Ventricular Fibrillation: Shock Me Baby!

Cardiac muscle contracts in a predictable, regular pattern, which allows it to generate enough force to eject blood to the body. However, in ventricular fibrillation the heart muscle “quivers” in a rapid, irregular, and unsynchronized manner. These feeble contractions are not strong, nor coordinated enough to eject blood from the heart. As a result, cardiac output drops and the body quickly goes into cardiogenic shock.

There are numerous causes of ventricular fibrillation. The most common cause of abnormal electrical activity occurs in diseased heart tissue that has lost its normal architecture. For example, muscle damage from heart attacks or disorganized heart structures seen in cardiomyopathies can serve as abnormal areas of electrical impulse formation; these irritated areas can predispose patients to develop ventricular fibrillation.

Other causes of ventricular fibrillation include electrolyte abnormalities. For example, hyperkalemia (ie: an elevated blood potassium level) can depolarize heart muscle cells and make them more likely to "fire" an action potential. In general, any electrolyte disturbance that makes the resting potential of the cardiac muscle fiber more positive (ie: more depolarized) can cause abnormal electrical impulse formation; these abnormal impulses can degenerate into ventricular fibrillation.

Signs and Symptoms

Ventricular fibrillation is a highly fatal rhythm because the heart fails to pump blood, and more specifically oxygen, to the bodies’ organs. As a result, every organ system in the body, including the heart becomes ischemic and dies.

The rapid decline in blood flow to the brain causes people to lose consciousness. If treatment is not sought quickly the patient will have anoxic brain injury (ie: a massive global stroke), which will lead to brain death.


Ventricular fibrillation is diagnosed by looking at an electrocardiogram (ECG). The ECG will show disorganized and chaotic electrical activity.

Ventricular fibrillation ECG
ECG of ventricular fibrillation


Treatment of ventricular fibrillation is with immediate un-synchronized electrical cardioversion (ie: the paddle "thingies" they use to shock someone’s heart). The goal of shocking the heart with electricity is to reset (ie: repolarize) all the cardiac muscle fibers at the same time. From there the sinus node should theoretically take over, and reset the heart back into a normal rhythm.

If a patient survives their first episode of ventricular fibrillation they often have a cardiac defibrillator implanted. Implantable cardiac defibrillators shock the heart when they detect an abnormal rhythm.


Ventricular fibrillation is a rapidly fatal, disorganized, and inefficient “quivering” of heart muscle. It causes cardiogenic shock and organ death if left untreated. It is most commonly due to underlying heart disease seen in people with coronary artery disease, previous heart attacks, and cardiomyopathies, although other causes exist. Treatment is with immediate electrical cardioversion (ie: “shocking” the heart).

Related Articles

References and Resources

  • Marcus GM, Scheinman MM, Keung E. The year in clinical cardiac electrophysiology. J Am Coll Cardiol. 2010 Aug 17;56(8):667-76.
  • Dosdall DJ, Fast VG, Ideker RE. Mechanisms of defibrillation. Annu Rev Biomed Eng. 2010 Aug 15;12:233-58.
  • Braunwald E. Hypertrophic cardiomyopathy: the early years. J Cardiovasc Transl Res. 2009 Dec;2(4):341-8. Epub 2009 Oct 7.
  • Rea TD, Page RL. Community approaches to improve resuscitation after out-of-hospital sudden cardiac arrest. Circulation. 2010 Mar 9;121(9):1134-40.
  • Schaer B, Kühne M, Koller MT, et al. Therapy with an implantable cardioverter defibrillator (ICD) in patients with coronary artery disease and dilated cardiomyopathy: benefits and disadvantages. Swiss Med Wkly. 2009 Nov 14;139(45-46):647-53.
  • Callans DJ. Out-of-hospital cardiac arrest–the solution is shocking. N Engl J Med. 2004 Aug 12;351(7):632-4.
  • Lilly LS, et al. Pathophysiology of Heart Disease: An Introduction to Cardiovascular Medicine. Seventh Edition. Lippincott Williams and Wilkins, 2020.

