Cardiology Notes PDF
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This document provides an overview of cardiology, covering topics such as the structure and function of the heart, cardiology technology, and various diagnostic tools. It details the role of cardiology technologists and includes information about electrocardiograms (ECG), Holter monitors, and exercise tolerance tests. The document also mentions different types of cardiac symptoms and rhythm disturbances.
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**Cardiology** is the study of the structure and function of the heart **Cardiology Technology**: Involves the non-invasive testing and monitoring of the functioning of the human heart under various conditions, the provision of basic patient care during these procedures, and the assessment and prog...
**Cardiology** is the study of the structure and function of the heart **Cardiology Technology**: Involves the non-invasive testing and monitoring of the functioning of the human heart under various conditions, the provision of basic patient care during these procedures, and the assessment and programming of implantable cardiac devices. **Cardiology Technologists:** Record electrocardiograms, hook up Holter monitors, analyze Holter monitors, perform exercise tolerance testing (stress test), and monitor and program cardiac pacemakers, implantable defibrillators, resynchronizers, implantable loop recorders and similar devices. They provide results and initial analysis to a physician for use in the prevention, diagnosis, and treatment of cardiac disease. In 1913, Einthoven, Fahr, and de Waart described the triangular frame of reference known as \"Einthoven\'s triangle\". This scheme assumed that the body was a large conducting medium Frank Wilson and his colleagues of Ann Arbor, Michigan. Wilson\'s group also developed the V (unipolar) leads. Unipolar leads provided a more exact measure of potential variation produced by the heart at any point on the body surface, virtually unaffected by the distant indifferent electrode. Until the late 1940s, the ECG was a cumbersome instrument that could rarely be used at the bedside. By 1950, the development of a portable film recording galvanometer and then a direct writing machine made the ECG a widely used clinical tool for diagnosis of coronary artery disease, ventricular hypertrophy, conduction problems and arrhythmias. The Electrocardiogram or **ECG** records the electrical activity of a large mass of atrial and ventricular cells as specific waveforms and complexes. ECG provides information about the orientation of the heart in the chest, conduction disturbances, electrical effects of medications and electrolytes, the mass of cardiac muscle, and the presence of ischemic damage (lack of oxygen to the heart). The electrocardiogram consists of **12** different leads or views of the heart in relation to the electrical potential of the heart muscle. The 12 leads are identified as Leads I, II, III, augmented leads aVR, aVL, aVF, and pre-cordial or chest leads V1, V2, V3, V4, V5 and V6. **Ambulatory ECG** (or **Holter** monitoring) employs a small, portable digital recorder that is used to obtain continuous electrocardiographic information over a long time interval (usually 24 hours) as the patient goes about his/her normal business. It is a qualitative and quantitative means of detecting and/or measuring cardiac events that may not be detected by a resting \"snapshot\" ECG. The long-term recording allows for a look at the patient\'s ECG during all levels of his/her typical daily activity (which are recorded by the patient in a diary There are 2 main components to the equipment: the **recorder** and **scanner** (analyzer) - - The most important diagnostic tool available is the patient\'s history. The patient\'s history should include information such as: - - - - - - - - - - - The correct diagnosis can be made in *[more than 50% of patient]* assessments after a carefully elicited history is taken The symptomatology should include both pathophysiological (i.e., the pathophysiological disturbance producing the symptoms) and empathetical (i.e., the effect these symptoms are having on the patient\'s quality of life) 1. 2. 3. 4. 5. 6. 7. **Cardiac Related Symptoms and Rhythm Disturbances** ---------------------------------------------------- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - **Dysrhythmia:** a problem with the rate or rhythm of your heartbeat caused by changes in your heart\'s normal sequence of electrical impulses. (Your heart may beat too quickly, called tachycardia. Or too slowly, called bradycardia; or with an irregular pattern) ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- - Dysrhythmias are the principal focus of the ambulatory ECG test, although ambulatory myocardial ischemia can also be detected ----------------------------------------------------------------------------------------------------------------------------- - - **Ischemia :**an inadequate blood supply to an organ or part of the body, especially the heart muscles ------------------------------------------------------------------------------------------------------ Episodic ST segment depression during ambulatory ECG monitoring often indicates myocardial ischemia. **Event Recorders:** Used to detect arrhythmias or to record the ECG during the development of infrequent, intermittent symptoms such as presyncope or palpitations. -------------------------------------------------------------------------------------------------------------------------------------------------------------------- **Exercise Tolerance Testing** (ETT): is frequently used in the diagnosis and follow-up of patients with ischemic heart disease (i.e., impairment of coronary perfusion usually as a result of atherosclerotic coronary artery disease) - Aside from the presence or absence of ST segment depression, diagnostic and prognostic conclusions can be drawn from the following factors and indicators: - - - - - - **Exercise Physiology:** Exercise tolerance testing is a sensitive and informative examination of the cardiovascular response to exercise. ------------------------------------------------------------------------------------------------------------------------------------------ - - There is a good correlation between the \"double product\" (blood pressure times heart rate \) and myocardial oxygen consumption during ETT. Since angina generally occurs at a constant double product in a given patient with IHD (independent of duration, intensity or type of exercise), ETT is designed to produce an increase in heart rate (HR), defined as a percentage of the maximal predicted HR of a normal population of matched age. Target HR=220-patients age With i**schemic heart disease (IHD)** there is constriction of the coronary arteries. Coronary blood flow cannot increase adequately to meet the demands of the myocardium. The constriction in flow results in ischemia, which is manifested by: - - - - **ETT Protocols** ----------------- **Cardiology Technologist Responsibilities** -------------------------------------------- - - - - - - - The purpose of the exercise test is to determine physiological responses to controlled exercise. Clinical applications include diagnostic, therapeutic, and functional goals. The ECG is monitored prior to ETT (supine and standing), at each step of the ETT protocol, immediately post exercise, and at pre-subscribed intervals post exercise for 6 to 10 minutes. Lead V5 is most often used because it provides the largest R wave and is most likely to detect ECG changes. Sensitivity is increased by using a 12-lead ECG system, which can detect ST segment changes from anterior and inferior walls. **Diagnostic Indications** -------------------------- Exercise testing may be used to evaluate medical therapy with antiarrhythmic, antianginal or antihypertensive drugs. Patients who are well controlled at rest may show abnormalities or limitations with exercise. - - - - - - - - - - - - - - - - - - - - - - - - - - **ETT Safety and Supervision** ------------------------------ - - - - - 1. 2. 3. 4. 5. 6. 7. 8. **Interpretation** ------------------ Using the criterion of 1 mm ST horizontal downsloping depression as an indication of IHD, conventional ETT has a/an: - - - ETT is not the definitive tool to verify IHD, as overall sensitivity is 64%. This means that 36% of IHD patients will have false-negative response. Note: Due to the sensor placement for ETT, the resultant ECG recording CANNOT be compared to a standard 12-lead ECG. The precordial leads may be similar, but leads I, II, III, aVR, aVL and aVF will be markedly different. - - - - - **ST Segment Changes** ST segment changes are the most reliable ECG indicators of myocardial ischemia. The depth of ST depression correlates roughly with the extent of coronary artery disease. The electrophysiological basis for ST changes during ETT is an imbalance between myocardial oxygen supply and demand. The imbalance can be caused by anemia, aortic stenosis, coronary spasm, severe hypotension, LVH and/or hypertrophic cardiomyopathy, among other causes. The imbalance results in an ST segment shift to the affected subendocardial area, and is manifested on the surface ECG as ST depression. 1. 2. 3. 4. 5. 6. - - - - - - - **Specialty Testing** The two types are tilt table testing and signal averaging ECG. Tilt table testing is used to evaluate recurrent, unexplained vasovagal or neurocardiogenic syncope in otherwise healthy persons. The test assesses the body\'s heart rate and blood pressure response to changes in position. In general, this test requires the patient to fast prior to testing. The room is often kept warm with dim lighting. The patient is strapped to a special table that is electronically raised to a 60 or 80° angle while continually monitoring ECG and blood pressure readings. In extreme cases, the patient will experience an episode of syncope immediately upon angling the table. If there are no symptoms of syncope or a drop in blood pressure, the patient may be administered a pharmaceutical (e.g., IV isoproterenol, sublingual nitroglycerin or IV adenosine) to try to instigate a response. The tilt table test is considered positive if a patient develops a drop in blood pressure associated with symptoms such as light-headedness, nausea, cold and clammy feeling, sweating, \"spacey feeling\" as if about to black out, or experiences a syncopal episode. **Signal Averaging ECG** ------------------------ Signal-averaged ECG (SAECG) uses a computer to detect each beat and to time-align each beat for a specified number of beats over a selected period of the cardiac cycle. This technique improves the signal-to-noise ratio, which enables recording of low-level cardiac signals. The low-level cardiac signals are not identifiable with standard ECG techniques. SAECG can be used to identify and analyze ventricular late potentials (VLP) and T wave alternans (TWA): - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Professionsalism Learning Outcomes: - - - - 1.the use by professionalizing groups of claims for superior knowledge and special moral integrity as devices by which they could secure some measure of control over the market for their services. 