Heart Attack and Sudden Cardiac Arrest

Heart attack and sudden cardiac arrest are two related but separate conditions of the same muscle of the body often mistakenly used interchangeably. Even though they are both cardiac related, prevention and treatment for each is different. Understanding the differences between the two most common and deadly heart conditions, and knowing how to recognize the signs and symptoms of each could mean the difference between life and death for the victim.

Physiology of a Heart Attack

A heart attack, also known as a myocardial infarction, is a sudden and complete blockage of one or more arteries which supply oxygen-rich blood to the heart. This kind of blockage is common in many forms of heart disease. One example is a condition known as atherosclerosis, which is clinically defined as “hardening of the arteries”. When arteries harden, “plaque” forms on the walls of the artery and ultimately blocks the artery completely. It can be thought of as a “plumbing problem”.

As more arteries become clogged completely, the circulatory system is unable to supply the heart with enough oxygen and the muscles within the heart begin to die. This condition, when it reaches its end-stage form, will generally result in a patient suffering a heart attack.   

Physiology of Sudden Cardiac Arrest

Conversely, sudden cardiac arrest (SCA), can be described as an “electrical problem.” It is a direct result of a lethal cardiac arrhythmia, generally ventricular fibrillation, which can occur in any person, at any time, regardless of health condition. Ventricular fibrillation is a rhythm defect in the heart, caused by an interruption of the natural electrical impulses produced by the sinoatrial node. The sinoatrial node acts as the heart’s natural pacemaker.

The lower chambers of the heart, known as ventricles, begin to beat in an irregular and often rapid pattern, which prevents the heart from pushing blood throughout the body. Without oxygenated blood flowing to the brain, heart and other vital organs, immediate clinical death occurs.

It is crucial to understand sudden cardiac arrest is not a condition which can be prevented entirely by lifestyle changes.  While exercise and a healthy diet help curb artery blockages, other causes of SCA include:

• An undiagnosed genetic condition such as Wolff Parkinson White Syndrome or Brugada Syndrome
• Choking
• Drowning
• Electrocution
• Excessive physical activity.

Symptoms of a Heart Attack

A heart attack has classic signs and symptoms a bystander can easily learn to recognize. Generally, someone in the midst of a heart attack will be alert, awake and able to tell you about these symptoms:

• Chest pain which can feel like intense burning or tightness (“clenched fist” feeling). This pain may radiate to the neck, between the shoulder blades, jaw, left arm, or the upper abdominal area.
• Occasionally nausea, clammy skin, fatigue, cold sweats, lightheadedness, and dizziness are present.
• Shortness of breath.
• Other symptoms, such as anxiety and a sense of impending doom, have been reported.
• Women sometimes report a stiff or painful jaw; this does not seem to be as prevalent in men.

Symptoms of Sudden Cardiac Arrest (SCA)

A person experiencing sudden cardiac arrest will not exhibit most of the symptoms present in a heart attack. SCA events truly are sudden, as the name implies. While heart attack symptoms can be gradual, sometimes occurring over days or even weeks, SCA occurs instantly when the heart goes into fibrillation and can no longer effectively pump blood. The signs and symptoms of sudden cardiac arrest include the following:

• Sudden loss of any and all responsiveness, which is defined as “no response to tapping on the shoulders or responding when asked if he/she is okay.”
• No pulse
• Not breathing (chest rising and falling). A victim may exhibit what is referred to as ‘agonal’ breathing – described as desperate gasping.  
• Some patients have reported a very brief sensation of nausea, irregular heartbeat, or rapid heartbeat prior to unconsciousness. The length of time between the patient feeling these sensations and becoming unconscious is so brief, it is immeasurable.

Treatment Options

Identifying which condition is occurring dictates which treatment needs to be administered.

Responding to a Heart Attack

Bystander Treatment of a Heart Attack

If you’re a bystander and you see someone experiencing heart attack symptoms, do the following:

• Call 911! It is not recommended you drive the person to the emergency room as this could actually delay treatment while you fill out forms and wait to get the person in to be seen.
• Stay close.  It is important to keep an eye on the person in case the heart attack turns to sudden cardiac arrest.  
• If the person has been prescribed nitroglycerin in the past, and it is close at hand, administer a dose.  
• If they have not been prescribed nitroglycerin, and you know for a fact they have no allergies or are taking medications which may interact badly with it, you can give regular aspirin.
  • Why: Since the arteries may be blocked, but not be completely closed, a blood thinner like aspirin can help blood continue to flow. The longer the heart is deprived of oxygen, the more damage is done. Thinning the blood as soon as possible will allow the heart to regain oxygenation much sooner than a patient who does not receive treatment until EMS arrives.
• Keep the patient comfortable and calm until EMS arrives.

Professional Treatment of a Heart Attack

• When professional responders arrive on the scene they will generally start an intravenous line to administer another blood thinner, such as heparin, which works via a different mechanism. They will also assess the patient and transport to the hospital if necessary.
• In the hospital, the patient will be assessed and will most likely undergo angioplasty to find and open any blocked arteries. Clot-busting drugs may also be given if the patient arrives at the hospital soon enough.
• Out-of-hospital, long-term treatments may include:
  • Medicines such as ACE inhibitors, anti-clotting, anticoagulants, beta blockers and statin drugs  
  • Additional medical procedures such as bypass surgeries to prevent further heart attacks
  • Lifestyle change recommendations including diet, safe exercise, stress management, limiting alcohol intake and quitting smoking (if relevant)
  • Cardiac rehabilitation, including education on heart disease, counseling, and training of the patient and loved ones on possible future signs and symptoms of possible future heart attacks.  
    

