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Cardiac Emergencies: Sudden Cardiac Death, Heart Failure, Acute Pericarditis, including Cardiac Tamponade
Author: David Tilton Click here for author information

 

Cardiac Emergencies: Sudden Cardiac Death, Heart Failure, Acute Pericarditis, including Cardiac Tamponade | Copyright © 2008 CEUFast.com


Course Contents

   Purpose
   Objectives
   Introduction
   Sudden Cardiac Death
   Heart Failure
   Pericarditis and Cardiac Tamponade
   Conclusion
   References

   Click any section in the index above to browse to the corresponding course section 

 

Purpose

This course is designed to inform and prepare you for the most lethal cardiac emergencies. It focuses on sudden cardiac death, heart failure, acute pericarditis, and cardiac tamponade.

 

Objectives

Following completion of this module, the student will be able to accomplish the following objectives:

1. Discuss the prevalence of sudden cardiac death, heart failure, and acute pericarditis.
   
2. Identify signs and symptoms of sudden cardiac death, heart failure, and acute pericarditis.
   
3. Describe an assessment of patients presenting with the signs and symptoms of sudden cardiac death, heart failure, or acute pericarditis,
   
4. Compare the causes of sudden cardiac death, heart failure, and acute pericarditis.
   
5. Recognize the usual treatments of sudden cardiac death, heart failure, and acute pericarditis.

 

Introduction

Cardiovascular disease is the number one killer of adults. Prompt recognition and initiation of appropriate treatment can save lives during three of the most deadly cardiac emergencies: sudden cardiac death, heart failure, and acute pericarditis. ("Heart Disease and Stroke Statistics", 2008)

 

Sudden Cardiac Death

When the heart ceases to beat effectively and breathing soon ceases, a person is said to have experienced sudden cardaic death (SCD). In order to meet the criteria for this diagnosis, the critical circulatory collapse must be; 1) unexpected, 2) it must relate in some manner to heart problems, and 3) it should occur with minimal warning or a complete absence of prelude symptoms. This means the event occurs proximal to any warnings, typically within one hour of the start of any type of cardiac related symptoms. In the past, this condition was often referred to by the terms cardiac arrest or sudden cardiac arrest, perhaps due to the fact that some individuals have experienced sudden cardiac death, and lived to tell about it.

Epidemiology of Sudden Cardiac Death

  325,000 cases of SCD occur in the U.S. annually.
  More deaths per year are accountable to SCD than to lung cancer, breast cancer, or AIDS.
  Some estimates place SCD as accountable for approximately 15 percent of the total mortality in the United States and other industrialized countries.
  SCD is often the first expression of coronary artery disease and is accountable for approx. 50-percent of the deaths that occur due to this disorder.
  A higher rate of SCD occurs in those with congestive heart failure, a recent myocardial infarction, and those having had a previous cardiac arrest.
  The incidence of SCD increases with age, is more common in blacks than whites, and is higher (3:1) among men than women.
  Is more common in those ages 45-75, though not limited to certain age ranges.
  Almost half of SCD's are unwitnessed (approx. 40-percent), with survival from SCD largely dependent on the immediate, proper response of those who witness the event.

(Sovari, 2006)

In sudden cardiac death the focus is on heart function. By that, I mean that actual death and sudden cardiac death are not, by definition, the same thing. In actual death the brain also dies, while in cardiac death though the heart ceases to function, the potential for resumption of cardiac function and effect remain intact. The important difference between death (i.e. irreversible brain and organ death) and sudden cardiac death is that SCD is potentially reversible. If sudden cardiac death is reversed quickly enough, the brain and other vital organs need not die.

Please be aware that a diagnosis of pre-existing heart disease is NOT necessary for sudden cardiac death to occur. However when SCD does occur it is common to find that an underlying pathology of coronary artery disease (CAD) is present. By most estimates the presence of coronary artery disease is a factor in approximately 80-percent of all instances of sudden cardiac death. (Sovari, 2006).

Good Heart Health Reduces Sudden Cardiac Death

Common sense is not a common phenomenon. Given that caveat, please realize that good cardiac health translates into a decrease in the chance that the lightening strike of sudden cardiac death will occur.
Good diet, exercise, and reduction of stress are all factors. The role that lifestyle and nutrition play becomes more evident as information becomes available.
One example is a recent study which showed that 1,000 milligrams of fish-oil capsules per day lowers the risk of sudden cardiac death by nearly half.

