Cardiac Electrophysiology, Cardiac Arrest, and First Aid

1. Brief Introduction to Cardiac Electrophysiology

Cardiac function can be broken down into three layers:

1.1 Electrical activity

The normal pacemaker is the sinoatrial node (SA node). The impulse travels in sequence through:

the atria
the atrioventricular node (AV node)
the bundle of His (His bundle)
the left and right bundle branches
the Purkinje fibers (Purkinje system)

completing orderly depolarization and repolarization.

1.2 Mechanical contraction

The electrical signal triggers excitation–contraction coupling in cardiomyocytes, producing atrial and ventricular contraction.

1.3 Hemodynamic output

The ultimate goal is not “having electricity” or “having contraction,” but:

effective stroke volume
effective arterial pressure
perfusion of vital organs

1.4 Clinical key points about the three layers

Electrical activity does not mean there is a pulse.
Weak myocardial contraction does not mean there is effective circulation.
Having a rhythm does not mean that rhythm can sustain perfusion.

This is the key to understanding PEA and pseudo-PEA (pulseless electrical activity, discussed below).

References:

NHLBI: How the Heart Beats

1.5 Cardiac vectors and ECG leads

When we look at the current in an ordinary wire, we can often simplify it as a vector propagating along the wire’s direction, because the wire is thin, regular, and the problem is essentially one-dimensional. But the human body is not like that. The body is not a single line, but a three-dimensional, irregularly shaped volume conductor in which different tissues have different electrical conductivities. Once the electrical activity generated by the heart reaches the body surface, it is no longer “current flowing along a single wire,” but rather forms a complex potential distribution throughout the torso. This cannot be simplified to a single vector; it is a vector field. What the surface electrodes measure is not “the direction of current in some wire,” but the potential difference between different positions on the body surface. To make things easier to understand clinically, we approximate the heart’s overall electrical activity at any instant as a single “instantaneous integrated cardiac vector,” and then look at how this vector projects onto each lead direction.

When we measure the ECG signal in a particular direction, what we get is necessarily the projection, in that direction, of the sum (a vector sum, obeying the parallelogram rule) of the cardiac vectors generated by all depolarizing myocytes. Of course, this vector obeys all the rules of spatial geometry (linear algebra), so we can also project first and then add or subtract algebraically.

References:

2. Distinguishing Different Cardiac Problems

2.1 Bradycardia

By definition, this usually refers to an adult heart rate < 60/min. But whether it constitutes a clinical problem depends not on the number itself, but on whether it causes hypoperfusion.

Possible manifestations

dizziness
fatigue
syncope
chest pain
hypotension
altered consciousness

Common causes

sinus node dysfunction
atrioventricular block
medications (β-blockers, non-dihydropyridine calcium channel blockers, digoxin, etc.)
ischemia
electrolyte disturbances
thyroid dysfunction
elevated vagal tone

Clinical essence

Bradycardia is “slow,” not “stopped.” As long as effective circulation is preserved, it is not cardiac arrest.

References:

2.2 Ventricular fibrillation (VF)

Definition: the ventricles exhibit extremely rapid, disorganized, fragmented electrical activity, and the ventricles cannot produce synchronized, effective contraction.

Physiological consequences

no effective cardiac output
no effective arterial pressure
loss of consciousness within a very short time
rapid death without intervention

Clinical classification

a cardiac arrest rhythm
a shockable rhythm

Core mechanism

The problem in VF is not “no electricity,” but that the electrical activity is too chaotic to organize effective mechanical pumping.

References:

2.3 Pulseless ventricular tachycardia (pVT)

Definition: a rapid ventricular rhythm is present, but because the rate is too fast or mechanical efficiency is extremely poor, no pulse can be palpated and there is no effective circulation.

Clinical classification

a cardiac arrest rhythm
a shockable rhythm

Difference from pulse-present VT

The difference does not lie in the ECG morphology itself, but in whether effective perfusion is present.

VT with a pulse: managed as unstable/stable tachyarrhythmia
Pulseless VT: managed as cardiac arrest

2.4 Pulseless electrical activity (PEA)

Definition: organized electrical activity is present, but there is no effective mechanical output — that is, no pulse and no effective circulation.

Clinical key points

PEA is the most easily misunderstood. It is not “the ECG looks like there’s something there, so the patient is okay.” On the contrary, it indicates:

Electrical activity is still present, but pumping has failed.

Common causes

Often related to reversible causes, classically remembered with Hs and Ts.

Clinical classification

a cardiac arrest rhythm
a non-shockable rhythm

2.5 Asystole

Definition: no recognizable organized cardiac electrical activity — colloquially, a “flatline.”

