Critical Care Emergency Medical Transport Program (CCEMTP) Study Guide

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A sealed, flexible gas pocket occupies 30 mL at an absolute pressure of 1,000 units. At 750 units, constant temperature predicts 40 mL. Identify vulnerable trapped gas spaces before accepting the planned cabin-pressure exposure.

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Compare dry air at total pressures of 760 and 600 mm Hg. Multiplying each by 0.21 gives oxygen partial pressures of about 160 and 126 mm Hg, despite the identical oxygen fraction.

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A patient has pH 7.25, PaCO2 60 mm Hg and bicarbonate 26 mmol/L. Increased carbon dioxide explains the acidemia, so identify a primary respiratory acidosis and investigate inadequate ventilation while assessing expected compensation.

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With bicarbonate 12 mmol/L, expected PaCO2 is 26 ±2 mm Hg. A measured PaCO2 of 40 is disproportionately high, indicating metabolic acidosis plus respiratory acidosis, even though 40 is within a usual reference range.

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Sodium is 140, chloride 104 and bicarbonate 12 mmol/L. The anion gap is 24 mmol/L. Investigate unmeasured acids while checking perfusion, ketones and the clinical history rather than naming the cause from arithmetic alone.

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A patient with PaCO2 60 and bicarbonate 31 may have chronic compensation if the history fits. A chronically hypercapnic patient whose PaCO2 abruptly rises further without a matching bicarbonate change may have acute respiratory acidosis superimposed on the chronic disorder.

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After the stretcher is raised, an arterial transducer remains below the patient’s reference level and the displayed pressure increases. Relevel the transducer and reassess before reducing a vasopressor solely because of that reading.

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A newly assembled pressure system has been placed at the correct reference height but has not been zeroed. Establish its atmospheric baseline according to the device instructions before using the displayed pressure to titrate treatment.

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Ten minutes after a red-cell transfusion begins, a patient develops rigors, back discomfort and hypotension. Stop the blood, assess and support circulation, preserve access appropriately, and initiate the reaction investigation rather than completing the unit.

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A catheter produces a venous waveform, but the radiograph shows its tip directed up the jugular vein toward the head. Identify malposition and obtain correction rather than accepting venous entry as proof of satisfactory positioning.

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Before starting a vasopressor through a newly placed neck catheter, transduction shows an arterial waveform. Withhold use of that catheter, obtain alternative appropriate access and urgently communicate that the vessel has been dilated.

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An arrest follows suspected overdose during interfacility care. Continue appropriate resuscitation and evaluation of reversible causes rather than automatically applying an adult field termination rule to this different population or stopping solely because end-tidal CO2 is low.

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A post-arrest patient has a reliable SpO2 of 100% on maximal oxygen and an arterial PaO2 well above the target range. Gradually titrate oxygen while continuously monitoring to maintain the recommended post-arrest oxygenation range.

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A post-arrest patient has PaCO2 25 mm Hg, pH 7.50 and bicarbonate 19 mmol/L, supporting inappropriate hypocapnia rather than compensation for severe metabolic acidemia. Reassess ventilation toward the usual target. Contrast this with bicarbonate 10 mmol/L, where Winter’s formula predicts PaCO2 near 23 ±2.

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A patient achieves return of circulation after ventricular fibrillation and remains hypotensive with persistent ST elevation. Obtain and communicate the diagnostic ECG while supporting perfusion so possible coronary occlusion informs urgent receiving-team evaluation.

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An awake, warm LVAD patient has no radial pulse. Assess device function and pressure using appropriate methods before diagnosing circulatory failure or initiating compressions solely because pulsatility is absent.

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An LVAD patient becomes unresponsive with abnormal breathing and poor peripheral perfusion. Start compressions while another rescuer checks external connections and alarms and communicates with the device team.

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A patient’s creatinine rises from 0.9 to 1.3 mg/dL in 36 hours. The 0.4 mg/dL increase meets the absolute-rise criterion even though the current value might appear only mildly abnormal in isolation.

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A regular monomorphic wide-complex rhythm causes hypotension and altered mentation. Prioritise synchronised cardioversion over prolonged diagnostic ECG acquisition. A stable patient permits diagnostic 12-lead assessment and monitored treatment planning.

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A vomiting patient has sodium 140, chloride 90 and bicarbonate 24 mmol/L. The gap is 26 mmol/L despite normal bicarbonate, suggesting an additional unmeasured-acid process concealed by alkalosis.