Atherosclerosis: Gruel and Hardening


What does the term atherosclerosis mean? If we break the term down into its components, "athero" is Greek for a gruel or paste, and sclerosis means hardening. This is precisely what is happening in the blood vessels of people with this disease; a paste-like material hardens to form a plaque. The specifics of how that paste-like material forms are much more complicated.

The paste-like material is composed of several different elements. The first, and perhaps most important element, is low density lipoprotein (ie: LDL). LDL, or the “bad cholesterol” as it is commonly referred, is a mixture of lipid (ie: fat and cholesterol) and protein. These molecules are highly atherogenic, which means they accelerate the plaque forming process.

How does LDL lead to a plaque? The first step involves disruption of part of the blood vessel known as the intima. Blood vessels have three layers: intima, media, and adventitia. The intimal layer is the portion of the vessel directly in contact with blood flow. It is composed of endothelial cells, which have numerous important functions. The medial layer is smooth muscle that controls the diameter of the blood vessel; the adventitial layer is a connective tissue coating (ie: similar to the plastic coating surrounding an electrical wire) that anchors the vessel to adjacent structures in the body.

Blood Vessel with Plaque

When the intimal layer is disrupted, LDL particles floating in the blood get trapped in the vessel wall. Once trapped, they start an inflammatory reaction. White blood cells (a key component of inflammation) known as macrophages are recruited to the vessel’s walland gobble up the intruding LDL particles. At this point the macrophages are known as “foam cells”. Foam cells get enmeshed in a web of scar and smooth muscle. All of this together becomes a "plaque".


The symptoms of atherosclerosis depend on how large the plaques are, and where they are located. The three common symptoms associated with atherosclerosis:

(1) Angina (chest pain) – read about acute coronary syndromes
(2) Transient ischemic attacks (TIA)
(3) Vascular claudication

Angina refers to chest pain that occurs with exercise (by exercise we refer to any activity above normal daily activity). The pain is a result of atherosclerotic plaque blocking the increased blood flow needed to supply the heart during strenuous activities. In essence, what is happening is that the heart is "starving" for oxygen, which results in chest pain. When the patient stops exercising the heart no longer needs as much oxygen; the amount of blood flow is again adequate, and the chest pain ceases. Angina is a harbinger of a potential heart attack.

Transient ischemic attacks are due to atherosclerosis in the blood vessels leading to the brain. The temporary decrease in blood flow to the brain caused by the blockages can result in stroke-like symptoms that resolve within twenty-four hours. TIAs are harbingers of potential strokes in the future.

If atherosclerosis develops in the vessels going to the lower extremities, vascular claudication occurs. Claudication refers to pain in the legs that worsens while walking (or running). Similar to angina, the pain is due to blocked blood flow to the legs secondary to the plaques. A condition known as "Leriche’s syndrome" occurs when there is decreased blood flow to not only the legs, but also the vessels leading to the penis. This causes not only lower extremity claudication, but also impotence.

The complications of atherosclerosis stem from the symptoms. They include myocardial infarction (eg: heart attack), of which angina is a warning sign; as well as cerebrovascular accidents (eg: strokes), of which transient ischemic attacks serve as a warning. Worsening disease in the lower extremities can lead to gangrenous limbs and the need for potential amputation.

(1) Myocardial infarction (eg: heart attack)
(2) Cerebrovascular accidents (eg: stroke)
(3) Worsening lower extremity disease -> amputations


Diagnosis of atherosclerotic disease depends on the location of symptoms. If anginal chest pain is the main symptom several different studies can be done. One such study is the “stress test”. There are several different permutations of the stress test.

All of them include two components. The first is a method of "visualizing" the heart. This can be done by ECG, echocardiography (ie: ultrasound of the heart), or nuclear/radioactive scans. The second component involves "stressing" the heart. This is most commonly done by exercising on a treadmill, but medications like dobutamine can also be used if the patient cannot exercise for whatever reason.

Stress Testing
Methods for visualizing the heart’s function – Electrocardiogram (ECG)
– Echocardiogram (echo)
– Nuclear studies
Methods for stressing the heart – Exercise (ie: treadmill)
– Medications (ie: dobutamine, persantine, etc.)

