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Ventricular Fibrillation

VF

Ventricular fibrillation is an abnormally irregular heart rhythm caused by rapid, ineffective, uncoordinated contraction of the ventricles which produce no peripheral pulse.


Presentation

Patients of ventricular fibrillation usually present with sudden loss of consciousness [10]. Signs and symptoms of ventricular fibrillation include chest pain, rapid heartbeat, dizziness, nausea, shortness of breath and collapse. If untreated, the person usually has a seizure and then becomes limp and unresponsive. The patient suddenly collapses, turns deathly pale, stops breathing, and has no detectable pulse, heartbeat, or blood pressure. The patient develops irreversible brain damage after 5 minutes because of lack of oxygen to the brain. This leads to sudden cardiac arrest and death of the patient.

Dyspnea
  • The most common presentation is acute substernal chest pain, although occasionally dyspnea and syncope, and rarely shock with ST-segment elevation and elevated cardiac biomarkers have been observed.[ncbi.nlm.nih.gov]
  • Three patients reported symptoms-primarily fatigue, nausea, and exertional dyspnea-that prompted evaluation. Serum chemistry analysis of blood drawn immediately after diagnosis showed no changes that suggested end-organ dysfunction.[ncbi.nlm.nih.gov]
  • An hour before the patient faints, symptoms that may indicate a possible heart condition: – Chest pain ( angina pain ); – Dyspnea (shortness of breath); – Fatigue – intense; – Palpitations; – Syncope; – Tachycardia (especially in serious cases).[heartupdate.com]
  • The following symptoms, while not necessarily specific for sudden cardiac death or VF, may develop before any major cardiac event: Chest pain and other angina equivalents Dyspnea Easy fatigue Palpitations Immediately preceding acute cardiac arrest, possible[emedicine.medscape.com]
  • […] cases of decompression sickness (Class IIa, LOE C-LD).updated for 20152015Oxygen Use in First AidFor first aid providers with specific training in the use of oxygen, the administration of supplementary oxygen to persons with known advanced cancer with dyspnea[doi.org]
Exertional Dyspnea
  • Three patients reported symptoms-primarily fatigue, nausea, and exertional dyspnea-that prompted evaluation. Serum chemistry analysis of blood drawn immediately after diagnosis showed no changes that suggested end-organ dysfunction.[ncbi.nlm.nih.gov]
Tachycardia
  • CONCLUSIONS: Adenosine remains a safe and highly efficacious therapy for supraventricular tachycardia.[ncbi.nlm.nih.gov]
  • BACKGROUND AND OBJECTIVE: To safely select the proper therapy for Ventricullar Fibrillation (VF) is essential to distinct it correctly from Ventricular Tachycardia (VT) and other rhythms.[ncbi.nlm.nih.gov]
  • tachycardia (diagnosis), ventricular tachycardia, V.tach, Tachycardia ventricular, Tachycardia, ventricular, Tachycardia, Ventricular [Disease/Finding], v tach, vt, ventricular tachyarrhythmia, ventricular tachycardia (V-tach), Ventricular tachycardia[fpnotebook.com]
  • CONCLUSIONS: Although usually benign, right ventricular outflow tract tachycardia can be life-threatening. Even the most malignant cases can be cured by ablation.[ncbi.nlm.nih.gov]
  • There are two other potential causes of ventricular tachycardia. The first is a special type of ventricular tachycardia called right ventricular outflow tract tachycardia (RVOT).[healthcentral.com]
Chest Pain
  • A 33-year-old man presented with waxing and waning severe substernal chest pain. The patient was on no prior medications, and had no risk factors for acute coronary syndrome.[ncbi.nlm.nih.gov]
  • The most common presentation is acute substernal chest pain, although occasionally dyspnea and syncope, and rarely shock with ST-segment elevation and elevated cardiac biomarkers have been observed.[ncbi.nlm.nih.gov]
  • CASE REPORT: A 56-year-old woman presented to the emergency department with complaints of chest pain, nausea, and vomiting.[ncbi.nlm.nih.gov]
  • A 60 year old man with 2 hours of "crushing" chest pain suddenly collapses.[ecglibrary.com]
  • Coronary artery bypass grafting (CABG): This surgery creates a bypass around your narrowed coronary arteries by grafting arteries or veins taken from other parts of your body to improve blood flow, stop chest pain and prevent a heart attack.[baptisthealth.com]
Palpitations
  • CASE PRESENTATION: A 26-year-old woman of Cypriot origin presented to our emergency department with a sudden onset of palpitations and chest discomfort. She was healthy, with no previous medical history and no regular medications.[ncbi.nlm.nih.gov]
  • On evaluation, the patient was conversant and without complaint of lightheadedness or palpitations. Bilateral radial and femoral pulses were absent. An automated cuff was unable to measure a brachial blood pressure in either arm.[jamanetwork.com]
  • Symptoms of VF may include palpitations (sensations of a racing heart), lightheadedness, chest tightness, shortness of breath, nausea and fainting.[scripps.org]
  • Signs and Symptoms Diagnosis Treatment Ventricular fibrillation may cause the following symptoms: Chest pressure or pain Fatigue Lightheadedness or dizziness Palpitations, which can be skipping, fluttering or pounding in the chest Shortness of breath[ucsfbenioffchildrens.org]
  • Presentation Patients may have a history of chest pain, fatigue, palpitations and other nonspecific complaints.[patient.info]
Cyanosis
  • This is also known as cyanosis. That's the blue-color skin when you're not circulating oxygen through the body. An EKG in someone in V-fib looks like this. You're going to see course squiggly lines.[khanacademy.org]
  • […] appears obstructed or if PPV is required (Class IIb, LOE C).not reviewed in 20152010Assessment of Oxygen Need and Administration of OxygenIt is recommended that oximetry be used when resuscitation can be anticipated, when PPV is administered, when central cyanosis[doi.org]
Contusion
  • Although we succeeded in defibrillation after percutaneous coronary intervention (PCI), a chest radiograph indicated a pneumothorax in the right lung and a pulmonic contusion in the left lung caused by cardiopulmonary resuscitation.[ncbi.nlm.nih.gov]

