NLE Emergency & Critical Care Nursing — Common Medical EmergenciesCheat Sheet

Common values

Important facts

• Universal signs of respiratory failure: ↑ RR, ↑ work of breathing, use of accessory muscles, restlessness/anxiety (early hypoxia), cyanosis, ↓ O2 sat, ↓ consciousness
• PRIORITY positioning: High Fowler's (upright) to maximize lung expansion and reduce work of breathing
• Acute asthma attack mainstays: short-acting beta-2 agonists (salbutamol/albuterol), anticholinergics (ipratropium), systemic corticosteroids
• Continuous reassessment of O2 sat, work of breathing, mental status guides escalation to non-invasive ventilation or intubation
• Accessory muscle use = escalating severity; prepare for intubation if patient tires
• Stridor (barking cough) = upper airway obstruction; drooling/inability to swallow = impending airway loss

Key definitions

Diagrams to know

• Respiratory distress progression: normal → tachypnea → accessory muscle use → silent chest → arrest
• Flow pattern in asthma: normal → wheezing → silent chest (obstruction too severe to move air)

Common values

Important facts

• Classic ACS: crushing substernal chest pain ± radiation to arm/jaw, diaphoresis, nausea, SOB
• 12-lead ECG within 10 minutes — mandatory; ECG changes guide diagnosis (ST elevation, ST depression, T-wave inversion, new LBBB)
• Troponin I or T elevation confirms myocardial injury; becomes detectable 3–4 hours post-infarction
• MONA components: Morphine (if pain unrelieved by nitrates), Oxygen (only if O2 sat <90%), Nitroglycerin (SL, repeat q5min), Aspirin (160–325 mg, chewed)
• CONTRAINDICATIONS to nitroglycerin: hypotension (SBP <90), RVI, PDE-5 inhibitor use (sildenafil, tadalafil) in past 24–48 hours
• Reperfusion therapy: ST elevation on ECG = urgent PCI (preferred) or fibrinolytic (if PCI unavailable); door-to-balloon <90 min, door-to-thrombolytic <30 min
• Continuous cardiac monitoring, IV access, serial troponins, and risk stratification essential
• Post-MI complications: arrhythmia, cardiogenic shock, pulmonary edema, mechanical rupture, VSD, free wall rupture

Key definitions

Diagrams to know

• Coronary artery anatomy: RCA (inferior wall, RV, AV node), LAD (anterior, septum, apex), LCx (lateral, posterior, SA node)
• ECG lead relationships to coronary territory: II/III/aVF (inferior/RCA), V1–V4 (anterior/LAD), V5–V6/I/aVL (lateral/LCx)

Common values

Important facts

• Classic triad of acute pulmonary edema: severe dyspnea + crackles + pink frothy sputum (or clear if mild)
• Associated signs: tachycardia, tachypnea, anxiety, diaphoresis, hypotension (cardiogenic shock) or hypertension
• PRIORITY nursing concept: 'Sit them up, dry them out, open them up'
• Position: HIGH FOWLER'S (upright) with legs dependent to reduce venous return and optimize ventilation
• Oxygen/NIPPV (CPAP/BiPAP): to improve oxygenation and reduce work of breathing
• IV loop diuretic (furosemide): mainstay of fluid offloading; onset 5–10 min IV; monitor urine output closely
• Vasodilators (nitroglycerin): reduce preload (venous dilation) and afterload (arterial dilation), improving cardiac output
• Monitor: O2 sat, BP, HR, breath sounds, urine output, weight, signs of cardiogenic shock
• Afterload reduction critical: IABP, inotropes if hypotensive; low BP limits diuretic and vasodilator use

Key definitions

Diagrams to know

• Pathophysiology chain: LV dysfunction → ↑ LV end-diastolic pressure → ↑ pulmonary venous pressure → pulmonary edema
• Treatment priorities: position → oxygen/NIPPV → diuretics → vasodilators → monitor response

