# Situation: The nurse is assigned as the circulating nurse in an operating room for a day of elective surgical cases. The first client is a 30-year-old man having laparoscopic abdominal surgery under general anesthesia with sevoflurane; succinylcholine was given for intubation, and carbon dioxide insufflation of the abdomen began 5 minutes after induction. The nurse notes these trends: 10 min: end-tidal carbon dioxide (ETCO2) 40 mmHg, heart rate 78/min, core temperature 36.8 °C 25 min: ETCO2 50 mmHg, heart rate 102/min, core temperature 36.9 °C; ventilation is then doubled 40 min: ETCO2 62 mmHg, heart rate 128/min, core temperature 37.2 °C, serum potassium 5.9 mEq/L (normal 3.5–5.0 mEq/L) Blood pressure is stable, there is no rash, wheeze, or subcutaneous crepitus, and the insufflation pressure is unchanged. Which problem do these findings MOST likely indicate?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=629869  
> language: ko  
> subject: Nursing Practice III — Care of Clients with Problems in Surgery, Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations

## 문제

Situation: The nurse is assigned as the circulating nurse in an operating room for a day of elective surgical cases.

The first client is a 30-year-old man having laparoscopic abdominal surgery under general anesthesia with sevoflurane; succinylcholine was given for intubation, and carbon dioxide insufflation of the abdomen began 5 minutes after induction. The nurse notes these trends:
10 min: end-tidal carbon dioxide (ETCO2) 40 mmHg, heart rate 78/min, core temperature 36.8 °C
25 min: ETCO2 50 mmHg, heart rate 102/min, core temperature 36.9 °C; ventilation is then doubled
40 min: ETCO2 62 mmHg, heart rate 128/min, core temperature 37.2 °C, serum potassium 5.9 mEq/L (normal 3.5–5.0 mEq/L)
Blood pressure is stable, there is no rash, wheeze, or subcutaneous crepitus, and the insufflation pressure is unchanged. Which problem do these findings MOST likely indicate?

## 보기

1. Inadequate depth of anesthesia
2. Malignant hyperthermia **✔ 정답**
3. Anaphylaxis to succinylcholine
4. Carbon dioxide absorbed from the insufflation

**정답: 2**

## 해설

Carbon dioxide absorbed from a pneumoperitoneum raises end-tidal carbon dioxide early and then responds to increased ventilation. Here ETCO2 keeps climbing after ventilation was doubled, with a rising heart rate and a new hyperkalemia after exposure to sevoflurane and succinylcholine: the pattern of malignant hyperthermia. Fever is a late sign, so a near-normal temperature does not rule it out.

## 심화 해설

Clinical picture and why it points to malignant hyperthermia

The patient received two classic MH triggers—sevoflurane (a potent volatile anesthetic) and succinylcholine (a depolarizing muscle relaxant)—and then developed a progressive, treatment-resistant rise in end-tidal carbon dioxide (ETCO2) with tachycardia and new hyperkalemia. In malignant hyperthermia, uncontrolled release of calcium from the sarcoplasmic reticulum of skeletal muscle drives sustained muscle hypermetabolism. That produces large amounts of CO2 and heat, consumes oxygen, and leads to acidosis, muscle rigidity, and rhabdomyolysis . The rising ETCO2 is therefore not simply a ventilation problem; it reflects massively increased CO2 production.

The key discriminator here is that ETCO2 continued to climb from 50 mmHg to 62 mmHg even after ventilation was doubled. With CO2 absorbed from a pneumoperitoneum, increased minute ventilation would be expected to lower or at least stabilize ETCO2. Instead, the CO2 kept rising, which signals ongoing endogenous CO2 production—the hallmark of an MH hypermetabolic crisis.

Watch out! Core temperature was only 37.2 °C at 40 minutes. Fever is a late sign of MH because the enormous heat production may initially be masked by redistribution and anesthetic-induced vasodilation. A near-normal temperature does not exclude MH .

