CEUFast - Angina
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3.00 Contact Hours:
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Author:    David Tilton (RN, BSN)


Angina is any pain of the anterior chest or throat that has a suffocating quality to it. It is essential that health care workers be able to recognize angina that is indicative of acutely life threatening conditions from among the other potential sources of similar pain.

Common Precipitating Factors in Typical Angina
Physical Factors:
Bathing, eating, dressing, sexual intercourse, straining during bowel movements, alcohol ingestion, cigarette smoking.
Environmental Factors:
Extreme cold, extreme heat, high altitudes.
Emotional Factors:
Stress, worry, anger, fear, excitement, any strong emotion.

Be aware that typical angina and stable angina are not the same thing. In typical angina, observation into the pattern of response to a causative event is the key. Attacks of chest discomfort will characteristically last between three to five minutes and rarely exceed 30 minutes. If an attack persists for 30 minutes or longer, particularly if this is a deviation to the typical presentation for this individual, it is wise to rule out a myocardial infarction.

Typical angina as a general rule responds to nitroglycerin. Most people with typical angina can predict fairly accurately when their angina will occur, as well as the manner in which it will progress or resolve. This sort of forecast is greatly helpful during diagnostic work-ups, allowing the use of a 12-lead ECG to document changes.

The discomfort or pain associated with typical angina is usually located in the sub or retrosternal area of the anterior chest. Do not expect the client to be able to pinpoint the exact location. Vagueness in relation to describing the source of the discomfort when describing symptoms is in fact typical of this form of angina, yet often you will observe a clenching of the fist over the sternal region. This is known as Levine's Sign, and is a useful diagnostic observation.

In typical angina the discomfort experienced is frequently transmitted to the left shoulder and radiates down one or both arms. It may also radiate to the throat, neck and jaw. On questioning the client regarding the quality of their feelings it is best to avoid using the actual word pain. Talking only about pain tends to lead people away from other descriptive terms and very well may cause the person not to mention or describe any other feelings that they are having such as heaviness, crushing, burning, or squeezing sensations.

Atypical angina, or angina equivalents, is so-named as they can manifest in unusual and at times bizarre fashions, often unique to that individual experiencing them. Equivalent sensations may be reported to the health professional as dyspnea, syncope with exertion, or epigastric sensations such as nausea and indigestion that occur even during rest periods while exercising.

Variant angina known as Prinzmetal's angina is a form of atypical constrictive chest pain that falls into the category of unstable angina, and is most frequently caused by a focal spasm of a normal coronary artery or by a spasm superimposed on a fixed lesion. It tends to be cyclic and occurs at rest without relation to effort. Often it is associated with ST segment elevation on the electrocardiogram (ECG) (Delehanty, 2008).

Equivalent angina encompasses the many forms of cardiac induced chest pain that do not present as expected. It may manifest as dyspnea, belching, fatigue or even faintness. This form of angina is often found in women who are experiencing an acute cardiac event. Do not neglect persistent symptoms just because they are not what might be expected in a middle aged, overweight, beer drinking, cigar smoking man.

Women's Angina Similar yet Not Identical to Male Chest Pain
Studies such as WISE, the National Institute of Health's Women's Ischemic Syndrome Evaluation, have been showing that in many women coronary artery disease is different than in men.

Coronary Microvascular Syndrome is when plaque evenly coats very small arteries instead of forming more obvious obstructions in large ones. The resultant narrowing of small coronary arteries, difficult to see on angiogram studies, is often missed during diagnostic workups. In addition to narrowing in the smallest arteries, many women experience a change in the endothelium of coronary vessels, preventing the blood vessel from dilating in response to stress or other increased oxygen demands.

Narrowed small arteries mean less oxygen flow to the heart, resulting in chest pain or other equivalent anginal symptoms found in many women such as back pain, fatigue or indigestion.
(MSNBC.com, 2006)

The classic description of chest pain from ischemia related cardiac sensations is most commonly seen in the male, middle aged population among those with risk factors for a coronary artery disease such as atherosclerosis. However, amongst the female population of all ages, clients with diabetes and in the elderly a large number of anginal events are described as different or atypical sensations.

In one study of 94 clients having cardiac distress 32 percent of those questioned, highest among female clients over the age of 65, reported anginal equivalent symptoms, abdominal pain being the most common, occurring in one-third of these clients. Still another non-typical symptom reported in this group was paroxysmal dyspnea in 17 percent of the clients. This suggests that our preconceptions of what angina should look like must change to avoid misdiagnosing those whose presenting symptoms differ from our classically trained expectations (Meisel, 2008).


Following completion of this course, the participant will be able to accomplish the following objectives:

  1. Discuss the prevalence of chest pain.
  2. Identify three potential causes of angina type chest pain.
  3. Discuss the classification of Angina Pectoris.
  4. Identify methods to diagnose cardiac related angina.
  5. Discuss treatment options for cardiac ischemia related angina.


Angina is the term we use for chest pain. When someone says, "I am having angina," we automatically assume they are referring to pain of cardiac origin. We further make the mental leap that ischemia, an inadequate supply of oxygen rich blood to tissues in the body, is at the heart of the matter.

