Electric motor:

An electric motor is a device using electrical energy to produce mechanical energy, nearly always by the interaction of magnetic fields and current-carrying conductors. The reverse process, that of using mechanical energy to produce electrical energy, is accomplished by a generator or dynamo. Traction motors used on vehicles often perform both tasks. In principle, all electric motors can run as generators and vice versa, although that is not practical with all types in all applications.
As a convention the term electric engine is not used for electric motors, but instead refers to a railroad electric locomotive.

Electric motors are found in a myriad of applications such as industrial fans, blowers and pumps, machine tools, household appliances, power tools, and computer disk drives, among many other applications. Electric motors may be operated by direct current from a battery in a portable device or motor vehicle, or from alternating current from a central electrical distribution grid. The smallest motors may be found in electric wristwatches. Medium-size motors of highly standardized dimensions and characteristics provide convenient mechanical power for industrial uses. The very largest electric motors are used for propulsion of large ships, and for such purposes as pipeline compressors, with ratings in the thousands of kilowatts. Electric motors may be classified by the source of electric power, by their internal construction, and by application.

The physical principle of production of mechanical force by the interactions of an electric current and a magnetic field was known as early as 1821. Electric motors of increasing efficiency were constructed throughout the 19th century, but commercial exploitation of electric motors on a large scale required efficient electrical generators and electrical distribution networks.

The principleThe principle of conversion of electrical energy into mechanical energy by electromagnetic means was demonstrated by the British scientist Michael Faraday in 1821 and consisted of a free-hanging wire dipping into a pool of mercury. A permanent magnet was placed in the middle of the pool of mercury. When a current was passed through the wire, the wire rotated around the magnet, showing that the current gave rise to a circular magnetic field around the wire. This motor is often demonstrated in school physics classes, but brine (salt water) is sometimes used in place of the toxic mercury. This is the simplest form of a class of electric motors called homopolar motors. A later refinement is the Barlow's Wheel. These were demonstration devices, unsuited to practical applications due to limited power.

In 1827, Hungarian Ányos Jedlik started experimenting with electromagnetic rotating devices he called "electromagnetic self-rotors". He used them for instructive purposes in universities, and in 1828 demonstrated the first device which contained the three main components of practical direct current motors: the stator, rotor and commutator. Again, the device had no practical application.

The first electric motors:

The first British commutator-type direct current electric motor capable of turning machinery was invented by the British scientist William Sturgeon in 1832. Following Sturgeon's work, a commutator-type direct-current electric motor made with the intention of commercial use was built by the American Thomas Davenport and patented in 1837. His motors ran at up to 600 revolutions per minute, and powered machine tools and a printing press. Due to the high cost of the zinc electrodes required by primary battery power, the motors were commercially unsuccessful and Davenport went bankrupt. Several inventors followed Sturgeon in the development of DC motors but all encountered the same cost issues with primary battery power. No electricity distribution had been developed at the time. Like Sturgeon's motor, there was no practical commercial market for these motors.

In 1855 Jedlik built a device using similar principles to those used in his electromagnetic self-rotors that was capable of useful work.He built a model electric motor-propelled vehicle that same year. There is no evidence that this experimentation was communicated to the wider scientific world at that time, or that it influenced the development of electric motors in the following decades.[citation needed].

The modern DC motor was invented by accident in 1873, when Zénobe Gramme connected the dynamo he had invented to a second similar unit, driving it as a motor. The Gramme machine was the first electric motor that was successful in the industry.

In 1888 Nikola Tesla invented the first practicable AC motor and with it the polyphase power transmission system. Tesla continued his work on the AC motor in the years to follow at the Westinghouse company.

The development of electric motors of acceptable efficiency was delayed for several decades by failure to recognize the extreme importance of a relatively-small air gap between rotor and stator. Early motors, for some rotor positions, had comparatively huge air gaps which constituted a very-high-reluctance magnetic circuit. They produced far-lower torque than an equivalent amount of power would produce with efficient designs. The cause of the lack of understanding seems to be that early designs were based on familiarity of distant attraction between a magnet and a piece of ferromagnetic material, or between two electromagnets. Efficient designs, as this article describes, are based on a rotor with a comparatively small air gap, and flux patterns that create torque.

The armature bars are at some distance (unknown) from the field pole pieces when power is fed to one of the field magnets; the air gap is likely to be considerable. The text tells of the inefficiency of the design. (Electricity was created, as a practical matter, by consuming zinc in wet primary cells!).

In his workshops Froment had an electromotive engine of one-horse power. But, though an interesting application of the transformation of energy, these machines will never be practically applied on the large scale in manufactures, for the expense of the acids and the zinc which they use very far exceeds that of the coal in steam-engines of the same force. [...] motors worked by electricity, independently of any question as to the cost of construction, or of the cost of the acids, are at least sixty times as dear to work as steam-engines.

Although Gramme's design was comparatively much more efficient, apparently the Froment motor was still considered illustrative, years later. It is of some interest that the St. Louis motor, long used in classrooms to illustrate motor principles, is extremely inefficient for the same reason, as well as appearing nothing like a modern motor. Photo of a traditional form of the motor. The prominent bar magnets, and the huge air gap at the ends opposite the rotor. Even modern versions still have big air gaps if the rotor poles are not aligned.

Application:

The electric motors revolutionized industry. Industrial processes were no longer limited by power transmission using shaft, belts, compressed air or hydraulic pressure. Instead every machine could be equipped with its own electric motor, providing easy control at the point of use, and improving power transmission efficiency. Electric motors applied in agriculture eliminated human and animal muscle power from such tasks as handling grain or pumping water. Household uses of electric motors reduced heavy labor in the home and made higher standards of convenience, comfort and safety possible. Today, electric motors consume more than half of all electric energy produced.