Workup

Ventricular fibrillation is always diagnosed in an emergency setting.

  • Cardiac monitor: A cardiac monitor reveals a very disorganized heart rhythm. In addition, there is no pulse.
  • Electrocardiogram: The presence of ventricular fibrillation can be confirmed only with an electrocardiogram which shows a chaotic, irregular pattern. In the begin of ventricular fibrillation, coarse and irregular waves are present. After a few seconds the electrocardiogram changes into a new pattern of low-voltage, irregular waves. The voltages of the waves in the electrocardiogram are usually about 0.5 millivolt when ventricular fibrillation begins, but they decrease to 0.2 or 0.3 millivolt. 0.1 millivolt or less may be seen 10 minutes or longer after ventricular fibrillation begins.
  • Echocardiogram: This test uses sound waves to produce video images of the heart, thereby detecting any underlying abnormality. A decrease in the ejection fraction and worsening wall-motion abnormalities may confer increased risk for the development of ventricular fibrillation.
  • Coronary angiography: It helps to determine if coronary arteries are narrowed or blocked. A liquid dye is injected through a long, thin tube that makes the arteries become visible on X-ray, revealing areas of blockage. Coronary angiography may precipitate ventricular fibrillation in susceptible individuals and should be used with caution [11] [12] [13].
  • Cardiac computerized tomography or magnetic resonance imaging: These tests are commonly used to diagnose heart failure due to sudden cardiac arrest. It helps detect the presence, extent and location of ischemia.
  • Chest X-ray: It helps check the size and shape of heart and blood vessels.
  • Blood tests: Blood samples are tested for the presence of certain cardiac enzymes that leak into circulation by damaged heart. Other laboratory studies may include serum electrolyte levels, arterial blood gases, thyroid stimulating hormone and B-type natriuretic peptide.
T Wave Alternans
  • RESULTS: Frequencies of history of syncope and spontaneous type 1 ECG, r-J interval in V1, QRS duration in V6, and LAS40, Tpeak-Tend dispersion, and max T-wave alternans were significantly associated with VF occurrence in univariate analyses.[ncbi.nlm.nih.gov]
  • alternans testing can also be done.[healthline.com]
T Wave Inversion
  • Presenting electrocardiogram (ECG) showed an old left bundle branch block and T-wave inversions in lateral leads (QTc 494ms) with no significant electrolyte abnormalities.[ncbi.nlm.nih.gov]
P Wave Absent
  • Answers Rhythm: Irregular Rate: Unable to determine P Wave: absent PR interval: absent QRS: absent Interpretation: Ventricular Fibrillation (Fine)[ekg.academy]
Myocardial Fibrosis
  • No correlation was seen between gender, age, heart weight, degree of coronary atherosclerosis, myocardial fibrosis, survival and MFB.[ncbi.nlm.nih.gov]
Electrocardiogram Change
  • After a few seconds the electrocardiogram changes into a new pattern of low-voltage, irregular waves.[symptoma.com]