Responding to Sudden Cardiac Arrest

Bystander Treatment of Sudden Cardiac Arrest

If you’re a bystander and observe someone experiencing SCA symptoms, immediately begin the Chain of Survival:

• Call 911 or have another bystander call 911
• Get an AED or send another bystander to get the AED
• Begin CPR
• Turn on the AED when it arrives and follow its directions
• For every minute defibrillation is delayed, the patient’s chances of survival decrease by 10%.
• Continual CPR and defibrillation should be continued until EMS transport arrives at the scene, or until the patient regains consciousness.
• The AED should be left attached to the patient until EMS arrives for use as a monitoring tool.

It is important to remember a patient in SCA is clinically dead. There is nothing you can do treatment-wise with an AED or with chest compressions which will result in any further damage to this individual. In fact, only positive outcomes can be achieved from this form of treatment. Use of an AED and CPR should be initiated in 100% of cases, as quickly as possible.

Professional Treatment of Sudden Cardiac Arrest

• In Hospital: post-arrest care usually includes most of the treatments above for heart attack
• In-Hospital Care: may also include additional tests to determine the cause of the SCA if it is not apparent at the time of the arrest.
  
• Long-term Treatment: may include the permanent placement of an implantable cardioverter-defibrillator. This device is connected to the heart via electrical leads and implanted just under the first couple of layers of the skin. Implanted defibrillators deliver the same type of shock as an AED directly to the heart anytime an arrhythmia is detected. 

Conclusion

When comparing a heart attack to sudden cardiac arrest, the information provided here demonstrates the signs and symptoms are not only different but markedly different. Starting the correct treatments outlined above quickly is key to increasing the chances of survival for both.

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Hypertrophic cardiomyopathy (HCM) is the leading cause of heart-related sudden death in people under the age of 40. According to the HCM Association website, publications from the 2000’s indicate that HCM is the most common of all genetic heart conditions affecting over 1 in 500 people in the general population. Based on these data we may estimate that between 700K and 725K people in the United States have HCM. Symptoms may be mild, and many times are dismissed as attributable to other conditions. An ECG (electrocardiogram) can identify this condition 90% of the time. Once detected, either through an ECG or a physical exam, an echocardiogram can confirm HCM.

Hypertrophic cardiomyopathy is a thickening of the heart muscle walls, making it more difficult to pump blood effectively.  While many people can have this condition but never experience symptoms and never even know they have it, for some, it is severely life-threatening. In HCM,  the cells which make up the heart are not aligned normally; this abnormality is called “myocardial disarray”. This disarray is usually not present in 100% of the heart muscle but affects it in patches.

It is theorized this patchy “disarray” is what interferes with the electrical impulses of the heart, causing abnormal heart rhythms (arrhythmia), which may lead to sudden cardiac arrest during times of physical exertion. This occurs most publicly among young male athletes, with basketball and soccer players leading the list. There are countless news stories about seemingly healthy individuals suddenly collapsing on the court or field. Around 14% of the time, autopsies reveal hypertrophic cardiomyopathy is the culprit – a condition which could have been identified with a routine ECG. In some cases, athletes are able to be revived through CPR and early defibrillation with an automated external defibrillator (AED), making the case not only for CPR training of anyone in a sports leadership position (athletic trainers, coaches, umpires, referees), but better access to AEDs, and more thorough prescreening procedures to identify those athletes at risk as well.

Hypertrophic cardiomyopathy does not have to be a death sentence. Knowing you have the condition is the best defense against an unexpected event. Most people with the condition live normal, active lives. It definitely does not mean you should not exercise at all. In fact, not exercising is detrimental to your overall health and may lead to obesity and other health concerns which could impact your heart such as high cholesterol and high blood pressure. However, high-impact and competitive sports are not recommended.

Treatments for HCM vary depending on the severity of the condition in individual patients. One of the most effective treatments for identified high-risk HCM patients is an implantable defibrillator which will administer a shock any time it senses the heart has gone into a shockable rhythm, ventricular fibrillation or ventricular tachycardia. Medications prescribed for HCM are designed to treat symptoms of the condition, rather than the condition itself for which there is no cure. Beta-blockers and calcium channel blockers help the heart contract and relax and may be prescribed to relieve pain in the chest and shortness of breath during exercise. Blood thinners are sometimes prescribed to reduce the risk of blood clots (if there is an arrhythmia present due to atrial fibrillation).   

Occasionally, circumstances or other conditions prevent patients from taking medications or receiving an implantable defibrillator.  In these instances, surgery may be an option. When blood flow out of the heart is severely blocked, symptoms can become severe. An operation called surgical myectomy may be done where a portion of the thickened heart muscle wall is removed to allow better blood flow. In other cases, patients may be given an injection of alcohol into the arteries which feed the thickened part of the heart (alcohol septal ablation). The bulging wall shrinks, allowing for better blood flow. People who have this procedure often show much improvement.

Since hypertrophic cardiomyopathy is genetic, it is recommended people with an immediate family (parents, siblings, children) history of sudden cardiac death be evaluated by their physician if they have exhibited any of the following symptoms (from the Cleveland Clinic website):

• Chest pain or pressure that usually occurs with exercise or physical activity, but also may occur with rest or after meals.
• Shortness of breath and fatigue, especially with exertion. These symptoms are more common in adults with hypertrophic cardiomyopathy and are most likely caused by a backup of pressure in the left atrium and lungs.
• Syncope (fainting or passing out) may affect HCM patients. Syncope with HCM may be caused by irregular heart rhythms, abnormal responses of the blood vessels during exercise, or no cause may be found.
• Palpitations (fluttering in the chest) due to abnormal heart rhythms (arrhythmias) such as atrial fibrillation or ventricular tachycardia. Atrial fibrillation occurs in about 25 percent of those with HCM and increases the risk for blood clots and heart failure.

There may be no cure for HCM, but understanding the implications of living with this condition are critical to survival for those who have it.