Pathophysiology:

A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, totally occluding the artery and preventing blood flow downstream.Main article: Acute coronary syndromeAcute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which are most frequently (but not always) a manifestation of coronary artery disease.

The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis.

Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction. As a result, the patient's heart will be permanently damaged. This Myocardial scarring also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.

Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

Diagnosis:

The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage). A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation, technetium-99m 2-methoxyisobutylisonitrile (Tc99m MIBI) or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmocologic stress. Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.

Diagnostic criteria:

WHO criteria[50] formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
Clinical history of ischaemic type chest pain lasting for more than 20 minutes Changes in serial ECG tracings Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

Physical examination:

The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can be become irregular.

If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung.

Electrocardiogram:

12-lead electrocardiogram showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative of an anterior wall myocardial infarction.The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture.

It is therefore desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. The standard 12 lead ECG also does not directly examine the right ventricle, and is relatively poor at examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.

The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.

The 12 lead ECG is used to classify patients into one of three groups:
those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI), those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG. A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation. In practice this is rarely seen, because it only exists for 2–30 minutes after the onset of infarction.

Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia. The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in the limb leads, and at least 2 mm elevation in the precordial leads. These elevations must be present in anatomically contiguous leads. (I, aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the anterior wall; II, III, aVF correspond to the inferior wall.) This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients.

Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.

Cardiac markers:

Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Now, the markers most widely used in detection of MI are MB subtype of the enzyme creatine kinase and cardiac troponins T and I as they are more specific for myocardial injury. The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity and are now the preferred markers for asssessing myocardial damage. Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future. New markers such as glycogen phosphorylase isoenzyme BB are under investigation.

The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.

Angiography Angiogram of the coronary arteries:

Coronary catheterizationIn difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings. It is performed by a physician trained in interventional cardiology.

Histopathology:

Timeline of myocardial infarction pathology Microscopy image (magn. ca 100x, H&E stain) from autopsy specimen of myocardial infarct (7 days post-infarction).Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.

Echocardiography:

An echocardiogram, often referred to in the medical community as a cardiac ECHO or simply an ECHO, is a sonogram of the heart. Also known as a cardiac ultrasound, it uses standard ultrasound techniques to image two-dimensional slices of the heart. The latest ultrasound systems now employ 3D real-time imaging.

In addition to creating two-dimensional pictures of the cardiovascular system, an echocardiogram can also produce accurate assessment of the velocity of blood and cardiac tissue at any arbitrary point using pulsed or continuous wave Doppler ultrasound. This allows assessment of cardiac valve areas and function, any abnormal communications between the left and right side of the heart, any leaking of blood through the valves (valvular regurgitation), and calculation of the cardiac output as well as the ejection fraction.

Echocardiography was an early medical application of ultrasound. Echocardiography was also the first application of intravenous contrast-enhanced ultrasound. This technique injects gas-filled microbubbles into the venous system to improve tissue and blood delineation. Contrast is also currently being evaluated for its effectiveness in evaluating myocardial perfusion. It can also be used with Doppler ultrasound to improve flow-related measurements (see Doppler echocardiography).

Echocardiography is either performed by cardiac sonographers or doctors trained in cardiology.

Purpose:
Echocardiography is used to diagnose cardiovascular diseases. In fact, it is one of the most widely used diagnostic tests for heart disease. It can provide a wealth of helpful information, including the size and shape of the heart, its pumping capacity and the location and extent of any damage to its tissues. It is especially useful for assessing diseases of the heart valves. It not only allows doctors to evaluate the heart valves, but it can detect abnormalities in the pattern of blood flow, such as the backward flow of blood through partly closed heart valves, known as regurgitation. By assessing the motion of the heart wall, echocardiography can help detect the presence and assess the severity of coronary artery disease, as well as help determine whether any chest pain is related to heart disease. Echocardiography can also help detect hypertrophic cardiomyopathy. The biggest advantage to echocardiography is that it is noninvasive (doesn't involve breaking the skin or entering body cavities) and has no known risks or side effects.

Transthoracic echocardiogram:
A standard echocardiogram is also known as a transthoracic echocardiogram (TTE), or cardiac ultrasound. In this case, the echocardiography transducer (or probe) is placed on the chest wall (or thorax) of the subject, and images are taken through the chest wall. This is a non-invasive, highly accurate and quick assessment of the overall health of the heart.

Transoesophageal echocardiogram:
This is an alternative way to perform an echocardiogram. A specialized probe containing an ultrasound transducer at its tip is passed into the patient's oesophagus. This allows image and Doppler evaluation which can be recorded. This is known as a transoesophageal echocardiogram, or TOE (TEE in the United States).

Cardiac cycle:
Cardiac cycle is the term referring to all or any of the events related to the flow or pressure of blood that occurs from the beginning of one heartbeat to the beginning of the next.[1] The frequency of the cardiac cycle is the heart rate. Every single 'beat' of the heart involves five major stages: First, "Late diastole" which is when the semilunar valves close, the Av valves open and the whole heart is relaxed. Second, "Atrial systole" when atria is contracting, AV valves open and blood flows from atrium to the ventricle.

Third, "Isovolumic ventricular contraction" it is when the ventricles begin to contract, AV valves close, as well as the semilunar valves and there is no change in volume. Fourth, "ventricular ejection", Ventricles are empty, they are still contracting and the semilunar valves are open. The fifth stage is: "Isovolumic ventricular relaxation", Pressure decreases, no blood is entering the ventricles, ventricles stop contracting and begin to relax, semilunars are shut because blood in the aorta is pushing them shut.

Throughout the cardiac cycle, the blood pressure increases and decreases. The cardiac cycle is coordinated by a series of electrical impulses that are produced by specialized heart cells found within the sino-atrial node and the atrioventricular node. The cardiac muscle is composed of myocytes which initiate their own contraction without help of external nerves (with the exception of modifying the heart rate due to metabolic demand). Under normal circumstances, each cycle takes approximately one second.

