1. Cardiac Arrest in Pregnancy
Cardiac arrest during pregnancy represents one of the most challenging resuscitation scenarios, requiring simultaneous management of two patients. The incidence is approximately 1 in 12,000 admissions for delivery. Maternal physiology undergoes profound changes that affect both the pathophysiology of arrest and the approach to resuscitation.
1.1 Key Physiological Changes Affecting Resuscitation
| Change | Effect on Resuscitation |
|---|
| Aortocaval compression | The gravid uterus (from approximately 20 weeks gestation) compresses the inferior vena cava and aorta in the supine position, reducing venous return by up to 25–30% and severely compromising cardiac output during CPR |
| Increased oxygen consumption | Maternal metabolic rate and oxygen consumption increase 20–30%; hypoxia develops more rapidly during apnea |
| Reduced functional residual capacity | Decreased FRC combined with increased oxygen consumption causes rapid desaturation; airway management must be prioritized |
| Increased blood volume | Expanded blood volume (30–50% increase) may mask hemorrhage initially |
| Difficult airway | Edema of upper airway, enlarged breasts, weight gain → higher rates of difficult intubation; use 6.0–6.5 mm ETT; consider video laryngoscopy first-line |
| Progesterone-mediated changes | Decreased lower esophageal sphincter tone → increased aspiration risk; hyperventilation at baseline (compensated respiratory alkalosis with normal PaCO2 ~30 mmHg) |
1.2 Modifications to Standard ACLS in Pregnancy
| Intervention | Modification |
|---|
| Chest compressions | Perform in standard supine position; hand placement may be slightly higher on the sternum if the uterus displaces the diaphragm cephalad |
| Left uterine displacement (LUD) | Critical intervention: Manually displace the uterus to the patient’s left to relieve aortocaval compression. A team member uses one or two hands to push the uterus leftward while the patient remains supine. This is preferred over left lateral tilt, which compromises CPR quality |
| Defibrillation | Standard energy levels; no dose modification required; remove fetal monitors before defibrillating; defibrillation is safe for the fetus |
| Medications | Standard ACLS medications at standard doses; epinephrine, amiodarone, and other drugs are used without modification; vasopressin and other vasoconstrictors may reduce uterine blood flow but are still indicated during cardiac arrest |
| Airway management | Early intubation is preferred due to high aspiration risk; use smaller ETT (6.0–6.5 mm); may be performed by the most experienced provider |
| IV access | Place IV above the diaphragm (to ensure drugs reach the heart without passing through the compressed IVC); avoid femoral lines |
| Sodium bicarbonate | Consider early use — fetal acidosis develops rapidly during maternal arrest |
1.3 Perimortem Cesarean Delivery (Resuscitative Hysterotomy)
| Parameter | Detail |
|---|
| Definition | Emergency cesarean delivery performed during maternal cardiac arrest to facilitate maternal resuscitation and improve fetal survival |
| Primary indication | Maternal cardiac arrest at ≥20 weeks gestational age (uterine fundus at or above the umbilicus) with failure to achieve ROSC within 4 minutes of arrest onset |
| Timing | Aim to deliver the infant by 5 minutes after arrest onset (meaning the decision and incision must occur by 4 minutes); this is a maternal intervention — the goal is to relieve aortocaval compression to improve maternal hemodynamics |
| Rationale | Emptying the uterus immediately relieves aortocaval compression, improves venous return, and increases the effectiveness of CPR; it may be the single most effective intervention for achieving maternal ROSC |
| Location | Perform at bedside (in the ED resuscitation bay, OR, or labor and delivery room); do NOT transport the patient to the OR — this causes unacceptable delay |