Clinical classification

a cardiac arrest rhythm
a non-shockable rhythm

Key point

Asystole is not “even more in need of a shock”; rather, it should not be defibrillated blindly. Its pathway is CPR + drugs + identifying the cause, not the defibrillation pathway.

2.6 Cardiac arrest

Cardiac arrest is a clinical state, not the name of any specific ECG.

Core definition:

the heart loses effective pumping function
there is no effective circulation
clinical presentation: unresponsive, no normal breathing/only agonal gasping, no pulse

Underlying rhythms can be

VF
pVT
PEA
asystole

Therefore:

VF is a rhythm; cardiac arrest is a state.

References:

3. The Core of Cardiac Arrest Management: “Is It Shockable?”

In ACLS, the most important distinction is not “fast or slow,” but:

3.1 Shockable rhythms

VF
pVT

Core management:

immediate defibrillation
immediately resume CPR afterward
repeat assessment and advanced life support per the algorithm

3.2 Non-shockable rhythms

PEA
asystole

Core management:

high-quality CPR
early epinephrine (in healthcare settings)
search for reversible causes
no routine defibrillation

References:

AHA Adult Cardiac Arrest Algorithm (2025)

4. Pacemaker vs. Defibrillator: Completely Different Mechanisms

4.1 Pacemaker

Essence

Delivers low-energy regular electrical pulses, providing rhythmic drive when the heart’s own pacing or conduction fails.

Main indications

symptomatic sinus bradycardia
high-grade or complete atrioventricular block
certain severe conduction system diseases

Physiological significance

From an electrophysiological standpoint, a pacemaker does not provide the mechanical force needed for cardiac contraction, but instead acts as an exogenous trigger pulse source.

The pacemaker’s “signal compensation” essence: why it works for bradycardia but not for asystole or VF

Mechanism for bradycardia (signal compensation): When the body’s own SA node (the master pacemaker) fires too slowly or there is conduction block, the cardiomyocytes’ resting membrane potential is usually normal, and the conduction pathways (such as the His–Purkinje system) retain their ability to conduct signals. At this point, the pacemaker delivers a low-energy electrical pulse, locally altering the transmembrane potential of the myocytes in contact with the electrode and bringing them to the threshold potential, thereby evoking an action potential. This local action potential then propagates along gap junctions between cardiomyocytes in a domino-like chain of depolarization, completing one heartbeat. Thus, the pacemaker, on the premise that the underlying network is intact, precisely fills in the missing “trigger signal.”
Why it cannot handle asystole or VF:
- Asystole: At this stage cardiomyocytes typically suffer severe ischemia and hypoxia; transmembrane ion pump function fails and the ion concentration gradients across the cell membrane are lost. Even if the pacemaker delivers a local stimulus, the cells cannot generate or conduct an action potential — the system has completely lost excitability.
- Ventricular fibrillation: The ventricles contain numerous chaotic micro-reentry circuits and ectopic pacemakers. The entire myocardial network is occupied by high-frequency, disorganized electrical signals. Inputting a weak pacing pulse here would simply be drowned out in the system’s enormous electrophysiological “noise,” and would never achieve global effective capture.

References:

NHLBI: Pacemakers - How They Work

4.2 Defibrillator

Essence

Delivers a high-energy electric shock with the goal of terminating life-threatening rapid ventricular arrhythmias by depolarizing the abnormal electrical activity en masse, creating the conditions for the SA node or another organized pacemaker to take over.

Main indications

VF
pVT

Device types

AED (automated external defibrillator)
ICD (implantable cardioverter-defibrillator)

Physiological significance

A defibrillator is not a device that “restarts a stopped heart”; rather:

It terminates chaotic electrical activity, creating the chance for an organized rhythm to resume. The reason it cannot “restart a stopped heart” is the same as in the previous section under “Why it cannot handle asystole or VF.” The main difference between a defibrillator and a pacemaker lies in the magnitude of electrical energy:

Electrophysiological basis of the energy threshold: the underlying logic of defibrillation vs. pacing

The vast difference in energy requirements between pacing and defibrillation arises because their goals in intervening on the electrophysiological system are fundamentally different: pacing aims at “local excitation,” whereas defibrillation aims at a “global forced reset.”

