Author Archives: Alila Medical Media

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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Thyroid Gland, Hormones and Thyroid Problems, with Animation

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The thyroid is a butterfly-shaped ENDOCRINE gland located in the neck. It is wrapped around the trachea, just below the thyroid cartilage –the Adam’s apple.

The two major hormones of the thyroid are triiodothyronine, T3 and thyroxine, T4. The numbers 3 and 4 indicate the number of iodine atoms present in a molecule of each hormone. T3 and T4 are collectively referred to as THYROID hormones.

Thyroid hormone secretion is under control of thyroid-stimulating hormone, TSH, from the anterior pituitary. TSH, in turn, is induced by thyrotropin-releasing hormone, TRH, produced by the hypothalamus. The amount of circulating thyroid hormones is regulated by a negative feedback loop: when their levels are too high, they SUPPRESS the production of TSH and TRH, consequently INHIBITING their own production.

Thyroid hormones act to INCREASE the body’s metabolic rate. They stimulate appetite, digestion, breakdown of nutrients and absorption. They also increase oxygen consumption, raise the breathing rate, heart rate and contraction strength. As a result, the body’s HEAT production is INCREASED. Thyroid hormone secretion usually rises in winter months to keep the body warm.

Thyroid hormones are also important for bone growth and fetal brain development.

There are 2 major groups of thyroid problems:

HYPOthyroidism: when the thyroid does NOT produce ENOUGH hormones, resulting in a LOW metabolic rate, combined with SLOW respiratory and cardiovascular activities. Common symptoms include fatigue, weight gain despite poor appetite, cold intolerance, slow heart rate, heavy menstrual bleeding and constipation. Iodine deficiency and Hashimoto’s thyroiditis are the most common causes. Hashimoto’s thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed by the body’s own immune system.

Hypothyroidism, especially when caused by iodine deficiency, may lead to swelling of the thyroid gland, known as GOITER. In an attempt to fix the low levels of thyroid hormones, the pituitary produces MORE TSH to further stimulate the thyroid gland. The thyroid, while UNable to make hormones WITHOUT iodine, responds to TSH by GROWING in size.

Hypothyroidism is managed with thyroxine hormone replacement.

HYPERthyroidism: when the thyroid gland produces TOO MUCH hormones, resulting in a TOO ACTIVE metabolism, together with respiratory and cardiovascular rates that are HIGHER than necessary. Common symptoms include irritability, insomnia, weight loss despite good appetite, heat intolerance, heart racing and diarrhea.

Hyperthyroidism is most commonly caused by Graves’ disease, another autoimmune disorder characterized by presence of an antibody, called thyroid stimulating immunoglobulin, TSI. TSI, similar to TSH, stimulates the thyroid gland to produce hormones. Unlike TSH, however, TSI is NOT regulated by  negative feedback mechanisms, leading to UNcontrolled production of thyroid hormones. TSI also stimulates the thyroid gland to grow, which MAY lead to formation of a goiter.

Hyperthyroidism may be managed with drugs that suppress thyroid function, radioactive iodine that selectively destroys the thyroid gland, or surgery that removes part of the gland.

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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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The Hypothalamus and Pituitary Gland, with Animation.

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The hypothalamus and the pituitary gland are at the center of endocrine function. The hypothalamus is part of the brain, while the pituitary, also called hypophysis (hy-POFF-ih-sis), is an endocrine gland. The hypothalamus links the nervous system to the endocrine system via the pituitary gland. The two structures are located at the base of the brain and are connected by a thin stalk.

The hypothalamus produces several hormones, known as neurohormones, which control the secretion of other hormones by the pituitary. Pituitary hormones, in turn, control the production of yet other hormones by other endocrine glands.

The pituitary has two distinct lobes:

The anterior pituitary, also called adenohypophysis (AD-eh-no-hy-POFF-ih-sis), communicates with the hypothalamus via a network of blood vessels known as the hypophyseal portal system. Several neurohormones produced by the hypothalamus are secreted into the portal system to reach the anterior pituitary, where they stimulate or inhibit production of pituitary hormones. Major hormones include:

  • Gonadotropin-releasing hormone, GnRH, a hypothalamic hormone, stimulates the anterior pituitary to producefollicle-stimulating hormone, FSH, and luteinizing hormone, FSH and LH, in turn, control the activities of the gonads – the ovaries and testes.
  • Corticotropin-releasing hormone, CRH,promotes the secretion of adrenocorticotropic hormone, ACTH, which in turn stimulates production of cortisol by the adrenal gland.
  • Thyrotropin-releasing hormone, TRH, promotes the release of thyroid-stimulating hormone, TSH, and prolactin. TSH, in turn, induces the thyroid gland to produce thyroid hormones. Prolactin stimulates the mammary glands to produce milk.
  • Prolactin-inhibiting hormone, PIH, inhibits production of prolactin.
  • Growth hormone–releasing hormone, GHRH, promotes production of growth hormone, or somatotropin, which has widespread effects on the growth of various tissues in the body.
  • Growth hormone–inhibiting hormone, GHIH, or somatostatin, inhibits production of growth hormone.

The posterior pituitary, also called neurohypophysis, communicates with the hypothalamus via a bundle of nerve fibers. These are essentially hypothalamic neurons with cell bodies located in the hypothalamus while their axons EXTENDED to posterior pituitary. These neurons produce hormones, transport them down the stalk, and store them at the nerve terminals within the posterior pituitary, where they wait for a nerve signal to trigger their release. Two hormones have been identified so far:

– Vasopressin, also known as antidiuretic hormone, ADH, acts on the kidneys to retain water.

– Oxytocin causes the uterus to contract during childbirth and stimulates contractions of the milk ducts in lactating women.