| Technique | Vertical midline incision; classical (vertical) uterine incision; delivery of infant; uterus left open (not closed during active arrest); continue CPR throughout |
| Do NOT delay for | Surgical scrub, sterile field preparation, informed consent (emergency exception applies), fetal heart rate assessment, transport to OR |
| Fetal viability | Perimortem cesarean delivery should be performed even if the fetus is non-viable (<24 weeks), as the primary goal is maternal resuscitation through relief of aortocaval compression; fetal survival is a secondary benefit |
1.4 Common Causes of Cardiac Arrest in Pregnancy
| Cause | Key Features | Specific Treatment |
|---|
| Hemorrhage | Postpartum hemorrhage, placental abruption, uterine rupture, ectopic pregnancy | Massive transfusion protocol; surgical hemostasis; uterotonics |
| Amniotic fluid embolism | Sudden cardiovascular collapse during labor/delivery or shortly after; DIC; respiratory failure | Supportive care; aggressive blood product replacement; consider ECMO |
| Pulmonary embolism | Pregnancy is a hypercoagulable state; may present with sudden PEA arrest | Systemic thrombolysis (alteplase 50–100 mg); surgical embolectomy; ECPR |
| Pre-eclampsia/eclampsia | Seizures, severe hypertension, HELLP syndrome | Magnesium sulfate 4–6 g IV loading dose; definitive treatment is delivery |
| Peripartum cardiomyopathy | Heart failure in late pregnancy or early postpartum; may precipitate VF or cardiogenic shock | Standard ACLS; inotropes; mechanical support; post-arrest cardiac evaluation |
| Sepsis | Chorioamnionitis, endometritis, pyelonephritis | Source control; antibiotics; vasopressors |
2. Cardiac Arrest Associated with Drowning
Drowning-related cardiac arrest is primarily a hypoxic event. The mechanism is respiratory failure leading to hypoxemia and subsequent cardiac arrest, in contrast to most adult cardiac arrests which are primarily cardiac in origin. This distinction has important implications for management priorities.
2.1 Key Principles
| Principle | Detail |
|---|
| Oxygenation and ventilation are the priority | Unlike other cardiac arrest etiologies, ventilation should be provided early and aggressively; the standard compression-first approach is modified to prioritize rescue breathing |
| Compression-to-ventilation ratio | Standard 30:2 with bag-mask ventilation; provide 2 initial rescue breaths before starting compressions if trained and willing |
| Presenting rhythm | Most commonly asystole or PEA (reflecting prolonged hypoxia); VF is uncommon in pure drowning (suggests concomitant hypothermia, underlying cardiac disease, or electrolyte abnormality) |
| Water in the lungs | Do NOT attempt to drain water from the lungs (Heimlich maneuver on drowning victims is NOT recommended); positive-pressure ventilation will overcome the water in the airways |
| Hypothermia | Prolonged submersion often causes concurrent hypothermia; follow hypothermia resuscitation principles (see Section 3); extended resuscitation may be warranted |
| Cervical spine | Routine cervical spine immobilization is NOT recommended unless there is a clear mechanism for spinal injury (diving, surfing, watercraft accident); immobilization delays airway management and effective CPR |
| Post-ROSC | Anticipate pulmonary edema, ARDS, aspiration pneumonia, and hypothermia; early intubation and mechanical ventilation; aggressive temperature management |
| Prognosis | Submersion time is the strongest predictor of outcome; submersion <5 minutes with early bystander CPR has the best outcomes; submersion >25 minutes in warm water is almost uniformly fatal |
3. Cardiac Arrest in Hypothermia
Accidental hypothermia is defined as an unintentional drop in core body temperature below 35°C. Severe hypothermia (<30°C) causes progressive bradycardia, loss of shivering, coma, and ultimately cardiac arrest. Hypothermic cardiac arrest is unique because the cold itself is neuroprotective, and patients may survive prolonged arrests with good neurologic outcomes if managed appropriately.
