Category Archives: Cardiology and Vascular diseases

Antiarrhythmic Drugs, Mechanism of Action, with Animation

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ANTI-Arrhythmic agents are drugs used to SUPPRESS abnormal rhythms of the heart. They act to either:

– interfere with the dynamics of cardiac action potentials by blocking a certain ion channel,


– block the sympathetic effects of the autonomic nervous system on the heart, to slow down heart rate.

There are 5 classes of antiarrhythmic drugs:

  • Class I: Sodium-channel blockers: these drugs bind to and block the fast sodium channels that are responsible for the DE-polarizing phase in contractile myocytes. The result is a SLOWER depolarization with a smaller amplitude. Slower influx of sodium results in a SMALLER flow of positive ions through gap junctions to adjacent cells; the adjacent cells take LONGER to reach the threshold required to generate a new action potential, ultimately resulting in a SLOWER propagation of action potentials through the myocardium. This REDUCED conduction velocity helps to SUPPRESS formation of re-entrant circuits, hence the use of these drugs for treating re-entrant tachycardias.

Class I agents are divided further into subclass IA, IB and IC. These subclasses differ in the STRENGTH of sodium channel blockage, and in their effect on the duration of action potentials and the effective refractory period, the ERP. While subclass IC has no effect on ERP, IA prolongs and IB shortens ERP, respectively. Changes in ERP may have different outcomes for different types of arrhythmias. A longer ERP generally reduces cardiac excitability, but prolonged repolarizations may increase the risk of torsades de pointes, a type of tachycardia caused by afterdepolarizations.

  • Class II: Beta-blockers: these drugs bind to beta1-adrenergic receptorsand block the sympathetic influences that act through these receptors. Sympathetic nerves release catecholamines which act to increase SA node firing rate and cardiac conductibility, especially at the AV node. These activities may precipitate arrhythmias. Beta-blockers SUPPRESS sympathetic effects, thereby decreasing heart rate and SLOWING down conduction through the AV node. The latter is particularly useful in treatment of tachycardias that originate upstream of the AV node, known as supraventricular tachycardias, or SVT. Note should be taken, however, that beta-blocker treatment may cause AV blocks.
  • Class III: Potassium-channel blockers: these agents block the potassium channels responsible for the repolarizing phase. The result is a SLOWED repolarization, hence a PROLONGED duration of action potentials and refractory period. This reduces the heart’s excitability and suppresses re-entrant However, these drugs may also CAUSE arrhythmias because slow repolarizations are associated with LONGER QT intervals and INcreased risks of torsades de pointes.
  • Class IV: Calcium-channel blockers: these drugs block calcium channels that are responsible for DE-polarization in SA and AV nodal cells. Blocking these channels results in a LOWER sinus rate and SLOWER conduction through the AV node. However, because calcium is also involved in cardiac myocyte contraction, these agents also reduce contractility of the heart and should not be used in case of systolic heart failures.
  • Class V includes all drugs that act by other or unknown mechanisms.
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Mitral Valve Prolapse and Regurgitation, with Animation

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The mitral valve serves to ensure ONE-WAY blood flow from the left atrium to the left ventricle of the heart. It OPENS during diastole when the left atrial pressure is higher than the left ventricular pressure, allowing blood to fill the left ventricle; and CLOSES during systole, when the pressure gradient is reversed, to prevent blood from flowing BACK to the atrium as the ventricles contract. The mitral valve has 2 flaps, known as anterior and posterior mitral leaflets, which are supported by a fibrous ring, called mitral annulus. During ventricular contraction, the leaflets are kept from opening in the wrong direction by the action of papillary muscles which attach to the leaflets via cord-like tendons called chordae tendineae, or tendinous chords.
The most common of all heart valve diseases is mitral valve prolapse, or MVP. In MVP, the mitral leaflets bulge into the left atrium every time the ventricles contract. In many people, the reason why this happens is unclear. In others, it is linked to connective tissue disorders such as Ehlers-Danlos or Marfan syndrome. Connective tissue problems are believed to weaken the leaflets, INcrease leaflet area and cause elongation of the chordae tendineae. In most people, MVP is Asymptomatic and does not require treatment. However, it does increase the risks of developing other heart diseases such as arrhythmias, endocarditis, and most frequently, mitral valve regurgitation. In fact, mitral valve prolapse is the most common cause of mitral regurgitation. The billowing leaflets may not fit together properly; elongated chords may also rupture, resulting in a LEAKY valve, which permits BACKflow of the blood to the left atrium when the ventricles contract. When the volume of regurgitated blood is significant, the left side of the heart experiences volume OVERLOAD and eventually fails; blood is backed up to the lungs, causing pulmonary congestion, a hallmark of left-sided heart failure.
Mitral valve prolapse and regurgitation produce characteristic ABNORMAL heart sounds, such as clicks and murmurs, which can be heard during auscultation. Diagnosis is usually confirmed by echocardiography, a procedure in which heart valves and blood flows can be visualized LIVE using ultrasound.
A leaky valve requires surgical repair or replacement. In a typical valve repair surgery, the floppy portion of the valve is removed and the remaining parts are REconnected. The procedure may also include tightening or replacing the mitral annulus, known as annuloplasty. Valve replacement is considered when repair is not possible. Artificial valves can be mechanical or bio-prosthetic. Mechanical valves last longer but usually require life-long administration of anticoagulant medications to prevent formation of blood clots.

