NLE Emergency & Critical Care Nursing — Shock, Sepsis & Multi-Organ DysfunctionCheat Sheet

Common Values

Section Title

Definition & Core Concept of Shock

Important Facts

• Shock is a SYNDROME, not a diagnosis — many different insults lead to the same final pathway of failing perfusion.
• Shock is MOST treatable in the compensatory stage, BEFORE blood pressure falls.
• A 'normal' or even 'high-normal' blood pressure can be falsely reassuring — compensatory mechanisms maintain BP until they fail.
• Rising respiratory rate and narrowing pulse pressure (difference between systolic and diastolic) are among the earliest reliable warnings of shock.
• Each shock class has a specific, class-appropriate treatment; what saves one class can be fatal in another.
• Untreated or late-treated shock leads to multi-organ dysfunction syndrome (MODS), refractory shock, and death.
• The window for successful intervention narrows at each stage of shock progression.

Key Definitions

Diagrams To Know

• Progression from adequate perfusion → initial stage → compensatory stage → progressive stage → refractory stage.
• Cell-level shift from aerobic (ATP-efficient) to anaerobic (lactate-producing) metabolism.

Common Values

Section Title

The Four Classes of Shock

Important Facts

• HYPOVOLEMIC SHOCK: Hallmarks are tachycardia, hypotension, cool clammy skin, FLAT neck veins, LOW CVP, and oliguria. TREAT WITH FLUIDS and blood products.
• CARDIOGENIC SHOCK: Hallmarks are hypotension, tachycardia, CRACKLES in lungs, JUGULAR VENOUS DISTENSION, cool skin, and ELEVATED CVP/wedge pressure. TREAT with inotropes (dobutamine), cautious diuresis or vasodilators; aggressive fluid loading can DROWN the patient.
• DISTRIBUTIVE SHOCK (all subtypes): Often WARM and FLUSHED early ('warm shock') because of vasodilation. This contrasts sharply with hypovolemic and cardiogenic shock.
• NEUROGENIC SHOCK: The ONLY shock with BRADYCARDIA (plus hypotension and warm dry skin) — every other shock is tachycardic. This is the cardinal distinguishing feature.
• ANAPHYLACTIC SHOCK: Priority drug is EPINEPHRINE 0.3 to 0.5 mg IM (1:1000 concentration). Do NOT use IV unless in a code situation with close monitoring.
• OBSTRUCTIVE SHOCK: Mechanical relief is MANDATORY — needle decompression and chest tube for tension pneumothorax, pericardiocentesis for tamponade, thrombolysis or embolectomy for massive PE. Fluids and drugs alone WILL NOT fix it.
• Flat neck veins in hypovolemic shock indicate inadequate preload; distended neck veins in cardiogenic shock indicate backup of blood into the pulmonary circulation.
• Cool, clammy skin in hypovolemic and cardiogenic shock reflects peripheral vasoconstriction from sympathetic activation; warm skin in distributive shock reflects vasodilation and loss of tone.
• CVP (central venous pressure) is LOW in hypovolemic shock (poor preload) but HIGH in cardiogenic shock (heart cannot eject the volume it receives).

Key Definitions

Diagrams To Know

• Cardiac output (CO) = Heart Rate (HR) × Stroke Volume (SV); in hypovolemic shock, SV is reduced so CO falls; in cardiogenic shock, the pump cannot contract forcefully despite adequate preload.
• Systemic Vascular Resistance (SVR) — HIGH in hypovolemic and cardiogenic shock (sympathetic compensation); LOW in distributive shock (vasodilation).
• Preload vs. Afterload vs. Contractility — the three determinants of cardiac output; understanding which is abnormal guides therapy.