3.1 Classification of Hypothermia
| Stage | Core Temperature | Clinical Features |
|---|
| Mild | 32–35°C (89.6–95°F) | Shivering, tachycardia, tachypnea, confusion, impaired judgment |
| Moderate | 28–32°C (82.4–89.6°F) | Shivering ceases, bradycardia, atrial fibrillation, decreased level of consciousness, paradoxical undressing |
| Severe | <28°C (<82.4°F) | Coma, very slow or absent pulse, VF susceptibility, risk of cardiac arrest |
| Profound | <24°C (<75.2°F) | Apparent death, may appear asystolic but recoverable |
3.2 Modifications to ACLS in Hypothermia
| Intervention | Modification |
|---|
| CPR | Standard high-quality CPR; if pulse assessment is difficult, begin CPR if no definite pulse is detected within 60 seconds (prolonged assessment allowed due to slow circulation) |
| Defibrillation | If VF is present, deliver one shock. If VF persists after one shock AND core temperature is <30°C, it is reasonable to defer further defibrillation until core temperature rises to ≥30°C. Once ≥30°C, standard defibrillation protocols apply |
| Medications | Below 30°C: withhold IV medications (epinephrine, amiodarone) — drugs are ineffective in the profoundly hypothermic myocardium and may accumulate to toxic levels as rewarming occurs. Between 30–35°C: administer medications at increased intervals (double the standard interval — e.g., epinephrine every 6–10 minutes instead of 3–5 minutes). Above 35°C: standard ACLS pharmacotherapy |
| Rewarming | Active rewarming is the definitive treatment; passive external rewarming for mild hypothermia; active external rewarming (forced warm air blankets, warm IV fluids) for moderate hypothermia; active internal (core) rewarming for severe hypothermia (warm IV fluids at 40–42°C, warm humidified oxygen, peritoneal lavage, pleural lavage, ECMO/cardiopulmonary bypass for severe/profound hypothermia with cardiac arrest) |
| Duration of resuscitation | Prolonged resuscitation is warranted — the cold brain is neuroprotected; patients have survived with good neurologic outcomes after hours of CPR in severe hypothermia; the rule “not dead until warm and dead” applies; resuscitation should generally continue until core temperature reaches 32–35°C or ECMO/bypass is initiated |
| ECMO/ECPR | Extracorporeal rewarming (ECMO or cardiopulmonary bypass) is the gold standard for severe hypothermic cardiac arrest; provides both circulatory support and rapid, controlled rewarming; survival rates of 50–100% have been reported in selected patients with hypothermic arrest |
3.3 Termination of Resuscitation in Hypothermia
- Do NOT terminate resuscitation in hypothermic patients using standard criteria
- Factors favoring continued resuscitation: witnessed arrest, submersion <60 minutes, no signs of obviously lethal injury, potassium <12 mEq/L
- Factors suggesting futility: potassium >12 mEq/L, completely buried in avalanche debris with packed airway, obvious signs of death (rigor mortis, decomposition)
4. Cardiac Arrest from Pulmonary Embolism
Massive pulmonary embolism is a common cause of PEA cardiac arrest and a potentially reversible etiology that warrants aggressive intervention including systemic thrombolysis during CPR.
4.1 Recognizing PE as the Cause of Arrest
| Clue | Details |
|---|
| Clinical history | Known DVT, recent surgery/immobilization, malignancy, hormonal therapy, prior PE/DVT, pregnancy |
| Arrest characteristics | Sudden PEA arrest (often narrow-complex PEA); sudden drop in ETCO2 (massive PE acutely reduces pulmonary blood flow); rapid cardiovascular collapse preceded by acute dyspnea |
| Point-of-care echo | Severe RV dilation; RV/LV ratio >1; McConnell sign (RV free wall akinesis with apical sparing); interventricular septum bowing into LV; may visualize thrombus in right heart or main pulmonary arteries |
| ETCO2 pattern | Very low ETCO2 despite good CPR quality (because blood is not reaching pulmonary vasculature for gas exchange); abrupt improvement in ETCO2 after thrombolysis suggests drug effect |
