This course is designed to inform and prepare the healthcare professional for cardiac emergencies. Cardiac assessment, angina, and acute myocardial infarction will be discussed.
Following completion of this module, the student will be able to:
Cardiovascular disease is the number one killer of adults in the United States. According to the American Heart Association, one in three American adults suffers from one or more types of cardiovascular disease (CVD). Of all reported deaths for 2004, the most current year in which complete numbers are available, 36.3 percent were due to cardiovascular causes. That is just over one out of every three deaths in this country. Cardiovascular problems cause the deaths of 2,400 Americans every day, or to put it another way, a cardiovascular related death occurs once every 37 seconds. Also, in 2001, more women died from cardiovascular disease than did men. ("Heart Disease and Stroke Statistics", 2008) ("Cardiovascular Disease in Women", 2007)
The good news is that despite these startling numbers, the rates of cardiovascular related deaths have shown a small but definite decrease in the last few years (Cardiovascular Death Rates Decline, 2007).
This decrease in cardiovascular related deaths has been, to a great extent, due to a vast improvement in the care and treatment of cardiac emergencies worldwide. In both pre-hospitalization situations and emergency care units, healthcare providers have rallied to the task with awareness, more effective methods and medications and have taken great strides forward in the care of emergent needs. However, more remains to be done in order to get this pervasive cause of death under control. Only by prompt recognition and initiation of appropriate treatment can we do our best in the battle to save lives from this deadly plight.
The key to successful handling of cardiac emergencies is a rapid assessment. Supportive treatment can and should be initiated while assessing the client. One key point is crucial; supplemental oxygen should be initiated on all individuals suspected of cardiac emergencies.
Mechanism of action: Increases hemoglobin saturation, increases oxygen tension, improves tissue oxygenation
Indications: Cardiac or pulmonary arrest, suspected hypoxemia, cardiac emergency, complaints of shortness of breath
When a cardiac emergency is suspected, place the client on a cardiac monitor, monitor the blood pressure and oximetry readings. Make sure a large bore IV, at least a 20 gauge, is started and a vacutainer tube of every color is drawn. Continue the physical assessment of the client while all the necessary equipment is being applied. Should the client become unconscious, check airway, breathing, and circulation and proceed with advanced cardiac life support if necessary.
A good place to start with a conscious client is their presenting signs and symptoms. While initiating supportive treatment, begin to dialog with the client. Find out what that person has to say about the situation. Speak in commonly used terms avoiding medical slang, abbreviations, and techno speak. Discuss the symptoms that he/she is experiencing. If prompting is needed mention the most common symptoms related to a cardiac emergency, being careful not to put your words into what the client is attempting to relate to you. The best place to start is with chest pain and related sensations. Here is a big caution - the information given by family members is invaluable, but be careful to get it separately from what you are asking the client. It is easy in the tension and excitement of the situation for a family member to put their perceptions of what may be happening forward as though it was the client's observation. As healthcare professionals we want to understand what the client is saying, and not lose that among the bustle of the moment.
Chest pain can be very deceptive. It is a subjective discomfort experienced by the individual which may be of cardiac or non-cardiac origin. In the short term, the safest course is to always assume it is cardiac until the prevalence of data convinces you otherwise.
Angina is the most commonly reported manifestation of cardiac chest pain. Typical angina is described as a pressure, heaviness, and/or a burning sensation. The discomfort of angina is the result of insufficient oxygen in one or more areas of the heart muscle.
Note the characteristic pattern of anginal pain spread. The sensation
may be described as heat, tingle, throb or any type of thing.
The true test is the pattern and location, not the word pain (Pfizer-India).
Cardiac and non-cardiac disorders can cause anginal sensations. 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, the American Heart Association preferred term for anginal pain or discomfort related directly to coronary heart disease.
