Arrhythmias before and during cardiac arrest
Cardiac arrest is a result of tachyarrhythmia, bradyarrhythmia or asystole. The tachyarrhythmias include ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). The bradyarrhythmias include all bradyarrhythmias, pulse-less electrical activity (PEA), and asystole.
Bradyarrhythmias are discussed in the chapter Management of Bradycardia (Bradyarrhythmia).
Initial rhythm and the course of arrhythmias during cardiac arrest
The initial rhythm in cardiac arrest is defined as the first electrocardiographically (ECG) recorded rhythm. In out-of-hospital cardiac arrest (OHCA) the initial rhythm is recorded by the EMS (emergency medical service) team upon their arrival at the scene. If an AED (automatic external defibrillator) has been connected, it should be interrogated (if possible) to determine whether it has recorded any shockable rhythms. In in-hospital cardiac arrest (IHCA) 20-30% of victims have continuous ECG monitoring (telemetry), which allows instantaneous identification of the initial rhythm (Thorén et al).
The initial rhythm has immense significance for survival in cardiac arrest, regardless of all other circumstances. The initial rhythm is an indicator of the underlying etiology, duration of cardiac arrest, quality of CPR, and a prognostic indicator for survival. In the nationwide Swedish Cardiopulmonary Resuscitation Registry, 30 days survival in OHCA, in relation to initial rhythm, is as follows (Rawshani et al):
- Overall survival: 11%.
- Shockable rhythm (VF, pulseless VT): 35%
- Pulseless electrical activity (PEA): 5%.
- Asystole: 1.6%
Pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electrical activity (PEA), and asystole can all occur in one patient. The typical depiction of sudden cardiac death as a gradual transition from sinus rhythm to ventricular tachycardia (VT), to ventricular fibrillation (VF) and ultimately asystole and death is not an absolute rule. While it often holds true for cardiac arrests caused by chronic or acute ischemic heart disease, it is often not true in other circumstances (e.g. pulmonary embolism, trauma, respiratory causes, drug overdoses, etc.).
Among victims in whom the cardiac arrest was caused by VT or VF (e.g acute or chronic myocardial ischemia, heart failure, etc.), it is clear that the earlier the initial ECG is recorded, the greater the likelihood that the rhythm will be VF or pulseless VT (i.e. shockable), and the probability of survival is higher (since these arrhythmias can be defibrillated). Likewise, the later the ECG is recorded, the greater the probability that the rhythm has deteriorated into PEA or asystole, and therefore the worse the prognosis. This does not always hold true. For example, in cardiac arrest due to pulmonary embolism the initial rhythm is typically PEA, which is explained by the fact that the embolus prevents blood from passing from the lungs to the left ventricle, which therefore contracts without pre-load (the ventricle is empty or nearly empty).
In patients with an initial shockable rhythm, compressions and ventilation can extend the duration of the shockable rhythm by several minutes, allowing for EMS or bystanders to connect a defibrillator or AED and defibrillate.
Watanabe et al studied 132 patients who unexpectedly experienced sudden cardiac arrest while being monitored with Holter ECG (the indications were palpitations, chest pain, syncope, etc.). The results were as follows:
- 73% were caused by ventricular tachyarrhythmias, of which 45% were VT degenerating into VF.
- 27% were caused by bradyarrhythmia, of which 74% were asystole and 26% were AV-blocks.
These findings should not be interpreted as representative of the population experiencing OHCA and IHCA.
Shockable and non-shockable rhythms
All healthcare professionals must be able to identify shockable rhythms, i.e. tachyarrhythmias that can be terminated by means of defibrillation (non-synchronized shock) or cardioversion (synchronized shock). Ventricular fibrillation (VF) and ventricular tachycardia (VT) are shockable rhythms. Asystole, bradyarrhythmias, and PEA are non-shockable rhythms. While there is no electrical therapy for PEA and asystole, bradyarrhythmias are effectively managed using any temporary pacing method (e.g. transcutaneous pacing).
Ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT)
- Survival to 30 days when the initial rhythm is VF/VT: 35%
- Percentage of witnessed cardiac arrests exhibiting VF/VT: 28%
- Percentage of unwitnessed cardiac arrest (OHCA) exhibiting VF/VT: 9%
The large difference in rates of VF/VT in witnessed and unwitnessed cardiac arrest is explained by the fact that VF/VT degenerate into asystole and PEA within a few minutes unless effective CPR is provided and maintained.
Ventricular contractions cease during ventricular fibrillation (VF), whereby tissue perfusion ceases immediately and the individual becomes unconscious. In ventricular tachycardia (VT), some contractility remains and the ventricular rate is high, which is often sufficient to generate cardiac output. However, VT can result in loss of consciousness and cardiac arrest in the following situations:
- If the VT is sustained it will drain myocardial energy resources and degenerate into VF and cardiac arrest.
- If the VT is very fast the pre-load and resulting ejection fractions become too small to maintain cardiac output, despite the ventricular rate.
- If ventricular dysfunction exists (e.g. heart failure) the ejection fraction during VT may be insufficient to maintain minimal cardiac output.
VT that results in loss of consciousness is referred to as pulseless VT. The systolic blood pressure is usually <60 mmHg during pulseless VT.
Pulseless VT is a rapid, regular rhythm with wide QRS complexes that does not generate pulse.
Ventricular fibrillation (VF) and ventricular tachycardia (VT) can mostly be defibrillated. The likelihood of successfully defibrillating ventricular fibrillation is a function of the state of myocardial metabolism. Early in the course of cardiac arrest, myocardial ATP concentrations are high and the VF waveform is coarse (large fibrillatory amplitudes). Coarse VF is relatively easy to defibrillate. However, as the duration of cardiac arrest (and VF) is prolonged, ATP concentrations diminish rapidly and the vF waveform transitions from coarse to fine VF, which is a precursor to asystole and very difficult to defibrillate. Fine VF is considered a non-shockable rhythm.
