Category Archives: Cardiology and Vascular diseases

Potencial de Ação Cardíaco, com Animação

Clique aqui para obter em nosso site a licença para este vídeo!

O coração é basicamente um músculo que contrai e bomba sangue. Consiste de células de músculo especializadas chamadas de miócitos cardiacos. A contração dessas células é iniciada por impulsos elétricos, conhecido como potenciais de ação. Os impulsos começam a partir de um pequeno grupo de miócitos chamados de células ‘MARCAPASSO’, que constituem o sistema de condução cardiaco. As células do nódulo sinoatrial dispara espontaneamente, gerando potenciais de ação que se espalham pelos miócitos contráteis dos átrios. Os miócitos são ligados por junções gap. Isso permite o acoplamento elétrico de células vizinhas.
As células ‘marcapasso’ e miócitos contráteis exibem formas diferentes do potenciais de ação.
As células ‘marcapasso’ do nódulo sinoatrial disparam espontaneamente em torno de 80 potenciais de ação por minute, sendo que cada uma desencadeia um batimento cardiaco. As células ‘marcapasso’ NÃO tem um potencial de repouso VERDADEIRO. A voltagem começa em torno de -60mV e se move para cima espontaneamente até alcançar o limiar de -40mV. Isso se deve a uma ação chamada de correntes ‘ENGRAÇADAS’, presente SOMENTE nas células ‘marcapasso’. Os canais ‘engraçado’ se abrem quando a voltagem da membrana se torna menor do que -40mV e permite um pequeno influxo de sódio. A despolarização resultante é conhecida como ‘potencial marcapasso’. No limiar, os canais de Cálcio se abrem, ións de cálcio fluem para dentro da célula, despolarizando mais ainda a membrana. Isso resulta na fase ascendente. No seu pico, canais de potássio se abrem, os canais de cálcio se tornam inativos e os ións de potássio deixam a célula e a voltagem retorna para -60mV. Essa é a fase descendente do potenciais de ação.
Miócitos contráteis tem um conjunto diferente de canais de ións. Seu retículo sarcoplasmático, o RS, aloja uma quantidade grande de cálcio. Elas também contém miofibrilas. As células contráteis tem um potencial de repouso estável de -90mV e despolariza APENAS quando estimulado. Quando a célula é DES-polarizada, tem mais sódio e cálcio dentro da célula. Estes ións positivos escapam através das junções gap até a célula adjacente e aumentam a voltagem da célula até o limiar de -70mV. Neste ponto, canais de sódio VELOZES se abrem, criando um influxo rápido de sódio e um aumento acentuado na voltagem. Essa é a fase despolarizadora. Canais de cálcio tipo-L também se abrem a -40mV, causando um influxo lento mas constante. No seu pico, canais de sódio se fecham rapidamente, e canais de potássio dependentes de voltagem se abrem, e isso resulta numa pequena diminuição de potencial de membrana, conhecida como a fase de repolarização PRECOCE. Os canais de cálcio se mantém abertos e o efluxo de potássio é equilibrado eventualmente pelo influxo de cálcio. Isso mantém o potencial de membrana relativamente estável por em torno de 200mseg, resultando na fase PLATEAU, característica de potenciais de ação cardiacos. O cálcio é crucial no acoplamento da excitação elétrica à contração muscular física. O influx de cálcio do fluído extracellular, no entanto, não é suficiente para induzir a contração. Em vez disso, ativa uma liberação de cálcio MUITO maior do RS, num processo conhecido como “Liberação de cálcio induzida por cálcio”. O cálcio ENTÃO desencadeia a contração muscular por o mecanismo de filamento deslizante. À medida que os canais de cálcio se fecham, o efluxo de potássio predomina e a voltagem da membrana retorna a seu valor de repouso. O período refractário absoluto é muito mais longo no músculo cardíaco. Isso é essencial para prevenção de somação e tétano.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Brain Stroke for Patient Education, with Animation

This video is available for licensing on our website. Click HERE!