Non-cardiac 'imposters' that produce angina can blur and confuse an initial diagnosis. These may include disease processes such as anemia, fever, hypoxia, thyrotoxicosis, aortic stenosis, sympathomimetic drug effects, general anxiety disorder/panic attack or cocaine use. The following is a list of some non-cardiac causes of angina type chest pain.
|Chest Wall Related Causes|
|Gastrointestinal Related Causes|
|Pulmonary Related Causes|
|Psychogenic Related Causes|
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. This results in an increased likelihood of experiencing chest pain related to oxygen deficit ischemia.
Idiopathic hypertrophic subaortic 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 congestive heart failure. 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 -- is 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 -- are 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 healthcare professionals are 'nausea', 'unusually severe fatigue', 'back pain', 'indigestion', 'and shortness of breath'.
Continue your assessment by asking about any difficulty in breathing, or dyspnea. Dyspnea can often be a clue that heart failure is present. Heart failure is a prime suspect especially if the person has the most trouble breathing when they lay down, a condition referred to as orthopnea. Ask your client how many pillows they use to prop themselves up with when sleeping. This question can help solidify a suspicion that long-standing heart failure may be present.
Ask about palpitations. Palpitations are often described as a pounding in the chest or an awareness of rapid or skipped heartbeats. These sensations can be caused by a wide variety of cardiac dysrhythmias. Narrow down the information by asking about duration, frequency and any precipitating factors that may be present.
Ask about syncope. Many clients are hesitant to report that they have experienced episodes of sudden dizziness, vertigo or brief loss of consciousness accompanied by weakness. If syncope has been experienced by the client you can start thinking about things that decrease perfusion to the brain. Dysrhythmias such as transient asystole, ventricular fibrillation, tachycardia, bradycardia or some less common rhythm disturbances can be the culprits. Other causes may be pulmonary hypertension, hyperventilation, cerebrovascular accidents or orthostatic hypotension.
It is never a mistake to ask about fatigue. Fatigue might be a clue pointing towards heart failure. It is also common when a person has anemia.
Fatigue is one of the key symptoms known as anginal equivalents that can be found in a large number of clients who have a slightly different subjective report of the myocardial oxygen deficit that creates the chest pressure and pain feelings of angina pectoris in others.
Ask the client if they have been experiencing frequent coughing recently. Cardiac related initiators of coughing could be pulmonary hypertension, pulmonary infarction or pulmonary edema. Ask about bloody sputum or hemoptysis. The presence of bloody sputum can signal the presence of mitral stenosis, a pulmonary infarct or pulmonary emboli. It can also be a clue to the presence of tuberculosis. Tuberculosis can also lead to the cardiac conditions of acute pericarditis or cardiac tamponade.
Be alert for the presence of cyanosis. Cyanosis is the dusky tissue discoloration resulting from lack of oxygenated blood flow. It can be an indication of cardiac involvement. A central cyanosis is most often due to the intracardiac shunting of blood and may be seen in the mucous membranes of the mouth and lips, the nail beds and the eye conjunctivae.
Peripheral cyanosis, on the other hand, is most often seen alone primarily in the nail beds of fingers and toes, as well as to a lesser extent, the lips. The presence of blunting, clubbing or hypertrophy of the fingertips (or toes) is worth noting. While it is associated with cyanosis, the condition of clubbing where the progressive taper of the distal portion of the fingers and toes transforms into a squaring off of the tissues is really indicative of long periods of peripheral oxygen deprivation and may be seen in those with congenital heart disease, cor pulmonale or endocarditis.
Look for edema. The tissue fluid engorgement of edema is caused by an elevation in venous pressure that forces fluid out of the vascular system through capillary walls and into the interstitial spaces in the lungs and the peripheral subcutaneous tissues. When edema is present, it can indicate heart failure.
Look closely at the skin surrounding the client's eyes. The presence of slightly raised, yellowish areas of tissue on a person's eyelids can be an important diagnostic clue. These small areas of discolored skin are known as xanthelasma, and are an indication of the presence of cholesterol plaques. While you are looking, pay attention to the eye field itself. If you see a light gray ring surrounding the iris of your client’s eyes, it may be arcus senilis, a finding that often accompanies the presence of existing heart disease and high cholesterol levels.