If the stress test is positive, or there is a high index of suspicion for atherosclerosis involving the coronary arteries, the next test performed is an angiogram. This involves injecting radio-opaque contrast material into the coronary arteries through a tiny catheter. The coronary arteries can then be visualized using x-rays. Areas where there is less contrast in the vessel indicate coronary atherosclerotic disease. The image below is an example of narrowing in the circumflex artery (indicated by the arrow).

Angiogram Circumflex Atherosclerosis

If the involved areas are the carotid arteries, a test known as "carotid artery duplex scanning" can be done. This involves using ultrasound to detect the amount of blood flow present in the vessel(s). Decreased rates are often attributable to atherosclerotic disease.

Finally, if disease is thought to be present in the lower extremities, a test known as the arterial brachial-ankle index (ABI) is obtained. This test involves taking the blood pressure in the arm and the leg and comparing the results. Blood pressure should be about equal in the upper and lower extremities resulting in a brachial to ankle ratio of 1.0. However, if there is atherosclerotic diseases in the lower extremities the ABI decreases to less than 1.0.

Location of suspected atherosclerotic disease: Initial test performed:
– Coronary arteries – Stress test
– Carotid arteries – Duplex scanning
– Arteries of lower extremities – Ankle-Brachial index (ABI)

Occasionally cardiologists or vascular surgeons will recommend a more invasive procedure known as a "catheterization". In this procedure a small catheter is threaded from a blood vessel in the groin to the area of interest (ie: the heart, carotids, vessels of the lower extremities). From there radio-opaque dye is injected. A fancy X-ray machine can then pick up locations of significant plaque formation.


Treatment is designed to prevent further plaque formation. Since LDL plays a crucial role in this process, it is a target of medical therapy, but in order to understand treatment we have to first understand how cholesterol gets into the body. Cholesterol is either (a) absorbed by the gut from your diet, or (b) produced naturally by your body through a series of biosynthetic reactions.

The first interventions for decreasing cholesterol in the body are, you guessed it, dietary modifications. By decreasing the amount of cholesterol in the diet it is possible to decrease the amount of cholesterol, either free or in the form of LDL, that is in the blood stream. There is also some evidence that replacing saturated fats with polyunsaturated fats (ie: α-linolenic acid, an ω-3 fatty acid) can decrease atherosclerotic plaque formation.

Unfortunately, diet and exercise are not always enough to decrease blood cholesterol levels to acceptable limits. Several medications have been developed, and as one could imagine, they target either cholesterol in the gut, or the biosynthetic machinery that produces cholesterol naturally.

There are several types of drugs that bind cholesterol in the gut to keep it from being absorbed. They are referred to as "bile acid binding medications" or "bile acid sequestrants". It is important to realize that bile acids, which are secreted by the liver and gallbladder, are rich in cholesterol.

Under normal circumstances they are reabsorbed by the gut and recycled back into the bile pathway. By inhibiting their re-absorption, cholesterol from the blood stream is recruited by the liver to replace the bile acids that were previously being recycled. The ultimate effect is that these drugs decrease the amount of cholesterol in the blood stream. There are three common medications in this category: colesevelam, cholestyramine, and colestipol.

Another medication, ezetimibe, directly binds to free cholesterol in the gut. As a result, less cholesterol is delivered to the liver. To compensate, the liver increases its ability to absorb LDL and other forms of cholesterol from the blood resulting in decreased plasma levels.


(1) diet and
(2) bile acid
(3) statins
(4) niacin
(5) fibrates
Perhaps the most widely used class of medications used to treat atherosclerosis are known as “statins.” Statins such as atorvastatin and pravastatin inhibit an enzyme (ie: HMG-CoA reductase) that normally produces cholesterol in the body. These medications dramatically reduce the risk of stroke and heart attack in patients with atherosclerotic disease.

A vitamin, niacin (ie: vitamin B3), can also lead to favorable effects on the lipid profile of the blood. It increases "good" cholesterol (ie: HDL). It is believed to perform these feats by increasing the activity of an enzyme, lipoprotein lipase, which normally breaks down VLDL particles (a precursor of LDL).