(Kirchheimer, 2006)

Sudden cardiac death, sometimes referred to by the older term sudden cardiac arrest (SCA), is not the same thing as a heart attack (myocardial infarction). With SCD or SCA, a cardiac electrical system failure is almost exclusively the fault, rather than the blocked blood flow to a portion of the heart muscle associated with a myocardial infarction. Infarction does not typically stop the heart from beating. Sudden cardiac death however may be associated with changes that occur during a heart attack, especially during the recovery period following an infarction.

The devastating loss of effective heart function that is sudden cardiac death revolves around what are often referred to as primary arrhythmias. Primary arrhythmias, a term often used yet rarely defined, is the establishment of a new and abnormal pattern of cardiac electrical stimulation which creates an ongoing sequence of unwanted or ineffective contractions for, and this is the key, no easily apparent reason. In sudden cardiac death ventricular fibrillation is considered the most devastating of primary arrhythmia, closely followed by ventricular tachycardia. Those instances of occurrence, when documentation is available, often show that rapid ventricular tachycardia precedes ventricular fibrillation in many instances of primary arrhythmia.

In ventricular tachycardia (also referred to as v-tach or VT) the lower chambers of the heart contract at such a rapid pace that effective blood flow is prevented. In ventricular fibrillation (v-fib or VF) the lower chamber of the heart quivers instead of pumping in an organized rhythm. Once started, v-fib rarely returns to a normal or even semifunctional rhythm spontaneously. In order to survive, immediate outside intervention is needed.

Medications Used to Manage Cardiac Arrhythmias

Medications used to slow fast cardiac rhythms or stabilize irregular rhythms are known as antiarrhythmics.

Antiarrhythmic medications are divided into classes by their primary mode of action.
 
  Class I agents: Sodium channel blockers that slow electrical conduction in the heart tissue. They are primarily used to treat rapid heart rhythms originating in the ventricles. This group is subdivided into;

Ia – Quinidine, Procainamide, Disopyramide
Ib – Lidocaine, Tocainide, Mexiletine, Phenytoin
Ic – Flecainide, Propafeone, Ecainide, Moricizine

  Class II agents: Beta blockers that reduce heart workload by blocking certain hormones that bind with beta receptors in the heart. This makes it harder for a rapid heartbeat to be triggered. Included in this class of antiarrhythmics are;
Metoprolol, Propranolol, Esmolol, Atenolol
  Class III agents: Potassium channel blockers which slow the use of potassium in heart cells. Included are;
Amiodarone, Sotalol, Azimilide, Bretylium,
Cloflium, Dofetilide, Tedisamil, Ibutilide,
Sematilide
  Class IV agents: Calcium channel blockers which slow blow vessel signals to contract, slowing overall heart rate. This class includes;
Verapamil, Diltiazem
  Class V agents: A category for those medications which fail to fit into other class descriptions. Included here are;
Magnesium, Digitalis (digoxin), Adenosine

(Verma, 2007)

When sudden cardiac death occurs, the highest priority goes to immediately summoning trained assistance equipped with the necessary equipment. This is done by calling emergency medical services or 911 when outside of the hospital, and following your facility’s appropriate emergency procedure when in the hospital. Next, work to establish some semblance of flow for oxygenated blood to the brain. Forcing air into the mouth in order to push oxygen into the lungs can do this. In order to get the oxygen to the brain, it is necessary to simulate the normal pumping of the heart as well. Rhythmically compressing the chest approximates the force of a beating heart and provides a small amount of blood flow to the lungs, brain, and coronary arteries. This is cardiopulmonary resuscitation. When the trained help you summoned arrives, they will attempt to establish a functioning heartbeat by using a defibrillator. Outside of the hospital an automatic external defibrillator (AED) will be used most commonly. As a general guide, cardiopulmonary resuscitation (CPR) should be initiated within four to six minutes and advanced cardiac life support (ACLS) measures should be within eight minutes to avoid damage to cells in the brain.