We all carry with us the experiences of a lifetime. As you assess, take a brief history of the present illness and past medical history. Remember you are dealing with an emergency situation. Avoid long genealogies and extended tales. Keep your client focused by asking leading questions like the following:
Angina pectoris is a clinical syndrome resulting from an oxygen deficit to the living tissue of the heart. It is the presence of chest pain or discomfort of a constricting or suffocating quality. Angina pectoris is commonly caused by myocardial ischemia and occurs when the cells of the heart muscle need more oxygen. For example, climbing a flight of stairs could trigger an attack of angina in one person while walking on flat ground might not in that same individual. Angina may happen during exercise, strong emotions or extreme temperatures.
Angina pectoris is a cardiac emergency as it indicates that the myocardial cells are experiencing a critical stress due to the lack of sufficient oxygen to the heart muscle. This ischemic event is usually due to a decrease in the blood flow to the cardiac tissue resulting from a physical constriction or blockage of one or more of the arteries that supply the tissues of the heart. When angina pectoris occurs, that person is at an increased risk of heart attack, cardiac arrest or sudden cardiac death.
Classic angina pectoris typically manifests as an uncomfortable pressure, squeezing or burning discomfort that may be felt in the neck, jaw, shoulder, back, or arms. Be aware, that some individuals will experience angina in ways differing from the classic presentation. Sensations differing from the typical or more common presentation are often referred to as atypical angina, or equivalent angina.
Atypical angina, or ‘angina equivalents’ are so-named as they can manifest in unusual and, at times, bizarre fashions, often unique to the individual experiencing them. Equivalent sensations may be reported to the healthcare professional as unusual fatigue, dyspnea, syncope with exertion or epigastric sensations such as nausea and indigestion.
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 mid-forties, overweight, beer drinking, cigar smoking man.
| 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. “Instead of the usual bulky clogs in main arteries”, as one article puts it, “these women have a hard-to-spot buildup in smaller blood vessels”.|
This condition, termed Coronary Microvascular Syndrome, is where plaque evenly coats very small arteries instead of forming more obvious obstructions in large arteries. The resultant narrowing of small coronary arteries which are 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.
|“Tests Miss Heart Disease in Women.” MSNBC.com, January 31, 2006.|
The classical 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 coronary artery disease such as atherosclerosis. In the female population of all ages, among clients with diabetes, and in the elderly a large number of anginal events are described as different, ‘atypical’ sensations.
In one study of 94 clients having cardiac distress, 32 percent of those questioned reported anginal equivalent symptoms of which abdominal pain was the most common. Still another non-typical symptom reported in this group was paroxysmal dyspnea, for 17 percent of the clients. This suggests that our preconceptions of what angina pectoris should look like must change to avoid misdiagnosing those whose presenting symptoms differ from our classically trained expectations (Meisel, 2008).
An accurate diagnosis of angina pectoris depends to a great extent on the results of a person’s history and physical examination. It is well known that angina does not always signal a myocardial infarction (MI), but due to the immediate threat to life that such a traumatic event causes, it is always best to rule out a myocardial infarction. In many instances true ischemic angina of cardiac origin can be readily ruled out by using the health history, physical examination and basic laboratory panels. CBC and electrolyte panels with BUN, creatinine and glucose levels are quick and helpful for isolating infectious or metabolic origins of chest pain. Laboratory results, as well as, chest x-ray findings are usually normal in those individuals with true angina pectoris. CXR may show evidence of cardiomegaly in those who have had a previous MI, ischemic cardiomyopathy, pericardial effusion or are experiencing acute pulmonary edema.
Angina pectoris is a result of an imbalance between the oxygen supply to the myocardium and the oxygen demands of the body. When the demand for oxygen is greater than the supply, chest pain occurs. The pain is from an insufficient supply of blood to the heart causing ischemia of the myocardium (inadequate oxygen supply to 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.