Physical basis of pacing’s low energy (threshold of local excitation): A pacemaker typically requires only microjoule-level energy. Its task is minimal — only to depolarize the cardiomyocytes within a few millimeters around the electrode tip. Once the local cellular potential threshold is exceeded, the subsequent spread of the signal depends entirely on the heart’s own ion channel cascade (i.e., the heart uses its own electrochemical potential to propagate the signal).
Why defibrillation requires high energy (global depolarization and state reset): A defibrillator typically delivers up to several hundred joules. The essence of defibrillation is not to start a heartbeat, but to forcibly terminate all chaotic electrical activity. A high-energy instantaneous direct-current pulse must create an electric field strong enough to instantaneously penetrate the entire heart, forcing the vast majority of cardiomyocytes to undergo global depolarization within the same millisecond and then collectively enter the absolute refractory period. This forceful “state reset” interrupts all abnormal reentrant discharges, creating a brief silent window in which the highest-level pacemaker (the SA node) can resume rhythm control of the system.
Why pacing energy cannot defibrillate: The electric field of a low-energy pacing pulse is extremely limited; it cannot cover the entire myocardial mass, much less force ectopic cell populations that are currently excited or refractory to synchronize. The pacemaker therefore cannot quell the electrophysiological storm of VF; this requires the high-voltage DC field of a defibrillator to produce a forced reset at the physical level.

References:

4.3 Side-by-side comparison

Item	Pacemaker	Defibrillator
Energy level	Low energy	High energy
Target problem	Too slow, poor conduction	Too chaotic, lethal ventricular tachyarrhythmias
Typical indications	Symptomatic bradyarrhythmias	VF / pVT
Physiological role	Provides the beat	Terminates abnormal rhythms
Routine use in asystole/PEA?	No	No

5. On-scene First-Aid Workflow for Cardiac Arrest

5.1 Recognition

Typical on-scene findings highly suggestive of cardiac arrest:

sudden collapse
unresponsive
no normal breathing or only agonal gasping
no pulse (assessed by trained personnel)

5.2 Activate the chain of survival

call emergency services
ask a bystander to fetch an AED
start CPR immediately

5.3 Key points of high-quality CPR

compression rate: 100 to 120 per minute
compression depth: at least 5 cm, avoid exceeding 6 cm
minimize interruptions
allow full chest recoil
trained rescuers can do 30:2
untrained rescuers should at least do Hands-Only CPR

The physiological role of CPR

The primary task of CPR is not “to restore the rhythm to normal,” but:

to provide minimal coronary perfusion
to maintain cerebral perfusion
to slow further myocardial energy depletion
to create the conditions for subsequent defibrillation or ROSC

References:

5.4 The role of the AED

The essence of an AED is not “an automatic resurrection machine,” but:

recognize the rhythm
determine whether it is a shockable rhythm
recommend a shock only when appropriate

When the AED says “shock advised”

clear contact
deliver the shock
immediately resume CPR

When the AED says “no shock advised”

continue CPR
do not assume that “no shock” means “no hope” or “nothing wrong”

References:

6. Three Categories of Outcomes After CPR

After every roughly 2 minutes of CPR, the core clinical questions are only two:

Is there ROSC?
If no ROSC, is the rhythm shockable?

So they naturally divide into three categories:

6.1 Category 1: ROSC (return of spontaneous circulation)

Definition: restoration of spontaneous circulation. What matters is not whether the ECG looks pretty, but whether effective perfusion has been achieved, for example:

a palpable pulse
a measurable blood pressure
recovery of an arterial waveform
improvement in circulatory signs

Management

Enter post-cardiac arrest care:

airway and oxygenation management
blood pressure support
12-lead ECG
search for the cause
ICU management
coronary evaluation/intervention as needed, etc.

References:

AHA Adult Post–Cardiac Arrest Care Algorithm

6.2 Category 2: No ROSC, but VF / pVT

This is shockable.

Management

defibrillate immediately
resume CPR immediately after the shock
under advanced life support, establish IV/IO access
pharmacotherapy
continue searching for the cause

Key point

The shock is not the endpoint. Resuming compressions immediately after the shock is the standard action.

6.3 Category 3: No ROSC, and PEA / asystole

This is non-shockable.

Management

continue high-quality CPR
early epinephrine (in healthcare settings)
repeat reassessment
search for and correct Hs and Ts
only switch to the shock pathway if the rhythm later truly converts to VF/pVT

Hs & Ts

“Hs and Ts” is a standardized framework in Advanced Cardiac Life Support (ACLS) for screening reversible causes, used mainly in resuscitation of non-shockable rhythms such as pulseless electrical activity (PEA) and asystole.

Its core significance: in these patients, the focus of treatment is usually not defibrillation, but rather identifying and correcting, as quickly as possible, the underlying causes of circulatory collapse, while sustaining high-quality CPR. In other words, resuscitation is not only “maintaining vital signs” but also “finding and fixing the underlying fault that caused the arrest.”

