The technique of usage the simplest physiotherapeutical procedures (compresses, cups, mustard plasters, ice bag, application of medical leeches. Usage of a pocket and stationary inhalers). Oxygenotherapy. The method and technique of taking wetted oxygen and using an oxygen pillow. Acquaintment with physiotherapeutic procedures (hydrotherapeutic, light, electromagnetic). A supervision after patients and rendering pre-doctor aid is in the case of worthening of patient’s codiion. Method and technique of registration of electrocardiogram. Simplest analysis it’s basic elements.
Simple Medical Procedures
Various procedures are used to produce the desired effect on a patient’s blood circulation, both local and general. These procedures include hot water-bottles, cups, mustard plasters, compresses, ice bags, etc. These procedures have their effect on both healthy and sick individuals through thermal, mechanical or chemical stimulation. The skin is the main site of application of these procedures. When irritated, various reflexes are activated in the skin. Ivan Pavlov showed that during thermal stimulation of the skin, inhibition develops in the cerebral cortex. For example, sleepiness develops after a warm bath or even after local application of heat. Thermal effects decrease or even remove pain, decrease skin sensitivity, and prevent transmission of pathological impulses into the central nervous system. Temperature stimulants reflectory change the lumen of the blood vessels to alter the blood
distribution in the body. When the cutaneous vessels dilate, the vessels of the abdominal organs contract, and vice versa, when the skin vessels narrow, the vessels of the abdominal viscera dilate.
The application of a warming compress is accompanied by local dilation of blood vessels and enlargement of blood circulation in tissues, that in this area of inflammatory processes produces painful and resorptional action. The warming compresses are used in treatment of various local infiltrations, for example, postinjection ones, some diseases of muscles and joints, chronic inflammatory diseases.
The warming compress can be dry or moist.
The dry warming compress (usual cotton-gauze bandage) is more often intended for protection of those or other sites of a body or head, for example neck or ear from cold exposure.
Moist warming compress is prepared from 4-th layers
Warming compress
At the beginning a piece of a tissue, moistened with warm water (50-
Warming compress
The duration of application of a moist warming compress is 6-8 hours. While taking off a compress the skin should be sponged with water or alcohol and then wiping with a towel to prevent maceration of the skin. If there is irritation of the skin, it is better to avoid further applying of moist compresses.
The contraindications for applying warming compresses are various skin diseases (dermatitises, furunculosis) and injuries of the skin.The local warming effect can be received with the help of a heater (hot water bottle). In its application, reflex dilatation of the blood vessels of the organs of abdominal cavity and the relaxation of a smooth musculature, that, in particular, is accompanied by disappearance of spastic pains will occur. In the treatment of a peptic ulcer, renal or hepatic colics, radiculitis, the effect of a heater may be painfull.
Hot water bottles in the volume from 1 to
Hot water bottle
The application of a mustard powder is based on the fact that evaporated etheral oil causes an irritation of a skin receptors and its hyperemia, resulting in a reflex dilation of blood vessels located deep in the internal organs and it causes resorption of some inflammatory processes.
Standard mustard plasters are sheets of a dense paper of the size
Mustard plasters are applied in treatment of neurologic diseases (myosites, neuralgia), catarrhal diseases (bronchites, pneumonia), in angina pectoris (on the left-hand half of thoracal cell) and headaches (on area of a nape).
Mustard plasters
The heaters are contraindicated in obscure abdominal pains (in such diseases, as an acute appendicitis, acute cholecystitis, acute pancreatitis), in malignant tumors, in the first day after a trauma, in outside and interior bleedings, in the patients with the impaired skin sensitivity, and also in unconscious patients.
If the skin is very sensitive mustard plasters should be applied over a thin sheet of paper or gauze. General mustard baths help alleviate catarrhs of the airways, bronchitis or pneumonia, usually in children. Mustard powder should be added to water in the bath, 40-
The cupping-glasses are contraindicated in tumors, active tuberculosis, pulmonary bleedings, diseases of a skin and its hypersensitivity.
Treatment with cold is called cryotherapy. Ice bags are commonly used. Cold causes contrac.ion of the blood vessels, thus decreasing the sensitivity of the peripheral nerves. Cold is applied as a first aid measure for acute inflammation of abdominal organs (acute appendicitis, pancreatitis, cholecystitis, etc.), for hemorrhage, contusion, bone fractures, delirium associated with fever, and also for anesthesia.
Moist cold compresses are used for the first hours with injuries, nasal and hemorrhoidal bleedings, high fever. Rolling some layers a piece of a soft tissue, it is moistened with cold water and put on the relevant area of the forehead or bridge (of the nose). As the moist cold compress soon reaches the temperature of the body, it is necessary to change it every 2 — 3 minutes.
