Circulatory arrest I46.9

• Ventilation:

In the 19th century, less effective measures for indirect ventilation through chest compressions such as Sylvester's arm movements were used, some of which were still taught until the 1970s (Ziegenfuß 2007).

The Austrian physician Peter Safar, together with D G Greene, developed the technique of modern respiratory resuscitation in the 1950s (Litzberski 2025).

• Cardiac massage:

Böhm first used external cardiac massage for poisoning with chloroform in 1874 and König performed it successfully in Göttingen in 1892. However, it was subsequently forgotten (Düben 1972).

It was not until 1960 that external cardiopulmonary resuscitation using chest compressions was published by Kouwenhoven, Jude and Knickerbocker. This was a milestone in modern medicine (Scholz 2017).

The combination of ventilation and cardiac massage was first recommended by P. Safar in 1961 (Ziegenfuß 2007),

In 1972, the European Resuscitation Council (ERC) published the first evidence-based European guidelines for the prevention and treatment of circulatory arrest and life-threatening emergencies. The last amendment dates from 2025 (Guidelines 2025).

During circulatory arrest, the macro- and microcirculation stops, which leads to hypoxia and thus damage to the end organs (Schwab 2015).

Consciousness is lost after 10 - 15 seconds, breathing stops after approx. 30 - 60 seconds (Ziegenfuß 2007) and pupils dilate after approx. 30 - 120 seconds (Schwab 2015).

Active intervention is usually required to restore spontaneous blood flow (Kasper 2015).

A distinction is made between respiratory and circulatory arrest. Circulatory arrest itself is also divided into primary and secondary circulatory arrest (Ziegenfuß 2007).

• In primary circulatory arrest:

If the blood circulation fails first

secondary respiratory arrest occurs within a few seconds

is usually a cardiogenic circulatory arrest ((Ziegenfuß 2007)

• In secondary circulatory arrest:

the first thing to fail is breathing (so-called primary respiratory arrest)

unconsciousness occurs within a few minutes

myocardial hypoxia leads to secondary circulatory arrest (Ziegenfuß 2007)

• A distinction is made in cardiovascular arrest between a:
  • Tachy-systolic cardiac arrest, also known as hyperdynamic cardiac arrest. It occurs in approx. 80% of cases and is due to previous ventricular fibrillation, ventricular flutter or pulseless ventricular tachycardia (Herold 2025).
  • -Adynamic cardiac arrest, also known as adynamic cardiac arrest. This is found in only 20% of those affected. It is characterized by pulseless electrical activity (Herold 2025).

In Europe, around 84 out of every 100,000 people suffer a cardiovascular arrest every year (Zumbrunn 2025). In the western world, cardiovascular death is the most common cause of death and is the first manifestation of previously unrecognized heart disease in around 55% of cases (Herold 2025).

The average age of patients is 67 years (plus/minus 17 years), of whom around 65% are male (Herold 2025).

The etiology of circulatory arrest may be due to:

• I. Cardiac causes:
  • 70 % due to CHD or myocardial infarction
  • 10 % due to cardiomyopathies
  • 5 % hypertensive heart disease
  • myocarditis
  • Vitia
  • Severe acidosis
  • Pericardial tamponade
  • Primary electrical diseases of the heart, so-called ion channel diseases
  • Electrical accident
  • Hypothermia
  • Hypo- or hyperkalemia
  • Drug toxicity (Herold 2025)
  • The decisive factor here is the severity of the insufficiency. Cardiac causes occur in > 90 % of all cases (Herold 2025).
• II Circulatory:
  • Circulatory shock of various origins is the trigger (Herold 2025).
• III. respiratory causes:
  • Aspiration
  • Obstruction of the airway
  • Central respiratory disorder
  • Neuromuscular causes
  • Intoxication
  • Tension pneumothorax
  • Oxygen deficiency of the respiratory air due to e.g. suffocation, drowning (Herold 2025)
• IV. Terminal stage of various diseases (Herold 2025)
• V. Severe trauma (Secchi 2009)

Reversible triggers of circulatory arrest are:

• HITS:
  • Pericardial tamponade
  • Intoxication
  • thromboembolism
  • Tension pneumothorax
• Four H's:
  • Hypovolemia
  • hypoxia
  • hypothermia
  • Hypo- or hyperkalemia (Herold 2025)