A final category of medications known as the "fibrates" decrease fat content in the blood. They do not necessarily affect LDL levels significantly, but they do decrease another atherosclerotic forming fat type known as triglycerides. The two common fibrates in use today are gemfibrozil and fenofibrate.


Atherosclerosis is due to LDL trapping in blood vessel walls. This trapping results in inflammation and the formation of a fibromuscular plaque. Symptoms include angina (ie: chest pain), lower extremity claudication, and transient ischemic attacks. Diagnosis is made by stress testing, carotid ultrasound, and ankle-brachial index; more invasive testing with groin catheters can be performed as well. Treatment is based on decreasing cholesterol absorption from the gut, or decreasing the bodies natural mechanism for creating cholesterol.

References and Resources

  • Negi S, Nambi V. Coronary heart disease risk stratification: pitfalls and possibilities. Methodist Debakey Cardiovasc J. 2010 Dec;6(4):26-32.
  • Amarenco P, Lavallée PC, Labreuche J, et al. Prevalence of Coronary Atherosclerosis in Patients With Cerebral Infarction. Stroke. 2010 Nov 18. [Epub ahead of print].
  • Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. Seventh Edition. Philadelphia: Elsevier Saunders, 2004.
  • Lilly LS, et al. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Fourth Edition. Lippincott Williams and Wilkins, 2006.
  • Flynn JA. Oxford American Handbook of Clinical Medicine (Oxford American Handbooks of Medicine). First Edition. Oxford University Press, 2007.

Atrioventricular Heart Block: PR, QRS, Mobitz

Heart block, also known as atrioventricular (AV) conduction system block, refers to decreased conduction of electrical impulses through the heart. This decreased conduction occurs at the atrioventricular node of the heart’s conduction system. Heart block occurs in three flavors: type 1, type 2, and type 3. Each type has different causes and different treatments.

Pathology and Types

In type 1 AV block the PR interval on an ECG is longer than normal (> 200 msec), but every QRS complex has a preceding P-wave indicating that the electrical impulses from the atria (ie: the top chambers in the heart) are "making" it through the AV node to the ventricles. In type 1 block, the AV nodal conduction is slowed compared to normal "healthy" individuals, but the impulses are still able to get all the way through the conduction system of the heart.

Type 1 AV node block = PR interval > 200 msec, no missed beats.

Type 2 heart block occurs in 2 flavors: Mobitz type 1 and type 2. In Mobitz type 1 the amount of delay between the P-wave and QRS complex (ie: the PR interval) gradually increases until a beat is dropped. It is caused by impaired conduction in the AV node. Mobitz type 2 occurs when the PR interval remains stable, and then out of the blue a missed beat occurs; this is caused most commonly by slowed conduction through the bundle of His or bundle branches of the heart’s conduction system.

Mobitz type 1 = increasing PR interval until dropped beat occurs (image below). Mobitz type 1 is also referred to as "Wenckeback" block.

Mobitz Type 1

Mobitz type 2 = PR interval remains the same until a dropped beat occurs (image below). Mobitz type 2 is also referred to as "Hay" block.

Mobitz Type 2

Finally, type 3 AV nodal block occurs when the atria and ventricles of the heart beat independently of one other. The most common causes of 3rd degree block are severe diseases of the AV nodal system due to age, previous heart attack, drug and medication toxicity (ie: digitalis), and untreated Lyme disease. The atria generally beat at a faster rate than the ventricles. In other words, the ECG will show more P-waves than QRS complexes. The QRS complexes may be narrow or wide depending on where in the conduction system the escape rhythm originates.

Type 3 heart block = atria (p-waves) and ventricles (QRS) beat independently of each other; no impulses from the atria make it to the ventricles (image below).

AV nodal block type 3


The symptoms of heart block depend on how slow the rate becomes. Patients with type 1 block rarely become symptomatic because the atria are still setting the pace of the entire hearts rhythm. However, in Mobitz type 2 and type 3 block the heart rate can become very slow. When this occurs symptoms such as syncope (ie: fainting), extreme fatigue, shortness of breath, and dizziness can occur. These symptoms occur because the heart is not pumping blood fast enough to keep up with the body’s demand; the result is a decrease in cardiac output.