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Bypass heart surgery is exactly what it sounds like. If you think about a highway bypass, which offers an alternative route to congested city driving, you get the general idea. In this case, it is blood, which needs to be rerouted due to clogged coronary arteries which normally supply oxygen-rich blood to the heart muscles. Blockages are generally caused by a buildup of plaque on the walls of the blood vessel.  If the plaque ruptures, a blood clot will form around the plaque.  This can significantly block blood flow through the artery, and the heart muscle supplied by this artery begins to die due to lack of oxygen and nutrients. This is called a heart attack or myocardial infarction.

In order to reroute the blood around the blockage, a strong, healthy, clear vein must be grafted to the existing coronary arteries before and after the block. If there is more than one blocked artery, multiple grafts may be needed – hence the terms “bypass” (one), double bypass (two), triple bypass (three) and quadruple bypass (four). It is very rare for a quintuple bypass to be performed, but it does occasionally happen.

In traditional, open-chest bypass surgery, a vein is harvested from the patient’s leg or wrist for the graft (the more bypasses which need to be made, the longer the vein must be). The patient’s sternum is cut open with a saw and the ribs spread. Blood is re-routed through a heart/lung machine to keep oxygenated blood flowing to the patient’s brain and vital organs, and the heart is stopped. The surgeon goes to work sewing the re-routed vein to the arteries before and after the blockages, opening up the pathways for blood to flow freely again. Recovery for this kind of surgery averages around two months, depending on the general health of the patient.

A new kind of bypass surgery, called Totally Endoscopic Coronary Artery Bypass (TECAB) Surgery is now being performed at some hospitals. This breakthrough surgery utilizes the Da Vinci Surgical System robot which accesses the heart through five finger-tip sized slits in the chest. There is no need to saw through the sternum or spread the ribs. According to the University of Chicago hospital website, with the Da Vinci Surgical System, “The surgeon sits in a console equipped with controls that direct robotic arms to perform the surgery. The robotic arms are very agile and work as an extension of the surgeon’s hands. A tiny camera attached to the robotic arms gives the surgeon a very detailed, three-dimensional view of the operating space inside the chest.” Advantages to this type of surgery include a much shorter recovery time, (according to the same website, “Most patients are back to work and/or other activities within a week, compared to four to eight weeks with open-chest bypass.”), shorter hospital stay, less chance for infection, minimal blood loss, minimal scarring, and sometimes, it can be performed without stopping the heart.

Dr. Vincent Gaudiani, a cardiologist at the California Pacific Medical Center, in his 3-part video series showing a live open-chest bypass, described surgery as “controlled injury that has a therapeutic aim.” TECAB would appear to minimize this injury to a significant degree.

Angioplasty & Stents

Sometimes bypass surgery is not necessary, and balloon angioplasty to open blocked arteries can be performed. With this procedure, a catheter is threaded through the patient’s groin or wrist arteries, the end of which is capped with a tiny balloon. When the constricted area is reached, the balloon is inflated and deflated in succession, inflating a little more each time to increase the cleared area. Sometimes a stent is inserted at the same time to hold the artery walls open. To install the stent, it is placed over the deflated balloon prior to insertion and, when the balloon is in place and inflated, the inflated balloon expands the stent, which locks in place. The balloon is deflated and removed, but the stent remains within the artery, hopefully keeping the artery clear indefinitely. Some stents are even coated with medications to prevent further clotting.

The procedure is minimally invasive and usually only requires a night or two in the hospital. The majority of experienced pain will be at the insertion site, and recovery is relatively quick.

If you suspect you may have heart-related issues, please take the time to visit your doctor. There are many options available, from surgical and medicinal, to relatively simple lifestyle changes, which can treat life-threatening heart problems before they become fatal.

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Too often, people tend to lump major life-threatening physical conditions together. While heart attack and stroke both get a lot of press, they are completely different conditions with very different symptoms, treatments, and outcomes. They do have two things in common – they are both commonly caused by blockages of arteries, and they can both result in death.

Heart Attacks are caused by a blockage in the arteries of the heart (as the name would imply). Without a supply of oxygenated blood, the part of the heart supplied by the blocked artery begins to die. This muscle death can cause a range of symptoms such as a feeling of crushing pain in the chest, numbness of the left arm, shortness of breath, shoulder or back pain, sweating, and nausea. The victim is typically awake and able to describe their pain. They need to get to a hospital without delay. If someone complaining of heart attack symptoms suddenly collapses and is no longer responsive or breathing normally, the heart attack has escalated into sudden cardiac arrest. Call 911 and begin CPR immediately. Defibrillation with an AED may be necessary to reset the heart’s rhythm. If one is available it should be utilized as soon as possible – ideally within 3 to 5 minutes. If no AED is available, continue CPR until EMS help arrives.

Stroke is typically caused by either a blockage of a blood vessel in the brain or by a rupture of a blood vessel in the brain. This can result in symptoms including “sudden difficulty seeing, speaking, or walking, and feelings of weakness, numbness, dizziness, and confusion.” (https://newsinhealth.nih.gov/issue/aug2014/feature1) Numbness or paralyzation on one side of the body is also a notable outward sign of stroke and observers will be able to see it most obviously in the victim’s facial muscles. If you suspect someone is having a stroke, you should administer a simple 4-part test: 1. Ask them to smile. 2. Ask them to speak a simple sentence such as “It is a very nice day.” 3. Ask them to raise both arms. 4. Ask them to stick out their tongue. If they are only able to smile on one side, their speech is slurred or they can’t remember the sentence, they are only able to raise one arm, and/or if their tongue automatically goes to one side or the other, they may be having a stroke. Call 911 immediately and wait for EMS to arrive. They can begin to administer treatment on the way to the hospital. Every minute counts!

