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Terms in this set (213)

Creatinine Kinase: Creatine kinase (CK) is a general marker of cellular injury. It is released from cells in the brain, skeletal muscle and cardiac tissue after muscle damage has occurred. One isoenzyme of CK, creatine kinase myocardial bands (CK-MB) is the marker specific to cardiac tissue. When myocardial damage occurs, CK-MB is released from the cells. Increased levels can be seen at 3 hours after myocardial damage and can remain elevated for up to 36 hours before returning to normal.

Troponin: The preferred method for diagnosing cardiac injury. It is a protein released from damaged tissue and, as with CK-MB, can elevate within 4 hours of injury. It can stay elevated for up to 10 days. Because it stays elevated longer than CK-MB, it is a valuable marker when attempting to diagnosis injury in the recent past.

Myoglobin: Released and elevated in muscle damage but is not specific for cardiac tissue. It can be used in conjunction with the other values to help rule out or rule in a myocardial infarction.

Brain natriuretic peptide: Brain natriuretic peptide (BNP) is released from overstretched ventricular tissue. Physiological responses to increased levels of BNP include venous dilation, which decreases preload; arterial dilation, which decreases after load; and diuresis. Elevations are an indicator of heart failure.

C-reactive protein (CRP)
-Marker for inflammation
-Linked to atherosclerosis

-Elevated levels increased risk for CVAD, peripheral vascular disease (PVD), and stroke

Cardiac Natriuretic Peptide Markers
-Three types:
-Atrial natriuretic peptide (ANP)
-B-Type natriuretic peptide (BNP)
-C-Type natriuretic peptide

-Increased levels of BNP levels signify heart failure
A. The endothelium (the inner lining of the vessel wall) is normally nonreactive to platelets and leukocytes and well as coagulation, fibrinolytic and complement factors. However, the endothelial lining can be injured as a result of tobacco use, hyperlipemia, hypertension, toxins, diabetes, hyperhomocysteinemia and infection causing a local inflammatory response
-CAD is a progressive disease that develops over many years. When it becomes symptomatic, the disease process is usually well advanced.
-The stages of development in atherosclerosis are (1) fatty streak, (2) fibrous plaque and (3) complicated lesion.

B. Fatty Streak
-Fatty streaks, the earliest lesions of atherosclerosis, are characterized by lipid-filled smooth muscle cells. As streaks of fat develop within the smooth muscle cells, a yellow tinge appears. Fatty streaks can be seen in the coronary arteries by age 15 and involve an increasing amount of surface area as one ages.

C. Fibrous Plaque
-The fibrous plaque stage is the beginning of progressive changes in the endothelium of the arterial wall. These changes can appear in the coronary arteries by age 30 and increase with age. Once endothelial injury has taken place, lipoproteins (carrier proteins within the bloodstream) transport cholesterol and other lipids into the arterial intimacy. Collage covers the fatty streak and forms a fibrous plaque with a grayish or whitish appearance. These plaques can form on one portion of the artery or in a circular fashion involving the entire lumen. The result is a narrowing of the vessel lumen and a reduction in blood flow to the distal tissues.

D. Complicated Lesion
-The final stage in the development of the atherosclerotic lesion is the most dangerous. As the fibrous plaque grows, continued inflammation can result in plaque instability, ulceration and rupture. Once the integrity of the artery's inner wall is compromised, platelets accumulate in large numbers, leading to a thrombus. The thrombus may adhere to the wall of the artery, leading to further narrowing or total occlusion of the artery. At this stage, the plaque is referred to as a complicated lesion.
Medical Management - Diagnosis
Total cholesterol, triglycerides, LDL HDL, CK. CK-MB, troponin
-Exercise stress test
-Coronary angiography

-Lipid profiles evaluate total cholesterol and triglyceride levels as well as LDL and high-density lipoprotein (HDL). Specific cardiac biomarkers are used to rule out MI. Creatine kinase (CK) or creatine kinase-muscle/brain (CK-MB) and troponin (I or T) levels rise when myocardial injury occurs and have been used to identify when ischemia has led to tissue damage.

