Stomach Blood supply

Nerve supply to anterior abdominal wall

Blood and lymph supply to skin and anterior abdominal wall

inferior vena cava tributaries

abdominal aorta branches

phenytoin

Phenytoin is used to prevent and control seizures (also called an anticonvulsant or antiepileptic drug). It works by reducing the spread of seizure activity in the brain.
OTHER USES: This section contains uses of this drug that are not listed in the approved professional labeling for the drug but that may be prescribed by your health care professional. Use this drug for a condition that is listed in this section only if it has been so prescribed by your health care professional.
This drug may also be used to treat certain types of irregular heartbeats.
How to use phenytoin oralRead the Medication Guide provided by your pharmacist before you start taking phenytoin and each time you get a refill. If you have any questions, ask your doctor or pharmacist.
Shake this medication well before each dose. Take this medication by mouth usually 2 or 3 times a day, or as directed by your doctor. This product is not recommended for use once a day. You may take it with food if stomach upset occurs.
Carefully measure the dose using a special measuring device/spoon/syringe. Do not use a household spoon because you may not get the correct dose.
Use this medication regularly in order to get the most benefit from it. It is important to take all doses on time to keep the amount of medicine in your body at a constant level. Remember to use it at the same times each day. Dosage is based on your medical condition and response to therapy.
Products that contain calcium (e.g., antacids, calcium supplements) and nutritional tube-feeding (enteral) products may decrease the absorption of phenytoin. Do not take these products at the same time as your phenytoin dose. Separate liquid nutritional products at least 1 hour before and 1 hour after your phenytoin dose, or as directed by your doctor.
Do not stop taking this medication without consulting your doctor. Seizures may become worse when the drug is suddenly stopped. Your dose may need to be gradually decreased.
Inform your doctor if your condition does not improve or worsens.

Heart Attacks and Heart Disease

Heart Attacks and Heart Disease

More than a million Americans have heart attacks each year. A heart attack, or myocardial infarction (MI), is permanent damage to the heart muscle. "Myo" means muscle, "cardial" refers to the heart, and "infarction" means death of tissue due to lack of blood supply.

What Happens During a Heart Attack?

The heart muscle requires a constant supply of oxygen-rich blood to nourish it. The coronary arteries provide the heart with this critical blood supply. If you have coronary artery disease, those arteries become narrow and blood cannot flow as well as they should. Fatty matter, calcium, proteins, and inflammatory cells build up within the arteries to form plaques of different sizes. The plaque deposits are hard on the outside and soft and mushy on the inside.

When the plaque is hard, the outer shell cracks (plaque rupture), platelets (disc-shaped particles in the blood that aid clotting) come to the area, and blood clotsform around the plaque. If a blood clot totally blocks the artery, the heart muscle becomes "starved" for oxygen. Within a short time, death of heart muscle cells occurs, causing permanent damage. This is a heart attack.

While it is unusual, a heart attack can also be caused by a spasm of a coronary artery. During a coronary spasm, the coronary arteries restrict or spasm on and off, reducing blood supply to the heart muscle (ischemia). It may occur at rest, and can even occur in people without significant coronary artery disease.

Each coronary artery supplies blood to a region of heart muscle. The amount of damage to the heart muscle depends on the size of the area supplied by the blocked artery and the time between injury and treatment.

Healing of the heart muscle begins soon after a heart attack and takes about eight weeks. Just like a skin wound, the heart's wound heals and a scar will form in the damaged area. But, the new scar tissue does not contract. So, the heart's pumping ability is lessened after a heart attack. The amount of lost pumping ability depends on the size and location of the scar.

Heart Attack Symptoms

Symptoms of a heart attack include:

• Discomfort, pressure, heaviness, or pain in the chest, arm, or below the breastbone
• Discomfort radiating to the back, jaw, throat, or arm
• Fullness, indigestion, or choking feeling (may feel like heartburn)
• Sweating, nausea, vomiting, or dizziness
• Extreme weakness, anxiety, or shortness of breath
• Rapid or irregular heartbeats

During a heart attack, symptoms last 30 minutes or longer and are not relieved by rest or nitroglycerin under the tongue.