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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.

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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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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Opioids/Opiates Mechanism of Action, with Animation

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Opioids refer to a class of drugs that act via opioid receptors in the nervous system to relieve pain. The term “opioid” includes:
– ENDOGENOUS opioids occurring naturally in the human body such as endorphins,
– OPIATES found in the opium poppy plant such as morphine,
– synthetic (methadone, fentanyl) and semi-synthetic opioids (heroin).
The major function of endogenous opioids is to modulate pain signals. They are synthesized in response to pain stimuli and exert their effects by binding to opioid receptors in the brain, spinal cord and peripheral nerves. In the brain, they also increase DOPAMINE release, producing EUPHORIC effects.
Opioid analgesics such as morphine and fentanyl mimic the action of endogenous opioids. They are powerful painkillers and are commonly used to manage severe pain. Continuous use, however, MAY lead to tolerance and dependence. Opioids slow down BREATHING and overdose can be FATAL. Their psychoactive effects also make them common drugs of abuse, with morphine being PARTICULARLY susceptible to addiction. Heroin, a semi-synthetic product made from morphine, is another drug that is highly popular among recreational users. Once administered, it is metabolized into morphine and 6-mono-acetyl-morphine, both of which are psychoactive. Heroin is rarely used in medicine.

How do opioids produce euphoric effects?
Dopamine neurotransmitter is at the basis of the brain reward pathway. Engaging in enjoyable activities causes dopamine release from dopamine-producing neurons into the synaptic space where it binds to and stimulates dopamine-receptors on the receiving neuron. This stimulation is believed to produce the pleasurable feelings or rewarding effect. Normally, GABA, another neurotransmitter, INHIBITS dopamine release in the nucleus accumbens. By binding to receptors on GABA inhibitory neurons, opioids REDUCE GABA’s activity, ultimately INCREASE dopamine release and induce pleasurable feelings.

Addiction, Dependence and Tolerance 
Continued use of opioids can result in dependence and addiction. As the body gets used to euphoric effects of the drug, it may become irritated if drug use is reduced or discontinued.
Tolerance develops following a typical sequence of events. A drug exerts its effect by INcreasing or DEcreasing a certain substance or activity in the brain to an ABNORMALLY high or low level. REPEATED exposure MAINTAINS this abnormal level for a period of time. The brain eventually ADAPTS by pulling it BACK to NORMAL level. This means the drug, at the current dosage, NO longer produces the desirable psychoactive effect; a higher dose is required to do so. This vicious cycle repeats itself and eventually leads to drug overdose.

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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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Long Term Potentiation and Memory, with Animation

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The process of learning begins with sensory signals being transcribed in the cortex. They are then transmitted to the hippocampus where new memories are believed to form. If a signal is strong, or repeated, a long-term memory is established and wired back to the cortex for storage. Lesions in the hippocampus impair formation of new memories, but do not affect the older ones.
The brain consists of billions of neurons. Neurons communicate with each other through a space between them, called a synapse. A typical neuron can have thousands of synapses, or connections, with other neurons. Together, they form extremely complex networks that are responsible for all brain’s functions. Synaptic connections can change over time, a phenomenon known as synaptic plasticity. Synaptic plasticity follows the “use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated. Synaptic plasticity is believed to underlie the process of learning and memory retention. New memories are formed when neurons establish new connections, or STRENGTHEN existing synapses. If a memory is no longer needed or rarely recalled, its corresponding synapses will slowly weaken and eventually disappear.
The strength of a synapse is measured by the level of excitability or responsiveness of the post-synaptic neuron in response to a GIVEN stimulus from the pre-synaptic neuron. High-frequency signals or repeated stimulations STRENGTHEN synaptic connections over time. This is known as long-term potentiation, or LTP, and is thought to be the cellular basis of memory formation. LTP can occur at most excitatory synapses all over the brain, but is best studied at the glutamate synapse of the hippocampus.
When a glutamatergic neuron is stimulated, action potentials travel down its axon and trigger the release of glutamate into the synaptic cleft. Glutamate then binds to its receptors on the post-synaptic neuron. The 2 main glutamate receptors that often co-exist in a synapse are AMPA and NMDA receptors. These are ion channels that activate upon binding to glutamate. When the pre-synaptic neuron is stimulated by a WEAK signal, only a small amount of glutamate is released. Although both receptors are bound by the glutamate, only AMPA is activated by weak stimulation. Sodium influx through the AMPA channel results in a SLIGHT DE-polarization of the post-synaptic membrane. The NMDA channel remains closed because its pore is blocked by magnesium ions.
When the pre-synaptic neuron is stimulated by a STRONG or REPEATING signal, a large amount of glutamate is released; the AMPA receptor stays open for a longer time, admitting more sodium into the cell, thus resulting in a GREATER DE-polarization. Increased influx of positive ions EXPELS magnesium from the NMDA channel, which NOW activates, allowing not only sodium but also CALCIUM into the cell. Calcium is the mediator of LTP induction. There are 2 distinct phases of LTP. In the early phase, calcium initiates signaling pathways that activate several protein kinases. These kinases enhance synaptic communication in 2 ways: they phosphorylate the existing AMPA receptors, thereby increasing AMPA conductance to sodium; and help to bring more AMPA receptors from intracellular stores to the post-synaptic membrane. This phase is thought to be the basis of short-term memory, which lasts for several hours. In the late phase, NEW proteins are made and gene expression is activated to further enhance the connection between the 2 neurons. These include newly synthesized AMPA receptors, and expression of other proteins that are involved in the growth of NEW dendritic spines and synaptic connections. The late phase may correlate with formation of long-term memory.

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