Treating a heart attack often includes anticoagulant drugs to thin the blood (liquids move through small openings quicker if they are thinner – the most common of these is simple aspirin) or other drug therapy, catheter procedures to open the arteries without opening the chest, or bypass surgery. Lifestyle changes are also often recommended as part of continuing treatment. Someone who suffers a heart attack can live a relatively “normal” life after leaving the hospital.

Since there are two different kinds of stroke – Ischemic (where the artery is blocked) and Hemorrhagic (where a blood vessel ruptures or leaks blood), there are two different treatments. For an ischemic stroke, treatment is similar to those of a heart attack – anti-clotting drugs or clot-busting drugs can be used to dissolve the clot, or a catheter procedure can be performed to physically open the blocked vessel. For a hemorrhagic stroke, the first thing the doctor will do is try to isolate the location of the bleed. Surgery may be needed. After leaving the hospital, recovery times can vary from days to years depending on the severity of the damage incurred during the stroke and may include both physical and speech therapy.

In cases of both heart attack and stroke, early intervention is the key to favorable outcomes. Heart attack symptoms can go on for hours, days or even weeks and can lead to sudden cardiac arrest if ignored. As strokes affect the brain, they can leave a victim with a road to recovery which involves relearning or improving how they move, think and speak. If there is any indication you are in the presence of someone experiencing a heart attack or a stroke, or if you think you may be having one yourself, the best advice is always to get medical help immediately!

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What is Sudden Cardiac Arrest?

While we like to romanticize the heart, the truth is the heart is nothing more than a pump, and its job is to pump blood to the brain and vital organs. Blood carries the necessary nutrients and oxygen to keep us alive. Sudden Cardiac Arrest (SCA) occurs when the heart suddenly stops pumping blood effectively, and a person whose heart suddenly stops pumping blood effectively loses consciousness and stops breathing normally. It is frequently caused by an abnormal, chaotic heart rhythm called ventricular fibrillation where the heart is just quivering and not moving blood through the heart and out to the body.

Once SCA occurs, the brain will start to die within 4-6 minutes of being deprived of oxygen, so immediate help is vital. For each minute which passes without oxygen being delivered to the brain and body, there is an incremental 10% decrease in the chance of survival. The average response time for paramedics can be anywhere from 8-15 minutes. Since the brain starts to die within 4-6 minutes of being deprived of oxygen, it is frequently too late to save the person and have them remain neurologically intact by the time paramedics arrive. Immediate CPR and early defibrillation using an Automated External Defibrillator (AED) can make the difference!

It may surprise you to know Sudden Cardiac Arrest is the single leading cause of death in America. It is killing more than 900 people in this country every day. More people die from SCA every year than all the deaths from breast cancer, prostate cancer, lung cancer and AIDs combined. It is a huge public health problem in this country, and it can be treated by you! Yes, you!

Who is at Risk?

Sudden Cardiac Arrest can happen to anyone, anywhere, at any time, but research shows African Americans and Hispanics have a higher risk than Caucasians. Also, a prior heart attack or heart failure is a major risk factor for SCA; and a family history of SCA in a parent, sibling or offspring is associated with a two-fold increase in SCA.

What are the Leading Causes?

There are many causes of Sudden Cardiac Arrest. The most common are:

1.) Heart Attack, also called a Myocardial Infarction

2.) Heart Muscle Thickening, such as Hypertrophic Cardiomyopathy and Arrhythmogenic
Right Ventricular Dysplasia

3.) Heart Rhythm Disorders, such as Brugada Syndrome, Long QT Syndrome, and Wolff
Parkinson White Syndrome.

4.) Some other common causes of SCA not related to having heart disease are:  
recreational drug use, electrocution, hypothermia, drowning, and commotio cordis
(which is a disruption in the heart rhythm due to a sudden blow to the chest).

Is SCA treatable?  

Yes, it frequently is, and with appropriate treatment, it is possible to greatly increase survival rates.  This is where you come in – you can help treat the leading killer in this country! Right now, the overall survival rate from SCA is only 10.4%. If the SCA is due to the chaotic rhythm of ventricular fibrillation, the survival rate is 31.7%. Survival rates increase significantly in places with strong AED programs and CPR training, such as Las Vegas casinos where survival rates jump to over 70%! Communities with strong CPR training programs and AEDs in police cars, local parks, recreation centers, schools and sporting fields, such as King County, Washington, have survival rates of 62%.

When a bystander witnesses an SCA event and has the confidence to begin CPR and deploy an AED, the victim’s chances of survival are greatly increased. Think of CPR as support – you are supporting the victim because every time you push on the chest, blood flows from the heart up to the brain and out to the vital organs. The AED, on the other hand, is treatment – it stills the chaotic rhythm of the ventricular fibrillation and allows the heart to restore its natural rhythm.

Arm yourself! Take a CPR course which includes AED use, and you will be able to recognize the signs of Sudden Cardiac Arrest and know what steps to take to help a victim of this quick, silent killer. Quality CPR and early defibrillation are crucial!

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A Case Study of One Woman’s Experience with Atrial Fibrillation

Patsy is a 64-year-old, otherwise healthy, Caucasian female with zero cardiac risk factors, save for about 15 excess pounds of body habitus.  Throughout the course of the past 25 years, she had experienced sporadic events which included heart palpitations, flutters, and intense heart racing.  She always correlated these events to anxiety attacks and related symptoms of the same – atrial fibrillation was the furthest item from her mind.  She was continually subjected to a quite demanding schedule, with a full-time executive position in the sales department of a major corporation as well as a busy family life with two children and a household to maintain.  As time went on, her children grew up and moved out, and she retired from her position.