For more prolonged local cooling it is more convenient to use an ice-bag, which represents a flat rubber bag with a wide hole filled with small pieces of ice. The ice-bag is expedient, but overcooHng should be avoided by to hanging it (above a head or a stomach), making ten-minutes breaks every half an hour.
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Ice bag
Cups give stronger vasculodilated activity, than mustard plasters and are applied widely in bronchites, pneumonia , neuralgias, neuritises, myosites.
Cups are represented glass vessels with a spherical bottom and thickened edges of volume 30 — 70 ml. They are put on the body with well developed muscular and subcutaneous fat, flattening bony formations (subclavial, subscapular, interscapular areas).
Cups
To avoid burns the skin is preliminarily sponged with vaselinum. Then a burning cotton plug moistened with alcohol is put on the inside of every cup for 2 — 3 sec. After that with prompt and vigorous motion the cupping-glasses are moved in a circle of a wide area over the surface of the skin. Due to reduction of the air inside a cup (cupping-glass) slight pulling of the skin occurs. The skin becomes a pink or purple color. Duration of cup application is usually from 10 to 15 minutes. The number of cups depends on the size of the surface to which they should be applied. To take it off, it is enough to press with a finger on the skin near to the edge of the cupping-glass, simultaneously wedging it from the bottom in the opposite side.
The patient should then be wrapped in blankets and allowed to lie for 30-60 minutes. If the cups remain attached for a longer time, dark red spots and even vesicles filled with fluid may develop on the skin.
Oxygen therapy is helpful in many diseases of the cardiovascular and respiratory system, especially if signs of hypoxia develop. Breathing an air-oxygen mixture quickly alleviates hypoxia.
Oxygen may be given to correct hypoxemia resulting from such disorders as chronic obstructive pulmonary disease, pulmonary edema, pneumonia, atelectasis, and adult respiratory distress syndrome. Supplemental oxygen increases the amount of alveolar oxygen available for diffusion across the alveolocapillary membrane. This, in turn, decreases the respiratory effort required to meet the body’s demand for oxygen.
In a cardiac emergency, oxygen therapy helps meet the increased myocardial work load as the heart tries to compensate for hypoxemia. Oxygen administration is particularly important for a patient whose myocardium is already compromised — perhaps from a myocardial infarction or cardiac arrhythmia.
When metabolic demand is high — in cases of massive trauma, burns, or high fever, for instance — oxygen administration supplies the body with enough oxygen to meet its cellular needs. For a better therapeutic effect, the mixture should contain about 50 % oxygen and be given to breathe for a
sufficiently long time.
Pure oxygen quickly inhibits the respiratory centre, and if inhaled for a long time, the patient may faint and develop convulsions. In this connection, a mixture of 95 per cent oxygen and 5 per cent carbon dioxide is given to inhale for 10-30 minutes in cases of CO poisoning, because carbon dioxide excites the respiratory centre. In all cases where the patient is given oxygen his condition should be watched attentively, and inhalation discontinued immediately if the patient complains of unpleasant sensations.
The oxygen must be moistened to prevent dryness and burning of the mucous. To that end we can use wrapped in several layers of wet gauze or a special bottle filled with water Bobrov’s apparatus is installed between the oxygen cylinder and the nasal tube or the mask.
The adequacy of oxygen therapy is determined by arterial blood gas analysis, oxymetry monitoring, and clinical examinations. The patient’s disease, physical condition, and age will help determine the most appropriate method of administration.
Methods of oxygen therapy
Oxygen can be giveot only for breathing. It can be given subcutaneously or in oxygen baths; it can be administered in the pleural and abdominal cavity, into the stomach and the intestine; it can be used for irrigating wounds. Oxygen partly compensates for hypoxia and also produces local and reflectory effects. Oxygen for medical use, contains 99 % pure oxygen and 1 % nitrogen. It is kept in cylinders that should be handled with care and protected from blows and jerks. It is necessary to remember that oxygen combines with oils and fats to produce an explosive mixture. The storage temperature should not exceed 35° C. No smoking or an open flame is allowed in the room where oxygen cylinders are stored. A jet of pure oxygen directed at the eye can impair vision.
Oxygen tent and chamber
The oxygen flow from the bag is controlled by the tap. When only a little oxygen remains in the bag, it can be expressed from it by hand. The disadvantage of an oxygen bag is that it is impossible to control the oxygen concentration and the rate of its
delivery into the lungs.