In the immediate interval following presentation of the symptoms of angina it is essential to initiate a strategy of care. The following is a sample of possible interventions that may be initiated in sequence when a patient presents with anginal type symptoms.
|Medical management may include:|
As oxygen availability to the myocardium is the crux of the matter in angina, acute interventions will gradually give way to longer lasting treatments, many of which may result in dramatic life style changes.
Supplemental oxygen administration is essential immediately and should be implemented first. Do not depend exclusively on oxygen administration as the source of the symptoms is generally related to blood supply constrictions and not oxygen uptake from the atmosphere.
It is therefore important to increase the oxygen availability to the cardiac muscle by means of medications whose purpose is to increase the flow of oxygenated blood to the myocardium and the tissues of the body. The following are medications commonly used in the treatment of angina.
|Antianginal and Anti-ischemic drugs:|
|(Alaeddini, 2007) (Brogden, 2008)|
A third choice for promoting oxygen flow to the tissue of the heart is that of emergency revascularization. These invasive procedures have the goal of mechanically opening partially occluded blood vessels or physically 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.
Angioplasty is a procedure that may be performed on an emergent or non-emergency basis for patients experiencing angina from blocked or clogged coronary arteries. The technique is similar to a cardiac catheterization except that a special catheter with a small inflatable balloon is inserted into the blockage and then expanded in order to compress the plaque toward the sides and open the lumen of 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 cylinder of fine mesh designed to expand and hold open the lumen of an artery is placed using another special catheter. These stents are springy, durable bundles which help provide renewed blood flow to ischemic tissue. Often angioplasty and stent placement occur 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.
Myocardial infarction (MI) is the loss of oxygenated blood flow to an area of the heart that produces dying (ischemic) areas of tissue and eventually dead (necrotic) areas in the muscular walls of the heart. As of the year 2005, over eight million living Americans are survivors of past myocardial infarctions. In 2004 one out of every five deaths in the United States was attributed to a cardiac ischemia related event, often referred to as coronary heart disease. Each year 310,000 deaths occur from coronary heart disease outside of the hospital or in a hospital or clinic emergency department, making cardiac ischemia/myocardial infarction one of the most critical emergency conditions we as healthcare professionals face (Heart Disease and Stroke Statistics, 2008).
Several suggested guidelines are available for the treatment of myocardial infarction with or without elevation of the ST segment on a 12-lead ECG. Consistent among the available guidelines is:
Experience has revealed that persons having the symptoms of an acute MI, the number one symptom being angina pectoris, tend to wait a minimum of two hours before seeking medical aid for their symptoms. A large portion of those who wait to seek assistance do so for twelve hours or longer, which minimizes benefits that may be gained from reperfusion therapies targeted to opening up newly formed heart artery blockages. Organizations devoted to research such as the American Heart Association (AHA) and the American College of Cardiology (ACC) have aggressively studied how to improve heart injury survival numbers. Findings from these, and other timely studies, have suggested the following as being chief components related to treatment delay from the time of symptom onset.
Of these time factors, the patient-related delay tends to be the longest. Yet every additional delay moves the clock along, making the ability to provide effective, time-sensitive treatment less likely. That is why it is so important to educate those individuals who we know are at risk for an acute cardiac event in how they should respond to symptoms of an acute myocardial infarction.
AHA and ACC guidelines emphasize the need for intense education of the persons and family members of those who have known existing heart disease. Verbal and written plans must be given to them covering the following aspects:
The prompt use of both aspirin and nitroglycerin if available.
How to access Emergency Medical Services.
The location of the nearest hospital offering 24-hour emergency cardiac care.
Nitroglycerin is an essential tool that should be provided to individuals with a history of cardiac disease. Current best practice is to instruct the person to take 1 nitroglycerin tablet sublingually at the onset of angina/ischemic type chest discomfort and to also take a single adult dosage aspirin. Another nitroglycerin tablet can then be used every 5 minutes for a total of three doses. Should symptoms persist, they should call 911 emergency services or obtain other emergency transport to the hospital. Please be sure to let clients know NOT to go to their physician’s office.