A stroke occurs when the blood supply to a certain part of the brain is reduced or interrupted. Without oxygen and nutrients from the blood, brain cells cannot function properly and eventually die.
There are 2 major types of strokes: ISCHEMIC stroke caused by a BLOCKED artery, and HEMORRHAGIC stroke caused by a RUPTURED artery.
Ischemic stroke happens when a blood clot OBSTRUCTS an artery. In some patients, the clot forms locally, inside the blood vessels that supply the brain. This occurs when fatty deposits in an artery, or cholesterol plaques, rupture and trigger blood clotting. In other cases, a clot may travel to the brain from elsewhere in the body. Most commonly, this happens in patients with atrial fibrillation, a heart condition in which the heart does not pump properly, blood stagnates in its chambers and this facilitates blood clotting. The clots may then pass into the bloodstream, get stuck in smaller arteries of the brain and block them.
Hemorrhagic stroke, on the other hand, occurs when an artery leaks or ruptures. This can result from high blood pressure, overuse of blood-thinners/anticoagulant drugs, or abnormal formations of blood vessels such as aneurysms and AVMs.
As a hemorrhage takes place, brain tissues located BEYOND the site of bleeding are deprived of blood supply. Bleeding also induces contraction of blood vessels, narrowing them and thus further limiting blood flow.
Stroke symptoms may include one or more of the following:
– Paralysis of muscles of the face, arms or legs: inability to smile, raise an arm, or difficulty walking.
– Slurred speech or inability to understand simple speech.
– Sudden and severe headache, vomiting, dizziness or reduced consciousness.
Cerebral stroke is a medical emergency and requires immediate attention. It is essential to determine if a stroke is ischemic or hemorrhagic before attempting treatment. This is because certain drugs used for treatment of ischemic strokes, such as blood thinners, may CRITICALLY aggravate bleeding in hemorrhagic strokes.
For ischemic strokes, emergency treatment aims to restore blood flow by removing blood clots. Medication, such as aspirin and tissue plasminogen activator, TPA, are usually the first options. TPA may be given intravenously, or, in the case the symptoms have advanced, delivered directly to the brain via a catheter inserted through an artery at the groin. Blood clots may also be removed mechanically by a special device delivered through a catheter.
Emergency treatment for hemorrhagic strokes, on the other hand, aims to stop bleeding, reduce blood pressure, and prevent vasospasm and seizures. These goals are usually achieved by a variety of drugs. If the bleeding is significant, surgery may be required to drain the blood and reduce intracranial pressure.
Preventive treatments for strokes include:
– Removal of cholesterol plaques in carotid arteries that supply the brain
– Widening of narrowed carotid arteries with a balloon, and sometimes, a stent. This is usually done with a catheter inserted at the groin.
– Various procedures to prevent rupturing of brain aneurysms, such as clipping and embolization.
– Removal or embolization of vascular malformations
– Bypassing the problematic artery

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Bloqueios de Ramo, com Animação

Clique aqui para obter em nosso site a licença para este vídeo!