AHA Chain of Survival

1. Recognize an Emergency
2. Early Access to Medical Care
(calling 9-1-1 immediately)
3. Early CPR
4. Early Defibrillation
5. Early Advanced Care

("The Links", 2008)

Of the estimated 325,000 deaths attributed to sudden cardiac death each year no witness is present in as many as 40-percent of these deaths. For the vast majority of individuals who experience SCD, survival depends on the presence of others who are competent in performing basic life support, as well as the rapid arrival of personnel and apparatus for defibrillation and advanced life support followed by transfer to a hospital able to provide advanced care. (Sovari, 2006)

Assessments on Arrival to Care following SCD

Lab Studies:
  Cardiac markers (creatine kinase, myoglobin, and troponin). – Remember cardiac tissue damage may occur prior, during or after the SCD event.
Electrolytes, calcium, and magnesium. - Severe metabolic acidosis, hypokalemia, hyperkalemia, hypocalcemia, and hypomagnesemia can dramatically increase the risk for arrhythmia and sudden death.
Quantitative drug levels (quinidine, procainamide, tricyclic antidepressants, digoxin). - Drug levels that are either higher or lower than the levels indicated in the therapeutic index may have a proarrhythmic effect. Most all of the antiarrhythmia medications also have a proarrhythmic effect!
Toxicology screen. – Look for drugs, such as cocaine that can lead to vasospasm, as a self-induced cardiac ischemia may exist.
Thyroid-stimulating hormone. - Hyperthyroidism can lead to tachycardia and tachyarrhythmias. Over a period of time, it also can lead to heart failure.
Brain natriuretic peptide (BNP). - Emerging data supports the notion that an elevated BNP level may provide prognostic information on the risk of SCD, independent of clinical information.
Imaging Studies:
Chest x-ray. - This may reveal heart failure.
Echocardiography.
Nuclear imaging techniques.
Other Tests:
Electrocardiogram.
Signal-averaged ECG (SAECG) - This may be of value in selected settings.
Genetic testing. - The value of genetic testing in conditions such as congenital long QT and HCM is still being evaluated. Some studies have recommended the testing of siblings and close relatives of people with SCD due to these conditions.
Procedures:
  Coronary angiography. - To assess the state of ventricular function and the severity and extent of damage.
  Ejection fraction. - This is the best predictor of significant cardiac events and survival.
  Revascularization. – This is the single greatest treatment for the underlying cause of VT/VF, ischemic myocardium.
  Electrophysiology studies.

(Sovari, 2006)

Even under ideal circumstances, only an estimated 20-percent of patients who have an out-of-hospital sudden cardiac arrest (SCD) will survive to be discharged from the hospital. One factor that is rapidly changing this rate of survival is the growing availability of automatic external defibrillators throughout communities and a larger number of citizens trained to use them. (Sovari, 2006)

Extracorporeal Life Support + CPR

New tools in the battle against sudden cardiac death are becoming available. One example is,

ELS = Extracorporeal Life Support.

Compared to CPR alone, adding extracorporeal life support doubles survival in hospital patients with cardiac arrest, concludes a study reported in the July 6, 2008 Lancet.

In extracorporeal life support (ELS), a catheter is inserted into a large blood vessel in a leg. In the patient receiving CPR once initiated ELS diverts a percentage of the returning blood volume through the catheter via a pump, heat exchanger and oxygenator before returning the blood to the body. The addition of ELS to CPR enhances oxygen rich coronary blood flow and helps keep heart and organ tissues alive while the cause of the sudden cardiac arrest is being dealt with.

Researchers assessed outcomes among cardiac arrest patients who had undergone CPR for more than 10 minutes. Patients who received ELS had a better survival rate to discharge, better 30-day survival, and better one-year survival. For each of these endpoints, patients who received ELS were about half as likely to die as those who received CPR alone.

("ELS Plus CPR Boosts Flow After Cardiac Arrest", July 9, 2008)

SCD is considered to be reversible in most people if treatment is begun quickly. However, of the people who do survive sudden cardiac death the risk of reoccurrence runs high, in the range of 20 to 25-percent each year. It is therefore essential that they receive appropriate treatment for the underlying cause of the episode, as well as the highest level of preventive measures.

