NLE Emergency & Critical Care Nursing — Common Medical EmergenciesRevision Notes

Exam Tips

• NLE favorite: 'A wheezing asthmatic suddenly becomes quiet' → your FIRST action is to reassess urgently and prepare for intubation, NOT to chart that the patient improved.
• First priority in any respiratory emergency: Airway → Breathing → Circulation (ABCs). Position upright FIRST, then O2.
• Salbutamol = bronchodilator (opens airways); ipratropium = anticholinergic (reduces secretions and bronchoconstriction); corticosteroids = anti-inflammatory (reduces mucosal edema long-term).
• NIPPV (BiPAP/CPAP) is a non-invasive bridge to prevent intubation — used in COPD exacerbation and pulmonary edema as well.
• For NLE: Distinguish the three pillars of asthma treatment — bronchodilator (salbutamol), anticholinergic (ipratropium), anti-inflammatory (corticosteroid).

Key Points

• Respiratory failure = inability to maintain adequate oxygenation (hypoxemia) or ventilation (hypercapnia). It is a final common pathway for asthma, COPD exacerbation, pulmonary edema, pneumonia, and pulmonary embolism.
• Universal signs: rising respiratory rate, use of accessory muscles, restlessness/anxiety (early hypoxia), then cyanosis, falling SpO2, and declining level of consciousness (late hypoxia).
• CRITICAL: A SILENT (QUIET) CHEST in a previously wheezing asthmatic is an OMINOUS sign — it means airflow is too poor to generate wheeze. This signals impending respiratory arrest, NOT improvement.
• Priority positioning: HIGH FOWLER'S (upright) to maximize lung expansion and reduce the work of breathing.
• Acute asthma priority drugs: (1) Inhaled short-acting beta-2 agonist — SALBUTAMOL (albuterol) via nebulizer or MDI; (2) Inhaled anticholinergic — IPRATROPIUM BROMIDE for severe attacks; (3) SYSTEMIC CORTICOSTEROIDS (e.g., hydrocortisone IV or prednisone PO) to reduce airway inflammation.
• Continuous reassessment: SpO2, work of breathing, mental status, and breath sounds after every nebulization.
• Escalation ladder: O2 therapy → nebulized bronchodilators → noninvasive positive-pressure ventilation (NIPPV/BiPAP) → endotracheal intubation.
• NANDA nursing diagnosis: Impaired Gas Exchange; Ineffective Airway Clearance; Ineffective Breathing Pattern.

Definitions

Section Title

Acute Respiratory Emergencies

Common Mistakes

• Mistaking a silent chest for improvement — this is a CRITICAL error. Absence of wheeze = worsening, not resolution.
• Positioning the dyspneic patient flat (supine) — always sit them upright (High Fowler's) first.
• Giving oxygen via low-flow nasal cannula to a severely hypoxic patient when high-flow O2 or NIPPV is needed.
• Forgetting to reassess the patient after each nebulization — continuous monitoring is essential.
• Delaying corticosteroids in a severe asthma attack — they take hours to work and must be given early.
• Confusing salbutamol (short-acting, for acute rescue) with salmeterol (long-acting, for maintenance — NOT for acute attacks).

Exam Tips

• The 12-lead ECG within 10 minutes is the single most testable priority action in ACS — do this FIRST among all diagnostics.
• Memorize the 3 nitroglycerin contraindications: hypotension, PDE-5 inhibitors, RV infarction. NLE loves to give one of these as a distractor.
• For pulmonary edema: remember 'sit them up, dry them out (furosemide), open them up (nitroglycerin).'
• Furosemide in pulmonary edema works by BOTH vasodilation (immediate, within minutes) AND diuresis (delayed, 15–30 min) — the vasodilatory effect provides faster relief.
• 'Time is muscle' applies to STEMI — for every 30 minutes of delay in reperfusion, mortality increases significantly.