Bloqueio de ramo acontece quando há uma obstrução em um dos ramos que conduz os impulsos elétricos. Os nomes “Bloqueio de Ramo Esquerdo” e “Bloqueio de Ramo Direito” indicam o lado que foi afetado.
Em um coração normal, os dois ventrículos são despolarizados simultaneamente pelos dois ramos e contraem ao mesmo tempo. No Bloqueio de ramo, o ventrículo NÃO AFETADO despolariza primeiro. Os impulsos elétricos então se movem através do miocárdio para o outro lado. Isto resulta numa despolarização RETARDADA e LENTA do ventrículo afetado, portanto, um complexo QRS mais largo – tipicamente mais longo do que 120 milissegundos; e uma perda na sincronia ventricular.
Os Bloqueios de ramo esquerdo e direito são diagnosticados e diferenciados observando os registros do eletrocardiograma, obtidas a partir das derivações precordiais, que mostram os movimentos de sinal num plano horizontal. Destes, os mais úteis são as derivações V1 e V6, uma vez que estão melhor localizadas para detectar impulsos que se deslocam entre os ventrículos esquerdo e direito.
A ativação dos ventrículos começa no septo interventricular. Na condução normal, a despolarização do septo é iniciada a partir do feixe esquerdo indo para o direito, EM DIREÇÃO A V1, e LONGE DE V6. Isso resulta em uma pequena deflexão positiva em V1 e uma deflexão negativa em V6. Os sinais, em seguida, movem se em ambas as direções para os dois ventrículos, mas como o ventrículo esquerdo é geralmente muito maior, o movimento resultante é para a esquerda, longe de V1, EM DIREÇÃO A V6. Isto corresponde a uma onda negativa em V1 e uma onda positiva em V6.
No bloqueio de ramo DIREITO, a ativação septal inicial permanece inalterada. O ventrículo esquerdo despolariza NORMALMENTE em direção a V6, longe de V1, produzindo uma deflexão positiva em V6, negativa em V1. Os impulsos então REVERTEM a direção com que se propagam para o ventrículo direito, gerando uma onda negativa em V6, positiva em V1. A derivação V1 gera um QRS em forma de “M” característico com uma onda R terminal, enquanto V6 vê uma onda S mais larga.
No bloqueio de ramo ESQUERDO, a despolarização septal é REVERTIDA, da direita para a esquerda, gerando uma onda negativa em V1. O ventrículo direito é ativado primeiro, com os sinais se movendo para a direita, gerando uma pequena deflexão para cima. A despolarização então se propaga para o ventrículo esquerdo maior, resultando em uma grande deflexão para baixo. A derivação V6 vê o oposto, produzindo um complexo QRS alargado, as “orelhas de coelho”, com duas ondas R. Em alguns casos, a despolarização ventricular direita pode não ser visível.
Algumas pessoas com Bloqueio de ramo nascem com esta condição. Eles geralmente não têm quaisquer sintomas e não requerem tratamento. Outros a adquirem como consequência de outra doença cardíaca. Esses pacientes necessitam de monitoramento, e em casos graves, um marca-passo pode ser necessário para restabelecer a sincronia ventricular.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Hypokalemia: Causes, Symptoms, Effects on the Heart, Pathophysiology, with Animation

This video is available for licensing on our website. Click HERE!

Hypokalemia refers to abnormally low levels of potassium in the blood.

In normal circumstances, more than 90% of the total body potassium is INTRA-cellular; the remaining is in the EXTRA-cellular fluid and blood plasma. The ratio of intracellular to extracellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must quickly and precisely react to keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms:
Excretion of potassium through the kidneys and intestines; with the kidneys playing a predominant role.
Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines.

Hypokalemia is defined as a serum potassium concentration LOWER than 3.5 mmol/L. Hypokalemia may result from INCREASED excretion, inadequate intake or shift of potassium from the extracellular fluid into the cells. Poor intake or intracellular shift ALONE rarely causes the disease, but may be a contributing factor. Most commonly, hypokalemia is caused by excessive loss of potassium in the urine, from the GI tract, or skin. The cause is usually apparent by the patient’s history of predisposing diseases or medication. Urine potassium levels are measured to differentiate between RENAL and NON-renal causes. Depending on the level of severity, symptoms may include muscle weakness, cramping, tremor, intestinal obstruction, hypotension, respiratory depression and abnormal heart rhythms.

As potassium levels decrease in the extracellular space, the MAGNITUDE of the potassium gradient across the cell membrane is INCREASED, causing HYPER-polarization. This moves the membrane voltage FURTHER from the threshold, and a GREATER than normal stimulus is required to generate an action potential. The result is a REDUCED excitability or responsiveness of the neurons and muscles. In the heart, however, HYPER-excitability is observed. This is because hyperpolarization ENHANCES the “FUNNY” currents in cardiac pacemaker cells, resulting in a FASTER phase-4 depolarization and thus a FASTER heart rate. The effect is greatest in Purkinje fibers as these are more sensitive to potassium levels, as compared to the SA node. Increased automaticity of Purkinje fibers may lead to the development of one or more ECTOPIC pacemaker sites in the ventricles, causing ventricular premature beats, tachycardia and fibrillation.

Reduced extracellular potassium, paradoxically, also inhibits the activity of some potassium channels, SLOWING down potassium EFflux during RE-polarization and thus DELAYS ventricular repolarization. As hypokalemia becomes more severe, especially in patients with other heart conditions, the inward current may exceed the outward current, resulting in EARLY afterdepolarization and consequently extra heartbeats. Prolonged repolarization may also promote re-entrant arrhythmias.

