Introduction
The emergency department (ED) technician (EDT) plays a critical role in the initial assessment, triage, workup, and management of patients with cardiac complaints. This chapter provides a framework for understanding and participating in the care of patients with cardiac emergencies.
Cardiac Anatomy
The heart is a four-chambered pump, each chamber separated from the other by two valves. The right atrium and right ventricle, receive deoxygenated blood from the body via the superior and inferior vena cava. This blood is pumped into the lungs from the heart via the pulmonary arteries through the heart’s pulmonic valve. The lungs oxygenate the blood and return the blood to the heart via the pulmonary veins. This blood is pumped through the left atrium and left ventricle, which then pump oxygenated blood through the aortic valve into the general circulation via the aorta. ( Fig. 9.1 ).
Understanding of Heart Disease
There are several areas of the heart that can be affected by disease, and although there is usually some overlap, a basic understanding of the specific disease targets will help contextualize the general topic of heart disease.
- 1.
Coronary artery disease: The coronary arteries supply the heart muscle cells with oxygen and nutrients. Blockages in the coronary arteries, depending on how rapidly they occur, can reduce the supply of blood to heart muscle cells and in extreme cases lead to cellular death (infarction). The scientific term for heart attack is myocardial infarction (MI). Identification of a patient having a large MI is often straightforward, relying on easily recognized electrical patterns on the electrocardiogram (ECG). However, many patients have much milder symptoms that precede their heart attack by several days, and initially, there may be any of the characteristic findings ( Fig. 9.2 ).
Fig. 9.2
Coronary arteries and cardiac veins
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(From Netter F. Atlas of Human Anatomy . 7th ed. Elsevier; 2018:plate 222.)
- 2.
Cardiac muscle disease: Although a lack of blood flow in the coronary arteries will affect muscular function, many other diseases directly attack and impair the muscle function itself without significant coronary artery blockages. The most frequent result of cardiac muscle disease is congestive heart failure, a condition in which the heart’s ability to pump blood is inadequate to meet the body’s demands.
- 3.
Valvular heart disease: The heart’s four chambers are separated from each other and the arteries leading from the heart by four valves, the normal functioning of which is required for adequate blood flow. Conditions that damage a valve can lead to a leaky (insufficient) valve or a tight (stenotic) valve. Both of these situations require greater muscular effort over time to meet the body’s demands and can lead to congestive heart failure ( Fig. 9.1 ).
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Pericardial disease: The pericardium is a tough membrane surrounding the heart separating it from the lungs and assisting the heart’s pumping function. When diseased, it can squeeze the heart, decreasing its function (pericardial effusion), and when inflamed, usually by a virus, it can cause chest pain that is hard to distinguish from a heart attack.
Initial Assessment and Triage of the Cardiac Patient
Appropriate prioritization of patients with potential cardiac complaints is important, as many more patients are evaluated for suspicion of heart disease than those who are actually experiencing a cardiac emergency. Patients with cardiac problems can be very unpredictable. A patient with an acute cardiac issue may have relatively minor complaints and normal vital signs initially but can become unstable very quickly; they should be regularly reassessed to quickly identify worsening of their clinical condition.
Initial assessment of all patients should focus on identifying patients who require emergent interventions. Heart disease kills by two major mechanisms:
- 1.
Arrhythmia: All forms of heart disease mentioned above can precipitate a sudden disturbance of heart rhythm (either fast or slow), which can suddenly depress or even stop heart function. It is therefore vital that anyone with suspected heart disease be placed on a cardiac monitor that will allow the early identification and intervention to identify an arrhythmia quickly.
- 2.
Loss of cardiac muscle cells: When the heart loses a significant number of muscle cells (usually from either coronary occlusion or other muscle disease), the heart will no longer be able to pump enough blood to meet the demands. When this happens gradually, a series of compensatory mechanisms ensues that allows some adaptation. If a large amount of muscle dies or ceases to function suddenly (as can happen with a heart attack), the patient can experience a condition called cardiogenic shock. In this situation, the patient often has a low blood pressure, high pulse rate, evidence of poor organ perfusion and appears acutely ill.