Emergency medical service (EMS) intervention has several advantages. More rapid transport to the hospital and quicker evaluation once at the hospital are the most widely recognized. Initial assessments being conducted while in route are a great help in getting prompt care to the acute MI client. The presence of EMS personnel with basic life support skills and an automated electronic defibrillator present is vital for quick intervention. In areas where advanced EMS services are available, the ability to monitor ECG changes, perform advanced cardiac life support and in some areas, especially in rural districts, even initiate thrombolytic therapy before reaching the hospital itself can be life saving.
The World Health Organization (WHO) definition of myocardial infarction calls on the presence of at least two of three hallmark criteria (Thygesen, 2007).
Please be aware that several proposed changes to the traditional definition of myocardial infarction are being prepared, specifically in relationship to the diagnostic weight placed on ECG changes versus cardiac biochemical markers of myocardial necrosis, i.e. cardiac enzymes and troponin levels. The changes proposed are more in the way of refinements to the currently used diagnostic definition rather than replacements for it.
Angina as manifested in an occurring or impending myocardial infarction is typically reported as prolonged chest pain even while at rest. Usually, in this occurrence, the characteristics of the pain include the following:
The electrocardiogram (ECG or EKG) is a key examination tool for both initial diagnosis and continuous monitoring of myocardial infarction, especially during the first 4 hours after pain onset. However, a normal ECG does not rule out an imminent infarction. The 12-lead ECG also allows distinction into subtypes of ischemic events in clients suspected of myocardial infarction. Three primary types or groups of ischemic events may be present:
In 2004 the ACC/AHA determined that in the presence of new ST-segment elevation (or new left bundle branch block) on ECG screening provides sufficient evidence to move forward with emergent reperfusion therapy such as thrombolysis or primary percutaneous coronary interventions without delaying care decisions for the return of laboratory cardiac markers. However, around half of those who have had a MI do not exhibit clear ST elevations, though they may display odd or nondiagnostic ECG changes. What this means in the real world of emergency medicine is that what is obvious can be caught quickly. The rest falls to experience and the laboratory for confirmation of diagnosis and planning of treatment (Reeder, 2008).
Studies have shown that mortality rates also increase with the number of ECG leads that show ST elevation. When no ST elevation (NSTEMI) waveforms are present it is recommended that thrombolytic agents be discouraged as current data suggests little or limited benefit to these individuals. However, early cardiac catheterization with or without revascularization is recommended for all but the lowest risk clients (Breall, 2008).
| Individuals without ST-segment elevation may require further diagnostic procedures, such as echocardiography, to rule out complications prior to consideration of emergency coronary angiography.|
Patients without significant ST-segment elevation who are hemodynamically unstable with or without ongoing chest pain may be considered for emergency coronary angiography if appropriate (i.e., no evidence of acute valvular dysfunction, which may necessitate emergency echocardiography).
After those first 4 critical hours, blood substances known as markers of myocardial injury (cardiac troponins "T" and "I", and creatine kinase-MB values) will start to rise in the presence of actual tissue injury or death. With angina of unknown origin, it is critical to wait for these laboratory values before ruling out heart damage as an increase of these markers is diagnostic of a myocardial infarction irrespective of electrocardiogram findings.
When heart cells (myocytes) suffer sufficient injury that they begin to die, they lose their membrane integrity. This allows intracellular macromolecules to diffuse into the circulation. The current term used to collectively describe these macromolecules is serum cardiac markers. Once free floating, it takes a while for the body to filter out the extraneous molecules. This allows peaks and ebbs in heart tissue damage to be measured indirectly.
|Cardiac Markers are measurable blood values used for diagnosis of acute coronary ischemia.|
|(Reeder, 2008) (Jaffe, 2008)|
The goal of emergency treatment in acute myocardial infarction is ALWAYS the preservation of injured, dying tissues. As the heart myocyte cells are blocked from the flow of oxygen rich blood, they begin to suffocate (ischemia) and die (necrosis). Our interventions must be aimed at preserving the life of the tissue at risk, toward restoring the needed oxygenation to that tissue. The following are treatment steps usually taken when an MI is suspected.
