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Premature ventricular contractions, PVCs, are premature heartbeats originating in one of the lower chambers of the heart, the ventricles.

PVCs can result from a variety of factors and conditions, including:

– consumption of alcohol, caffeine, tobacco or drugs

– certain medications

– physical exercise, stress, or anything that increases adrenaline levels

– certain electrolyte deficiencies

– and damaged cardiac tissue caused by other heart diseases.

PVCs are very common, but often produce no or few symptoms. When present, symptoms may include skipped heart beats, palpitations, and lightheadedness.

In normal conduction, electrical impulses start in the SA node, depolarize the atria, then pass through the AV node to activate the ventricles. A PVC happens when the ventricles are activated prematurely, by an abnormal firing site, called ectopic site, located in one of the ventricles. Because ventricular depolarization does not come from the atria, PVC complexes are not preceded by P waves. Unlike the normal conduction carried out by specialized cells of the conduction pathway, the signal in PVC is conducted through the myocytes of the heart muscle, and propagates more slowly, producing a broader QRS complex. Depending on the location of the ectopic site, the resulting QRS complex may also be taller, or deeper than usual. PVCs typically do not conduct back to the atria, so SA node firing is usually not affected, and PP intervals remain unchanged. But the P wave that follows a PVC may not result in a beat if it happens too closely to the PVC, when the ventricles are still in their refractory period. This is referred to as a compensatory pause.

There are 3 mechanisms by which a PVC may occur:

• Increased automaticity. The ability of ventricular myocytes to spontaneously depolarize and generate action potentials is associated with intracellular calcium overload caused by excess catecholamines, drugs such as digoxin, and certain electrolyte deficiencies, such as hypokalemia or hypomagnesemia.
• Re-entry circuit in a ventricle. This usually happens when there is a damage to the heart muscle, such as a scar from a previous heart attack, or other heart conditions. The damaged tissue conducts at a slower speed, causing the electrical signal to go around it, creating a self-perpetuating loop.
• Triggered beats. These are extra-beats produced by early or delayed after-depolarizations. Early after-depolarization may occur when the duration of action potentials is abnormally long, in conditions such as long QT syndrome, hypokalemia, or as an effect of drugs such as potassium channel blockers. Delayed after-depolarizations can be caused by digoxin toxicity or excess catecholamines.

Most people do not need treatment for PVC itself, but the underlying factor or condition must be addressed.

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The heart pumps out oxygen-rich blood through the aorta to nourish the entire body. It also supplies itself via a network of blood vessels called the coronary circulation. The two main vessels – the left and right coronary arteries – branch out from the aorta shortly after it exits the heart, right above the aortic valve.
The right coronary artery provides blood supply to the right atrium, and gives rise to:
– the marginal artery nourishing the lateral aspect of the right side of the heart,
– and the posterior interventricular artery, or posterior descending artery, supplying the posterior aspect of both ventricles and part of the interventricular septum.
The right coronary artery also supplies the SA node and AV node in the majority of people.
The left coronary artery splits into 2 major branches:
– the anterior interventricular artery, or anterior descending artery, supplying the anterior walls of both ventricles and most of the interventricular septum. This artery contributes the most to the left ventricle and is therefore the most critical vessel of the heart.
– the circumflex artery curves toward the posterior surface, providing for the left atrium and posterior walls of the left ventricle.
Coronary circulation is of utmost importance as it is required for normal function of the heart, which supplies blood to the entire body. A blocked coronary artery may cause life-threatening myocardial infarction, or heart attack. The most common cause of blockage is the accumulation of fat deposits on the wall of blood vessels, in a condition known as coronary heart disease.
Several procedures are available to treat coronary heart disease and restore normal blood supply to the heart. The most commonly performed are angioplasty and vascular bypass surgery.
Coronary angioplasty, also known as percutaneous coronary intervention, PCI, is a minimally invasive endovascular procedure used to widen narrowed or blocked coronary arteries. A deflated balloon attached to a catheter is passed through the femoral artery in the groin to the site of blockage, where the balloon is inflated, opening the artery. A stent may also be inserted together with the balloon and left in place to keep the artery open permanently. PCI is the procedure of choice for emergency treatment.
Coronary bypass, or vascular bypass, is a surgical procedure performed to create an alternative route for the blood to flow beyond the site of blockage. An artery graft from the patient’s chest, or a vein graft from the patient’s leg may be used for this purpose. Vascular bypass is usually performed in patients with severe coronary heart disease to prevent heart attacks, but it may also be used during or after a heart attack.