Atrial systole:

Atrial systoleAtrial systole is the contraction of the heart muscle (myocardia) of the left and right atria. Normally, both atria contract at the same time. The term systole is synonymous with contraction (movement or shortening) of a muscle. Electrical systole is the electrical activity that stimulates the myocardium of the chambers of the heart to make them contract. This is soon followed by Mechanical systole, which is the mechanical contraction of the heart.
As the atria contract, the blood pressure in each atrium increases, forcing additional blood into the ventricles. The additional flow of blood is called atrial kick.

70% of the blood flows passively down to the ventricles, so the atria do not have to contract a great amount. Atrial kick is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation, atrial flutter, and complete heart block. Atrial kick is also different in character depending on the condition of the heart, such as stiff heart, which is found in patients with diastolic dysfunction.

Detection of atrial systole:

Electrical systole of the atria begins with the onset of the P wave on the ECG. The wave of bipolarization (or depolarization) that stimulates both atria to contract at the same time is due to sinoatrial node which is located on the upper wall of the right atrium. 30% of the ventricles are filled during this phase.

Ventricular systole:

Ventricular systole is the contraction of the muscles (myocardia) of the left and right ventricles. At the later part of the ejection phase, although the ventricular pressure falls below the aortic pressure, the aortic valve remains patent because of the inertial energy of the ejected blood.

The graph of aortic pressure throughout the cardiac cycle displays a small dip which coincides with the aortic valve closure. The dip in the graph is immediately followed by a brief rise then gradual decline. The small rise in the graph is known as the "dicrotic notch" or "incisure", and represents a transient increase in aortic pressure. Just as the ventricles enter into diastole, the brief reversal of flow from the aorta back into the left ventricle causes the aortic valves to shut. This results in the slight increase in aortic pressure caused by the elastic recoil of the semilunar valves and aorta.

Detection of ventricular systole:

Heart sounds:
The closing of the mitral and tricuspid valves (known together as the atrioventricular valves) at the beginning of ventricular systole cause the first part of the "lub-dub" sound made by the heart as it beats. Formally, this sound is known as the First Heart Tone, or S1. This first heart tone is created by the closure of mitral and tricuspid valve and is actually a two component sound, M1, T1.

The second part of the "lub-dub" (the Second Heart Tone, or S2), is caused by the closure of the aortic and pulmonary valves at the end of ventricular systole. As the left ventricle empties, its pressure falls below the pressure in the aorta, and the aortic valve closes. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The second heart sound is also two components, A2, P2. The aortic valve closes earlier than the pulmonary valve and they are audibly separated from each other in the second heart sound. This "splitting" of S2 is only audible during inhalation.

ElectrocardiogramIn an electrocardiogram, electrical systole of the ventricles begins at the beginning of the QRS complex.

Diastole:

Cardiac diastoleCardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing. Together they are known as complete cardiac diastole.

During ventricular diastole, the pressure in the (left and right) ventricles drops from the peak that it reaches in systole. When the pressure in the left ventricle drops to below the pressure in the left atrium, the mitral valve opens, and the left ventricle fills with blood that was accumulating in the left atrium. Likewise, when the pressure in the right ventricle drops below that in the right atrium, the tricuspid valve opens, and the right ventricle fills with blood that was accumulating in the right atrium. During diastole the pressure within the myocardium is lower than that in aorta, allowing blood to circulate in the heart itself via the coronary arteries.

Regulation of the cardiac cycle:
Cardiac muscle has automaticity, which means that it is self-exciting. This is in contrast with skeletal muscle, which requires either conscious or reflex nervous stimuli for excitation. The heart's rhythmic contractions occur spontaneously, although the rate of contraction can be changed by nervous or hormonal influences, exercise and emotions. For example, the sympathetic nerves to heart accelerate heart rate and the vagus nerve decelerates heart rate.

The rhythmic sequence of contractions is coordinated by the sinoatrial (SA) and atrioventricular (AV) nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation that initiates atrial contraction by creating an action potential. Once the wave reaches the AV node, situated in the lower right atrium, it is delayed there before being conducted through the bundles of His and back up the Purkinje fibers, leading to a contraction of the ventricles.

The delay at the AV node allows enough time for all of the blood in the atria to fill their respective ventricles. In the event of severe pathology, the AV node can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the pacemaker cells in the SA node and hence is overridden.

Cardiac monitoring:
The phrase cardiac monitoring generally refers to continuous electrocardiography with assessment of the patients condition relative to their cardiac rhythm. It is different from hemodynamic monitoring which monitors the pressure and flow of blood within the circulatory system. The two may be performed simultaneously on critical heart patients. It is different from neurological monitoring of intracranial pressure and electroencephalography A small monitor worn by an ambulatory patient is known as a Holter monitor Transmitting data from a monitor to a distant monitoring station is known as Telemetry or Biotelemetry.

Emergency Medical Services:

Ambulance services and other emergency medical services providers utilize heart monitors to assess the patient's cardiac rhythm. Providers licensed or certified at the Intermediate or Paramedic level are qualified to interpret EKGs. The finding of a cardiac dysrhythmia (or for that matter, a normal sinus rhythm) may give additional information about the patients condition or may be a sufficient diagnosis on its own to guide treatment.

Treatment for specific cardiac rhythms is guided by ACLS. Basic EMTs are allowed to apply the electrodes and physically operate the monitor but not interpret the rhythm. The most common monitors used in the United States are made by Philips Healthcare (Heartstart Series) Physio-Control (Lifepak series) and ZOLL (E and M series), but other brands exist.

Electrolyte:
An electrolyte is any substance containing free ions that behaves as an electrically conductive medium. Because they generally consist of ions in solution, electrolytes are also known as ionic solutions, but molten electrolytes and solid electrolytes are also possible.