Early ECG changes in hypokalemia are mainly due to delayed ventricular repolarization. These include flattening or inversion of T wave, increasingly prominent U wave, ST-segment depression, and prolonged QU interval.

Hypokalemia-induced arrhythmias require immediate potassium replacement. Oral administration is safer but may not be effective in severe cases. If potassium infusion is indicated, continuous cardiac monitoring and hourly serum potassium determinations must be performed to avoid hyperkalemia complications. In the long-term, the underlying causes must be addressed.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Hyperkalemia: Causes, Effects on the Heart, Pathophysiology, Treatment, with Animation.

This video is available for licensing on our website. Click HERE!

Hyperkalemia refers to abnormally high levels of potassium in the blood. In normal circumstances, more than 90% of the total body potassium is INTRAcellular; the remaining is in the EXTRAcellular fluid and blood plasma. The ratio of INTRAcellular to EXTRAcellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must quickly and precisely react to keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms:
Excretion of potassium through the kidneys and intestines; with the kidneys playing a predominant role.
Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines.

Hyperkalemia is defined as a serum potassium concentration HIGHER than 5mmol/L. Hyperkalemia may result from decreased excretion, excessive intake, or shift of potassium from INSIDE the cells to EXTRA-cellular space. Usually, a combination of factors is responsible. The most common scenario is a RENAL INsufficiency combined with excessive potassium supplements OR administration of certain drugs. Impaired kidney function is most prominent; excessive intake or extracellular shift is rarely the only cause.
Mild hyperkalemia is often without symptoms, although some patients may develop muscle weakness. Slow or chronic increase in potassium levels is less dangerous, as the kidneys eventually adapt by excreting more potassium. Sudden onset and rapid progression of hyperkalemia, on the other hand, can be fatal. Primary cause of mortality is the effect of potassium on cardiac functions. As potassium levels INcrease in the EXTRAcellular space, the MAGNITUDE of potassium gradient across the cell membrane is REDUCED, and so is the ABSOLUTE value of the resting membrane potential. Membrane voltage becomes less negative, moving closer to the threshold potential, making it EASIER to initiate an action potential. The effect this has on excitability of myocytes, however, is complex. While initial changes seem to increase myocyte excitability; further rise of potassium has the OPPOSITE effect. This is because the value of membrane potential at the onset of an action potential DETERMINES the number of voltage-gated sodium channels activated during depolarization. As this value becomes less negative in hyperkalemia, the number of available sodium channels DEcreases, resulting in a SLOWER influx of sodium and subsequently SLOWER impulse conduction.
In experimental models, ECG changes produced by hyperkalemia follow a typical pattern that correlates with serum potassium levels: peaked T-wave, P wave widens and flattens, PR interval lengthens, QRS complex widens and eventually blends with T-wave. In practice, however, this pattern is present only in a fraction of hyperkalemia patients and does NOT always correlate with potassium levels. This makes diagnosis on the basis of ECG alone very difficult. Given the dangerous nature of acute hyperkalemia, it must be suspected in any patient having new bradycardia or conduction block, especially in those with renal problems.
Severe hyperkalemia is treated in 3 steps:
– Calcium infusion is given to rapidly REVERSE conduction abnormalities. Calcium antagonizes the effect of potassium at the cellular level, stabilizing membrane potential. However, it does not remove potassium, and should not be used in the case of digoxin toxicity.
– Insulin is administered to stimulate the sodium/potassium pump, promoting INTRA-cellular shift of potassium.
– Hemodialysis is performed to remove potassium from the body.
Longer term treatment for hyperkalemia without conduction problems consists of reducing intake and increasing excretion.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Cardiac Action Potential, with Animation.

This video is available for licensing on our website. Click HERE!