Medical Treatment for Sudden Cardiac Death

  Advanced cardiac life support (ACLS): In the event of SCD the immediate implementation of ACLS guidelines is indicated. Widespread interest in improving rates of public ACLS training with a special emphasis on use of early defibrillation by public service personnel (e.g., police, fire, airline attendants) exists. Through these measures, the greatest public health benefits can be achieved in the fight against sudden death.
  Once the patient is resuscitated, the clinical course is largely dependent on the presentation of hemodynamic stability in the emergency department, early neurologic recovery, and the duration of the resuscitation.
  Medical stabilization: Careful post resuscitative care is essential to survival because studies have shown a 50-percent repeat in-hospital arrest rate for people admitted after an SCD event. Beta-blockers are reasonable in many circumstances because of favorable properties. Antiarrythmics, including amiodarone, should not supersede ICD implantation unless control of recurrent VT is needed while the patient is in the hospital.
Surgical Care:
  Radiofrequency ablation: Radiofrequency ablation, now routinely available, is indicated for patients with self caused arrhythmias initiated by irritable spots or foci in their heart tissue.
  Implantable Cardiac Defibrillators (ICDs): Implanted sensing and defibrillating devices are a great advance in care of those individuals who are at risk for SCD.
  Surgical excision of VT foci is being performed with decreasing frequency, because of perioperative mortality and the alternative, transvenous ICD implantation.
  Patients with long QT syndrome who do not respond to beta-blockers are candidates for ICD implantation.

(Sovari, 2006)

 

Heart Failure

Heart failure provides some of the most difficult cardiac emergencies to stabilize. Due to the progressive nature of the disease state and the actual cellular changes that occur in the myocardium, especially with those who have experienced cardiac remodeling with the accompanying left ventricular cardiomegaly, little emergency reserve is left for their heart to work with. This means in real life that the day-to-day struggle to push blood against sluggish resistance has drained the cardiac tissue of its ability to snap back and readily compensate in times of crises. When pushed beyond its abilities, the heart of a failure client seems to be more resistant to rescue attempts.

Heart Failure is ALL About - CARDIAC OUTPUT

Preload =
  The amount of force stretching the cardiac muscle before contraction. (Like a child filling a balloon with water, a little stretch and springiness is good, too much pressure stretch has the potential for disaster)
Afterload =
  Pressure against which the heart must push to move blood. (Peripheral vascular resistance – slight resistance is good, yet too much brings trouble)
  Integral to afterload is the size of the ventricular chamber doing the pushing. (Smaller is BETTER!)
Contractility =
  The strength of the muscle fibers in the heart chambers.
  Dependent on the supply of oxygen and glucose TO the cardiac muscle fibers. (Ischemia drastically cuts function)
  Reflective of the presence of influencing medications.
Heart rate =
  Not too fast. (Tachycardia tires heart muscle causing cardiomegaly ~ BAD)
  Not too slow. (Bradycardia decreases needed perfusion)

Nearly 5 million Americans live with heart failure (often referred to as Congestive Heart Failure or CHF), with 550,000 new cases diagnosed each year. Of those hearing these words applied to them for the first time, nearly half will die of complications related to this condition within the first 5 years after diagnosis, bringing the annual death rate to nearly 300,000 cases in the United States each and every year. Despite such horrendous statistics, new studies show that the actual number of Americans receiving a new diagnosis of heart failure is very slightly on the decline! As though to balance this however, the continuing increase as more individuals live longer has brought the total number of those who are struggling to live with congestive heart failure to new, record highs. (Preidt, 2008).

In 2005 CHF was the listed diagnosis in 1,064,000 hospital discharges, and remains the most common diagnosis in hospital patients age 65 years and older. In that age group, one fifth of all hospitalizations have a primary or secondary diagnosis of heart failure. The rate of hospitalizations for heart failure increased more than three times between 1970 and 1994, with a large absolute increase in the 65+ age group. This seems likely to be a result of better diagnosis of the condition rather than an actual increase of disease incidence. Based on the follow-up 44 years after the initial National Heart Lung and Blood Institute’s Framingham Heart Study 80-percent of men and 70-percent of women under the age of 65 who are diagnosed with heart failure will die within eight years. In individuals diagnosed with heart failure, sudden cardiac death will occur at six to nine times the rate experienced by the general population. ("Heart Disease and Stroke Statistics – Update 2008").

The cruel fact about heart failure is that basically every individual who has experienced traumatic cardiac injury or a disease to their heart tissue runs a heightened risk for developing some degree of heart failure within his or her lifetime.

Emergency presentation of heart failure can vary from person to person, from instance to instance, due to factors such as right-sided failure versus left-sided failure, or a combination of both. Please remain mindful that in an emergency presentation of heart failure a large amount of information must be gathered, however the focus of treatment must initially be that of acute rescue.

Presentations of angina with heart failure focus on oxygenation and rescue of at risk ischemic heart tissue. People with pulmonary congestion must have external, sometimes extreme assistance to restore a semblance of internal fluid and perfusion pressure balance.

All treatment tracts for heart failure emergencies converge on restoring the maximum amount of function to the cardiovascular system, at the least expense to other organs and tissues.