Refractory VF/VT is defined as VF/VT that resists 3 consecutive defibrillations. The approach to refractory VF/VT is discussed in the chapter Advanced Cardiovascular Life Support.
Pulseless Electrical Activity (PEA)
Pulseless Electrical Activity (PEA) was previously called Electromechanical Dissociation (EMD)
- Survival to 30 days when the initial rhythm is PEA: 6%
- Percentage of witnessed cardiac arrest: 22%
- Percentage of witnessed and unwitnessed cardiac arrest: 9%
Pulseless electrical activity (PEA) exists if organized electrical activity (QRS complex on ECG) does not produce effective contractions and pulse. Thus, in PEA there are QRS complexes indicating myocardial electrical activity, but there are no meaningful ejections from the ventricles. There are two types of pulseless electrical activity.
Primary PEA: In primary PEA the right and left ventricles are filled with blood but the depolarization does not result in any contraction. Primary PEA is usually an end-stage and suggests highly advanced heart disease as the underlying cause, or prolonged cardiac arrest in the absence of advanced heart disease.
Secondary PEA: In secondary PEA the left and/or right ventricle is not filled with blood. This can be explained by massive pulmonary embolism, bleeding, tamponade (with or without hemopericardium), or acute prosthetic dysfunction leading to flow obstruction through the prosthesis.
ECG in pulseless electrical activity (PEA)
QRS complexes may be narrow or wide in PEA, and the heart rate can be very slow (agonal rhythm), normal, fast, regular or irregular. The ventricular rate (assessed on the ECG) in PEA usually does not exceed 130 beats/min and it is not possible to defibrillate PEA.
Bradycardia leading to cardiac arrest requires the ventricular frequency to be lower than 20 beats/min. In this scenario, ventricular contractions exist but the frequency is insufficient to maintain adequate cerebral perfusion, whereby the individual becomes unconscious. Sinus bradycardia, sinus arrest, SA block, AV block 2 and AV block 3 are the most common bradyarrhythmias leading to loss of consciousness. For details, refer to the chapter Management of bradycardia.
- Survival to 30 days when the initial rhythm is asystole: 1.5%.
- Percentage of witnessed cardiac arrest: 50%
- Percentage of unwitnessed cardiac arrest: 82%
Asystole is defined as the absence of electrical activity and the cessation of contractions. Asystole is the end stage of any cardiac arrest because all fatal rhythms degenerate into asystole. A cardiac arrest may also begin with asystole, which speaks for advanced underlying heart disease.
Sinus tachycardia (supraventricular tachyarrhythmia)
Sinus tachycardia or other supraventricular tachyarrhythmias just before and/or during cardiac arrest suggests hypovolemia, insufficient preload (pulmonary embolism, hemorrhage) or outflow obstruction.
Typical arrhythmias in cardiac arrest
- Cardiac arrest can begin with ventricular fibrillation, without other arrhythmias preceding the ventricular fibrillation.
- Cardiac arrest can begin with asystole, without other arrhythmias preceding the asystole. This implies that there is advanced underlying heart disease.
- Ventricular fibrillation virtually always transitions to asystole unless defibrillation is attempted and successful. Spontaneous conversion of ventricular fibrillation to organized rhythm is rare.
- Ventricular fibrillation is often preceded by ventricular tachycardia, especially in myocardial ischemia, heart failure, cardiomyopathies, and long QT syndrome (congenital or acquired).
- Occasionally ventricular fibrillation transitions to PEA before asystole occurs.
Tachyarrhythmias in coronary artery disease
In order for ischemia or infarction to induce life-threatening tachyarrhythmias, both a trigger and a substrate (i.e. vulnerable myocardium) are required. Experimental all studies and clinical experience show that a trigger is rarely sufficient to induce ventricular fibrillation or ventricular tachycardia in normal myocardium. It is also clear that myocardial ischemia is rarely sufficient to induce ventricular tachycardia or ventricular fibrillation. This is evidenced by the following observations:
- Among individuals with stable coronary heart disease, daily episodes of angina pectoris (i.e. symptomatic ischemia) are common, and asymptomatic ischemic episodes are even more common. Despite this, ventricular fibrillation and ventricular tachycardia are unusual. In light of the large number of ischemic episodes, it is clear that cardiac arrest is a rare consequence of ischemia.
- The purpose of cardiopulmonary exercise testing is to induce ischemia gradually by increasing myocardial oxygen demand. Ventricular tachycardia, ventricular fibrillation and cardiac arrest are extremely rare during the exercise test (<1/50000 examinations).
As compared with stable angina (ischemia), VF and VT are significantly more common (with regard to the proportion of instances leading to VF/VT) in acute coronary syndrome (ACS). The explanation for this is that the acute event induces a series of electrophysiological and biochemical changes that immediately induce electrical instability. These changes include disturbances in intracellular calcium flow (accumulation of intracellular calcium), potassium flow (profuse efflux of potassium), high concentration extracellular potassium, decreased extracellular pH, increased sympathetic tone, and altered adrenoreceptor function. The risk of tachyarrhythmias is highest in the first 30 minutes and then gradually decreases. The risk of tachyarrhythmias is highest in abnormal myocardium (previous infarction, remodeling, hypertrophy).
It should also be mentioned that abrupt increases in myocardial perfusion may also induce electrical instability, as evidenced by the high risk of ventricular tachycardia seen during and immediately after reperfusion (after PCI, thrombolysis and spontaneous reperfusion) and after coronary vasospasm has resolved.
Libby P et al: Braunwald’s Heart Disease, Chapter 70, Cardiac arrest and sudden cardiac death.
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