The initial use of sublingual nitroglycerin then IV nitrates have the positive effect of dilating or expanding blood vessels that may be blocked due to spasm or constriction. This is a good start towards our goal of preserving tissue through oxygenation. The taking of a single aspirin early on has the benefits of acting as a mild blood thinner to slow the clotting process that may start on the turbid flow of blood in the compromised coronary arteries. Aspirin also has the benefit of having few significant adverse effects. Supplemental oxygen should be initiated as soon as possible to increase the quantity of free flowing oxygen in the arterial blood supply, the thought being that if any blood flow is trickling through the blocked areas at all (such as may occur during a NSTEMI event), it should be as oxygen rich as possible.
Once enough information is available to make the clinical decision that an acute myocardial infarction is present, the effort to preserve tissue viability and restore blood flow to the heart can be accelerated.
When available, primary percutaneous coronary intervention (PCI) is preferred for the majority of patients experiencing an acute ST elevation myocardial infarction. In areas where this intervention is available, an experienced clinician can perform PCI within the first 90 minutes after a patient arrives into the emergency department. In areas where PCI is not available, or in clients better served by alternative treatment, fibrinolysis (thrombolytic or fibrinolytic) therapy remains an important option.
Percutaneous coronary intervention as a reperfusion strategy centers on mechanically moving or compressing the offending blockage that is present in the coronary artery. One such revascularization procedure is Directional Coronary Atherectomy (DCA). This is the insertion of a specialized catheter into the compromised coronary artery allowing mechanical removal of plaque in order to decrease vessel blockage.
Still another PCI revascularization procedure is balloon angioplasty, with or without the placement of stents to hold open a diseased cardiac artery, such as is used for the treatment of angina pectoris in selected clients.
Of all the variables that come into play with thrombolytics, one of the most interesting is that of weight. Low patient weight has been identified as an ongoing risk factor for the significant complication of intracranial hemorrhage when thrombolytics are administered. It is therefore imperative to accurately estimate the weight of patients with acute myocardial infarction so as to determine the proper dose of thrombolytic and minimize such risks as intracranial hemorrhage (Levin, 2008).
Sustained hypertension (poorly controlled or chronic) = systolic blood pressure >180 mmHg
Ischemic stroke or other intracranial pathology
Prolonged cardiopulmonary resuscitation (>10 minutes) or recent major surgery (<3 weeks)
Recent history of (within two to four weeks) of internal bleeding
Noncompressible vascular puncture
For streptokinase or anistreplase: history of prior exposure (more than five days previously) or prior allergic reaction to these agents
Active peptic ulcer
Current use of anticoagulants = the higher the INR, the higher the risk of bleeding
Beta-blockers have consistently been recognized as a good choice for use in individuals with an acute myocardial infarction as these medications tend to slow the heartbeat while working to regulate and conserve myocardial strength. The calming effects promoted by these antihypertensives help conserve heart strength and decrease the overall oxygen demand placed on the myocardial tissue. A short-acting beta-blocker such as IV esmolol may be considered if the clinician is concerned about potential adverse effects of beta-blockers (Fenton, 2007).
|Beta-blockers such as metoprolol (Lopressor) can be useful in the treatment of an acute MI. |
Optimally all patients with known or suspected myocardial infarction should be admitted for close observation into a cardiac care or intensive care unit in order to facilitate response to rapid changes of condition.
As their individual condition warrants, patients should continue to receive nitrates, beta-blockers, and heparin during the immediate post admission phase of follow-up care.
Consideration should be given to the use of ACE inhibitors in this client base due to the improvement in survival rates that have been shown following a myocardial infarction. Effects of these medications help to decrease the heart workload by lowering afterload pressure to the heart which in turn lowers oxygen use and impacts the potential for ischemic damage. Other benefits are a lessened chance of developing congestive heart failure or experiencing sudden death, which makes the risk benefit profile for use of ACE inhibitors in the post myocardial infarction period a definite. Use them!