Principles:

Electrolytes commonly exist as solutions of acids, bases or salts. Furthermore, some gases may act as electrolytes under conditions of high temperature or low pressure. Electrolyte solutions can also result from the dissolution of some biological (e.g., DNA, polypeptides) and synthetic polymers (e.g., polystyrene sulfonate), termed polyelectrolytes, which contain multiple charged moieties.

Electrolyte solutions are normally formed when a salt is placed into a solvent such as water and the individual components dissociate due to the thermodynamic interactions between solvent and solute molecules, in a process called solvation. For example, when table salt, NaCl, is placed in water, the salt (a solid) dissolves into its component elements, according to the dissociation reaction
NaCl(s) ? Na+(aq) + Cl-(aq).

It is also possible for substances to react with water when they are added to it, producing ions, e.g., carbon dioxide gas dissolves in water to produce a solution which contains hydronium, carbonate, and hydrogen carbonate ions.
The molten salts can be electrolytes as well. For instance, when sodium chloride is molten, the liquid conducts electricity.

An electrolyte in a solution may be described as concentrated if it has a high concentration of ions, or dilute if it has a low concentration. If a high proportion of the solute dissociates to form free ions, the electrolyte is strong; if most of the solute does not dissociate, the electrolyte is weak. The properties of electrolytes may be exploited using electrolysis to extract constituent elements and compounds contained within the solution.

Physiological importanceIn physiology, the primary ions of electrolytes are sodium (Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), chloride (Cl-), hydrogen phosphate (HPO42-), and hydrogen carbonate (HCO3-). The electric charge symbols of plus (+) and minus (-) indicate that the substance in question is ionic in nature and has an imbalanced distribution of electrons, which is the result of chemical dissociation.

All known higher lifeforms require a subtle and complex electrolyte balance between the intracellular and extracellular milieu. In particular, the maintenance of precise osmotic gradients of electrolytes is important. Such gradients affect and regulate the hydration of the body, blood pH, and are critical for nerve and muscle function. Various mechanisms exist in living species that keep the concentrations of different electrolytes under tight control.
Both muscle tissue and neurons are considered electric tissues of the body.

Muscles and neurons are activated by electrolyte activity between the extracellular fluid or interstitial fluid, and intracellular fluid. Electrolytes may enter or leave the cell membrane through specialized protein structures embedded in the plasma membrane called ion channels. For example, muscle contraction is dependent upon the presence of calcium (Ca2+), sodium (Na+), and potassium (K+). Without sufficient levels of these key electrolytes, muscle weakness or severe muscle contractions may occur.

Electrolyte balance is maintained by oral, or in emergencies, intravenous (IV) intake of electrolyte-containing substances, and is regulated by hormones, generally with the kidneys flushing out excess levels. In humans, electrolyte homeostasis is regulated by hormones such as antidiuretic hormone, aldosterone and parathyroid hormone. Serious electrolyte disturbances, such as dehydration and overhydration, may lead to cardiac and neurological complications and, unless they are rapidly resolved, will result in a medical emergency.

Why do I need an electrical adapter when I travel overseas?

Although technology is helping to make the world seem a lot smaller, there are still major differences between countries. Electrical standardization is one area where not much has changed since the original national standards were set by each country. If you travel a lot, this can make things very frustrating! The United States and most of the Western hemisphere use electrical systems operating at 110-120 volts.

Almost every other country uses 220-240 volts as a standard. The 110v systems have a 60Hz cycle while most of the 220v systems operate at 50Hz. This difference in cycles per second is not normally a big deal but it can make certain items like electric clocks run faster or slower. With a few exceptions, most notably Brazil and South Africa, alternating current (AC) is the method used to deliver electricity. But be aware of those countries that use direct current (DC) -- it can easily destroy any equipment plugged in that wasn't made to operate in that system.

There are three items you may need to switch between the different power systems:
Adapters Converters Transformers The adapter is simply a connector that changes the plug shape to match the outlet. It does not change the voltage or electrical output in any way. If you know that the plug shape is the only difference between your equipment and the electrical system you are planning to use, then an adapter is all you need. Some items come with ability to use either 110v or 220v built right in. In fact, most computers now have smart power supplies that are switchable between the two. Look at the different plug shapes shown below for various countries.

If your equipment requires a specific voltage, then you need a converter or a transformer. Converters use an electronic switch to approximate 110v by rapidly cutting on and off the current received from a 220v source. This is okay for some electrical items like hair dryers but not good for anything electronic (something with a computer chip in it). Also, converters should not be used for anything that is going to be plugged in longer than a few minutes.
Electronic items need a transformer.

You will also want to use a transformer if you are stepping up from 110 to 220. Where a converter would simply limit the amount of electrical output without really reducing it, a transformer actually reduces the voltage of the electricity going through it. This is a very important distinction. Always use a transformer with electronics!

Electrical Admittance:

The Admittance (Y) is the inverse of the Impedance (Z). The SI unit of admittance is the Siemens.
Admittance means calculation of how a device or circuit admits or allows Electric Current to flow through it. Admittance is concerned with easy flowing of current through a circuit. An Impedance can be thought of as the "inverse" of admittance.
Y=Inverse of Z=1/Z
where
Y is the admittance, it is measured in siemens Z is the impedance, measured in ohms

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Gas hose, fans, duct, vaporizers, lights, and portable self-contained heaters.

Electrical alternans:

Electrical alternans is an electrocardiographic phenomenon of alternation of QRS complex amplitude or axis between beats. Also a wandering baseline may be seen. It is seen in cardiac tamponade and is thought to be related to changes in the ventricular electrical axis due to fluid in the pericardium.

Cardiac tamponade:

Cardiac tamponade, also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of blood, shock, and often death.

Causes:

Cardiac tamponade occurs when the pericardial space fills up with fluid faster than the pericardial sac can stretch. If the amount of fluid increases slowly (such as in hypothyroidism) the pericardial sac can expand to contain a liter or more of fluid prior to tamponade occurring. If the fluid occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 ml can cause tamponade.