Why the other options are less likely

| Option | Why it does not fit this case |
| --- | --- |
| 1. Inadequate depth of anesthesia | Light anesthesia can cause tachycardia and hypertension, but it does not cause progressive hypercapnia that worsens despite doubling ventilation, nor does it produce hyperkalemia. |
| 3. Anaphylaxis to succinylcholine | Anaphylaxis typically presents with hypotension, rash, bronchospasm/wheeze, and angioedema. This patient had stable blood pressure, no rash, and no wheeze, making anaphylaxis unlikely. |
| 4. CO2 absorbed from insufflation | Absorbed CO2 raises ETCO2 early, but it responds to increased ventilation. The continued rise despite doubling ventilation, plus the new hyperkalemia and tachycardia, argues against absorption as the sole cause. |

Pathophysiology of the key findings

MH is a pharmacogenetic disorder of skeletal muscle calcium regulation. Trigger agents cause abnormal, sustained release of calcium from the sarcoplasmic reticulum, which produces persistent muscle contraction and a hypermetabolic state . The clinical consequences include increased CO2 production, increased oxygen consumption, tachycardia, tachypnea, acidosis, muscle rigidity, and rhabdomyolysis . The hyperkalemia (5.9 mEq/L; normal 3.5–5.0 mEq/L) results from potassium leaking out of damaged, hypermetabolic muscle cells and from rhabdomyolysis. This is a critical finding because hyperkalemia can precipitate life-threatening arrhythmias.

The combination of sevoflurane and succinylcholine exposure, progressively rising ETCO2 unresponsive to increased ventilation, tachycardia, and new hyperkalemia is the classic early pattern of an MH crisis. The absence of fever, rash, wheeze, and subcutaneous crepitus helps exclude anaphylaxis and insufflation-related CO2 absorption as the primary problem.

Clinical timing and delayed onset

MH can present during induction or later in the anesthetic course. Although many reactions occur shortly after exposure, delayed onset after sevoflurane and succinylcholine has been reported . In this case, the progressive worsening from 10 to 40 minutes—despite an initial doubling of ventilation—fits a developing hypermetabolic crisis rather than a transient response to intubation or insufflation. The circulating nurse must recognize that early MH may present with unexplained rising ETCO2 and tachycardia before fever or rigidity appears, and that prompt recognition triggers immediate discontinuation of the triggering agent, hyperventilation with 100% oxygen, and administration of dantrolene .

Key point! In the operating room, an unexplained, persistent rise in ETCO2 after exposure to volatile anesthetics or succinylcholine should be treated as malignant hyperthermia until proven otherwise, even when temperature is normal and no rigidity is yet evident.

## 임상 시나리오

Malignant Hyperthermia RecognitionRising ETCO2 despite ventilation is a crisis sign
After exposure to sevoflurane and succinylcholine, a progressive rise in end-tidal CO2 that continues despite doubling ventilation signals increased CO2 production, not hypoventilation.

New hyperkalemia (5.9 mEq/L) with tachycardia supports muscle breakdown and a hypermetabolic state. Fever is a late sign; a near-normal temperature does not rule out malignant hyperthermia.

CautionDo not attribute rising ETCO2 to CO2 insufflation if increased ventilation fails to lower it. Call for help, stop trigger agents, and initiate the MH protocol immediately.

## 핵심 개념

- **Malignant hyperthermia** — A hypermetabolic crisis of skeletal muscle triggered by volatile anesthetics or succinylcholine, causing increased CO2 production, acidosis, tachycardia, and hyperkalemia.
- **End-tidal CO2** — The partial pressure of carbon dioxide at the end of expiration, reflecting ventilation and CO2 production; a rising trend despite increased ventilation suggests increased production.
- **Succinylcholine** — A depolarizing neuromuscular blocker used for intubation that is a known trigger for malignant hyperthermia.
- **Sevoflurane** — A volatile halogenated anesthetic gas that is a potent trigger for malignant hyperthermia.
- **Hyperkalemia** — Elevated serum potassium; in malignant hyperthermia it results from rhabdomyolysis and muscle cell breakdown.

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