock appear, look for CRACKLES and NECK VEIN DISTENSION to identify cardiogenic.
• The warm, flushed skin early in distributive shock is a classic NLE trick — it is the opposite of what you expect in shock.

Key points

• MEMORIZE the 4 classes: Hypovolemic, Cardiogenic, Distributive (Septic/Neurogenic/Anaphylactic), and Obstructive.
• CLASS determines TREATMENT — the wrong fluid or drug for the wrong class can be fatal.
• HYPOVOLEMIC: Low preload → Low CO → Treat with FLUIDS/BLOOD and control the source of loss.
• CARDIOGENIC: Pump failure → Low CO despite normal/high filling pressures → Treat with INOTROPES (dobutamine); do NOT fluid-overload.
• DISTRIBUTIVE: Loss of vascular tone → Blood pools in dilated vessels → Early sign is WARM FLUSHED SKIN ('warm shock').
• SEPTIC SHOCK: Most common and most lethal distributive shock — vasodilation + capillary leak from overwhelming infection.
• NEUROGENIC SHOCK: Classic triad = HYPOTENSION + BRADYCARDIA + WARM DRY SKIN — the ONLY shock with bradycardia.
• ANAPHYLACTIC SHOCK: IgE-mediated massive histamine release → vasodilation + capillary leak + BRONCHOSPASM → Priority drug: EPINEPHRINE 0.3–0.5 mg IM (1:1000).
• OBSTRUCTIVE SHOCK: Mechanical block to blood flow (tension pneumothorax, cardiac tamponade, massive PE) → Needs MECHANICAL RELIEF, not just drugs or fluids.
• In hypovolemic shock: neck veins are FLAT (low CVP); in cardiogenic shock: neck veins are DISTENDED (high CVP) — this distinction is tested frequently.
• Cardiogenic shock produces CRACKLES (pulmonary congestion); hypovolemic shock does NOT.
• For tension pneumothorax: needle decompression (2nd intercostal space, midclavicular line), then chest tube.
• For cardiac tamponade (Beck's Triad: hypotension, JVD, muffled heart sounds): pericardiocentesis.
• For massive PE: thrombolysis or embolectomy.

Definitions

Common mistakes

• Giving large amounts of IV fluids to a cardiogenic shock patient — this worsens pulmonary edema and can cause death.
• Giving antihistamines (diphenhydramine) FIRST in anaphylaxis — epinephrine is ALWAYS the priority drug.
• Forgetting that neurogenic shock has BRADYCARDIA — every other shock type causes tachycardia.
• Thinking tension pneumothorax needs only medication — it requires immediate needle decompression.
• Mixing up the position for neck veins: flat/collapsed = hypovolemic; distended/full = cardiogenic or obstructive.

Formulas

Exam tips

• NLE questions on stages of shock often present a patient with normal BP but tachycardia, restlessness, and cool skin — this is COMPENSATORY stage, not 'no shock.'
• If the scenario shows a patient with a slightly rising RR and narrowing pulse pressure but 'stable' BP, the NLE expects you to recognize early shock and act.
• Remember: in the initial stage, the ONLY abnormality is a rising serum lactate — no clinical signs yet.

Key points

• All shock progresses through 4 predictable stages: Initial → Compensatory → Progressive → Refractory.
• STAGE 1 (INITIAL): Cellular shift to anaerobic metabolism; NO visible clinical signs yet — changes are BIOCHEMICAL only (rising lactate).
• STAGE 2 (COMPENSATORY): The body activates protective reflexes; BP may still be NORMAL — this is the most treatable stage.
• Compensatory mechanisms: SNS activation (tachycardia, vasoconstriction), RAAS activation (oliguria, sodium and water retention), increased respiratory rate.
• EARLY WARNING SIGNS in compensatory stage: rising respiratory rate, narrowing pulse pressure, mild anxiety or restlessness, cool clammy skin, decreased urine output.
• STAGE 3 (PROGRESSIVE): Compensation FAILS — BP falls, frank tissue ischemia, worsening acidosis, decreasing mentation, organ failure begins.
• STAGE 4 (REFRACTORY/IRREVERSIBLE): Cellular and organ damage is so severe that no therapy can reverse it — death follows despite maximal support.
• KEY TEACHING: Shock is MOST TREATABLE in the COMPENSATORY STAGE, BEFORE blood pressure falls.
• Waiting for hypotension to intervene means you are already in the PROGRESSIVE stage — the window is closing.
• A narrowing pulse pressure (difference between SBP and DBP getting smaller) is one of the earliest hemodynamic warnings of compensatory shock.
• Pulse pressure narrows in compensatory shock because DBP rises (vasoconstriction) while SBP is maintained or slightly drops.