Treatment

Ventricular fibrillation is treated by delivering a quick electric shock through the chest, within a few minutes of attack, using a device called an external defibrillator. Although a moderate alternating-current voltage applied directly to the ventricles almost invariably throws the ventricles into fibrillation, a strong high-voltage alternating electrical current passed through the ventricles for a fraction of second can stop fibrillation by throwing all the ventricular muscle into refractoriness simultaneously. This is accomplished by passing intense current through large electrodes placed on two sides of the heart. The current penetrates most of the fibers of the ventricles at the same time, thus stimulating essentially all parts of the ventricles simultaneously and causing them to become refractory. All action potentials stop, and the heart remains quiescent for 3 to 5 seconds, after which it begins to beat again, usually with the sinus node or some other part of the heart becoming the pacemaker. When electrodes are applied directly to the two sides of the heart, fibrillation can usually be stopped using 110 volts of 60-cycle alternating current applied for 0.1 second or 1000 volts of direct current applied for a few thousandth of a second. When applied through two electrodes on the chest wall, the usual procedure is to charge a large electrical capacitor up to several thousand volts and then to cause the capacitor to discharge for a few thousandth of a second through the electrodes and through the heart.

Unless ventricular fibrillation is defibrillated within a minute from its onset, the heart is usually too weak to be revived because of the lack of nutrition from coronary blood flow. A technique for pumping the heart without opening the chest consists of intermittent thrusts of pressure on the chest wall along with artificial respiration. This technique in combination with the use of a defibrillation is called cardiopulmonary resuscitation.

Prognosis

The prognosis of ventricular fibrillation involves consideration of the underlying cause of cardiac arrest and presence of co-morbidities such as metastatic cancer and dementia [5] [6]. The chances of survival after an acute attack of ventricular fibrillation depend on cardiopulmonary resuscitation rapid availability, advanced life support and transport to a hospital. The probability of success generally declines at a rate of 2-10% per minute. An estimated 20% of patients with cardiac arrest survive to hospital discharge. After return of heart function, there is a moderately higher risk of death due to recurrent ventricular fibrillation when compared to myocardial infarction patients [7] [8] [9]. With immediate angioplasty and stent placement, the prognosis is good.

Etiology

The most common cause of ventricular fibrillation is myocardial infarction, particularly due to inadequate blood flow to the heart muscle because of coronary artery disease [2]. The patients with a previous episode of ventricular fibrillation or a previous heart attack are more prone to develop this condition. Moreover, increased risk for the development of ventricular fibrillation is also found in conditions such as congenital heart disease, cardiomyopathy, myocarditis, heart surgery, hypoxic ischemia, narrowed coronary arteries, damage to the heart muscles by electrocution, use of illegal drugs (such as cocaine and methamphetamine), commotio cordis in athletes and electrolyte abnormalities involving potassium and magnesium [3].

A number of people with ventricular fibrillation have no history of heart disease. However, they often have risk factors of cardiovascular disease, such as smoking, high blood pressure, obesity, dyslipidemia, sedentary lifestyle and diabetes.

Epidemiology

Sudden cardiac arrest is the leading cause of death in the developed world. The World Health Organization estimates a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom with survival rates of only 2%. Up to 30% survivors of cardiac arrest may experience recurrent ventricular fibrillation in the first year after the heart complication [4]. According to one study, 31% of deaths are sudden in people aged between 20 to 29 years and a greater proportion have been common in blacks than in whites. The incidence of ventricular fibrillation is usually higher in men than in women. If prompt treatment is not given, death usually occurs within minutes.

Sex distribution
Age distribution

Pathophysiology

Ventricular fibrillation is a life-threatening cardiac arrhythmia which results from cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating one portion of the ventricular muscle, then another portion, then another, and eventually feeding back onto itself to re-excite the same ventricular muscle over and over again without never stopping. When this happens, many small portions of the ventricular muscle will be contracting at the same time, while as many other portions will be relaxing. Thus, there is never a coordinated contraction of all the ventricular mass at once, which is required for a normal pumping cycle of the heart. Despite massive movement of stimulatory signals throughout the ventricles, the ventricular chambers neither enlarge nor contract but remain in an indeterminate stage of partial contractions, pumping either no blood or negative amounts of it. Therefore, after fibrillation begins, unconsciousness occurs within 4 to 5 seconds due to lack of blood flow to the brain, and irretrievable death of tissues begins to occur throughout the body within a few minutes.
Ventricular fibrillation is based upon the phenomenon of re-entry that leads to “circus movements”.

It is a condition that causes the cardiac impulse to continue to travel around in a circle resulting in the”re-entry” of the impulse into muscle that has already been excited. A long conductive pathway and decreased rate of conduction frequency results in repetitive electrical stimulation. Thus, in many cardiac disturbances, re-entry can cause abnormal patterns of cardiac contraction that ignore the pace-setting effects of the sinus node.

Prevention

People who are successfully resuscitated from ventricular fibrillation and survive are at high risk of another episode. In order to reduce the risk of future ventricular fibrillation, the treatment options include the following.