Some people have a heart attack without having any symptoms (a "silent" myocardial infarction). A silent MI can occur in anyone, but it is more common among people with diabetes.

What Do I Do if I Have a Heart Attack?

After a heart attack, quick treatment to open the blocked artery is essential to lessen the amount of damage. At the first signs of a heart attack, call for emergency treatment (usually 911). The best time to treat a heart attack is within one to two hours of the first onset of symptoms. Waiting longer increases the damage to your heart and reduces your chance of survival.

Keep in mind that chest discomfort can be described in many ways. It can occur in the chest or in the arms, back, or jaw. If you have symptoms, take notice. These are your heart disease warning signs. Seek medical care immediately.

How Is a Heart Attack Diagnosed?

To diagnose a heart attack, an emergency care team will ask you about your symptoms and begin to evaluate you. The diagnosis of the heart attack is based on your symptoms and test results. The goal of treatment is to treat you quickly and limit heart muscle damage.

Tests to Diagnose a Heart Attack

• ECG. The ECG (also known as EKG or electrocardiogram) can tell how much damage has occurred to your heart muscle and where it has occurred. In addition, your heart rate and rhythm can be monitored.
• Blood tests. Blood may be drawn to measure levels of cardiac enzymes that indicate heart muscle damage. These enzymes are normally found inside the cells of your heart and are needed for their function. When your heart muscle cells are injured, their contents -- including the enzymes -- are released into your bloodstream. By measuring the levels of these enzymes, the doctor can determine the size of the heart attack and approximately when the heart attack started. Troponin levels will also be measured. Troponins are proteins found inside of heart cells that are released when they are damaged by the lack of blood supply to the heart. Detecting troponin in the blood may indicate a heart attack.
• Echocardiography. Echocardiography is an imaging test that can be used during and after a heart attack to learn how the heart is pumping and what areas are not pumping normally. The "echo" can also tell if any structures of the heart (valves, septum, etc.) have been injured during the heart attack.
• Cardiac catheterization. Cardiac catheterization, also called cardiac cath, may be used during the first hours of a heart attack if medications are not relieving the ischemia or symptoms. The cardiac cath can be used to directly visualize the blocked artery and help your doctor determine which procedure is needed to treat the blockage.

What Is the Treatment for a Heart Attack? 

What Drugs Are Used to Treat a Heart Attack?

The goals of drug therapy are to break up or prevent blood clots, prevent platelets from gathering and sticking to the plaque, stabilize the plaque, and prevent further ischemia.

These medications must be given as soon as possible (within one to two hours from the start of your heart attack) to decrease the amount of heart damage. The longer the delay in starting these drugs, the more damage can occur and the less benefit they can provide.

Drugs used during a heart attack may include:

• Aspirin to prevent blood clotting that may worsen the heart attack
• Other antiplatelets, such as Brilinta, Effient, or Plavix, to prevent blood clotting
• Thrombolytic therapy ("clot busters") to dissolve any blood clots in the heart's arteries
• Any combination of the above

Other drugs, given during or after a heart attack, lessen your heart's work, improve the functioning of the heart, widen or dilate your blood vessels, decrease your pain, and guard against any life-threatening heart rhythms.

Are There Other Treatment Options for a Heart Attack?

During or shortly after a heart attack, you may go to the cardiac cath lab for direct evaluation of the status of your heart, arteries, and the amount of heart damage. In some cases, procedures (such as angioplasty or stents) are used to open up your narrowed or blocked arteries. 

If necessary, bypass surgery may be performed in the days following the heart attack to restore the heart muscle's supply of blood.

