The “T” causes of reversible cardiac arrest are five conditions that emergency teams systematically check for when someone’s heart stops. They come from a well-known mnemonic called the “Hs and Ts,” which lists 12 total reversible causes of cardiac arrest: seven starting with H and five starting with T. The five Ts are tension pneumothorax, cardiac tamponade, toxins, thrombosis from a pulmonary embolism, and thrombosis from a heart attack. Each one has a specific treatment that can restart the heart if identified quickly enough.
Tension Pneumothorax
A tension pneumothorax happens when air leaks into the space between the lung and the chest wall, then gets trapped. With each breath, more air accumulates but can’t escape, creating increasing pressure that compresses the heart and the opposite lung. This pressure eventually prevents blood from returning to the heart, leading to cardiac arrest.
The physical signs are distinctive: absent breath sounds on the affected side, a chest that sounds hollow when tapped, visible neck vein swelling, and sometimes the windpipe shifting away from the affected side. Severe respiratory distress, low blood pressure, and a rapid heart rate develop quickly. In some cases, air leaks under the skin, creating a crackling sensation you can feel.
Treatment is immediate decompression, meaning releasing that trapped air. In an emergency, a needle is inserted into the chest at the second rib space along the midclavicular line (roughly below the collarbone). When time allows, the fifth rib space along the front of the armpit is preferred because it has higher success rates and fewer complications. This is followed by placement of a chest tube for ongoing drainage.
Cardiac Tamponade
Cardiac tamponade occurs when fluid, usually blood, fills the sac surrounding the heart. As fluid accumulates, it squeezes the heart from the outside, preventing the chambers from filling properly. Eventually the heart can’t pump enough blood to sustain life.
The classic presentation is known as Beck’s triad: low blood pressure, swollen neck veins, and muffled heart sounds. In practice, all three signs aren’t always present, which is why bedside ultrasound has become essential during resuscitation. On ultrasound, the earliest sign is collapse of the right atrium, which is 94% sensitive and nearly 100% specific when it lasts more than one-third of the heartbeat cycle. A swollen, non-collapsing vena cava (the large vein feeding the heart) is another strong clue, with sensitivity around 95-97%.
The fix is pericardiocentesis: draining the fluid from around the heart with a needle. Once pressure is relieved, the heart can fill and pump again, sometimes producing an immediate return of circulation.
Toxins
Toxin-related cardiac arrest covers a broad category, from drug overdoses to chemical exposures. What makes this cause unique among the Ts is that the treatment depends entirely on identifying the specific substance involved. Several common culprits have direct reversal agents.
Opioid overdoses can be reversed with naloxone. Older antidepressant overdoses (tricyclics) cause dangerous heart rhythm changes that respond to sodium bicarbonate. Beta-blocker and calcium channel blocker overdoses, both common heart medications, can cause the heart to slow dangerously or stop. Treatment involves calcium, glucagon, and high-dose insulin therapy. Digoxin toxicity, which causes life-threatening rhythm problems, is treated with a specific antibody fragment that binds and neutralizes the drug.
Cyanide poisoning, whether from industrial exposure or smoke inhalation, has its own antidote kit. One agent binds cyanide to form vitamin B12, while others work through different chemical pathways to neutralize it. Organophosphate poisoning from pesticides or nerve agents is treated with atropine to block the toxic buildup of a nerve-signaling chemical, plus a second drug to reactivate the enzyme that’s been disabled.
The key point for toxin-related arrest is that standard resuscitation alone often won’t work. The underlying poisoning must be identified and counteracted. Emergency teams look for clues like pill bottles, track marks, chemical odors, or bystander information to guide treatment.
Thrombosis: Pulmonary Embolism
A massive pulmonary embolism occurs when a large blood clot blocks the arteries feeding the lungs. The right side of the heart suddenly can’t push blood through, pressure builds, and the heart fails. This is one of the more common causes of cardiac arrest that initially looks unexplained, especially in patients with risk factors like recent surgery, prolonged immobility, or a history of blood clots.
Diagnosing a massive PE during cardiac arrest is challenging. Bedside ultrasound can show an enlarged right ventricle, a flattened wall between the heart’s chambers (called the D-sign), and sometimes a visible clot in the right side of the heart. A very low reading on the carbon dioxide monitor attached to the breathing tube also suggests massive PE, since blood isn’t reaching the lungs to exchange gases. However, the absence of these findings doesn’t rule it out, so clinical suspicion matters enormously.
Treatment involves clot-dissolving drugs given during CPR. The most commonly used approach is a 50 mg bolus of alteplase, based on British Thoracic Society guidelines, which can be started on clinical suspicion alone when cardiac arrest is imminent. Other protocols use 100 mg infused over two hours. CPR should continue for an extended period after these drugs are given, as it can take time for the clot to dissolve. This is one situation where prolonged resuscitation efforts are specifically justified.
Thrombosis: Heart Attack
A heart attack, or myocardial infarction, happens when a blood clot blocks a coronary artery and cuts off blood flow to part of the heart muscle. If enough muscle is affected, the heart can develop a fatal rhythm or simply stop pumping effectively. Heart attacks are among the most common triggers of cardiac arrest overall.
When a heart attack is suspected as the cause of cardiac arrest, the priority after restoring a heartbeat is getting the blocked artery open. Percutaneous coronary intervention, a procedure where a catheter is threaded to the blockage and a stent is placed, is the preferred approach. Multiple studies have shown that immediate catheterization after return of a heartbeat is safe and associated with significantly better survival, particularly when the heart tracing shows the classic pattern of ST-elevation (a specific electrical change indicating a major blockage).
This means that after successful resuscitation, patients are often taken directly to the cardiac catheterization lab rather than an intensive care unit. Speed matters: the longer heart muscle goes without blood flow, the more permanent damage occurs.
How These Causes Are Identified During CPR
Emergency teams don’t work through the Ts randomly. Bedside ultrasound has transformed how quickly these causes can be identified during active chest compressions. Several structured protocols exist, all sharing the same principle: during brief pauses in CPR, a quick ultrasound view of the heart and lungs can reveal tamponade, tension pneumothorax, massive PE, or signs of severe blood loss within seconds.
For pneumothorax, a single ultrasound view of the upper chest can detect the absence of normal lung sliding, a finding that’s fast and reliable. For tamponade, the subxiphoid view (looking at the heart from just below the breastbone) is preferred because it doesn’t interfere with chest compressions. For PE, an enlarged right ventricle with a flattened septum points toward the diagnosis. Toxin exposure and heart attack are identified more through clinical context, medication history, and ECG patterns than through ultrasound.
The Ts are called “reversible” for a reason: each one has a targeted intervention that addresses the root cause rather than just supporting the heart. Identifying which T is responsible is often the difference between a resuscitation that succeeds and one that doesn’t.