bubble_chart Overview

Sudden death refers to a natural, unexpected, and abrupt death. Most scholars advocate that deaths occurring within 1 hour of onset should be classified as sudden death, while the World Health Organization defines it as deaths occurring within 6 hours of onset. Many organic heart diseases can lead to sudden death, with more than half of cases caused by coronary heart disease, which can be considered a type of coronary heart disease.

The report by the International Society and Federation of Cardiology and the World Health Organization's Task Force on Standardization of Clinical Nomenclature deliberately omitted the definition of sudden death, instead referring to it as primary cardiac arrest, because sudden death is the result of cardiac arrest. Deaths occurring within a short time due to acute myocardial infarction are not classified under this category.

bubble_chart Etiology

In this type of patient, cardiac arrest occurs due to coronary artery spasm or microcirculatory embolism on the basis of atherosclerotic plaque, leading to myocardial ischemia and hypoxia. The uneven repolarization of ischemic myocardium predisposes to micro-reentry. Ischemia and hypoxia cause intracellular potassium to leak out, resulting in extracellular hyperkalemia, reduced resting membrane potential, inhibition of fast sodium channels, and induction of slow responses, all of which facilitate the formation of reentrant excitation. Additionally, ischemia and hypoxia can enhance the excitability of ectopic cardiac pacemakers. These changes collectively render the myocardial electrophysiology unstable, thereby triggering ventricular tachycardia or ventricular fibrillation, with a minority of patients presenting asystole.

bubble_chart Diagnosis

1. Sudden loss of consciousness, often accompanied by convulsions.
2. The pulse disappears, and heart sounds cannot be heard.
3. Breathing stops shortly afterward.
4. Pupils dilate, mucous membranes and skin become cyanotic.
5. If an electrocardiogram can be recorded immediately, ventricular fibrillation is visible in 85% of cases. Ventricular asystole may also be observed, where the ventricles completely lose electrical activity and remain in a static state.

bubble_chart Treatment Measures

The electrophysiological mechanisms of ventricular fibrillation and cardiac arrest differ, leading to varying prognoses and treatments for patients. The former, if treated promptly, has a relatively better prognosis, whereas those presenting with extremely slow rhythms or arrest have an extremely poor prognosis.

The entire rescue and treatment process can be broadly divided into the following four stages:

1. **Stage 1: Immediate Response Period** Irreversible brain injury occurs after 4–6 minutes of circulatory interruption, so decisive action must be taken without delay. Ideally, resuscitation should begin within 1 minute of cardiac arrest.
   1. Using appropriate force, strike the middle of the patient’s sternum with the ulnar side of a clenched fist, repeating 2–3 times. This may terminate ventricular fibrillation and restore sinus rhythm.
   2. If fist percussion is ineffective, immediately place the patient in a supine position. Support the neck with one hand while using the other hand to press the forehead with moderate force, tilting the head back as far as possible. This fully opens the airway (Figure 3-5-9). If vomit, dentures, or other obstructions are present in the mouth, remove them quickly. After these steps, some patients may regain adequate breathing or even achieve cardiopulmonary resuscitation.
   If a foreign object is lodged in the trachea, immediately place the patient in a lateral position and forcefully slap the interscapular region to dislodge it. If unsuccessful, switch to the Heimlich maneuver: - For a standing patient, stand behind them, wrap arms below the ribcage, and deliver a rapid upward thrust to the abdomen with a clenched fist. - For a supine patient, place the left palm on the upper abdomen between the xiphoid process and navel, cover it with the right palm, and deliver a rapid upward thrust. These methods sharply increase airway pressure, forcing the object out.
2. **Stage 2: Basic Life Support**

   **(1) Artificial Respiration** The goal is to ensure oxygen intake and carbon dioxide expulsion to maintain vital organ function.

   1. **Mouth-to-Mouth Respiration** Position the patient supine. Support the neck with one hand to keep the head tilted back, ensuring an unobstructed airway. Pinch the nostrils with the other hand, take a deep breath, and deliver four forceful breaths into the patient’s mouth to prevent lung collapse. Seal the lips tightly around the patient’s mouth to prevent air leakage. Inflate until the chest rises slightly (Grade I expansion), lasting about 2 seconds. Release the nostrils to allow passive exhalation (~3 seconds). Repeat at 12 breaths per minute (Figure 3-5-10).
      **2. Mouth-to-Nose Respiration** If mouth-to-mouth is ineffective or the patient’s jaw is clenched, switch to mouth-to-nose respiration. The principle is the same: close the patient’s mouth and deliver breaths through the nose.
      These methods may cause gastric distension. To prevent this: - Apply pressure to the upper abdomen during breaths. - Use an esophageal obturator to block gas entry into the stomach. - Insert a nasogastric tube and intermittently compress the upper abdomen to expel gastric air.
   2. If possible, endotracheal intubation with pressurized oxygen administration should be performed immediately, as this method yields better results.
   (II) External Chest Cardiac Compression Cardiac compression is a crucial measure to maintain the patient's blood circulation. The specific method is as shown in Figure 3-5-11: Place the patient in a supine position on a hard board bed, with the operator's chest level higher than the patient's waist. The operator places the base of the left hand on the lower third of the patient's sternum, with the right hand stacked on top of the left hand for emetic therapy. The elbow joint should be extended vertically, and the arm should be perpendicular to the sternum. Using the force of the body, rhythmically compress the sternum and then quickly release. The compression frequency should be 80–100 times per minute, and continuous, uninterrupted compressions are necessary. The duration of each compression and release should be roughly the same, approximately 0.5 seconds each. When suddenly releasing after compression, there should be elasticity to facilitate blood reflux into the heart. However, the base of the hand should not leave the compression site to ensure more adequate cardiac output.
3. Phase Three: Electrical Defibrillation and Drug Therapy