Oxygen can be given through a tube directly from an oxygen cylinder. The cylinders should be kept outside the ward in a special room and delivered to the bed-side by a pipeline. Each oxygen cylinder is provided with a reducing valve which lowers the oxygen pressure from 150 atm to 1.5-5 atm. The cylinder is also provided with a flowmeter which controls the oxygen delivery to the patient. Within the
hospital, the cylinders should be earned on special shock-absorbing carts. Each oxygen delivery system has particular indications, advantages and disadvantages and delivers different concentrations of oxygen. Safe effective therapy hinges on choosing the proper delivery system and the correct mix of oxygen and humidity for each patient.
Oxygen delivery systems come in two basic types: low-flow and high-flow. Low-flow systems supplement room air with oxygen, providing an approximate concentration of oxygen to the patient. These systems include nasal cannulas, simple face masks, trach collars , face tents, and T tubes
High-flow systems deliver oxygen at more precise concentrations. They include Venturi masks and continuous positive airway pressures (CPAP) masks. Although the face tent and T tube are essentially low-flow systems, they can function as high-flow systems when attached to a Venturi jet nebulizer.
Some oxygen delivery devices are designed for neonates and children. These include Isolettes, oxygen hoods, and croup tents, all of which completely envelop the patient in an oxygen-enriched atmosphere.
|
Delivery system |
Advantages |
Disadvantages |
|
Nasal cannula |
-safe and simple -comfortable and easily tolerated -tubing molds to facial contour -effectively delivers low oxygen concentrations -allows freedom of movement doesn’t interfere with eating or talking -inexpensive and disposable -can provide continuous positive airway pressure(CPAP) for infants and children. |
-easily dislodged with movement -can’t be used when patient has complete nasal obstruction ,such as mucosal edema or polyps – headaches or dry mucous membranes may result if flow rate exceeds 6 liters/minute, -strap may pinch patient’s chin if adjusted too tightly. |
|
Simple face mask |
–may be useful for patient with nasal obstruction -effectively delivers oxygen to mouth-breathing patients. |
-hot and confining; may irritate patient’s skin -higher oxygen concentration requires a tight seal,which may be difficult to maintain and may cause discomfort -interferes with eating and talking -impractical for long- term therapy because of inability to deliver precise oxygen concentration. |
Venturi mask – a type of disposable face mask used to deliver a controlled oxygen concentration to a patient.
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Venturi system -substitutes for face mask if patient can’t tolerate a covered nose — for example, because of a brokeose or facial burns – doesn’t dry mucous membranes -oxygen can be heated or cooled |
concentrations without Venturi attachment; patient can rebreathe carbon dioxide unless a Venturi system is used – impractical for long-term therapy |
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Tube |
-offers high humidity when connected to a nebulizer -helps when weaning patient from mechanical ventilation -can be used when patient has a tracheostomy tube or an endotracheal tube – can function as high-flow system when attached to a Venturi system -oxygen can be heated or coole |
-any condensation collected in tube may drain into tracheostomy -weight of T tube can pull on the tracheostomy (or endotracheal) tube |
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Venturі mask |
-delivers highly accurate oxygen concentrations despite patient’s respiratory pattern because mask always entrains same amount of air -can vary oxygen concentrations by changing diluter jets or setting dial – doesn’t dry mucous membranes -can add humidity or aerosol to the air stream |
–confining;may irritate skin -oxygen concentrations may be altered if mask doesn’t fit snugly, if tubing kinks, if oxygen intake ports are blocked, if flow rate is lower than recomended, or if patient has hyperpnea -interferes with eating and talking |
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CPAP mask |
-noninvasively improves arterial oxygenation by increasing functional residual capacity – provides CPAP to a |
-uncomfortable and confining;may irritate skin -may lose CPAP if mask doesn’t fit snugly -increased risk of aspiration if |
CPAP mask. Full Facemask.
This mask covers both your nose and your mouth. This type of mask may help if you have air leaks when using a nasal mask.
Method of registration and coding of electrocardiogram (ECG).
The conduction system of the heart consists of four structures:
1. The sinoatrial (SA) node, located within the rig atrial wall near the opening of the superior vena cava
2. The atrioventricular (AV) node, also located within the right atrium but near the lower end of the septum
3. The atrioventricular bundle (bundle of His), which extends from the atrioventricular node along each side of the interventricular septum
4. Purkinje fibers, which extend from the atrioventricular bundle into the walls of the ventricles. The electric impulses from this conduction system can be recorded on an electrocardiogram.