2\. the issue of cultural and social authority, arguing that the market success of fields such as medicine have been ultimately, and crucially, dependent on their ability to establish their claims to possess the authority to define and control a specific area of expertise 3.instead the emergence of professionalism as an ideology of social reform - - **Assessing the cardiac patient** Basic components include: - - - - - - Other components may include vital signs and allied tests such as chest x-ray, electrocardiogram, and common blood tests (e.g., a lipid profile). The stethoscope is an acoustic medical device used in auscultation of the lungs and heart. Many have two sides, the bell and the diaphragm, as shown in the images below. The bell is used to hear low frequency sounds while the diaphragm is used to hear high frequency sounds. **Identify the Patient** ------------------------ It is important to ensure you have the correct patient before you begin an assessment. this can be achieved by confirming the identity of a patient based on their ID band, which may be located on the wrist or ankle. The most important diagnostic tool available to the health professional is the patient\'s history. The patient\'s history should include such information as: - - - - - - - - - - - **Body Mass Index (BMI)** ------------------------- The BMI of a patient is a graph that is derived by dividing the patient\'s body weight in kilograms by the square of the patient\'s height in meters. ----------------------------------------------------------------------------------------------------------------------------------------------------- Body Mass Index (BMI) = Kg/m2 A \"normal\" BMI is considered to be between **18.5 and 24.9** for both sexes. **Physical Examination :** The cardiovascular examination includes a general inspection of physical appearance, taking the pulse, assessing the blood pressure, assessing the jugular venous pressure, palpation, and auscultation. **General Inspection of Physical Appearance:** ---------------------------------------------- Patients with acute cardiac illness can show signs of cyanosis, pallor, and sweatiness. It is important to ask yourself, \"How does the patient look? Do they look well? In more stable patients, the most common visual feature is cachexia, since it is a prognostic sign of heart failure. Palpation is necessary to determine edema. Other genetic disorders may have characteristic physical findings that should suggest to the skilled clinician to investigate for specific cardiac abnormalities. Note: Cachexia is the loss of weight, muscle atrophy, fatigue, weakness and loss of appetite, which is seen in pathologically ill patients who are not trying to actively lose weight.  **Pulse Rate** -------------- Taking a person\'s pulse is one of the simplest and most informative aspects of the cardiovascular exam. It is important to document the rate and rhythm of the pulse. It can also be useful to note the character and volume of the pulse. The most common sites to measure a pulse from are: ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- - - - The pulse rate is best determined by gently but firmly placing your first and second finger tips on the artery until you can feel a pulse. Use a watch with a second hand and count the number of pulses that are felt in 60 seconds. Alternatively, if the pulse is regular you can count the number of pulses in 15 seconds and multiply by 4. In either case, use the first pulse in the timing as 0. Aortic dissection screening can be accomplished by checking both radial pulses simultaneously. Coarctation can be assessed by looking at the radiofemoral delay. **Blood Pressure Measurement** ------------------------------ In non-invasive procedures, blood pressure is usually measured with a blood pressure cuff wrapped snugly around an upper limb. The cuff is attached to a sphygmomanometer (aneroid or mercury). ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- - - **Measurement:** Blood pressure is measured in standard units of millimeters of mercury (mmHg). The standard brachial arterial pressure consists of two (2) numbers: systolic and diastolic. The numbers are usually recorded as systolic/diastolic (e.g., 120/80). - - **Guidelines for Measuring Blood Pressure:** -------------------------------------------- - - - - - - - - - - - - - - - - - - - - - - - - -  **The jugular venous pressure (JVP)** can be a useful diagnostic tool in identifying right heart failure and pulmonary embolism. It should be assessed with the patient reclined at a 45 degree angle. The height of the waveform in centimetres above the sternal angle is defined as the JVP. In the table below, note the probable cause associated with each JVP abnormality  **Palpation** is the process of examining by applying the hands or fingers to the external surface of the body to detect evidence of disease or abnormality in the various organs. This is usually done at the apex of the heart that is located about the fifth intercostal space in the midclavicular line. Some examples of apex beats include: - - Note: Visually look for scars that may be a sign of open heart surgery (e.g., coronary artery bypasses or valve repair/replacement). **Cardiac auscultation** is the process of listening with a **stethoscope** for heart sounds within the body to detect some abnormal conditions. This is accomplished using a stethoscope. The diagram below (Figure 2-7) shows the standard positions of stethoscope placement for cardiac auscultation. ### **First Heart Sound (S1)** The first heart sound is usually loudest at the apex. Because it is high frequency, it is best heard using the diaphragm of the stethoscope. **The first heart sound is produced by the closing of the mitral and tricuspid valves**. The two sounds are separated by such a small amount of time that they are usually heard as a single heart sound. Some exceptions would include patients with right bundle branch blocks. ### **Second Heart Sound (S2)** The second heart sound is usually best heard in the second intercostal space to the left of the sternum. It is best heard using the diaphragm of the stethoscope since it is a high frequency sound. S2 is related to the closure of the semilunar aortic and fractionally-delayed pulmonary valves. Normally it is heard as a single sound on expiration but splits into its earlier aortic (A2) and delayed pulmonary (P2) components on inspiration. This physiological splitting of the second heart sound may be due to a more negative intrathoracic pressure, which increases the capacitance of the intrathoracic pulmonary vessels when the chest expands during inspiration. The opposite occurs during expiration and with a decreased venous return and a reduced stroke volume; the time to empty the left ventricle is also shortened, which makes aortic valve closure slightly sooner. A summary of this is found in the table below. ### **Third Heart Sound (S3 or Ventricular Gallop)** The third heart sound is an extra diastolic sound that is generated during the rapid ventricular filling phase of early diastole, following the opening of the atrioventricular valves. It is best heard at the apex as a dull, low-pitched sound, with the bell of the stethoscope. Although a normal finding in children and young adults, the third heart sound is a pathological finding in the middle-aged and elderly. An audible third heart sound indicates an abnormally large diastolic flow into a normal ventricle or a normal flow into an abnormal ventricle. Its presence implies either congestive heart failure (i.e., abnormal ventricle), or abnormally rapid filling of the ventricle, as in advanced mitral or tricuspid regurgitation. ### **Fourth Heart Sound (S4 or Atrial Gallop)** The fourth heart sound is an extra diastolic heart sound that resembles the third heart sound; it is low-pitched and is best heard at the apex. This sound results from atrial contraction in late diastole. The sound occurs as a result of an atrium (right or left) vigorously contracting against a rigid ventricle. It is rarely heard in the healthy individual, and is usually a sign of either ischemia or hypertrophy.  **Pulmonary Auscultation and Respiration Rate** ----------------------------------------------- **Pulmonary auscultation** is the process of listening with a stethoscope for breath sounds within the body to detect abnormal conditions. Most stethoscopes have two chest pieces: bell and diaphragm. In general, you can only pick up the sound that is directly underneath the stethoscope. Therefore, to listen to all lung fields, you should try to listen to a minimum of six places on the anterior chest and six places on the posterior chest. --------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- **Normal breath** sounds are described as vesicular, bronchial, and bronchovesicular. It is the same as saying the patient has clear lungs. In normal breathing, air moves into the airway during inspiration and it branches into progressively smaller airways. The movement through the branching airways causes turbulence that produces the sound. During expiration, the air is flowing from small airways to much larger ones; there is much less turbulence created, therefore less sound. The stethoscope's diaphragm is the preferred chest piece in listening to the lungs. The characteristics of normal breath sounds are described in the table below. Breath sounds are usually classified in three groups: normal, abnormal, and adventitious. Adventitious means \"added\" or \"extra\" sounds.  **Common abnormal breath sounds** include: consolidation, crackles or rales, rhonchi, wheezes, stridor, and pleural friction rubs. **Consolidation** occurs when normally aerated tissues are filled with fluid, mucus, pus, or cellular debris allowing only bronchial sounds to be heard. The bronchial sounds are different than normal bronchial sounds because they are louder than normal and over the entire lung periphery. Other consolidation sounds include bronchophony, egophony and whispered pectoriloquy. ### ### **Crackles or Rales** are common adventitious (abnormal) breath sounds that are discontinued sounds heard at the end of inspiration when terminal airways pop open late in inspiration due to fluid or secretion build up. Crackles are heard most commonly over the lung bases and may be a result of congestive heart failure or pneumonia. ### **Rhonchi** is defined by the American Thoracic Society as deeper, rumbling sounds that are more pronounced on expiration. Rhonchi are likely to be continuous and occur as a result of air passing through a partial obstructed airway. Possible causes include thick secretions and airway narrowing caused by a spasm or tumor. ### **Wheezes** are musical or whistling in nature that may persist throughout the respiratory cycle. They are caused by air passing through a narrowed airway, for example a bronchospasm caused by asthma, but may also be associated with congestive heart failure or foreign body aspiration. ### **Stridor** is a crowing sound heard after extubation that is commonly caused by inflammation and edema of the larynx and trachea. ### **Pleural Friction Rubs** are produced when visceral and parietal pleurae become inflamed and can no longer gently slide amongst one another, rather they rub. The sound may be intermittent and the result of pleural effusion or infection of the pleural cavity. **Accessory Muscles:** Back, neck, and abdominal muscles are accessory muscles for respiration. Under normal circumstances, they don\'t play a major role in respiration but they become more prominent during exercise or respiratory distress. Retraction (sucking in of respiratory structures) suggests a barrier to inspiration somewhere along the respiratory tract. This can be overcome by a more negative intrapleural pressure that results from vigorous contraction of the accessory muscles. The **respiration rate** is measured by observing or by placing the hand lightly on the chest and counting the number of breaths, as is done with the pulse. Also, note whether the respirations are shallow or deep. The normal rate at rest for adults is in the range of 12 to 20 breaths per minute. **Cardiac Symptoms** 1. - - - 2. 