Free NREMT Paramedic Exam Flashcards

Give the induction (sedative) agent first to produce unconsciousness, then immediately the paralytic. A common pairing is etomidate followed by rocuronium or succinylcholine. Analgesia/sedation for maintenance comes AFTER the tube is confirmed, not during the RSI push.

Succinylcholine: fast onset (~45-60 s), short duration (~5-10 min), but contraindicated with hyperkalemia, crush/burn >24-48 h old, and malignant hyperthermia history. Rocuronium: similar onset at higher dose but long duration (~30-45 min) with no hyperkalemia risk.

Continuous waveform capnography is the most reliable confirmation of correct ET tube placement and ongoing monitoring. A persistent square-wave ETCO2 tracing confirms tracheal placement; sustained near-zero ETCO2 after good CPR suggests esophageal placement or no circulation.

Indicated in a 'cannot intubate, cannot oxygenate/ventilate' failed-airway situation where BVM, supraglottic, and intubation attempts have failed. The cricothyroid membrane (between thyroid and cricoid cartilage) is the landmark. It is a rescue procedure, not a first-line technique.

Anticipate difficulty with limited mouth opening, short thyromental distance, large tongue/obesity, neck immobility or C-collar, facial/airway trauma, and blood/vomit. Plan a backup (supraglottic, surgical) and optimize positioning and preoxygenation BEFORE the first attempt.

Normal ETCO2 is 35-45 mmHg. A sudden drop toward zero signals tube dislodgement, circuit disconnection, complete obstruction, or loss of cardiac output (arrest). A gradual rise suggests hypoventilation; a gradual fall suggests hyperventilation or falling perfusion.

ETCO2 below ~10 mmHg during CPR indicates inadequate compressions or poor perfusion—improve compression quality. A sudden, sustained rise (often >35-40 mmHg) is an early sign of return of spontaneous circulation (ROSC) before a pulse check.

Over-ventilation raises intrathoracic pressure, reduces venous return and coronary perfusion, and worsens outcomes. With an advanced airway in cardiac arrest, deliver about 1 breath every 6 seconds (~10/min) with continuous compressions—do not bag fast.

Severe dyspnea, hypotension, distended neck veins, tracheal deviation (late), absent breath sounds and hyperresonance on the affected side. Treat immediately with needle decompression (large-bore catheter, 2nd intercostal space midclavicular or 5th midaxillary line)—do not wait for X-ray.

CPAP is first-line for acute pulmonary edema (CHF) and severe COPD/asthma in an awake, cooperative, spontaneously breathing patient with adequate BP. Contraindicated with apnea/inadequate respiratory drive, hypotension, decreased LOC, vomiting, or suspected pneumothorax.

Inferior wall: ST elevation in leads II, III, and aVF. Always obtain a right-sided lead (V4R) because inferior MI is frequently associated with right ventricular infarction, which changes management (nitrates can cause profound hypotension).

STEMI is generally ST elevation ≥1 mm in two contiguous limb leads (or ≥2 mm in precordial leads V2-V3). Reciprocal ST depression in the opposite wall increases specificity. Anterior MI = V1-V4 (LAD); lateral = I, aVL, V5-V6; inferior = II, III, aVF.

RV infarction makes cardiac output preload-dependent. Nitroglycerin (a venodilator) drops preload and can cause severe, refractory hypotension. Manage RV MI with cautious fluid boluses to support preload instead of routine nitrates.

Monomorphic VT: uniform wide QRS complexes—treat per stable/unstable VT pathway. Torsades de pointes (polymorphic VT with twisting axis, often long QT): treat with IV magnesium sulfate; defibrillate if pulseless.

P waves and QRS complexes are completely dissociated—no relationship between atrial and ventricular rates. Often symptomatic bradycardia. Atropine is usually ineffective in high-grade/3rd-degree block; prepare for transcutaneous pacing.

For symptomatic unstable bradycardia: atropine 1 mg IV every 3-5 minutes, max total 3 mg. If atropine is ineffective, move to transcutaneous pacing and/or a chronotropic infusion (dopamine or epinephrine). Atropine is generally ineffective in high-grade AV block.