Diagnosis of heart block can be made by looking at the characteristic findings on ECG.


Treatment of AV nodal dysfunction is dependent on the type. Most patients with type 1 heart block do not need treatment. Type 1 heart block can be considered a "healthy" variant of AV nodal conduction, which is slower than most people in the population. The only instance where type 1 block may need further work up is in elderly patients who have other signs or symptoms of coronary artery disease.

Type Treatment
Type 1

Usually none, look for causes such as coronary artery disease in elderly patients

Type 2 – Mobitz type 1

Usually none, but pacemaker if symptomatic. Also discontinue any drugs that slow AV node.
Type 2 – Mobitz type 2 Pacemaker
Type 3 Pacemaker

Mobitz type 1 (ie: one of the 2 subgroups of type 2 heart block) also generally requires no treatment. If patients are symptomatic pacemaker insertion may be considered. Mobitz type 2 is more worrisome because it often progresses to 3rd degree heart block. In these patients, pacemakers are often inserted to ensure that the heart beats at a pre-defined and safe rate.

Type 3 heart block is almost always controlled with pacemaker insertion. The reason is that the ventricles often beat at a rate that is too slow for normal daily activity. A pacemaker will keep the heart beating at a pre-defined rate to ensure that symptoms do not develop.


Heart block (aka: atrioventricular block) occurs when impulses travel too slowly, or not at all through the AV node. There are different types depending on how severe the block is. In type 1 AV block impulses are slowed, but cause no conduction block. In type 2 missed beats can occur, and in type 3 the atria beat independently of the ventricles indicating complete conduction block. Symptoms depend on the severity of block but can include fainting, shortness of breath, dizziness, and fatigue. Diagnosis is made by ECG. Treatment is dependent on the type of block, but can include placement of a pacemaker.

References and Resources

Hypertension: Understanding and Managing High Blood Pressure

The pathology of essential hypertension is not well understood. However, there are numerous theories, each with supporting evidence.

Genetic causes are supported by the fact that children of hypertensive parents have an increased risk of developing the disease. However, specific known genetic mutations are not common. When mutations are responsible for essential hypertension they often involve the sodium and chloride channels in kidney cells, or mutations in the genes responsible for producing the proteins of the renin-angiotensin-aldosterone system. Sodium, renin, angiotensin, and other molecules play a vital role in blood pressure. In some hypertensive patients these systems are abnormal and can lead to elevated blood pressure.

Some patients with essential hypertension appear to be “salt sensitive”. Salt, or more specifically sodium, appears to play a role in the development of hypertension. Some patients likely have a genetic predisposition to retain sodium. Excess sodium enters the blood stream where it exerts an osmotic pull on water in adjacent tissues. Fluid from body tissues is "sucked" into the blood stream resulting in increased blood volumes. The expanded blood volume increases the pressure within the blood vessel causing hypertension. Although salt plays a role in hypertension, new research has shown its importance may not be as clear as once thought.

There are other known causes of hypertension, but they constitute a relatively small proportion of cases. They are discussed in separate articles.

Signs and Symptoms

Essential hypertension in its earliest stages does not cause any signs or symptoms. Many people do not know they have high blood pressure. However, if left untreated hypertension can cause serious long term consequences.

One such consequence is an increase in the risk of cardiovascular disease. The risk of cardiovascular disease doubles with each 20/10 mmHg increase in blood pressure beyond a "baseline" of 115/75 mmHg! After years of pumping at elevated pressures the heart undergoes physical changes. Like any good muscle, it becomes larger because it is having to pump harder than normal. The result is a process known as concentric hypertrophy. The added muscle mass of the heart results in increased oxygen demand and the potential for heart attacks and heart failure.

Overall, nearly a third of heart attacks are attributable to high blood pressure. In addition, the risk of stroke is also dramatically higher in untreated hypertensive patients. The small blood vessels in the kidney and retina can also be damaged by years of high blood pressure resulting in kidney failure (hypertensive nephropathy) and blindness (hypertensive retinopathy).