This is not always the case. The term angina is not exclusive to a specific bodily organ, nor is a sensation of chest tightness or pain limited to the heart! Even those symptoms which are related to cardiac distress can be experienced in diverse ways other than one stereotyped image of angina. This means that descriptions which nicely fit into our concept of pain of cardiac origin may have nothing to do with the heart at all.

This course seeks to expand awareness of alternative causes of angina and will review the types of pathologies which may cause this feeling; look at various means to distinguish between them; and then discuss methods which may be employed to treat this pain in the neck, and chest when it does relate to cardiac distress. So hang on tight as we look at some of the hidden meaning that rests behind the term, "angina".

Angina Constricts

Angina, and the "anginal equivalents", are seen in clients by health professionals much too often. The occurrence of distressing discomfort and constrictive pain characteristic of angina may originate from many different conditions. Some causes require prompt medical attention (e.g. tearing of the aortic blood vessel, ischemic heart attack, or pulmonary embolism), while other sources of angina type pain may allow more time for accurate diagnosis and establishment of a treatment regimen (e.g. gallbladder attacks, esophageal spasm, pericarditis, panic attacks).

Angina (noun) A disease marked by spasmodic attacks of intense suffocative pain (Merriam-Webster Online, 2005).

The term Angina does not mean heart. Angina is a descriptive word focused on the sensation being experienced. The word angina can, and is, applied to a wide range of conditions which manifest in a painful intermittent strangling sensation reminiscent of suffocative constriction or anoxic spasms. Differentiating between causes of angina type sensations can be complex and taxing, and we will discuss some of the more common disease processes that are observed in conjunction with the sensation of angina and those individually unique variant symptoms which are being referred to in recent literature as anginal equivalents.

In common medical use, the term angina is automatically associated with the chest discomfort accompanying a decrease in the supply of oxygenated blood flow to the heart muscle in relation to demand. The reason for this association is frankly, prevalence. According to the American Heart Association Heart Disease and Stroke Statistics - 2008 Update, more than nine million Americans experienced angina related directly to cardiovascular disease (American Heart Association, 2008).

  • An estimated 80,700,000 Americans (one in three) have one or more types of cardiovascular disease
  • An estimated 9,100,000 Americans have angina pectoris
  • Only 18% of coronary attacks are preceded by long standing angina
  • Nearly 2,400 Americans die each day from cardiovascular disease an average of one death every 37 seconds
(American Heart Association, Heart Disease and Stroke Statistics, 2008)

In 2012 according to CDC Angina Facts more than 6 million people in the United States have angina.

While cardiac ischemia related chest pain is both life-threatening and prevalent, other causes of angina type pain are frequently encountered by health professionals as well. One example of this is a report focused on clients seen by primary care physicians. Of those clients they encountered experiencing anginal type pain some 36-percent of the instances were related not to cardiac problems, but to musculoskeletal causes (Meisel, 2008).

Causes of Chest Pain

Cardiac and non-cardiac disorders can cause angina. It is therefore important to have an awareness of possible alternative causes of anginal sensations, as well as to be able to differentiate serious, imminently life-threatening conditions from sources of discomfort that are still serious yet less emergent. It should also be emphasized that factors and conditions not directly related to the heart itself can increase myocardial oxygen demand and present credibly as angina pectoris.

Non-cardiac imposters that produce angina can blur and confuse an initial diagnosis include disease processes such as anemia, fever, hypoxia, thyrotoxicosis (extreme hyperthyroidism), aortic stenosis, sympathomimetic drug effects, general anxiety disorder/ panic attack, or cocaine use. The following is a listing of some non-cardiac causes of angina type chest pain.

Possible Non-cardiac Causes of Angina or Anginal Type Pain
Chest Wall Related Causes
  • Musculoskeletal pain
  • Isolated musculoskeletal chest pain syndromes
    • Costochondritis
    • Costovertebral joint dysfunction syndrome
  • Rheumatic diseases
    • Rheumatoid arthritis
    • Ankylosing spondylitis
    • Psoriatic arthritis
    • Fibromyalgia
  • Nonrheumatic systemic diseases
    • Stress fractures
    • Neoplasms including pathologic fractures
    • Sickle cell anemia
    • Infections such as septic arthritis or osteomyelitis
  • Skin and sensory nerves
    • Herpes zoster (shingles)
    • Postherpetic or postradiation neuralgia
Gastrointestinal Related Causes
  • Gastroesophageal reflux disease
  • Esophageal hyperalgesia
  • Esophageal spasm
  • Esophageal rupture
  • Medication-induced esophagitis
  • Radiating or referred visceral pain
    • Peptic ulcer disease
    • Cholecystitis
    • Pancreatitis
    • Kidney stones
    • Appendicitis
Pulmonary Related Causes
  • Acute pulmonary thromboembolism
  • Pulmonary hypertension, cor pulmonale
  • Pneumonia
  • Cancer
  • Sarcoidosis
  • Pneumothorax
  • Pleuritis
  • Pleural effusion
Psychogenic Related Causes
  • General anxiety disorder
  • Panic disorder
  • Depression
  • Hypochondriasis
  • Munchausen syndrome
  • Phobias
(Meisel, 2008)

Cardiac or cardiac associated chest pain can by itself have many different etiologies other than coronary artery disease. One example is in aortic valve disease where the aortic orifice is obstructed to some degree in its function. This occurrence can readily increase systolic pressure and result in a deficit in the level of myocardial oxygenation. The end result of such an aortic valve disease is often hypertrophy with a chronic increase in myocardial oxygen demand, and chest pain.