-An electrocardiogram (ECG) is often the initial test when CAD is suspected. During anginas episodes or symptoms of ACS, the ECG may show ST segment depression of greater than 0.5 mm or flat or inverted T waves that are indicative of ischemia. These changes return to normal when chest pain is relieved. It is important to note that ischemia in some patients may be electrically silent, with an ECG that appears normal. Serial ECGs may be done with cardiac biomarkers to rule out an infarction

-If cardiac biomarkers and ECGs are normal, a patient may then undergo an exercise stress test. This is done to assess the function of the heart during exercise. Alternatively, for those who are unable to use treadmill or stationary bicycle, pharmacological agents such as dobutamine can be used to increase HR, mimicking the effects of exercise on the heart. Stress echocardiograms are another option. Stress testing can be combined with nuclear imaging, such as thallium or technetium studies, to further evaluate perfusion to the heart.

-The gold standard for diagnosing CAD is coronary angiography, a left-sided cardiac catheterization with the purpose of evaluating the coronary arteries for blockage. This is performed to determine the location of the plaque within the coronary circulation, the degree of occlusion, and whether the area can be treated with percutaneous transluminal coronary angioplasty.
Diagnostic studies
-Chest x-ray
-12 lead ECG
-Laboratory studies
-Exercise stress test

-When CAD is suspected in a patient or when a patient with chronic stable angina has a change in the anginas pattern, a variety of studies are completed.
-After a detailed health history and physical examination, a chest x-ray is done to look for cardiac enlargement, aortic calcifications and pulmonary congestion.
-A 12 lead ECG is done and compared with a previous ECG whenever possible to look for any changes.
-Laboratory tests (lipid profile, C-reactive protein) are done to identify specific risk factors for CAD
-An echocardiogram may be done to look for resting LV wall motion abnormalities, which may suggest evidence of CAD.
-An exercise stress test with or without echocardiography or nuclear imaging may be ordered. For patients with physical limitations in walking, a pharmacologic (adenosine [Adenocard] or dipyridamole [Persantine]) stress test with nuclear imaging, or a pharmacologic (dobutamine [Dobutrex]) stress echocardiogram may be ordered. Coronary blockages less than 70% are not usually detected with stress testing.
-The electron beam computed tomography (EBCT) scan locates and measures coronary calcification. However, additional testing (stress testing or cardiac catheterization) is needed to further assess the impact of the lesion on coronary blood flow. Further studies are needed to determine the accuracy of the EBCT scan to diagnose high-grade blockages because many atherosclerotic plaques are not calcified.
-Coronary computed tomography angiography (CCTA) may be considered. Using IV contrast radiation, CCTA can detect calcified and non calcified plaques in the artery, as well as other heart conditions. Limitations of using CCTA include patients with rapid HRs (greater than 90 beats per minute), extensive coronary artery calcifications, obesity, and a history of prior coronary after stent. Patients allergic to IV contrast dye must be premeditated with corticosteroids. Patients with chronic kidney disease need hydration pre-and post-procedure. A baseline serum creatine level should be obtained as the IV contrast dye can worsen renal function.
-Angiotensin-converting enzyme
inhibitors (ACE) and angiotensin receptor blockers (ARBs)
-Calcium channel blockers