Key Points

• ACUTE CORONARY SYNDROME (ACS) includes unstable angina, NSTEMI, and STEMI. All require immediate response.
• Classic presentation: crushing substernal chest pain, radiation to left arm or jaw, diaphoresis, nausea, shortness of breath. ATYPICAL presentations (women, elderly, diabetics): fatigue, epigastric pain, jaw pain only, dyspnea without pain.
• FIRST PRIORITY: Obtain a 12-LEAD ECG within 10 MINUTES of arrival. 'Time is muscle' — every minute of ischemia = more cardiomyocyte death.
• MONA mnemonic (given as indicated, not in rigid sequence): Morphine, Oxygen (only if SpO2 <94%), Nitroglycerin (SL), Aspirin (chewed 160–325 mg).
• NITROGLYCERIN CONTRAINDICATIONS (must memorize): (1) Hypotension (SBP <90 mmHg); (2) Patient took a PDE-5 inhibitor (sildenafil/Viagra, tadalafil) within 24–48 hours; (3) Right ventricular (inferior) infarction — these patients depend on preload.
• ASPIRIN: given CHEWED (not swallowed whole) for faster absorption and antiplatelet effect. Standard dose: 160–325 mg.
• For STEMI: reperfusion is the goal — either percutaneous coronary intervention (PCI, preferred if available within 90 min of arrival) or fibrinolytic therapy (within 30 min if PCI unavailable).
• ACUTE DECOMPENSATED HEART FAILURE (ADHF) / ACUTE PULMONARY EDEMA: Left ventricular failure causes pulmonary congestion. Signs: severe dyspnea, orthopnea, crackles throughout lung fields, pink frothy sputum, tachycardia, profuse diaphoresis.
• Pulmonary edema PRIORITY management: Sit UP (High Fowler's with legs DEPENDENT to reduce venous return) → High-flow O2 or NIPPV → IV Furosemide (loop diuretic) → IV/SL Nitroglycerin (vasodilator to reduce preload and afterload).
• NANDA nursing diagnoses: Decreased Cardiac Output; Acute Pain; Activity Intolerance; Excess Fluid Volume (pulmonary edema).

Definitions

Section Title

Acute Cardiac Emergencies

Common Mistakes

• Giving nitroglycerin to a hypotensive patient — this causes further vasodilation and can cause cardiovascular collapse.
• Giving nitroglycerin to a patient who took sildenafil — catastrophic hypotension can result.
• Forgetting to chew the aspirin — swallowing it whole delays absorption and antiplatelet effect.
• Positioning the pulmonary edema patient flat — they must be upright with legs dangling to reduce preload.
• Waiting for the ECG before starting MONA — the ECG and interventions should begin simultaneously (12 min).
• Giving oxygen to all ACS patients regardless of SpO2 — current evidence says give O2 ONLY if SpO2 <94% (hyperoxia worsens myocardial injury).
• Confusing STEMI (ST elevation, complete occlusion, needs immediate reperfusion) with NSTEMI (no ST elevation, partial occlusion, managed urgently but differently).

Exam Tips

• The NLE will always have an anaphylaxis question. The FIRST and PRIORITY drug = EPINEPHRINE IM (1:1000) to the thigh.
• Memorize the dosing contrast: ANAPHYLAXIS = 0.3–0.5 mg IM, 1:1000 | CARDIAC ARREST = 1 mg IV, 1:10,000. This is a classic NLE trap.
• Antihistamines (diphenhydramine) treat SKIN symptoms only; they do NOT reverse shock or bronchospasm. Never listed as priority.
• Corticosteroids prevent the LATE (biphasic) reaction; they take hours to work — not for the acute phase.
• Biphasic reaction = major NLE rationale for why patients are NOT sent home immediately after anaphylaxis resolves.

Key Points

• Anaphylaxis = rapidly progressive, life-threatening systemic allergic reaction. Onset: usually within MINUTES of allergen exposure.
• Four systems involved: (A) Airway — laryngeal edema, stridor; (B) Breathing — bronchospasm, wheeze; (C) Circulation — distributive shock (vasodilation + capillary leak); (D) Skin — urticaria, angioedema, flushing. GI symptoms (nausea, vomiting, cramping) also common.
• SINGLE PRIORITY INTERVENTION = EPINEPHRINE. Do NOT delay for antihistamines or steroids.
• EPINEPHRINE DOSING FOR ANAPHYLAXIS: 0.3 to 0.5 mg INTRAMUSCULARLY (IM), 1:1000 concentration, injected into the ANTEROLATERAL THIGH (vastus lateralis). Can repeat every 5–15 minutes as needed.
• WHY epinephrine: (1) Vasoconstriction — counteracts vasodilation and shock; (2) Bronchodilation — reverses bronchospasm; (3) Reduces mediator release — blunts ongoing reaction.
• CRITICAL DOSING COMPARISON (highest-yield NLE distinction): ANAPHYLAXIS = 0.3–0.5 mg IM, 1:1000 concentration. CARDIAC ARREST = 1 mg IV, 1:10,000 concentration. Confusing these is dangerous.
• ADJUNCTS (secondary to epinephrine, NEVER instead of it): (1) High-flow O2; (2) IV fluids (aggressive, for hypotension/shock); (3) Antihistamine — diphenhydramine (H1 blocker) for skin symptoms; (4) Corticosteroids (e.g., hydrocortisone) to blunt the late-phase reaction.
• POSITIONING: Hypotensive patient → SUPINE with legs elevated (shock position). Respiratory distress → more upright. Pregnant patient → left lateral decubitus.
• BIPHASIC REACTION: Anaphylaxis can RECUR 1–72 hours after apparent recovery even without re-exposure. Observe patient for at least 4–8 hours (or admit for monitoring).
• NANDA nursing diagnoses: Ineffective Airway Clearance; Impaired Gas Exchange; Decreased Cardiac Output; Risk for Shock.