Heart Failure Emergencies Call for Alphabet Therapy

ABC’s
  Airway – Check and secure
  Breathing – Monitor
  Circulation – Start advanced life support if needed
LMNOP’s
  Lasix – Reduce fluid congestion
  Morphine – Decrease stress on myocardium
  Nitroglycerin – Insure cardiac circulation
  Oxygen – Oxygen to heart and brain
  Positioning – Sit person up to avoid lungs filling with fluid

Individuals suffering from heart failure consistently report that two of the major factors during a crisis are shortness of breath, and chest pain. One of the initial means of managing such symptoms is by the use of nitroglycerin to open cardiac supply vessels, combined with supplemental oxygen provision and the aggressive use of diuretics to pull fluid away from lung and heart thereby decreasing the congestion that is impeding general circulation. This is where all the pre-load after-load dynamics come into play as it is often fluid retention (fluid overload) combined with the lack of heart-pumping capability (low cardiac output) that is causing this type of emergency in heart failure clients. Treatment around heart failure focuses primarily on decreasing the things impeding heart function while increasing heart-pumping ability.

Medical Therapies for Heart Failure
~The Fab Four~

  Diuretics help reduce fluid buildup in the lungs and peripheral edema.
  ACE Inhibitors lower blood pressure and reduce the strain on the heart. (These medications also may reduce the risk of a future heart attack)
  Beta-blockers slow heart rate and lower blood pressure to decrease the cardiac workload.
  Digoxin makes the heart beat stronger and pump more blood.

One essential medical regimen for heart failure sufferers in acute crisis is the ability to shift fluid by the means of diuretics.

Lasix

  Generic name: Furosemide
  Classification: Diuretic
  Mechanism of action: Inhibits reabsorption of sodium and water in the kidney
  Effect: Begins approx. 10 minutes after administration and lasts up to 6 hours.
  Result: Lowers preload pressures.
  Uses: Emergency treatment of congestive heart failure (i.e. cardiogenic pulmonary edema) in persons with normal or high blood pressures.
  Dosing: IV = 20-40+mg injected slowly over 1 to 2 minutes.
  Precautions: Dehydration, hypotension, electrolyte imbalances, may precipitate renal failure.
  Contraindications: Hypotension, Sulfa allergy.

An implantable cardioverter defibrillator (ICD) is the treatment of choice in heart failure clients with known ventricular remodeling or a history of past cardiac arrhythmias. The implantable cardioverter serves the purpose of constantly monitoring the heart rhythm, and being able to deliver a small micro shock should a dangerous rhythm be detected.

Like an implantable pacemaker the ICD consists of a pulse generator, battery, and implanted electrodes capable of delivering any needed shock. Also present is a sophisticated processor allowing recognition of tachy arrhythmias such as ventricular tachycardia, and also fibrillation.

  
 


Implantable Cardioveeter/Defibrillator
When the ICD senses an abnormal heart rhythm, it delivers an electrical shock
to reset the heart to a normal rhythm.
 

 

Pericarditis and Cardiac Tamponade

Pericarditis is one of the less frequently encountered cardiac emergencies. When it does present in an acute emergency it makes work tricky for healthcare providers due to the unanticipated nature of the condition. Pericarditis and its close associate cardiac tamponade are clinical problems involving the space surrounding the heart, which is known as the pericardium. Pericarditis results from fluid accumulation in this space while cardiac tamponade is the hemodynamic culmination of that fluid accumulation.

The pericardium, also known as the pericardial complex, consists of an outer fibrous layer and an inner serous layer. The outer fibrous pericardium is best described as flask-shaped. It is a tough sac with anchoring attachments to the diaphragm, sternum, and costal cartilage. The inner serous layer is delicate, thin, and is proximal to the surface of the heart. The combined pericardium serves primarily as a protective barrier from the spread of infection or inflammation from adjacent structures.

  
 


Image compliments of the National Heart Lung and
Blood Institute of the National Institutes of Health.
 

Normally, the pericardial lining floats free above the heart surface. In pericarditis an inflammatory process either produces exudate which serves to balloon out this virtual cavity, or begins a process of inflammatory adhesion of the pericardium to the outermost tissue of the heart itself. Neither process is healthy.

