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Tetralogy of Fallot, or TOF, is a CONGENITAL heart disease, classically known as a combination of FOUR defects that disrupt the normal blood flow in the heart.

In normal circulation, oxygen-poor blood from the body returns to the right side of the heart where it is pumped into the pulmonary artery and to the lungs. After being oxygenated, oxygen-RICH blood from the lungs returns to the left side of the heart to be pumped into the aorta and out to the body.

Infants born with TOF are presented with 4 major structural defects:

• NARROWING of the PULMONARY output
• Ventricular septal defect: an OPENING in the interventricular septum
• Displacement of the aorta: it now connects to both ventricles

and

• Hypertrophy of the right ventricle

The 4 defects, however, are likely the result of a SINGLE incident during embryonic development – the MAL-alignment of the upper part of the ventricular septum, known as the conal septum, with the rest of it. As the conal septum moves rightward and anteriorly, it creates an opening in the septum; blocks the right ventricular outflow tract; and pulls the aorta over the ventricular septum. Finally, because the output to the lungs is obstructed, the right ventricle develops thicker muscle to push harder, resulting in right ventricular hypertrophy.

The cause of TOF remains largely unknown but several genetic disorders and prenatal factors are thought to be associated with increased risks of this condition.

Connected ventricles in TOF allow blood to flow from one side to the other. The DIRECTION of this flow, however, depends on the DEGREE of pulmonary tract obstruction. When the obstruction is minimal, the flow is LEFT-to-RIGHT, because the LEFT ventricular pressure is usually HIGHER. While some of the already oxygenated blood leaks back to the lungs, most of it goes the usual route to the aorta, and the baby appears “pink” as normal. However, in the long-term, if too much blood flows to the lungs, patients may develop congestive heart failure.

On the other hand, when pulmonary stenosis is severe, blood in the right ventricle has to escape through the septal defect during ventricular contraction, and a RIGHT-to-LEFT shunt results. The MIXED blood, which is LOW in oxygen, is then pumped into the aorta and to the body, causing oxygen deprivation in body’s tissues, or hypoxia. This may result in a BLUISH skin color, known as CYANOSIS. The greater the pulmonary obstruction, the more deoxygenated blood enters the systemic circulation, the more severe the symptoms.

Children with TOF may develop acute episodes of hypoxia, known as “tet spells”, during activities that demand more oxygen. These episodes are characterized by: shortness of breath, increased cyanosis, loss of consciousness, and may result in hypoxic brain injury and death. Tet spell is a medical emergency but simple procedures such as squatting and the knee chest position, which increase systemic vascular resistance and therefore decrease right-to-left shunting, can help to temporarily relieve symptoms.

Diagnosis is by echocardiography and can be done prenatally. Treatment is usually by repair surgery within the first year of life. The surgery involves enlargement of the pulmonary tract and closure of the septal defect.

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Blood pressure is the force the circulating blood EXERTS on the walls of blood vessels. It is different in different types of vessels, but the term ”blood pressure”, when not specified otherwise, refers to ARTERIAL pressure in the SYSTEMIC circulation.
When the heart contracts and pumps blood into the aorta, during systole, the aortic pressure RISES, and so does the systemic arterial pressure. The maximum pressure following an ejection is called the SYSTOLIC pressure. In between heart beats, when the ventricles refill, blood pressure FALLS to its lowest value called the DIASTOLIC pressure. THESE are the 2 numbers on a blood pressure reading.
Blood pressure normally shows a daily pattern and is usually lower at night. During day-time, it fluctuates with physical activities and emotional states.
Hypertension refers to a PERSISTENT HIGH blood pressure. In the US, high blood pressure used to be defined as greater than 140/90, but recent guidelines have changed these values to 130/80 to better prevent and treat the condition. Normal blood pressure is BELOW 120/80. In practice, blood pressure is considered TOO low ONLY if it produces symptoms.
Hypertension does NOT cause symptoms on its own, but it slowly DAMAGES blood vessels, and in the long-term, is a MAJOR risk factor for a variety of cardiovascular diseases such as stroke, aneurysm and heart attack; as well as end organ damage such as renal failure or vision loss. For this reason, hypertension is known as the “SILENT killer”.
Hypertension can be classified as primary or secondary, with the former being responsible for over 90% of cases. Primary hypertension has NO apparent cause and may develop as a result of old age, obesity, high-salt diet, lack of exercise, smoking and drinking. Most commonly, the blood vessels are hardened with age or unhealthy diets, making it harder for blood to flow.
Secondary hypertension, on the other hand, is caused by an underlying condition. Many conditions and factors can cause hypertension; most notable are kidney problems and endocrine disturbances.
Regardless of the cause, the increase in blood pressure is produced by EITHER an increase in vascular resistance – narrower or stiffer blood vessels; OR an increase in cardiac output – larger volume of blood pumped out by the heart. These 2 factors are the targets of antihypertensive drugs.
Treatments must start with life style changes such as healthy, low-sodium diets, physical exercise and stress management. On top of that, antihypertensive agents may be used to control hypertension. These include:
– Vasodilators: these drugs DILATE blood vessels, thereby DEcreasing vascular resistance and reducing blood pressure.
– Diuretics: diuretics promote sodium and water removal by the kidneys and thereby DEcrease blood volume.
– Drugs that decrease cardiac output by decreasing heart rate or contractility, may also be used to treat hypertension.

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As arritmias cardíacas podem ser classificadas de acordo com o local de origem: ritmos sinusais são originários no nódulo sinoatrial ou nódulo SA; os ritmos atriais são originários nos átrios; ritmos ventriculares são originários nos ventrículos.