  • Medications: Various anti-arrhythmic drugs may help control rhythm disturbances. Beta blockers are commonly used in people at risk of ventricular fibrillation.
  • Implantable cardioverter-defibrillator: It is a device that can be implanted in the chest wall of people at increased risk of rhythm disorder. It detects the dangerous heart rhythm and sends out energy shocks to reset the heart to a normal rhythm.
  • Coronary angioplasty and stent placement: The procedure is used for the treatment of severe coronary heart disease and thus reduces the risk of future episodes of ventricular fibrillation.
  • Coronary bypass surgery: This also improves blood supply to the heart and reduces the risk of rhythm disorder.

Summary

Ventricular fibrillation is an abnormally irregular heart rhythm caused by rapid, ineffective, uncoordinated contraction of the ventricles; producing no peripheral pulse. It is a life-threatening medical emergency which, if not stopped within 1 to 3 minutes, is almost invariably fatal [1]. The lower chambers of the heart quiver and it fails to pump any blood to the vital organs, causing cardiac arrest. The patient can sustain irreversible brain damage and possibly become brain-dead due to effects of cerebral hypoxia. Ventricular fibrillation is very common during electric shock and during ischemia of conductive system. It also occurs in conditions like coronary artery disease, chloroform anesthesia, heart muscle disease and trauma to heart. Emergency treatment includes cardiopulmonary resuscitation and shocks delivered to the heart with a defibrillator.

Patient Information

Ventricular fibrillation is a severely abnormal heart rhythm. It is a life-threatening emergency and causes death within few minutes. Emergency treatment requires immediate resuscitation and defibrillation. Drug therapy and defibrillators can correct abnormal rhythms in high-risk patients.

References

Article

  1. Otto CM, Tauxe RV, Cobb LA, et al. Ventricular fibrillation causes sudden death in Southeast Asian immigrants. Annals of internal medicine. Jul 1984;101(1):45-47.
  2. Micchia MT, Beccia F, Ariano M. Etiology and pathogenesis of ventricular fibrillation. Acta anaesthesiologica. 1968;19:Suppl 9:224+.
  3. Pevzner I, Gorshkova TV, Eppel MM. Histoxic hypoxia as one of the causes of ventricular fibrillation and decreased myocardial contractility. Kardiologiia. Jul 1975;15(7):88-93.
  4. Volpi A, Cavalli A, Franzosi MG, et al. One-year prognosis of primary ventricular fibrillation complicating acute myocardial infarction. The GISSI (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto miocardico) investigators. The American journal of cardiology. May 15 1989;63(17):1174-1178.
  5. Trappe HJ, Brugada P, Talajic M, et al. Prognosis of patients with ventricular tachycardia and ventricular fibrillation: role of the underlying etiology. Journal of the American College of Cardiology. Jul 1988;12(1):166-174.
  6. Willems AR, Tijssen JG, van Capelle FJ, et al. Determinants of prognosis in symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction. The Dutch Ventricular Tachycardia Study Group of the Interuniversity Cardiology Institute of The Netherlands. Journal of the American College of Cardiology. Sep 1990;16(3):521-530.
  7. Inkovaara J, Ruosteenoja R. Long-term prognosis after ventricular fibrillation in acute myocardial infarction. Duodecim; laaketieteellinen aikakauskirja. 1971;87(14):1046-1052.
  8. McNamee BT, Robinson TJ, Adgey AA, Scott ME, Geddes JS, Pantridge JF. Long-term prognosis following ventricular fibrillation in acute ischaemic heart disease. British medical journal. Oct 24 1970;4(5729):204-206.
  9. Volpi A, Cavalli A, Santoro L, Negri E. Incidence and prognosis of early primary ventricular fibrillation in acute myocardial infarction - results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI-2) database. The American journal of cardiology. Aug 1 1998;82(3):265-271.
  10. Saxon LA, Uretz EF, Denes P. Significance of the clinical presentation in ventricular tachycardia/fibrillation. American heart journal. Oct 1989;118(4):695-701.
  11. Murdock DK, Lawless CE, Loeb HS, Furiasse JG, Pagano S, Scanion PJ. Characterization of ventricular fibrillation during coronary angiography. The American journal of cardiology. Jan 1 1985;55(1):249.
  12. Murdock DK, Euler DE, Becker DM, Murdock JD, Scanlon PJ, Gunnar RM. Ventricular fibrillation during coronary angiography: an analysis of mechanisms. American heart journal. Feb 1985;109(2):265-273.
  13. Wolf GL, Le Veen RF, Mulry C, Kilzer K. The influence of contrast media additives upon ventricular fibrillation thresholds during coronary angiography in ischemic and normal canine hearts. Cardiovascular and interventional radiology. 1981;4(3):145-147.

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Last updated: 2018-06-21 22:37