However, she was still the first person to be contacted when it came to supervising grandchildren and was also expected to complete most of the daily upkeep tasks in the home she shares with her fiance.  To compound this, her oldest son was incarcerated in state prison for a period of three years, and her life became consumed with this situation, leaving her in a constant state of anxiety and mental anguish.  As such, with these events being attributed to anxiety, Patsy never sought medical treatment for them; and even when she went to her primary provider for health maintenance visits, her vital signs were always within normal range, and all of her preventive screening tests were always normal.  With the belief her condition was a complication of anxiety, Patsy was determined not to take a sedative-hypnotic drug such as Valium or Xanax to combat these suspected panic attacks, and as such, attempted to always practice psychological methods such as deep breathing and meditation to alleviate these spells.  With this train of thought, the focus on any sort of follow-up treatment for these anxiety attacks faded from her mental process.  However, she would soon learn things were not as they appeared.

Abruptly, on September 3, 2015, Patsy was awakened at approximately 4:30 a.m. with an inability to swallow or form words.  Her son, who had been released from prison, noticed the dysarthria and a bit of a facial droop and took her to the local hospital.  The symptoms were pronounced to Patsy, but subtle to observing hospital staff and treating physicians, and as such, they did not think there was a serious neurologic etiology to them.  During routine testing, a heart rate of 145 beats per minute was observed along with an irregular rhythm, and atrial fibrillation was felt to be the culprit and was diagnosed as such.  At this point, Patsy’s youngest son was contacted and notified of these events.  Having a medical background, he promptly suggested to the admitting physician it was simply an impossibility to have neurologic symptoms such as dysphagia and dysarthria with atrial fibrillation unless a thromboembolic stroke had occurred as a result of a traveling blood clot.  The treating team ignored this, and consequently, did not perform a CT scan or MRI of the brain upon presentation to the emergency room.  Therefore, new, potentially life-saving treatments, such at the administration of TPA and other articles of stroke protocol, were not considered.

During the first day of hospitalization, Patsy’s youngest son visited her in the hospital, at which time the right-sided weakness and dysarthria became worse.  Critical care staff members were consulted, yet they still felt this was not stroke-related, for some reason unknown.  She continued through the night with these symptoms worsening.  Then, upon morning rounds, the hospitalist physician took one look at his patient and immediately ordered an MRI of the brain, which confirmed the presence of four old, small-vessel, lacunar-type infarctions, with one acute — or new — stroke happening that morning.  Patsy was immediately transferred to a certified stroke center’s intensive care unit, where she was sufficiently anticoagulated and released within 8 days with the residual effects greatly diminished.

Moving along, about a month after the hospital admission and diagnosis, Patsy returned to the cardiology department for a routine follow-up appointment.  At this visit, her heart rate was 84 and regular.  Just as the cardiologist was leaving the room to otherwise give her a clean bill of health with instructions to return in one year, he decided to repeat her manual cardiac examination and found she had spontaneously converted to atrial fibrillation.  She was then sent for an EKG and admitted back to the hospital, with the physician concerned for a new-onset, and extremely lethal form of ventricular tachycardia occurring concurrently with the atrial fibrillation.  Needless to say, her level of care was upgraded to include 24-hour close observation in the Cardiac Critical Care Unit of the University of Florida Hospital.  Fortunately, the ventricular origin of the arrhythmias was eventually ruled out after cardiac catheterization and CT angiography.  However, upon identification of the cells responsible for the atrial fibrillation, it was determined the risk of further complication was too great to proceed with a curative procedure such as ablation, yet implantation of an AICD was not something Patsy was ready to consider unless there was no hope of medical management.  Today, she is sufficiently managed with a new-generation anticoagulant called Eliquis as well as heart rate/rhythm controlled with metoprolol and Cardizem.  She also received statin therapy as a secondary prevention method to prevent harmful low-density lipoprotein, the so-called “bad cholesterol,” accumulation which can contribute to vessel stenosis.

Bearing this in mind, it is clear there were so many factors which contributed to Patsy’s situation.  First of all, the stress in her personal life masked the symptoms of atrial fibrillation, including the palpitations she, otherwise, would have discussed with her primary physician.  Secondly, because her atrial fibrillation is paroxysmal and intermittent, it was up to chance the irregular rhythm would be detected at a routine visit, and chance ruled against such detection.  Additionally, during the beginning stages of hospitalization with the stroke symptoms, the treating physicians failed to treat the patient according to stroke protocol, and as such, her atrial fibrillation caused her to “throw” another clot that evening.  Had she been evaluated for and deemed to be a candidate for TPA administration, there is a high probability the final lacunar infarction would have been prevented.  In spite of these systemic failures, Patsy has made a 95% recovery in less than 6 months.  However, the risk of a future stroke is now increased astronomically, and she will be on lifelong medication unless said medication eventually fails to suppress the arrhythmia, at which time she will require implantation of an AICD device in order to maintain normal sinus rhythm.

Unfortunately, many patients are not so fortunate.  Many times, due to the unique challenges of identifying this intermittent form of atrial fibrillation and consequent challenges of treatment of the same, these patients may suffer from a larger vessel stroke, perhaps of the middle cerebral artery (MCA), which causes profound, permanent, debilitating residual neurologic symptoms and even death.  In cases such as these, however, the patient will present to the hospital with such profound symptoms treating staff immediately begin stroke protocol and evaluation for clinical indication of TPA administration, which can greatly reduce the likelihood of stroke evolution, and in turn, can increase the patient’s chance of survival and recovery.

In summary, the lessons from Patsy’s story are profound, to say the least.  In this presentation, all of the challenges associated with a proper diagnosis of atrial fibrillation were present.  Because Patsy had no cardiac symptoms or risk factors of any kind and because of the stress level in her personal life, atrial fibrillation went undiagnosed, therefore leading to a series of strokes and further cardiac events.  Had this been identified, proper medical management had a very real probability of preventing these strokes.  This story illustrates the unique challenges atrial fibrillation creates, as well as the complications which can occur when the proper diagnosis does not happen.  Therefore, it is important every member of a patient’s treatment team remain watchful for differential possibilities when a patient presents with symptoms such as palpitations with no other symptomatology, so as not to discount such symptoms as “anxiety.”  Furthermore, it is equally important for the general population to be educated in the warning signs of major cardiac irregularities, such as atrial fibrillation and other ventricular events.  Sadly, this is a case in which education and information could have prevented a number of complications from the condition, and it is ever-so-important misinformation and miscommunication such as this are precluded.