On the subject of risk, please be reminded that prophylactic lidocaine administration to prevent ventricular dysrhythmias is now contraindicated. Should dysrhythmias manifest themselves try amiodarone first and then lidocaine if needed, for the management of ventricular tachycardia and ventricular fibrillation.
Angina may be an entirely separate entity from the physiologic process of an acute myocardial infarction. It is important to be aware in what ways it is related and in what ways it is unrelated to an actual infarction. Excellent assessment skills make the distinction, or the connection, in each individual person who needs our services. The blurring of the boundaries of these two conditions is one of the most frustrating challenges that face healthcare providers facing a cardiac emergency. With few exceptions, those being instances where the underlying cause of the discomfort is obvious, it is best to treat the presence of suffocating pain or pressure in the chest and angina manifestation areas as though an acute myocardial infarction is occurring. As the assessment process proceeds, evidence to support or refute the acute myocardial assumption will present itself and lead to appropriate treatment pathways for the type of injury that is occurring. Be open to the clues that may not agree with your assumption of myocardial injury. Check things out while remaining alert as sudden cardiac death waits for no one.
"Cardiovascular Death Rates Decline But Risk Factors Still Exact Heavy Toll." (December 21, 2007). ScienceDaily. (Visit Source). Accessed April 14, 2008.
"Cardiovascular Disease in Women Module 1: Epidemiology." (August 30, 2007). National Institute of Health. (Visit Source). Accessed April 14, 2008.
"Heart Disease and Stroke Statistics – Update 2008." (2008). American Heart Association. Dallas, Texas.
“Tests Miss Heart Disease in Women.” (January 31, 2006). MSNBC.com. (Visit Source). Accessed on March 6, 2008.
Alaeddini, Jamshid. (December 19, 2007). “Angina Pectoris.” eMedicine. (Visit Source). Accessed March 6, 2008.
Brogden, Nicole., Dunn, Steven., Macaulay, Tracy. (February 1, 2008). “Advances in the Treatment of Chronic Stable Angina.” US Pharmacist.com. Accessed March 10, 2008.
Breall, Jeffrey. Aroesty, Julian, Simons, Michael. (February 15, 2008). "Overview of the Management of Unstable Angina and Acute Non-ST Elevation (non-Q wave) Myocardial Infarction." UpToDate 16.1. Accessed April 18, 2008.
Fenton, Drew. (September 10, 2007). "Myocardial Infarction." eMedicine. (Visit Source). Accessed June 18, 2008.
Jaffe, Allan. (February 15, 2008). "Troponins, Creatine Kinase, and CK Isoforms as Biomarkers of Cardiac Injury." UpToDate 16.1. (Visit Source). Accessed April 18, 2008.
Kennedy, Harald. Reeder, Guy., Rosenson, Robert. (February 15, 2008). "Overview of the Management of Acute ST Elevation Myocardial Infarction." UpToDate 16.1. Accessed on April 29, 2008.
Levin, Thomas. Gibson, C Michael. (February 12, 2008). "Fibrinolytic (Thrombolytic) Agents in Acute ST Elevation (Q Wave) Myocardial Infarction." UpToDate 16.1. (Visit Source). Accessed April 20, 2008.
Meisel, James. (2008). "Differential Diagnosis of Chest Pain in Adults." UpToDate15.3. (Visit Source). Accessed on February 27, 2008.
Reeder, Guy., Kennedy, Harold. (January 23, 2008). "Diagnosis of an Acute Myocardial Infarction." UpToDate 16.1. (Visit Source). Accessed April 18, 2008.
Rosenson, Robert, Reeder, Guy., Kennedy, Harold. (February 15, 2008). "Overview of the Management of Acute ST Elevation (Q Wave) Myocardial Infarction." UpToDate 16.1. (Visit Source). Accessed June 18, 2008.
Thygesen, Kristian., Alpert, Joseph., White, Harvey. (October 19, 2007). "Universal Definition of Myocardial Infarction." Circulation. American Heart Association. (Visit Source). Accessed April 18, 2008.