The heart is essentially a muscle that contracts and pumps blood. It consists of specialized muscle cells called cardiac myocytes. The contraction of these cells is initiated by electrical impulses, known as action potentials. Unlike skeletal muscles, which have to be stimulated by the nervous system, the heart generates its OWN electrical stimulation. In fact, a heart can keep on beating even when taken out of the body. The nervous system can make the heartbeats go faster or slower, but cannot generate them. The impulses start from a small group of myocytes called the PACEMAKER cells, which constitute the cardiac conduction system. These are modified myocytes that lose the ability to contract and become specialized for initiating and conducting action potentials. The SA node is the primary pacemaker of the heart. It initiates all heartbeats and controls heart rate. If the SA node is damaged, other parts of the conduction system may take over this role. The cells of the SA node fire SPONTANEOUSLY, generating action potentials that spread though the contractile myocytes of the atria. The myocytes are connected by gap junctions, which form channels that allow ions to flow from one cell to another. This enables electrical coupling of neighboring cells. An action potential in one cell triggers another action potential in its neighbor and the signals propagate rapidly. The impulses reach the AV node, slow down a little to allow the atria to contract, then follow the conduction pathway  and spread though the ventricular myocytes. Action potential generation and conduction are essential for all myocytes to act in synchrony.

Pacemaker cells and contractile myocytes exhibit different forms of action potentials.

Cells are polarized, meaning there is an electrical voltage across the cell membrane. In a resting cell, the membrane voltage, known as the RESTING membrane potential, is usually negative. This means the cell is more NEGATIVE on the INSIDE. At this resting state, there are concentration gradients of several ions across the cell membrane: more sodium and calcium OUTSIDE the cell, and more potassium INSIDE the cell. These gradients are maintained by several pumps that bring sodium and calcium OUT, and potassium IN. An action potential is essentially a brief REVERSAL of electric polarity of the cell membrane and is produced by VOLTAGE-gated ion channels. These channels are passageways for ions in and out of the cell, and as their names suggest, are regulated by membrane voltage. They open at some values of membrane potential and close at others.

When membrane voltage INCREASES and becomes LESS negative, the cell is LESS polarized, and is said to be DE-polarized. Reversely, when membrane potential becomes MORE negative, the cell is RE-polarized. For an action potential to be generated, the membrane voltage must DE-polarize to a critical value called the THRESHOLD.

The pacemaker cells of the SA node SPONTANEOUSLY fire about 80 action potentials per minute, each of which sets off a heartbeat, resulting in an average heart rate of 80 beats per minute. Pacemaker cells do NOT have a TRUE RESTING potential. The voltage starts at about -60mV and SPONTANEOUSLY moves upward until it reaches the threshold of -40mV. This is due to action of so-called “FUNNY” currents present ONLY in pacemaker cells. Funny channels open when membrane voltage becomes lower than     -40mV and allow slow influx of sodium. The resulting DE-polarization is known as “pacemaker potential”. At threshold, calcium channels open, calcium ions flow into the cell further DE-polarizing the membrane. This results in the rising phase of the action potential. At the peak of depolarization, potassium channels open, calcium channels inactivate, potassium ions leave the cell and the voltage returns to -60mV. This corresponds to the falling phase of the action potential. The original ionic gradients are restored thanks to several ionic pumps, and the cycle starts over.

Electrical impulses from the SA node spread through the conduction system and to the contractile myocytes. These myocytes have a different set of ion channels. In addition, their sarcoplasmic reticulum, the SR, stores a large amount of calcium. They also contain myofibrils. The contractile cells have a stable resting potential of -90mV and depolarize ONLY when stimulated, usually by a neighboring myocyte. When a cell is DE-polarized, it has more sodium and calcium inside the cell. These positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage of this cell up to the threshold of -70mV. At threshold, FAST sodium channels open creating a rapid sodium influx and a sharp rise in voltage. This is the depolarizing phase. L-type, or SLOW, calcium channels also open at -40mV, causing a slow but steady influx. As the action potential nears its peak, sodium channels close quickly, voltage-gated potassium channels open and these result in a small decrease in membrane potential, known as EARLY RE-polarization phase. The calcium channels, however, remain open and the potassium efflux is eventually balanced by the calcium influx. This keeps the membrane potential relatively stable for about 200 msec resulting in the PLATEAU phase, characteristic of cardiac action potentials. Calcium is crucial in coupling electrical excitation to physical muscle contraction. The influx of calcium from the extracellular fluid, however, is NOT enough to induce contraction. Instead, it triggers a MUCH greater calcium release from the SR, in a process known as “calcium-induced calcium release”. Calcium THEN sets off muscle contraction by the same “sliding filament mechanism” described for skeletal muscle. The contraction starts about half way through the plateau phase and lasts till the end of this phase.