The potential space found between the layers of pericardium normally contains roughly 20 ml of soothing fluid rich with electrolytes and proteins, that when analyzed possesses a profile similar to plasma. In addition to this normal vestige of liquid, about 120 ml of extra fluid is able to accumulate in the pericardium without any adverse increase in pressure. Further fluid accumulation beyond this amount however can result in marked increases in pericardial pressure, causing decreased cardiac output and hypotension. This is cardiac tamponade. The rapidity of fluid accumulation influences the hemodynamic effect.

Pericarditis Crisis Point Flow Chart

Fluid within the pericardium presses the heart tissue
This pressure keeps the heart from expanding fully
Less blood can fill or leave the heart
Diminished oxygen reaches the brain or organs
Tachycardia
Dropping blood pressure
Tachypnea
Anxiety / Panic
Swollen neck veins
Loss of consciousness

SCD = Sudden Cardiac Death

As with many conditions, early diagnosis and treatment greatly increases the survival rates in acute pericarditis with or without cardiac tamponade. The epidemiology of pericarditis is that it is more common in males than in females. It is also more common in adolescents and young adults. The most common symptom of acute pericarditis is precordial or retrosternal chest pain, usually described as sharp or stabbing. Like angina pectoris, the pain may be of either sudden or gradual onset and may radiate to the back (left trapezial ridge), neck, left shoulder, or arm. The process of taking a deep breath or movement in general may serve to aggravate the pain.

The pain of pericarditis may be most severe when that person is supine and relief can often be found when the person leans forward while sitting. Common associated signs and symptoms can include a low-grade intermittent fever, dyspnea, cough, and dysphagia. In tuberculous pericarditis, fever, night sweats, and weight loss tend to be common (80-percent). Be aware that individuals with pericarditis may also present with a primary symptom of acute abdominal pain. Fevers usually are low grade, but they occasionally reach 104F. Cardiac arrhythmias tend to arise from the irritation and inflammation processes as well as increased heart constriction. Premature atrial and ventricular contractions occasionally are present.

In cardiac tamponade without pericarditis it is more common for individuals to present with symptoms of anxiety, dyspnea, fatigue, and/or altered mental status. Tamponade sufferers need to be questioned thoroughly as they may have a history of medical illnesses associated with pericardial involvement, particularly end-stage renal disease (ESRD). If it is a traumatic tamponade, it is common that the individual presents with acute dyspnea and/or altered mental status reflective of a reduction in total vascular flow. A waxing and waning clinical picture may be present with the presence of an intermittently decompressing tamponade.

Beck’s Triad

3 features of acute tamponade
  Decline in systemic arterial pressure
  Elevation in systemic venous pressure (e.g. distended neck vein)
  A small, quiet heart

During a physical assessment the most common and important physical finding is that of a pericardial friction rub, which is best heard at the lower left sternal border or apex when the individual is positioned sitting forward or on hands and knees. A friction rub may be transient from one hour to the next and is present in only about 50-percent of cases. Friction rubs may be distinguished from a cardiac murmur by its changing character from heartbeat to heartbeat and as the person changes position. A friction rub can be said to be closer to the ear with regard to sound quality on auscultation than a murmur.

Acute Pericarditis Diagnostics

Lab Studies:
  CBC with differential
  Elevated erythrocyte sedimentation rate (ESR)
  Creatine kinase and isoenzymes
  Elevated lactate dehydrogenase and serum glutamic-oxaloacetic transaminase
  HIV testing
  Tuberculosis skin testing
  Thyroid function tests
  Antinuclear antibody, rheumatoid factor
Imaging Studies:
  Chest radiography
  Echocardiography
  CT Scanning
  MRI
Other:
  Electrocardiography
  Pericardiocentesis
  Central venous pressure measurement

Infectious disease is the most common cause of pericardial effusion with tamponade. Outside of the United States, the presence of tuberculosis should be considered when clients present with acute pericarditis. In addition, the reported incidence of acute pericardial tamponade is approximately 2-percent in penetrating chest traumas, though the condition is rarely seen in blunt chest traumas.

Causes of Pericarditis

Irritation or inflammation
  Myocardial infarction (heart attack)
  Radiation treatment
  Surgical complications
  Reaction to certain medications.
Infection
  Bacterial
  Parasites
  Protozoa
  Viral
  Fungal
Other diseases
  Kidney failure
  Tuberculosis
  Cancer
  Rheumatoid arthritis
  Rheumatic fever
  Lupus
  Scleroderma
Injury or trauma
  Gunshot wounds
  Stab wounds
  Blunt (nonpenetrating) impacts
  Motor vehicle accidents

Acute pericarditis can be caused by noninfectious inflammation such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). This is known as serous pericarditis. The fluid found in these instances contains few polymorphonuclear neutrophils, lymphocytes, or histiocytes. The usual volume is 50-200 mL and accumulates slowly. Fibrous adhesions rarely occur with noninfectious serous pericarditis.