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Shock, also called circulatory shock, is a life-threatening clinical state characterized by body-wide deficiency of blood supply, causing oxygen deprivation, buildup of waste products, and eventual organ failure if untreated.
Shock may have different causes and hence its classification into different types:
– Hypovolemic, or low volume shock happens when the circulating blood volume is severely reduced. This can be caused by:
+ External blood loss, such as after an injury,
+ Internal blood loss such as that results from a ruptured blood vessel, ruptured ectopic pregnancy, pancreatitis …
+ Or fluid loss from major burns, excessive vomiting, diarrhea or urination.
– Cardiogenic shock occurs when the heart fails to pump sufficiently. This can result from a sudden heart attack, or an end-stage development in various heart conditions.
– Obstructive shock is caused by an obstruction of blood flow in a major circulatory circuit.
– Distributive shock results from excessive dilation of blood vessels, or vasodilation, which decreases blood pressures. Distribution shock can have different causes, the most common being sepsis, anaphylaxis and damage to the central nervous system (neurogenic):
+ In sepsis, the immune system is overwhelmed by an infection that gets out of control, and responds with a systemic cytokine release that causes vasodilation and fluid leakage from capillaries.
+ In anaphylaxis, the immune system overreacts to an allergen, releasing massive amounts of histamine, which has similar effects to cytokines. Peanut allergy is a common cause of anaphylaxis.
+ Neurogenic shock typically occurs as a result of a spinal cord injury. As the autonomic nervous system is damaged, the sympathetic tone that normally keeps blood vessels constricted is lost, causing vasodilation and hypotension.
Common symptoms of shock include low blood pressures and signs of organ damage such as confusion, reduced urine output and cold, sweaty, mottled or bluish skin, although distributive shocks due to sepsis or anaphylaxis may initially produce warm or flushed skin. This is because the infection in sepsis usually comes with fever, and the allergic reaction in anaphylaxis is accompanied by hives. Distributive shocks may also differ from other types of shock by having, at least initially, normal or high cardiac output.
As the body tries to compensate for hypotension, fast heart rates and rapid breathing may be observed. Diagnosis may also be assisted by blood tests for blood lactate levels. This is because in the absence of oxygen, the body switches to an alternative way of producing cellular energy, called anaerobic metabolism, in which glucose is broken down only partially producing lactic acid. Blood tests may also indicate signs of organ damage, or infection in case of sepsis.
Shock is a medical emergency and requires immediate treatments which aim to increase blood pressures and treat the underlying cause.

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The heart electrical signals are initiated in its natural pacemaker – the sinoatrial node, or SA node, and travel through the atria to reach the atrioventricular node, or AV node. The AV node passes the signals onto the bundle of His, which then splits into two branches that conduct the impulses to the two ventricles.

The SA node is composed of two major cell types: P, for pacemaker, cells generate electrical impulses; and T, for transitional, cells transmit these signals to the right atrium and subsequently to the rest of the cardiac conduction system. Sinus node dysfunction occurs when any of these cells cease to function properly: failure to produce electrical impulses by P cells leads to sinus pause or sinus arrest, while delay or failure of signal transmission by T cells results in SA exit blocks.

On an ECG, sinus pause or arrest can be seen as a brief absence of P waves, which can last for seconds to minutes. In most cases, a downstream pacemaker in the atria, atrioventricular junction, or ventricles, will take over the pacing function, producing so-called escape beats or rhythms, and thus preserving heart rate and function until the SA node recovers and fires again; but long pauses may cause dizziness, fainting and possibly cardiac arrest.

In SA exit blocks, the SA node discharges normally, but the impulses are slow to reach the atrium, or completely interrupted before reaching the atrium. There are three degrees of SA blocks, similar to the 3 degrees observed with AV blocks.

• In first-degree SA block, there is an abnormal delay between the firing of the SA node and transmission to the atrium. Because SA node firing is not significant enough to be seen on a standard 12-lead ECG, this type of block cannot be detected on a surface ECG.
• In second-degree SA block type I, the electrical signals are delayed further and further with each heartbeat until a P wave is missing altogether. Due to the diminution in the increment of the delay, the P-P intervals are progressively shortened before the dropped P wave. This pattern results in pauses and the appearance of grouped beats. The duration of each pause is less than two P-P cycles.
• In second-degree SA block type II, some of the electrical signals do not reach the atrium. On an ECG, this is seen as intermittent dropped P waves; the pauses are multiple, usually twice, of the P-P interval.
• Third-degree SA block is a complete block; P waves are absent. This type of SA exit block is indistinguishable from a sinus arrest.

Sinus node dysfunction is most commonly due to degeneration or scarring of the SA node tissue, which can result from aging, other heart diseases or diabetes. Other causes may include certain medications or an excessive vagal tone.

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Cardiomyopathy is a group of diseases that weaken the heart muscle – the myocardium, making it harder for the heart to pump blood. Cardiomyopathy reduces blood output, and may lead to heart failure. The condition may be inherited from a parent, or develop as a consequence of another disease or factor. Some patients do not experience any symptoms. When present, symptoms may include: shortness of breath, fatigue, rapid heartbeats, chest pain, swelling of lower limbs, dizziness and fainting. Progression of the disease varies greatly from person to person. In some people, symptoms may appear suddenly, and worsen quickly; while others see a gradual development over a long period of time.