Another cardiac related origin of chest pain can be seen in mitral valve prolapse where valvular function is compromised by an overabundance of mitral valve leaflet tissue. The result to that person is an increased opportunity to experience chest pain related to oxygen deficit.

Cardiac Associated Causes of Angina
  • Coronary heart disease
    • Coronary artery disease
      • Unstable angina
      • Non-ST elevation myocardial infarction
      • ST elevation myocardial infarction
  • Aortic dissection
  • Valvular heart disease
    • Aortic stenosis
    • Mitral stenosis
    • Pulmonic stenosis
  • Pericarditis
  • Myocarditis
  • Stress-induced cardiomyopathy
  • Cardiac syndrome X
  • Coronary vasospasm
  • Idiopathic hypertrophic subaortic stenosis
(Meisel, 2008)

Idiopathic hypertrophic sub-aortic stenosis (IHSS) is another example of an unexpected angina producer. IHSS is a type of gross obstruction of the left ventricular outflow tract originating from a hypertrophied heart septum, not uncommon in a congestive heart. The increase in muscle mass that accompanies congestive heart failure produces an increased oxygen demand at the same time that a hyper-contractile state exists. This leads to a resultant overall decrease in blood volume flow, and the experience of constrictive chest pain, angina.

When present, pulmonary hypertension can result in anginal symptoms. This can occur first by dilatation of the pulmonary arteries, or secondly by the varying degree of right ventricular ischemia which results from pulmonary hypertension.

Angina Pectoris Classifications

Angina pectoris is a clinical syndrome that is the result of an imbalance between the oxygen demand present in heart tissue and an insufficient supply of oxygen carrying blood due to changes in the coronary arteries supplying the heart itself. This imbalance, or oxygen starvation, results in myocardial ischemia. The supply of oxygenated blood can be impaired for a variety of reasons. These range from actual blood flow blockage due to coronary atherosclerosis or coronary spasm to reduction of available supply due to such things as hypotension and anemia. Vascular processes such as preload, afterload, and heart rate affect the demand side of the equation. Preload is the volume of blood waiting to be pumped by the heart, or from another angle, it is the resident pressure that distends the ventricle prior to ventricular contraction. Afterload is the resistance against which the left ventricle of the heart must push the blood that is being pumped.

Angina Pectoris -- The expected companion of ischemic heart disease. The oxygen deficit created by a reduced blood flow in the arteries feeding the myocardium typically results in what is often described as a vice-like squeezing, burning, elephant on the chest, crushing, heaviness that is located behind the mid-sternum and may radiate into the arms, neck or jaw.

Anginal Equivalents -- Alternate symptoms which may represent the same oxygen deficit condition that is being experienced in the cardiac tissues. Some of the more common anginal equivalents conveyed to health professionals are nausea, unusual strong fatigue, back pain, upper epigastric discomfort, or shortness of breath.

Currently the exact process that results in angina pectoris is not known. It is thought to be related to an increase in excitement of sympathetic and vagal efferent nerve fibers following the release of bradykinin and adenosine from ischemic tissues of the myocardium. A better understanding of the mechanism generating cardiac specific angina will greatly enhance rapid differential diagnosis of angina.

Angina pectoris is itself broken into categories in order to better describe the qualities and conditions of the term.

Stable vs. Unstable Angina Pectoris

Stable angina: chest pain occurs when the myocardial oxygen demand exceeds the ability of a coronary artery to supply oxygenated blood to the heart muscle itself. As a person exercises, myocardial work increases and is accompanied by an increase in myocardial oxygen demand. Normal coronary arteries dilate in response to this demand and coronary blood flow increases.

Stable angina is found frequently in an individual with a fixed obstruction in their coronary vessels, such as is often seen in coronary artery disease. This fixed disease condition limits the blood flow in a consistent manner as it flows through the diseased artery regardless of tissue demand requirements. The result is a consistently reproducible oxygen deficit during activities such as exercise which increase myocardial oxygen demand. For even though demand has increased the oxygen supply remains fixed, resulting in chest pain secondary to mounting ischemia. With rest, myocardial oxygen demand again falls within the limit of supply and the pain is relieved as the deficit decreases (Gersh, 2007). Therefore these triggers initiating "Stable angina" occurs when the heart is working harder than usual such as when exercising, doing yard work, experiencing emotional stress, eating a large meal, or going out into cold weather (Henshaw, 2012). The pain associated with stable angina usually goes away after a few minutes of rest or after taking a medication for angina. Often these attacks last from one to 15 minutes (Henshaw, 2012).
Angina Pain

Angina Pain

Because stable angina occurs in a repetitive pattern it is sometimes referred to as chronic stable angina or brief myocardial ischemia. A diagnostic history of this type of chest pain is characterized by the presence of the same precipitating factors, repetition in quality or duration, and/or a consistent response to the same modes of treatment such as rest or use of nitroglycerin. As a general rule for diagnosis the angina pattern of presentation should remain unchanged for at least one month.