The sinoatrial node initiates the heart’s conduction system. It also possesses –an intrinsic rhythm that maintains a constant heart rate. For these reasons it is called the body’s pacemaker. The sinoatrial impulse spreads throughout the atria to cause depolarization. As the atria contract, impulses spread to the atrioventricular node to stimulate the ventricles. The atrioventricular node is the only normal pathway by which the impulses from the atria can be transmitted to the ventricles. The impulses then spread to the atrioventricular bundle and Purkinje fibers to cause simultaneous depolarization of the ventricles.
Heart conductive system
A cardiac cycle is composed of sequential contraction (systole) and relaxation (diastole) of both the atria and ventricles. First, the atria contract, ejecting blood into the relaxed ventricles. Then, as the atria relax, the ventricles contract to eject blood into the pulmonary artery and aorta. During the period of atrial diastole blood enters the atria from the systemic and pulmonary veins, thus completing one cardiac cycle.
Electrocardiography is the method of graphic registration of operating heart biopotentials from the body surface. Potential difference appears at this moment between stimulated part of myocardium and the area at the state of rest. This potential difference is fixed by electrocardiograph in the form of EGG waves.
Electrocardiography (ECG or EKG) records the electrical impulses generated from the heart muscle and provides a graphic illustration of the summation of these impulses and their sequence and magnitude.
This method occupies one of the first places in the store of instrumental methods of patient examination. Due to it we are able to determine pathology of heart automatism, stimulation and conductivity.
Heart systole is preceded by its stimulation. During this time physical-chemical properties of cellular membrane are changed. ionic composition of intercellular and intercellular liguid undergoes changes accompanied by electric current generation.
Modern electrocardiographs are of the same structure as voltage measuring instruments. They have the following parts: perceiving device, amplifiers, galvanometer, registrating device, apparatus supply unit. The main principle of operation is based on the perception of potential difference oscillations prodused during myocardium stimulation by electrodes located on the body of examined patient. This low voltage is amplified 600-700 times by electron tubes.
Electrodes are put on lower one third of both forearms and left shin. Red wire with one relief ring is connected to the electrode on the right arm, yellow wire with two relief rings is connected to the electrode on the left arm, green wire with three relief rings is connected to the electrode on the left leg.
Augmented unipolar leads from extremities are aVR, aVL, aVF; a being the first letter of the English word “augmenteg” which means amplified; V being the first letter of the English word “Voltage”; R,L,F are the first letters of the English words “Right”, “Left”, “Foot”; aVR is an active electrode on the right arm, indifferent from connected left arm and left leg; aVL is an active electrode on the left arm, indifferent from connected right arm and left leg; aVF is an active electrode on the left leg, indifferent from connected right and left arms.
Chest leads are used for more accurate diagnostics of myocardium diseases, they are:
1) electrode is located on the left edge of breast – bone in IV intercostal space;
2) electrode is located on the right edge of breast – bone in IV intercostal space;
3) electrode is situated on the left peristernum line between IV and V intercostal space;
4) electrode is put on the left medium clavicle line in V intercostal space;
5) electrode is located on the left front axial line in V intercostal space;
6) electrode is placed on the left axial line in V intercostal space.
The P wave represents the electric activity associated with the sinoatrial node and the spread of the impulse over the atria. It is a wave of depolarization.
The QRS complex (wave) is actually composed of three separate waves: the Q wave, the R wave, and the S wave. They are all caused by currents generated when the ventricles depolarize before their contraction. Because ventricular depolarization requires septal and right and left ventricular depolarization, the electrical wave depicting these events is more complex than the smooth P wave.
The P-R interval is measured from the beginning of the P wave to the beginning of the QRS complex. It is termed P-R instead of PQ because frequently the Q wave is absent. This interval represents the time that elapses from the begin Q-T intervalning of atrial depolarization to the beginning of ventricular depolarization.
The T wave represents repolarization of the ventricles. The Q-T interval begins with the QRS complex and ends with the completion of the T wave. It represents ventricular j depolarization and repolarization. This interval varies with j the heart rate. The faster the rate, the shorter the Q-T interval. Therefore in children this interval is normally shorter than in adults.
The S-T segment is normally an isoelectric (flat) line that I connects the end of the S wave to the beginning of the T wave. The T-P interval represents atrial and ventricular polarization in anticipation of the next cardiac cycle.
An electrocardiogram is taken by placing leads or electrodes on the skin to transmit elective impulses back to a recording machine. By means of telemetry the pattern of electrical impulses can be demonstrated on an oscilloscope. The position of the electrodes on the body and the manner in which they are attached to the electrocardiogram machine influence the type of recording. Usually the electrodes are attached to the body with a rubber strap or a type of adhesive (for continuous monitoring). An electrolyte lubricant or electrolyte-soaked gauze is placed between the skin and lead to increase conductivity.