Definitions

Section Title

Anaphylaxis

Common Mistakes

• Giving antihistamines or steroids FIRST instead of epinephrine — antihistamines treat itching, not shock or airway compromise. Epinephrine FIRST, always.
• Using the wrong epinephrine route (IV instead of IM for anaphylaxis) or wrong concentration (1:10,000 instead of 1:1000).
• Giving IM epinephrine in the deltoid instead of the anterolateral thigh — the thigh (vastus lateralis) has better blood flow and faster absorption.
• Discharging the patient as soon as symptoms resolve, without observing for biphasic reaction.
• Positioning all anaphylaxis patients the same way — hypotensive = supine with legs up; respiratory distress = upright.
• Forgetting to assess and secure the airway early — laryngeal edema can progress rapidly and completely obstruct the airway.

Formulas

Exam Tips

• NLE question stem will describe a hypertensive patient — look for signs of organ damage (headache + confusion = encephalopathy, chest pain = cardiac, decreased urine = renal). If present = EMERGENCY.
• The 25% MAP reduction in the first hour is the most testable number. Memorize it.
• Mnemonic for target organs: BRAIN-HEART-AORTA-KIDNEY-EYE (BHAKE) — these define a hypertensive emergency.
• Sodium nitroprusside requires protection from light and is metabolized to cyanide with prolonged use — an NLE pharmacology favorite.
• Never give sublingual nifedipine (causes uncontrolled rapid BP drop) — it was used in the past but is now contraindicated for hypertensive crisis.

Key Points

• Hypertensive crisis = severe BP elevation, generally SBP >180 mmHg or DBP >120 mmHg.
• CRITICAL DISTINCTION — TWO TYPES: (1) HYPERTENSIVE URGENCY = severely elevated BP WITHOUT acute target-organ damage. Managed gradually over 24–48 hours with ORAL agents. Not immediately life-threatening. (2) HYPERTENSIVE EMERGENCY = severely elevated BP WITH ACUTE TARGET-ORGAN DAMAGE. Requires IMMEDIATE CONTROLLED IV blood pressure reduction. Life-threatening.
• Target organs damaged in HYPERTENSIVE EMERGENCY (memorize): Brain (encephalopathy — headache, confusion, seizures, stroke), Heart (acute heart failure, myocardial ischemia), Aorta (aortic dissection), Kidneys (acute kidney injury), Eyes (papilledema/retinal hemorrhage).
• IV AGENTS for hypertensive emergency: Labetalol (alpha/beta blocker), Nicardipine (calcium channel blocker), Sodium Nitroprusside (potent vasodilator — used for severe cases/aortic dissection).
• THE OVERRIDING PRINCIPLE: LOWER BLOOD PRESSURE GRADUALLY, NOT ABRUPTLY. Target: reduce MAP by no more than 25% in the FIRST HOUR. Dropping too fast causes ischemic stroke, MI, or acute renal failure (cerebral autoregulation is impaired in chronic hypertension).
• EXCEPTION: Aortic dissection requires MORE RAPID and aggressive BP control (target SBP <120 mmHg within minutes) to prevent propagation.
• Monitoring: Continuous BP monitoring (ideally via arterial line in ICU), frequent neurologic checks (GCS, pupil response), urine output.
• NANDA nursing diagnoses: Risk for Decreased Cardiac Tissue Perfusion; Risk for Ineffective Cerebral Tissue Perfusion; Acute Pain (headache).