Unstable angina, in contrast, implies a precipitous and critical reduction in coronary artery blood flow. Key factors that relate to the potential for diminution in coronary blood flow should be considered for diagnosis of unstable angina. Unstable angina can occur at any time, even when a person is at rest. It can happen with or without physical exertion (Henshaw, 2012).

The known presence of pre-existing arterial plaque, especially plaque rich in foam cells as plaque composed of these cells can be easily fractured or dislodged. This easily dislodged plaque may result in a debris fragment that partially occludes a coronary artery. Such non-occlusive, partial blockages may be identified on angiography and coronary angioscopy. This type of occurrence is the presumed etiology for the majority of the individuals who present with unstable angina (Tan, 2005).

Atherosclerotic plaque contains varying levels of high lipid macrophages known as foam cells. As arterial plaque accumulates, the production of macrophage proteases and neutrophil elastases may increase instability in foam cell rich atherosclerotic plaque leading to fissuring or rupture and the creation of occlusive debris. Moderate to large plaque disruptions commonly result in unstable angina or acute infarction (Tan, 2012).

Prinzmetal's variant angina is a focal spasm of a coronary artery that can be caused by adrenergic input, hyperventilation, emotional stress, cold stimuli, or street drugs such as cocaine. Coronary artery vasospasm may also explain ischemia associated with microcirculatory angina, in which only the small intramural branches of coronary vessels constrict and lead to pain, while the larger epicardial supply arteries remain unaffected.

Prinzmetal's angina is relatively rare, affecting people between 51 and 57 years old and has fewer risk factors for heart disease, unless they are smokers. It is estimated that 4 out of every 100,000 Americans have it and men more than women suffer from Prinzmetal's Angina (70% to 90%). More Japanese men than Caucasian men and more Caucasian women than Japanese women suffer from this form of angina (HeartHealthyWomen.org, 2012).

Scenario: Kathy is a nurse and a returning veteran who has completed two tours of duty in Iraq. While there she started smoking to help relieve the stress of not knowing when a bomb would explode. She just turned 51 years old and at night started waking up with a crushing sensation in her chest radiating to her left arm. Kathy is not a diabetic and considers herself physically fit. She has had this sensation for the past two weeks and finally decided to see her physician after the pain lasted about 30 minutes and radiated to her shoulder and jaw. She told the physician she ended up having a cigarette to relieve the tension. Kathy is not pregnant and had not gone through menopause. She did notice when menstruating she never had chest discomfort. She has no known allergies.

Her father died of a heart attack at the age of 71 years of age and was a diabetic. Her mother had no history of heart disease; however her mother did have a stroke at the age of 70, is a diabetic and is still alive.

Her vital signs were checked and her oxygen saturation was 98%. Her heart rate was 82 and blood pressure 128/70. The ER physician immediately ordered an EKG, a cardiac workup, chest X-ray and labs. Kathy's' EKG was normal, chest X-ray, cardiac enzymes, and labs were normal. She was scheduled for a glucose tolerance test and stress test. Her physician suggested she stop smoking and recommended a class she could attend. He did not want to prescribe any anti-smoking medications at this time.

Kathy's physician told her he thought she had Prinzmetal's angina and prescribed the following:

  1. Nitroglycerin to stop the coronary spasm and pain,
  2. Long-acting nitrates and a calcium channel blocker to help open the blood vessels and improve blood and oxygen flow to the heart muscle. He said she may have to change the calcium channel blocker or long acting nitrate depending on her response.
  3. If the above was not effective he would order, Alpha blockers to lower

Blood pressure and reduce blood vessel narrowing by blocking the action of stress hormones.

She was told that medicines can help to control the coronary spasms and drugs such as calcium antagonists and nitrates are used as the mainstays of treatment. If she continued to have discomfort and there is a blockage, an angioplasty or another surgical procedure may be needed. Spasms tend to come in cycles appearing and them disappearing. Her physician said that normally after 6 to 12 months of treatment the medication would be reduced, but this is considered a chronic condition.

In summary this is a form of unstable angina and occurs at rest often without a predictable pattern. Episodes usually occur in clusters, with periods lasting for a few months followed by months or weeks without any episodes of chest pain.

Symptoms of Prinzmetal's angina have these characteristics:

  • Chest pain is located under the breast bone
  • Pain described as a tightness, pressure, squeezing, or crushing sensation with discomfort radiating to the neck, jaw, arm, or shoulder
  • Often times occurs at rest between the hours of 12:00 midnight and 8:00 AM
  • Pain may last from 5 to 30 minutes
  • Nitroglycerin relieves the pain
  • Loss of consciousness or fainting could occur

(HeartHealthyWomen.org, 2012).

