Angina

Angina is an attack of spasmodic pain of the anterior chest or throat that has a suffocating quality. Healthcare workers must recognize suffocating angina pain indicative of acutely life-threatening conditions from other sources of similar pain.

Angina is the term medical professionals have agreed to use for ischemic chest pain of cardiac origin. When someone says, "I am having angina" or "the client has angina," we automatically assume it is all about the heart. We further make the mental leap that an inadequate supply of oxygen-rich blood to tissues, e.g., ischemia, is at the heart of the pain (Aroesty, 2020).

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

This course seeks to expand awareness of alternative causes of angina and review the types of pathologies that may cause this feeling. We will look at various means to distinguish between them and then discuss methods employed to treat this pain in the neck and chest when it relates to cardiac distress. So, deep breaths and hang on tight as we discover some of the hidden meanings that rest behind the term "angina."

We will refer to angina as the "anginal equivalents" seen in clients by health professionals much too frequently. The occurrence of distressing discomfort and constrictive pain characteristic of angina spasms 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). At the same time, 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, etc.).

The term angina does not mean heart. Angina is a descriptive word focused on the sensation being experienced, regardless of its source. The word angina can, and is, applied to a wide range of conditions that 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. We will discuss some of the more common disease processes observed in conjunction with the feeling of angina and those individually unique variant symptoms referred to in recent literature as anginal equivalents.

In its most common medical use, the term angina is automatically associated with chest discomfort accompanying a decrease in the supply of oxygenated blood flow to the heart muscle in relation to oxygen demand. The reason for this association is, frankly, prevalence. According to the American Heart Association Heart Disease and Stroke Statistics 2021 Update, more than eleven million Americans experienced angina related to cardiovascular disease (Virani, 2021).

While cardiac ischemia-related chest pain is both life-threatening and prevalent, other causes of angina-type pain are frequently encountered by health professionals.

Both cardiac and noncardiac disorders can cause angina. Therefore, it is crucial to have an awareness of possible alternative causes of anginal sensations and differentiate serious, imminently life-threatening conditions from sources of discomfort that, while still serious, are less emergent. It should also be emphasized that factors and conditions not directly related to the heart can increase myocardial oxygen demand and present credibly as angina pectoris.

Noncardiac Chest Pain (NCCP) accounts for an estimated 50% of all clients presenting at the emergency department and 80% of those seen in primary care with complaints of chest pain (Teragawa, 2020) (Newman, 2020).

These noncardiac imposters may produce believable anginal symptoms that can blur and confuse an initial diagnosis. NCCPs include disease processes such as GERD, 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 noncardiac causes of angina-type chest pain.

Cardiac or cardiac-associated chest pain can by itself have many different etiologies other than coronary artery disease. One example is 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. Such an aortic valve impairment is frequently heart muscle hypertrophy with a chronic increase in myocardial oxygen demand and subsequent chest pain.

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

Angina pectoris is a clinical syndrome resulting from 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 to coronary atherosclerosis or coronary spasm to reduce available supply due to 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 before ventricular contraction. Afterload is the resistance against which the heart's left ventricle must push the blood that is being pumped.

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

A heightened platelet tendency to activate and adhere to coronary arteries can be affected, leading to progressive arterial narrowing until the resultant stenosis is sufficiently severe to produce pain, even at rest. This mechanism is sometimes observed following balloon angioplasty, stent placement, or other revascularization procedures when restenosis, the recurrence of narrowing, is observed. The gradual return to stenosis's stricture happens most often between 3 to 12 months after revascularization procedures such as stent placement. Typically, recurrent angina is a primary indication. However, an acute myocardial infarction may occur in around 10 percent of restenosis patients (Levin, 2020).

Patients with a history of acute coronary syndrome often have a recurrent transient reduction in coronary blood supply due to vasoconstriction and thrombus formation at an atherosclerotic plaque rupture site. This is due to episodic platelet aggregation and complex interactions among the vascular wall, atherogenic lipoproteins, platelets, and leukocytes (Levin, 2020).

Evidence suggests that chronic low-grade inflammation plays an important role in atherogenesis and thrombogenesis. Experts are unsure exactly what role inflammation of the blood vessels takes in the atherosclerotic build-up. Evidence does show inflammation as the initiating event in many heart attacks and strokes. 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 (Narula, 2020).

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.

Be aware that typical angina and stable angina are not the same things. Stable angina – a.k.a. angina pectoris brought about by decreased blood supply to the heart muscle has a gradual initiation, consistent symptoms, and tapered relief with rest. In typical angina, observation into the pattern of response to a causative event is the key. Physical exertion or intense emotional stress tends to be the consistent initiator of typical angina. Attacks of classic substernal chest discomfort accompany typical angina, which will last between three to five minutes and rarely exceed 30 minutes. Either rest or use of nitroglycerin works to end an episode. Suppose an angina attack persists for 30 minutes or longer, particularly if this is a deviation from this individual's typical presentation. In that case, it is wise to rule out myocardial infarction.

Typical angina, as a general rule, responds well to sublingual nitroglycerin. Most people with typical angina can predict fairly accurately when their angina will occur, responding to what provocation and how it will progress or resolve. This sort of forecast is beneficial during diagnostic workups, 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 is typical of this form of angina. Yet, you may often observe a clenching of the fist over the sternal region. This is known as Levine's Sign and is a useful diagnostic observation (Alaeddini, 2018).

