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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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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.
Management
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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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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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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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 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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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.
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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.
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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
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.
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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.
