Cardiac Arrest: Causes

Pathogenesis (development of disease)

Pathogenesis depends on the particular cause of cardiac arrest or sudden cardiac death (PHT). A large autopsy study (postmortem examination; cadaver dissection) demonstrates that in approx. 40 percent of patients with sudden cardiac death had a prior unrecognized myocardial infarction/heart attack (silent infarction); in three-quarters of cases, PHT was related to coronary artery disease (CAD; coronary artery disease); those with silent infarction more often had left ventricular hypertrophy/enlargement compared to those with unrecognized CAD (71 vs. 54 percent) and PHT was more likely to have occurred during physical activity (18 vs. 12 percent).

Etiology (Causes)

Biographical Causes

  • Genetic burden
    • Family history: long QT syndrome (LQTS; prolonged QT syndrome; see below); hypertrophic cardiomyopathy.
    • Genetic risk dependent on gene polymorphisms:
      • Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
        • Genes: IL18
        • SNP: rs187238 in the gene IL18
          • Allele constellation: GG (in hypertension, 3.75-fold).
          • Allele constellation: CG (0.49-fold).
          • Allele constellation: CC (0.49-fold)
        • SNP: rs16847548 in an intergenic region.
          • Allele constellation: CT (1.3-fold).
          • Allele constellation: CC (2.6-fold)

Behavioral causes

  • Nutrition
    • Ingredients of energy drinks (prolongations of the QTc interval) ?
    • Micronutrient deficiency (vital substances).
      • Low potassium
      • Low magnesium
  • Stimulant consumption
    • Alcohol excesses at the weekend → accumulation of sudden deaths on Monday.
    • Tobacco – men with sudden cardiac death were about 60% more likely to be smokers
  • Drug use
    • Cocaine
  • Physical activity
    • Ambitious recreational athletes (average age: 47 years; for soccer and running); extremely rare professional competitive athletes.
    • Triathlon (fatal incidents: 1.47/100,000; marathons: 1.00/100,000):
      • Age
        • > 40 years: 6.08/100,000; up to 50 years: 9.61/100,000
        • 60 years and older 18.61/100,000)
      • Deaths and cardiac arrests occurred in.
        • 67% of those during swimming
        • 16% during cycling
        • 11 % while running
        • 6 % during the recovery phase after the competition

      In one study, evidence of myocardial fibrosis (muscle tissue of the heart is replaced by connective tissue) was found in nearly one in five male triathletes in a cardiac magnetic resonance imaging scan; in the long term, this results in ischemic cardiomyopathy (heart muscle disease that causes the heart and heart muscle to lack an adequate supply of blood and nutrients) and heart failure (cardiac insufficiency).

  • Psycho-social situation
    • Pessimism
  • Overweight (BMI ≥ 25; obesity) in combination with.
    • Diabetes mellitus type 2
    • Hypercholesterolemia
    • Hypertension (high blood pressure)

Disease-related causes

Congenital malformations, deformities and chromosomal abnormalities (Q00-Q99).

  • Malformations of the heart, unspecified

Respiratory system (J00-J99)

  • Chronic obstructive pulmonary disease (COPD):
    • Esp. older COPD patients.
    • Independent risk factor

Endocrine, nutritional and metabolic diseases (E00-E90).

  • Acidosis – hyperacidity of the blood.
  • Diabetes mellitus
    • Type 2 diabetes represents the most common cause of death (nearly 25% of all deaths), but not in type 1 diabetics; autopsy-confirmed causes of death are: coronary heart disease (47%), followed by the so-called “sudden arrhythmic death” syndrome (26%) and hypertrophic heart disease (11%)
    • Men with PHT were about 3 times more likely to have hypertension
  • Electrolyte disturbances, unspecified

Cardiovascular system (I00-I99)