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An oliguric patient has worsening pulmonary oedema and persistent dangerous hyperkalaemia despite initial treatment. Escalate urgently for renal-replacement evaluation and an appropriate receiving service instead of waiting for creatinine to cross an arbitrary numerical threshold.

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A person with known diabetes has glucose 180 mg/dL, beta-hydroxybutyrate 4.5 mmol/L and bicarbonate 14 mmol/L. The history, ketosis and acidosis support DKA despite glucose remaining below the traditional marked-hyperglycaemia pattern.

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A patient with confirmed DKA has potassium 3.2 mmol/L before insulin begins. Recognise the immediate potassium hazard, arrange monitored replacement and defer insulin until potassium has been corrected above the consensus threshold under the treatment protocol.

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New cyanosis follows benzocaine exposure with discordant saturation findings. Consider haemoglobin dysfunction, communicate the exposure and obtain appropriate diagnostic evaluation while supporting oxygenation rather than assuming isolated ventilation failure.

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Glucose falls to 170 mg/dL, but beta-hydroxybutyrate remains 2.5 mmol/L and venous pH is 7.24. DKA has not resolved; ongoing protocol-directed management must address persistent ketosis while preventing hypoglycaemia as glucose falls.

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Two occupants of an enclosed workshop develop headache and confusion near a combustion heater. Both have SpO2 readings of 99%. Treat the exposure history as significant, provide appropriate oxygen and seek blood co-oximetry rather than dismissing poisoning.

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A patient’s headache resolves after oxygen following an enclosed-space exposure. Before discharge planning is completed, ensure the receiving team knows the earlier confusion and that the patient receives instructions about delayed neurological symptoms and follow-up evaluation.

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A patient was speaking normally at 22:00, went to sleep and was found aphasic at 06:30. Record 22:00 as last known well and 06:30 as discovery, then communicate both during stroke-system activation and handoff.

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A patient develops unilateral weakness and has a low bedside glucose. Correct the glucose promptly under protocol, then repeat the neurological examination. Persistent focal weakness still requires urgent stroke evaluation with clearly documented timing and treatment response.

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Before a necessary transfer, place a surgical mask on the patient if tolerated, communicate airborne precautions to the receiving team and assess whether close care or procedures require additional respiratory protection.

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Chest movement occurs after intubation, but the CO2 trace is absent or diminishing. Immediately evaluate tracheal versus oesophageal location while maintaining effective oxygenation; check the sampling connection and circulation concurrently.

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A ventilated patient’s end-tidal carbon dioxide suddenly falls while settings remain unchanged and blood pressure deteriorates. Check the airway and circuit, but also investigate reduced pulmonary perfusion rather than automatically lowering the respiratory rate as the first interpretation.

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An unresponsive adult has a clearly palpable pulse at 72/min but is apnoeic. Open the airway and provide effective assisted breaths at approximately ten per minute while reassessing the pulse and preparing further airway support as required.

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An adult with ARDS has predicted body weight 60 kg and actual weight 105 kg. A starting tidal volume near 360 mL corresponds to 6 mL/kg predicted weight; 630 mL would incorrectly use actual weight.

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A passive ARDS patient has plateau pressure 33 cm H2O on a reliable inspiratory hold. Reassess tidal volume and respiratory-system mechanics as part of lung-protective management rather than assuming an acceptable peak-pressure alarm guarantees safe distending pressure.

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With unchanged tidal volume, inspiratory flow and total PEEP, peak pressure rises from 25 to 40 cm H2O while valid plateau pressure remains 20. Inspect the tube, circuit and airway for resistance problems.

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A passive patient has plateau pressure 28 cm H2O, total PEEP 12 and set PEEP 6. Driving pressure is 16 cm H2O, while intrinsic PEEP is 6; subtracting set PEEP alone would give the wrong driving pressure.

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Persistent expiratory flow prompts a valid hold showing total PEEP 14 cm H2O with set PEEP 5. Intrinsic PEEP is 9 cm H2O; relate it to obstruction, ventilator timing and circulation.

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An obstructed patient becomes hypotensive after respiratory rate is increased. Persistent expiratory flow suggests trapping; reassess timing and resistance while evaluating other causes of shock.

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Repeated intubation attempts interrupt compressions while mask ventilation remains effective. Continue effective ventilation, minimise interruptions and use an appropriate alternative airway strategy rather than persisting with unsuccessful attempts.