Definitions

Section Title

Hypertensive Crisis

Common Mistakes

• Aggressively lowering BP too fast (e.g., normalizing it in minutes) — this causes watershed ischemia, stroke, or MI.
• Confusing hypertensive urgency with hypertensive emergency — the KEY differentiator is the presence of acute target-organ damage.
• Using oral agents for a hypertensive emergency — IV agents with titratability are required.
• Forgetting neurologic monitoring — BP numbers alone are insufficient; patient's mental status and symptoms guide management.
• Not recognizing aortic dissection as requiring faster BP control — the general 25% rule does NOT apply here.

Exam Tips

• NLE will describe a patient with severe abdominal pain — your FIRST priority nursing action = KEEP NPO.
• Three things NEVER to do in acute abdomen (NLE favorites): no heat, no laxatives, no enemas.
• Board-like rigidity = peritoneal irritation = likely surgical emergency — escalate immediately.
• For bowel obstruction: NGT for decompression, IV fluids for hydration, strict NPO, prepare for surgery.
• Ruptured ectopic pregnancy and AAA rupture = hemorrhagic shock + acute abdomen — prioritize circulation (IV fluids, blood products, emergency OR) alongside the NPO rule.

Key Points

• Acute abdomen = sudden onset of severe abdominal pain suggesting a potential surgical emergency.
• Common causes: Appendicitis, GI perforation (perforated ulcer), bowel obstruction, mesenteric ischemia, ruptured ectopic pregnancy, ruptured abdominal aortic aneurysm (AAA).
• RED FLAG SIGNS: Rigid, board-like abdomen (peritoneal irritation), rebound tenderness (worsening pain when pressure is released), involuntary guarding, abdominal distension, absent bowel sounds (ileus), signs of shock (tachycardia, hypotension, pallor).
• PRIORITY NURSING ACTIONS: (1) KEEP NPO (nothing by mouth) — patient may need emergency surgery; (2) Establish IV access and administer IV fluids; (3) Monitor vital signs and pain continuously; (4) Prepare for diagnostics (CBC, serum amylase/lipase, upright abdominal X-ray, ultrasound, CT abdomen); (5) Position of comfort (usually knees-to-chest or side-lying to reduce pain).
• WHAT TO AVOID — CRITICAL: NO HEAT APPLICATION to the abdomen (increases circulation, may worsen inflammation). NO LAXATIVES OR ENEMAS (can rupture an inflamed appendix or worsen obstruction). NO ENEMAS FOR SUSPECTED APPENDICITIS.
• Pain management: Historically, analgesics were withheld to preserve examination findings, but current guidelines allow judicious use of analgesics once surgical assessment is completed — HOWEVER, for NLE purposes, 'do NOT mask the abdominal assessment' is still a testable principle.
• Nasogastric (NGT) insertion may be ordered for bowel obstruction to decompress the stomach and reduce vomiting.
• NANDA nursing diagnoses: Acute Pain; Risk for Deficient Fluid Volume; Risk for Infection (peritonitis); Anxiety.

Definitions

Section Title

Acute Abdomen

Common Mistakes

• Applying a hot water bag to the abdomen to relieve pain — NEVER do this in acute abdomen; it can rupture the appendix.
• Giving a laxative or enema for constipation-like abdominal pain without ruling out appendicitis — can cause perforation.
• Giving the patient water or food 'to soothe the stomach' — this violates NPO and delays emergency surgery.
• Neglecting to assess for signs of shock — abdominal emergencies can cause rapid hemorrhage (AAA rupture, ectopic pregnancy).
• Forgetting that a rigid abdomen = late peritonitis — do not wait for this sign before escalating care.

Formulas

Exam Tips

• NLE TRAP: The question will describe an unconscious diabetic patient. Do NOT select 'give oral glucose.' Answer = IV D50W or IM glucagon.
• DKA management order: FLUIDS → INSULIN → POTASSIUM. Water before insulin is the most testable principle.
• Kussmaul respirations + fruity breath + high glucose + acidosis = DKA diagnosis. If there is no fruity breath or Kussmaul = think HHS.
• Hypokalemia is the most dangerous DKA complication from insulin therapy — always check potassium before and during insulin infusion.
• Hypoglycemia is the MORE RAPIDLY DANGEROUS of the two because neurons cannot store glucose and begin dying within 4–6 minutes of severe hypoglycemia.