Treatments (medications, open heart surgery, and interventional procedures, like angioplasty) do not cure coronary artery disease. Having had a heart attack or treatment does not mean you will never have another heart attack; it can happen again. But, there are several steps you can take to prevent further attacks.

How Are Future Heart Attacks Prevented?

The goal after your heart attack is to keep your heart healthy and reduce your risks of having another heart attack. Your best bet to ward off future attacks are to take your medications, change your lifestyle, and see you doctor for regular heart checkups.

Why Do I Need to Take Drugs After a Heart Attack?

Drugs are prescribed after a heart attack to:

• Prevent future blood clots
• Lessen the work of your heart and improve your heart's performance and recovery
• Prevent plaques by lowering cholesterol

Other drugs may be prescribed if needed. These include medications to treat irregular heartbeats, lower blood pressure, control angina, and treat heart failure.

It is important to know the names of your medications, what they are used for, and how often and at what times you need to take them. Your doctor or nurse should review your medications with you. Keep a list of your medications and bring them to each of your doctor visits. If you have questions about them, ask your doctor or pharmacist.

What Lifestyle Changes Are Needed After a Heart Attack?

There is no cure for coronary artery disease. In order to prevent the progression of heart disease and another heart attack, you must follow your doctor's advice and make necessary lifestyle changes -- quitting smoking, lowering your bloodcholesterol, controlling your diabetes and high blood pressure, following an exerciseplan, maintaining an ideal body weight, and controlling stress.

When Will I See My Doctor Again After I Leave the Hospital?

Make a doctor's appointment for four to six weeks after you leave the hospital following a heart attack. Your doctor will want to check the progress of your recovery. Your doctor may ask you to undergo diagnostic tests such as an exercise stress test at regular intervals. These tests can help your doctor diagnose the presence or progression of blockages in your coronary arteries and plan treatment.

Call your doctor sooner if you have symptoms such as chest pain that becomes more frequent, increases in intensity, lasts longer, or spreads to other areas; shortness of breath, especially at rest; dizziness, or irregular heartbeats

IHD

Ischemic Heart Disease Notes

Heart disease is responsible for 40% of all U.S. deaths, about 750,000 annually.  The major causes of heart disease, in descending order, are 1) IHD, CHD 2) HTN heart disease 3) valvular HD, 4) NIHD, and 5) congenital HD.  IHD is responsible for 80-90% of deaths due to cardiac causes.

Normal heart: ~300 gm, RV wall 3-5 mm, LV wall 1.3-1.5 cm

Valves:  semilunar valves have three cusps which overlap about 30% in the closed state.  Semilunar = aortic and pulmonic.  Mitral valve closure marks the beginning of systole.

Atrioventricular valves:  mitral and tricuspid.  Mitral is a bicuspid valve.

25% of cells in myocardium are myocytes, but these comprise 90% of heart volume since they are large cells.  The remainder are ECs associated with capillaries and some connective tissue cells. Purkinje cells with few myofibers help to regulate contraction and disruption of these areas leads to rhythm disturbances.  These include the 1) SA node (at right atrium near SVC opening), 2) the AV node (right atrium near IV septum), and 3) the bundle of His that runs down the IV septum into branches that divide into each ventricle.

Blood Supply:  coronary circulation occurs mostly during diastole when cardiac relaxation diminishes the pressure in the vasculature.  There are three main coronary arteries with specific areas of the heart that they perfuse.

1. Left Anterior Descending branch of left coronary artery:  supplies anterior LV wall, anterior 2/3 of IV septum, apex of the heart
2. Right Coronary artery supplies the RV wall, posterior wall of LV and posterior 1/3 of IV septum
3. Left Circumflex artery supplies the lateral LV wall

In 80% of people, there is right dominant circulation, which means that the RCA supplies 1/3 of septum and thus right heart circulatory problems can cause serious LV damage.  In 20% of people, the Left Circumflex (LCX) also supplies the posterior 1/3 of the IV septum, called left dominant circulation.