3. 4. - - - - 5. 6. 7.  **Heart Murmurs** **cardiac murmurs** appear to result from vibrations cause by turbulent blood flow. In children and young people a murmur may be the result of turbulent blood flow in a healthy and dynamic heart; however, it may also be the sign of some hemodynamic and/or structural abnormality. Some mechanisms may include: - - - - - **Murmurs are classified on the basis of their timing in the cardiac cycle**: Systolic, Diastolic or Continuous **[Systolic]** murmurs may occur in patients in whom no evidence of heart disease can be found. The timing of systolic murmurs can be further subdivided in 3: - - - **[Diastolic]** murmurs are divided into two main varieties: - - [**Continuous**] murmurs start during systole and continue into diastole and are heard throughout the cardiac cycle. The most common 2 types of continuous murmurs are: - - **Module 3: Cardiac Anatomy and Physiology** **The heart:**  The heart is a hollow, muscular organ composed of two halves that function as a double pump. Each side consists of a passive, filling chamber called the atrium (the top) and a muscular pumping chamber called the ventricle (the bottom). Figure 3-2 highlights and labels the four main chambers of the heart: the left atrium, left ventricle, right atrium, and right ventricle. Blood returning from circulation through the body (low in oxygen, high in carbon dioxide, dark red in color) enters the right side of the heart and is pumped on to the pulmonary circulation, where blood is carried to the lungs for re-oxygenation. Blood then returns to the left side of the heart (now rich in oxygen, low in carbon dioxide, bright red in colour), where it is pumped back into circulation through the body. The heart sits posterior to the sternum, anterior to the spine, and slightly to the left. -The heart is about the size of a man\'s fist, weighs less than 500 grams, and is somewhat conical in shape. -When resting, the heart pumps about 75 milliliters of blood into circulation with each beat or contraction. -The typical adult has an average heart rate of 60 to 90 beats per minute \-- over 85,000 beats in one day. -The heart pumps 5 to 30 liters of blood per minute. **Chambers of the Heart** **Right Atrium:** (Top left) The right atrium acts as a **reservoir**, receiving deoxygenated blood from the superior vena cava, inferior vena cava, and coronary sinus. The coronary sinus returns venous blood from the circulation of the myocardial muscle. The superior vena cava receives deoxygenated blood from the head, neck, and upper extremities, while the inferior vena cava receives deoxygenated blood from the torso and lower extremities. During ventricular diastole, venous blood flows through the open tricuspid valve to fill the right ventricle. Approximately 80% of the venous return to the right atrium flows passively into the right ventricle. Another 20% of ventricular filling occurs during atrial contraction. This active contribution is called the atrial kick. **Atrial kick** is an important part of assessing a patient\'s ventricular output when specific types of cardiac arrhythmias occur. Note the location of the right atrium **Right Ventricle:** (lower left) --------------------------------- The right ventricle is a roughly triangular-shaped chamber. The superior aspect of the chamber forms a cone shaped outflow tract. It pumps its contents via the pulmonic valve into the pulmonary artery. The right ventricular chamber has a low pressure in comparison to the left ventricle, and has a bellow-like contraction.The chamber is divided into two parts: - - **Left Atrium: (top right)** ---------------------------- The left ventricle is approximately cone shaped and longer than the right ventricle. It has thick muscular walls of about 9 to 11 mm. Like the right ventricle, it has a smooth outflow tract (aortic vestibule) and heavily trabeculated inferior region with even more numerous and thicker trabeculae than the right ventricle. Oxygenated blood is literally wrung out of the chamber after the left ventricle has generated enough pressure to overcome the high resistance of the aorta. **Interventricular Septum** ---------------------------  Even the **interventricular septum**---the wall separating the left ventricle from the right ventricle---contributes by becoming rigid just before contraction, thereby serving as a fixed fulcrum at each ventricle\'s end. ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- **How the Chambers Work -- Coordinated Pumps** ---------------------------------------------- Although they function essentially independently of each other, each atrium and its ventricle must be coordinated to pump in a rhythm and to pump equal volumes. The atria contract simultaneously, and after a timed interval (to allow for ventricular filling to be completed) the ventricles contract. The volume of blood received and ejected by the right side is the same as that of the left side; otherwise an imbalance in the system would be created. **Great Vessels of the Heart** The great vessels of the heart are the venae cavae (inferior and superior), the pulmonary veins, the pulmonary artery, and the aorta. DEf: The great vessels connect the heart to the arteries and veins of the systemic and pulmonary circulation, which connect to smaller arteries, veins, arterioles, venules, and capillaries. **Inferior Vena Cava and Superior Vena Cava:**  The venae cavae empty the deoxygenated blood from systemic circulation into the right atrium. The inferior vena cava receives venous blood from the internal organs and lower extremities while the superior vena cava receives venous blood from the head and upper extremities. **Pulmonary Veins** ------------------- The four pulmonary veins empty the oxygenated blood from the pulmonary circulation into the left atrium. **Pulmonary Artery** --------------------  The pulmonary artery receives deoxygenated blood from the right ventricle. Upon leaving the heart, the pulmonary artery bifurcates to become the right and left pulmonary arteries. The right and left branches connect to the pulmonary circulation in the lungs for gas exchange at the alveolar membrane. Figure 3-12 highlights the main pulmonary artery from the annulus of the pulmonic valve to the bifurcation of the branches. **Aorta** The aorta carries oxygenated blood from the left ventricle to the systemic circulation. --------------------------------------------------------------------------------------- Several smaller arteries branch off the main aortic stem soon after the vessel leaves the heart, to supply the arms and the head. These are the brachiocephalic trunk (innominate artery), the left common carotid artery, and the left subclavian artery. Figure 3-13 highlights the ascending aorta, aortic arch, and bifurcation of the brachiocephalic artery, left common carotid artery and left subclavian, from left to right respectively. **Heart Valves** The heart has four main valves, which in the normal heart serve to direct blood in an antegrade direction and prevent backward leakage. There are two **atrioventricular valves (tricuspid and mitral)** that, as the name implies, separate the atria from the ventricle, and two **semilunar valves (pulmonic and aortic)** that separate the ventricle from the great vessels. All four valves are attached to the fibrous cardiac skeleton and respond to pressure changes caused by the changes in fluid volume in the chambers. They passively open and close accordingly. In the case of a defective valve, blood may flow back into the chamber that it just left (retrograde or regurgitant flow). **Tricuspid Valve** -------------------  The tricuspid valve is the three-cusped valve located between the right atrium and the right ventricle. It prevents the backflow of blood to the right atrium during right ventricular systole. Figure 3-14 highlights the location of the tricuspid valve, more specifically the anterior and superior leaflets from left to right. Movement of the valve leaflets is controlled by tension of the chordae tendineae, which are thin strands of fibrous tissue that extend to the papillary muscles. Without the tension of the chordae tendineae during ventricular systole, the valve cusps would be forced into the atria. Disease or infarction can rupture the chordae tendineae, permitting retrograde flow or regurgitation of blood into the atrium during ventricular contraction. Because it is situated between an atrium and a ventricle, the tricuspid valve is called an atrioventricular, or A-V valve. **Mitral Valve** ---------------- The mitral valve is a two-cusped valve located between the left atrium and the left ventricle. It prevents backflow of blood to the left atrium during left ventricular systole. Figure 3-15 highlights the position of the mitral valve, in particular the anterior and posterior leaflets from left to right. Movement of the valve is controlled by the chordae tendineae, as is done with the tricuspid valve. However, the chordae tendineae associated with the mitral valve are much more numerous. They are thicker and stronger than those of the tricuspid valve. Since the mitral valve is situated between an atrium and a ventricle, it is one of the atrioventricular (A-V) valves. **Pulmonary (Pulmonic) Valve** ------------------------------  The pulmonary valve is a three-cusped valve, located between the right ventricle and the pulmonary artery. It prevents backflow from the pulmonary artery during right ventricular diastole. Unlike the A-V valves, the pulmonic valve is not supported by chordae tendineae or papillary muscles. The pulmonic valve is referred to as one of the semilunar valves, because the three cusps are semilunar shaped. Figure 3-16 highlights the position of the pulmonic valve. **Aortic Valve** ---------------- The aortic valve is a three-cusped valve, located between the left ventricle and the aorta. It prevents backflow from the aorta during left ventricular diastole. Figure 3-17 highlights the position of the aortic valve. The coronary arteries originate above the cusps of this valve at the three outpouchings of the aortic wall, called the sinuses of Valsalva. Like the pulmonary valve, the aortic valve is not supported by chordae tendineae or papillary muscles. These valves are instead secured by a fibrous ring that surrounds the valve. The aortic valve is also referred to as one of the semilunar valves, because the three cusps are semilunar shaped. The Endocardium, Myocardium, and Pericardium This topic describes the endocardium, myocardial wall, and the pericardium. The pericardium consists of the parietal and visceral layers; it is synonymous with epicardium. From the inside out, the layers of the heart are the endocardium, myocardium, and epicardium, which are demonstrated in the image below.  **Endocardial Layer (Endocardium)** ----------------------------------- The endocardium is the innermost layer of the cardiac chambers, valves, and blood vessels. It is a smooth, delicate single layer lining. The endocardial layer functions to minimize trauma to red blood cells and the accumulation of platelets that would form clots. Tissue containing fibroblasts, elastic and collagenous fibers, veins, nerves, and branches of the conducting system can be found in the subendocardium, which is continuous with the connective tissue of the myocardium. **Myocardial Layer (Myocardium)** The middle layer of the cardiac wall, the myocardium, is the heart muscle and is responsible for mechanical contraction. It is striated like skeletal muscle and is also involuntary like smooth muscle. This unique structure provides some distinctive properties. Electrical excitation spreads faster in the myocardium than in other types of muscle fibers. The cardiac muscle has the ability to produce self-excitation: to initiate its own electrical impulse to stimulate the muscle and cause contraction. Atrial and ventricular muscle fibers are completely separated from each other by fibrous tissue. The only connection between the two muscle fibers is an electrical one, via the conduction system. **Pericardial Layer (Pericardium)** ----------------------------------- The pericardium is comprised of two layers. The first layer is the inner visceral pericardium (epicardium), which adheres to the external wall of the heart before reflecting back on itself to form a second layer that lines the outer fibrous layer. This second layer is known as the parietal pericardium. The space between the parietal and visceral layers of the pericardium is normally filled with a thin film of pericardial fluid that helps to minimize friction. The epicardium is synonymous with visceral pericardium, the outermost layer of the heart. The epicardium offers minor protection and secures the heart within the thorax by attaching to the sternum and mediastinal portions of the right and left pleurae. Multiple connections ensure that the heart is firmly anchored and maintained in position. Composed of connective tissue and adipose (fat) tissue, the epicardium allows the passage of larger blood vessels and nerves that supply the heart. Note the layers of the heart in Figure 3-18 inner to outer: the endocardium, the myocardium and the pericardium, which is further separated into the visceral (epicardium) and parietal layers. Position and Borders of the Heart The heart sits semi-horizontally, with the apex directed downward, forward, and to the left, toward the left hypochondrium (upper left lateral region beneath the ribs). The ability to identify the structures of the heart that face each respective surface is an important aid to the understanding of abnormalities. - - - - The anatomical long axis is defined as a line passing through the apex from the left hypochondrium toward the right shoulder. Internally this line roughly corresponds to the orientation of the septa dividing the right and left hearts and passes from base to apex. The short axis on the other hand lies at right angles to the long axis and is approximately in line with the A-V valve plane. Figure 3-20 demonstrates the anatomical axis of the heart. It is important to recognize the difference between the anatomic long axis and the electrical axis of the heart. The electrical axis will be discussed in different parts of the Cardiology Technology Diploma program. Coronary Circulation, Arteries, Artery Disease, and Veins **Coronary Circulation**  The heart muscle has its own blood supply delivered by the coronary arteries. The coronary arteries branch out into smaller arteries and capillaries, and lie within the loose connective tissue in the epicardial fat. Figure 3-21 is a labeled diagram that shows the general configuration of many of the main coronary arteries tracing the surface of the heart. Blood is circulated to the heart muscle almost completely during ventricular diastole, when the muscle is at rest. Thus, the heart muscle is very efficient, being able to meet all of its metabolic needs during the brief rest interval of the cardiac cycle. Coronary blood flow increases with oxygen demand, such as when the person is febrile (i.e., feverish), or with exercise. When coronary blood flow does not meet oxygen need, compensatory mechanisms and symptoms develop. There are two main coronary arteries, the left coronary artery and the right coronary artery. The coronary arteries originate from the root of the aorta just above the cusps of the aortic valve, where the blood is oxygen-rich. It is the left coronary artery that passes between the left atrium and pulmonary trunk where it eventually divides to become two large branches: the left anterior descending artery (LAD) and the left circumflex (LC) artery. The coronary arteries divide into smaller and smaller branches, until they become so small that only one blood cell at a time can flow through them. These very small vessels are called capillaries. In the capillaries, the myocardial tissues extract oxygen and release carbon dioxide and metabolites. The blood, now deoxygenated, flows into veins that become increasingly larger. The veins empty directly into the right atrium by way of the coronary sinus. **Right Coronary Artery (RCA)** ------------------------------- The right coronary artery (RCA) courses the right A-V groove posteriorly between the right atrium and ventricle. It supplies the right ventricle via marginal branches. In the majority of individuals, the RCA branches to form the posterior descending artery, which supplies the inferior and posterior walls of the ventricles as well as the posterior one third of the interventricular septum. Branches of the RCA supply blood to the following parts of the cardiac conduction system: - - **Left Main Coronary Artery** ----------------------------- The left main coronary artery travels between the pulmonary trunk and left atrium to reach the AV groove. It bifurcates to form the left anterior descending coronary artery and the circumflex artery. **Left Anterior Descending Coronary Artery (LAD)** -------------------------------------------------- The LAD courses the anterior interventricular groove towards the apex. It gives rise to septal branches that supply the anterior two thirds of the interventricular septum and diagonal branches that supply the anterior surface of the left ventricle. **The Circumflex Artery** ------------------------- The circumflex artery travels the left AV groove and branches to form the large obtuse marginal branches to supply the lateral and posterior wall of the left ventricle. In 8% of the population the circumflex branches to form the posterior descending coronary artery and AV nodal artery supplying the AV node. These individuals are considered left dominant. In some cases (25% of the normal population), the SA nodal artery may arise from the circumflex and supply the SA node. Note: A very small percentage (5%) of the population has dual supply to the SA node in which the RCA and circumflex both contribute to the SA nodal artery. **Coronary Artery Disease** --------------------------- When a coronary artery becomes narrowed or obstructed, blood flow to specific areas of the myocardium (muscle) and cardiac structures (e.g., papillary muscles and conduction system) becomes temporarily or permanently damaged. It is, therefore, important to remember the structures that each of the coronary arteries supply. **Coronary Veins** ------------------ Venous drainage follows a distribution similar to that of the coronary arteries. However, the vessels return blood from the myocardial capillaries to the coronary sinus, which empties into the right atrium. The major veins most often lie superficial to the arterial counterpart within the epicardial fat. Cardiac Cycle and Cardiac Output  A cardiac cycle is the sequence of one systole (the contraction phase of a chamber of the heart) and one diastole (the relaxation phase of a chamber of the heart). During sedentary activity, the cycle is about 0.8 seconds. With exercise and increased heart rate, the cardiac cycle is completed in a shorter time. The time reduction is largely at the expense of diastole, the rest period for the heart. The path of **blood in the cardiac cycle** is as follows: - - - - Note Figure 3-22 demonstrates the normal pressures taken in the aorta and left atrium during cardiac catheterization. The pressures are superimposed with an ECG, which correlates the phases of the cardiac cycle as well as the opening and closure of the aortic and mitral valve. **Cardiac Output (CO)** ----------------------- Cardiac output (CO) is defined as the volume of blood ejected from the left ventricle to the aorta in one minute. Cardiac output is the product of the heart rate (HR) or number of beats per minute, and the stroke volume (SV) or the volume of blood ejected from the ventricle in a single beat. CO = HR x SV The three main factors that determine **stroke volume are preload, afterload, and myocardial contractility** 1. 2. 3. Heart rate (HR) is determined by the balance between sympathetic and parasympathetic (or vagal) tone of the nervous system. Sympathetic tone increases HR whereas parasympathetic tone has the opposite effect and slows HR. Cardiac Index (CI) is used to compare cardiac outputs amongst individuals since CO is dependent on body size. It is calculated by dividing the cardiac output by the body surface area (BSA). FYI: Cardiac output is measured by the thermodilution technique or the Fick technique during cardiac catheterization. Conduction System The conduction system is the pacing system of the heart that is responsible for the electrical activity that controls every heartbeat. This unique system consists of specialized cells and fibers that are collectively known as nodes or bundles. An understanding of the conduction system is an essential component of learning and understanding an electrocardiogram. Function: 1. 