  • Arrhythmogenic right ventricular cardiomyopathy (ARVCM; synonyms: Arrhythmogenic right ventricular dysplasia cardiomyopathy; ARVD; ARVC) – the musculature of the right ventricle is altered.
  • Electrophysiologic disorders of the heart such as conduction disorders or pathologic conduction pathways
  • Familial clustered diseases such as.
    • Brugada syndrome – is classified as “primary congenital (congenital) cardiomyopathies” and there the so-called ion channel diseases; in 20% of cases of the disease is based on an autosomal dominant point mutation of the SCN5 gene; Characteristic are the occurrence of syncope (brief loss of consciousness) and cardiac arrest, which first occurs due to cardiac arrhythmias such as polymorphic ventricular tachycardia or ventricular fibrillation; patients with this disease are apparently completely heart healthy, but can already suffer sudden cardiac death (PHT) in adolescence and early adulthood.
    • Long-QT syndrome (LQTS) – belongs to the group of ion channel diseases (channelopathies); heart disease with pathologically prolonged QT interval in the electrocardiogram (ECG); disease is either congenital (inherited) or acquired, then usually as a result of an adverse drug reaction (see below “Cardiac arrhythmia due to drugs“); can lead to sudden cardiac death (PHT) in otherwise heart-healthy people.
  • Hypertension (high blood pressure) – men were about 3.5 times more likely to have hypertension.
  • Hypertrophic cardiomyopathy (HCM) – The thickness of the myocardium (heart muscle), especially the left ventricular wall, increases. With and without obstruction (narrowing) of the left ventricular outflow tract:
    • Hypertrophic non-obstructive cardiomyopathy (HNCM) – Cardiomyopathy (heart muscle disease) that may present with the following symptoms and complications: Dyspnea (shortness of breath), angina (“chest tightness”; sudden pain in the heart area), cardiac arrhythmias, syncope (brief loss of consciousness), and sudden cardiac death; approximately one-third of cases;
    • Hypertrophic obstructive cardiomyopathy (HOCM; synonym: Idiopathic hypertrophic subaortic stenosis (IHSS) – The muscles of the left ventricle, especially the ventricular septum (ventricular septum), thicken; about two-thirds of cases.
    • Notice: A meta-analysis of a total of 34 studies of 4,600 under 35-year-old individuals who died of sudden cardiac death demonstrated that only 10.3% of deaths were due to HCM; in 76.7% of cases, no structural heart disease was detectable postmortem.
    • Cause of sudden cardiac death in the younger athlete (<35 years).
  • Heart failure (cardiac insufficiency), acute or chronic.
    • Systolic heart failure: at approximately 40%, PHT is the leading cause of death.
    • Diastolic heart failure (heart failure with preserved ejection fraction; HFpEF: Heart Failure with preserved Ejection Fraction): about 20% PHT.
    • Men were about 5 times more likely to have heart failure
    • 24% of women over 55 with sudden cardiac death had heart failure (control group: 1.15%)
  • Valvular heart disease, unspecified; among others
      .