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Phases of the Cardiac Cycle, with Animation

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The cardiac cycle refers to the sequence of events that occur and repeat with every heartbeat. It can be divided into 2 major phases: SYSTOLE and DIASTOLE, each of which SUBdivides into several smaller phases. Systole and diastole, when not specified otherwise, refer to VENTRICULAR contraction and relaxation, respectively.

Basic principles:

– Blood flows from HIGHER to lower pressure.

– Contraction INcreases the pressure within a chamber, while relaxation lowers the pressure.

– AV valves OPEN when atrial pressures are HIGHER than ventricular pressures and CLOSE when the pressure gradient is REVERSED. Similarly, semilunar valves OPEN when ventricular pressures are HIGHER than aortic/pulmonary pressures, and close when the reverse is true.

The cycle is initiated with the firing of the SA node that stimulates the atria to depolarize. This is represented by the P-wave on the ECG. Atrial contraction starts shortly after the P-wave begins, and causes the pressure within the atria to increase, FORCING blood into the ventricles. Atrial contraction, however, only accounts for a FRACTION of ventricular filling, because at this point, the ventricles are ALREADY almost full due to PASSIVE blood flow DOWN the ventricles through the OPEN AV valves.

As atrial contraction completes, atrial pressure begins to FALL, REVERSING the pressure gradient across the AV valves, causing them to CLOSE. The closing of the AV valves produces the first heart sound, S1, and marks the beginning of SYSTOLE. At this point, ventricular DE-polarization, represented by the QRS complex, is half way through, and the ventricles start to contract, RAPIDLY building UP pressures inside the ventricles. For a moment, however, the semilunar valves remain closed, and the ventricles contract within a CLOSED space. This phase is referred to as isovolumetric contraction, because NO blood is ejected and ventricular volume is unchanged.

Ventricular ejection starts when ventricular pressures EXCEED the pressures within the aorta and pulmonary artery; the aortic and pulmonic valves OPEN and blood is EJECTED out of the ventricles. This is the RAPID ejection phase.

As ventricular RE-polarization, reflected by the T-wave, begins, ventricular pressure starts to FALL and the force of ejection is REDUCED.

When ventricular pressures drop BELOW aortic and pulmonary pressures, the semilunar valves CLOSE, marking the end of systole and beginning of diastole. Closure of semilunar valves produces the second heart sound, S2.

The first part of diastole is, again, isovolumetric, as the ventricles relax with ALL valves CLOSED. Ventricular pressure drops RAPIDLY but their volumes remain unchanged.

Meanwhile, the atria are being filled with blood and atrial pressures RISE slowly.  Ventricular FILLING starts when ventricular pressures drop BELOW atrial pressures, causing the AV valve to open, allowing blood to flow DOWN the ventricles PASSIVELY.

The atria contract to finish the filling phase and the cycle repeats itself.

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Heart Sounds and Heart Murmurs, with Animation.