The causes of coronary spasms is not exactly known and theories related to problems with the thin lining of the blood vessels' endothelium and the chemical produced by the lining called nitric oxide is being researched. Nitric oxide widens the blood vessel allowing blood to easily flow. When there is a decrease in this chemical a coronary spasm occurs. Levels of this artery widening chemical are higher when estrogen levels are also high at specific stages of the women's menstrual cycle and women have fewer signs of Prinzmetal's angina. Smokers tend to have a lower level of nitric oxide in their blood vessels than nonsmokers (HeartHealthyWomen.org, 2012).

Other research studies suggest the following:

  • Atherosclerosis impairs the release of the artery widening nitric oxide because of the buildup of fatty plaque and coronary spasms could occur.
  • Problems in the nervous system (brain and spinal cord) or muscle tissue involved in making the arteries narrow and widen could contribute to coronary spasms.
  • Another theory is that injuries to the lining of the arteries expose the muscle to chemicals that could cause the vessels to narrow

(Cardiovascular Research Foundation, 2013).

Increased thrombosis

A heightened platelet tendency to activate and adhere can affect a coronary artery leading to progressive narrowing until the resultant stenosis is sufficiently severe to produce pain even at rest. This mechanism is sometimes observed following balloon angioplasty or other revascularization procedures when restenosis is observed. Focal treatments such as percutaneous coronary intervention (PCI), is incomplete and medical therapy to protect the entire vascular tree is complementary and crucial (Tan, 2012).

Increased thrombosis in coronary arteries can result from exposure of subendothelial components of the vessel triggering an increase in platelet adhesion and activation. Activated platelets aggregate in response to exposed vessel wall collagen or an increase in chemical aggregate triggers (e.g. thromboxane, adenosine diphosphate) (Tan, 2005).

Patients with a history of acute coronary syndrome often times have recurrent transient reduction in coronary blood supply due to vasoconstriction and thrombus formation at the site of the atherosclerotic plaque rupture. This is due to episodic platelet aggregation and complex interactions among the vascular wall, atherogenic lipoproteins, platelets, and leukocytes (Tan, 2012).

Coronary inflammation

Evidence suggests that inflammation plays an important role in atherogenesis and thrombogenesis. Inflammatory markers, such as C-reactive protein and amyloid A, have proven to be predictive of mortality and future cardiac events in unstable coronary syndromes. There are also reports of an association between Helicobactor pylori infection and coronary heart disease, as well as an association between Chlamydia pneumoniae antibodies and coronary vascular disease (Alavi, 2008).

Coronary Inflammation

Coronary Inflammation

A Clinical Research project in 2012 was conducted with combined positron emission tomography and computed tomography. This was done to investigate coronary arterial uptake of 18F-sodium fluoride (18F-NaF) and 18F-fluorodeozyglucose as markers of active plaque calcification and inflammation. The research study indicated that 18F-NaF uptake provides different information, relating to metabolically active calcific plaque and developing micro-calcification. This information seems to be of clinical significance in relation to symptomatic status, prior major adverse cardiac events (MACE), and cardiovascular risk scores. Prospective studies to determine the relationship between 18F-NaF uptake, morphological plaque characteristics, and future cardiovascular events are needed in subjects with stable and unstable Coronary Artery Disease (CAD) (Dweck, 2012).

The study concluded that the noninvasive assessment of coronary artery plaque biology would help identify vulnerable plaques, which are associated with specific pathological characteristics, including micro-calcification and inflammation. 18F-NaF holds promise as a noninvasive method for investigating the role of active calcification in coronary atherosclerosis
(Dweck, 2012).

Typical vs. Atypical Angina

Angina may also be classified as either typical or atypical. Typical angina has a gradual onset and is brought on by predictable precipitating factors such as exercise, shoveling snow, or chasing down a taxi.

Common Precipitating Factors in Typical Angina
Physical Factors:
Bathing, eating, dressing, sexual intercourse, straining during bowel movements, alcohol ingestion, cigarette smoking.
Environmental Factors:
Extreme cold, extreme heat, high altitudes.
Emotional Factors:
Stress, worry, anger, fear, excitement, any strong emotion.

Angina Classification Tools

The following are two commonly used classification tools for describing angina. Chances are good that you will see one or both of these tools in active use in your local area of practice.

Canadian Cardiovascular Society Angina Scale
The Canadian Cardiovascular Society grading scale is commonly used for the classification of angina severity:
  • Class I Angina only during strenuous or prolonged physical activity
  • Class II Slight limitation, with angina only during vigorous physical activity (walking uphill, climbing stairs rapidly, etc)
  • Class III Symptoms with everyday living activities, i.e., moderate limitation (walking 1 to 2 blocks on level surface, climbing 1 flight of stairs under normal conditions)
  • Class IV Inability to perform any activity without angina or angina at rest, i.e., severe limitation
(Watcher, 2005)
New York Heart Association Functional Classification System
The New York Heart Association classification system quantifies quality of life issues such as the functional limitation imposed by patients' symptoms from difficulty breathing and angina. It is an especially useful basis of comparison between current and previous episodes.
  • Class I (Mild) No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).
  • Class II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.
  • Class III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.
  • Class IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.
(Heart Failure Society of America, 2006)

Diagnosing Angina Pectoris

Prompt diagnosis of cardiac ischemic angina combines the results of a person's history and their physical presentation. The following are the most common signs and symptoms of an acute episode of cardiac ischemic angina.