    • Asymptomatic severe aortic stenosis (5-year cumulative incidence for PHT: 7.2%; annual incidence: 1.4
      • Risk of sudden cardiac death is particularly high with severe aortic stenosis and anemia (anemia) (75% increased all-cause mortality (all-cause death rate) and 42% increased risk of sudden cardiac death).
    • Mitral valve prolapse (prevalence in general population: 1, 2%); calculated incidence of sudden cardiac death in patients with mitral prolapse: 0.14 per 100 person-years vs. overall incidence: 0.06-0.08 per 100 person-years; patients with bileaflet prolapse, ventricular ectopy, ST-T wave abnormalities, and ventricular fibrosis appear to be particularly at risk
  • Cardiac arrhythmias, such as ventricular fibrillation, ventricular flutter [80% of cases in the setting of unpredictable myocardial infarction].
  • Cardiac ion channel disease (“channelopathies”).
  • Cardiomyopathy (heart muscle disease).
  • Carotid sinus syndrome (synonym: hyperresponsiveness of the carotid sinus/initial dilation at the origin of the internal carotid artery; Engl. Carotid sinus syndrome, CSS); the vascular wall of the carotid sinus contains baroreceptors that register blood pressure in the vasculature); clinical picture: bradycardia (heartbeat too slow: < 60 beats per minute), short-term asystole (cessation of electrical and mechanical cardiac action when no replacement rhythm occurs!)and/or a drop in blood pressure, accompanied by syncope (brief loss of consciousness) and even cardiac arrest; relatively common in the elderly (-41% of those over 80)
  • Coronary artery disease (CAD) – atherosclerosis (arteriosclerosis, hardening of the arteries) of the coronary vessels; especially if risk factors such as smoking, obesity persist [most common cause].
    • 70% of all sudden cardiac deaths in CHD patients whose LVEF (left ventricular ejection fraction) >35%; cumulative incidence for sudden cardiac death was 2.1% compared with 7.7% for other causes of death; most at risk were CHD patients whose LVEF was already moderately impaired (30-40%) and those with advanced heart failure symptoms
    • 10.5% of heart-dead men younger than 55 years and 22.3% older than 55 years had a CHD diagnosis – 5 and 3 times as many as in the control group (2.2 and 8.3%, respectively); nearly 12% of women older than 55 years had a CHD diagnosis
  • Pulmonary embolism – blockage of a pulmonary artery by a blood clot.
  • Myocardial infarction (heart attack)
  • Myocarditis (inflammation of the heart muscle) (also as a complication of apoplexy/stroke).
  • Myocardial rupture – rupture of the heart muscle.
  • Pericardial tamponade – restriction of the heart muscle due to fluid accumulation in the pericardium.
  • Stress cardiomyopathy (synonyms: Broken heart syndrome), Tako-Tsubo cardiomyopathy (Takotsubo cardiomyopathy), Tako-Tsubo cardiomyopathy (TTC), Tako-Tsubo syndrome (Takotsubo syndrome, TTS), transient left ventricular apical ballooning) – primary cardiomyopathy (myocardial disease) characterized by short-term impairment of myocardial (heart muscle) function in the presence of overall unremarkable coronary arteries; clinical symptoms: Symptoms of acute myocardial infarction (heart attack) with acute chest pain (chest pain), typical ECG changes, and increase in myocardial markers in the blood; in approx. 1-2% of patients with a suspected diagnosis of acute coronary syndrome are found to have TTC on cardiac catheterization instead of a presumed diagnosis of coronary artery disease (CAD); nearly 90% of patients affected by TTC are postmenopausal women; Increased mortality (death rate) in younger patients, especially men, largely due to increased rates of cerebral hemorrhage (brain bleeding) and epileptic seizures; possible triggers include stress, anxiety, heavy physical work, asthma attack, or gastroscopy (gastroscopy); risk factors for sudden cardiac death in TTC include: Male gender, younger age, prolonged QTc interval, apical TTS type, and acute neurological disorders; long-term incidence for apoplexy (stroke) after five years was significantly higher in patients with Takotsubo syndrome, 6.5%, than in patients with myocardial infarction (heart attack), 3.2

Neoplasms – Tumor Diseases (C00-D48).

  • Cardiac metastases (daughter tumors affecting the heart) – affecting the epicardium (outermost layer of the heart wall), pericardium (heart sac), myocardium (heart muscle), endocardium (inner lining of the heart), or coronary vessels (coronary arteries)
  • Unrecognized neoplasms in children (0.54% of autopsied children with sudden death)

Psyche – nervous system (F00-F99; G00-G99).

  • Epilepsy (SUDEP, sudden unexpected death in epilepsy: sudden unexplained death in epilepsy without evidence of relevant trauma).
  • Drug abuse: opiate addicts take loperamide (e.g., for hope of relieving withdrawal symptoms), which inhibits intestinal peristalsis by stimulating opioid receptors in the myenteric plexus; extreme overdose leads to cardiac arrhythmias and thus sudden cardiac death
  • Sniffing deodorant spray with butane as propellant gas.