Core logic: shifting from rhythm management to cause management

For shockable rhythms (VF / pVT): the focus is to defibrillate as quickly as possible, terminating the lethal ventricular tachyarrhythmia.
For non-shockable rhythms (PEA / asystole): the focus is high-quality CPR, drug support, and a systematic search for reversible causes.

It is worth emphasizing that PEA does not mean “no electrical activity.” PEA is defined as: organized electrical activity present on the monitor, but no palpable pulse or effective circulation. Asystole, on the other hand, is the absence of any recognizable organized cardiac electrical activity.

The 5 H’s: common physiological and metabolic causes

Abbreviation	Full term	Clinical meaning
Hypovolemia	Low blood volume	Insufficient circulating volume, e.g., from major hemorrhage or severe dehydration, leading to inadequate cardiac preload and perfusion.
Hypoxia	Hypoxia	Severely inadequate oxygen delivery, leaving the myocardium and vital organs unable to maintain normal metabolism.
Hydrogen ion (acidosis)	Acidosis	Severe acidosis can suppress myocardial contractility and the stability of electrical activity.
Hypo-/Hyperkalemia	Hypokalemia / Hyperkalemia	Electrolyte disturbances can substantially affect cardiomyocyte membrane potential and conduction.
Hypothermia	Hypothermia	Low body temperature can slow metabolism, cause conduction abnormalities, and impair myocardial function.

The 5 T’s: common mechanical, structural, or toxicological causes

Abbreviation	Full term	Clinical meaning
Tension pneumothorax	Tension pneumothorax	High intrathoracic pressure compresses the lungs and great vessels, sharply reducing venous return and cardiac output.
Tamponade (cardiac)	Cardiac tamponade	Pericardial fluid or blood compresses the heart, preventing adequate diastolic filling.
Toxins	Toxins / drug poisoning	Certain drugs or toxins can directly suppress the myocardium, the conduction system, or respiration and circulation.
Thrombosis (pulmonary)	Pulmonary embolism	A massive pulmonary artery embolism can cause right heart failure and circulatory arrest.
Thrombosis (coronary)	Coronary thrombosis	Acute coronary occlusion can trigger severe ischemia, malignant arrhythmias, or pump failure.

How to apply this on scene

In each round of CPR, the team typically maintains standard resuscitation operations while in parallel thinking through the Hs and Ts:

Is there evidence of significant blood loss, dehydration, or impaired venous return?
Is there hypoxia, inadequate ventilation, or an airway problem?
Are there clues to hyperkalemia, acidosis, or other metabolic disturbances?
Could there be tension pneumothorax, cardiac tamponade, pulmonary embolism, or an acute coronary event?
Is there a history of drug overdose, poisoning, or unusual exposure?

When necessary, bedside ultrasound, blood gas, electrolytes, history, and on-scene clues can be used for rapid assessment, provided this does not significantly interrupt high-quality CPR.

References

AHA Adult Cardiac Arrest Algorithm (2025)

7. The “Proportions” of the Three Outcomes After CPR

7.1 What do public databases usually report?

Large out-of-hospital cardiac arrest registries most commonly report:

initial rhythm
whether ROSC was ultimately achieved
outcomes such as survival to hospital admission and hospital discharge

They usually do not directly provide:

a real-time, mutually exclusive, round-by-round table of “what proportion of each of the three states is present after each round of CPR.”

So any “precise proportions table for the three categories after CPR” that is stated too categorically often suffers from definitional inconsistency.

7.2 Based on large adult OHCA samples

Take CARES 2024 as an example:

Initial rhythm distribution

initial shockable rhythm: about 18.1%
initial non-shockable rhythm: about 81.9%

Of the non-shockable cases, roughly:

asystole: 50.6%
PEA/idioventricular: 22.5%
unknown unshockable: 8.8%

Outcomes during resuscitation

sustained ROSC: about 25.4%

References:

CARES 2024 Non-Traumatic National Summary Report

7.3 Interpreting these proportions

18.1% / 81.9%: answer the question “what rhythm did the patient have to begin with?”
25.4%: answers the question “did spontaneous circulation later return?”

These are overlapping, not mutually exclusive bins.

Example

A given patient:

initial rhythm of asystole
achieved ROSC after CPR

This patient simultaneously belongs to:

initial non-shockable
ultimate ROSC

7.4 On-scene experience

about 1/4 of patients will reach ROSC at some point during resuscitation
those who have not yet achieved ROSC are mostly still on the non-shockable pathway
those who actually need defibrillation — VF/pVT — are a minority, but must be identified and treated as quickly as possible

8. Differences Between Underlying Causes and Hs & Ts

Coronary artery disease, pre-excitation syndrome, long QT syndrome, and myocarditis are all important causes of, or risk factors for, sudden cardiac death (SCD).