Causes of increased pericardial effusion include hypothyroidism, physical trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and myocardial rupture.

Cardiac tamponade is caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardium. This commonly occurs as a result of chest trauma (both blunt and penetrating), but can also be caused by myocardial rupture, cancer, uraemia, pericarditis, or cardiac surgery, and rarely occurs during retrograde aortic dissection, or whilst the patient is taking anticoagulant therapy. The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood, but pus is also found in some circumstances.

Myocardial rupture is a somewhat uncommon cause of pericardial tamponade. It typically happens in the subacute setting after a myocardial infarction (heart attack), in which the infarcted muscle of the heart thins out and tears. Myocardial rupture is more likely to happen in elderly individuals without any previous cardiac history who suffer from their first heart attack and are not revascularized either with thrombolytic therapy or with percutaneous coronary intervention or with coronary artery bypass graft surgery.

One of the most common settings for cardiac tamponade is in the first 24 to 48 hours after heart surgery. After heart surgery, chest tubes are placed to drain blood. These chest tubes, however, are prone to clot formation. When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade. Nurses will frequently milk clots from the tubes, or strip the tubes, but even with these efforts chest tubes can become clogged. Thus, after heart surgery it is critical to be on the watch for chest tube clogging.

Pathophysiology:

The outer pericardium is made of fibrous tissue which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase.

If fluid continues to accumulate, then with each successive diastolic period, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to decreased stroke volume. This causes obstructive shock to develop, and if left untreated then cardiac arrest may occur (in which case the presenting rhythm is likely to be pulseless electrical activity).

Diagnosis:

Initial diagnosis can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, and acute heart failure.[citation needed] In a trauma patient presenting with PEA in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade.

Classical cardiac tamponade presents three signs, known as Beck's triad. Hypotension occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid inside the pericardium.

Other signs of tamponade include pulsus paradoxus (a drop of at least 10mmHg in arterial blood pressure on inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes, as well as general signs & symptoms of shock (such as tachycardia, breathlessness and decreasing level of consciousness).
Tamponade can often be diagnosed radiographically, if time allows. Echocardiography often demonstrates an enlarged pericardium or collapsed ventricles, and a chest x-ray of a large cardiac tamponade will show a large, globular heart.

Treatment-Pre-hospital care:

Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. A number of the Helicopter Emergency Medical Services (HEMS) in the UK, which have doctor/paramedic teams, have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.
Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.

Hospital management:

Initial management in hospital is by pericardiocentesis.[3] This involves the insertion of a needle through the skin and into the pericardium and through the fifth intercostal space, and aspirating fluid. Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead,[3] during which the pericardium is cut open to allow fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium.

Pericardial effusion:

Pericardial effusion ("fluid around the heart") is an abnormal accumulation of fluid in the pericardial cavity. Because of the limited amount of space in the pericardial cavity, fluid accumulation will lead to an increased intrapericardial pressure and this can negatively affect heart function. When there is a pericardial effusion with enough pressure to adversely affect heart function, this is called cardiac tamponade. Pericardial effusion usually results from a disturbed equilibrium between the production and re-absorption of pericardial fluid, or from a structural abnormality that allows fluid to enter the pericardial cavity.

Normal levels of pericardial fluid are from 15 to 50 mL.

Typestransudative (congestive heart failure, myxoedema, nephrotic syndrome), exudative (tuberculosis, spread from empyema) haemorrhagic (trauma, rupture of aneurysms, malignant effusion). malignant (due to fluid accumulation caused by metastasis)

Causes:

Pericarditis Viral infection(coxsackie virus) Infection Inflammatory disorders, such as lupus and post myocardial infarction pericarditis(Dressler's syndrome) Cancer that has spread to the pericardium Trichinosis Kidney failure with excessive blood levels of urea nitrogen Heart surgery.

Symptoms:

Chest pain, pressure symptoms. A small effusion may have no symptoms. Pericardial effusion is also present after a specific type of heart defect repair. An Atrial Septal Defect Secundum, or ASD, when repaired will most likely produce a pericardial effusion due to one of the methods of repair. One repair method of an ASD is to take a piece of the pericardial tissue and use it as a patch for the hole in the atrial cavity.

The so-called "water-bottle heart" is a radiographic sign of pericardial effusion, in which the cardiopericardial silhouette is enlarged and assumes the shape of a flask or water bottle.It can be associated with Ewart's sign.
Treatment:Treatment depends on the underlying cause and the severity of the heart impairment. Pericardial effusion due to a viral infection usually goes away within a few weeks without treatment.

Some pericardial effusions remain small and never need treatment. If the pericardial effusion is due to a condition such as lupus, treatment with anti-inflammatory medications may help. If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space. A drainage tube is often left in place for several days. In some cases, surgical drainage may be required by pericardiocentesis, in which a needle, and sometimes a catheter are used to drain excess fluid.

Tamponade:

Tamponade is a condition of blood flow stoppage into a blood vessel by a constriction of the vessel by an outside force.
Tamponade is a useful method of stopping a hemorrhage. This can be achieved by applying an absorbent dressing directly onto a wound, thereby absorbing excess blood and creating a blockage, or by applying direct pressure with a hand or a tourniquet.

There can, however, be disastrous consequences when tamponade occurs as a result of health problems, as in the case of cardiac tamponade. In this situation, fluid collects between the heart muscle and the pericardial sac. The pressure within the sac prevents the heart from expanding fully and filling the ventricles, with the result that a significantly reduced amount of blood circulates within the body. If left unchecked, this condition will result in death.