4.2 Thrombolysis During CPR for Suspected PE
| Parameter | Detail |
|---|
| Indication | Cardiac arrest with high clinical suspicion for massive PE (do not delay for confirmatory imaging — treat empirically based on clinical suspicion and ultrasound findings) |
| Alteplase (tPA) | 50 mg IV bolus (rapid infusion over 2–5 minutes); may give a second 50 mg bolus if no improvement after 15–30 minutes. Some protocols use 100 mg over 15 minutes (standard PE dosing), but the 50 mg bolus approach is preferred during arrest for simplicity and speed |
| Tenecteplase | 0.5 mg/kg IV bolus (single weight-based dose); max 50 mg; practical advantage of single-dose administration |
| Continue CPR | CPR must continue for at least 60–90 minutes after thrombolysis to allow the drug time to work; do NOT terminate resuscitation prematurely after thrombolytic administration |
| Bleeding risk | Thrombolysis during CPR increases bleeding risk, but in the setting of cardiac arrest this risk is acceptable given the alternative is certain death; CPR itself is NOT a contraindication to thrombolysis |
| Adjunctive heparin | Consider unfractionated heparin 80 units/kg IV bolus (or 5,000 units empiric bolus) concurrent with thrombolysis, though this is secondary to thrombolytic administration |
| Alternatives | Surgical embolectomy (if available and patient can be transported with ongoing CPR or mechanical CPR); catheter-directed therapy; ECPR as a bridge |
5. Cardiac Arrest from Tension Pneumothorax
Tension pneumothorax is a rapidly lethal condition in which progressive air accumulation in the pleural space causes mediastinal shift, compression of the contralateral lung, kinking of the great vessels, and obstruction of venous return. It is a common reversible cause of PEA arrest, particularly in trauma, mechanical ventilation, and central line placement.
5.1 Recognition During Cardiac Arrest
| Finding | Notes |
|---|
| Clinical | Unilateral absent breath sounds; tracheal deviation (late sign, may be absent during arrest); distended neck veins (may be absent if hypovolemic); difficulty ventilating (high airway pressures); subcutaneous emphysema |
| Ultrasound | Absent lung sliding on the affected side; absence of B-lines; presence of lung point (100% specific); stratosphere (barcode) sign on M-mode |
| In the intubated patient | Sudden increase in peak airway pressures; sudden decrease in ETCO2; hypotension; cardiac arrest |
5.2 Treatment During Cardiac Arrest
| Intervention | Technique |
|---|
| Needle decompression | 14-gauge, 3.25-inch (8 cm) angiocatheter inserted at the 4th–5th intercostal space, anterior axillary line (preferred site — better success rate and lower risk of mediastinal injury than the traditional 2nd intercostal space midclavicular line) or at the 2nd intercostal space midclavicular line; advance the needle over the top of the rib (to avoid the neurovascular bundle on the inferior rib margin); a rush of air confirms decompression |
| Finger thoracostomy | Preferred over needle decompression in the arrest setting (more definitive, higher success rate): make a 3–5 cm horizontal incision at the 4th–5th intercostal space anterior axillary line; blunt dissection through intercostal muscles; finger sweep into the pleural space; immediate release of tension |
| Tube thoracostomy | Definitive treatment; 28–36 Fr chest tube placed after initial decompression; connect to drainage system |
| Bilateral decompression | In traumatic cardiac arrest, consider bilateral finger thoracostomy empirically as part of the traumatic cardiac arrest protocol even without confirmed tension pneumothorax |
6. Cardiac Arrest from Cardiac Tamponade
Cardiac tamponade is the accumulation of fluid (blood, effusion) in the pericardial space causing compression of cardiac chambers and impaired filling. When it causes cardiac arrest, emergency pericardial decompression is the only potentially lifesaving intervention.
6.1 Recognition
| Finding | Details |
|---|
| Clinical (Beck’s triad) | Hypotension, muffled heart sounds, distended neck veins — though in cardiac arrest, these may be difficult to assess |
| Context | Penetrating thoracic trauma, blunt thoracic trauma, post-cardiac surgery, post-cardiac catheterization, malignant pericardial effusion, aortic dissection with rupture into pericardium, uremic pericarditis |
| Ultrasound | Pericardial effusion with right atrial and/or right ventricular diastolic collapse; IVC plethora; swinging heart |
6.2 Treatment During Cardiac Arrest
| Intervention | Technique |
|---|
| Pericardiocentesis | Ultrasound-guided subxiphoid approach: 18-gauge spinal needle or catheter-over-needle advanced at 30–45° angle toward the left shoulder, aspirating continuously; withdrawal of even 15–25 mL of blood may restore cardiac function; leave a catheter in place for ongoing drainage |
| Emergency thoracotomy | In traumatic cardiac tamponade (penetrating trauma), emergency department thoracotomy with pericardotomy is the definitive intervention; left anterolateral thoracotomy → pericardotomy → direct cardiac repair if needed |
| Considerations | CPR is relatively ineffective in cardiac tamponade (the heart cannot fill despite compressions); early decompression is the only effective therapy; do not delay for additional diagnostic studies |
7. Cardiac Arrest Associated with Opioid Overdose
The opioid epidemic has dramatically increased the incidence of opioid-related cardiac arrests. The primary mechanism is respiratory depression leading to hypoxemia, hypercarbia, and respiratory arrest, which if untreated progresses to cardiac arrest.
7.1 Key Principles
| Principle | Detail |
|---|
| Mechanism | Opioids → respiratory depression → hypoxemia → respiratory arrest → cardiac arrest (hypoxic mechanism, similar to drowning) |
| Presenting rhythm | Typically asystole or PEA (reflecting prolonged hypoxia); VF is uncommon |
| Priority | Ventilation and oxygenation are the immediate priorities; provide rescue breaths/bag-mask ventilation; secure the airway |
| Standard ACLS is required | Naloxone alone does not reverse cardiac arrest; once the patient is in full cardiac arrest (pulseless), standard ACLS with CPR, defibrillation (if shockable rhythm), and epinephrine is required |
7.2 Naloxone Administration
| Parameter | Detail |
|---|
| Mechanism | Competitive mu-opioid receptor antagonist; reverses respiratory depression, sedation, and hypotension |
| Dose — respiratory arrest (not yet cardiac arrest) | 0.4–2 mg IV/IO/IM/SC/IN; titrate to restore adequate ventilation (not necessarily full consciousness); repeat every 2–3 minutes as needed |
| Dose — during cardiac arrest | 2 mg IV/IO; administer as an adjunct to standard ACLS; continue CPR — naloxone is not a substitute for chest compressions and defibrillation |
| Intranasal (IN) route | 4 mg IN (using commercially available nasal atomizer device); useful for bystander and first-responder administration |
| Intramuscular (IM) route | 0.4 mg IM (standard dose) or auto-injector formulations (0.4 mg or 2 mg IM); onset approximately 5 minutes |
| Duration of action | 30–90 minutes; shorter than most opioids → re-sedation and recurrent respiratory depression may occur; observe patient for extended period (at least 4 hours for short-acting opioids, longer for long-acting opioids or sustained-release formulations) |
| Cautions | May precipitate acute withdrawal in opioid-dependent patients (agitation, vomiting, tachycardia, hypertension); in cardiac arrest, this is not a concern; pulmonary edema may occur after naloxone reversal (mechanism debated — may be related to massive sympathetic surge) |
8. Cardiac Arrest from Hyperkalemia
Hyperkalemia is one of the most common and treatable metabolic causes of cardiac arrest. It primarily affects patients with renal failure, adrenal insufficiency, rhabdomyolysis, tumor lysis syndrome, and those taking potassium-sparing diuretics, ACE inhibitors, or potassium supplements.
8.1 ECG Progression of Hyperkalemia
| Potassium Level | ECG Changes |
|---|
| 5.5–6.5 mEq/L | Peaked, narrow, symmetrical T waves (earliest sign) |
| 6.5–7.5 mEq/L | PR prolongation; flattened P waves; widened QRS |
| 7.5–8.0 mEq/L | Loss of P waves; further QRS widening; intraventricular conduction delay |
| >8.0 mEq/L | Sine wave pattern (merging of widened QRS with T wave); VF; asystole |
8.2 Treatment of Hyperkalemia During Cardiac Arrest
| Intervention | Dose | Onset | Mechanism | Notes |
|---|
| Calcium chloride 10% | 1–2 g (10–20 mL) IV over 2–5 minutes (push during arrest) | 1–3 minutes | Membrane stabilization — does NOT lower potassium; protects myocardium from effects of hyperkalemia | First-line treatment — administer immediately; may repeat if ECG changes persist; calcium gluconate (3 g IV) is an alternative but provides less ionized calcium per dose |
| Sodium bicarbonate | 50 mEq (1 ampule of 8.4%) IV | 15–30 minutes | Drives potassium intracellularly via alkalinization | Most effective when preexisting acidosis is present; flush line between calcium and bicarbonate (precipitation risk) |
| Insulin + dextrose | Regular insulin 10 units IV + 25 g dextrose (50 mL D50W) IV | 15–30 minutes | Drives potassium intracellularly via insulin-mediated Na/K-ATPase stimulation | Monitor glucose; if patient has blood glucose >250 mg/dL, insulin may be given without concurrent dextrose |
| Albuterol | 10–20 mg nebulized (or 0.5 mg IV — IV preparation not available in all countries) | 15–30 minutes | Beta-2 stimulation drives potassium intracellularly | Additive effect with insulin/dextrose; may cause tachycardia |
| Sodium polystyrene sulfonate (Kayexalate) | 15–30 g PO or per rectum | Hours | Ion exchange resin; removes potassium from body | NOT useful in acute cardiac arrest (too slow onset); primarily for post-ROSC management |
| Emergent hemodialysis | — | Immediate (once initiated) | Directly removes potassium from blood | Definitive treatment; arrange emergently; consider in refractory hyperkalemia or anuric renal failure |
8.3 Order of Treatment During Arrest
- Calcium (immediate membrane stabilization)
- Sodium bicarbonate (if acidotic or prolonged arrest)
- Insulin + dextrose (intracellular shift)
- Standard ACLS (CPR, epinephrine, defibrillation if shockable)
- Arrange emergent dialysis (definitive treatment)
9. Cardiac Arrest from Anaphylaxis
Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction that can cause cardiovascular collapse and cardiac arrest through massive vasodilation, capillary leak, bronchospasm, and direct myocardial depression.
9.1 Management During Cardiac Arrest
| Intervention | Dose/Details |
|---|
| Epinephrine — cardiac arrest dose | 1 mg (1:1,000 concentration or 1 mg/mL) IV/IO every 3–5 minutes per standard cardiac arrest protocol; this is the standard ACLS dose, NOT the IM anaphylaxis dose |
| Epinephrine — pre-arrest (anaphylaxis dose) | 0.3–0.5 mg IM (1:1,000 or 1 mg/mL) into the anterolateral thigh; repeat every 5–15 minutes as needed; the IM route is first-line for anaphylaxis that has not yet progressed to cardiac arrest |
| Volume resuscitation | Aggressive crystalloid boluses (1–2 L or more); massive capillary leak in anaphylaxis can cause distributive shock requiring 4–8 L of crystalloid in severe cases |
| Airway management | Early intubation if angioedema is present — laryngeal edema may progress rapidly, making subsequent intubation impossible; consider surgical airway (cricothyrotomy) if unable to intubate |
| Vasopressin | 40 units IV bolus; consider for refractory vasodilatory shock in anaphylaxis (not standard in cardiac arrest, but may be useful as adjunct in anaphylaxis-specific distributive shock) |
| Glucagon | 1–5 mg IV over 5 minutes; useful in patients taking beta-blockers who are refractory to epinephrine (glucagon has positive chronotropic and inotropic effects independent of beta-receptors) |
| Antihistamines (H1 + H2) | Diphenhydramine 25–50 mg IV + ranitidine 50 mg IV (or famotidine 20 mg IV); adjunctive only — do NOT give instead of epinephrine; these do not reverse anaphylaxis but reduce ongoing histamine effects |