The PQRST complex is plotted on graph paper. Each small block represents 0.04 second horizontally and I mv (millivolt) vertically. By counting the number of squares intersected by the complex, one can calculate the various intervals, such as the P-R or Q-T interval, and the amplitude (height) of each wave. Other information supplied by electrocardiogram includes heart rate, rhythm, abnormalities; of conduction, muscular damage (ischemia), hypertrophy, effects of electrolyte imbalance, influence of various drugs, and pericardial disease. However, the electrocardiogram gives no direct information concerning the mechanical performance of the heart as a pump triumph and satisfaction in having gone through the experience.
Electrocardiogram of a healthy person is distinguished by considerable variability that is why general regularities typical for all ECGs were conclude:
1) wave P – stimulation of right (ascending part) and left (descending part of wave) atrium;
2) interval P-Q – time of impulse passage from atriums to ventricules;
3) wave Q – stimulation of right ventricle basis, interventricle membrane;
4) wave R – stimulation transition to left ventricle basis;
5) wave S – stimulation of both ventricles;
6) waveT – ventricular repolarisation;
7) interval T-P – heart diastole;
8) interval Q-T – ventricle systole;
9) interval R-R – complete cycle of heart operation.
Acute anterior myocardial infarction.
Acute inferior myocardial infarction
Posterolateral myocardial infarction
Electrocardiography is necessary to detect ischaemic changes or arrhythmias. It should be noted that the initial ECG has a low sensitivity for ACS, and a normal ECG does not rule out ACS. However, the ECG is the sole test required to select patients for emergency reperfusion (fibrinolytic therapy or direct PCI). Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should have a reperfusion strategy implemented promptly (grade A recommendation).
Many people who have had a prior MI will have an ECG that appears normal. There may however be typical features of previous MI, and the most conspicuous of these is Q waves. A simplistic explanation of these prominent Q waves is that an appropriately placed lead “sees through” the dead tissue, and visualises the normal depolarisation of the viable myocardial wall directly opposite the infarcted area. Because, in the normal myocardium, depolarisation moves from the chamber outwards, this normal depolarisation is seen as a Q wave
Another feature of previous MI is loss of R wave amplitude. It’s easy to imagine that if muscle is lost, amplitude must be diminished. (Having a pre-infarction ECG for comparison is invaluable).
One can get some idea of the site of infarction from the lead in which abnormalities are seen – inferior, lateral, or anterior.
Ischaemic heart disease – ST changes
One should always remember that more than a quarter of people presenting with an acute myocardial infarction will have no ECG evidence of ischaemia or infarction! The ECG on its own is a blunt-edged tool in the detection of coronary artery disease. Exercise testing to elicit ischaemia is also not very sensitive in detecting this common disease.
Acute myocardial infarction — the `hyperacute phase’
There are four main features of early myocardial infarction (as per Schamroth):
1. increased VAT
2. increased R wave amplitude (!)
3. ST elevation which is sloped upwards!
4. Tall, widened T waves (The ST segment often merges with these)
We now lay great emphasis on ST segment elevation in diagnosing acute MI (In the past, Q waves were remarked on, but as noted above, these are often absent, early on). The features of `full blown’ MI may be:
1. prominent Q waves;
2. elevated ST segments;
3. Inverted `arrowhead‘ T waves.
Remember our previous warning, that a significant proportion of people having an acute MI will have a normal ECG, so do not rely on any of these features to Posterior MI
The trick in diagnosing this is to realise that posterior wall changes will be mirrored in the leads opposite to the lesion — V1 and V2. S we’ll see a tall R (corresponding to a Q), ST depression, and upright arrowhead T waves:
Right ventricular infarction
This occurs in about 1/3 of patients with inferior MI, but is often missed. It would be distinctly unusual in the absence of inferior MI. Sensitivity can be improved by looking at V4R — V4, but put the lead on the right side of the chest! Look for ST elevation which is higher than that in V1 — V3. Another suggestive feature is lack of ST depression in V1 with evidence of MI in the inferior leads (look for ST depression in V2 under 50% of the ST elevation in AVF).
Non-ST elevation MI
There are no reliable correlates of “subendocardial” or non-ST elevation MI, and the diagnosis is based on the combination of clinical and laboratory criteria (troponin elevation being important). There may be no ECG changes, or even ST segment depression and/or T wave abnormalities.