Emergency medicine:

Emergency medicine is a medical specialty in which a physician receives practical training to provide patients with acute illnesses or injuries which require immediate medical attention. While not usually providing long-term or continuing care, emergency medicine physicians diagnose a variety of illnesses and undertake acute interventions to stabilize the patient. Emergency medicine physicians practice in hospital emergency departments, in pre-hospital settings via emergency medical service, other locations where initial medical treatment of illness takes place, and recently the Intensive-care unit.

Just as clinicians operate by immediacy rules under large emergency systems, emergency practitioners aim to diagnose emergent conditions and stabilize the patient for definitive care.Urgent care centers are staffed by physicians, physician assistants, and nurses including nurse practitioners. Such practitioners may or may not be formally trained in emergency medicine. The centers offer primary care treatment to patients who desire or require immediate care, but who do not reach the acuity that requires care in an emergency department or admission to a hospital.

Scope:

Emergency medicine has evolved to treat conditions that pose a threat to life, limb, or have a significant risk of morbidity. In the word of the International Federation for Emergency Medicine:
"Emergency medicine is a medical specialty—a field of practice based on the knowledge and skills required for the prevention, diagnosis and management of acute and urgent aspects of illness and injury affecting patients of all age groups with a full spectrum of undifferentiated physical and behavioral disorders. It further encompasses an understanding of the development of pre-hospital and in-hospital emergency medical systems and the skills necessary for this development."

Emergency Medicine encompasses a large amount of general medicine but involves virtually all fields of medicine and surgery including the surgical sub-specialties. Emergency physicians are tasked with seeing a large number of patients, treating their illnesses and arranging for disposition—either admitting them to the hospital or releasing them after treatment as necessary. The emergency physician requires a broad field of knowledge and advanced procedural skills often including surgical procedures, trauma resuscitation, advanced cardiac life support and advanced airway management.

Emergency physicians ideally have the skills of many specialists—the ability to manage a difficult airway (anesthesia), suture a complex laceration (plastic surgery), reduce (set) a fractured bone or dislocated joint (orthopedic surgery), treat a heart attack (internist), work-up a pregnant patient with vaginal bleeding (Obstetrics and Gynecology), stop a bad nosebleed (ENT), and place a chest tube (Cardiothoracic Surgery).

History:

During the French Revolution, after seeing the speed with which the carriages of the French flying artillery maneuvered across the battlefields, French military surgeon Dominique Jean Larrey applied the idea of ambulances, or "flying carriages", for rapid transport of wounded soldiers to a central place where medical care was more accessible and effective. Larrey manned ambulances with trained crews of drivers, corpsmen and litter-bearers and had them bring the wounded to centralized field hospitals, effectively creating a forerunner of the modern MASH units. Dominique Jean Larrey is sometimes called the father of emergency medicine for his strategies during the French wars.

Emergency medicine (EM) as a medical specialty is relatively young. Prior to the 1960s and 70s, hospital emergency departments were generally staffed by physicians on staff at the hospital on a rotating basis, among them general surgeons, internists, psychiatrists, and dermatologists. Physicians in training (interns and residents), foreign medical graduates and sometimes nurses also staffed the Emergency Department (ED). EM was born as a specialty in order to fill the time commitment required by physicians on staff to work in the increasingly chaotic emergency departments (EDs) of the time. During this period, groups of physicians began to emerge who had left their respective practices in order to devote their work completely to the ED.

The first of such groups was headed by Dr. James DeWitt Mills who, along with four associate physicians; Dr. Chalmers A. Loughridge, Dr. William Weaver, Dr. John McDade, and Dr. Steven Bednar at Alexandria Hospital, VA established 24/7 year round emergency care which became known as the "Alexandria Plan". Soon, the problem of the "ER", propagated by published reports and media coverage of the poor state of affairs for emergency medical care had culminated with the establishment of the first emergency medicine training program at Cincinnati General Hospital, with Bruce Janiak, M.D. being the first emergency medicine resident in 1970.

During the 1970s, several other residency programs developed throughout the country. At this time, EM was not yet a recognized specialty and hence had no primary board certification exam. It was not until the establishment of American College of Emergency Physicians (ACEP), the recognition of emergency medicine training programs by the AMA and the AOA, and in 1979 a historical vote by the American Board of Medical Specialties that EM became a recognized medical specialty.

Development of emergency medicine as a specialty in the UK:Emergency medicine traces its development as a specialty in UK to 1952 when Mr Maurice Ellis was appointed as the first consultant in Emergency Medicine in the UK at Leeds General Infirmary. In 1967 the Casualty Surgeons Association was established with Maurice Ellis as its first President. The name of the Association was changed twice, in 1990, to the British Association for Accident and Emergency Medicine, and later on in 2004, to British Association for Emergency Medicine (BAEM).

In 1993, Intercollegiate Faculty of Accident and Emergency Medicine (FAEM) was formed at the Royal College of Surgeons of England, London. In 2005, the BAEM and the FAEM were merged to form College of Emergency Medicine (CEM). The College of Emergency Medicine is the single authoritative body for emergency medicine in the UK. It conducts its fellowship and membership exams, publishes guidelines and standards for the practise of emergency medicine, and has its own journal, called the Emergency Medicine Journal (EMJ).

Organizations around the world:

United Kingdom and Ireland:

In the United Kingdom and Ireland, the College of Emergency Medicine sets the examinations that trainees in Emergency Medicine take in order to become consultants (fully-trained emergency physicians).

Australasia:

In Australia and New Zealand, advanced training in Emergency Medicine is overseen by the Australasian College for Emergency Medicine (ACEM).

Canada:

In Canada, there are two routes to certification in emergency medicine. However, more than two-thirds of the physicians currently practicing emergency medicine across Canada have no specific emergency medicine residency training or certification.[citation needed] Emergency physicians who tend to work in more community-based settings complete a residency specializing in Family Medicine and then proceed to obtain an additional year of training in emergency medicine to obtain a Certificate of Special Competence in Emergency Medicine from the College of Family Physicians of Canada (CCFP-EM).