Aging:  The aging heart accumulates increased connective tissue and has fewer myocytes with some deposition of amyloid.  In addition, myocytes may accumulate lipofuscin and undergo atrophy which leads to the term "brown atrophy" for a smaller and lipofuscin colored heart.  Mitral and aortic valves may calcify, leading to stenosis.

Congestive Heart Failure:  defined as inability of heart to pump adequately to meet metabolic needs, or the heart becomes effective only at elevated pressures.  300,000 deaths in the US per year, 50% mortality within five years of diagnosis.  CHF is the leading diagnosis upon discharge from hospitalization in those over 65.  Failure of the heart may arise from inability to eject venous return (backward failure) or "high" output failure where heart cannot eject enough blood to meet elevated systemic demands (forward failure).  Another way to classify CHF is as systolic dysfunction that results from LV failure due to ischemia, pressure or volume overload, dilated cardiomyopathy, or as diastolic dysfunction that results from the inability to fill the heart and may occur with excessive LV hypertrophy, fibrosis and constrictive diseases, or amyloid deposits.  Many forms of heart disease eventually lead to CHF which can result from left or right sided failure.

Hypertrophy may precede the development of CHF as first the heart tries to compensate either for increased outflow pressure (HTN) or increased fluid load by increasing muscle fiber size and contractile force.  Pressure hypertrophy, due to either HTN or aortic stenosis, develops concentrically with a diminished lumen size whereas volume hypertrophy occurs with chamber dilation and may exist with normal wall thickness.  Therefore, wall thickness alone cannot indicate the severity of disease. 

Decreased CO leads to dilation of chambers from increased volume, stretching of myofibers (eventually past maximal contractile length), and hypertrophy.  CHF is considered to be compensated when dilation, hypertrophy, release of catecholamines and increased contractile strength maintains output and decompensated when these mechanisms are no longer adequate.   As the compensatory adaptations fail, decreased perfusion coinciding with the stimulus to increase gene expression and upregulate metabolic machinery may accelerate apoptosis of myocytes. 

Left ventricular hypertrophy itself is a risk factor for sudden death, independent of CHF, HTN, or atherosclerosis.  The enlarged heart has increased metabolic needs in a context of inadequate perfusion.  But the pathologic hypertrophy of the ailing heart differs from that of exercise induced cardiac response, which is not associated with increased risks.

Left sided failure: caused by IHD, HTN, valvular disease, dilated LV and reduced compliance.  All these increase pulmonary pressure which leads to pulmonary edema, hemosiderin laden macrophages in alveoli("heart failure cells"), brown induration (hemosiderin and fibrosis), soggy lungs and increased risk of pulmonary infection.

Sx:  dyspnea, orthopnea, PND, hemoptysis and eventually cerebral hypoxia, decreased renal perfusion, pre-renal azotemia.  Pre-renal azotemia is uremia (BUN (blood urea nitrogen) elevations) that occurs secondary to dysfunction in organs other that diminishes kidney perfusion.  In this case, decreased perfusion to the kidneys will activate the renin-angiotensin system which will lead to volume overload in an already failing heart.  The heart cannot compensate for the increased load and kidney perfusion will be further diminished, leading to acute tubular necrosis and loss of kidney function causing BUN elevations.

Right sided failure:  usually secondary to left sided failure but can be primary from mitral stenosis, congenital left-to-right shunt, cor pulmonale.  Causes systemic fluid overload leading to organ damage, including nutmeg liver, splenomegaly, severe prerenal azotemia, peripheral edema, pleural effusions, and DVT with pulmonary embolism.

Patients with clinically significant CHF will often present with signs of both left and right-sided heart failure.

IHD (clinicians usually call this CHD):  defined as myocardial oxygen demand that exceeds supply. Single most common cause of death in developed nations, about 500,000 annually in the US.  Major cause is coronary AS to with significant lumen reduction.  Greater than 90% of IHD patients have severe coronary AS, usually with reduction in lumen size of a major epicardial vessel of greater than 75%. 