The diagnostic parameters of hypertension are constantly shifting. Currently the diagnosis can be made if a patient presents with a severely elevated blood pressure (systolic blood pressure > 200 and/or a diastolic blood pressure > 120) and/or signs or symptoms referable to the elevated blood pressure.

Severity Classification:
(1) Pre-hypertensive:
(2) Grade 1:
(3) Grade 2:
In patients with less severe elevations, it is generally recommended that the blood pressure be measured several times over a period of multiple weeks. If the average of these readings is a systolic blood pressure of 140 or greater, or a diastolic blood pressure of 90 or greater than the diagnosis can be made. If the blood pressue stays between 120 and 130 systolic, and 80 to 90 diastolic the diagnosis of "pre-hypertension" is made meaning the patient is at risk of becoming hypertensive.

Some patients may have "white coat" hypertension simply by being in a doctor’s office (and the anxiety that this can provoke! Gosh, I hate going to the doctor’s office!). If this is the case the patient should be instructed to take their blood pressure at home and keep a log of the results.


Treatment of hypertension consists of lifestyle modifications and/or using medications from several different pharmacologic categories. These medications may be used alone, or in combination, depending on each individual patient’s needs.

Patients who are pre-hypertensive or have stage 1 hypertension should be started on “lifestyle” modification therapy for at least 6 months prior to starting medicines (assuming there are no other health issues like diabetes or coronary artery disease). Lifestyle therapy consists of increasing aerobic exercise, as well as adhering to the “DASH” diet. DASH stands for "dietary approaches to stop hypertension" and consists of eating fruits, vegetables, low-fat dairy, whole grains, poultry and fish while reducing (or eliminating) red meat and sugars. This intervention alone can decrease systolic pressures over 10 mmHg and diastolic pressures over 5 mmHg.

Sometimes diet and exercise aren’t enough so we may have to resort to medications to control blood pressure. The first category of medications are known as diuretics, most commonly of the thiazide class. Thiazide diuretics work by inhibiting the re-absorption of sodium at the distal convoluted tubule of the kidney. Less sodium means less circulating blood volume, and therefore decreased blood pressure. Hydrochlorothiazide is a commonly used thiazide diuretic.

The second category of medications is known as β-blockers. β-blockers lower blood pressure by slowing the heart rate and indirectly lowering the amount of angiotensin II (angiotensin II is a potent natural blood vessel constrictor produced by the body). β-blockers reduce renin synthesis by specialized cells in the kidney.

A third category of medications known as angiotensin converting enzyme inhibitors (ACEIs) interfere with the formation of angiotensin II. ACEIs inhibit an enzyme present in the lung, which converts angiotensin I into the more potent vasoconstrictor angiotensin II. Interestingly, ACEIs also increase the level of bradykinin; this molecule causes blood vessels to dilate, which helps to further lower pressure.

There are also medications called direct angiotensin receptor blockers (ARBs), which inhibit the actions of angiotensin II. They do this by blocking angiotensin IIs ability to bind to its normal receptor sites.

Some medications, the calcium channel blockers (CCBs), lower blood pressure by inhibiting the contraction of smooth muscle cells that line the blood vessel walls. A specific subcategory of calcium channel blockers known as dihydropyridines block calcium from flowing into vascular smooth muscle cells. This results in decreased contraction of the muscle surrounding the vessel. As a result the vessel remains dilated, which lowers pressure.


The pathology of essential hypertension is not well understood. Several theories have been postulated, but it is likely a combination of genetic predispositions that result in this type of high blood pressure. Years of elevated blood pressure lead to cardiovascular disease including heart failure, heart attacks, and stroke, as well as damage to the kidneys and retinas. Treatment is with lifestyle modifications, diuretics, β-blockers, calcium channel blockers, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers.

References and Resources

The Basics of Myocardial Infarction (Heart Attack)


An acute coronary syndrome refers to any process where heart muscle receives less oxygen than it needs. It encompasses three separate, but overlapping pathologies: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). Therefore, acute coronary syndrome represents a continuum of severity, which if severe enough, can lead to irreversible cardiac muscle death.