Cardiac Ischemic Angina
  • Retrosternal chest discomfort rather than frank pain (i.e. pressure, heaviness, squeezing, burning, choking)
  • Positive Levine sign (presence of fist clenched over the sternum when describing the discomfort)
  • Diaphoresis with cold, clammy skin
  • Indigestion, nausea or vomiting
  • Shortness of breath (dyspnea)
  • Lightheadedness
  • Anxiety with increased heart rate
  • Pain localized primarily in the epigastrium, back, neck, jaw, or shoulders
  • Report of recent exertion, eating, exposure to cold, or emotional stress
  • Discomfort duration approximately 1-5 minutes with relief following rest or nitroglycerin
(Alaeddini, 2007)

Generally speaking, the first thing an emergency room visit with angina will bring is a search for a myocardial infarction. It is well known that angina does not always signal an myocardial infarction (MI), yet due to the immediate threat to life that such a emergent event causes, suspicion of a heart attack always takes precedence when the cause of angina symptoms are unknown.

Acute Management of Angina of Unknown Origins

Initial Management

  • Monitoring of vital signs and oxygen saturation
  • Establishing intravenous access
  • Draw blood specimens: CBC, chemistry, coagulation studies, cardiac markers (CK-MB, myoglobin, troponin)
  • 12 lead electrocardiogram
  • Take a targeted history

Medical management may include

  • Administering oxygen
  • Aspirin
  • Nitroglycerin or morphine to relieve chest pain
  • Assessing for thrombolytics

Diagnostic work-up

  • Cardiac stress testing
  • Cardiac catheterization

In many instances ischemic angina of cardiac origin can be readily ruled out by using history, physical examination findings, and basic laboratory panels. A complete blood count and electrolyte panels with BUN, creatinine, and glucose levels provide quick assistance for isolating infectious or metabolic origins of chest pain. Such lab results, as well as chest x-ray findings are usually normal in those individuals with true angina pectoris. Chest x-rays may also show evidence of cardiomegaly in those who have had a previous MI, ischemic cardiomyopathy, pericardial effusion, or are experiencing acute pulmonary edema.

A cardiac stress test is a tool the physician may utilize to determine if the heart is getting the blood it needs under external stress, even if the patient has no signs of a problem when the heart is "at rest". When a patient has arthritis or another medical condition that prevents the patient from exercising during a stress test the physician may give a medication which makes the heart work hard, as it would during exercise. This is called a pharmacological stress test (Wilson, 2012).

On a less urgent event note, graded exercise stress testing is the most widely used diagnostic test for the evaluation of patients presenting with chest pain. In those who have an established stable angina pectoris, it also can provide prognostic information about the extent of disease. Exercise stress testing has the ability to be performed alone or in conjunction with echocardiography and myocardial perfusion scintigraphy studies. For detection of cardiac ischemic processes related to angina, stress echocardiography has shown an overall sensitivity of 78 percent with a specificity of 86 percent. While exercise stress testing alone generally has a somewhat lower diagnostic sensitivity, it is less expensive and therefore a reasonable choice in certain circumstances (Alaeddini, 2007).

Stress echocardiography testing can be very useful in the evaluation of segmental wall motion during exercise. Visualization of the cardiac structure makes it possible to detect changes in the regional wall movements that tend to occur during myocardial ischemia. Experience has shown that during ischemia, normal myocardium becomes hyperdynamic in response to stresses such as exercise, while affected ischemic segments become hypokinetic or akinetic. Stress echocardiography also has the benefit of allowing simultaneous evaluation of left ventricular function, cardiac dimensions, and visualization of any valvular disease affects. It is especially useful in patients with baseline ECG abnormalities and those with systolic murmurs suggestive of aortic stenosis or hypertrophic cardiomyopathy. Most useful of all perhaps is its help in the localization of ischemia and evaluation of its severity.

Thallium-201 and technetium-99m sestamibi are the most frequently used myocardial perfusion scintigraphy tests. These tests are very useful in individuals with unstable chest pain and baseline ECG abnormalities to localize the region of ischemic changes, and as prognostic indicators (Alaeddini, 2007).

During the scan, a camera takes pictures of the heart after a special test medicine (radioactive tracer) is given through an IV. The tracer travels through the blood and into the heart muscle. As the tracer moves through the heart muscle, areas that have good blood flow absorb the tracer. Areas that do not absorb tracer may not be getting enough blood or may have been damaged by a heart attack (Heartwise, 2011).

In essence this type of testing is used to:

  • Assess the amount of blood reaching the heart muscle.
  • To identify areas of heart muscle lacking an adequate blood supply as a result of a heart attack.
  • To identify blocked coronary arteries and evaluate the effectiveness of coronary bypass grafts of angioplasty.