Definitions

Common mistakes

• Assuming a normal blood pressure means the patient is NOT in shock — in the compensatory stage, BP is maintained by tachycardia and vasoconstriction.
• Missing the early warning signs: rising RR, mild restlessness, slightly decreased urine output, cool skin — these precede hypotension.
• Treating the progressive stage as early shock and underestimating urgency of intervention.
• Forgetting that the refractory stage is irreversible — the clinical goal is ALWAYS to intervene before this stage.

Exam tips

• In NLE questions, if the scenario says 'blood cultures and antibiotics' — the correct nursing action is blood cultures FIRST, then antibiotics immediately after.
• qSOFA is the BEDSIDE tool; SOFA is the full scoring system requiring labs. NLE bedside scenarios use qSOFA.
• When a septic shock patient remains hypotensive after 30 mL/kg fluids, the next step is vasopressors (norepinephrine) — NOT more fluids indefinitely.
• SIRS criteria: remember the fever OR hypothermia — both are included; hypothermia is often missed.
• Lactate ≥ 4 mmol/L = trigger for 30 mL/kg fluid bolus even if BP is 'normal' (cryptic shock).

Key points

• Sepsis sits on a CONTINUUM: SIRS → Sepsis → Septic Shock → MODS.
• SIRS (Systemic Inflammatory Response Syndrome): ≥ 2 of: Temp > 38°C or < 36°C; HR > 90/min; RR > 20/min; WBC > 12,000 or < 4,000 or > 10% bands.
• SIRS can be triggered by BOTH infectious AND non-infectious causes (trauma, pancreatitis, burns).
• SEPSIS: Life-threatening organ dysfunction caused by a DYSREGULATED host response to INFECTION.
• Bedside screening for sepsis: qSOFA score — 1 point each for: RR ≥ 22/min, altered mentation, SBP ≤ 100 mmHg. Score ≥ 2 = high risk for sepsis.
• SEPTIC SHOCK: Sepsis + vasopressors needed to maintain MAP ≥ 65 mmHg + serum lactate > 2 mmol/L despite adequate fluid resuscitation.
• Septic shock mortality is HIGH — early recognition and bundle compliance are the key nursing interventions.
• The HOUR-1 BUNDLE (Surviving Sepsis Campaign) is the standard of care in managing sepsis.
• BUNDLE SEQUENCE: (1) Measure lactate → (2) Blood cultures BEFORE antibiotics → (3) Broad-spectrum antibiotics ASAP → (4) 30 mL/kg IV crystalloid for hypotension or lactate ≥ 4 mmol/L → (5) Vasopressors if MAP < 65 despite fluids.
• NOREPINEPHRINE is the FIRST-LINE vasopressor in septic shock.
• Blood cultures MUST be drawn BEFORE starting antibiotics — cultures drawn after antibiotics are far less useful for identifying the organism.
• However, antibiotics must NOT be delayed waiting for diagnostic results — each hour of antibiotic delay increases mortality.
• Common sources of sepsis in Philippine settings: pneumonia, urinary tract infection, abdominal source (peritonitis), wounds.
• Lactate remeasurement after initial resuscitation guides adequacy of resuscitation — lactate clearance is a treatment goal.
• A lactate ≥ 4 mmol/L indicates tissue hypoperfusion even without overt hypotension (cryptic shock).

Definitions

Common mistakes

• Drawing blood cultures AFTER starting antibiotics — this is the most common clinical and NLE-tested error in sepsis management.
• Waiting too long to start antibiotics while chasing laboratory results — antibiotics must be given early even if blood cultures have not resulted.
• Confusing SIRS criteria with qSOFA — SIRS has 4 criteria including WBC; qSOFA has only 3 clinical criteria and no labs.
• Using dopamine instead of norepinephrine as the first vasopressor in septic shock — norepinephrine is first-line.
• Giving the sepsis fluid bolus to a patient with cardiogenic shock — always assess for signs of fluid overload before resuscitation.

Exam tips

• When an NLE question mentions a sepsis patient who now has low urine output, rising creatinine, AND worsening oxygenation — think MODS (≥ 2 organs failing).
• ARDS is the most commonly tested organ complication in MODS — recognize it as refractory hypoxemia with bilateral infiltrates on CXR.
• NLE questions on MODS priorities often test Maslow's hierarchy: airway and oxygenation (physiologic needs) are ALWAYS the top priority — address respiratory failure first.
• Lung-protective ventilation (low tidal volumes) is the standard for ARDS — a common NLE critical care question.