Clinical presentation does not correlate well with extent of atherosclerosis, however, leading to the hypothesis that acute plaque disruption with plaque hemorrhage, fissuring, ulceration or thrombus formation may cause most of the clinical manifestations of IHD.  AMI tends to occur in the a.m. when blood pressure, platelet reactivity, and adrenergic stimulation of the myocardium is high.  Smaller and less advanced plaques (50-75% lumen reduction) may be at higher risk of acute events than very severe or advanced ones.  In more severe stenosis, there may be more fibrosis, a less dense lipid core, and more lumen occlusion that decreases blood flow and pulsatile stress on the lesion.  Other possible causes of acute clinical symptoms include thrombosis and vasospasm.  Four distinct IHD clinical syndromes discussed below are angina, MI, CIHD, SCD. Transmural AMI usually arises from a thrombus that leads to complete occlusion of a vessel and subsequent areas of cardiac death.  However, angina, subendocardial infarcts, and SCD usually occur when there is less than total occlusion of the vessel by a thrombus.

Angina = reversible chest pain caused by narrowed coronary artery lumen.  Stable (or typical angina pectoris) is caused by severe AS and exercise induced, improved by rest and nitroglycerin.  Occlusive AS lesions progressively limit the supply of oxygen to the heart.  As demand increases with exercise, oxygen delivery cannot keep pace.  Stable angina is therefore associated with progressive AS and not with acute events such as thrombosis or plaque rupture. 

Prinzmetal's (variant angina) occurs at rest from vasospasm and is unrelated to changes in BP, heart rate or oxygen demand.  Responds to nitroglycerin.  Unstable (crescendo) angina gets progressively worse and more frequent.  May occur at rest and last longer than stable angina.  Usually arises an acute change in status such as thrombosis of a fissured AS plaque.  Unstable angina signals worsening heart disease and indicates that infarction is likely.

MI = leading cause of US death, occurs at any age but more frequent in men than women, although this differential decreases at increased ages, increased risk in smokers HTN, DM, and hypercholesterolemia.  1.5 million in the US per year, about 500,000 deaths, of which about half occur before arrival at a hospital.  Typically presents with chest pain, rapid, weak pulse, sweating, dyspnea, nausea.  About 15% are clinically silent.

90% of AMI stems from coronary artery disease with “sudden change” involving fissure and plaque disruption, thrombus formation as platelets aggregate to the subendothelial collagen with eventual occlusion of the arterial lumen.  The remaining 10% may result from vasospasm, emboli, or unknown causes.  Restoration of blood flow within 20-40 minutes may prevent any significant necrosis.  Obstruction of blood flow for longer than 40 minutes normally kills the affected myocardial cells.

Angina precedes MI in 50% of patients.  Subendocardial types involve only inner 1/3 to 1/2 of wall.  These infarcts may result from severe AS without an acute event such as thrombus formation.  Transmural type associated with AS, plaque rupture, platelet aggregation, vasospasm, and occlusive thrombus.  Most occur in early a.m. with high platelet counts.  Begin in subendocardial myocardium of LV = least well perfused area and once begun, the infarct may spread across the entire wall during the next six hours.  If the thrombus is partial and flow is re-established after the occlusion, an AMI will tend to be subendocardial, but if a thrombus is complete, an AMI will tend to be transmural.  Most all transmural infarcts involve the LV wall.  Most common sites are within proximal 2 cm of LAD.  40-50% or total occur in LAD (affects anterior LV and anterior 2/3 of ventricular septum) 30-40% RCA (posterior LV wall, posterior 1/3 of septum), 15-20% LCX (lateral wall of LV). 