The most frequent type of pericarditis is fibrous and serofibrinous pericarditis. Common causes of this type of rapidly forming condition are acute myocardial infarction (AMI), postinfarction (including Dressler syndrome), uremia, radiation, RA, SLE, and trauma. Severe infections also may cause a fibrinous reaction, and this fibrinous response can be a sequeli following routine cardiac surgery.

Dressler’s Syndrome

  Fever, pericarditis, pleuritis
(typically with a low grade fever and a pericardial friction rub)
  Occurs in the first few days to several weeks following MI or heart surgery
  Incidence of 6-25 percent of post MI and heart surgery clients
  Treat with high-dose aspirin or other NSAIDs

With purulent or suppurative pericarditis invasive organisms may originate from direct extension, hematogenous seeding, lymphatic extension, or by direct introduction during a cardiotomy. Immunosuppression accelerates to this condition. The fluid found in the pericardial sac may be as much as 400-500 ml in volume and tends to show as a thin to creamy pus. Clinical features include fever, chills, and spiking temperatures. Constrictive pericarditis is a serious complication.

In hemorrhagic pericarditis blood is present. Tuberculosis or direct neoplastic invasion most commonly lead to this blood mix found in a fibrinous or suppurative effusion. It also can occur in severe bacterial infections. Hemorrhagic pericarditis can be found after cardiac surgery or trauma and tends to cause tamponade.

Both adhesive mediastinopericarditis and constrictive pericarditis are chronic conditions. They often follow an infective pericarditis, cardiac surgery, or irradiation. The pericardial potential space is obliterated, and adhesion of the external surface of the parietal layer to surrounding structures occurs. The increased workload may cause massive cardiac hypertrophy and dilatation, which can mimic an idiopathic cardiomyopathy. The heart may also become encased in a 0.5 to 1.0 cm-thick layer of scar or calcification (concretio cordis), resembling a plaster mold. In this presentation the heart cannot expand, become hypertrophic or dilate because of insufficient space.

 


Note the adhesive exudate on both
inner pericardial lining  and heart
tissue. Inflammation can  lead
to greatly limited heart expansion.

The cardiac emergency of pericarditis with cardiac tamponade is most common in individuals with malignant pericarditis. Effusions caused by tumors often progress to tamponade, eliciting bleeding in the pericardium. In these instances blood accumulates more rapidly than does transudate or exudate and more commonly causes tamponade.

When discussing pericarditis it is necessary to mention the importance of appropriate emergency care of penetrating cardiac injuries. Identification of any pericardial fluid in the setting of penetrating injury to the thorax or upper abdomen requires immediate aggressive ACLS intervention.

Hemopericardium is the most common feature of penetrating cardiac injuries. In acute massive hemopericardium, there is insufficient time for a defibrination response to occur. The hemopericardium may partially clot, resulting in a pericardial hematoma.

Often, it is in the hospital setting that penetrating cardiac injuries occur. Some potential sources of cardiac perforation include central line placement, pacemaker insertion, cardiac catheterization, sternal bone marrow biopsies, and pericardiocentesis. The right atrium is the most common site of perforation from catheter placement. Cardiac wall perforation, as well as direct catheter infusion of fluids, can cause tamponade. Formation of a tamponade has been known to occur immediately, or from hours to days after injury secondary to catheter misplacement.

Emergency pharmacologic therapy in pericarditis and cardiac tamponade revolve mainly around pain control, primarily fast acting opiods supplemented with NSAIDs to reduce inflammation. As it is the physical problem of too much fluid in too tight a space, there is not a whole lot that drugs can do to resolve it rapidly. Corticosteriods are helpful, but it takes time for them to work. Always consider the need for supportive oxygenation, IV access, and preparation should advanced life support be needed.

Acute pericarditis can manifest with alarming rapidity or very slowly until cardiac function is compressed to literally a standstill. It is so interwoven into the fabric of other emergency cardiac conditions that rapid recognition is essential in order to begin emergency pericardial decompression, should that be indicated. Decompression of the pericardium can be considered a cardiac emergency, and can be accomplished by the insertion of a large bore needle through the chest wall and into the fluid engorged pericardial sac.