There are 3 MAJOR types of cardiomyopathy:

• Hypertrophic cardiomyopathy, or HCM, is the thickening of the heart muscle. Most commonly, this occurs in the inter-ventricular septum facing the left ventricle. The thickened septum obstructs blood flow to the aorta, a condition called “outflow tract obstruction” or “obstructive hypertrophic cardiomyopathy”.Thickening elsewhere in the heart muscle causes non-obstructive HCM. In both cases, cardiac output is reduced. While HCM can develop as a result of high blood pressure or aging, it is most commonly inherited as an autosomal dominant trait: children of an affected parent have a 50% chance of inheriting the disease. Multiple mutations have been identified in genes encoding for proteins of the heart muscle. Genetic screening is recommended as the disease may progress rapidly, from asymptomatic to heart failure and cardiac arrest. In fact, HCM is the major cause of sudden cardiac death among young a People who test positive for HCM are advised to avoid high-intensity activities.
• Dilated cardiomyopathy, DCM, is the thinning of the myocardium and enlargement of a heart chamber, most commonly the left ventricle. DCM is usually acquired and the cause is unknown in most cases. Risk factors include high blood pressure; damage to the myocardium caused by previous heart attacks, alcohol or cocaine use, toxins or infections; and obesity or diabetes. While DCM may develop in anyone at any age, it is more common in men of middle age. Some DCM cases are inherited.
• Restrictive cardiomyopathy, RCM, is when the heart muscle becomes rigid, lacking the elasticity required to properly fill and pump blood. RCM usually results from building-up of scar tissues or abnormal proteins, caused by a variety of conditions. RCM is more likely in older people.

Less common types of cardiomyopathy include: arrhythmogenic right ventricular dysplasia, a condition in which the right ventricle tissue is scarred, causing arrhythmias; and stress cardiomyopathy, or broken heart syndrome: a sudden temporary weakening of the heart muscle triggered by excessive emotional or physical stress.

Treatment varies depending on the type of cardiomyopathy, the underlying cause and severity of symptoms, and can range from life style changes, to medications and surgeries.

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Wolff-Parkinson-White, or WPW, syndrome is a congenital heart disease characterized by presence of an ABnormal electrical CONNECTION between the atria and ventricles of the heart. WPW typical symptom is an abnormally FAST heart rate, or TACHYCARDIA.
In normal conduction, electrical signals are initiated in the SA node, and travel throughout the atria before they reach the AV node. The AV node is the GATEWAY to the ventricles. It DELAYS the passage of electrical impulses to the ventricles to ensure that the atria have ejected all the blood into the ventricles before the ventricles contract. This REFRACTORY property of the AV node is essential in LIMITING electrical activities that reach the ventricles. In situations where the ATRIAL rate is EXCESSIVELY high, such as during atrial fibrillation or atrial flutter, the AV node BLOCKS most of the impulses from passing to the ventricles, keeping the heart rate under control.
In WPW, there is an ADDITIONAL connection between the atria and the ventricles, called the ACCESSORY pathway, or bundle of Kent. This pathway is essentially a patch of conductive tissue that provides a SHORTCUT to the ventricles, BYPASSING the AV node. It allows PART of electrical impulses to arrive to the ventricles SOONER, causing a so-called “PRE-excitation”. This can be seen as a SHORTENED PR interval on an ECG. Because part of the ventricles depolarize EARLIER, ventricular depolarization develops in a more GRADUAL fashion and lasts LONGER, resulting in a SLURRING slow rise of the initial portion of the QRS complex, known as DELTA wave, and QRS prolongation.
To note, however, that the presence of an accessory pathway ALONE does NOT cause tachycardia. In fact, most people with a WPW pathway NEVER develop any symptoms. They are said to have a WPW PATTERN, as opposed to WPW SYNDROME in symptomatic patients.
There are 2 mechanisms by which tachycardia can happen in WPW:
– Most commonly, tachycardia develops when electrical impulses travel DOWN one pathway, either the normal or accessory, then BACK UP via the OTHER, creating a SELF-perpetuating LOOP, or a RE-ENTRANT circuit. The frequency of this loop determines heart rate and CAN be very fast, ranging from 150 to 250 beats per minute. This is known as Atrioventricular Re-entry Tachycardia, or AVRT. AVRT can be orthodromic or antidromic depending on the direction of the loop.
– Another scenario is when WPW patients ALSO suffer from Atrial Fibrillation. In this condition, the atria contract at a VERY HIGH rate but most of the electrical impulses do NOT make it through the AV node to the ventricles. This is where a WPW pathway can have a detrimental effect. It provides a BYPASS to let MORE impulses reach the ventricles, causing a FASTER heart rate that could potentially be fatal.
The severity of WPW tachycardia depends on how FAST the accessory pathway is able to conduct. This varies from person to person and can be evaluated in a procedure called Programmed Electrical Stimulation, in which the atria are stimulated to produce progressively HIGHER rates and the atrial-to-ventricular conduction ratio is monitored. Patients are at high risk of developing LETHAL tachycardia if their accessory pathway CONTINUES to conduct at 1-to-1 ratio with dangerously high atrial rates. High-risk patients are usually treated with catheter ablation to destroy the conductive tissue of the accessory pathway.