Key points

• MODS = Progressive, potentially reversible dysfunction of TWO OR MORE organ systems following severe shock, sepsis, or systemic inflammation.
• The trigger is UNCONTROLLED SYSTEMIC INFLAMMATION and MICROVASCULAR INJURY — microthrombi and inflammatory mediators destroy organ function.
• ORGANS FAIL IN SEQUENCE (typical order): Lungs first (ARDS) → Kidneys (AKI) → Liver → Coagulation system (DIC) → GI tract → Heart.
• ARDS (Acute Respiratory Distress Syndrome): lungs are the 'sentinel organ' in MODS — refractory hypoxemia despite high FiO2 is the hallmark.
• AKI in MODS: rising creatinine, rising BUN, falling urine output (oliguria/anuria).
• Mortality CLIMBS STEEPLY with EACH additional failing organ — 2 organs: ~40–50%; 3 organs: ~70–80%; 4+ organs: >90%.
• There is NO SPECIFIC CURE for MODS — management is aggressive SUPPORT of each failing organ system.
• The 3 pillars of MODS management: (1) Treat/eliminate the underlying source, (2) Support each failing organ, (3) Prevent further insults (infections, hypoxia, hypoperfusion).
• PREVENTION is the most effective strategy — treat shock and sepsis EARLY and WELL before MODS develops.
• NANDA Nursing Diagnoses relevant to MODS: Impaired Gas Exchange, Decreased Cardiac Output, Risk for Infection, Impaired Urinary Elimination, Imbalanced Nutrition.
• ICU nursing care in MODS includes: mechanical ventilation management (lung-protective ventilation), renal replacement therapy monitoring, strict I&O, nutritional support (enteral nutrition preferred over parenteral), infection control.

Definitions

Common mistakes

• Thinking MODS has a specific treatment protocol like the sepsis bundle — MODS has NO specific cure, only organ support and source elimination.
• Forgetting that the LUNGS fail first in MODS (ARDS) — not the kidneys or heart.
• Underestimating how quickly mortality escalates with each additional organ failure.
• Neglecting enteral nutrition — early enteral feeding preserves gut mucosal integrity and prevents gut bacterial translocation, which can worsen MODS.

Exam tips

• NLE questions on DIC always test the PARADOX: simultaneous clotting AND bleeding — the key concept is CONSUMPTION of clotting factors.
• The 4 DIC lab values to memorize: Prolonged PT/aPTT + Low platelets + Low fibrinogen + High D-dimer.
• When the NLE asks the PRIORITY TREATMENT for DIC: TREAT THE UNDERLYING CAUSE is always the correct priority answer.
• Obstetric DIC (abruptio placenta, amniotic fluid embolism) is commonly tested in NLE — recognize that delivery of the fetus/placenta removes the DIC trigger.
• The blood products for DIC: FFP = clotting factors; Cryoprecipitate = fibrinogen; Platelet concentrate = platelets — know which product replaces what.

Key points

• DIC is a PARADOXICAL disorder: SIMULTANEOUS widespread microvascular clotting AND diffuse systemic BLEEDING.
• DIC is ALWAYS SECONDARY to another condition — it is NEVER a primary diagnosis.
• Common triggers: SEPSIS (most common), major trauma, obstetric emergencies (amniotic fluid embolism, abruptio placenta, HELLP syndrome), malignancy, massive blood transfusion.
• PATHOPHYSIOLOGY: Trigger activates coagulation cascade → microthrombi form throughout circulation → platelets and clotting factors get CONSUMED → diffuse bleeding occurs because the clotting system is depleted.
• CLINICAL FINDINGS: Bleeding from IV sites, mucous membranes, surgical wounds, petechiae, purpura AND signs of organ ischemia from microthrombi.
• LAB FINDINGS (all 4 must be memorized):
• → PROLONGED PT and aPTT (clotting factors consumed)
• → LOW platelets (thrombocytopenia — consumed in clot formation)
• → LOW fibrinogen (consumed in clot formation)
• → ELEVATED D-dimer and fibrin degradation products (FDPs) (evidence of clot breakdown).
• CORNERSTONE OF TREATMENT: CORRECT THE UNDERLYING CAUSE (e.g., treat the sepsis, deliver the baby, manage the tumor).
• SUPPORTIVE TREATMENT: Fresh Frozen Plasma (FFP) to replace clotting factors; Cryoprecipitate to replace fibrinogen; Platelet transfusion for severe thrombocytopenia.
• ANTICOAGULATION (heparin) is reserved for thrombosis-predominant DIC — used cautiously.
• Nursing priority: Monitor for bleeding from ALL sites (IV sites, nasogastric tube, urine, stool, skin); minimize invasive procedures; apply pressure to all puncture sites.
• NANDA Nursing Diagnosis: Risk for Bleeding; Impaired Tissue Perfusion; Risk for Injury.