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When a healthy heart beats, it makes a “lub-dub” sound. The first heart sound “lub”, also known as S1, is caused by the closing of the AV valves after the atria have pumped blood into the ventricles. The second heart sound “dub”, or S2, originates from the closing of the aortic and pulmonary valves, right after the ventricles have ejected the blood. The time interval between S1 and S2 is when the ventricles contract, called SYSTOLE. The interval between S2 and the NEXT S1 is when the ventricles relax and are filled with blood, called DIASTOLE. Diastole is longer than systole, hence the lub-dub, lub-dub, lub-dub…
Heart sounds are auscultated at 4 different sites on the chest wall which correspond to the location of blood flow as it passes through the aortic, pulmonic, tricuspid, and mitral valves, respectively. This is how SIMILAR defects associated with DIFFERENT valves are differentiated.
Heart murmurs are whooshing sounds produced by turbulent flow of blood. Murmurs are diagnosed based on the TIME they occur in the cardiac cycle, their changes in INTENSITY over time, and the auscultation SITE where they are best heard.
Examples of conditions associated with common systolic murmurs include:
– MITRAL valve regurgitation, when the mitral valve does NOT CLOSE properly and blood surges back to the left atrium during systole. The murmur starts at S1, when the AV valves close, and maintains the same intensity for the entire duration of systole. This holosystolic murmur is best heard at the mitral region -the apex, with radiation to the left axilla. Because the valve closure in mitral regurgitation is INcomplete, S1 is often quieter. On the other side of the heart, a TRICUSPID valve regurgitation has similar timing and shape, but it is loudest in the tricuspid area and the sound radiates up, along the left sternal border.
– AORTIC valve stenosis, when the aortic valve does NOT OPEN properly and blood is forced through a narrow opening. The blood flow starts small, rises to a maximum in mid-systole at the peak of ventricular contraction, then attenuates toward the end of systole. This results in a crescendo-decrescendo, or a diamond-shaped, murmur which starts a short moment after S1. It is often preceded by an ejection click caused by the opening of the STENOTIC valve. Aortic stenosis murmur is loudest in the aortic area and the sound radiates to the carotid arteries in the neck following the direction of blood flow. Again, on the other side of the heart, a PULMONIC stenosis has the same characteristics but is best heard in the pulmonic area and does NOT radiate to the neck.
Other conditions that cause audible systolic murmurs include ventricular septal defect and mitral valve prolapse.
An example of diastolic murmurs is aortic valve regurgitation. This is when the aortic valve does NOT CLOSE properly, resulting in blood flowing back to the left ventricle during diastole- the filling phase. As the blood flows in the REVERSE direction, the murmur is best heard NOT in the aortic area, but rather along the left sternal border. It peaks at the beginning of diastole when the pressure difference is highest, then rapidly decreases as the equilibrium is reached.
Other common diastolic murmurs are associated with pulmonic regurgitation, mitral stenosis and tricuspid stenosis.

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Cardiac Physiology Basic Terms Explained with Animation

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CARDIAC OUTPUT is the amount of blood pumped by each ventricle in one minute. It is the product of STROKE VOLUME – the amount of blood pumped in one heartbeat, and HEART RATE – the number of beats in one minute. An INcrease in either stroke volume or heart rate results in INcreased cardiac output, and vice versa. For example, during physical exercises, the heart beats faster to put out more blood in response to higher demand of the body.

It is noteworthy that the ventricles do NOT eject ALL the blood they contain in one beat. In a typical example, a ventricle is filled with about 100ml of blood at the end of its load, but only 60ml is ejected during contraction. This corresponds to an EJECTION fraction of 60%. The 100ml is the end-DIASTOLIC volume, or EDV. The 40ml that remains in the ventricle after contraction is the end-SYSTOLIC volume, or ESV. The stroke volume equals EDV minus ESV, and is dependent on 3 factors: contractility, preload, and afterload. 

Contractility refers to the force of the contraction of the heart muscle. The more forceful the contraction, the more blood it ejects.

PRELOAD is RELATED to the end-diastolic volume. Preload, by definition, is the degree of STRETCH of cardiac myocytes at the end of ventricular filling, but since this parameter is not readily measurable in patients, EDV is used instead. This is because the stretch level of the wall of a ventricle INcreases as it’s filled with more and more blood; just like a balloon – the more air it contains, the more stretched it is. According to the Frank-Starling mechanism, the greater the stretch, the greater the force of contraction. In the balloon analogy, the more inflated the balloon, the more forceful it releases air when deflated.

AFTERLOAD, on the other hand, is the RESISTANCE that the ventricle must overcome to eject blood. Afterload includes 2 major components:

  • Vascular pressure: The pressure in the left ventricle must be GREATER than the systemic pressure for the aorticvalve to open. Similarly, the pressure in the right ventricle must exceed pulmonary pressure to open the pulmonary valve. In hypertension for example, higher vascular pressures make it more difficult for the valves to open, resulting in a REDUCED amount of ejected blood.
  • Damage to the valves, such as stenosis, also presents higher resistance and leads to lower blood output.
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Congestive Heart Failure, Explained with Animation.