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Atrial Fibrillation:  Analysis of the Causes, Treatments, and Challenges

Atrial fibrillation, in its most basic of definitions, is a form of cardiac arrhythmia or “irregular heartbeat.”  A more detailed definition of this condition can be described as an arrhythmia in which the upper chambers of the heart, or atria, beat irregularly, thus potentially disrupting the normal blood flow of the heart by not allowing the lower chambers of the heart, or ventricles, to completely fill with blood.  This can lead to major complications, usually resulting in the “throwing” of a blood clot, leading to strokes of an ischemic (oxygen-depriving) nature, or alternatively, resulting in heart failure due to decreased ventricular function — commonly known as congestive heart failure.

Now, this arrhythmia is the most common type of irregular heartbeat worldwide, with estimates showing the affected population in the United States to be between 2.7 and 6.1 million individuals [1] as of 2014.  Now, the difference in the conservative estimate of 2.7 million and the liberal estimate of 6.1 million demonstrates the unpredictable — and often diagnosed — nature of this condition.  Atrial fibrillation can be intermittent, sensed as a bit of a palpitation or flutter in the patient, and may resolve spontaneously without any intervention whatsoever.  Because of this, the afflicted patient may not seek treatment, and in turn, may never be diagnosed with atrial fibrillation altogether.  These characteristics present some very unique challenges to the treatment and management of what can be a lifelong condition.

Variants of Atrial Fibrillation

First, it is important to understand the differing variants of atrial fibrillation, and what each type entails.  The American Heart Association classifies atrial fibrillation in the 2014 AHA/ACC/HRS Guidelines into several distinct iterations of the condition.[2]  With paroxysmal atrial fibrillation, “the faulty electrical signals and rapid heart rate begin suddenly and then stop on their own.”[3]  Generally, paroxysmal atrial fibrillation can be erratic and will stop in less than a week.  However, most episodes convert back to the heart’s normal rhythm, called sinus rhythm, within 24 hours.  The challenges with treating this variant of atrial fibrillation rest mainly on correct identification and diagnosis.  Because of the erratic and spontaneous nature of this type of atrial fibrillation, patients may go years without a correct diagnosis, despite maintaining regular health maintenance visits with their primary care physician.  Many times this will occur because the patient is not in atrial fibrillation at the time of the scheduled appointment, and with good vital signs, the brief episode of palpitations may slide under the proverbial radar as simply an anxiety attack.  Many times, this spontaneous irregular heartbeat will cause a thromboembolic event, leading to a series of different possible ischemic strokes.  However, if paroxysmal atrial fibrillation is diagnosed, the treatment options are many, with conservative, medical management being the most preferred method of treatment.

Conversely, with persistent atrial fibrillation, the abnormal rhythm continues uninterrupted for more than a week. This too has the potential to abruptly convert back to normal sinus rhythm. The persistent nature of this variant is more easily identifiable — and therefore, treatable — than paroxysmal atrial fibrillation. Healthcare providers are able to identify the rapid rate via standard pulse readings, visualize the irregularity through ECG, diagnose persistent atrial fibrillation through subjective and objective examinations, and properly treat the symptoms. The same risks are associated with both the intermittent and persistent types of atrial fibrillation, with the former representing a more challenging presentation than the latter, due to missed diagnoses and sporadic symptomatology.

Finally, permanent atrial fibrillation occurs when sinus rhythm cannot be restored, even with treatment.  It is important to note that both variants above have the possibility to progress in frequency as time moves along, resulting in this permanent arrhythmia.  When a patient reaches this point, the normal methods of treatment, including anticoagulation and rate/rhythm control medication as well as more invasive methods, have failed to reduce the patient’s symptoms, and the decision has been made by the patient and provider not to attempt restoration of sinus rhythm whatsoever.  At this point, the patient’s life quality can diminish, and the patient may feel increasingly tired, out of breath, and lifeless.  When these symptoms become omnipresent, there is a good chance that the patient’s heart has become weak, enlarged, and unable to pump out precious oxygenated blood into the body.  The end result here is congestive heart failure, which can only be cured by heart transplantation, although symptomatic treatment is available.[4]

Complications Associated with Atrial Fibrillation

As noted above, the two main complications that can arise from atrial fibrillation are stroke and congestive heart failure.  The majority of the population is familiar with these two conditions, but in order to understand the risks associated, it is important to understand the etiology of both of these when in the setting of atrial fibrillation.

Congestive Heart Failure

As such, congestive heart failure occurs when the heart is overworked.  In the setting of atrial fibrillation, the irregular and erratic impulses that cause the arrhythmia cause the heart to work too hard, rendering it enlarged, ineffective, and weak.  When atrial fibrillation compounded with other heart problems, such as valvular disease and aortic stenosis, the resultant congestive heart failure becomes increasingly severe and hard to treat.  As the heart is unable to pump out the oxygenated blood, the lungs begin to fill with fluid in a condition called pulmonary edema.  This causes fluid retention throughout the body, but mainly in the lower extremities.  When this happens, electrolyte balance can be significantly out of control, leading to very serious conditions such as toxic metabolic encephalopathy.  Weight gain, shortness or breath, and extreme fatigue are also symptoms.  In order to treat this, providers must decrease the fluid retention.  This is done by using diuresis to rapidly eliminate the fluid through reducing the volume of fluid in the body by increasing urination.  The risk of complication with diuresis is significant, in that if a patient is over-diuresed, damage to the kidneys can easily occur.  Therefore, as evidenced by this lone example of the many complications that can arise in treating congestive heart failure, it becomes clear that this is one of the most significant — and life-threatening — conditions that can develop as a progression of disease due to atrial fibrillation and its increased stress on the heart.