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The aortic valve serves to ensure ONE-WAY flow of oxygen-RICH blood from the LEFT ventricle to the aorta and to the body. It OPENS when the left ventricle contracts and pumps blood; and CLOSES when the ventricles refill, to prevent blood from flowing BACK to the left ventricle. The aortic valve consists of three leaflets, or cusps.

A defective valve is one that FAILS to either OPEN or CLOSE properly. Aortic STENOSIS happens when the aortic valve does not OPEN fully, REDUCING blood flow. Aortic REGURGITATION, on the other hand, occurs when the valve does not CLOSE tightly, causing BACKWARD flow to the ventricle.

The common outcome of both situations is that the heart does NOT pump enough blood to the body, and heart failure may result. Symptoms may develop suddenly or SLOWLY over decades, and may include: fatigue, shortness of breath, especially when exercising; chest pain or tightness; dizziness, fainting, swelling in the ankles and feet; and poor feeding and growth in children.

In attempts to compensate for the low blood output, the left ventricle grows LARGER to generate higher pressures and pump harder. This enlargement may help to relieve symptoms at first, but eventually it causes the ventricle to become weak and fail.

Risk factors for both conditions include:

– Congenital heart valve disease: some people are born with ABnormal structures that increase the risks of valve MALfunctioning. Common defects include having two leaflets, instead of three; fused leaflets, and dilation of the aortic root.

– STIFFENED valve due to calcium deposits, as a result of AGING.

– and valve DAMAGE due to infection or inflammation in conditions such as endocarditis and rheumatic fever.

Aortic valve diseases produce characteristic heart murmurs that are useful for diagnosis.

Aortic stenosis gives rise to a crescendo-decrescendo systolic murmur which starts shortly after the first heart sound. It is often preceded by an ejection click caused by the opening of the STENOTIC valve. The murmur is loudest in the aortic area and the sound radiates to the neck.

Aortic regurgitation produces a diastolic murmur which is heard along the left sternal border. It peaks at the beginning of diastole when the flow is largest, then rapidly decreases as the ventricles are filled.

Diagnosis is usually confirmed by echocardiography.

A damaged valve usually requires surgical repair or replacement. Several repair procedures are available depending on the type of defect. Valve replacement is often preferred as a long-term solution, especially for aortic stenosis, in which the valve tends to become narrow again after a repair procedure. 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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Ventricular septal defect, or VSD, refers to an OPENING in the interventricular septum that separates the two ventricles of 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.
Pathology: A VSD allows abnormal blood flow between the two ventricles. The NET flow of blood, called a SHUNT, is usually from LEFT to RIGHT due to significantly HIGHER blood pressure in the LEFT side of the heart. This is because the left side has to pump blood all over the body while the right side only needs to send it to the lungs. If the defect is small, the shunt is negligible and does not result in any symptoms. A large defect, on the other hand, may OVERLOAD the right side of the heart, causing it to FAIL. Heart failure symptoms usually appear during the first few weeks of life and include: fatigue, shortness of breath, difficulty feeding and poor growth.
Without treatment, other complications may also occur. As the right ventricle continuously pumps MORE blood to the lungs, the entire pulmonary vasculature may be overloaded and pulmonary Hypertension may result. To OVERCOME the high pressure in the lungs, the right ventricle has to generate even HIGHER pressure, which eventually becomes GREATER than that of the LEFT ventricle. This REVERSES the direction of the shunt, causing oxygen-POOR blood to flow from RIGHT to LEFT and be sent to all tissues of the body. The resulting oxygen DEPRIVATION may be seen as a BLUISH skin color, known as CYANOSIS.
A VSD can happen alone or in combination with other congenital defects in conditions such as Down syndrome, or tetralogy of Fallot. The cause is unknown but likely to involve both genetic and environmental factors.
The turbulence of abnormal blood flow in VSD produces heart murmurs, which can be heard using a stethoscope. Diagnosis is confirmed by echocardiography.
VSD is the most common congenital heart defect in infants, but the defect is small in most cases. Small defects usually close on their own in early childhood and no treatment is needed. Large defects that produce symptoms usually require surgical closure in the first year of life.