Why are they not listed under the Hs and Ts? Because they are not at the same level of classification as Hs and Ts.

8.1 What category do these diseases belong to?

They are better categorized as underlying cardiac disease / sudden death substrate, that is, they answer:

“Why is this person at higher probability of developing a lethal arrhythmia or sudden cardiac death?”

For example:

Coronary artery disease (CAD): one of the most important causes of sudden cardiac death in middle-aged and older adults, particularly closely related to myocardial ischemia, post-infarction scar, and ventricular arrhythmias.
Wolff–Parkinson–White syndrome (WPW): can trigger rapid arrhythmias via accessory-pathway conduction and, in rare cases, lead to sudden death.
Long QT syndrome (LQTS): an inherited or acquired electrophysiological abnormality that can induce torsades de pointes, ventricular fibrillation, and sudden death.
Myocarditis: can lead to sudden death through inflammation, scarring, conduction abnormalities, or ventricular arrhythmias — particularly worth attention in young people and athletes.

About LQTS

I don’t know much about the others, so I won’t go into detail; but the QT interval is closely tied to the cardiac electrophysiology discussed above. From the electrophysiological standpoint, the cardiac action potential depends on the movement of sodium, potassium, and calcium ions in and out of the cell. The length of the QT interval is mainly determined by the speed of myocardial repolarization, which depends primarily on potassium ions flowing out of the cell.

Potassium channel “loss of function”: this is the most common cause. The channels responsible for letting potassium out (such as I*{Ks} or I*{Kr}, like discharging a capacitor) work inefficiently, so the cell potential cannot drop down and repolarization time is forced to lengthen.
Sodium channel “gain of function”: in theory, sodium channels should close rapidly after firing, but if they “don’t close tightly” and allow sodium to keep flowing in, this counteracts the work of potassium and likewise slows repolarization.

When the repolarization process (i.e., phases 2 and 3 of the action potential) is significantly delayed, cardiomyocytes enter a highly unstable state.

“Misfiring” of calcium channels: because repolarization is too slow, L-type calcium channels that have already closed may unexpectedly reopen because the membrane potential has stayed elevated for too long.
Early after-depolarization (EAD): this unexpected calcium current produces an additional small voltage fluctuation. If the fluctuation is large enough, it can forcibly trigger a premature “discharge” before the heart has fully completed its previous “recharge.”

8.2 What are Hs and Ts?

Hs and Ts belong to the reversible-causes checklist in ACLS (Advanced Cardiac Life Support), which mainly answers a different question:

“This person is already in cardiac arrest — at the CPR/resuscitation scene, is there an immediately identifiable and treatable reversible cause?”

In the AHA adult cardiac arrest algorithm, Hs and Ts are placed under “Treat reversible causes,” with emphasis on resuscitation of non-shockable rhythms such as PEA (pulseless electrical activity) and asystole.

8.3 The core difference between the two categories

You can think of them as answering two different questions:

(1) SCD causes

This is the upstream etiological perspective, focused on:

Why is this person inherently prone to lethal ventricular arrhythmias?
Are there long-term risk factors such as structural heart disease, inherited arrhythmia syndromes, inflammation, or ischemia?

This layer would include:

CAD
WPW
LQTS
myocarditis
various cardiomyopathies
coronary artery anomalies, etc.

(2) Hs and Ts

This is the on-scene resuscitation management perspective, focused on:

the patient is already in arrest or in PEA/asystole
is there a direct trigger that could potentially be corrected within minutes?
is there a problem that must be addressed in a targeted way immediately?

So, Hs and Ts is not “an encyclopedia of sudden death causes,” but rather “a quick-reference list of reversible causes at the cardiac arrest scene.”

Why does CAD partly “show up” in Hs and Ts, while WPW/LQTS/myocarditis usually do not? Because:

Chronic CAD is an underlying disease, but its acute event form — for example, coronary thrombosis — falls precisely under the T in Hs and Ts.
WPW, LQTS, and myocarditis are more like upstream disease states that “predispose patients to malignant arrhythmias or sudden death,” and they are usually not standard Hs and Ts items that can be reversed within the few minutes of on-scene resuscitation.

In other words:

CAD can be both a long-term problem and, in an acute presentation, manifest as coronary thrombosis in Hs and Ts.
WPW / LQTS / myocarditis are more often “arrhythmogenic substrates” rather than “immediately reversible triggers” of the Hs and Ts type.