Coronary Syndrome
Coronary syndrome is the spectrum of illness that occurs from acute, subacute, or chronic blockages of the coronary arteries. These blockages generally occur at locations where there is a disruption of the wall of the artery by deposition of cells, fats, and cholesterol into a coronary plaque. These plaques can occur in all types of arteries, and the process guiding the plaque development is called atherosclerosis. Major risk factors for atherosclerosis include elevated cholesterol, hypertension, and smoking. Other risk factors include diabetes, kidney disease, male sex, and family history. The arterial walls are in a constant state of motion, responding to differing metabolic needs of the heart muscle. At times, a plaque ruptures, and the body’s clotting mechanisms will respond to the plaque rupture by forming a clot at the site of the rupture. There then ensues a dynamic process resulting in either clot expansion (propagation) or dissolution via a natural system that dissolves clots preventing excess clotting (thrombolysis).
When a clot at the site of plaque rupture occurs, the clinical syndrome that ensues will be related to the clot’s location in the arterial system, whether the blockage caused by the clot is complete or partial, and how much muscle is supplied by that portion of the artery where flow is impeded. Because both blood supply and the demand of the heart muscle are variable and dynamic, the patient can be expected to have a wide range of symptoms. The three clinical syndromes associated with coronary syndrome are:
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Angina pectoris , in which pain results from ischemic heart tissue, where the heart cells have not yet died.
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ST-elevation myocardial infarction (STEMI) , where the clot occludes the entire arterial blood supply, severely impairing blood flow and leading to extensive cell death.
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Non–ST-elevation myocardial infarction (nSTEMI) , where blood flow at the clot is decreased; there is some cell death but less extensive damage to the heart wall.
Common presenting symptoms of coronary syndrome include the following:
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Chest pain: This is a common symptom that can be caused by issues in the heart, lungs, chest wall, pericardium, pleura (membrane surrounding the lungs), ribs, or even problems in the abdomen. The pain from coronary syndrome is generally milder and often has a pressure-like quality. The pain may radiate to the jaw, neck, or down the arm on the ulnar (pinky finger) side. Other symptoms associated with it are shortness of breath and, when severe, nausea, vomiting, and diaphoresis (sweating).
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Other symptoms could include syncope (fainting), palpitations (sensation of irregular heart beats), pallor , and a feeling of “impending sense of doom.” Of note, coronary syndrome in woman may present with atypical chest pain or other less specific symptoms, such as excessive fatigue .
Therefore it is important to maintain a high index of a suspicion toward all patients during triage of a potential cardiac emergency.
Heart failure symptoms are variable, but those more frequently expressed by patients include shortness of breath either at rest or on exertion, awakening in the middle of the night with breathlessness, exertional fatigue, and dizziness related to low blood pressure. Heart failure patients often have evidence of fluid retention in the legs (seen on physical exam) or in the lungs (seen on chest x-ray or bedside sonogram).
In patients with all cardiac complaints, the ECG is an early diagnostic test in which a physician analyzes the heart’s electrical activity and compares it to normal activity (see Chapter 8 ).
Measuring leakage of an enzyme only found in heart muscle (troponin) has become an important part of heart disease evaluation. Finding elevated levels of this enzyme in the bloodstream will indicate cardiac cell death (or extreme metabolic strain on heart cells) and will help the physician prioritize the treatment response. This test can either be done as a point-of-care (POC) test or in the hospital lab.
Cardiac Arrest
Cardiac muscle that is diseased or not getting enough blood (ischemic) can become electrically unstable. The heart rhythm can suddenly change from normal to a highly disorganized rhythm called ventricular fibrillation, which leads to a cessation of the heart’s organized pumping activity and circulatory collapse (no blood flow to any tissues). Without brain perfusion, respiration will soon stop, and the patient will be in full cardiac arrest (no heart contraction, leading to no pulse or blood pressure and no breathing, or respiratory arrest). These patients are most frequently brought in by emergency medical services; in many systems, they will have their airway controlled and intravenous (IV) access started in the field. For patients who are brought in by basic life support or code in the ED, most EDs have a team approach that includes the EDT, who is often assigned to do chest compressions or obtain an IV line while the physician manages the airway. For those who arrest in the ED, determining their cardiac rhythm and attempting to defibrillate them quickly is of paramount importance ( Fig. 9.3 ).