Symptoms and abnormal clinical and laboratory findings not elsewhere classified (R00-R99).

  • Hypothermia (hypothermia)
  • Sudden infant death syndrome
  • Subclinical inflammation (English “silent inflammation”) – permanent systemic inflammation (inflammation that affects the whole organism), which runs without clinical symptoms.

Injuries, poisoning and other consequences of external causes (S00-T98).

  • Bolus death (death due to reflex cardiac arrest triggered by a larger bolus (foreign body) in the area of the pharynx (throat) or larynx (larynx)) – life-saving immediate measure in case of imminent asphyxiation or bolus death is the Heimlich maneuver, also called Heimlich maneuver.Procedure: The rescuer grasps the patient’s upper abdomen from behind with his arms, forming a fist with one hand and placing it below the ribs and sternum. He then grips the fist with the other hand and pulls it straight back toward his body in a jerky manner. This creates an increase in pressure in the lungs, which is intended to move the foreign body out of the trachea. The maneuver may be performed up to five times.Contraindications: unconsciousness, condition after drowning, airway not completely closed (eg, by fish bone), age < 1 year.
  • Blow to the thorax/chest, more violent (commotio cordis; cardiac concussion); risk increases the smaller and harder the contact of an object with the chest → ventricular fibrillation
  • Shock, caused by anaphylaxis (acute, pathological (pathological) reaction of the immune system to chemical stimuli, the picture of anaphylactic reactions ranges from mild skin reactions to disturbances of organ functions, circulatory shock with organ failure to fatal circulatory failure), sepsis (blood poisoning), etc.
  • Electricity accident

Laboratory diagnoses – laboratory parameters that are considered independent risk factors.

  • BNP or NT-proBNP ↑
  • C-reactive protein (CRP) ↑
  • Cystatin C ↑
  • Free thyroxine (fT4) (≥ upper normal range) (hazard ratio: 2.28 for each 1 ng/dl increase in FT4 (95% confidence interval: 1.31-3.97; association was significant)).
  • Hyperkalemia (excess potassium).
  • Hypokalemia (potassium deficiency)
  • Hypomagnesemia (magnesium deficiency)

Medication

  • Drug intoxication, unspecified; e.g., digitalis – drug used in heart failure.
  • Cotrimoxazole (trimethoprim plus sulfmethoxazole) + RASB (renin-angiotensin system blockers; inhibitors of the renin-angiotensin system) – associated with sudden cardiac death in elderly patients (in the 14-day period after antibiotic treatment)
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) – also nonsteroidal anti-inflammatory drugs (NSAPs) or NSAIDs) increase the risk of sudden cardiac death:
  • X-ray contrast media (as an immediate reaction).
  • See also under: “Cardiac arrhythmias caused by drugs”

Environmental pollution – intoxications (poisoning).

  • Cocaine
  • Ice cold (+49%) + coronary artery disease (CAD)Note: Patients taking acetylsalicylic acid (ASA), beta-blockers, or nitrates alone or in combination were partially protected from cold-associated cardiac death.

Other causes

  • Tight wetsuit (→ cardiac arrest during diving); attempt at explanation: possibly the wetsuit fitting tightly around the patient’s neck caused irritation of the baroreceptors located in the carotid sinus when the patient was immersed in the water (carotid sinus syndrome: see below Cardiovascular system).
  • Increased platelet aggregation tendency (tendency of platelets to clump together).
  • Malfunction of implantable cardioverter defibrillators (ICDs) (6.4% of pacemaker deaths)
  • Intraoperative neuromonitoring to protect the recurrent laryngeal nerve; cardiac arrest after vagus stimulation: first bradycardia, then asystole.