Stroke

Additionally, stroke is the other major, life-changing, medical condition that can occur as a result of atrial fibrillation.  However, different than congestive heart failure, the cause of an acute stroke in the setting of atrial fibrillation does not occur as gradual and systematically as the weakening of the heart with congestive heart failure, but rather, it is spontaneous and unpredictable by the very nature of the physiology of the event.  That is to say, every time the heart converts into atrial fibrillation, the atria has a very high probability of pooling blood, as the normal cycle of pumping to fill the ventricles is interrupted.  This pooled blood had the potential to begin coagulation — forming a clot.  Once a clot is formed in the heart, there exists a very real, highly-probably chance of said clot “breaking off” or “throwing,” which releases one or several into the arterial circulatory system.  What happens next literally amounts to a stroke of good luck or a stroke of bad luck, no pun intended.  The clot can block off one of the arteries leading to the blood flow in the brain, causing cerebral ischemia — a stroke.  In this case, the size of the clot determines the severity of the stroke.  In some instances, the stroke can occur as a sudden, debilitating loss of speech and motor function, but in other cases, these clots can block smaller vessels in the brain, and the loss of function is not as pronounced and/or more gradual.  However, while the extent of the damage is generally the gold standard in determining the severity of the attack, it is just as equally important to understand that, in most cases, this damage cannot be reversed.  The patient may end up with a condition known as hemiparesis, where one side of the body is affected and the other side functions normally.  With that said, it is important to understand the multiplicity in stroke probability that exists as a result of atrial fibrillation.  While statistical data suggest that a person with atrial fibrillation is five times more likely to have a stroke,[5] a more realistic understanding is possible when considering that each time the heart experiences arrhythmia from atrial fibrillation, there exists a very good possibility of a clot being “thrown” and causing a stroke.  In fact, many patients who experience this phenomenon can be treated for atrial fibrillation for years, have successful procedures and underestimate this risk.  The same patients can be discharged from the hospital in stable condition, only to have a massive stroke the following day from a brief episode of atrial fibrillation.  Fortunately, there are many treatment options that can be employed when atrial fibrillation is diagnosed which act as stroke-prevention agents by keeping the heart at a regular rate and rhythm, thereby practically lowering the risk back to that of a patient who does not suffer from arrhythmia.

Treatments

As mentioned above, there are many different treatment options available for the patient who suffers from atrial fibrillation.  These range from medical management and conservative treatment to semi-invasive techniques such as cardioversion, to even more invasive procedures with very high cure rates, such as catheter ablation or pacemaker/AICD (Automatic Implantable Cardioverter-Defibrillator) implantation.  The clinical indication for each type of treatment is a very individualized approach, as not everyone with atrial fibrillation is a candidate for the cure procedure – nor does every candidate wish for invasive treatment.  The most prominent and preferred approach to treatment by providers and patients alike is conservative medical prevention.  Using this technique, patients are started on a medical regimen that usually consists of a medication to thin the blood (an anticoagulant, such as warfarin), along with a rate-control medication (beta-blockers such as metoprolol), and rhythm-control medications (such as amiodarone).  Additionally, cholesterol-lowering medications known as statins, are routinely introduced as a secondary prevention strategy to decrease stenosis of the blood vessel walls, as is caused by the accumulation of LDL-type cholesterol.  For many patients, this type of prevention regimen works amazingly well.  However, as with all medications, there exists the chance of severe side effects occurring.  With these types of regimens, the most serious and common side effect can be the increased risk of bleeding associated with the anticoagulant medications and risk of major long-term complications associated with amiodarone, including lung toxicity.  Therefore, it is very important that the provider treating the patient have a clear picture of the individual’s overall health, so as not to prescribe a medical regimen that is contraindicated with another condition.

Unfortunately, conservative medical management is not indicated for and is not effective for every patient with atrial fibrillation.  In many instances, a patient will have palpitations so severe that he/she feels it necessary to sojourn to the emergency room for treatment.  At this point, the decision will be made to start the patient on medical management or to hold medical management.  In the event that the medication is not working or is not indicated, another option is a procedure known as electrical cardioversion or electrocardioversion.  This is a planned procedure, many times done in a specialty suite (electrophysiology suite), where the heart is effectively shocked back into normal sinus rhythm, using the same logic behind the electrical impulses used in AED devices to deliver shocks to restart a heart that has stopped beating during defibrillation.  The main difference between these two techniques is that electrocardioversion delivers the electrical impulse at a specific portion of the cardiac cycle, whereas resuscitation is deployed at a random point of the same.  If not done in an emergent manner, it is ideal for the patient receiving electrocardioversion to receive anticoagulation therapy for some period of time before the event to ensure that there are no clots that may break away during the procedure.  Electrocardioversion can be very effective for converting back to normal sinus rhythm, although sustained maintenance of sinus rhythm with this procedure is only around 20% to 30%, but increases when rate-control medications are taken afterward.[6]
Conversely, the invasive forms of treatment are generally done when conservative management has failed, the patient is not indicated for conservative management, or the patient has the desire to attempt to cure the underlying etiology of the atrial fibrillation above all else.  The two main types of these invasive treatments are known as ablation or AICD/pacemaker device implantation.  Both are performed via cardiac catheterization, in which an instrument enters the heart through a hollow catheter that is introduced through a blood vessel in the femoral or groin area.  With ablation, the electrophysiology specialist will attempt to find the defect in the heart that is causing the irregular rhythm and will then attempt to destroy – or ablate – the defect.  When this can be performed safely and successfully, the rate of cure for atrial fibrillation is very high.  Unfortunately, this is not a procedure that is indicated in every situation, as much depends on the location and type of defect as well as safety protocol.  Additionally, another permanent form of treatment is the implantation of an automatic implantable cardioverter-defibrillator device (AICD).  The leads of this are delivered peripherally into the heart, usually via a subclavian portal, and the device is implanted under the skin on the patient’s chest.  This device has the ability to monitor for changes in rhythm and electrocardiovert the heart back to normal sinus rhythm upon detection of the arrhythmia.  The major drawback to this procedure, besides the surgical portion involved, is the size of the device, which becomes clearly visible and protrudes from under the patient’s skin.  However, it is likely that as technology advances and components are reduced in size, this aesthetic drawback will become nonexistent.  The function provided by an AICD does not cure the underlying cause of the atrial fibrillation, but rather corrects the rhythm in an instant.