Physicians wanting to practice in major urban/tertiary care hospitals will often pursue a 5 year specialist residency in Emergency Medicine, certified by the Royal College of Physicians and Surgeons of Canada. These members typically spend more time in academic and leadership roles within emergency medicine, EMS, research, and other avenues. There is no significant difference in remuneration or clinical practice type between physicians certified via either route.

United States:

In the United States, there are many member organizations for emergency physicians:
The American College of Emergency Physicians (ACEP) is the oldest and largest professional organization. Originally founded in 1968, it now has over 25,000 members.

The American College of Osteopathic Emergency Physicians (ACOEP) was founded in 1975 and is open only to D.O. emergency physicians. The Association of Emergency Physicians (AEP) offers membership to any practicing emergency physician regardless of training. The American Academy of Emergency Medicine (AAEM) is focused on the "corporate practice of medicine" and the negative consequences related to patient care. There are three ways to become board certified:
The American Board of Emergency Medicine (ABEM) is the oldest and largest. The Board of Certification in Emergency Medicine (BCEM) is the second-largest. It is the only board that still certifies doctors trained in other types of primary care. The American Osteopathic Board of Emergency Medicine (AOBEM) certifies only emergency physicians with a D.O. degree.

Education:

In the U.S., Emergency Medicine is a moderately competitive specialty for medical graduates to enter, ranking 7 of 16 specialties in terms of percentage of U.S. graduates whose applications are successful. However, over 90% of applicants from U.S. medical schools to U.S. Emergency Medicine residencies are successful. [9] Emergency medicine residencies (M.D., D.O., M.B.B.S.,MBChB) can be three or four years in length, depending on the training institution. In addition to the didactic exposure, much of an emergency medicine residency involves rotating through other specialties with a majority of such rotations through the emergency department itself. By the end of their training, emergency physicians are expected to handle a vast field of medical, surgical, and psychiatric emergencies, and are considered specialists in the stabilization and treatment of emergent condition. Emergency physicians are therefore both clinical generalists and well-rounded diagnosticians.

A number of fellowships are available for emergency medicine graduates including prehospital medicine (emergency medical services), research, toxicology, hyperbaric medicine, sports medicine, ultrasound, and pediatric emergency medicine.

In the United Kingdom, emergency medical trainees enter training after five years of medical school and two-years of the Foundation Programme. During the three year core training programme (Acute Care Common Stem), doctors will complete training in anaesthesia, acute medicine, intensive care, emergency medicine, emergency medicine (paediatric focus) and musculo-skeletal emergency medicine. They must also pass the Membership of the College of Emergency Medicine (MCEM) examination. Trainees will then go onto Higher Training, lasting a further 3 years. Before the end of higher training, the final examination—the FCEM must be passed. Upon completion of training the doctor will be eligible for entry on the GMC Specialist Register and allowed to apply for a post as a Consultant in Emergency Medicine. Emergency Medicine training in the UK is emerging.

Traditionally emergency medics have been drawn from anaesthesia, medicine and surgery. The majority of A&E consultants are surgically trained; some hold the Fellowship of Royal College of Surgeons of Edinburgh in Accident and Emergency—FRCSEd(A&E). Some of these consultants will be referred to as 'Mister' whilst others choose either not to change from 'Doctor' or to change back to 'Doctor' after passing the FCEM exam. Medical consultants will be holders of the MRCP and anaesthetic trained consultants will hold the FRCA and some may hold both FRCA and MRCP. A&E Consultants may dual accredit in Intensive Care Medicine.

Working:

The employment arrangement of emergency physician practices are either private (a democratic group of EPs staff an ED under contract), institutional (EPs with an independent contractor relationship with the hospital), corporate (EPs with an independent contractor relationship with a third party staffing company that services multiple emergency departments) or governmental (employed by the US armed forces, the US public health service, the Veteran's Administration or other government agency).

Most emergency physicians staff hospital emergency departments in shifts, a job structure necessitated by the 24/7 nature of the emergency department. By its very nature, emergency medicine is considered one of the most grueling and intensive fields to train and practice in. 100-hour work weeks for residents are not uncommon. As emergency medicine practitioners often act as primary care providers for those who are uninsured, they are expected to be competent in treating, diagnosing, and managing a wide array of illnesses and conditions, both chronic and acute. Emergency department physicians experience a high rate of patient death, more than any other group except oncologists. As a result, burn-out and depression are not uncommon.

In the United Kingdom all Consultants in Emergency Medicine work in the NHS. There is little scope for private emergency practice.

Pulmonary contusion:

A pulmonary contusion (or lung contusion) is a contusion (bruise) of the lung, caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia). Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue.

A pulmonary contusion is usually caused directly by blunt trauma but can also result from explosion injuries or a shock wave associated with penetrating trauma. With the use of explosives during World Wars I and II, pulmonary contusion resulting from blasts gained recognition. In the 1960s its occurrence in civilians began to receive wider recognition, in which cases it is usually caused by traffic accidents. The use of seat belts and airbags reduces the risk to vehicle occupants.

Diagnosis is made by studying the cause of the injury, physical examination and chest radiography. Typical signs and symptoms include direct effects of the physical trauma, such as chest pain and coughing up blood, as well as signs that the body is not receiving enough oxygen, such as cyanosis. The contusion frequently heals on its own with supportive care. Often nothing more than supplemental oxygen and close monitoring is needed; however, intensive care may be required. For example, if breathing is severely compromised, mechanical ventilation may be necessary. Fluid replacement may be required to ensure adequate blood volume, but fluids are given carefully since fluid overload can worsen pulmonary edema, which may be lethal.