2. The conduction system of the heart is composed of the specialized cells that form the Sinoatrial Node (SA Node), the intermodal conduction tracts, the atrioventricular node (AV Node), the Bundle of His, the left and right bundle branches, and the Purkinje network. ### **[Sinoatrial Node]** The Sinoatrial node (SA node) is located in the upper posterior portion of the right atrial wall of the heart, near the opening of the superior vena cava. The SA node is commonly referred to as the primary pacemaker of the heart because it normally depolarizes more rapidly than any other part of the conduction system. It is normally the primary pacemaker of the heart. The SA node initiates electrical impulses at a rate of 60-100 bpm. If, for any reason, the SA node fails to be the dominant pacemaker of the heart, other areas of the conduction system can take over control by discharging impulses. ### **[Internodal Tracts]** The intermodal tracts receive the electrical impulse as it leaves the SA node. These tracts distribute the electrical impulse throughout the atria and transmit the impulse from the SA node to the AV node. ### **[Atrioventricular Node]** The atrioventricular node (AV Node) is located in the posterior wall of the right atrium immediately behind the tricuspid valve and near the opening of the coronary sinus. In most individuals the AV node is supplied by the right coronary artery. In the remainder, the circumflex artery provides the blood supply. As an impulse from the atria enters the AV node, there is a delay in conduction of the impulse to the ventricles. This delay in conduction allows time for the atria to empty their contents into the ventricles before the next ventricular contraction begins. The AV node has the ability to act as a pacemaker, if needed, and will pace the heart at 40-60 bpm. ### **[Bundle of His]** After passing through the AV node, the electrical impulse enters the Bundle of His. The Bundle of His is usually the only electrical connection between the atria and the ventricles. It is located in the upper portion of the interventricular septum and connects the AV node with the two bundle branches. ### **[Bundle Branches]** The bundle of His divides into two main branches at the top of the interventricular septum. These branches are the right bundle branch and the left bundle branch. The right bundle branch innervates the right ventricle. The left bundle branch spreads the electrical impulse to the interventricular septum and left ventricle, which is thicker and more muscular than the right. The left bundle branch further divides into three fascicles. ### **[Purkinje Network]** The right and left bundle branches divide into smaller and smaller branches and then into a special network of fibers called the Purkinje fibers. This network of fibers carries electrical impulses directly to ventricular muscle cells. Conduction through the Purkinje system precedes ventricular contraction. The electrical impulse spreads from the endocardium to the myocardium. The Purkinje fibers have an intrinsic pacemaker ability of 20-40 bpm. **Electrical Pathway of the Conduction System** ----------------------------------------------- In a normal heart, the SA node initiates the impulse for the conduction system. The electrical impulse leaves the SA node at a rate of 60-100 bpm and travels through the atria via the internodal pathways to the AV node, resulting in atrial depolarization/contraction. The electrical impulse continues onto the Bundle of His, down the Left and Right Bundle Branches, and finally to the Purkinje fibres, which results in ventricular depolarization/contraction. ### **Different Pacemaker Cells**  Module 4: Basic ECG and Arrhythmia - - - - - - - - How ECGs Work The cardiac conduction system is composed of highly specialized cells. These specialized cells have unique characteristics and functions that allow the creation and propagation of electrical impulses throughout the cardiac muscle. - - - - - - The standard electrocardiogram is the summation of the many electrical potentials generated by the heart: that is, cardiac electrical activity. These electrical potentials are viewed and recorded from specific sites, known as leads. Note that the terms sensor, electrode, and lead are often interchanged. ECG components, the P, QRS, and T waves, represent the electrical activity needed to bring about certain physiological events. The electrical activity is either myocardial depolarization or repolarization. Note that by convention, electrical activity **directed upwards is a positive** deflection while a **downward deflection is negative**. Twelve-lead ECG Sensor (Electrode) Placement -------------------------------------------- To record a standard 12-lead ECG, it is necessary to place all six precordial sensors in their assigned positions: - - - - - - The right and left arm sensors are located at the wrists. The right and left leg sensors are located just above the ankles. The right leg sensor acts as the ground lead.  The lead or lead wire is an insulated wire that attaches to the sensor (electrode) with an alligator clip. The lead wires come together to form the main patient cable that connects to the main ECG machine. Specific leads in a standard 12-lead ECG reflect activity in specific parts of the heart. Recording Paper/Speeds/Calibration/Signal filtering/Measurements ---------------------------------------------------------------- - - - It is possible to determine the heart rate on an ECG from these measurements. A standard ECG usually consists of 4 columns and 3 rows. Each ECG tracing is printed on a separate sheet by the machine. A 4th row is sometimes included as a rhythm strip of one specific ECG lead: lead II or V1. - - The standard format for a normal ECG with normal columns and rows is shown in the image below. #### **GAIN (or Standard)** On a standard ECG, each vertical millimeter of paper equals 0.1 millivolt. The standard calibration for an ECG is 10 mm (i.e., 1 millivolt). Calibrations can be changed to adjust for too large a deflection or too small a deflection. Alternate gains are 1/2 and x2. - - Some ECG recorders will allow for a \"split\" calibration. A split calibration is usually normal standard for the limb and augmented leads, and 1/2-standard for the chest (precordial) leads. #### **Paper speed** The standard ECG recording speed is 25 mm/sec. Alternate paper speeds are 12.5 mm/sec and 50 mm/sec. - - #### **Signal filtering** ECG recording filters for adults, as recommended by the American Heart Association (AHA), are 0.05 to 150 Hz. These are programmed into the ECG recording device.  Components and Normal Readings An ECG is made up of a series of waveforms, segments, and intervals that represent a cardiac cycle: P wave, PR segment, PR interval, QRS complex, J point, ST segment, T wave, QT interval, U wave. The U wave is not usually visible. P Wave ------ The P wave is the first waveform in the normal cardiac cycle. In Lead II of the ECG, it is normally smooth, rounded and upright or positive. The P wave is the complete depolarization of the right and left atrium. The P wave: - - The mean P wave depolarization vector of the two atria occurs from right to left and from superior to inferior. Remember: Electrical activation must precede contraction. Therefore, the P wave represents the electrical activation sequence of the atria. Contraction of the atria follows immediately. PR Segment ---------- The PR segment is the period immediately after the P wave, up to the beginning of the QRS complex. This is an electrically silent period when the impulse slowly traverses the AV node. During this time, the atria contract. PR Interval ----------- The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It measures the time it takes for the impulse to travel from the atrial myocardium near the sinoatrial node to the ventricular myocardium. The normal PR interval is 0.12 to 0.20 seconds. The PR rate varies with heart rate because the PR segment is the transmission of the impulse across the AV node, which is controlled by the sympathetic and parasympathetic divisions of the autonomic nervous system. It also varies with age. Note the PR interval in the following image. QRS Complex ----------- The QRS complex represents ventricular depolarization. Atrial repolarization occurs during this time, but is usually obscured on the ECG by the larger ventricular depolarization. The QRS duration is the time taken for complete ventricular depolarization. Duration is normally in the range of 0.08 to 0.12 sec. Although (by convention) the ventricular depolarization is called the QRS, certain ECG complexes may not have a Q, an R or an S component, depending on the lead being examined. All three waves on a normal ECG can be appreciated in V5 and V6. - - - J Point ------- The J point is the precise point (junction) where the QRS and ST segment meet. This point is relevant to hypothermia, hypercalcemia, stress testing, and the Brugada Syndrome. Later modules will discuss these conditions in relation to the J point in more detail. ST Segment ---------- The ST segment of the electrocardiogram typically represents a period when the ventricular myocardium remains in a depolarized state. It is measured from the end of the QRS complex to the beginning of the T wave. Normally, the ST segment is flat (isoelectric). It may be slightly upsloping, downsloping, or horizontally depressed. The ST segment is a very sensitive indicator of myocardial ischemia or infarction (heart attack). By comparing the relationship of the isoelectric PR segment with that of the ST segment, you can determine whether there is significant ST elevation or depression. Elevation or depression of the ST segment by 1 mm (0.1 mV) from the isoelectric baseline is considered \"abnormal\". T Wave ------ The T wave represents ventricular repolarization. Usually, the T wave is upright and positive (except in aVR), as illustrated in the following image. The duration by itself is not usually measured; rather it is measured within the QT or QTc interval, as defined below. QT Interval ----------- The QT interval consists of the QRS, ST segment, and T wave. Together these represent the entire depolarization and repolarization of the ventricles, also known as the electrical activity and recovery. The QT interval is measured from the beginning of the QRS complex to the end of the T wave and varies with heart rate, gender and age. The QT interval is corrected (QTc) for heart rate by a specific formula:  Note: the RR interval is in seconds. The QT interval is of interest due to its predisposition for causing ventricular arrhythmias. U Wave ------ The U wave is usually absent from the ECG. Its electrophysiologic origin is uncertain. The U wave normally mimics the T wave in polarity. Interpreting the ECG and Arrhythmias 1. - - 2. - - - 3. - - - - 4. 5. 6. Heart Rate Calculation ---------------------- This is best for irregular rhythms and is the least accurate of all the methods. The method is to count the number of QRS complexes on a 6-second rhythm strip and multiply by 10. The Large Square method is best for regular rhythms. Count the number of large squares between 2 consecutive QRS complexes and dividing into 300, since there are 300 large squares in one minute. It is easiest to start on a dark line. If the rhythm is irregular, you take the longest R-R interval and the shortest R-R interval and give a range. The R-R value is referring to two consecutive QRS complexes. The concept is the same as the large square method, except small squares are used, instead of large squares. The method is to count the amount of small squares between two consecutive QRS complexes, and divide into 1500. The memory method is handy if you don't have a ruler or a calculator. The method involves counting the number of large squares between two QRS complexes and using the rates that you have memorized. Sinus Rhythms The normal cardiac rhythm originates in the sinus node and is therefore called, \"sinus rhythm.\" It is generally regular but has some continual variation due to the input of the sympathetic and parasympathetic aspects of the autonomic nervous system. Sinus rhythm is usually between 60 and 100 bpm. However, you must consider situation factors to determine if the rate is in fact normal (e.g., your HR should not be 100 bpm while sleeping, unless you are having a nightmare).  