Try vagal maneuvers first. If unsuccessful, give adenosine 6 mg rapid IV push followed by a saline flush; if no conversion, give 12 mg. Warn the patient about a brief pause/flushing. Use synchronized cardioversion if the patient is unstable.

Unstable patient WITH a pulse (and serious signs from the rate) → synchronized cardioversion (shock timed to the R wave). Pulseless VT or VF → unsynchronized defibrillation. Sync mode prevents an R-on-T shock that could induce VF.

If stable, regular, monomorphic and likely VT, consider an antiarrhythmic such as amiodarone or procainamide and seek expert consultation. If the patient becomes unstable at any point, proceed to synchronized cardioversion.

Establish last-known-well time, perform a validated stroke scale, check glucose (rule out hypoglycemia mimicking stroke), avoid aggressive BP lowering, keep airway protected, and provide early pre-arrival notification to a stroke-capable center.

Ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) are shockable—defibrillate immediately. Asystole and pulseless electrical activity (PEA) are NOT shockable; treat with high-quality CPR, epinephrine, and reversible-cause correction.

Epinephrine 1 mg IV/IO (1:10,000) every 3-5 minutes throughout the arrest. In shockable rhythms it is given after the second shock; in non-shockable rhythms it is given as soon as access is obtained.

For VF/pVT that persists after defibrillation and epinephrine, give amiodarone 300 mg IV/IO first dose, then 150 mg for a second dose. Lidocaine 1-1.5 mg/kg is an acceptable alternative if amiodarone is unavailable.

H's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/Hyperkalemia, Hypothermia. T's: Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary or coronary). Actively search for and correct these, especially in PEA/asystole.

Optimize oxygenation (target SpO2 ~94-99%, avoid hyperoxia), support BP (treat hypotension with fluids/vasopressors), obtain a 12-lead for STEMI, maintain normocapnia, avoid routine hyperventilation, and consider targeted temperature management at the receiving facility.

Beck's triad: hypotension, muffled heart sounds, jugular venous distension. Pulsus paradoxus may be present. Tamponade is a reversible 'T' cause of PEA arrest; definitive treatment is pericardiocentesis at the hospital—rapid transport is key.

Sit the patient upright, apply CPAP, give high-flow oxygen, and use nitroglycerin to reduce preload/afterload if BP is adequate. Avoid large fluid boluses. Diuretics may be given per protocol but airway/CPAP and nitrates drive early field improvement.

Hypotension with signs of poor perfusion (cool, mottled skin, altered mentation, oliguria) due to pump failure—often after large MI. Unlike hypovolemic shock, lungs may be wet; aggressive fluids can worsen pulmonary edema. May need inotropes/pressors and rapid transport for revascularization.

Set a rate (commonly 60-80/min), increase milliamps until electrical capture (a wide QRS after each pacer spike) AND mechanical capture (a palpable pulse matching the set rate) are confirmed. Provide analgesia/sedation for the pain of pacing in a conscious patient.

Withhold nitroglycerin with hypotension/SBP below protocol threshold, suspected right ventricular infarction, severe bradycardia/tachycardia, and recent phosphodiesterase inhibitor use (sildenafil/tadalafil/vardenafil) due to risk of profound, refractory hypotension.

Adenosine briefly blocks AV node conduction to break reentrant SVT; expect a short asystolic pause then conversion. Give rapid push with immediate flush. Less effective and use caution in patients on theophylline; dipyridamole/carbamazepine potentiate it. Not effective for atrial fibrillation/flutter.

Amiodarone: broad antiarrhythmic for refractory VF/pVT (300 mg then 150 mg) and stable VT. Lidocaine (1-1.5 mg/kg, then 0.5-0.75 mg/kg repeats) is the alternative for VF/pVT. Watch for hypotension with amiodarone and CNS toxicity (slurred speech, seizures) with lidocaine.

Diltiazem (a calcium channel blocker) controls rate in stable atrial fibrillation/flutter with rapid ventricular response. Avoid AV-nodal blockers in WPW with pre-excited AFib (can accelerate conduction) and in wide-complex tachycardia of uncertain origin.

Before definitive hemorrhage control, titrate fluids to a lower target (e.g., a palpable radial pulse / SBP ~80-90) rather than normalizing BP. Over-resuscitation can pop clots, dilute clotting factors, and worsen bleeding. Rapid transport to surgery is the priority.