-Patients with chronic stable angina who have an ejection fraction (EF) of 40% or less, diabetes, hypertension or chronic kidney disease should take an ACE inhibitor (Iisinoprin [Zestril]) indefinitely, unless contraindicated. Patients with chronic stable angina and a normal EF, diabetes and one other CAD risk factor should take an ACE inhibitor to decrease the risk of MI, stroke and death.
-Theses drugs result in vasodilation and reduced blood volume. Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI. For patients who are intolerant of ACE inhibitors (cough, angioedema), ARBs (Iosartan [Cozaar] are used.
-B-Blockers are ordered for relief of angina symptoms in patients with chronic stable angina. Patients who have LV dysfunction, elevated BP or have had an MI should start and continue B-Blockers indefinitely, unless contradicted. These drugs decrease myocardial contractility, HR, SVR and BP, all of which reduce the myocardial oxygen demand. B-Blockers that have been shown to reduce the risk of death in patients with LV dysfunction, heart failure (HF) or MI are carvedilol (Coreg), metoprolol (Lopressor, Toprol XL) and bisoprolol (Zebeta).
-B-Blockers have many side effects and can be poorly tolerated. Side effects may include bradycardia, hypotension, wheezing from bronchospasm and GI complaints. Many patients also complain of weight gain, depression, fatigue and sexual dysfunction. Absolute contradictions to using B-blockers include severe bradycardia and acute HF. Patients with asthma should avoid B-Blockers include severe bradycardia and acute HF. Patients with asthma should avoid B-Blockers. They are used cautiously in patients with diabetes, since they mask signs of hypoglycemia. B-Blockers should not be stopped abruptly without medical supervision as this may result in an increase in the number and intensity of angina attacks.
-If B-Blockers are contradicted, are poorly tolerated, or do not control anginal symptoms, calcium channel blockers are used. The primary effects of calcium channel blockers are (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary vasodilation, and (4) decreased HR. There are 2 groups of calcium channel blockers - those which have more vasodilatory effects and those which have more rate and contractility effects. Teach patients that they increase serum digoxin levels and therefore levels should be closely monitored.
-A stent is an expandable mesh like structure designed to keep the vessel open after balloon angioplasty.
-Because stents are thrombogenic, many different types of drugs are used to prevent platelet aggregation within the stent. Drugs commonly used during PCI are unfractionated heparin (UH) or low-molecular-weight heparin (LMWH), a direct thrombin inhibitor (bivalirudin [Angiomax]), and/or a glycoprotein IIb/IIIa inhibitor (eptifbatide [Integrillin]). After PCI, the patient is treated with dual antiplatelet drugs (aspirin [indefinitely] and clopidogrel) up to 12 months or longer, until the intimal lining grows over the stent and provides a smooth vascular surface.
-There are two types of stents: bare metal stents (BMS) and drug-eluting stents (DES). DESs are coated with a drug (paclitaxel, sirolimus) to reduce the risk of overgrowth of the intimal lining (neointimal hyperplasia) within the stent. This is the primary cause of in-stent restenosis (ISR). Following DES placement, dual anti platelet drugs are taken to prevent thrombus formation within the stent (stent thrombosis) for a minimum of 12 months or longer. The duration of dual anti platelet drugs for patients with BMS is a minimum of 1 month but ideally one full year after PCI.
-The most serious complications from stent placement are abrupt closure from coronary artery dissection and vascular injury at the artery access site (femoral or radial), acute MI, stent embolization, coronary spasm, dye allergy, renal compromise, bleeding (retroperitoneal) infection, stroke and emergent coronary artery bypass graft (CABG) surgery. The possibility of dysrhythmias during and after the procedure is always present.
-Infection of endocardium affecting heart valves
-Usually bacterial

Risk Factors
-IV drug use
-Diabetes mellitus
-Prosthetic heart valves
-Prior history endocarditis
-Congenital/structural heart defect
-Intravascular access or cardiac device

-Ineffective endocarditis is defined as an infection of the innermost later of the heart, the endocardium, most typically affecting the heart valves. Ineffective endocarditis begins with damage to the endocardial lining of the heart, which can occur as a result of turbulent blood flow. Turbulent blood flow is often caused by valve dysfunction. Platelet and fibrin deposit deposit onto the injured area, forming what is known as a nonbacterial thrombotic endocardial lesion. Microorganism introduced into the bloodstream through patient exposures circulate and can become trapped under the layers of platelet and fibrin deposits. These microorganisms and deposits grow into clumps known as vegetation. This vegetation can severely damage the valves of the heart.

-The etiology of IE is generally of bacterial origin, although other pathogens have been reported. The most common causative microorganisms are Staphylococcus aureus and streptococcus. Ineffective endocarditis can also be caused by other bacteria, viruses, and fungi. The source of exposure to microorganisms in the blood has been historically linked to dental and other invasive procedures. However, it has been suggested that repeated exposures to microorganisms are more likely to cause IE than random exposure during a single dental or other invasive procedure. Strong evidence is lacking for the routine use of antibiotics to prevent IE. For this reason, routine prophylactic use of antimicrobials is recommended only for those at increased risk.
Risk factors
-CAD, hypertension, DM, metabolic syndrome, obesity, smoking, high sodium intake

Clinical Manifestations
-Weight gain - fluid retention
-Hypo- or hypertension

-Other conditions that can cause HF include valvular dysfunction; cardiomyopathies; infectious and inflammatory heart disorders, such as pericarditis and endocarditis; dysrhythmias; and cardiotoxic substance exposure, such as alcohol, chemotherapy, and illicit drugs. With advances in management, mortality rates are declining but remain high at about 40% after 5 years from the times of diagnosis. HF is a leading cause of hospitalizations amount persons older than 65.
-Clinical manifestations of HF vary depending on the type, onset and severity of the failure. The timing of onset and severity of symptoms can be used to determine if HF is acute or chronic. Acute HF has a sudden onset of symptoms and requires immediate intervention. Chronic HF describes the baseline set of symptoms and limitations that are relatively stable with treatment and self-management.