As calcium channels slowly close, potassium efflux predominates and membrane voltage returns to its resting value. Calcium is actively transported out of the cell and also back to the SR. The sodium/potassium pump then restores the ionic balance across the membrane.

Because of the plateau phase, cardiac muscle stays contracted longer than skeletal muscle. This is necessary for expulsion of blood from the heart chambers. The absolute refractory period is also much longer – 250 msec compared to 1 msec in skeletal muscle. This long refractory period is to make sure the muscle has relaxed before it can respond to a new stimulus and is essential in preventing summation and tetanus, which would stop the heart from beating.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

QRS Transitional Zone and R Wave Progression Explained, with Animation.

This video is available for licensing on our website. Click HERE!


The chest leads look at the heart in a horizontal plane. V1 represents the rightmost view, and V6 – the leftmost. The QRS complex represents depolarization of the ventricles which starts with the interventricular septum. In normal conduction, depolarization of the septum is initiated from the left bundle going to the right, TOWARD V1 and AWAY from V6. This results in a small positive deflection in V1 and a negative deflection in V6. The signals then move both directions to the two ventricles, but as the left ventricle is usually much larger, the NET movement is to the left, AWAY from V1, TOWARD V6. This corresponds to a negative wave in V1 and a positive wave in V6. Thus, the QRS complex starts as predominantly negative in V1, and ends as predominantly positive in V6. Somewhere in between, usually from V3 to V4, it is isoelectric, with equal positive and negative deflections. This is known as the transitional zone. In addition, there is a gradual increase in amplitude of R wave from V1 to V5. This is known as R wave progression.

The normal transitional zone is between V3 and V4. When transition happens at or before V2, it is referred to as early transition, rightward shift, or counter-clockwise rotation. This is because these ECG patterns would have been generated if the heart had rotated counter-clockwise around the longitudinal axis. Reversely, when the transition occurs after V4, it is referred to as late transition, leftward shift, or clockwise rotation. These shifts may or may not be signs of heart diseases. In many cases, these are simply artefacts, resulting from incorrect placement of the chest electrodes – too low or too high. In other cases, they are due to normal anatomical variations of the heart’s shape and orientation. Clockwise rotation is more commonly associated with cardiovascular diseases while counter-clockwise rotation is more common in healthy individuals.

Some clinical causes of clockwise rotation include:

  • Physical rotation of the heart in conditions such as chronic obstructive pulmonary disease
  • Conduction problems due to anterior myocardial infarction
  • Heart chambers dilatation (Dilated cardiomyopathy)

Some clinical causes of counter-clockwise rotation include:

  • Conduction problems due to posterior myocardial infarction
  • Electrical shift to the right in conditions such as right ventricular hypertrophy

When the transitional zone is absent, or is not clear, it is usually clinical. In this case it may be helpful to look at R wave progression.

Non-progression or poor progression of R wave – R wave stays low and S wave remains deep throughout all chest leads. This is an extreme case of clockwise rotation and is suggestive of extensive anterior myocardial infarction.

Reverse progression of R wave – tall R wave in V1, tallest in V1 or V2 – is usually seen in right ventricular hypertrophy. Increased muscle mass in the right ventricle results in net electrical movement towards the right chest leads.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Fibrilación Auricular e Ictus, con Animación.

¡Haz clic aquí para poder acceder a nuestro video y otras imágenes/videos similares en nuestra página web!