Common values

Important facts

• SINGLE priority intervention: IM epinephrine FIRST — do NOT delay for adjuncts (antihistamines, steroids)
• Epinephrine dose for anaphylaxis: 0.3–0.5 mg IM of 1:1000 (0.3–0.5 mL), into anterolateral thigh (vastus lateralis)
• Repeat epinephrine every 5–15 minutes if no response (hypotension, continued dyspnea, stridor)
• CRITICAL DISTINCTION: Anaphylaxis ≠ cardiac arrest dosing — NOT 1 mg IV of 1:10,000 (that is for ACLS); confusing these is a dangerous error
• Adjuncts (secondary, never instead of epinephrine): high-flow O2, aggressive IV fluids for hypotension, antihistamines (diphenhydramine), corticosteroids
• Position: hypotensive patient supine with legs elevated; dyspneic patient more upright
• Airway management: anticipate rapid airway swelling; have equipment at bedside; intubate early if stridor or oropharyngeal swelling
• Watch for biphasic reaction — observe for ≥4–24 hours (some protocols); repeat epinephrine if symptoms recur
• Common triggers in Philippines: antibiotics (penicillins, cephalosporins), NSAIDs, contrast dye, foods (shellfish, peanuts), insect venom, latex
• Prevention: obtain detailed allergy history, use hypoallergenic gloves, have epinephrine auto-injector available for at-risk patients

Key definitions

Diagrams to know

• Anaphylaxis cascade: allergen exposure → IgE-mast cell crosslink → degranulation → histamine/tryptase/heparin/kinins/leukotrienes → systemic vasodilation, bronchoconstriction, angioedema
• ABCDE assessment in anaphylaxis: Airway (stridor, edema), Breathing (wheezing, dyspnea), Circulation (hypotension, shock), Disability (syncope, confusion), Exposure (rash, urticaria)

Common values

Important facts

• KEY PRINCIPLE: lower BP gradually, NOT abruptly — rapid drops cause ischemic stroke, MI, or acute kidney injury from reduced perfusion
• Target: reduce Mean Arterial Pressure (MAP) by approximately ≤25% in the first hour (exception: aortic dissection, which needs faster control)
• MAP calculation: MAP = (SBP + 2×DBP) / 3; example: if SBP 200, DBP 120, MAP = (200 + 240)/3 = 147 mmHg
• First-line IV agents: labetalol (combined alpha/beta blocker), nicardipine (calcium channel blocker), sodium nitroprusside (direct vasodilator, requires ICU monitoring)
• Withhold or avoid: sudden nitroprusside boluses, immediate-release nifedipine (unpredictable drop), IV hydralazine monotherapy (causes reflex tachycardia)
• Hypertensive urgency: oral therapy (e.g., amlodipine, ACE inhibitor, diuretic) over hours, close follow-up
• Hypertensive emergency: admit to ICU, continuous IV infusion + arterial line BP monitoring, frequent neuro checks
• Monitor end-organs: check urine (proteinuria, RBCs), creatinine (acute renal injury), troponin (ACS), neurologic status q15–30 min
• Common causes: medication non-adherence, NSAID use, cocaine, sympathomimetics, renal disease, preeclampsia
• Aortic dissection special case: target SBP <120 and HR <60 (use labetalol then nitroprusside or nicardipine)

Key definitions

Diagrams to know

• Autoregulation curve: cerebral blood flow maintained at MAP 50–150 mmHg; outside this range, ischemia (low) or edema (high) occurs
• Hypertensive crisis decision tree: SBP >180/DBP >120 → assess for target-organ damage (neuro, cardiac, renal, pulmonary) → urgency vs emergency → oral vs IV therapy

Reactions or equations

Common values

Important facts

• Red flags: severe pain, rigid (board-like) abdomen, rebound tenderness, guarding, distension, hypotension, fever, elevated WBC
• PRIORITY nursing actions: keep NPO (nothing by mouth) for possible surgery, establish IV access, give IV fluids, assess pain continuously, prepare for diagnostics (CT, US, labs)
• CRITICAL — DO NOT apply heat, give laxatives/enemas, or use aggressive massage — these can rupture inflamed organs (e.g., appendix) and cause peritonitis
• Insert nasogastric tube if ordered for decompression in bowel obstruction; monitor NG output (character, volume)
• Avoid opioid analgesia only per protocol (some institutions allow judicious analgesia AFTER surgical evaluation) — do not mask the clinical picture inappropriately
• Bowel obstruction signs: severe crampy pain, vomiting, abdominal distension, high-pitched bowel sounds (early) or silent (late), visible peristaltic waves
• Ruptured AAA presentation: sudden severe abdominal/back pain, hypotension, pulsatile abdominal mass, shock — mortality high; requires immediate vascular surgery
• Ectopic pregnancy rupture: young woman with amenorrhea, sudden severe lower abdominal pain, shoulder pain, hemodynamic instability, ↓ Hgb
• Appendicitis: RLQ pain (often begins periumbilical then localizes), nausea, fever; McBurney's point tenderness, rebound > direct tenderness (McBurney's is more painful)
• Monitor vital signs closely; shock (hypotension, tachycardia, altered mental status) indicates need for emergency surgery