Early compensated shock shows tachycardia, narrowing pulse pressure, anxiety, and cool/pale skin with a still-normal systolic BP. Hypotension is a LATE finding (often after ~30% blood loss). Treat based on perfusion signs, not on a normal blood pressure alone.

Direct pressure first; if life-threatening extremity bleeding is uncontrolled, apply a tourniquet high and tight proximal to the wound, tighten until bleeding stops, and note the application time. Use hemostatic-gauge packing for junctional wounds not amenable to a tourniquet.

Always record the exact time a tourniquet is applied (often written on the device and the patient). Prolonged ischemia time guides hospital limb-salvage and reperfusion decisions; never loosen a tourniquet in the field once a hemorrhage is controlled unless ordered.

Cushing's triad = hypertension (widening pulse pressure), bradycardia, and irregular respirations—a late sign of rising intracranial pressure/impending herniation. Manage with oxygenation, normocapnia (avoid routine hyperventilation), and head elevation; brief controlled hyperventilation only for active herniation signs.

Two or more adjacent ribs fractured in two or more places create a free segment with paradoxical movement. The main threat is the underlying pulmonary contusion and hypoventilation. Support oxygenation/ventilation (consider positive pressure) and watch for respiratory failure.

Use the Rule of Nines and depth to estimate TBSA. Significant burns require warmed isotonic fluid resuscitation (parkland-type formula at the hospital), early airway assessment for inhalation injury (singed nasal hair, soot, stridor, hoarseness), and pain control.

Hypoglycemia: rapid onset, diaphoretic, altered/combative, may seize—treat with glucose (oral if able, otherwise IV dextrose or glucagon). DKA: gradual onset, dehydration, Kussmaul respirations, fruity breath, hyperglycemia—needs IV fluids and hospital insulin, NOT field glucose.

Suspect sepsis with infection plus hypotension, tachycardia, tachypnea, altered mentation, and high or low temperature. Field priorities: high-flow oxygen, large-bore IV access, isotonic fluid resuscitation for hypoperfusion, and early pre-arrival notification for time-sensitive treatment.

Epinephrine 0.3 mg (adult) of 1:1,000 IM in the anterolateral thigh is first-line and given EARLY—do not delay for antihistamines or steroids. Repeat every 5-15 minutes as needed; add fluids for hypotension and consider an epinephrine infusion for refractory shock.

Escalate: continuous nebulized albuterol + ipratropium, IM/IV epinephrine for severe/impending failure, IV/IM steroids, and magnesium sulfate as an adjunct bronchodilator. A 'silent chest' with rising CO2 and exhaustion signals impending respiratory failure—prepare for ventilatory support.

Titrate naloxone to restore adequate ventilation (rate/tidal volume), NOT full alertness—abrupt full reversal can precipitate severe withdrawal and agitation. Support ventilation with BVM first; re-dosing may be needed because naloxone's duration is shorter than many opioids.

Look for a widening QRS, tachycardia, hypotension, seizures, and altered mentation. A QRS widening (often >100 ms) signals cardiotoxicity—treat with sodium bicarbonate. Manage seizures and airway aggressively; TCA overdose can deteriorate rapidly.

After delivery, the most common cause is uterine atony. Perform vigorous fundal massage, encourage the newborn to breastfeed if possible, ensure the placenta is delivered, give isotonic fluids for shock, and transport rapidly; uterotonics (e.g., oxytocin) per protocol.

Eclampsia is seizures in pregnancy/postpartum with preeclampsia features (hypertension, edema, headache, visual changes). Position left-lateral, protect the airway, control the seizure, and treat with magnesium sulfate per protocol. Definitive treatment is delivery—transport without delay.

Most newborns need only warming, drying, stimulation, and airway positioning/suctioning. If HR stays below 100 with apnea/gasping → positive-pressure ventilation. If HR remains below 60 despite 30 s of effective PPV → start chest compressions (3:1 with ventilations), then epinephrine.

Computerized adaptive test of 110-150 items (20 unscored pilot) in 3.5 hours; pass at a scaled score of 950 on the 100-1500 scale. Fee is $175/attempt via Pearson VUE, certification valid 2 years; retest 15 days after results, six attempts allowed with remediation after three failures.