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Heart failure occurs when the heart is unable to provide sufficient blood to meet the body’s needs. Heart failure is not a disease on its own but rather a consequence of other underlying conditions.
The impairment of the heart function can be due to an inability to PUMP effectively during systole, called SYSTOLIC heart failure, or inability to FILL properly during diastole, called DIASTOLIC heart failure.
Heart failure can be right-sided or left-sided depending on the side that is affected.
About two thirds of all left–sided heart failures are caused by systolic dysfunction.

Left-sided SYSTOLIC heart failure
In systolic heart failure, ventricular contraction is compromised. This may be caused by any condition that weakens the heart muscle or creates more difficulty for the ventricle to pump. The most common include:
Coronary artery disease and its consequences: Plaque buildup narrows the coronary artery, reducing blood supply to the heart muscle. Complete blockage can cause heart attacks which often leave behind non-functional scar tissue.
Dilated cardiomyopathy: The Ventricular wall is dilated, becomes thin and weak.
Hypertension: higher systemic pressure makes it harder for the ventricle to eject blood. This is because the pressure in the left ventricle must EXCEED the systemic pressure for the aortic valve to open.
Valvular heart disease: Damage to the valves, such as stenosis, also makes it more difficult for the ventricle to pump.
The effectiveness of ventricular contraction is measured by the EJECTION fraction. Typically, the left ventricle is filled with about 100ml of blood, but only 60ml is ejected during contraction. This corresponds to an ejection fraction of 60%. The normal range of the ejection fraction is between 50 and 70%. When ventricular contraction is impaired, the volume of ejected blood is REDUCED, and so is the value of the ejection fraction. In systolic heart failure, it drops below 40%.

Left sided DIASTOLIC heart failure
In DIASTOLIC heart failure, the ventricle is filled with LESS blood. This may be because it is smaller than usual, or it has lost the ability to relax. The ejection fraction may be normal, but the blood output is reduced. The ejection fraction is therefore commonly used to differentiate between SYSTOLIC and DIASTOLIC dysfunction.
Examples of conditions that can lead to diastolic heart failure include:
Hypertrophic cardiomyopathy: the heart muscle grows thicker than usual, leaving LESS room for blood filling.
Restrictive cardiomyopathy: the heart muscle becomes rigid, unable to stretch.
Hypertension can also cause diastolic dysfunction indirectly, via compensation mechanisms. As higher systemic pressures make it more difficult for the ventricle to pump, the heart compensates by growing thicker muscle to try harder. Larger muscle means REDUCED space for blood filling.
Regardless of being systolic or diastolic in nature, left-sided heart failures share a common outcome: LESS blood pumped out from the heart. As a result, blood flows back to the lungs, where it came from, causing CONGESTION and INCREASED pulmonary pressure. As this happens, fluid leaks from the blood vessels into the lung tissue, resulting in PULMONARY EDEMA, a hallmark of left-sided heart failure. Accumulation of fluid in the alveoli IMPEDES the gas exchange process, resulting in respiratory symptoms such as shortness of breath, which worsens when lying down, and chest crackles.
RIGHT-sided heart failure is most commonly caused by LEFT-sided heart failure. This is because the INCREASED pulmonary pressure caused by left-sided heart failure makes it harder for the right ventricle to pump INTO the pulmonary artery. This results in SYSTOLIC dysfunction. In compensation, the right ventricle grows thicker to pump harder, which reduces the space available for filling, eventually leading to DIASTOLIC dysfunction. Other common causes of right-sided heart failure include chronic lung diseases which also raise pulmonary blood pressure.
As the right ventricle pumps out less blood, the blood, again, backs up to where it came from, and in this case, the SYSTEMIC circulation. This results in abnormal fluid accumulation in various organs, most notable in the feet when standing, sacral area when lying down, abdominal cavity and liver. The fluid status can be assessed by examining the distension level of the jugular vein.


Heart failure is usually managed by treating the underlying condition, together with a combination of drugs. ACE inhibitors, beta blockers are used to reduce blood pressure in patients with systolic dysfunction. Diuretics are used to reduce water retention.

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Potencial de Ação Cardíaco, com Animação

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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.

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Brain Stroke for Patient Education, with Animation

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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

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Bloqueios de Ramo, com Animação

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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.

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

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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.

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