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. It may cause the person not to mention or describe any other feelings they are having, such as heaviness, crushing, burning, or squeezing sensations.

Clinical tools are employed to help determine heart damage and make informed decisions regarding care. The following are two commonly used classification tools for describing angina. The chances are good that you will see one or both of these tools in active use in your local area of practice.

In clients graded with low severity of the damage, or damage risk, lifestyle changes may focus on treatment. For higher grades of risk/ damage, immediate cardiac surgery in conjunction with medical intervention may be appropriate.

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

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

In many instances, cardiac origin's ischemic angina can be readily ruled out by 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 chest pain's infectious or metabolic origins. Such lab results and chest x-ray findings are usually normal in those with true angina pectoris. Chest x-rays may also show cardiomegaly evidence 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 that makes the heart work hard, as it would during exercise. This is called a pharmacological stress test.

On a less urgent event note, graded exercise stress testing is the most widely used diagnostic test for evaluating patients presenting chest pain. Those who have an established stable angina pectoris can also provide prognostic information about the disease's extent. Exercise stress testing can be performed alone or in conjunction with echocardiography and myocardial perfusion scintigraphy studies. For detecting cardiac ischemic processes, stress echocardiography has shown an overall sensitivity of 79 percent with a specificity of around 91 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 (Sicari, 2017).

Stress echocardiography testing can be beneficial 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 normal myocardium becomes hyperdynamic during ischemia in response to stresses such as exercise, while affected ischemic segments become hypokinetic or akinetic. Stress echocardiography also benefits from allowing simultaneous evaluation of left ventricular function, cardiac dimensions, and visualization of any valvular disease effects. It is especially useful in patients with baseline ECG abnormalities and those with systolic murmurs suggestive of aortic stenosis or hypertrophic cardiomyopathy. Perhaps, most valuable of all is its help in the localization of ischemia and evaluation of its severity.

Thallium-201 (TI-201) and technetium-99m sestamibi (Tc-99m) are the most frequently used myocardial perfusion scintigraphy (imaging) tests. These tests are widely available and useful in individuals with unstable chest pain and baseline ECG abnormalities to localize the region of ischemic changes and prognostic indicators.

During the imaging 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.

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.

Contrary to many in the health professions, electrocardiography (EKG or ECG) is not definitive when attempting to determine the cause of acute angina. About 50 percent of patients experiencing angina specifically related to an ischemic cardiac process have normal findings on a resting ECG (Alaeddini, 2018).

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 chest pain.

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

Dramatic lifestyle 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 essential role in the dialog between clients and health professionals. We will discuss five methods for increasing the supply of needed oxygen to the heart's muscle itself.

The first, increasing the concentrations of oxygen present in the carrying medium, is mostly of aid on an acute basis. A small number of angina sufferers use oxygen routinely as part of their treatment regimen. Oxygen administration is undoubtedly a valid complementary treatment for the most challenging angina cases associated with ischemia, whether it is the cardiac or noncardiac origin.

The second method of increasing oxygen flow to the heart muscle is using medications to increase flow availability by the carrying medium. One way 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.

The third choice for promoting increased oxygen flow to the heart tissue 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 a 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 to decrease vessel blockage.

Another revascularization procedure is balloon angioplasty with or without stents placement 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. A special catheter with a small balloon is inserted into the blockage and inflated to compress the plaque and open the artery. The uninflated balloon catheter is advanced to the area of blockage. The balloon is inflated and deflated several times until the blockage is compressed and the artery is widened. When using a stent, a fine wire mesh designed to expand and hold open the lumen of an artery is placed using a special catheter. These stents are springy, durable bundles that help provide renewed blood flow to ischemic tissue. Often angioplasty and stent placement occur during the same procedure, though either can certainly be done independently. These procedures have proven effective in the revascularization of ischemic cardiac tissues.

A fourth option is that of TMR. Transmyocardial laser revascularization is available for clients with persistent angina, considered inoperable or poor risks for the more traditional revascularization procedures. In this procedure, a surgeon exposes the heart's muscles. Using a special high-energy computerized CO2 laser creates between twenty and forty, one-millimeter wide channels (think of the width of a pinhead) in the muscle of the left heart ventricle. Body responses to these perforations close the outside of the channels. Yet, the cardiac muscle's unique characteristics allow the channels inside to remain open, providing new blood flow to ischemic tissue (Alaeddini, 2018).

The mechanism by which this works is not entirely 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 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 are 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
2. Unload systolic cardiac workload volumes and therefore decrease myocardial oxygen demand
3. Increase venous return and, subsequently, cardiac output.

This pressure shift sequence works to displace the pressure of flowing blood backward into the coronary arteries during heart diastole when the cardiac tissue is in a state of relaxation. Resistance to backpressure 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. 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 the traditional treatment of cardiac ischemic-related angina. The investigation is being done concerning EECP's strong potential for treating other severe cardiac pathologies (Caceres, 2021).

Angina is the strangling, compressive discomfort common to a broad spectrum of disease processes. It may be the first visible sign of a disorder warranting emergency attention, including but not limited to anoxia and ischemia of the heart muscle. 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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