-In left-sided HF, the weakened contraction results in poor peripheral perfusion and back flow of blood that causes fluid accumulation in the lungs. This produces classic symptoms such as SOB (dyspnea), orthopnea, fatigue and crackles heard on auscultation. Other symptoms of left-sided failure include fatigue, poor color, weak pulses and cool temperature in the extremities.
-The weakened contraction of the right ventricle, right-sided HF, results in a back flow of blood into the right atrium and venous circulation and is characterized by JVD, generalized dependent edema, hepatomegaly, and ascites. Left sided HF can eventually cause right sided HF or the entire heart may be initially affected. If that happens, the symptom classification becomes less clear. In severe HF exacerbations, the patient may present with hypotension, cool extremities, decreased or no urine output and poor or decreasing mentation. In such cases, both S3 and S4 may be heard

-There are several classification of HF. The AHA and American College of Cardiology (ACC) classify the stages of HF development from A though D. The NY Heart Association (NYHA) classifies functional status as I through IV according to the clinical manifestations of HF. It is important to note that a patient can fluctuate between NYHA classes I and IV with interventions such as diuresis; however, patients do not regress back to a previous stage in the AHA/ACC classification.
Medical Management - Diagnosis
-Physical assessment
-Chest X-ray
- Multigated acquisition scans (MUGA)
-Biomarker - BNP

-The diagnosis of HF is heavily depended on history and physical assessment. The symptoms are fairly nonspecific, so diagnostic tests are done to rule out other disorders and determine the underlying cause. Diagnostic tools include chest x-ray, echocardiogram and ECG to assess the presence of structural disease, ejection fraction, heart size, pulmonary congestion or dysrhythmias. Multigated acquisition (MUGA) scans can also determine EF. Nuclear imagine studies, stress testing and coronary angiography to evaluate blood flow to the heart are performed when coronary artery disease is suspected. In severe acute HF, hemodynamic monitoring with a pulmonary artery catheter can be useful.

-Laboratory testing includes cardiac biomarkers, serum electrolytes, a CBC, urinalysis, glucose level, fasting lipid profile, liver function testing and renal function tests. Electrolytes can be outside the normal range as a result go decreased kidney perfusion or medication. For example, potassium might be low because of diuretic therapy. Also, inadequate flow to the kidneys may impair renal function, resulting in elevated creatine and blood urea nitrogen (BUN) levels.
-Decreased hemoglobin and hematocrit levels may indicate anemia, which may be a result of decreased blood flow to the kidneys. Cardiac biomarkers such as troponin I or T are used to rule out an acute ischemic event. Other biomarkers, BNP and N-terminal pro-B-type natriuretic peptide (NT-proBNP), are increased because of the overstitching of the ventricles. Increased values in these tests can be used to diagnose HF; BNP and NT-proBNP can also guide clinical decision making and track a patients response to therapy as well as indicate disease progression.
-Beta blockers
-Aldosterone antagonist diuretics/loop diuretics
-ACE inhibitors
-Calcium channel blockers

Surgical management
-Internal cardiac defibrillator
-Ventricular assist device

-Beta blockers are used to control the sympathetic nervous system compensatory response in HF, such as tachycardia, in order to decrease cardiac workload. Ivabradine, a new medication that slows sinus-node firing, can be added for greater control of HR in patients taking maximal doses of beta blocker or who do not tolerate beta blockers.

-Preload is the amount of stretch in the heart at the end of diastole and is affected by the amount and pressure of blood returning to the heart. Aldosterone antagonist diuretics such as spironolactone (Aldactone) as well as loop diuretics such as furosemide (Lasix) are essential medications to decrease preload in patients with fluid retention. The use of spironolactone should be cautioned in patients in with renal insufficiency because of the potential complication of hyperkalemia. In contrast, furosemide can cause hypokalemia and is often paired with a potassium replacement medication.

-Afterload refers to the resistance within the vasculature. Increased after load intensifies the workload on the heart, further impairing cardiac output. Afterload reduction is a main goal of medical management. Angiotensin-converting enzyme (ACE) inhibitors are usually the first line of medications used to control the RAAS compensatory response and reduce after load. Angiotensin receptor blockers (ARBs) have a similar effect and can be used in patients who are intolerant of ACE inhibitors. Other medications that may be prescribed to reduce after load include vasodilators such as hydralazine and isosorbide denigrate. Calcium channel blockers, with the exception of amlodipine, should be avoided in HF due to their myocardial depressant effect and lack of demonstrated efficacy.