NSTEMI and STEMI are distinguished from unstable angina by the presence of heart muscle death. NSTEMI occurs when the inner most portion of the heart wall dies, and is generally due to a partially occlusive thrombus (blood clot) in one of the coronary arteries or their branches. An NSTEMI can, in some ways, be thought of as a "partial" heart attack.

On the other hand, STEMI occurs when a coronary blood vessel becomes fully blocked by thrombus. If untreated, the result is transmural (full wall) death of the heart muscle that the occluded vessel serves. A STEMI, in non-technical terms, can be thought of as a "full blown" heart attack.

Coronary thrombi (blood clots) form after rupture of an atherosclerotic plaque. The exposed plaque surface is highly thrombogenic, which means that blood clots form easily on it. The exposed surface causes platelet and coagulation cascade activation, which results in a thrombus that can occlude the entire vessel diameter resulting in decreased, or in the worst case scenario, no blood flow to the heart muscle. This is the basis of a "heart attack" or myocardial "infarction".

Signs, Symptoms, and Complications

Symptoms of acute coronary syndrome are consistent with anginal chest pain. If angina occurs at rest, or with less activity than it normally does, this is referred to as "unstable" angina, and signifies increased narrowing (ie: decreased diameter) of a coronary blood vessel.

Substernal “crushing” chest pain is the classic description of a heart attack (either NSTEMI or STEMI) and is usually accompanied by diaphoresis (ie: excessive sweating). In addition, nausea and vomiting can also occur. Pain from the chest can sometimes radiate into the arm (usually the left arm) or the jaw. Numbness and tingling in the arm and jaw are also common features. Shortness of breath is another symptom of heart attack, and is usually due to the acute back up of blood into the vessels of the lung, which leads to pulmonary edema.

Complications of infarction are due to mechanical changes in the heart. Damage of the electrical conduction system can lead to arrhythmias (abnormal heart rhythms), which are common in the first few days after an infarction.

If enough heart muscle is destroyed cardiogenic shock can occur. This happens when the heart is no longer able to pump enough blood to the rest of the body. Decreased blood flow to the other organs can lead to ischemia of these organs and multi-organ failure.

Myocardial infarction
and "heart attack"
refer to the same thing –
death of heart muscle.
Other complications are a result of the scarring process that occurs hours to days after the initial heart attack. Dead heart muscle is slowly replaced by scar tissue in a process called fibrosis. During the scarring process there are periods in which the scar and adjacent tissue is weaker than normal. This weakness can cause various complications such as rupture of the heart wall, interventricular septum rupture, or papillary muscle rupture. All of these complications occur roughly 5 to 10 days after the initial heart attack, and are due to structural instability in the newly formed fibrotic area(s). In addition, aneurysm (ie: a ballooning out of the heart) formation may occur several weeks after myocardial infarction.

Finally pericarditis, or inflammation of the sack that the heart sits in, can also occur. A condition known as Dressler’s syndrome is pericarditis that occurs after a heart attack. It usually occurs two weeks to several months after the infarction.

Long term complications of myocardial infarction include heart failure. Ultimately the damaged heart is unable to beat as well as it did in the past. This leads to the back up of blood and fluid in the lungs causing shortness of breath, amongst other symptoms.


Diagnostic studies can confirm NSTEMI or STEMI. An electrocardiogram (ECG) is the gold standard. It will show ST segment depression in NSTEMI, and ST segment elevation in STEMI. Q-waves are also seen, but may represent previous infarction.

Image (left) – An ECG of someone with a STEMI would look like the image to the left. Note how the ST segment is elevated relative to the baseline.

Blood tests can also show elevations in specific proteins released by the dying heart muscle. Cardiac troponin I is one of these markers, and is the most specific for heart muscle injury. It begins to rise 4 hours after the initial thrombus formation and stays elevated for 7-10 days. CK-MB (creatine kinase myocardial band) is another protein released by damaged heart tissue; it is useful in that it is cleared relatively quickly compared to troponin; this is useful in that it can aid in detection of early re-infarction.

Image (right) – An ECG of someone with an NSTEMI. Notice how the NSTEMI ECGST segment is depressed below baseline.