Key definitions

Diagrams to know

• Acute abdomen assessment: pain character/location → peritoneal signs (rebound, guarding, rigidity) → organ-specific signs → imaging/labs → surgical consult
• Bowel obstruction chain: mechanical block → proximal bowel dilation → vomiting → dehydration → shock → perforation/peritonitis

Common values

Important facts

• Hypoglycemia is MORE immediately dangerous than hyperglycemia — brain dies within minutes of severe glucose deficit
• Rapid onset distinguishes hypoglycemia from DKA/HHS (which are gradual, hours to days)
• Early signs: adrenergic (tremor, diaphoresis, palpitations, anxiety, hunger) — patient usually still alert and able to communicate
• Late signs: neuroglycopenic (confusion, slurred speech, altered behavior, seizures, coma) — patient at risk of injury
• CRITICAL: NEVER give oral carbohydrate to unconscious or unalert patient — aspiration risk is fatal; use IV dextrose or IM glucagon
• Conscious patient protocol (Rule of 15): 15 g fast-acting carbs (glucose tablets, juice, hard candy, honey) → wait 15 min → recheck → repeat if <70 → then complex carb (bread, crackers, protein)
• Unconscious/unable-to-swallow protocol: IV dextrose 25 g (50 mL of D50) or IM glucagon 1 mg (onset 5–15 min, lasts 60–90 min); follow with oral carbs when alert
• Glucagon is less effective in depleted glycogen stores (starvation, ethanol abuse); if no response to first dose, use IV dextrose
• After hypoglycemia episode: review cause (missed meal, overdose, excessive exercise), adjust diet or insulin dose, educate on prevention
• Patient should carry glucose source at all times; wear medical alert identification; teach family to recognize and treat hypoglycemia

Key definitions

Diagrams to know

• Hypoglycemia symptom progression: normal → adrenergic (tremor, sweat) → neuroglycopenic (confusion) → seizure → coma → death
• Hypoglycemia treatment algorithm: conscious & alert → Rule of 15 (oral carbs) vs unconscious/altered → IV dextrose or IM glucagon

Common values

Important facts

• DKA onset is GRADUAL (hours to days) — distinguishes it from rapid-onset hypoglycemia
• Classic DKA triad: hyperglycemia (BG >250 mg/dL, often 300–600), metabolic acidosis (pH <7.3, HCO3 <15), positive serum and urine ketones
• Classic presentation: polydipsia, polyuria, nausea, abdominal pain, Kussmaul respirations, fruity/acetone breath odor, altered consciousness
• Total-body potassium is DEPLETED in DKA despite normal serum K+ — insulin shifts K+ into cells, causing dangerous hypokalemia as treatment begins
• PRIORITY management sequence: (1) FLUIDS FIRST — aggressive IV normal saline to correct severe volume deficit (often 5–10 L); (2) INSULIN — IV regular insulin infusion (not bolus) to shut off ketogenesis; (3) POTASSIUM — monitor K+ closely, replace if <5.5 mEq/L before starting insulin, then add to IV fluids once insulin is infusing
• DO NOT start insulin if serum K+ is severely low (<3.0 mEq/L) — will cause cardiac arrhythmias; replace K+ first
• Add dextrose (D5 or D10) to IV fluids once glucose falls to 200–250 mg/dL to prevent hypoglycemia while acidosis resolves
• Insulin dose: 0.05–0.1 units/kg/hr IV infusion; titrate to lower BG by 50–75 mg/dL/hr (not faster)
• Monitor: BG q1h, VBG/ABG for pH/HCO3, electrolytes (especially K+) q2–4h initially, urine output, mental status, signs of cerebral edema
• Cerebral edema risk: young patients, severe acidosis, rapid correction — manifests as altered consciousness, seizures; mortality >50% if occurs
• Precipitants: missed insulin, infection (UTI, pneumonia), MI, new-onset diabetes, stress; always investigate cause
• HHS management identical to DKA (fluids → insulin → K+) but mortality higher due to severe dehydration and older age; slower glucose correction needed

Key definitions

Diagrams to know

• DKA pathophysiology: insulin deficiency → gluconeogenesis, lipolysis → ↑ BG, ↑ ketones → metabolic acidosis → Kussmaul respirations → osmotic diuresis → severe dehydration → shock
• DKA management flowchart: fluids → lab assessment (BG, K+, HCO3, pH) → start insulin (after K+ >3.0) → add dextrose when BG 200–250 → monitor q1–2h → resolution when pH >7.3, HCO3 >15, patient eating