-Contractility is the force of the myocardial muscle contraction. A past mainstay of HF management has been digoxin (Lanoxin), an oral positive inotropic medication used to increase cardiac contractility and reduce HR. Its use is being questioned. Although patients realize a reduction in symptoms, overall mortality is not decreased.
Vital signs
-Hypertension is present because of the increased afterload. Hypotension may be caused acute heart failure or be an adverse effect of medications. Tachycardia can be present as the heart attempts to compensate for decreased cardiac output. Tachypnea and decreased oxygen saturation may be present when fluid accumulates in the lungs because of left-sided HF.

Breath sounds
-Crackles indicate pulmonary congestion

Monitoring for irregular heart rhythm or dysthymias
-Dysrhythmias are a common adverse effect of HF and medications used to treat HF

Dry persistent cough
-Common complication of ACE inhibitors

Activity tolerance
-Dyspnea on exertion, weakness and fatigue indicate decreased cardiac output and worsening HF

Urine Output
-Output may be reduced with decreased renal perfusion and also can be used to assess the effectiveness of diuretic therapy. Less than 30 mL/hr should be reported to the provider

Daily weight
-To evaluate fluid retention and effectiveness of diuresis

Lab Data
-Elevated BNP and NT - proBNP indicate overstitching of heart tissue. Elevated creatine and BUN may be indicative of prerenal failure due to decreased cardiac output or overdiuresis. Elevated hepatic enzymes can be indicative of hepatomegaly; hypokalemia is a common complication of diuretic administration. Anemia can be caused by reduced kidney perfusion.

Depression screening and mood
-high rates of depression and anxiety are noted in the HF population. These can impact self-management

Social support
-SOcial isolation has been shown to be independent predictor of mortality among HF patients
-High BP is known as the "silent killer" because it can cause considerable damage to the heart, brain and kidneys (target organs) before symptoms are apparent. The heart is most commonly affected by HTN. When arterial pressure is high, the heart uses more energy to pump against the increased after load caused by the elevated pressure in the aorta. Because of the increased after load, the left ventricle gradually hypertrophies, causing diastolic dysfunction. The ventricle eventually dilates, causing dilated cardiomyopathy and HF due to systolic dysfunction.

-HTN also compromises kidney function. The principal site of damage is in the arterioles leading to the renal system. The continual high pressures exerting force against the walls cause them to thicken, which narrows the lumen. The blood supply to the kidneys is gradually reduced. In response to the reduction in blood supply, the kidneys secrete more renin, which elevates the BP even more, complicating the problem. Eventually, the reduced blood flow may lead to the death of the kidney cells.

-Stroke is a very serious complication of HTN. Prolonged increases in BP may cause vessel rupture, which leads to hemorrhage and a sudden loss of function, resulting from a disruption of the blood supply to the part of the brain. It is the fourth-leading cause of death in the US and the leading cause of disability.
-HTN is the most important but modifiable risk factor related to stroke. In clinical trials, antihypertensive therapy has been associated with reductions in stroke incidence averaging 35% to 40%. An aneurysm is another very serious complication of hypertension. An intracranial aneurysm is a dilation of the walls of the cerebral artery that develops as a result of weakness in the arterial wall. The aneurysm pressures on nearby cranial nerves of brain tissue causing damage or ruptures causing subarachnoid hemorrhage and stroke.

-Hypertensive crisis is an umbrella term for acute, severe elevations in BP. It comprises two conditions on a continuum: hypertensive urgency and hypertensive emergency. Hypertensive urgency is severely elevated BP (diastolic BP greater than or equal to 120 mm Hg) with no obvious, acute TOD, which may include signs of stroke, papilledema, HF, or aortic dissection.
-Hypertensive emergency is the most serious but least common form of hypertensive crisis, representing only 5% of cases. It requires emergent attention. Blood pressure must be lowered immediately to halt TOD. The incidence is higher in older adults, African Americans and men.
-Most patients seen in hypertensive crisis have a prior history of HTN and have been prescribed antihypertensive medications at some point. Sudden escelation of essential, chronic HTN is a common precipitant of hypertensive crisis. Medication interactions and/or withdrawal of treatment are also frequently precipitating factors.
Medical management - Diagnosis
-Compression ultrasonography