(Heartwise, 2011)

Stress testing is quite helpful in the determining the pathophysiology underlying angina. Although useful for most clients, the risk of death during a stress test is around 1 per 10,000 tests. Absolute contraindications to testing include severe aortic stenosis, symptomatic cardiac arrhythmias, acute MI within the previous 2 days, acute myocarditis, or pericarditis. It is also advisable to discontinue the exercise stress test in the presence of chest pain, a drop in systolic blood pressure of more than 10 mm Hg, severe shortness of breath, fatigue, dizziness or near syncope, ST depression of more than 2 mm, ST elevation of at least 1 mm without diagnostic Q waves, or development of ventricular tachyarrhythmia.

Contrary to the belief of many in the health professions electrocardiography (EKG or ECG) is not absolutely definitive when attempting to determine the cause of acute angina. In fact, about 50 percent of patients experiencing angina specifically related to an ischemic cardiac process have normal findings on a resting ECG (Alaeddini, 2007).

Information obtained from an ECG is very helpful as it can provide evidence of prior MI, intraventricular conduction delay, various degrees of atrioventricular block, arrhythmias, or ST-T wave changes. The point is simply not to dismiss chest pain in the presence of a normal ECG, as evidenced by those patients with known coronary artery disease who have been documented as showing pseudonormalization of a resting ECG, even during active monitoring of chest pain.

Cardiac catheterization is an invasive procedure that involves aspects of both diagnosis and the potential for treating some types of ischemic cardiac disorders. Catheterization assesses angina by taking a close look at coronary hemodynamics. A cardiac cath (cardiac angiography) is usually performed in a special area under local anesthesia and sterile conditions. A flexible catheter is introduced into the heart via an artery and/or vein located in the groin or arm and advanced into the target area. Dye is injected through the catheter into the coronary arteries and/or heart's chambers, while an x-ray is taken and recorded on film. This procedure allows the physician to visualize the coronary arteries, as well as the function of the heart and its valves. Indications for cardiac catheterization include the following:

  • Confirm or exclude coronary atherosclerosis
  • Assess the feasibility of surgical correction of lesions
  • Detect valvular disease
  • Evaluate left ventricular hemodynamics
  • Assess for congenital cardiac anomalies
  • Confirm the presence of tumors, cardiomyopathies or anomalous coronary arteries

Treating Angina Pectoris

Angina pectoris is a result of an imbalance between the oxygen supply to the heart and the demand. When the demand for oxygen is greater than the supply, chest pain occurs. The pain is caused by an insufficient supply of blood to the heart causing a temporary ischemia of the myocardium (inadequate oxygen for the myocardium to meet its metabolic needs). The coronary arteries are unable to provide enough oxygen carrying blood to meet the oxygen requirements of the heart muscle.

Dramatic life style changes often accompany the onset of angina in a person's life. Treatment options for angina, particularly angina that is cardiac ischemic in origin, play an important role in the dialog between clients and health professionals. We will discuss five methods for increasing the supply of needed oxygen to the muscle of the heart itself.

The first, increasing the concentrations of oxygen present in the carrying medium, is mostly of aid on an acute basis. There are a small number of angina sufferers who use oxygen routinely as part of their individual treatment regimen. Oxygen administration is certainly a valid complementary treatment for the most difficult cases of angina associated with ischemia whether it is of cardiac or non-cardiac origin.

The second method of increasing oxygen flow to the heart muscle is by use of medications whose purpose is to increase availability of flow by the carrying medium. In one manner of speaking the goal of pharmacologic intervention here is to convert unstable angina into stable, predictable angina. The following are medications commonly used in the treatment of angina.

Medications Used in Treatment of Angina Pectoris
Anti-anginal and Anti-ischemic drugs
  • Aspirin - Aspirin inhibits blood clotting, helping to maintain blood flow through narrowed heart arteries. Frequently given when presenting with angina, especially during a suspected heart attack, aspirin can decrease death rates by 25 percent. Chewing the aspirin hastens its absorption.
  •  Clopidogrel (Plavix) - Selectively inhibits ADP binding to platelet receptor, thereby inhibiting platelet aggregation. Consider use in patients with contraindication to aspirin.
  •  Nitroglycerine - This medication for treating angina temporarily opens narrowed blood vessels, improving blood flow to and from your heart. It comes in a small sublingual pill, or sublingual spray form. Either form promotes vascular dilatation, allowing an increase in blood flow through coronary arteries.
  •  Beta-blockers - A form of blood pressure medication that helps relax the heart muscle, slow the heart rate and decrease overall oxygen demands.
  •  Angiotensin-converting enzyme (ACE) inhibitors - These drugs allow blood to flow from the heart more easily. For instance, a doctor may prescribe ACE inhibitors if a person has had a moderate to severe heart attack that has reduced the heart's overall pumping capacity.
  •  Calcium channel blockers - When treating coronary artery spasms, heart medications such as calcium channel blockers work to relax the coronary arteries and prevent the spasms.
  •  Ranolazine (Ranexa) - Cardio selective anti-ischemic agent (piperazine derivative) that partially inhibits fatty acid oxidation. Indicated for chronic angina unresponsive to other antianginal treatments. Unlike beta-blockers, calcium channel blockers, and nitrates, ranolazine does not reduce blood pressure or heart rate.
(Alaeddini, 2007) (Brogden, 2008)

The third choice for promoting increased oxygen flow to the tissue of the heart is that of revascularization procedures. These invasive procedures have the goal of opening partially occluded blood vessels, or replacing completely blocked vessels. Coronary Artery Bypass Graft surgery (CABG) is a surgical procedure that involves the removal of a portion of healthy blood vessel, such as a vein from the leg or the internal mammary artery (located in the chest) and using it to bypass the blockage(s) that are present in the coronary arteries.