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After airway placement, assign one rescuer to coordinate ten effective breaths per minute while another maintains continuous compressions. Reassess the circuit, chest movement and capnography if ventilation becomes difficult.

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After PEEP is increased, an ARDS patient’s saturation improves but blood pressure falls and plateau pressure rises markedly. Reassess the balance between oxygenation benefit, distending pressure and circulatory effects instead of accepting saturation as the sole endpoint.

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MAP 82 mm Hg and ICP 24 mm Hg give CPP 58 mm Hg. Identify both contributions to the low gradient. MAP 86 with the same ICP gives CPP 62, within the guideline range.

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After thoracic trauma, ventilation suddenly becomes difficult and blood pressure falls. Rapidly assess the chest, airway and circuit, and institute indicated emergency treatment for suspected tension physiology without allowing a routine imaging process to delay necessary care.

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A severe-TBI patient has no evidence of acute herniation, but a proposed transport plan targets PaCO2 24 mm Hg throughout the journey. Recognise this as prolonged prophylactic hyperventilation and seek a ventilation strategy consistent with cerebral perfusion protection.

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One burn is red, dry and blanching without blisters; another is moist and blistered. Distinguish superficial from partial-thickness injury before estimating burn size, while recognising that a pale, insensate area may represent deeper damage.

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An adult has the entire anterior trunk affected, but only half is blistered partial-thickness injury; the remainder is superficial erythema. Using the adult anterior-trunk estimate of 18%, count approximately 9% TBSA rather than the whole 18%.

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A patient has a small but clearly deep burn across the hand and a finger joint. Seek immediate burn-centre consultation with consideration for transfer based on depth and location even though TBSA is well below 10%.

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A septic patient remains poorly perfused after initial treatment. A passive leg raise produces no meaningful change in a reliable stroke-volume measurement. Reconsider further empirical fluid and assess other support needs rather than infusing solely because blood pressure remains low.

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In sepsis without TBI, consider the conditional balanced-crystalloid preference when fluid is indicated. In sepsis with traumatic brain injury, recognise the saline exception. Rising chloride with improving lactate can explain persistent bicarbonate reduction after saline exposure.

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A septic patient’s blood pressure improves, yet capillary refill remains prolonged and urine output is falling. Communicate the discordant perfusion findings and reassess the overall resuscitation response rather than declaring shock resolved from the pressure alone.

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Over several hours, a patient with infection develops increasing oxygen requirements, reduced urine output and new confusion. Recognise an expanding organ-dysfunction pattern and escalate the receiving-team handoff even if the latest blood pressure is acceptable.

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Several days after delivery, a patient develops severe headache, visual symptoms and a generalised seizure. Recognise possible postpartum eclampsia, support airway and circulation, and initiate urgent obstetric escalation rather than dismissing it because pregnancy has ended.

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A pregnant patient with upper abdominal pain has evidence of haemolysis, rising aminotransferases and thrombocytopenia. Communicate the complete HELLP pattern and need for urgent obstetric care rather than handing over only an abnormal liver-function result.

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A child has heart rate 48/min, weak pulses and altered responsiveness despite effective bag-mask ventilation and oxygenation. Begin CPR according to the paediatric bradycardia pathway while arranging further treatment and identifying the cause of the persistent compromise.

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A child develops a slow rhythm associated with a clear vagal trigger. After assessing airway, breathing and perfusion, recognise why atropine may fit this mechanism; contrast it with a hypoxic child whose immediate need is effective respiratory support.

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An awake patient with a tachyarrhythmia needs cardioversion. Prepare appropriate procedural medication alongside the electrical treatment. If hypotension and altered mentation develop, expedite cardioversion while maintaining airway and circulatory support.

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An adult with suspected opioid exposure has a definite pulse but only occasional shallow breaths. Open the airway and provide effective assisted ventilation while naloxone is prepared and administered, then reassess breathing and circulation rather than waiting for the drug response.

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A patient awakens after naloxone but becomes progressively drowsy with shallow breathing during transfer. Recognise recurrent opioid toxicity as a possibility, support ventilation immediately and reassess the need for further antagonist treatment under the clinical protocol.

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An unresponsive adult near opioid packaging has no normal breathing and no definite pulse within the recommended assessment interval. Begin CPR and use an AED promptly; incorporate an antagonist only without delaying the core resuscitation actions.