La fibrilación auricular es la arritmia cardíaca más común. En un corazón sano, el nodo sinoatrial o nódulo SA inicia todos los impulsos eléctricos en las aurículas. En la fibrilación auricular, los impulsos eléctricos se inician al azar en muchos otros sitios llamados sitios ectópicos, dentro y alrededor de las aurículas, comúnmente cerca de las raíces de las venas pulmonares. Estas señales eléctricas caóticas desincronizadas, hacen que las aurículas tiemblen o fibrilen en lugar de contraerse.
Aunque la frecuencia auricular durante la fibrilación auricular puede ser extremadamente alta, la mayor parte de los impulsos eléctricos no pasan por el nódulo auriculoventricular – nodo AV – a los ventrículos. Esto es debido a las propiedades refractarias de las células del nodo AV. Aquellas que vienen a través del mismo son irregulares. La frecuencia ventricular o la frecuencia cardíaca es, por lo tanto irregular y pueden variar desde lenta – menos de 60 – a rápida -más de 100 – latidos por minuto.
En el ECG, la fibrilación auricular se caracteriza por la ausencia de ondas P y complejos QRS estrechos e irregulares. Recordatorio: la onda P representa la actividad eléctrica del nodo SA que es ahora oscurecida por las actividades de varios sitios ectópicos. La línea de base puede aparecer ondulada o totalmente plana en función del número de sitios ectópicos en las aurículas. En general, un mayor número de sitios ectópicos resulta en una línea de base plana.
A medida que las aurículas no funcionan correctamente, el corazón bombea menos sangre, y puede provocar una insuficiencia cardíaca. La complicación más común de la fibrilación auricular, sin embargo, es la formación de coágulos de sangre en las aurículas. A medida que las aurículas no se vacían por completo en los ventrículos, la sangre puede estancarse dentro de las aurículas y puede formar coágulos de sangre. Estos coágulos pueden entonces pasar al torrente sanguíneo, atascarse en las arterias pequeñas y bloquearlas. Así que cuando un coágulo de sangre bloquea una arteria en el cerebro, puede provocar un ictus, o infarto cerebral.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

ECG/EKG Reading Made Easy with Animation

The videos on this page are available for licensing here!

Lead 2 is most popular among the 12 leads. This is because the net movement of the heart’s impulses is toward lead II, making it the best general view. Unless otherwise specified, we will be looking at lead 2.

Our analysis will include the following: heart rate, heart rhythm, P wave, PR interval, QRS complex, ST segment.

For heart rate: Identify the QRS complex – usually the biggest on an ECG; count the number of small squares between two consecutive QRS complexes and calculate the heart rate with this formula. If this number is variable, count the number of QRS complexes on a 6 second strip and multiply by 10. A normal heart rate is between 60 and 100 beats per minute. A rate of less than 60 bpm is bradycardia; heart rate of more than 100 bpm is tachycardia.

For rhythm: measure the intervals between the R waves. If these intervals vary by less than 1.5 small squares, the rhythm is regular; if the variation is greater than 1.5 small squares, the rhythm is irregular.

P wave represents depolarization of the atria initiated by the SA node. Presence of a normal P wave therefore indicates sinus rhythm. P waves are most prominent in leads II, III, aVF and V1.

Absence of P waves indicates non-sinus rhythms. Absence of P waves and presence of irregular narrow QRS complexes are the hallmark of atrial fibrillation. The baseline may be undulating or totally flat.

A sawtooth pattern instead of regular P waves signifies atrial flutter. These are called flutter waves. The number of flutter waves preceding a QRS complex corresponds to number of atrial contractions to one ventricular contraction.

P wave is the summation of 2 smaller waves resulting from depolarization of the right atrium followed by that of the left atrium. Normal P waves are rounded, smooth and upright in most leads. In V1, P wave is biphasic, with an initial positive deflection corresponding to activation of the right atrium, and a subsequent negative deflection, resulting from activation of the left atrium.

Unusual morphology of P waves is indicative of atrial enlargement. In right atrial enlargement, depolarization of the right atrium lasts longer than normal and its waveform extends to the end of that of the left atrium. This results in a P wave that is taller than normal, more than 2.5 small squares. Its duration remains unchanged, less than 120ms. In V1, this is seen as a taller initial positive deflection of the P wave, more than 1.5 small squares. Right atrial enlargement is usually due to pulmonary hypertension.

In left atrial enlargement, depolarization of the left atrium lasts longer than normal. This results in a wider P wave, of more than 3 small squares. The waveform may also be notched. In V1 the negative portion of P wave is deeper and wider. Left atrial enlargement is commonly due to mitral stenosis.

P-wave inversion in the inferior leads indicates a non-sinus rhythm. When this happens measure the PR interval. If the PR interval is less than 3 small squares, the rhythm is started in the AV junction – AV nodal junctional rhythm. If the PR interval is more than 3 small squares, the origin of the rhythm is within the atria – ectopic atrial rhythm.