   (1) Electrical Defibrillation If a defibrillator is available at the rescue site, defibrillation should be performed first. The earlier the defibrillation, the higher the success rate of resuscitation, so every second counts. Generally, asynchronous electrical shocks of 200–300J are used. If unsuccessful, the power can be increased, but the maximum should not exceed 350J. Patients who restore sinus rhythm after 1–2 shocks have a better prognosis. If conditions permit, blood gas and electrolyte tests should be conducted during resuscitation, and corresponding measures should be taken based on the results.

   (2) Drug Therapy For all patients with cardiac arrest, an intravenous infusion channel should be rapidly established during the above resuscitation process. Appropriate drugs, including lidocaine, epinephrine, procainamide, atropine, etc., should be selected based on the type of arrhythmia. If an intravenous channel has not yet been established, drug administration through an endotracheal tube is most effective for those who have undergone intubation.

4. Phase Four: Post-Resuscitation Management

   Patients who have been successfully resuscitated may still experience recurrent arrhythmias. Moreover, since the functions of the heart, brain, and kidneys have been injured to varying degrees, continuous ECG monitoring for at least 48–72 hours is recommended if conditions allow, to promptly detect and manage various arrhythmias and complications.

(1) Maintaining Circulation: Post-resuscitation, patients may suffer from insufficient blood volume, acidosis, electrolyte imbalances, weak myocardial contractions, or microcirculatory disturbances. These should be corrected based on the specific situation, and vasopressors may be administered if necessary.

(2) Preventing Brain Injury: Brain tissue is most sensitive to hypoxia and prone to injury. Cooling measures should be initiated from the start of resuscitation, typically by placing an ice cap on the head. If necessary, artificial hibernation may be employed, with the rectal temperature maintained at 31–32°C for 3–5 days, by which time the peak of cerebral edema has passed. During cooling, dehydrating agents such as 20% mannitol (250ml) may be administered intravenously every 8 hours, supplemented with dexamethasone (20–40mg/day) in doses of 4–5mg every 6–8 hours if needed. Dehydration therapy generally lasts about a week. Avoid sudden rewarming at the end of artificial hibernation; gradual rewarming is preferable. Continuous oxygen supply during the entire resuscitation and post-resuscitation cooling process is also crucial for preventing brain injury.

(3) Preventing Renal Insufficiency: If a patient's urine output does not exceed 20ml/h and the urine specific gravity is fixed below 1.012, acute renal insufficiency should be suspected. Rapid intravenous infusion of 50% glucose (100–200ml) or injection of furosemide is recommended. If urine output does not significantly improve after treatment, manage as acute renal insufficiency.

(4) Preventing Secondary Infections: During resuscitation, aspiration of vomitus into the respiratory tract often leads to aspiration pneumonia. Therefore, post-resuscitation patients should routinely receive antibiotics to prevent secondary infections.

bubble_chart Prevention

Risk factors: Patients with coronary heart disease should be considered at risk for sudden death if they currently exhibit the following conditions:

1. Ventricular premature beats, especially frequent ones (more than 5 per minute), or premature beats occurring during early diastole (RonT phenomenon). Recent clinical observations indicate that advanced diastolic (RonP) premature beats can also trigger ventricular premature beats, with a higher incidence than those in early diastole. Moreover, the ventricular tachycardia induced by RonP appears to have a more severe clinical course and prognosis, with a higher likelihood of ventricular fibrillation and sudden death.
2. Persistent sinus bradycardia, especially in cases with organic lesions in the sinoatrial node or conduction system, significantly increases the risk of sudden death.
3. Acute myocardial infarction with right bundle branch block: Patients who have recently experienced acute myocardial infarction and exhibit ischemia in myocardium distant from the infarct zone are more prone to sudden death than those with ischemia only at the infarct border zone. During cardiac stress testing, such patients may show ST-segment depression of 1–2 mm; the more pronounced the ST-segment elevation during coronary artery spasm, the higher the likelihood of cardiac arrest.
4. Others who have survived a prior cardiac arrest but continue to smoke face a significantly increased risk of sudden death. Coronary heart disease patients who smoke have a higher risk of sudden death than non-smokers.
5. Those with left ventricular hypertrophy or dilation.

Warning signs: Most patients experience sudden collapse and loss of consciousness without any prior warning. Some may feel sudden, pronounced fatigue, palpitations, chest tightness, shortness of breath, or gastrointestinal symptoms such as abdominal pain or vomiting within half an hour before the onset.