with rhabdomyolysis during primary HIV infection. Miltiadis Douvoyiannis .. steroids had previously failed A patient with cauda equina syndrome improved 5. Request PDF on ResearchGate | Rhabdomyolysis: A review, with emphasis on the pediatric population | Rhabdomyolysis is a common clinical syndrome and. Palavras-chave: adaptação, enzimas, equino, fisiologia do .. equinos Puro Sangue Árabe submetidos a exercício . exertional rhabdomyolysis in endurance.

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Cerivastatin monotherapy-induced muscle weakness, rhabdomyolysis and acute renal A cauda equina lesion was suspected. Download full-size image. There has been no case report of traumatic cauda equina syndrome resulted in paraparesis among Key Words: Achondroplasia, Cauda equina syndrome, Spinal stenosis. TOOLS. PDF Links; Full text via DOI; Download Citation · CrossRef TDM; E-Mail Bilateral Sciatic Neuropathy associated with Rhabdomyolysis in an. divergente em equinos Quarto de Milha de corrida e trabalho / Camila rhabdomyolysis, in addition to defective glucose transport in skeletal muscle and.

The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy.

La fatiga muscular aguda, puede ser definida como la incapacidad para seguir Miositis benigna aguda: una inusual causa de impotencia funcional La debilidad muscular se debe al dolor muscular y no a la inhabilidad Los trastornos que Ver cuadro Cuadro favorito Descargar.

Debilidad Muscular Aguda - es. Flag for inappropriate content. Fragilidad en el adulto mayor Ricardo Jauregui Distrofia Muscular - Impcna.

Cardiología equina.pdf

Low-yield topics to remove. Diagrams, tables, partial entries, updates, corrections, and study hints are also appreciated, and significant contributions will be compensated at the discretion of the authors. Also let us know about material in this edition that you feel is low yield and should be deleted. Please include name, address, school affiliation, phone number, and e-mail address if different from the address of origin.

Please verify all data and spellings carefully. In the event that similar or duplicate entries are received, only the first entry received will be used. Include a reference to a standard textbook to facilitate verification of the fact. Please follow the style, punctuation, and format of this edition if possible. Initially, this is a result of changes in the length of sarcomeres.

Later the myocytes themselves lengthen and the number of sarcomeres increases. The change in ventricular geometry allows a more efficient contraction and an increased stroke volume can be produced. There is no change in the efficiency of the myocardium until this compensation fails to meet demands and myocardial failure ensues, or if the dilation is sufficient to effect the efficiency of the AV valve apparatus.

A consequence of increased ventricular diameter is increased wall tension This relationship is described by the law of Laplace. In a simplified form, this states that wall tension is proportional to the radius of the chamber and the pressure within it, and inversely proportional to the wall thickness. The ventricles therefore respond to increased tension by increasing wall thickness. Pressure overload results in increased wall thickness with no change in the radius of the chamber concentric hypertrophy and is rare in the horse.

If increased tension is due to volume overload, the ventricle responds within limits by increasing in radius without a change in wall thickness. This means that oxygen consumption will not increase unduly and is termed eccentric hypertrophy.

The equation summarising the law of Laplace demonstrates this relationship Figure 1. Wall stress oc internal radius x ventricular pressure 2 x wall thickness Fig. The law of Laplace describes the relationship of the radius of a sphere, the pressure within it, the thickness of the wall and the wall stress.

This process of hypertrophy is a normal, healthy response to increased load.

In the horse, such loads are normally imposed by exercise training, or by increased preload related to a substantial regurgitant volume. Only at the point of myofailure does the wall thickness begin to decrease, resulting in increased tension and oxygen consumption.

Control of the system by internal and higher homeostatic mechanisms results in a normal cardiac rhythm and alters heart rate to maintain an appropriate cardiac output.

A knowledge of the anatomy of the normal conduction pathway and the basis of excitation of cells is fundamental to understanding normal and abnormal cardiac function and abnormalities of conduction and rhythm. An appreciation of the differences in the activation process in horses compared with humans and small animals is essential in order that the many misconceptions regarding interpretation of equine ECGs electrocardiograms are avoided.

Topics The normal activation process within the heart and within each individual myocyte is dependent on specialised cellular physiology. Cardiac tissue has four important characteristics. These properties are present to differing degrees in different cells within the heart.

Conductivity: Cardiac cells are joined in a functional syncytium that allows excitation to pass from cell to cell.

Specialised cardiac cells have fast or slow conducting properties which govern the rate of spread of the electrical impulse through them.

Excitability: Like nervous tissue, individual cardiac cells exhibit the all-or-none phenomenon, i. Automaticity: Specialised cardiac cells possess automaticity. This means that they will spontaneously depolarise due to the membrane potential grabecoming less negative until the threshold potential is reached.

The rate at which this occurs depends on the type of cardiac tissue and on autonomic nervous control. It is also affected by disease, electrolyte conand by drug therapy.