Emergency Pericardial Decompression
(pericardiocentesis)

  Should cardiac compromise be suspected in pericarditis (falling BP, shock-like state) pericardial decompression (pericardiocentesis) becomes essential.
  Suspicion of purulent pericarditis also warrants immediate pericardiocentesis with culture of exudates.
  Except in emergencies, pericardiocentesis, a procedure with potential for high risk complications, should be performed under the supervision of a cardiologist or thoracic surgeon and in the cardiac catheterization laboratory if possible, under echocardiographic guidance.
  Thoracotomy is generally considered safer, should time and circumstances allow.
  Resuscitation equipment must be at hand.
  Premedication with pain medication such as morphine or meperidine is desirable in non-urgent situations.
  IV sedation preferred.
  The client should be placed in a recumbent position, with the head elevated 30 from the horizontal.
  Under aseptic conditions, the skin and subcutaneous tissues should be infiltrated with lidocaine.
  A 75-mm (3-in) short-beveled, 16-gauge needle is attached via a three-way stopcock to a 30- or 50-mL syringe.
  The pericardial sac may be entered via the right or left xiphocostal angle or from the tip of the xiphoid process with the needle directed inward, upward, and close to the chest wall.
  The needle is advanced with constant suction applied to the syringe in order to determine the time of contact with pericardial fluid.
  Echocardiography may be used to guide the needle.
  Once in place, the needle should be clamped next to the skin to prevent it from entering further than necessary and possibly puncturing the heart or injuring a coronary vessel.
  ECG monitoring is essential for detecting arrhythmias produced when the myocardium is touched or punctured.
  Fluid is withdrawn until intrapericardial pressure falls below right atrial pressure, usually to subatmospheric levels.
  A plastic catheter may be passed through the needle into the sac and the needle withdrawn if continued drainage is needed. This may be left in place for 2 to 4 days.
  Consideration should be given to treating recurrent effusion due to malignant tumor invasion with sclerosing drugs (such as tetracycline).

(Holt, 2006)

 

Conclusion

Cardiac emergencies happen all around us. Though they are the number one killer of our time, they rarely make the evening news, or the papers. Despite this tacit conspiracy of silence they occur frequently, and no doubt have happened to someone close to each of you. Every one of us is one single beat of our heart away from a cardiac emergency. It pays to be aware of what is going on around us, how to recognize the presence of a cardiac emergency, and quickly differentiate between the various causes. When confronted with a cardiac emergency, do not panic. Take a deep breath and summon help. Remember the American Heart Association Chain of Survival. You are not alone in dealing with cardiac emergencies. Be alert, assess the situation, and get the help you need.

 

References

"ELS Plus CPR Boosts Flow After Cardiac Arrest". (July 9, 2008). Healthfinder.gov. http://healthfinder.gov/news/newsstory.asp?docid=617220. Accessed July 9, 2008.

"Heart Disease and Stroke Statistics – Update 2008." (2008). American Heart Association. Dallas, Texas.

"Sudden Cardiac Arrest." (August 2006). National Heart Lung and Blood Institute. http://www.nhlbi.nih.gov/health/dci/Diseases/scda/scda_whatis.html. Accessed June 24, 2008.

"The Links in the Chain of Survival". (April 21, 2008). American Heart Association. http://www.americanheart.org/presenter.jhtml?identifier=3012016. Accessed July 2, 2008.

Kirchheimer, Sid. (January 12, 2006). "Shield Your Heart". AARP.org. http://www.aarp.org/health/conditions/articles/shield_your_heart.html. Accessed July 9, 2008.

Preidt, Robert. February 25, 2008. “More Elderly Americans Living With Heart Failure.” HealthDay. U.S. National Library of Medicine. http://www.nlm.nih.gov/medlineplus/news/fullstory_61540.html. Accessed March 13, 2008.

Holt, Brian. (September 2006). "Pericarditis". Merck Manual Professional. http://www.merck.com/mmpe/sec07/ch078/ch078a.html. Accessed July 8, 2008.

Sovari, Ali. (July 17, 2006). "Sudden Cardiac Death." eMedicine.com. http://www.emedicine.com/med/fulltopic/topic276.htm. Accessed June 23, 2008.

Verma, Sumit., Hamby, Robert., Cohen, Kenneth. (January 10, 2007). "Antiarrhythmics." Your Total Health. http://yourtotalhealth.ivillage.com. Accessed July 2, 2008.