Angina and stress testing
The most important component of an effort ECG that indicates the presence of coronary artery disease is where exercise reproduces the patient’s chest discomfort or pain. Other findings may be:
· ST segment depression (It is customary to apply the Sheffield criteria, that is, 1mm (0.1mV) ST depression 0.08s after the J point;
· failure of suppression of ventricular ectopy, or (especially) development of ectopy in the recovery period;
· Failure of the blood pressure to rise with exercise (an ominous finding);
· ST segment elevation
· T-wave changes (which may be rather nonspecific)
· Development of inverted U waves, which, although subtle, is said to be specific for the presence of ischaemia
A) Shows the normal QRS complex in a lead.
B C) Within hours of the clinical onset of an MI, there is ST segment elevation. At this stage no QRS or T wave changes have occurred. This indicates myocardial damage only, not definitive evidence of infarction.
D) Within days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before.
E) Within one or more weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical T wave inversion may develop at this stage.
F) Months after the MI, the T waves may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist.
Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.
Because primary ECG changes occur in leads overlying the infarct, the location of an infarct can be derived by looking at the primary changes occurring in such leads. This is depicted in the following table:
|
Location of infarction |
Leads showing primary changes |
|
|
Typical changes |
|
Anterior infarction |
|
|
Antero-septal |
V1, V2, V3 |
|
Anterior |
Some of V1-V3 plus some of V4-V6 |
|
Anterior extensive |
V1, V2, V3, V4, V5, V6,I, aVL |
|
Antero-lateral |
V4, V5, V6, I, aVL, possibly II |
|
High lateral |
aVL and/or I |
|
Inferior infarction |
|
|
Inferior |
II, III, aVF |
|
Infero-lateral (= apical) |
II, III, aVF, V5, V6 & sometimes also I, aVL |
|
Infero-septal |
II, III, aVF, V1, V2, V3 |
|
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Other changes |
|
Posterior infarction |
V1, V2 (inverse of usual changes elsewhere) |
|
Subendocardial infarction |
Any lead (usually multiple leads) |
Diagnostic criteria for MI
A definitive diagnosis of MI from the ECG can only be made on the basis of abnormalities in the QRS complex. The following changes are seen:
1. q waves which are either 0.04 s or longer in duration (excluding aVR and lead III) or have a depth which is more than 25% of the height of the following R wave (excluding aVR and lead III).
2. qs or QS complexes (excluding aVR and lead III).
3. Local area of inappropriately low R wave voltage.
4. Additional changes frequently associated with MI are:
5. ST segment elevation (convex upwards) in leads facing the infarcted zone.
6. ST segment depression occurs as a reciprocal change in leads mutually opposite to the primary leads showing evidence of infarction.
7. Horizontal ST segment depression may occur as a primary change in subendocardial infarction.
Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA), right coronary artery = RCA
Did you notice the ST segment depression in our section on voltage and timing, above? Prinzmetal’s angina
The simple (and possibly even correct) explanation of why you see ST segment elevation with this variant form of angina is that the predominant area of ischaemia is epicardial. This disorder is thought to be related to vascular spasm, and angiography shows coronaries without a significant burden of atheroma. Many other morphological abnormalities have been described with this disorder.
T waves
T wave abnormalities are common and often rather nonspecific. T-wave changes that suggest ischaemia are a very sudden junction between the ST segment and the T wave, and very symmetrical T waves. A variety of changes may be seen with cardiomyopathies, intracranial haemorrhage and so on. Symmetrical deep T-wave changes most prominent in V3 and V4 suggest ischaemia in the territory of the left anterior descending artery (LAD T0-waves). We should all know the features of hypo- and hyper-kalaemia.
Introduction to ECG Recognition of Myocardial Infarction
When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with subendocardial or transmural ischemia, followed by necrosis, and eventual fibrosis (scarring) if the blood supply isn’t restored in an appropriate period of time. Rupture of an atherosclerotic plaque followed by acute coronary thrombosis is the usual mechanism of acute MI. The ECG changes reflecting this sequence usually follow a well-known pattern depending on the location and size of the MI. MI’s resulting from total coronary occlusion result in more homogeneous tissue damage and are usually reflected by a Q-wave MI pattern on the ECG. MI’s resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave MI pattern on the ECG. Two-thirds of MI’s presenting to emergency rooms evolve to non-Q wave MI’s, most having ST segment depression or T wave inversion.
Most MI’s are located in the left ventricle. In the setting of a proximal right coronary artery occlusion, however, up to 50% may also have a component of right ventricular infarction as well. Right-sided chest leads are necessary to recognize RV MI.