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Refractoriness: This property ensures that all cardiac cells have a period after activation during which no level of further stimulus will cause an action potential. It is an important feature of myocardial cells because it prevents tetanic spasm of cardiac muscle. The duration of the refractory period also depends on the type of cardiac tissue, autonomic nervous control, disease states and drug therapy.

These electrophysiological features result from specific properties of the cardiac cell membrane. The most notable feature is a very high concentration of potassium and low level of sodium within the resting cell. The different concentrations of ions and proeither side of the membrane result in a potential difference in electrical charge across the cell membrane.

The intracellular potential of a resting myocell is mV in comparison with the extracellular fluid. Depolarisation results in a reversal of this potential difference, and is then followed by repoThe process has been divided into five phases, Figure 1. The action potential of myocardial cells has a defined pattern known as phases The slope of the phases depends on the exact cell type, autonomic tone, electrolytes, drugs and disease. During each phase, specific channels and pumps are responsible for movement of different ions, each of which affect the membrane potential.

The relative contributions of the different currents which result from this ion movement vary in different tissues within the conduction pathways.

1 Cardiac Anatomy and Physiology

This determines the different properties of each specialised cell, and the effects of changes in extracellular ion concentrations, disease and drugs on the cell. In fast-conducting cells such as the Purkinje network and the myocardium, a rapid influx of sodium is responsible for this change in potential.

In the slower conducting pacemaker tissues of the SA and AV nodes, the resting potential of the cell membrane is less negative than non-pacemaker cells around mV. This results in a decreased rate of phase 0 depolarisation and relatively slow conduction. In pacemaker cells, during phase 0 the contribution of the fast inward current carried by sodium is small, and the relatively slow depolarisation process is largely due to movement of calcium ions.

Consequently, these tissues are relatively sensitive to changes in calcium concentration and drugs which affect calcium channels. The plateau phase The depolarisation phase is followed by a relatively small but sharp drop in potential phase 1 and a plateau phase phase 2 , during which a complex interaction of ion movements involving sodium, potassium, calcium, magnesium and chloride, associated with different channels and pumps, results in some decrease of the intracellular potential towards zero.

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After the plateau phase, repolarisation takes place. Sodium is pumped out of the cell in exchange for potassium, resulting in a return of the membrane potential to the resting level phase 3. Repolarisation must occur before another impulse can be transmitted, or before the myocardial cells can contract again. This gives cardiac tissue the property of refractoriness. Abnormalities of the rate of repo and therefore the degree of refractoriness have a very important role in the generation of some arrhythmias section 7.

An important property of certain specialised conducting cells and to a lesser extent all conducting tissues within the heart is that they are capable of spondepolarisation and repolarisation independent of external neural stiThis property is known as automaticity.

The cells with the fastest rate of automaticity are known as pacemaker cells. There is a hierarchy of cells with different rates of automaticity.

Under normal circumstances, the SA node has the highest rate and it therefore acts as the pacemaker.

Encyclopedia of the Neurological Sciences

Automaticity depends on phase 4 of the cardiac action potential. The rate of change in potential is dependent on a time-related change in membrane potassium permeability and is influenced by autonomic tone, electrolytes, drugs and disease.

The steeper the slope, the faster the rate of automaticity. Phase 4 is steepest in SA nodal cells but, if these cells fail to depolarise, other tissues which have automaticity will spontaneously depolarise to initiate an impulse.

The AV node and junctional tissue also have automaticity and will become the dominant pacemaker if the SA node fails to depolarise. In some disease states, Purkinje tissue may also act as a pacemaker and abnormal automaticity may also occur in other cells. The conduction process follows a predictable pathway in the normal heart, passing along specialised conduction fibres, leading to a coordinated contraction of atrial and then ventricular muscle Figure 1.

The contractile cells of the heart are found in two syncytia, the atria and the ventricles. These syncytia are normally electrically separated except at the atrioventricular AV node. The SA node governs the rate of the normal heart. The normal rhythm is therefore called sinus rhythm. The SA node is a crescent-shaped structure located at the site where the cranial vena cava enters the right atrium.

The impulse is formed in the SA node and spreads across the atria to the AV node. Conduction occurs along specialised fibres; however, the impulse also leads to contraction of atrial muscle.

The right and then the left atrium are depolarised.This process of hypertrophy is a normal, healthy response to increased load. The electrical activity associated with depolarisation of this muscle mass results ina sufficiently large electrical field for it to be detected at the body surface as a P wave. The almost instantaneous increase in heart rate to increased demand for cardiac output results from a fall in vagal tone and from the release of noradrenaline from sympathetic fibres, mediated by BI receptors.

A knowledge of the anatomy of the normal conduction pathway and the basis of excitation of cells is fundamental to understanding normal and abnormal cardiac function and abnormalities of conduction and rhythm.

We also offer paid internships in medical education and publishing ranging from three months to one year see below for details. In fact, changes in cardiac output in the horse are usually mediated by changes in heart rate.