Key Points

• TWO DIABETIC EMERGENCIES: HYPOGLYCEMIA (low glucose, rapid onset, more immediately dangerous to the brain) vs. HYPERGLYCEMIC EMERGENCIES — DKA and HHS (high glucose, gradual onset).
• HYPOGLYCEMIA: Blood glucose <70 mg/dL (3.9 mmol/L). ONSET: RAPID (minutes to hours). Signs: adrenergic (shakiness, sweating, palpitations, hunger) + neuroglycopenic (confusion, irritability, slurred speech, seizures, coma). The brain depends entirely on glucose — prolonged hypoglycemia causes irreversible brain damage.
• HYPOGLYCEMIA TREATMENT — RULE OF 15: CONSCIOUS patient who can swallow → give 15 g of fast-acting oral carbohydrate (3 glucose tablets, 4 oz fruit juice, 3 tsp sugar) → recheck glucose after 15 minutes → repeat if still <70 mg/dL → once normalized, give complex carbohydrate to prevent recurrence.
• HYPOGLYCEMIA in UNCONSCIOUS patient or unable to swallow: NEVER give oral carbs (aspiration risk) → give IV DEXTROSE (25 g of D50W = 50 mL of 50% dextrose) OR INTRAMUSCULAR GLUCAGON. Monitor for rebound hypoglycemia.
• DIABETIC KETOACIDOSIS (DKA): Mostly TYPE 1 diabetes. Caused by insulin deficiency → fat breakdown → ketoacid production. ONSET: GRADUAL (hours to days). Signs: BG >250 mg/dL, metabolic acidosis (low pH, low HCO3), ketonuria/ketonemia, KUSSMAUL RESPIRATIONS (deep, rapid breathing — compensatory for metabolic acidosis), FRUITY/ACETONE BREATH (ketones exhaled), polyuria, polydipsia, dehydration, abdominal pain, nausea, altered consciousness.
• DKA MANAGEMENT PRIORITY ORDER — MEMORIZE: (1) FLUIDS FIRST — IV normal saline (0.9% NaCl) aggressively to correct dehydration and improve renal perfusion; (2) INSULIN — continuous IV regular insulin infusion (0.1 unit/kg/hr) to suppress ketogenesis and lower glucose — DO NOT start insulin if K+ is very low (<3.3 mEq/L); (3) POTASSIUM — monitor closely; insulin drives K+ into cells → dangerous hypokalemia. Replace K+ before starting insulin if low; add dextrose to IV fluids when BG falls to 200–250 mg/dL to prevent hypoglycemia while clearing acidosis.
• HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS): TYPE 2 diabetes, elderly. VERY HIGH glucose (often >600 mg/dL), SEVERE dehydration, MINIMAL or NO ketosis (some insulin present prevents fat breakdown), no Kussmaul respirations, no fruity breath. Managed with the same fluids-insulin-potassium principles but more gradual fluid replacement.
• COMPARISON TABLE: DKA = Type 1, BG 250–500, ketones present, acidosis, Kussmaul respirations, fruity breath, younger. HHS = Type 2, BG >600, minimal ketones, no acidosis, no Kussmaul, older/more dehydrated, higher mortality.
• NANDA nursing diagnoses: Deficient Fluid Volume; Impaired Gas Exchange (DKA); Risk for Electrolyte Imbalance; Acute Confusion.

Definitions

Section Title

Diabetic Emergencies: Hypoglycemia and DKA

Common Mistakes

• Giving oral glucose/juice to an unconscious or confused hypoglycemic patient — aspiration risk. ONLY IV dextrose or IM glucagon for unconscious patients.
• Starting insulin in DKA before checking/correcting potassium — insulin shifts K+ into cells; if K+ is already low, insulin can cause fatal hypokalemia.
• Dropping glucose too fast in DKA — when BG reaches 200–250 mg/dL, dextrose should be added to IV fluids to prevent hypoglycemia while continuing to correct the acidosis.
• Confusing DKA with HHS — DKA has ketones + acidosis + Kussmaul + fruity breath (Type 1); HHS has none of those but has much higher glucose and more severe dehydration (Type 2).
• Treating hypoglycemia then discharging without finding the CAUSE — hypoglycemia can recur if the underlying cause (excess insulin, missed meal) is not addressed.
• Forgetting that DKA can occur with a NORMAL blood glucose in pregnant patients (euglycemic DKA) — less common but important.