In general, the more leads of the 12-lead ECG with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis. Additional leads on the back, V7-9 (horizontal to V6), may be used to improve the recognition of true posterior MI.
The left anterior descending coronary artery (LAD) and it’s branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum. The left circumflex coronary artery (LCX) and its branches usually supply the posterolateral wall of the left ventricle. The right coronary artery (RCA) supplies the right ventricle, the inferior
Basically, there can be three types of problems – ischemia is a relative lack of blood supply (not yet an infarct), injury is acute damage occurring right now, and finally, infarct is an area of dead myocardium. It is important to realize that certain leads represent certain areas of the left ventricle; by noting which leads are involved, you can localize the process. The prognosis often varies depending on which area of the left ventricle is involved (i.e. anterior wall myocardial infarct generally has a worse prognosis than an inferior wall infarct).
Diaphragmatic and true posterior walls of the left ventricle, and the posterior third of the septum. The RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX.
Usual ECG evolution of a Q-wave MI; not all of the following patterns may be seen; the time from onset of MI to the final pattern is quite variable and related to the size of MI, the rapidity of reperfusion (if any), and the location of the MI.
A. Normal ECG prior to MI
B. Hyperacute T wave changes – increased T wave amplitude and width; may also see ST elevation
C. Marked ST elevation with hyperacute T wave changes (transmural injury)
D. Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis) (Pathologic Q waves are usually defined as duration >0.04 s or >25% of R-wave amplitude)
E. Pathologic Q waves, T wave inversion (necrosis and fibrosis)
F. Pathologic Q waves, upright T waves (fibrosis)
Inferior MI Family of Q-wave MI’s
Inferior STEMI with sinus node dysfunction (either sinus arrest or extreme sinus bradycardia) and a slow junctional escape rhythm.
Right Ventricular Infarction
Clinical Significance
v Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
v Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
v Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.
The ECG changes of RV infarction are subtle and easily missed!
How to spot right ventricular infarction
The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI!
In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:
v ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
v ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
Other useful tips for spotting right ventricular MI (as described by Amal Mattu and William Brady in ECGs for the Emergency Physician):
v If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.
v If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed.
v NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.
Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided leads (V3R-V6R).
Right-sided leads
There are several different approaches to recording a right-sided ECG:
v A complete set of right-sided leads is obtained by placing leads V1-
v It may be simpler to leave V1 and V2 in their usual positions and just transfer leads V3-6 to the right side of the chest (i.e. V3R to V6R).
The most useful lead is V4R, which is obtained by placing the V4 electrode in the 5th right intercostal space in the midclavicular line. ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% in the diagnosis of RV MI.
Inferior STEMI. Right ventricular infarction is suggested by:
v ST elevation in V1
v ST elevation in lead III > lead II
Repeat ECG of the same patient with V4R electrode position:
v There is ST elevation in V4R consistent with RV infarction
This ECG shows a full set of right-sided leads (V3R-V6R), with V1 and V2 in their original positions. RV infarction is diagnosed based on the following findings:
v There is an inferior STEMI with ST elevation in lead III > lead II.
v V1 is isoelectric while V2 is significantly depressed.
v There is ST elevation throughout the right-sided leads V3R-V6R.
Posterior Myocardial Infarction
Clinical Significance
v Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.
v Isolated posterior MI is less common (3-11% of infarcts).
v Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.
v Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.
Be vigilant for evidence of posterior MI in any patient with an inferior or lateral STEMI.
How to spot posterior infarction
As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3:
v Posterior MI is suggested by the following changes in V1-3:
v Horizontal ST depression
v Tall, broad R waves (>30ms)
v Upright T waves
v Dominant R wave (R/S ratio > 1) in V2
In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.
Typical appearance of posterior infarction in V2
v Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9).
Explanation of the ECG changes in V1-3
The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:
v ST elevation becomes ST depression
v Q waves become R waves
v Terminal T-wave inversion becomes an upright T wave
The progressive development of pathological R waves in posterior infarction (the “Q wave equivalent”) mirrors the development of Q waves in anteroseptal STEMI.
This picture illustrates the reciprocal relationship between the ECG changes seen in STEMI and those seen with posterior infarction. The previous image (depicting posterior infarction in V2) has been inverted. See how the ECG now resembles a typical STEMI!
Posterior leads
Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram below):
v V7 – Left posterior axillary line, in the same horizontal plane as V6.
v V8 – Tip of the left scapula, in the same horizontal plane as V6.
v V9 – Left paraspinal region, in the same horizontal plane as V6.
The degree of ST elevation seen in V7-9 is typically modest – note that only
Inferolateral STEMI. Posterior extension is suggested by:
v Horizontal ST depression in V1-3
v Tall, broad R waves (> 30ms) in V2-3
v Dominant R wave (R/S ratio > 1) in V2
v Upright T waves in V2-3
The same patient, with posterior leads recorded:
v Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall, making this an inferior-lateral-posterior STEMI (= big territory infarct!).
In this ECG, posterior MI is suggested by the presence of:
v ST depression in V2-3
v Tall, broad R waves (> 30ms) in V2-3
v Dominant R wave (R/S ratio > 1) in V2
v Upright terminal portions of the T waves in V2-3
Inferior MI
v Pathologic Q waves and evolving ST-T changes in leads II, III, aVF
v Q waves usually largest in lead III, next largest in lead aVF, and smallest in lead II
v Example #1: frontal plane leads with fully evolved inferior MI (note Q-waves, residual ST elevation, and T inversion in II, III, aVF)
True posterior MI
ECG changes are seen in anterior precordial leads V1-3, but are the mirror image of an anteroseptal MI:
v Increased R wave amplitude and duration (i.e., a “pathologic R wave” is a mirror image of a pathologic Q)
v R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)
v Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3
v Late normalization of ST-T with symmetrical upright T waves in V1-3
Often seen with inferior MI (i.e., “inferoposterior MI”)
Right Ventricular MI (only seen with proximal right coronary occlusion; i.e., with inferior family MI’s)
ECG findings usually require additional leads on right chest (V1R to V6R, analogous to the left chest leads)
ST elevation, >1mm, in right chest leads, especially V4R (see below)
Anterior Family of Q-wave MI’s
Anterior Myocardial Infarction
Clinical Relevance
Anterior STEMI results from occlusion of the left anterior descending artery (LAD).
Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size.
A study comparing outcomes from anterior and inferior infarctions (STEMI + NSTEMI) found that on average, patients with anterior MI had higher incidences of in-hospital mortality (11.9 vs 2.8%), total mortality (27 vs 11%), heart failure (41 vs 15%) and significant ventricular ectopic activity (70 vs 59%) and a lower ejection fraction on admission (38 vs 55%) compared to patients with inferior MI.
In addition to anterior STEMI, other high-risk presentations of anterior ischaemia include left main coronary artery (LMCA) occlusion and Wellens’ syndrome.
How to recognise anterior STEMI
v ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).
v Reciprocal ST depression in the inferior leads (mainly III and aVF).
NB. The magnitude of the reciprocal change in the inferior leads is determined by the magnitude of the ST elevation in I and aVL (as these leads are electrically opposite to III and aVF), hence may be minimal or absent in anterior STEMIs that do not involve the high lateral leads.
Patterns of anterior infarction
The nomenclature of anterior infarction can be confusing, with multiple different terms used for the various infarction patterns. The following is a simplified approach to naming the different types of anterior MI.
The precordial leads can be classified as follows:
v Septal leads = V1-2
v Anterior leads = V3-4
v Lateral leads = V5-6
The different infarct patterns are named according to the leads with maximal ST elevation:
v Septal = V1-2
v Anterior = V2-5
v Anteroseptal = V1-4
v Anterolateral = V3-6, I + aVL
v Extensive anterior / anterolateral = V1-6, I + aVL
(NB. While these definitions are intuitive, there is often a poor correlation between ECG features and precise infarct location as determined by imaging or autopsy. For an alternative approach to the naming of myocardial infarctions, take a look at this 2006 article from Circulation)
Three other important ECG patterns to be aware of:
v Anterior-inferior STEMI due to occlusion of a “wraparound” LAD: simultaneous ST elevation in the precordial and inferior leads due to occlusion of a variant (“type III”) LAD that wraps around the cardiac apex to supply both the anterior and inferior walls of the left ventricle.
v Left main coronary artery occlusion: widespread ST depression with ST elevation in aVR ≥ V1
v Wellens’ syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a warning sign of imminent anterior infarction)
v ST elevation is maximal in the anteroseptal leads (V1-4).
v Q waves are present in the septal leads (V1-2).
v There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III.
v There are hyperacute (peaked ) T waves in V2-4.
v These features indicate a hyperacute anteroseptal STEMI
Anterior-inferior STEMI
v ST elevation is present throughout the precordial and inferior leads.
v There are hyperacute T waves, most prominent in V1-3.
v Q waves are forming in V1-3, as well as leads III and aVF.
v This pattern is suggestive of occlusion occurring in “type III” or “wraparound” LAD (i.e. one that wraps around the cardiac apex to supply the inferior wall)