Common Values

Section Title

Stages of Shock Progression

Important Facts

• COMPENSATORY STAGE is when shock is MOST TREATABLE — BEFORE blood pressure falls.
• Rising respiratory rate (>20/min) is one of the earliest reliable warnings of shock compensating for metabolic acidosis.
• Narrowing pulse pressure (difference between systolic and diastolic) indicates vasoconstriction and is an early sign.
• A 'normal' blood pressure in the compensatory stage is DECEPTIVE; the patient is already in shock but compensation is masking it.
• Waiting for hypotension to confirm shock means intervening in the PROGRESSIVE STAGE — too late for many patients.
• Mentation deteriorates in the progressive stage because cerebral perfusion pressure falls and the brain becomes ischemic.
• Oliguria (urine output <0.5 mL/kg/hr) in the compensatory stage is a sign that the kidneys are already hypoperfused.
• Skin becomes mottled and gray in the progressive stage as peripheral vasoconstriction worsens and microvascular stasis occurs.
• Lactic acidosis worsens progressively through stages 1–3 because anaerobic metabolism persists and lactate clearance by the liver is impaired.

Key Definitions

Diagrams To Know

• Timeline from initial stage (biochemical changes only) → compensatory (vital sign changes) → progressive (BP falls, organ dysfunction) → refractory (no response to therapy).
• Sympathetic cascade: low perfusion → baroreceptor reflex → sympathetic outflow → catecholamine release → tachycardia, vasoconstriction, increased RR.

Common Values

Section Title

SIRS, Sepsis, Septic Shock, and Sepsis Bundle

Important Facts

• SIRS criteria: Temp >38°C or <36°C, HR >90, RR >20, WBC >12,000 or <4,000. Two or more = SIRS. NOT specific to infection.
• qSOFA: RR ≥22 (not just >20), ALTERED MENTATION (confusion, disorientation), SBP ≤100 mmHg. Score ≥2 predicts high mortality risk.
• Sepsis ≠ infection; sepsis is the ORGAN DYSFUNCTION caused by dysregulated response TO infection.
• Septic shock is the most LETHAL and MOST COMMON type of distributive shock.
• HOUR-1 BUNDLE (Sepsis Bundle core elements, ideally within 60 minutes):
• 1. Measure serum lactate AND remeasure if initially elevated.
• 2. Obtain BLOOD CULTURES BEFORE starting antibiotics — cultures drawn after antibiotics are far less useful.
• 3. Administer BROAD-SPECTRUM ANTIBIOTICS early; each hour of delay increases mortality.
• 4. Begin RAPID CRYSTALLOID FLUID resuscitation (typically 30 mL/kg) for hypotension or lactate ≥4 mmol/L.
• 5. Start VASOPRESSORS if hypotension persists during or after fluid resuscitation to maintain MAP ≥65 mmHg.
• NOREPINEPHRINE is the FIRST-LINE vasopressor in septic shock.
• Time is tissue in sepsis — the survival benefit of the bundle depends entirely on SPEED of implementation.
• Septic shock mortality is HIGH even with optimal treatment; early recognition and aggressive intervention are critical.
• Source control (draining an abscess, removing infected catheter, etc.) is as important as antibiotics and fluids.
• Lactate >2 mmol/L in the setting of infection and hypotension defines septic shock and indicates microvascular dysfunction and anaerobic metabolism.
• Persistent lactate elevation despite 30 mL/kg fluids is an indicator for vasopressor therapy.

Key Definitions

Diagrams To Know

• Sepsis progression: infection → dysregulated host response → SIRS criteria → organ dysfunction → sepsis → septic shock (if vasopressors needed).
• Hour-1 Bundle sequence: lactate measurement → blood cultures → antibiotics + fluids → vasopressors (if needed).
• Pathophysiology: bacterial endotoxin (LPS) → TLR4 activation → cytokine storm → vasodilation, capillary leak, microvascular dysfunction → shock.

Common Values

Section Title

Multi-Organ Dysfunction Syndrome (MODS) and DIC

Important Facts

• MODS develops in sequence: LUNGS first (ARDS) → KIDNEYS (AKI) → LIVER → COAGULATION → GUT → HEART.
• Mortality climbs STEEPLY with each additional failing organ — 1 organ ~15%, 2 organs ~60%, 3+ organs >80%.
• There is NO specific cure for MODS; management is aggressive SUPPORT of each failing system, eradication of the SOURCE, and prevention of further injury.
• PREVENTION of MODS by treating shock and sepsis EARLY and WELL is far more effective than treating established MODS.
• DIC is ALWAYS secondary to another condition — sepsis (most common), major trauma, obstetric emergencies (placental abruption, amniotic fluid embolism), or malignancy.
• DIC laboratory findings: PROLONGED PT and aPTT (factor consumption), LOW platelets, LOW fibrinogen, ELEVATED D-dimer and fibrin degradation products (FDP).
• Clinical signs of DIC: bleeding from IV sites, mucous membranes, surgical wounds (diffuse bleeding) PLUS signs of thrombosis (ischemic digits, skin necrosis).
• CORNERSTONE of DIC treatment: Correct the underlying cause (treat sepsis, stop hemorrhage, deliver placenta, etc.).
• Supportive care in DIC: replace consumed components with FFP (fresh frozen plasma), cryoprecipitate (fibrinogen), and platelets.
• Anticoagulation in DIC is CONTROVERSIAL and reserved for thrombotic-predominant cases (not routine); the primary goal is source control.
• Organ-specific support in MODS: mechanical ventilation for ARDS, dialysis for AKI, vasopressors and inotropes for circulatory failure, glucose control, and stress ulcer prophylaxis.
• The gut becomes a source of further infection in MODS when barrier function fails — called 'bacterial translocation'; this perpetuates inflammation and organ failure.

Key Definitions

Diagrams To Know

• MODS organ failure sequence and timeline: shock → SIRS → ARDS (day 1–2) → AKI (day 2–3) → hepatic/coagulation failure (day 3–5) → refractory shock and death.
• DIC paradox: simultaneous activation of coagulation (forming microthrombi and consuming factors) and fibrinolysis (degrading clots and bleeding).
• Pathophysiology cascade: shock/sepsis → endothelial injury → capillary leak → microvascular stasis → ischemia-reperfusion injury → MODS.

Common Values

Section Title

Nursing Management & Priority Interventions Across All Shock

Important Facts

• POSITION most shock patients SUPINE with LEGS ELEVATED to promote venous return — EXCEPT cardiogenic with pulmonary congestion (keep more UPRIGHT to ease breathing).
• OXYGENATE and prepare for ventilatory support — target SpO₂ >94%, use non-rebreather mask, intubate if needed.
• RESTORE VOLUME with rapid crystalloids via LARGE-BORE IV access (18-gauge or central line) — EXCEPT cardiogenic shock (fluid given cautiously).
• Use LACTATED RINGER'S or NORMAL SALINE; LR is preferred in trauma (contains potassium, calcium, more physiologic) but NS is acceptable.
• TITRATE VASOACTIVE DRUGS to MAP ≥65 mmHg; norepinephrine is FIRST-LINE in septic shock.
• MONITOR hourly: urine output (target ≥0.5 mL/kg/hr), lactate trend (should fall with successful resuscitation), mental status, skin perfusion, and hemodynamic numbers (BP, HR, CVP if available).
• MATCH THERAPY TO THE CLASS: fluids + source control for hypovolemic; inotropes (dobutamine, milrinone) + reduce load for cardiogenic; fluids + vasopressors + antibiotics for septic; epinephrine for anaphylactic; mechanical relief for obstructive.
• Cool, clammy skin improves with successful resuscitation (vasoconstriction eases); persistent cool skin despite therapy suggests inadequate perfusion.
• Rising lactate despite fluids and vasopressors indicates ongoing tissue hypoxia and is a sign of treatment failure or disease progression.
• Reassess the patient FREQUENTLY — shock evolves rapidly and therapy must be adjusted continuously based on response.
• Prepare for ICU admission, invasive monitoring (arterial line, central line, Swan-Ganz catheter if available), and potential mechanical ventilation.
• Communicate with the team — the nurse is often the first to notice deterioration and must escalate care promptly.
• In the Philippines, many rural hospitals lack advanced monitoring (central lines, arterial lines); use clinical assessment (skin, mental status, urine output) as your primary guide.

Key Definitions

Diagrams To Know

• Shock recognition and initial nursing steps: Check airway → Ensure oxygenation → Establish IV access → Obtain labs (lactate, cultures if sepsis) → Position appropriately → Monitor continuously.
• Class-specific treatment flowchart: Assess shock class (vital signs, skin, CVP if available) → Match to hypovolemic/cardiogenic/distributive/obstructive → Implement class-appropriate therapy.

Common Values

Section Title

Specific Drug Therapy & Monitoring Parameters

Important Facts

• ANAPHYLACTIC SHOCK: Epinephrine 0.3–0.5 mg IM (1:1000 concentration) is the PRIORITY drug — do NOT delay for IV access. Give IM into the vastus lateralis or deltoid, can repeat every 5–15 min if needed.
• If anaphylaxis occurs in a patient already on beta-blockers, epinephrine may be less effective; higher doses or IV epinephrine may be needed (risky — use in code setting with close monitoring).
• SEPTIC SHOCK: Norepinephrine (4–12 mcg/min, titrate to MAP ≥65) is FIRST-LINE; some sources recommend adding dobutamine if lactate remains elevated despite norepinephrine + fluids (but this is debated).
• CARDIOGENIC SHOCK: Dobutamine (2.5–10 mcg/kg/min) to improve contractility OR milrinone (phosphodiesterase inhibitor) for inodilation (improves contractility AND reduces afterload). Avoid norepinephrine (too much peripheral vasoconstriction).
• HYPOVOLEMIC SHOCK: Crystalloids (LR or NS) FIRST, blood products (PRBCs, FFP, platelets) per damage control resuscitation protocols if hemorrhage.
• In hypovolemic shock, give fluids RAPIDLY — do NOT restrict fluids to 'prevent overload.' The patient is already hypovolemic; the risk is underfilling, not overfilling.
• In cardiogenic shock with pulmonary edema, restrict fluids and use vasodilators (nitroprusside, nicardipine) or diuretics carefully to reduce preload and afterload.
• MONITORING: Every shock requires continuous pulse oximetry, cardiac monitor, and frequent vital signs; insert Foley catheter to quantify urine output hourly; consider central line for CVP if available.
• LACTATE CLEARANCE: If initial lactate is elevated, recheck at 3–6 hours; failure to clear lactate despite fluids and vasopressors indicates poor prognosis.
• BLOOD CULTURES before antibiotics in sepsis — delay of minutes is acceptable if cultures are obtained cleanly. Contaminated cultures lead to unnecessary broad-spectrum coverage.
• In the Philippines, broad-spectrum choices depend on local resistance patterns; amoxicillin-clavulanate or cephalosporins for community-acquired; imipenem or fluoroquinolones for nosocomial until cultures return.

Key Definitions

Diagrams To Know

• Vasoactive drug selection by shock class and mechanism: hypovolemic (crystalloids) → cardiogenic (dobutamine or milrinone, reduce afterload) → septic (fluids, norepinephrine) → anaphylactic (epinephrine IM).
• Monitoring cascade: vital signs every 5–15 min → lactate at 0 and 3–6 hours → urine output hourly → hemodynamics (BP, HR, CVP) continuously.

Section Title

NLE High-Yield Facts & Exam Patterns

Important Facts

• Shock = INADEQUATE TISSUE PERFUSION; it is the FINAL COMMON PATHWAY of many different insults.
• Four shock classes: HYPOVOLEMIC (low volume), CARDIOGENIC (bad pump), DISTRIBUTIVE (lost tone), OBSTRUCTIVE (mechanical block).
• Hypovolemic → FLAT neck veins, LOW CVP. Cardiogenic → DISTENDED neck veins, HIGH CVP, CRACKLES. DO NOT confuse them — treatment is opposite.
• NEUROGENIC shock is BRADYCARDIC (unlike all others); classic triad is hypotension, BRADYCARDIA, and warm dry skin. High cervical spine injury.
• ANAPHYLACTIC shock requires EPINEPHRINE 0.3–0.5 mg IM (1:1000) as FIRST-LINE; antihistamines and steroids are supportive only.
• OBSTRUCTIVE shock (tension pneumothorax, tamponade, massive PE) requires MECHANICAL RELIEF (needle decompression, pericardiocentesis, thrombolysis), not just fluids/drugs.
• Shock is MOST TREATABLE in the COMPENSATORY STAGE (before BP falls); rising RR and narrowing pulse pressure are EARLY WARNINGS.
• SIRS = ≥2 criteria; SEPSIS = organ dysfunction; SEPTIC SHOCK = needs vasopressors for MAP ≥65 + lactate >2 despite fluids.
• qSOFA for sepsis: RR ≥22, ALTERED MENTATION, SBP ≤100 — score ≥2 is HIGH RISK.
• SEPSIS BUNDLE (Hour-1): measure lactate, draw BLOOD CULTURES BEFORE antibiotics, give BROAD-SPECTRUM ANTIBIOTICS EARLY, fluid bolus ~30 mL/kg, vasopressors if needed. SPEED MATTERS.
• NOREPINEPHRINE is FIRST-LINE vasopressor in septic shock.
• MODS = ≥2 organ failure; no cure, only support + source control. Lungs fail first (ARDS), kidneys second (AKI).
• DIC = simultaneous clotting (microthrombi) and bleeding (factor consumption); labs show prolonged PT/aPTT, low platelets, low fibrinogen, high D-dimer. Treat the underlying cause.
• Target MAP ≥65 mmHg, urine output ≥0.5 mL/kg/hr, lactate should FALL with successful resuscitation.
• Cool clammy skin in hypovolemic/cardiogenic; warm flushed skin in distributive.
• Common NLE trap: 'normal' BP in compensatory shock is FALSELY REASSURING — patient is already in shock.
• Permissive hypotension in hemorrhagic shock means tolerating SBP 80–90 mmHg until hemorrhage control to minimize fluid resuscitation and 'wash out clots.'
• In Philippines, sepsis from dengue, leptospirosis, or meningococcemia is common; always think about local pathogens and resistance patterns.

Diagrams To Know

• Shock classification decision tree: inadequate perfusion → assess vital signs, CVP, skin → classify (hypovolemic/cardiogenic/distributive/obstructive) → treat accordingly.
• Sepsis progression and timeline: infection → SIRS → organ dysfunction → sepsis → septic shock (if vasopressors needed) → MODS → death.

Item

SHOCK = inadequate tissue perfusion → cells shift to anaerobic metabolism → lactic acid accumulates → if untreated, organs fail and die. It is a SYNDROME from many different causes, not a diagnosis.

Number

1

Item

FOUR SHOCK CLASSES: (1) HYPOVOLEMIC = low volume → treat with fluids; (2) CARDIOGENIC = bad pump → treat with inotropes, NOT fluids; (3) DISTRIBUTIVE = lost tone (septic/neurogenic/anaphylactic) → treat class-specifically; (4) OBSTRUCTIVE = mechanical block → mechanical relief mandatory.

Number

2

Item

HYPOVOLEMIC SHOCK hallmarks: flat neck veins, LOW CVP, tachycardia, hypotension, cool clammy skin, oliguria. CARDIOGENIC hallmarks: DISTENDED neck veins, HIGH CVP, CRACKLES. DO NOT confuse — treatment is opposite (fluids vs. inotropes).

Number

3

Item

NEUROGENIC SHOCK = ONLY shock with BRADYCARDIA (plus hypotension and warm dry skin). Every other shock is tachycardic. This is the distinguishing feature. Causes: high spinal cord injury (T6 or above).

Number

4

Item

ANAPHYLACTIC SHOCK: Epinephrine 0.3–0.5 mg IM (1:1000 concentration) is FIRST-LINE — give immediately, do NOT delay for IV access. Can repeat every 5–15 minutes if needed. Antihistamines and steroids are supportive only.