Sinus Bradycardia (less than 60bpm) ----------------------------------- Sinus bradycardia can be defined as a sinus rhythm of less than 60 beats per minute (bpm). Treatment with atropine can be indicated if the patient is symptomatic. Sinus Arrhythmia ---------------- Commonly, young people experience an exaggeration of the normal variation of heart rate with respiration (i.e., the slowing down and speeding up that occurs with normal breathing) known as sinus arrhythmia. It is benign and usually of no clinical significance. However, marked sinus arrhythmia is a sign of increased vagal tone, which can be an indicator of cause for vasovagal syncope. Sinus Tachycardia(above 100 bpm) -------------------------------- Sinus tachycardia can be defined as a sinus rhythm in excess of 100 bpm. Sinus tachycardia is typically the result of a physiological demand, but may be caused by pain, anxiety, hypovolemia, left ventricular dysfunction, fever, pulmonary embolism, hyperthyroidism, or drug withdrawal. These are just some examples. Treatment is for the cause (e.g., pain, anxiety, hypovolemia, left ventricular dysfunction, fever, drug toxicity, anemia) of the sinus tachycardia, not the rhythm.  Atrial Rhythms: **Premature atrial contraction (PAC)** originates in an ectopic focus in the atria outside of the SA node. PAC is often the result of catecholamine, nicotine, and caffeine influences. In some cases, it is associated with drug toxicity and rarely with pericarditis. The P wave may be premature and hidden in the T wave of the preceding beat. The contour of the P wave is usually different from that of a sinus beat; it depends on the origin of the ectopic focus. Three or more premature atrial contractions (PACs) establish the criteria for supraventricular tachycardia (SVT). Supraventricular tachycardias are often called paroxysmal due to their sudden onset and termination and run in the neighborhood of 140 to 220 bpm. **Supraventricular tachycardia (SVT)** is a term used to describe tachycardias that originate above the level of the ventricle. Examples of SVTs include: - - - - - - The distinguishing characteristics of atrial flutter are the recognizable flutter waves (f waves). These waves combined with the preceding QRS complexes appear to have a saw-tooth configuration. There is usually an associated physiological AV block of at least 2:1. More commonly the ratio is 4:1, and sometimes 6:1. When the conduction ratio is 2:1 and the flutter waves are obscured, it is difficult to recognize atrial flutter. Vagal maneuvers (e.g., carotid sinus massage or the Valsalva maneuver) may help to unmask the rhythm by slowing conduction and increasing the degree of AV block. - The number of impulses reaching the ventricles can be in excess of 140 to 180 bpm by the refractory period of the atrioventricular (AV) node; in this case it is considered a rapid ventricular response. The ECG characteristics of atrial fibrillation are: - - **Atrial fibrillation (AF) with an irregular ventricular response (RR interval) is characterized by the:** - - - AF is thought to be a result of myocardial tissue damage/injury and elevated atrial pressure. Other common causes include: - - -  Heart Blocks Four Atrioventricular conduction defects are discussed below. These are the First degree, Second degree Type I, Second degree Type II, and Third degree AV blocks. ### **First-degree AV Block** With first-degree AV block, the refractory period of the AV node is delayed. The ECG characteristic of first-degree AV block is a PR interval exceeding 0.20 seconds. ### **Second-degree AV Block** With second-degree AV block, the conduction of sinus or other supraventricular impulses fail to be conducted to the ventricles. There are two types of second-degree AV block: Type I (Wenckebach) and Type II (Mobitz II) and they may be intermittent or continuous. [Type I (Wenckebach)] is characterized by a progressive prolongation of the PR interval until a P wave is not conducted to the ventricles. This is because the impulse conducted to the ventricles becomes progressively more difficult to propagate.  [Type II (Mobitz II)] is characterized by a conduction pattern in which the PR interval remains constant, but intermittently, a P wave is blocked (i.e., not conducted to the ventricle). ### **Third-degree AV Block** Third-degree AV block, or **complete heart block**, implies that all sinus or supraventricular impulses fail to conduct through the AV node and penetrate the ventricles. To prevent cardiac standstill, a latent subsidiary pacemaker is necessary. Often there is sinus activity and subsidiary pacemaker activity that are totally independent of each other. This rhythm is often described as P waves marching through the QRS, which implies that there is no relationship between the P wave and the QRS complexes, as they beat independently. This results in no consistent PR interval. The resulting QRS width and rate indicate whether the subsidiary pacemaker is junctional (i.e., AV node) or infranodal (i.e., bundle branch-Purkinje system in ventricle) in origin. - - Symptoms associated with complete heart block may range from none to Stokes-Adams attacks. Stokes-Adams attacks are the result of diminished cardiac output and blood flow to the brain and cause fatigue, difficult breathing, loss of consciousness, and even convulsions.  Ventricular Rhythms There are 4 Ventricular arrhythmias; Premature Ventricular Contractions or PVCs, Ventricular tachycardia, Ventricular fibrillation, and Ventricular flutter. ### **Premature Ventricular Contraction (PVC)** A PVC is a premature impulse of ventricular origin occurring before the next expected sinus beat. In most instances, a PVC is easy to recognize by its widened QRS complex (greater than 0.12 seconds). PVCs may have either a right bundle branch block (RBBB), a left bundle branch block (LBBB), or near-normal morphology depending on the origin of the impulse. The delay that follows most PVCs is called the compensatory pause. This pause demonstrates the inability of the ectopic ventricular impulse to penetrate the AV node retrogradely, so the sinus node activity is unaffected. A PVC can also be "interpolated." In this case, the PVC occurs between two normal beats without an associated compensatory pause. ### **Ventricular Tachycardia** When three or more PVCs occur in succession at a rate exceeding 100 to 250 bpm, the term Ventricular Tachycardia (VT) is applied. The sequence of ventricular depolarization and repolarization is abnormal, resulting in a widened QRS complex. ST segments and T waves may not be distinct. Most VT results from a PVC, or PVCs, generated by a re-entry mechanism in the setting of myocardial infarction (MI) and coronary artery disease (CAD). Torsades de Pointes ("twisting of the points") is a ventricular tachycardia with the unusual characteristic of showing cycles of alternating QRS polarity. The peaks of the QRS complexes appear to be twisting around the isoelectric line of the recording in sinusoid fashion. Torsades de Pointes is also characterized by frequent spontaneous conversion and recurrence.  ### **Ventricular Fibrillation and Ventricular Flutter** By far, ventricular flutter and ventricular fibrillation are 2 of the worst arrhythmias you will encounter. It is not uncommon for these arrhythmias to co-exist. Ventricular fibrillation (150 to 500 bpm) generates a grossly irregular waveform with varying amplitudes. As cardiac function deteriorates, the waves tend to diminish. Atrial activity is difficult to determine, but it is assumed there is complete AV dissociation. With ventricular flutter (150 to 300 bpm), the waveform appears to be regular (sinusoidal - waveform looks the same whether read right side up or upside down). Large flutter waves tend to indicate a healthier heart. As the flutter waves become smaller, ventricular fibrillation becomes more imminent. Myocardial Infarction Serial ECGs during the acute phases of a suspected acute myocardial infarction are of critical importance because they allow you to determine the stage of myocardial infarction. ST Segment Elevation Myocardial Infarction **(STEMI)** The ST elevated myocardial infarction is an infarction that penetrates the entire width of the myocardial wall (transmural). The ECG criteria for STEMI is ST segment elevation of 1 mm or more (0.1 mV) in two or more ECG leads that look at the same ventricular wall segment (e.g., inferior wall). ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- ST segment elevation alone is not specific to transmural acute myocardial infarction (AMI). It is also seen in other conditions, such as pericarditis, and early repolarization. STEMI results in pathologic Q waves over the area of infarct. These Q waves have a width of ≥ 1 mm and a depth 25% the height of the QRS complex and occur as a result of the inability of the impulse to travel through dead or necrotic muscle. Left bundle branch block (LBBB) may conceal changes resulting from an acute myocardial infarction. Non-ST Segment Elevation Myocardial Infarction **(NSTEMI)** ----------------------------------------------------------- Non-ST segment elevation myocardial infarction typically does not penetrate the entire width of the myocardium (non-transmural). In NSTEMI, the ECG changes are variable, but they most commonly include: - - - Abnormal Q waves do not usually develop during the course of NSTEMI. Since ECG changes are nonspecific, ancillary studies (e.g., enzymes or imaging) are necessary to confirm myocardial damage. ST-T wave changes are not specific to NSTEMI. Patients with unstable angina also transiently exhibit similar abnormalities. Localization of Site and Age of an Old Myocardial Infarction ------------------------------------------------------------ The ECG is able to localize the site of probable old infarction/injury with considerable accuracy. The localization is based on identifying which leads have abnormal pathological Q waves for lateral or inferior walls, or noting if there is poor (or no) R wave progression in the precordial leads (old anterior wall).  **Module 5: Cardiac Diagnostic Imaging Technology** **Chest Radiography (X-ray):** Penetration of x-rays is inversely proportional to tissue density; therefore, air-filled structures absorb few waves and appear black (underlying film) whereas denser materials like bone are able to absorb more radiation and appear white. x rays offer a silhouette of the heart and surrounding structures. - There are two main views used to routinely assess the heart and lungs: - - The **frontal** view is used for accurate assessment of overall size. The x-rays are transmitted from behind the pati ent to a film placed against their chest, producing a posterior-anterior image. In the **lateral** view the x-rays pass from right to left and are transmitted to a film that is on the patient\'s left side. A clinical use of radiography is to evaluate the size of chambers and to visualize pulmonary signs of heart failure. The cardiac silhouette is a good indicator of chamber size. In adults, the normal heart should occupy less than or equal to 50% of the width of the thorax. A cardiothoracic ratio is used to account for variation in body habitus. The following image shows a normal chest x-ray: **Pericardial effusion or cardiac tamponade** can give a misrepresentation of heart size because the fluid causes absorption of x rays. **Hypertrophy (i.e., hypertrophic cardiomyopathy)** is not usually detectable on the x-ray because it results in an overall increase in muscle mass rather than chamber size. The main causes of chamber and great vessel dilatation include: - - - - The pattern of chamber enlargement and the shape of the dilated chamber can offer clues into the specific underlying disease and etiology. Heart failure has several key pulmonary radiographic findings: - - - - - Changes in pulmonary blood flow patterns can suggest pulmonary embolism, whereas changes in appearance can suggest pulmonary hypertension. **Echochardiography** - - - There are several main types of echocardiographic techniques, which include: - - - - As you will see, there are four main echocardiographic modes that include: 1. 