The PR interval is measured from the start of the P wave to the start of the QRS complex and reflects the conduction through the AV node.

A longer than normal PR interval signifies an abnormal delay in the AV node, or an AV block. A consistent long PR interval of more than 5 small squares constitutes first-degree heart block. It might be a sign of hyperkalemia or digoxin toxicity. A progressive prolongation of PR interval followed by a P wave WITHOUT a QRS complex is the hallmark of second-degree AV block type I.

A shorter than normal PR interval, of less than 3 small squares, signifies that the ventricles depolarize too early. There are 2 scenarios for this to happen:

  • Pre-excitation syndrome: presence of an accessory pathway bypassing the AV node.
  • AV nodal (junctional) rhythm: Non-sinus rhythm initiated from around the AV node area instead of the SA node. In this case, P waves are either absent or inverted in the inferior leads.

The QRS complex represents depolarization of the ventricles. A normal QRS complex is narrow, between 70 and 100 ms. A wider QRS complex, resulting from an abnormally slow ventricular depolarization, may be caused by:

–          A ventricular rhythm: rhythms originated from ectopic sites in the ventricles. OR

–          An impaired conduction within the ventricles in conditions such as bundle branch block, hyperkalemia or sodium-channel blockade.

A QRS complex wider than three small squares despite sinus rhythm is the hallmark of bundle branch block. When bundle branch block is suspected, check leads V1 and V6 for characteristic patterns of the QRS complex.

The ST segment extends from the end of the S wave to the start of the T wave. A normal ST segment is mostly flat and level with the baseline. Elevation of more than two small squares in the chest leads or one small square in the limb leads, indicates the possibility of myocardial infarction.

Pericarditis causes a characteristic “saddleback” ST segment elevation and PR segment depression in all leads except aVR and V1, where the reverse – ST depression and PR elevation – are seen.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn

Cardiac Axis Explained, with Animation.

This video is available for licensing on Alila Medical Media website. Click HERE!

Cardiac axis is the net direction of electrical activity during depolarization. In a healthy heart, the net movement is downward and slightly left. This axis is altered, or deviated, in certain conditions. For example, in left ventricular hypertrophy the axis is skewed further left; while right ventricular hypertrophy results in a deviation to the right.

Cardiac axis can be determined by examining the 6 limb leads, which look at the heart from different angles in a vertical plane. The QRS axis is the most important, and also the easiest to be determined, as it represents ventricular depolarization. The QRS axis is considered normal when it is between -30 and +90 degrees. Left axis deviation is between -30 and -90 degrees. Right axis deviation goes between +90 and +180 degrees. The rest is known as northwest axis or extreme axis deviation.

Remember that depolarization TOWARD a lead produces a POSITIVE deflection; depolarization AWAY from a lead gives a NEGATIVE deflection. Impulses moving at a 90 degree angle relative to a lead produce an isoelectric, or equiphasic result with positive and negative deflections of similar amplitude.

There are several methods to estimate the QRS axis; we here discuss 2 of them.

The quadrant method.

This method looks at the QRS complex in lead 1 and lead aVF. If the QRS complex is mostly positive in both leads, the axis is somewhere in between the 2 leads, which is in the normal range. If it’s negative in lead I and positive in aVF, the axis is running away from lead I but toward aVF and is thus in the lower right quadrant. The diagnosis is right axis deviation. A positive value in lead I and negative in lead aVF, place the axis in the upper left quadrant, which interprets as possible left axis deviation. A more accurate method will be needed to further determine if it is borderline normal or left deviation. Negative values of the QRS complex in both leads are indicative of extreme axis deviation.

The isoelectric lead method

This method consists of finding the isoelectric or equiphasic lead – the one with equal, or closest to equal, negative and positive deflections. In other words, the one with zero, or nearest to zero, net amplitude.  The axis line is perpendicular to the direction of the isoelectric lead. Now, look at the lead that runs nearest to this line. If the QRS complex is positive in that lead, the axis points to roughly the same direction as the lead. If it is negative, the axis points to the opposite direction.

There is also a method for exact calculation of the heart axis but it is rarely used in clinical practice.

Email this to someoneShare on FacebookTweet about this on TwitterShare on Google+Share on LinkedIn