The severity ranges from mild to deadly—small contusions may have little or no impact on the patient's health—yet pulmonary contusion is the most common type of potentially lethal chest trauma. It occurs in 30–75% of severe chest injuries. With an estimated mortality rate of 14–40%, pulmonary contusion plays a key role in determining whether an individual will die or suffer serious ill effects as the result of trauma. Pulmonary contusion is usually accompanied by other injuries. Although associated injuries are often the cause of death, pulmonary contusion is thought to cause death directly in a quarter to half of cases. Children are at especially high risk for the injury because the relative flexibility of their bones prevents the chest wall from absorbing force from an impact, causing it to be transmitted instead to the lung. Pulmonary contusion is associated with complications including pneumonia and acute respiratory distress syndrome, and it can cause long-term respiratory disability.

Epidemiology:

Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma. Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%. It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself. Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury. It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries.

The mortality rate of pulmonary contusion is estimated to range from 14–40%, depending on the severity of the contusion itself and on associated injuries. When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion. One study found that 35% of people with multiple significant injuries including pulmonary contusion die. In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries. An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone. Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with polytrauma who die.

Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents, and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions. As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries. However an increase in the number of airbags installed in modern cars may be decreasing the incidence of pulmonary contusion. Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.

Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are, and it is more common in children than in adults for that reason. Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures. Pulmonary contusion has been found in 53% of children with significant chest injuries (those requiring hospitalization). The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars when they are pedestrians.

Differences in the bodies of children and adults also lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma to multiple body systems. Some differences in children's physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome. However, despite these differences, children with pulmonary contusion have similar mortality rates to adults.

Associated injuries:

Severe pulmonary contusion with pneumothorax and hemothorax following severe chest traumaA large amount of force is required to cause pulmonary contusion; a person injured with such force is likely to have other types of injuries as well, and pulmonary contusion can be used to gauge the severity of trauma. Up to three quarters of cases are accompanied by other chest injuries, the most common of these being hemothorax and pneumothorax. Flail chest is usually associated with pulmonary contusion, and the contusion, rather than the chest wall injury, is often the main cause of respiratory failure in people with these injuries.

Other indications of thoracic trauma may be associated, including fracture of the sternum and bruising of the chest wall. Over half of fractures of the scapula are associated with pulmonary contusion. The contusion is frequently found underlying fracture sites. When accompanied by a fracture, it is usually concentrated into a specific location—the contusion is more diffuse when there is no fracture. Pulmonary lacerations may result from the same blunt or penetrating forces that cause pulmonary contusion. Lacerations can result in pulmonary hematomas; these are reported to develop in 4–11% of pulmonary contusions.

History:

Giovanni Battista Morgagni, credited with having first described lung trauma without chest wall traumaIn 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century.

It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs. Studies of World War I injuries by D.R. Hooker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.

Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries.These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, Buford and Burbank described what they called "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it. They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.

During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment. The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described. Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion.

For example, positive pressure ventilation was used to stabilize the flail segment from within the chest. It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall, and a group led by J.K. Trinkle confirmed this hypothesis in 1975. Hence the modern treatment prioritizes the management of pulmonary contusion.Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion.

Epidemiology:

Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma. Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%. It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself. Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury. It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries. The mortality rate of pulmonary contusion is estimated to range from 14–40%, depending on the severity of the contusion itself and on associated injuries.

When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion. One study found that 35% of people with multiple significant injuries including pulmonary contusion die. In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries. An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone. Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with polytrauma who die.

Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents, and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions. As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries. However an increase in the number of airbags installed in modern cars may be decreasing the incidence of pulmonary contusion. Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.

Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are, and it is more common in children than in adults for that reason. Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures. Pulmonary contusion has been found in 53% of children with significant chest injuries (those requiring hospitalization). The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars when they are pedestrians.

Differences in the bodies of children and adults also lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma to multiple body systems. Some differences in children's physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome. However, despite these differences, children with pulmonary contusion have similar mortality rates to adults.

Associated injuries:

Severe pulmonary contusion with pneumothorax and hemothorax following severe chest traumaA large amount of force is required to cause pulmonary contusion; a person injured with such force is likely to have other types of injuries as well, and pulmonary contusion can be used to gauge the severity of trauma. Up to three quarters of cases are accompanied by other chest injuries, the most common of these being hemothorax and pneumothorax. Flail chest is usually associated with pulmonary contusion, and the contusion, rather than the chest wall injury, is often the main cause of respiratory failure in people with these injuries.

Other indications of thoracic trauma may be associated, including fracture of the sternum and bruising of the chest wall. Over half of fractures of the scapula are associated with pulmonary contusion. The contusion is frequently found underlying fracture sites. When accompanied by a fracture, it is usually concentrated into a specific location—the contusion is more diffuse when there is no fracture. Pulmonary lacerations may result from the same blunt or penetrating forces that cause pulmonary contusion. Lacerations can result in pulmonary hematomas; these are reported to develop in 4–11% of pulmonary contusions.

History:

Giovanni Battista Morgagni, credited with having first described lung trauma without chest wall traumaIn 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century. It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs. Studies of World War I injuries by D.R. Hooker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.

Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries.These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, Buford and Burbank described what they called "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it.

They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.

During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment. The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described. Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion. For example, positive pressure ventilation was used to stabilize the flail segment from within the chest.

It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall, and a group led by J.K. Trinkle confirmed this hypothesis in 1975. Hence the modern treatment prioritizes the management of pulmonary contusion.Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion.

History:

Giovanni Battista Morgagni, credited with having first described lung trauma without chest wall traumaIn 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century.

It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs. Studies of World War I injuries by D.R. Hoo

ker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.
Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries.These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, Buford and Burbank described what they called "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it.

They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.

During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment. The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described. Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion.

For example, positive pressure ventilation was used to stabilize the flail segment from within the chest. It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall, and a group led by J.K. Trinkle confirmed this hypothesis in 1975. Hence the modern treatment prioritizes the management of pulmonary contusion.Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion.