Every ACLS provider can recite the H's and T's. Hypovolemia, Hypoxia, Hydrogen ion, Hypo/Hyperkalemia, Hypothermia. Tension pneumothorax, Tamponade, Toxins, Thrombosis pulmonary, Thrombosis coronary.
But reciting a list is not the same as recognizing one at the bedside during a code.
"Reciting a list under fluorescent classroom lights is not the same skill as finding the cause under a strip of red-flashing monitor alarms."
In a PEA arrest, the rhythm on the monitor tells you almost nothing. There is organized electrical activity and no pulse — which means the problem is not the conduction system. Something is stopping the heart from filling, from emptying, or from contracting at all. Compressions and epinephrine buy you time. Finding the cause is the treatment.
The 10 causes at a glance
Hypovolemia
Hemorrhage, GI losses, sepsis, burns. Fluids and blood.
Hypoxia
Airway obstruction, failed oxygenation, respiratory arrest preceding the code. Confirm the tube, confirm the chest rises.
Hydrogen ion (acidosis)
Prolonged arrest, DKA, renal failure. Ventilation first; bicarbonate is situational, not routine.
Hypo/Hyperkalemia
Dialysis patients, crush injury, DKA. Calcium stabilizes the membrane before anything else.
Hypothermia
Environmental exposure, drowning, prolonged extrication. Warm aggressively; do not call it early.
Tension pneumothorax
Trauma, central line, barotrauma on the vent. Needle decompression, then a chest tube.
Tamponade, cardiac
Post-cardiac-surgery, malignancy, uremia, penetrating trauma. Pericardiocentesis.
Toxins
Beta-blockers, calcium channel blockers, tricyclics, local anesthetic, opioids. Each has a specific antidote.
Thrombosis, pulmonary
Massive PE. Sudden collapse, RV strain, often a recent surgery or immobility history.
Thrombosis, coronary
Massive MI. The arrest is the presentation; the cath lab is the treatment.
Stop searching all ten. Search the likely three.
Ten causes is too many to work through while someone is doing compressions. Under stress, a ten-item list becomes no list at all — you freeze, or you default to the one you happen to remember.
The clinicians who actually find reversible causes do something different: they let the patient's story narrow the list before they start looking. A dialysis patient who misses a session and arrests is hyperkalemia until proven otherwise. A trauma patient who arrests after intubation is a tension pneumothorax until you decompress. A post-op cardiac surgery patient who arrests on the unit is tamponade until you open the chest.
The H's and T's are not a checklist to recite in order. They are a differential to be weighted by the history you already have. Two or three causes will account for nearly every reversible arrest you personally witness — and which two or three depends entirely on where you work.
The QRS gives you a shortcut
In PEA, the width of the complex is one of the few free pieces of information you get, and most providers never use it.
A narrow-complex PEA generally points to a mechanical or obstructive problem — the heart is contracting but has nothing to pump, or cannot fill. Think tamponade, tension pneumothorax, massive PE, and severe hypovolemia. These are right-ventricular problems, and several of them are visible on ultrasound within seconds.
A wide-complex PEA generally points to a metabolic or toxic problem — the myocardium itself is poisoned. Think hyperkalemia, sodium channel blocker toxicity, and profound acidosis. These are treated pharmacologically, and calcium is often the first move.
Narrow and empty, wide and poisoned. It is not an absolute rule, but as a first cut under pressure it directs your hands to the right half of the list in about two seconds — which is roughly all the thinking time you have.
Look during the rhythm check, not between codes
The single biggest change in how reversible causes get found is point-of-care ultrasound used during the pulse check, in the ten seconds you already stop compressions. A subxiphoid or parasternal view answers several questions at once, and it answers them faster than any lab.
- Is there a pericardial effusion? A large effusion with a collapsing right ventricle is tamponade. This is the finding that changes management immediately — and it is the easiest one to see.
- Is the right ventricle huge? A dilated, strained RV with a small underfilled LV suggests massive PE. In the right clinical context this is the moment to discuss thrombolysis during the arrest.
- Is the heart moving at all? True cardiac standstill on ultrasound carries a very poor prognosis and informs how long you continue. Coordinated contraction with no palpable pulse is pseudo-PEA — that patient needs pressure support, not just more epinephrine.
- Is the IVC flat? A collapsed IVC supports hypovolemia and points you toward volume and blood rather than more drugs.
- Is there lung sliding on both sides? Absent sliding on one side, in a patient who is hard to bag and has tracheal deviation or a recent line, is your tension pneumothorax. Decompress before you finish the discussion.
None of this replaces compressions, and none of it justifies a longer pause. If the look takes more than ten seconds, the look is hurting the patient. That constraint is exactly why it must be practised before it matters.
The three that reward you most
Hyperkalemia is the reversible cause most often missed and most dramatically fixed. If the history fits — dialysis, crush injury, renal failure, a wide bizarre complex — give calcium immediately to stabilize the myocardium, then move potassium intracellularly. You do not wait for a confirmatory lab in an arrest.
Tension pneumothorax is the one where hesitation costs the most. If the clinical picture fits, decompress. A needle in a chest that did not need one is a small harm; a missed tension is a dead patient.
Hypovolemia is the one people treat too timidly. In haemorrhagic arrest, crystalloid is a holding measure — the treatment is blood and control of the bleeding source. Do not run litres of saline into a patient who needs an operating room.
PEA scenarios where the cause is hidden in the history and the vitals respond to what you actually do. You can give epinephrine on a metronome and watch the patient die, or find the hyperkalemia and watch the complex narrow. Failing safely, repeatedly, is what builds the reflex.
What every clinician should remember
- In PEA, compressions and epinephrine buy time — identifying the cause is the actual treatment
- Weight the differential by the patient's history before you start searching; two or three causes cover most real arrests
- Narrow-complex PEA suggests obstructive or mechanical causes; wide-complex suggests metabolic or toxic
- Use point-of-care ultrasound during the pulse check you are already taking — never lengthen the pause
- Hyperkalemia, tension pneumothorax and hypovolemia are the highest-yield finds; treat on clinical suspicion, not on confirmation