Pathophysiological triggers of circulatory arrest can be:

• in 60 % ventricular tachycardia with degeneration into ventricular fibrillation
• in 20 % bradycardia or asystole
• in 10 % torsades de pointes tachycardia
• 10% primary ventricular fibrillation (Herold 2025)

Clinical signs are

• Deep unconsciousness, which occurs after approx. 10 - 15 sec.
• respiratory arrest after 30 - 60 sec
• dilated pupils after approx. 2 min (Herold 2025)

The diagnosis of circulatory arrest can be made if:

• non-responsiveness
• if there is no reaction to pain stimuli
• respiratory movements are no longer visible
• Breathing can no longer be felt
• Breathing noises are no longer audible
• the carotid artery pulse can no longer be felt (although this sign is imprecise) (Herold 2025). The carotid pulse should always be palpated, but never both carotids at the same time. Peripheral pulses can no longer be palpated at this stage due to centralization (Schwab 2015).
• pupils are wide and unresponsive (however, interfering factors such as the administration of atropine or adrenaline should be taken into account here) (Herold 2025)

• Neuron-specific enolase (NSE)

These should be measured 48-72 hours after the event. Elevated values (> 60 µg/L according to ERC guidelines and > 90 µg/L according to S1 guidelines) indicate a poor neurological prognosis (Zumbrunn 2025).

• Neurofilament light chains (NfL)

NfL is another prognostic marker, although this marker has not yet been sufficiently researched. An assessment is possible as early as 24 hours after the event (Zumbrunn 2025).

• Complications due to circulatory arrest include:
  • "Post Intensive Care Syndrome (PICS). This occurs in approx. 14 - 45 % of survivors of cardiac arrest. It is characterized by symptoms of depression similar to those of post-traumatic stress disorder (Zumbrunn 2025).
  • Cerebral damage up to brain death
  • Acute kidney failure (Herold 2025)
• Complications caused by the resuscitation measures include:
  • Rib fractures with injuries to the lungs and/or heart
  • Sternum fracture
  • Liver injury
  • Spleen injury
  • Aortic or cardiac rupture
  • Pericardial effusion
  • Gastric hyperinflation (Herold 2025)

Any gasping breaths should not be misinterpreted as sufficient breathing. However, breath control can be difficult even for experienced rescuers, which is why resuscitation should be started as soon as there is no pulse (Schwab 2015).

• Basic measures (basic life support = BLS):

The basic measure in the event of circulatory arrest is cardiopulmonary resuscitation (CPR). It should be carried out for at least 30 minutes, or even up to an hour in the event of hypothermia caused by accidents (Herold 2025).

If a cardiovascular arrest occurs in a public place, resuscitation should ALWAYS be initiated without a clear advance directive or clear medical exclusion criteria. In hospital, however, possible scenarios can be discussed beforehand (Zumbrunn 2025).

The basic measures of CPR consist of:

- C = Chest compression

- A = Airway

- B = Breathing (Herold 2025)

After recognizing a circulatory arrest, both the rescue service and an emergency doctor should be notified (Herold 2025)

CPR should be started on any person who is unresponsive and not breathing or not breathing normally. Abnormal breathing also includes slow labored breathing, so-called gasping (Herold 2025)

First, chest compressions should be started on as hard a surface as possible. This involves compressing the lower half of the sternum with a compression depth of approx. 5 - 6 cm, the frequency should be between 100 - 200 / min (Herold 2025)

Chest compression can also be performed mechanically, whereby the compression depth of the plunger can be adjusted (Ziegenfuß 2007).

For mouth-to-mouth resuscitation, the patient's head should be hyperextended and the chin raised. The nasal opening should be closed with the fingers. Then exhale into the patient's lungs for approx. 1 second until the chest rises visibly (Ziegenfuß 2007)

For endotracheal intubation, the pause in chest compressions should be < 5 sec (Herold 2025)

The subsequent rate of chest compressions: ventilation should be 30: 2, with no pause in chest compressions during ventilation. The rescuers should be changed every 2 min if possible (Herold 2025)

Use the AED. The patient should not be touched during the AED cardiac rhythm analysis (Herold 2025)

If mouth-to-mouth resuscitation is rejected for psychological or infection prevention reasons, only chest compressions are permitted (Herold 2025).