Conclusion

In summary, it is apparent that there are some monumental challenges that apply to effective treatment and management of atrial fibrillation.  As stated above, the first of these obstacles is correct diagnosis of the condition, followed by appropriate choices as indicated for each individual patient situation regarding treatment options, methods, and efficacy.  The end goal in all of these treatment options is that of reducing the risk of the two major complications that can occur due to atrial fibrillation — congestive heart failure and stroke.  Taking all of this into account, the patient and treating provider must work together to create an individual treatment plan that will address the issues of stroke risk, medication side effects, the patient’s preference of conservative management versus highly-invasive possible cure, as well as the unique circumstances that make up each individual picture of the patient’s entire panoramic state of health.  However, when this type of creative approach is incorporated, the successful reduction of symptoms and stroke risks are very attainable, and with new treatments continuing to be introduced into this exciting field, there may be a time soon where these risks and complications can be reduced even further, to a point to where patients can say, “Atrial fibrillation?  Oh yeah, I used to have that.”

Footnote1:

[1] January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Journal of the American College of Cardiology. 2014;64(21):2246–80.

Footnote2:

[2] 2014 AHA/ACC/HRS Guidelines for the Management of Patients with Atrial Fibrillation <https://circ.ahajournals.org/content/early/2014/04/10/CIR.0000000000000041.full.pdf >, Circulation, 2014; published online before print March 28 2014, doi:10.1161/CIR.0000000000000041.

Footnote3:

[3] National Heart, Lung, and Blood Institute (2014).  Atrial Fibrillation.  Retrieved from:  https://www.nhlbi.nih.gov/health/health-topics/topics/af/types.

Footnote4:

[4] StopAfib.org.  Why is Atrial fibrillation a Problem?  Retrieved from:  https://www.stopafib.org/why.cfm.

Footnote5:

[5] StopAfib.org. Retrieved from https://www.stopafib.org.

Footnote6:

[6] Russo, Andrea M., MD, “Overview of the Contemporary Evaluation and Management of Patients with Atrial Fibrillation: What Every General Practitioner Should Know”, American Heart Association, Copyright, 2006.

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The heart is the most vital organ of the body. The fist-sized bundle of muscle lives under the ribcage (slightly to the left of the sternum) and between the lungs. While the heart only weighs about 10oz, it is a complex maze of pumps, valves, and electrical signals which carries nutrients, blood, and oxygen throughout the body. How does the heart work? Well unlike most pumps, which only transport fluid from one location to another, the heart pulls vital fluids in, passes them through the lungs so they can be re-oxygenated and then passes new, oxygen-rich blood throughout the body.

Technically, the heart is a large muscle made up of four chambers. There are valves, or “doors,” leading to each of the chambers which regulate the amount of blood flowing into each chamber at any given moment and make sure blood only travels in one direction through the heart. In a process known as systole, the muscle contracts and pumps blood from the largest chamber, known as the left ventricle, into the arteries. The heart then relaxes – blood fills up in the heart again and the process is repeated – in milliseconds. The arteries carry this fresh, bright red, oxygen-rich blood through a network of branches of blood vessels ending in capillaries, so it reaches every part of the body. De-oxygenated blood flows back to the heart through veins.

Blood which is depleted of its oxygen content comes into the right side of the heart via two very large veins. It is first pumped into the right atrium, and then the right ventricle. From there, the blood is sent to the lungs where it is re-oxygenated and carbon dioxide is released into the lungs (the reason you breathe out). Oxygen-rich blood comes back into the heart from the lungs via the left atrium. It is then pumped into the left ventricle, and out to the body via a very large artery called the aorta.

The heart muscle pumps because of its built-in electrical system. This electrical system signals the heart when to contract and pump the blood from one chamber to another.

The electrical system begins in the right atrium at the SA (Sinoatrial) node. The electrical impulse is first generated in specialized pacemaker cells.

The impulse then travels from the SA node to the AV (Atrioventricular) node. The AV node is at the junction of the right atrium and right ventricle. From there, the impulse travels through the right and left ventricles via specialized tissue called the bundle of HIS, then down the right and left bundle branches ending in the Purkinje fibers.

The ECG (Electrocardiogram), sometimes called an EKG, is a snapshot of the electrical system of the heart at work. The P wave occurs as the right and left atria contract, pumping blood into the right and left ventricles. The QRS complex occurs as the right and left ventricles contract sending blood either to the lungs or the body. The T wave is the relaxation phase of the ventricles.

Since the ECG tracks all of the major electrical impulses of a normal heart rhythm, it is a very useful clinical tool. An ECG can identify many heart problems including, abnormal heart rhythms, heart enlargement and injury to the heart. In fact, through the use of electrode pads on a patient’s chest, an ECG is how AED units determine if a patient is in a normal sinus rhythm (as seen above) or if the heart isn’t working properly.

 From here out you’ll hopefully have a better understanding if you ever are wondering “

Did this answer your question: “How does the heart work?” if so please feel free to share this article with friends and family. If you want to learn even more about the heart and its functions, Heart.org has a variety of resources available.

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