| Corticosteroids | Methylprednisolone 125 mg IV or hydrocortisone 200 mg IV; do NOT delay epinephrine for steroids; steroids have no acute effect but may help prevent biphasic reactions (4–12 hours later) |
| Bronchodilators | Albuterol 2.5–5 mg nebulized for bronchospasm refractory to epinephrine |
| Prolonged CPR | Anaphylactic cardiac arrest patients may respond to prolonged resuscitation; the underlying cause is vasodilation/volume depletion rather than irreversible myocardial injury; aggressive epinephrine and volume may restore perfusion |
10. Cardiac Arrest from Electrolyte Emergencies
10.1 Hypokalemia
| Parameter | Detail |
|---|
| Cardiac arrest mechanism | Severe hypokalemia (<2.5 mEq/L) causes QT prolongation, U waves, ventricular ectopy, torsades de pointes, VF |
| Treatment during arrest | Potassium chloride 40 mEq IV; may infuse rapidly through central line (10 mEq over 5 minutes through central line is acceptable during arrest); 2 mEq/min through peripheral IV is generally considered the maximum safe rate; concurrent magnesium sulfate 2 g IV (hypomagnesemia frequently accompanies hypokalemia and prevents potassium correction until magnesium is repleted) |
10.2 Hypomagnesemia
| Parameter | Detail |
|---|
| Cardiac arrest mechanism | Severe hypomagnesemia causes QT prolongation, torsades de pointes, refractory hypokalemia, refractory hypocalcemia |
| Treatment during arrest | Magnesium sulfate 1–2 g IV push; may repeat |
10.3 Hypocalcemia
| Parameter | Detail |
|---|
| Cardiac arrest mechanism | Severe hypocalcemia (ionized calcium <0.5 mmol/L) causes QT prolongation, hypotension, cardiomyopathy |
| Treatment during arrest | Calcium chloride 10% 1 g IV or calcium gluconate 10% 3 g IV; repeat as needed guided by ionized calcium levels |
| Common causes in critical illness | Massive transfusion (citrate chelation), pancreatitis, sepsis, tumor lysis syndrome |
10.4 Hypermagnesemia
| Parameter | Detail |
|---|
| Cardiac arrest mechanism | Severe hypermagnesemia (>8 mg/dL) causes progressive neuromuscular blockade, respiratory depression, bradycardia, heart block, cardiac arrest |
| Treatment during arrest | Calcium chloride 10% 1–2 g IV (directly antagonizes magnesium at the neuromuscular junction and cardiac membrane); IV normal saline for renal magnesium excretion; emergent dialysis if renal failure |
| Context | Most commonly iatrogenic (magnesium sulfate infusion for pre-eclampsia or tocolysis); renal failure with magnesium-containing antacids or laxatives |
11. Cardiac Arrest in Asthma (Status Asthmaticus)
Cardiac arrest in severe asthma is caused by hypoxemia, dynamic hyperinflation (auto-PEEP/breath stacking), and tension physiology from air trapping.
11.1 Modifications to ACLS
| Intervention | Detail |
|---|
| Ventilation | In intubated patients: disconnect from ventilator and allow complete passive exhalation (bilateral manual chest compression may help expel trapped air); reduce ventilation rate; extend expiratory time |
| Auto-PEEP | Severe auto-PEEP mimics tension pneumothorax hemodynamically; disconnecting the circuit allows decompression |
| Bilateral decompression | Consider empiric bilateral needle decompression/finger thoracostomy if auto-PEEP management fails (pneumothorax is common in severe asthma) |
| Epinephrine | Standard dosing; epinephrine’s bronchodilating properties (beta-2 effect) provide additional benefit |
| Magnesium | Magnesium sulfate 2 g IV (bronchodilatory effect); reasonable to administer during arrest |
| Bronchodilators | Continuous albuterol nebulization; ipratropium; may be administered via ETT during CPR if ventilation circuit is in place |
| Ketamine | Ketamine 1–2 mg/kg IV has bronchodilatory properties; may be used for sedation/induction if needed; some practitioners use it as a rescue bronchodilator |
| ECPR | Consider for refractory cardiac arrest from asthma; the underlying process is reversible if the patient can be supported through the acute episode |
References