O ritmo sinusal é o ritmo normal do coração definido pelo marcapasso natural no nódulo SA. Em um coração saudável, o nódulo SA dispara 60 a 100 vezes por minuto, resultando na frequência cardíaca normal de 60 a 100 batimentos por minuto. As variações mais comuns do ritmo sinusal incluem:

* Bradicardia sinusal: quando o nódulo SA dispara menos de 60 vezes por minuto, resultando em uma frequência cardíaca mais lenta, com menos de 60 batimentos por minuto.

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* Taquicardia sinusal: quando o nódulo SA dispara mais de 100 vezes por minuto, gerando uma frequência cardíaca mais rápida, com mais de 100 batimentos por minuto.

A bradicardia sinusal e a taquicardia sinusal podem ser normais ou clínicas, dependendo da causa subjacente. Por exemplo, a bradicardia sinusal é considerada normal durante o sono e a taquicardia sinusal pode ser normal durante os exercícios físicos.

As arritmias cardíacas originárias de outras partes dos átrios são sempre patológicas. As mais comuns incluem: flutter atrial, fibrilação atrial e Taquicardia atrioventricular Reentrante Nodal. Estas são formas de taquicardia supraventricular ou TSV.

O flutter atrial ou flutter auricular é causado por um impulso elétrico que gira em torno de um ciclo localizado que se autoperpetua, mais comumente localizado no átrio direito. Isso é chamado de circuito REENTRANTE. Para cada ciclo, há uma contração dos átrios. A frequência atrial é regular e rápida, entre 250 e 400 batimentos por minuto. A frequência ventricular, ou frequência cardíaca, no entanto, é mais lenta, graças às propriedades REFRATÁRIAS do nódulo AV. O nódulo AV evita que parte dos impulsos atriais cheguem aos ventrículos. Neste exemplo, apenas um em cada TRÊS impulsos atriais segue o caminho para os ventrículos. Portanto, a frequência ventricular é 3 vezes MENOR do que a frequência atrial. A frequência ventricular em flutter atrial geralmente é regular, mas também pode ser IRREGULAR. Em um ECG, flutter atrial é caracterizado pela ausência de ondas P normais. Em vez disso, são observadas ondas flutter ou ondas f com um padrão serrilhado.

A fibrilação atrial é causada por múltiplos impulsos elétricos que são iniciados ALEATORIAMENTE de muitos focos ECTÓPICOS, dentro e ao redor dos átrios, geralmente perto das raízes das veias pulmonares. Esses sinais elétricos caóticos e não sincronizados fazem com que os átrios tremem ou fibrilhem ao invés de se contraírem. A frequência atrial durante a fibrilação pode ser EXTREMAMENTE alta, mas a maioria dos impulsos elétricos NÃO passam através do nódulo AV para os ventrículos, novamente, graças às propriedades refratárias do nódulo AV. Aqueles que passam são IRREGULARES. A frequência ventricular ou frequência cardíaca é, portanto, IRREGULAR e pode variar de lento, menor que 60, a rápido, mais de 100 batimentos por minuto. Em um ECG, a fibrilação atrial caracteriza-se por ausência de ondas P e presença de complexos QRS ESTREITOS e irregulares. A linha de base pode parecer ondulada ou totalmente plana, dependendo do número de focos ectópicos nos átrios. Em geral, um número maior de focos ectópicos resulta em uma linha de base mais plana.

A Taquicardia Atrioventricular Reentrante Nodal, ou TAVRN, é causada por um pequeno circuito de reentrada que envolve DIRETAMENTE o nódulo AV. Toda vez que o impulso passa através do nódulo  AV, ele é transmitido para os ventrículos. A frequência atrial e a frequência ventricular são, portanto, idênticas. A frequência cardíaca é regular e rápida, variando de 150 a 250 batimentos por minuto.

Os ritmos ventriculares são os mais perigosos, sendo ameaças para a vida.

A taquicardia ventricular é mais comumente causada por um foco de disparo ou circuito, sendo FORTE e ÚNICO em um dos ventrículos. Geralmente ocorre em pessoas com problemas cardíacos estruturais, como cicatrizes de um ataque cardíaco prévio ou anormalidades nos músculos cardíacos. Os impulsos que começam nos ventrículos produzem batimentos ventriculares PREMATUROS que são regulares e rápidos, variando de 100 a 250 batimentos por minuto. Em um ECG, a taquicardia ventricular é caracterizada por complexos QRS largos e estranhos. A onda P está ausente. A taquicardia ventricular pode ocorrer com episódios curtos de menos de 30 segundos e não causar nenhum ou poucos sintomas. A taquicardia ventricular SUSTENTADA dura mais de 30 segundos e requer tratamento imediato para prevenir uma parada cardíaca. A taquicardia ventricular também pode progredir para a fibrilação ventricular.

A fibrilação ventricular, ou FV, é causada por MÚLTIPLOS e FRACOS focos ectópicos nos ventrículos. Esses sinais elétricos não sincronizados fazem com que os ventrículos sofram FIBRILAÇÃO em vez de se contraírem. O coração bombeia pouco ou nenhum sangue. A FV pode rapidamente levar a uma parada cardíaca. O ECG da FV é caracterizado por formas de onda IRREGULAR e aleatória de amplitude variável, NÃO é possível identificar a onda P, o complexo QRS ou onda T. A amplitude diminui com o tempo, desde a FV GROSSEIRA inicial até a FV FINA e, finalmente, até a linha plana.

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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,

or

– 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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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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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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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.