Medical Management - Medications
-Unfractionated heparin
-Low molecular weight heparin
-Direct factor Xa inhibitors

-Medical therapy typically consists of anticoagulation with unfractioned heparin or low molecular weight heparin (LMWH) followed by long-term oral anticoagulation with warfarin. These conventional anticoagulant therapies are widely used but have limitations. They require regular monitoring to maintain safe levels (see safety alert).
-Newer oral anticoagulant agents, including direct thrombin inhibitors (dabigatran etexilate) and direct factor Xa inhibitors (ribaroxaban, apixaban and edoxaban) have been developed to overcome some of the limitations conventional anticoagulant therapy.
-These new oral agents have been evaluated for safety and efficacy in large, randomized clinical trials in the treatment and secondary prevention of VTE with results that are comparable to conventional therapy. These medications are important new treatment options for patients with VTE because of they are effective and do not require regular monitoring.

-The use of thrombolytic therapy such as tissue plasminogen activator (tPA) is not routinely administered in patients with DVT. These thrombolytic agents have a more rapid and complete thrombolysis, thus potentially preventing PE and decreasing the incidence of recurring DVT but are not associated with decreased mortality and are associated with increased risks for bleeding.
-Because of this, thrombolytics are only used under certain circumstances. They include patients who have failed conventional therapy with a clot that has been present for fewer than 14 days and have a low bleeding risk.
-Further assessment is made based on individual patient circumstances such as size and location of the clot and preexisting conditions.
-Sleep history
-Polysomnography (sleep study)
-Continuous positive airway pressure
-Weight management

-Diagnostic testing begins with a sleep history, which include gathering information on sleep patterns, a history of snoring and daytime sleepiness Polysomnography (a sleep study) is performed to diagnose OSA and can be conducted in an overnight sleep laboratory or using home portable monitoring. Numerous biophysiological measurements are obtained during sleep, including an electrocardiogram, pulse oximetry, respiratory airflow, eye and skeletal muscle movement, and an electroencephalogram. A key value obtained during the sleep study is the apnea-hypopnea index value, the number of apnea events each hour. It can be used to characterize the severity of OSA.

-Treatment of OSA requires multiple interventions and the active participation of the patient. The use of continuous positive airway pressure (CPAP) is the treatment of choice. Continuous positive airway pressure prevents collapse of the upper airway through the use of pressure delivered through the use of a nasal, oral or oronasal mask during sleep. A CPAP machine delivers a continuous treat of positive pressure, keeping the airway open and providing an unobstructed airway. Patients are taught about the operation, care and maintenance of the CPAP machine. Follow-up care is conducted for problem solving and to evaluate the effectiveness of therapy

-Weight management and loss are encouraged as a first-line intervention in conjunction with the use of CPAP. Positioning during sleep in a non supine position by using pillows is an effective secondary intervention. The avoidance of alcohol and sedatives before bedtime is an additional intervention. Oral appliances that are custom-made for the patient may be used to maintain airway potency. Oral appliances assist with mandibular repositioning to hold the mandible in a forward position to keep the airway open. Forward positioning of the tongue is accomplished with tongue retaining devices.
-Highly contagious
-Droplet transmission

Risk Factors
-Immune compromise
-Chronic illness

-Human influenza viruses are divided into 3 types, designated as A, B and C. Influenza types A and B are responsible for epidemics of respiratory illness that occur mostly during the winter months and are often associated with increased hospitalizations and deaths.

-The primary event that initiates an influenza infection is the aerosolization of small droplets (particles less than 5 um that settle within 3-6 feet from point of release) from an infected individual's sneezing or coughing or by direct contact with fomites that are inhaled and become deposited on the epithelial cells of the upper respiratory tract

-Fomites are inanimate objects that can carry organisms and facilitate their transfer from one person to another, such as stethoscopes, scissors or pens. Over a period of approximately 4-6 hours, these infected cells reproduce and spread the virus to other respiratory cells, extending the infection through the respiratory tract

-The incubation period (from the time of initial droplet inhalation to symptom development) lasts approximately 18-72 hours. The severity of the symptoms and subsequent illness are dependent on the amount of viruses shed during the replication phase and the dependent on the amount of viruses shed during the replication phase and the number of respiratory cells affected. Virus shedding usually ends 2-5 days after symptoms first appear; therefore, it is important to remember that individuals are infectious for up to 7-10 days.