• Advanced measures after ECG analysis (Advanced Life Support = ALS):
  • In the event of pulseless ventricular tachycardia, ventricular fibrillation or ventricular flutter:
  • Immediate defibrillation at the highest energy level required
  • If this is unsuccessful, the same cycle of CPR should be repeated for 2 minutes, followed by defibrillation at the highest energy level. If unsuccessful again, an alternative patch position may be considered.
  • Establish venous access without interrupting HDM. If venous access cannot be achieved, create intraosseous access.
  • If a defibrillatable rhythm still cannot be achieved, a maximum of 1 mg adrenaline (adrenaline 10 µg /kg [2025 guidelines]) plus 9 mg NaCl should be administered intravenously.
  • If the rhythm can be defibrillated, 1 mg adrenaline should be administered after the 3rd defibrillation. This therapy should be repeated every 3 - 5 minutes. In the case of intraosseous access, additional rinsing with 20 ml isotonic solution is required.
  • If VF or polymorphic VT is still present after 3 defibrillations, a maximum of 300 mg amiodarone should be administered intravenously(amiodarone 5 mg /kg [Guidelines 2025]). After 5 defibrillations and continued VF or polymorphic VT, inject 150 mg amiodarone once.
  • Intubation and ventilation: If the interruption of HDM does not last longer than 5 seconds, the patient can be intubated at an early stage. As an alternative to intubation, a supraglottic breathing aid can also be used (Herold 2025)
  • The measurement of CO2 in the exhaled air, known as capnography, is recommended to check the correct position of the endotracheal tube. The ventilation rate should be 10/min.
  • The resuscitation itself is carried out under high oxygen levels. After successful resuscitation, SpO2 values should be limited to normal values between 94-96%. Hyperoxemia should be avoided at all costs after the return of spontaneous circulation (Herold 2025).

• In asystole and electromechanical dissociation:
  • CPR for 2 min and subsequent administration of 1mg adrenaline i.v. every 3 - 5 min (as for ventricular fibrillation).
  • If this is unsuccessful, transthoracic electrical stimulation should be used as pacemaker therapy.
  • 50 mmol sodium bicarbonate should be administered in case of circulatory arrest due to hyperkalemia or overdose of tricyclic antidepressants
  • The use of thrombolytics should be considered if there is an urgent suspicion of pulmonary embolism. CPR should then be continued.
  • If the cause of the circulatory arrest is a myocardial infarction/acute coronary syndrome (ACS), prompt percutaneous coronary intervention is recommended (Herold 2025)

• Post-resuscitation treatment

After successful resuscitation, the following target values should be aimed for:

▪ SaO2 94-98%

▪ PaO2 10-13 kPa

▪ etCO2 (end-tidal CO2) 4.7-6.0 kPa

▪ MAP (mean arterial blood pressure) 60-65 mmHg

▪ Temperature ≤ 37.5 °C (2025 guidelines)

Rescue services in Germany attempt around 55,000 resuscitations every year. However, 74.3% of these die shortly before or after reaching the hospital. But even after reaching the hospital, the prognosis remains serious, as the 1-year survival rate is only 7.7% worldwide (Zumbrunn 2025).

The chances of successful resuscitation after primary circulatory arrest are significantly better than after secondary circulatory arrest, as in secondary circulatory arrest the organs are usually already severely hypoxic (Secchi 2009).

If defibrillation is performed immediately after the onset of ventricular fibrillation (e.g. in the intensive care unit), it can be successful in up to 95% of cases. For every minute that defibrillation is delayed, the chances of survival are reduced by 10% (Herold 2025).

Within a hospital (IHCA) between 15-34% of those affected survive a cardiac arrest, outside (OHCA) only around 10%. Among the survivors, around 22.9% of IHCA patients ultimately die from severe neurological damage and around 67.7% of the OHAC group. In patients who survive the first year after such an incident, up to 83.3% have a good neurological outcome (Zumbrunn 2025).

In OHCA cases under 50 years of age, a clinically relevant pathogenic variant in a gene that is probably associated with sudden circulatory arrest was identified in up to 25% of cases (Guidelines 2025).

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