2. 3. 4. ### **2-D Echocardiography:** also known as B-mode is used to obtain cross sectional, real-time images of the heart. Images are obtained on modern machines by electronically sweeping the ultrasound beam across the tomographic plane. The quality of the image depends on the frequency of the transducer and the frame rate. ### **M-mode:** imaging was the original mode of ultrasound and is still part of routine assessment today. Two-dimensional imaging is used to guide the placement of the M-mode cursor, which ensures that the image is on axis. The amplitude of the signal is recorded along the length of a single beam with the distance on the vertical axis and the time on the horizontal axis. The high frame rate of m-mode allows for good resolution. It is also useful for evaluating the opening and closing of valves. ### **Doppler:** ultrasound is used to detect the direction and average speed of blood flow; essentially the velocity. It is based on the difference in frequency between the transmitted frequency from the transducer and the scattered signal reflected off moving blood cells that return to the transducer. This is known as the Doppler shift.  The following image is an example of pulsed wave Doppler sampling the left ventricular outflow tract: Tissue Doppler imaging tracks the movement of cardiac tissue and is of low velocity. It is a useful method of assessing regional differences in cardiac wall function. ### **3-D Echocardiography:** allows the visualization of cardiac structures and function in three dimensions. It can be used to obtain 3D volumes of systole and diastole to determine a quantitative ejection fraction, taking all walls into account. It is also useful in determining the structure of valves prior to surgery. This technology initially required a larger probe, which was difficult to maneuver and was difficult to image between small intercostal spaces. Over time, the technology has been integrated into regular 2-D probes. The post-processing work to crop and analyze three-dimensional images can still be time consuming. The 4 Techniques: **Transthoracic Echocardiography** ---------------------------------- Images are obtained by placing a probe on the chest of a patient lying, ideally, on their left hand side. A gel is placed on the probe to allow the transmission of sound to the patient. Images are found using five standard windows located on the chest and abdomen. These spaces are useful in observing the heart without the obstruction of the ribs and lungs. These windows include: - - - - - The following is an example of the aortic arch and descending aorta taken from the suprasternal window: Aortic arch and descending aorta  **Contrast Echocardiography** Is useful in patients with suboptimal TTE images as it enhances endocardial border definition. A contrast agent (usually gas microbubbles with a fat coating) that enters the heart is administered intravenously. Contrast is particularly useful to help assess ejection fractions and visualize cardiac thrombus but can also be used to assess myocardial perfusion. **Stress Echocardiography** --------------------------- Is primarily used to diagnose coronary artery disease by determining if there are any wall motion abnormalities as the result of physical exercise or drug induced stress (Dobutamine), which may indicate ischemia. Generally, ultrasound images are taken before and after exercise for comparison. In cases where a stationary bicycle or Dobutamine is used, images may be taken at various stages within the exercise protocol. In some cases a contrast agent may be administered if image quality is suboptimal. **Transesophageal Echocardiography** ------------------------------------ Involves the passage of a probe down the esophagus posterior to the heart. It usually provides clearer images than TTE without interference from lungs or bones. Because the procedure requires the use of a topical anesthetic to reduce the gag reflex and IV sedation, it is performed by a physician who administers pharmaceuticals and manipulates the probe. Most patients have had a previous TTE which was inconclusive and TEE is used to get a closer look. It is most useful for detection of endocarditis, examination of a prosthetic valve, pre-operative assessment, exclusion of embolism and detection of septal defects. Some modern probes have 3-D capabilities, which are useful to obtain a surgical view prior to valve replacement. Clinical applications of echocardiography include but are not limited to: - - - - - **Nuclear Cardiology** - There are 3 types of nuclear cardiac imaging procedures: 1. 2. 3. **1.Myocardial perfusion imaging:** is a useful way to determine ischemia and infarction from coronary artery disease. This technique involves the injection of radioactive isotopes, generally thallium-201 and technetium 99m sestamibi, and image acquisition using single photon emission computer tomography (SPECT). The uptake of thallium in the myocardium is proportional to blood flow. The intracellular concentration of thallium is estimated based on the density of the image and depends primarily on two factors: (1) vascular supply and (2) membrane function. To evaluate for ischemia, an initial set of images is taken right after exercise (controlled physical or pharmacological) and thallium injection, and then acquisition of images several hours later. A normal heart should show homogenous distribution of radioactive tracer throughout the myocardium. In comparison, areas of scarred (due to previous infarct) or reduced perfusion with exercise (ischemia) causes a lack of thallium accumulation and will be indicated on the images as light spots, also referred to as \"cold spots.\" If after the second set of images with the \"cold spots" have resolved, this indicates ischemia and is considered reversible. In the case of scarring, the \"cold spots\" will persist, which is considered irreversible. Note: Hibernating myocardium occurs when both initial and secondary images show persistence of \"cold spots\" in the absence of scarring due to a chronic reduction in coronary flow. It can be differentiated from irreversible changes by repeated images at rest. The difference is that the repeated images at rest will show normal coronary blood flow. 99m sestamibi (also referred to as MIBI) demonstrates the relationship between the amount absorbed by the myocardium in relation to the blood flow. Images are usually taken at rest with a low dose of tracer and then post exercise (controlled physical or pharmacological) with a higher dose of tracer. Due to the difference in uptake mechanisms, the distribution of MIBI reflects perfusion at the time of injection, allowing more flexibility with time when acquiring the post exercise images (4 to 6 hours). The following image shows an example of images from a nuclear stress test: **Clinical Application of Myocardial Perfusion Imaging** The uses of **nuclear "cold spot" myocardial imaging** include: - - - - - - - - 2.**Radionuclide ventriculography**, also referred to as multi-unit gated acquisition (MUGA) nuclear scan, is used to evaluate ventricular function. A radioactive isotope, for example technetium 99m, is injected intravenously by bolus, which then binds to red blood cells or serum albumin. Sequential nuclear images at fixed intervals are obtained while labeled cells move through the heart and associated blood vessels. Information from studies can be used to determine ejection fraction. MUGA is commonly used to follow patients undergoing potentially cardiotoxic chemotherapy to assess cardiac function. It can also be used to assess abnormal cardiac and vascular shunts. The two types of radionuclide angiography, first pass, and gated-equilibrium, are described below: - Obtains rapid, sequential cardiac images during the initial passage of the radio-tracer through the great vessels and chambers of the heart. This can assess the presence and extent of left to right or right to left cardiac shunts. - Allows continuous imaging of the heart chambers at a predetermined time (gate) after the QRS complex. ### **Clinical Applications of Radionuclide Ventriculography** Radionuclide angiography can be used to: - - - **Positron emission tomography (PET)** is a specialized nuclear imaging technique that uses positron emitting isotopes (i.e., Rubidium-82) attached to metabolic tracers (i.e., 18-Fluorodeoxyglucose (FDG)). A detector is then used to measure the positron emission from the tracer molecules. It is able to assess the myocardial metabolism and perfusion simultaneously. Areas of reduced blood flow are characterized by increased FDG uptake. ### **Clinical Applications of PET** Positron emission tomography can be used to: - - **Computed Tomography (CT)** is a radiologic technique that produces remarkably detailed anatomic cross sections of the thorax. X-ray beams rotate around the body and are absorbed by tissues, while the remaining beams are captured by electronic detectors that electronically compose a visual representation by computer. Electrocardiographic gating and intravenous administration of radiographic contrast media enhance the clarity of the images despite the continuous motion of the heart and great vessels. The size, shape and wall thickness of the cardiac chambers and great vessels are clearly visualized. ### **Clinical Applications of Computed Tomography** Computed tomography can be used: - - - The Magnetic resonance imaging (MRI) technique applies powerful magnetic fields and radio-frequency non-ionized radiation to the body. When the radio-frequency radiation is suddenly discontinued, the energy released from the atoms within the field can be detected, quantitated and converted into cross-sectional images. MRI can delineate the proximal portions of the coronary arterial tree and differentiate small contrasts in tissue. MRI images have an even greater clarity than those obtained by CT. **Coronary magnetic resonance angiography** is a non-invasive, contrast free angiographic method of differentiating laminar blood flow versus turbulent blood flow that may be a result of obstructions or narrowing due to stenosis. **Contrast-enhanced MRI** can be used to differentiate between impaired but viable tissue from scarred and unviable tissues. ### **Clinical Applications of (MRI)** Computed tomography can be used for: - - - - - **Module 6: Ischemic Heart Disease** **Ischemic Heart Disease:** is the result of the myocardial oxygen demand exceeding the supply. It is typically caused by the **inability of atherosclerotic coronary arteries to perfuse the heart under conditions of increased myocardial oxygen consumption (demand).