Changes seen in light microscopy:

0-30 minutes = none

1-4 hours = cell swelling, fiber waviness (normal cells are stretched when adjacent dead cells fail to contract) may be visible.  CKMB rises by 4 hours.  CKMB is extremely sensitive but not very specific.  Also, it peaks at 24 hours and returns to normal within 72 hours so you can't test for it later.  LDH1 rises by 18-36 hours.  Troponins (cTn1 and cTnT) are extremely specific and rise in about four hours and stay elevated for 4-7 days.

4-12 hours = coagulation necrosis, edema

12-24 hours = intercellular edema and intense eosinophilia evident on histology, pyknosis of nuclei

24-72 hours = intense inflammatory response with lots of neutrophils visible between myocardial fibers

72 hours - 10 days = organization and lots of granulation tissue

weeks = collagen deposition and loss of vascularity and contraction

2 months = dense collagenous scar without further modification (i.e., you cannot tell a 5 year old infarct from a 2 month old one)

Gross changes:  At 0-12 hours, the infarct is not visible.  at 12-24 hours, there is pallor and blotchiness in the affected area.  At 24-72 hours, the area is soft and pale to yellow.  At 3-10 days, the infarct is yellow with a hyperemic border indicating granulation tissue and new vascularity.  At several weeks, the infarct is pale gray to whitish, firmer and well demarcated.

Treatment:  streptokinase and tissue plasminogen activator can be given early in an MI in order to help thrombolysis.  PTCA can both help destroy a thrombus and clear out some of the AS plaque as well.

Complications:  Those who survive an initial AMI are at risk for developing further life-threatening complications.  80-90% of patients who survive initially experience complications including arrhythmias (85%) which are especially common with posterior infarcts that may affect the AV node.  LV failure may develop if a large portion of the LV wall is compromised and leads to pulmonary edema (60%).  Rupture of the ventricular wall usually about 3-7 days after the event occurs when blood ruptures either the exterior LV wall leading to rapid death from cardiac tamponade or rarely through the LV septum, causing a left to right shunt.  Rupture occurs in roughly 5% of cases.  Mural thrombus may develop over the inflamed and necrotic area in about 30% of patients, leading to concern about emboli traveling to kidney, brain, and GIT.  Cardiogenic shock is also a potential complication in 10% of patients and is usually fatal.  Left ventricular aneurysm may also develop over the scar in about 10% of long-term survivors.

CIHD:  progressive CHF from chronic ischemia.  Occurs insidiously in elderly with a long history of angina, often with previous MI.  There is gradual loss of cardiac reserve and cardiac atrophy, scarring, and lipofuscin in myocytes.  Diagnose by exclusion of other causes only.

Sudden cardiac death:  Death within 24 hours of onset of acute sx, usually from IHD and severe AS, usually death occurs within the first hour.  First sign of IHD in 50% of patients.  Occurs in 25% of acute MI.  Obesity and HTN predispose to SCD.  Many other causes are not related to AMI such as hypertrophic cardiomyopathy, congenital heart abnormalities, pulmonary hypertension.  Mechanism= lethal arrhythmia such as ventricular fibrillation, usually due to irritable myocardium from ongoing ischemia.

Hypertensive Heart Disease:  hx of HTN and otherwise unexplained LV hypertrophy caused by HTN which increases O2 demand.  LV compliance is reduced, increased myofiber size increases diffusion distance for O2.  May occur with sustained BP levels of 140/90.  Sx: concentric hypertrophy of LV wall without other causes, headache, dizziness, a-fib, IHD. 

Cor Pulmonale:  RV enlargement due to primary pulmonary HTN or other primary pulmonary causes.  Acute = RV dilation following massive pulmonary embolism but not associated with RV hypertrophy which takes time to develop.  Chronic = RV hypertrophy and dilation due to pressure overload, usually secondary to COPD.  RV wall enlarges to > 1.0 cm.  Associated with chronic bronchitis and emphysema.  Causes 10-30% of hospital cardiac admissions.