Another revascularization procedure is Directional Coronary Atherectomy (DCA). This is the insertion of a specialized catheter into a compromised coronary artery, similar to an angioplasty, except that plaque is mechanically removed in order to decrease vessel blockage.

Still another revascularization procedure is balloon angioplasty with or without the placement of stents to hold open a diseased cardiac artery.

An angioplasty is a procedure performed on patients with blocked or clogged coronary arteries. The technique is similar to a cardiac catheterization except that a special catheter with a small balloon is inserted into the blockage and inflated in order to compress the plaque and open the artery. The uninflated balloon catheter is advanced to the area of blockage. The balloon is then inflated and deflated several times until the blockage is compressed and the artery is widened. When using a stent, a fine wire mesh that is designed to expand and hold open the lumen of an artery is placed using a special catheter. These stents are springy, durable bundles which help provide renewed blood flow to ischemic tissue. Often angioplasty and stent placement occurs during the same procedure, though either can certainly be done on its own. These procedures have proven effective in the revascularization of ischemic cardiac tissues.
Balloon Angioplasty

Balloon Angioplasty

A fourth option called TMR, Transmyocardial Laser Revascularization, is available for clients with persistent angina who are considered inoperable or poor risks for the more traditional revascularization procedures. In this procedure a surgeon exposes the muscle of the heart, and using a special high energy computerized CO2 laser, creates between twenty and forty one-millimeter wide channels (think of the width of a pin head) in the muscle of the left heart ventricle. Body responses to these perforations close the outside of the channels, yet the unique characteristics of the cardiac muscle allow the channels inside to remain open, providing new blood flow to ischemic tissue (Bhimiji, 2006).

The mechanism by which this works is not completely understood even by those specialists who perform TMR. Evidence that has been gathered suggests that coronary blood flow is improved however, and it may be that the procedure promotes angiogenesis, the growth of new, very small, blood vessels that contribute to improved oxygenation of the heart.

A fifth and somewhat exciting option increasingly available for achieving improved oxygenation to the myocardium in cardiac ischemic angina sufferers is that of Enhanced External Counter pulsation (EECP). EECP is a noninvasive treatment using carefully timed, sequential inflations of pressure cuffs placed onto the client's calves, thighs and buttocks. Inflation and deflation of these cuffs is timed to the patient's ECG, and the effectiveness is observed by noninvasive arterial pressure waveform monitoring.

The overall hemodynamic effect of EECP compressions is to 1) provide diastolic augmentation and thus increase coronary perfusion pressure; to 2) unload systolic cardiac workload volumes and therefore decrease myocardial oxygen demand; and to 3) increase venous return and subsequently, cardiac output. This sequence of pressure shifts works to displace the pressure of flowing blood backwards into the coronary arteries during heart diastole, when the cardiac tissue is in a state of relaxation and resistance to back pressure in the coronary arteries is at its lowest point.

Remarkably, coronary collateral vessel development appears to be stimulated by this noninvasive increase in artery perfusion pressures, and with time a noticeable increase in perfusion capacities can be seen in both the new and pre-existing coronary arteries. Currently this therapy is gaining favor as an exciting adjunct to traditional treatment of cardiac ischemic related angina, and investigation is being done concerning EECP's strong potential for treating other severe cardiac pathologies (Doctors Guide, 2006).

The FDA approved EECP for treatment of angina in 1995, and later for treatment of congestive heart failure in 2002. Current treatment regimens vary, however for many clients who suffer from angina resistant to conventional approaches, a series of 35 daily one-hour sessions of EECP appears to promote growth in the collateral coronary artery circulation with reduction of ischemic angina symptoms.


The strangling, compressive discomfort of angina is a common presentation in a wide spectrum of disease processes. It may be the first visible sign of a disease warranting emergency attention. Angina must always be carefully investigated to identify the underlying cause. Awareness of both typical angina, and anginal equivalent symptoms, must be present to aid in the prompt recognition of cardiac ischemic angina and allow timely intervention to restore adequate oxygenation to tissues in distress. By our awareness of what angina is and the alert observations we make, we as health care workers can begin to get a firmer grip on this terrible pain in the neck, and chest, that angina is to us all.


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This course is applicable for the following professions:

Advanced Registered Nurse Practitioner (ARNP), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Registered Nurse (RN)


Cardiology, CPD: Practice Effectively, Critical Care / Emergency Care, Geriatrics, Medical Surgical

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