** The clinical representation of ischemic heart disease can vary from individual to individual and between genders. Angina pectoris, the most common symptom of myocardial ischemia, is chest pain as a result of myocardial oxygen demand exceeding supply. -------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- The metabolic needs and delivery of blood to the myocardial cells require a continuous balance. During exercise the delivery of oxygen increases as the metabolic demands increase. Myocardial oxygen supply and demand can be altered by the occurrence of atherosclerosis. **Myocardial oxygen** supply depends primarily on two things: the quantity of oxygen carried by red blood cells and the rate at which coronary blood is flowing. - - - - - - - - - **Myocardial oxygen demand depends primarily on three** main factors: ventricular wall stress, heart rate, and contractility. Coronary atherosclerosis is characterized not only by focal narrowing of coronary arteries by fixed atherosclerotic plaque but also abnormal vascular tone, which leads to obstruction (or near occlusion) of the lumen of a coronary vessel. The degree of hemodynamic significance is determined by the degree of vessel narrowing and the length of the lesion. **Atherosclerosis** ------------------- Distal vessels of the coronary arteries are able to dilate in response to increased metabolic demands. Therefore, even if the coronary artery is partially occluded, it can dilate at rest or during exercise to meet metabolic demands and avoid ischemia. However, if the vessel is occluded by stenosis greater than approximately 90%, then dilation may not be adequate to prevent ischemia and meet metabolic demands, even at rest. Collateral vessels may develop between unobstructed coronary arteries and areas distal to obstruction; however, during times of increased metabolic demand, this may not be enough to ensure adequate perfusion. **Endothelial Dysfunction** --------------------------- Abnormal endothelial cell function can contribute to ischemia by causing inappropriate vasoconstriction of coronary arteries and by loss of normal antithrombotic properties. Vasoconstriction occurs as a result of impairment of nitric oxide release, a potent vasodilator. The lack of vasodilation can be amplified in individuals with already notably reduced vasoconstriction as a result of coronary artery disease (CAD) risk factors. **Atherosclerosis Risk Factors** -------------------------------- Coronary atherosclerosis is a multifactorial disease. Several risk factors have been identified. There are **three identified non-modifiable** risk factors---that is, factors which cannot be changed---and **seven identified modifiable** risk factors, which can be changed for primary and secondary prevention of atherosclerosis. **Risk factors for atherosclerosis** --------------------------------------------------- ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------ *Non-modifiable risk factors (can\'t be changed)* 1\. Age Atherosclerosis gradually worsens with age. Almost all elderly individuals show some evidence of the disease, and after middle age, complications from it account for many deaths. Coronary artery disease increases nearly linearly with age. 2\. Gender Because women are somewhat protected during their reproductive lives (i.e., pre-menopause) males have a significantly higher age-matched risk. After menopause, the age-matched risk for women starts to approach that of men. By 75 years of age, the prevalence is nearly equal. 3\. Family history There is a strong hereditary predisposition to atherosclerosis. A family history of premature coronary artery disease is defined as a definite MI or sudden death before 55 years of age in a male first relative, or before 65 years of age in a female first relative. +-----------------------------------+-----------------------------------+ | **Modifiable risk factors (can be | | | changed for primary and secondary | | | prevention of atherosclerosis)** | | +===================================+===================================+ | 4\. Smoking | Smoking is an important risk | | | factor and is the leading | | | preventable cause of death in | | | Canada. It has many roles in the | | | development of atherosclerosis | | | including: modification of | | | low-density lipoproteins (LDL) | | | levels, decreased high-density | | | lipoproteins (HDL) levels, | | | endothelial dysfunction, | | | increased platelet adhesion, | | | increased leukocyte adhesion | | | molecule differentiation, | | | inappropriate stimulation of the | | | sympathetic nervous system, and | | | displacement of oxygen by carbon | | | monoxide from hemoglobin. Smoking | | | cessation can reverse some | | | adverse outcomes. | +-----------------------------------+-----------------------------------+ | 5\. Hypertension | The risk of atherosclerosis is | | | directly proportional to the | | | duration and severity of | | | hypertension. Systolic blood | | | pressure is a more reliable | | | predictor of an adverse outcome | | | than diastolic blood pressure. | | | Elevated blood pressure may lead | | | to atherosclerosis as a result of | | | vascular endothelium injury, | | | increased numbers of macrophages | | | and development of foam cells as | | | a result of the inflammatory | | | response. Control of hypertension | | | involves lifestyle modifications | | | (diet and exercise) and drug | | | therapy (principally diuretics, | | | beta-adrenergic receptor | | | antagonists (beta blockers), | | | calcium channel blockers, | | | angiotensin-converting enzyme | | | inhibitors, and alpha-adrenergic | | | receptor antagonists). | +-----------------------------------+-----------------------------------+ | 6\. Dyslipidemia | A high lipid intake and high | | | blood lipids contribute to | | | atherosclerosis. Low-density | | | lipoproteins (LDL) elevated in | | | serum levels correlate to the | | | incidence of atherosclerosis and | | | coronary artery disease. | | | High-density lipoproteins (HDL) | | | are considered protection against | | | atherosclerosis as they transport | | | cholesterol away from the | | | peripheral tissue and back to the | | | liver for disposal. | | | | | | Angiographic studies have shown | | | that therapeutic lowering of LDL | | | cholesterol levels by | | | lipid-lowering therapy combined | | | with a low-fat diet can impede | | | progression or bring about | | | regression of atherosclerosis | | | lesions. Therefore, lowering LDL | | | cholesterol levels can be highly | | | effective in primary and | | | secondary prevention. | | | | | | According to the Mayo Clinic, | | | Canadian guidelines suggest total | | | cholesterol levels should be | | | below 5.2 mmol/L for the general | | | population and LDL should be | | | below 2.6 mmol/L for those at | | | risk of heart disease. The total | | | cholesterol to HDL ratio is the | | | best guide when determining | | | dyslipidemia as a risk factor. | +-----------------------------------+-----------------------------------+ | 7\. Diabetes mellitus | Diabetes mellitus causes rapid | | | advancement of atherosclerosis | | | that results in the complications | | | of coronary artery disease, renal | | | failure, gangrene in the limbs | | | and blindness. | | | | | | There is strong epidemiologic and | | | clinical evidence indicating that | | | diabetes mellitus is a major risk | | | factor in coronary artery | | | disease. | | | | | | Diabetes is related to an | | | increase in cholesterol uptake by | | | macrophages, pro-thrombotic | | | tendencies and anti-fibrinolysis, | | | which in turn may explain its | | | connection to atherosclerosis. | | | | | | The treatment of diabetes | | | includes careful monitoring and | | | control of blood glucose levels | | | and control of hypertension and | | | dyslipidemia. | +-----------------------------------+-----------------------------------+ | 8\. Estrogen deficiency | Premenopausal estrogen has been | | | shown to raise HDL levels and | | | lower LDL. Research findings | | | support the theory that | | | endogenous estrogen protects | | | women against vascular injury due | | | to potentially beneficial | | | antioxidant and antiplatelet | | | actions, as well as improved | | | endothelium-dependent | | | vasodilation. This protection is | | | lost after natural menopause, due | | | to estrogen deficiency. Hormone | | | replacement therapy is not | | | indicated solely for the | | | reduction of HDL as a risk factor | | | in cardiovascular disease. | +-----------------------------------+-----------------------------------+ | 9\. Inactivity | Decreased physical activity | | | adversely influences lipoprotein | | | levels, blood pressure, weight | | | and glucose tolerance, as well as | | | cardiovascular and pulmonary | | | functional capacity. | +-----------------------------------+-----------------------------------+ | 10\. Obesity | Being overweight predisposes you | | | to hyperlipidemia, diabetes, and | | | hypertension. | +-----------------------------------+-----------------------------------+ Several biomarkers, referred to as novel markers, have been linked to the risk of atherosclerosis, including: increased levels of the amino acid homocysteine, lipoprotein(a) and the presence of C-reactive proteins, fibrinogen, and serum amyloid A. **Angina pectoris:** a prominent symptom of myocardial ischemia, is chest pain as a result of the imbalance between myocardial oxygen demand and supply. It is typically caused by the inability of atherosclerotic coronary arteries to perfuse the heart under conditions of increased myocardial oxygen consumption (demand). Angina pectoris is specifically the uncomfortable sensation felt in the chest and neighboring structures as a result of inadequate blood supply. It is usually triggered by exercise, emotion, or physiological stress. It is typically relieved by rest or by cessation of stimulus. The pain may radiate to the left arm, shoulder, neck, and jaw. (angina pectoris, can be termed as stable angina, unstable angina, variant angina, silent ischemia, and syndrome x) **Stable angina**, also referred to as typical angina, the pattern tends to be chronic and extremely predictable, precipitated by exertion or emotional stress. It is typically caused by fixed and obstructive plaque in one or multiple arteries. In general, the pattern of symptoms is related to the progress of the underlying disease. The location of the pain is typically diffuse rather than localized, occurring most often behind the middle or upper part of the sternum (i.e., substernal area). It can radiate to other parts of the chest (usually on the left side) or to the lower jaw, the neck, left arm, and shoulder. Individuals with stable angina experience a retrosternal tightness or pressure that does not vary with movements of the chest (e.g., breathing). An important indicator of typical angina is its duration: an attack is rarely longer than 10 minutes. During the attacks there are often characteristic changes in the ECG: temporary ST depression without permanent myocardial damage. Stable angina is relieved within a few minutes by rest or by administration of nitroglycerin (venodilator). **Unstable Angina**: When stable angina suddenly exhibits an increase in frequency and duration of episodes and is precipitated by a lesser degree of exercise,