The main goals of treatment are to restore blood flow, and to decrease the amount of work the heart is doing. Both of these measures help provide oxygen to the dying heart muscle. One of the main problems in myocardial infarction is that the heart is working harder than usual, and is doing so under decreased oxygen delivery (ie: decreased blood flow). This deadly combination increases the rate of heart muscle death. Therefore, treatment is designed to increase oxygen flow (ie: by restoring blood flow), or by decreasing the work of the heart, and therefore the amount of oxygen the heart needs to survive.

Treatment of any patient with suspected acute coronary syndrome should include pain control. For example, morphine controls the pain associated with heart attacks, and this indirectly lowers the heart rate. Lowering the heart rate decreases the amount of work the heart muscle is doing, and therefore decreases the amount of oxygen that must be delivered for muscle survival.

In addition, nitroglycerin is given because it decreases preload. Preload refers to the amount of blood inside the left ventricle just before contraction of the heart. A larger preload means that the heart must work harder because, in essence, it is pumping more blood per beat. Nitroglycerin dilates blood vessels (mostly veins) in the body and effectively decreases the amount of blood within the heart itself. Less blood to pump, equals less work the heart must do.

Oxygen therapy should also be started to help improve blood oxygen levels. This will ensure that any blood getting to the myocardium will have as much oxygen as possible.

There are several methods for restoring blood flow. The preferred method is through percutaneous coronary interventions (PCI). In this procedure a small catheter is inserted into blood vessels in the groin and threaded up towards the heart; once in the blood vessels of the heart the catheter can be used to mechanically remove any blockage. This is known as "angioplasty" or "thrombectomy". Percutaneous coronary intervention should occur in a reasonable amount of time. There is debate about the exact timing and depends on the type of acute coronary syndrome (ie: STEMI vs NSTEMI).

If the hospital does not have the capacity to do PCI then medications can be used to "break up" the blood clot/thrombus. All patients with suspected infarction should receive an aspirin. Aspirin works by inhibiting platelet plug formation. This helps slow the rate of thrombus formation. First line medications for restoring flow in myocardial infarction are intravenous unfractionated heparin or subcutaneous enoxaparin. Fibrinolytics like tissue plasminogen activator (tPa), reteplase, streptokinase, and urokinase are also sometimes used to try and restore blood flow.

Finally, revascularization operations (ie: coronary artery bypass grafting) may also be necessary depending on the level of disease in the other coronary vessels.


Acute coronary syndrome refers to a continuum of coronary blood vessel blockage. On the least extreme end is unstable angina; on the most extreme (ie: most dangerous) end is ST elevation myocardial infarction. Symptoms are usually crushing chest pain that radiates to the jaw and arm, but may also include nausea, vomiting, dizziness/fainting, and sweating. Diagnosis is based of ECG and blood tests for heart muscle damage. Treatment is aimed at increasing blood flow, and therefore oxygen delivery, to the heart muscle. This is done by decreasing the amount of work the heart is doing, increasing the amount of oxygen present in blood, and breaking up the blood clot via mechanical or medical means.

References and Resources

  • Husted SE, Nielsen HK. Unfractionated heparin and low molecular weight heparin for acute coronary syndromes–assessment of a Cochrane review. Ugeskr Laeger. 2010 Sep 13;172(37):2522-6.
  • Lepor NE, McCullough PA. Differential diagnosis and overlap of acute chest discomfort and dyspnea in the emergency department. Rev Cardiovasc Med. 2010;11 Suppl 2:S13-23.
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  • Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. Seventh Edition. Philadelphia: Elsevier Saunders, 2004.
  • >
  • Lilly LS, et al. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Fourth Edition. Lippincott Williams and Wilkins, 2006.
  • Flynn JA. Oxford American Handbook of Clinical Medicine (Oxford American Handbooks of Medicine). First Edition. Oxford University Press, 2007.
  • Ferguson JJ, Califf RM, Antman EM, et al. Enoxaparin vs unfractionated heparin in high-risk patients with non-ST-segment elevation acute coronary syndromes managed with an intended early invasive strategy: primary results of the SYNERGY randomized trial. JAMA. 2004 Jul 7;292(1):45-54.