Definitions

Common mistakes

• Thinking DIC is a primary disease — it is ALWAYS secondary; you must identify and treat the trigger.
• Mixing up the DIC lab pattern: confusing which values are HIGH vs. LOW — D-dimer is HIGH; platelets and fibrinogen are LOW; PT/aPTT are PROLONGED.
• Giving heparin routinely to all DIC patients — anticoagulation is only for thrombosis-predominant DIC and is used cautiously.
• Forgetting to monitor all possible bleeding sites including IV insertion sites, urine (hematuria), and stool (melena) — DIC causes bleeding EVERYWHERE.
• Treating only the bleeding without addressing the underlying cause — the bleeding will continue until the trigger is corrected.

Exam tips

• NLE always tests PRIORITY nursing action — in shock, the sequence is: AIRWAY first, then BREATHING, then CIRCULATION.
• When asked about positioning in cardiogenic shock with pulmonary congestion, the answer is UPRIGHT (semi-Fowler's), not legs elevated.
• When asked about vasopressor administration, remember CENTRAL LINE for vasopressors — this is a safety principle tested in NLE.
• Maslow's hierarchy in NLE: physiologic needs (airway, breathing, circulation) ALWAYS rank above psychological or safety needs in acute shock scenarios.
• NANDA diagnosis 'Decreased Cardiac Output' is the primary nursing diagnosis for cardiogenic shock — be able to match diagnoses to shock classes.

Key points

• NURSING PROCESS in shock follows the ABC framework with Maslow's hierarchy: Airway → Breathing → Circulation → Safety → then higher needs.
• AIRWAY AND OXYGENATION: Ensure patent airway; apply high-flow O2 (10–15 L/min via non-rebreather mask); prepare for intubation in progressive/refractory shock.
• CIRCULATION: Establish large-bore IV access (at least 2 large-bore peripheral IVs or central venous access); rapid fluid administration as appropriate.
• POSITIONING: Most shock → supine with legs elevated 20–30° (modified Trendelenburg) to enhance venous return. EXCEPTION: Cardiogenic shock or pulmonary edema → Semi-Fowler's or upright position to ease breathing.
• MONITORING: Continuous hemodynamic monitoring — BP, HR, RR, SpO2, urine output (hourly, via Foley catheter), skin color and temperature, mentation.
• PERFUSION TARGETS: MAP ≥ 65 mmHg; Urine output ≥ 0.5 mL/kg/hr; Lactate trending down; improving mentation.
• VASOPRESSORS: Administered via CENTRAL VENOUS ACCESS — peripheral infiltration causes tissue necrosis. Norepinephrine is first-line for septic shock.
• MATCH TREATMENT TO CLASS: Fluids for hypovolemia; Inotropes for cardiogenic; Epinephrine + fluids + antihistamine for anaphylaxis; Fluids + vasopressors + antibiotics for septic; Mechanical relief for obstructive; Atropine/vasopressors + fluids for neurogenic.
• NANDA Nursing Diagnoses in Shock: Decreased Cardiac Output; Ineffective Tissue Perfusion; Deficient Fluid Volume (hypovolemic); Excess Fluid Volume risk (cardiogenic); Impaired Gas Exchange; Anxiety; Risk for Infection (septic).
• Under RA 9173, the nurse collaborates with the physician team but independently monitors vital signs, executes orders, and reports deterioration promptly.
• DOCUMENTATION: Accurate and timely documentation of all interventions and patient responses is both a legal duty under RA 9173 and a clinical necessity in shock management.
• KEEP THE PATIENT WARM: Hypothermia worsens acidosis, coagulopathy, and cardiac arrhythmias — use warm blankets or warmed IV fluids.
• FAMILY EDUCATION: Early recognition of warning signs of infection and dehydration; importance of antibiotic completion; prompt care-seeking in Philippine community and barangay health centers.

Definitions

Common mistakes

• Using the Trendelenburg (head-down) position — current evidence does NOT support classic Trendelenburg; modified Trendelenburg (legs elevated, body flat) is the accepted position.
• Administering vasopressors via peripheral IV — always use central venous access for vasopressors to prevent extravasation injury.
• Failing to insert a Foley catheter for hourly urine monitoring — urine output is the most accessible bedside perfusion indicator.
• Delaying oxygen administration while trying to determine shock class — O2 is a UNIVERSAL first step in all shock types.
• Not keeping the patient warm — hypothermia worsens all aspects of shock physiology (acidosis, coagulopathy, arrhythmias).