Number

5

Item

SHOCK IS MOST TREATABLE IN THE COMPENSATORY STAGE, BEFORE BLOOD PRESSURE FALLS. A 'normal' or 'high-normal' BP with rising RR and narrowing pulse pressure = shock compensating. Waiting for hypotension means intervening too late.

Number

6

Item

SEPSIS BUNDLE (Hour-1): (1) Measure serum lactate; (2) Blood cultures BEFORE antibiotics; (3) Broad-spectrum antibiotics EARLY (each hour delay increases mortality); (4) Crystalloid bolus ~30 mL/kg for hypotension or lactate ≥4; (5) Vasopressors if hypotension persists. NOREPINEPHRINE is first-line.

Number

7

Item

SEPTIC SHOCK = sepsis + circulatory/metabolic failure requiring vasopressors for MAP ≥65 AND persistent lactate >2 despite adequate fluids. qSOFA (RR ≥22, altered mentation, SBP ≤100): score ≥2 = high risk. Mortality is high even with optimal treatment.

Number

8

Item

MODS = progressive dysfunction of ≥2 organ systems; sequence is lungs (ARDS) → kidneys (AKI) → liver → coagulation → gut → heart. Mortality climbs steeply with each failing organ. No cure — only support, source control, and prevention.

Number

9

Item

PERFUSION TARGETS: MAP ≥65 mmHg, urine output ≥0.5 mL/kg/hr, lactate should FALL with successful resuscitation. Cool clammy skin in hypovolemic/cardiogenic; warm flushed skin in distributive (early). Reassess frequently — shock evolves rapidly.

Number

10

Tip

NLE TRAP: A patient with a 'normal' systolic BP (110–120 mmHg) but rising heart rate, fast breathing, and cool skin IS IN SHOCK (compensatory stage). Do NOT be falsely reassured by a 'normal' BP. Look for the rising respiratory rate and narrowing pulse pressure — these are the real warning signs.

Tip Number

1

Tip

CARDIOGENIC vs. HYPOVOLEMIC in 10 seconds: Check NECK VEINS. Distended = cardiogenic (high preload, bad pump) → inotropes. Flat = hypovolemic (low preload) → fluids. If you see CRACKLES in lungs + distended neck veins + hypotension = cardiogenic shock, fluid bolus will KILL the patient.

Tip Number

2

Tip

ANAPHYLAXIS EMERGENCY: Do NOT wait for IV access — give epinephrine 0.3–0.5 mg IM (vastus lateralis or deltoid) FIRST. Then get IV access and prepare for second dose, antihistamines, steroids, and airway management. Speed of IM epi is life-saving.

Tip Number

3

Tip

SEPSIS BUNDLE SEQUENCE MATTERS: Blood cultures must come BEFORE antibiotics, but do NOT delay antibiotics chasing every test. If you can draw cultures in <15 minutes without delaying antibiotics, do it. If there will be a delay, start antibiotics first — the cultures are not worth the delay in antimicrobial therapy.

Tip Number

4

Tip

NLE QUESTION PATTERN: If a question asks 'What is the most likely diagnosis?' in a patient with fever, tachycardia, tachypnea, and altered mentation, think SEPSIS first. If you see 'vasopressors needed,' think SEPTIC SHOCK. The qSOFA score (RR ≥22, altered mentation, SBP ≤100) is the bedside tool — memorize it, it appears on exams.

Tip Number

5

Rows

Columns

• Class
• Cause
• CVP/Preload
• Skin
• Neck Veins
• Key Findings
• Treatment

Table Title

Four Shock Classes at a Glance

Rows

Columns

• Stage
• Cellular Changes
• Vital Signs
• Blood Pressure
• Urine Output
• Mental Status
• Skin
• Lactate
• Prognosis

Table Title

Stages of Shock: Clinical Progression

Rows

Columns

• Condition
• Criteria
• Trigger
• Organ Dysfunction
• Vasopressor Need
• Mortality

Table Title

SIRS vs. Sepsis vs. Septic Shock

Rows

Columns

• Parameter
• Cardiogenic Shock
• Hypovolemic Shock

Table Title

Cardiogenic vs. Hypovolemic Shock: Distinguishing Features