-The electrical activity of the heart can be detected on the body surface using electrodes and is recorded on an electrocardiogram (ECG). The letters P, QRS, T and U are used to identify the separate waveforms.
-The first wave form, the P wave, begins with the firing of the SA node and represents depolarization of the atria.
-The ORS complex represents depolarization from the AV node throughout the ventricles. Impulse transmission through the AV node is delayed, which accounts for the time interval between the end of the P wave and beginning of the ORS wave.
-The T wave represents depolarization of the Purkinje fibers, or it may be associated with
-The U wave, if seen, may represent depolarization of the Purkinje fibers, or it may be associated with hypokalemia.
-Intervals between these waves (PR, QRS, QT intervals) reflect the length of time it takes for the signal to travel from one area of the heart to another. These time intervals are measured, and changes from these time references often indicate pathology.
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
-Atrial natriuretic peptide (ANP)
-B-Type natriuretic peptide (BNP)
-C-Type natriuretic peptide
-Increased levels of BNP levels signify heart failure
Laboratory Markers as Predictors of Heart Disease
-A lipid panel includes total cholesterol, low-density lipoproteins (LDLs), high-density lipoproteins (HDLs), and triglycerides.
-Cholesterol is a lipid necessary for the synthesis of hormones and cell walls. It is available through the ingestion of animal products (Meat) and though synthesis in the liver. It is not soluble in blood, so it combines with proteins to form lipoproteins, LDLs and HDLs, to facilitate transport through the vascular system.
-Low-density lipoproteins primarily transport cholesterol into the cell but can also deposit it on the walls of arterial vessels.
-Elevated levels, greater than 100 mg/dL, are associated with an increased risk of heart disease. High-density lipoproteins, protective lipoproteins, transport cholesterol away from the cells to the liver for excretion.
-Therefore, opposite of LDLs, decreased levels of HDLs, less than 40-60 mg/dL, are a risk factor for heart disease.
-A total cholesterol level includes both LDLs and HDLs. Normal levels are 200 mg/dL or less.
-Increased levels are a risk factor for atherosclerotic vessel disease. Triglycerides, another lipid, store ensued ingested calories in fat cells, which may be later released as an energy source between meals.
-Elevated levels, greater than 150 mg/dL, are another risk factor for heart disease.
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
-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.
-12 lead ECG
-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.
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.
-Severe chest pain not relieved by rest, position change, or nitrate administration
-Heaviness, pressure, tightness, burning, constriction, crushing
-Substernal or epigastric
-May radiate to neck, lower jaw, arms, back
-Often occurs in early morning
-Atypical in women, elderly
-No pain if cardiac neuropathy (diabetes)
Acute care: Hospitalization -> antibiotic therapy -> once stable, continue antibiotics at home (total antibiotic therapy as long as 4-6 weeks). Home teaching re: IV care
-Fever: ASA, acetaminophen, fluids
-Avoid persons with infections, flu, etc.
-Plan and maintain rest periods, good oral hygiene
-Monitor temp, assess heart sounds, assess for s/sx HF, s/sx emboli
-Assess lab data, blood cultures
-Prophylactic antibiotic therapy before invasive procedures
Nursing Management - Assessment and analysis
-S/s due to weakened or damaged heart muscle
Nursing Interventions - Assessments
-Assess for signs of heart failure
-Administer medications as ordered
-Provide emotional support
Nursing interventions - Teaching
-Complete full medication treatment regimen
-Avoid strenuous activities
-Clinical manifestations of myocarditis, such as SOB, chest pain, fatigue and dysrhythmias, are due to the weakened or damaged heart muscle typical of the manifestations of HF.
-Vital Signs: Hypotension, hypertension, tachycardia, tachypnea, and hypoxia are signs of HF. Fever is indicative of infection.
-Cardiac rhythm: Dysrhythmias are a common and dangerous clinical manifestation and must be identified and treated promptly
-Assess for crackles, edema, jugular vein distention (JVD), weight gain and decreased urine output. These are evidence of the weakened heart muscle seen with heart failure.
-CAD, hypertension, DM, metabolic syndrome, obesity, smoking, high sodium intake
-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
- 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.
-Aldosterone antagonist diuretics/loop diuretics
-Calcium channel blockers
-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.
-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: Prevention
-Venous thromboembolism prophylaxis
-Low molecular weight heparin
Low dose Unfactionated Heparin subcutaneously
-Antidote: Protamine sulfate
Low molecular weight Heparin (LMWH) subcutaneously (mg/kg)
-The first step in treatment is prevention. In low risk patients, early ambulation may be all that is necessary. VTE prophylaxis is indicated in at-risk hospitalized populations. In patients with a low bleeding risk pharmacological prevention is recommended. Preferred medications include low molecular weight heparin (LMWH), unfractionated heparin, or, in patients with heparin induced thrombocytopenia (HIT), fondaparinux can be used.
-In patients with a higher risk of bleeding mechanical VTE prophylaxis is indicated. This includes the use of graduated compression stockings, venous foot pumps and active external intermittent compression devices. The benefits of these methods include their effectiveness, ease of application, and safety especially in respect to bleeding.
-Intermittent compression devices apply external pressure to the limn which promotes blood flow velocity, reduces venous stasis, and increases levels of systemic fibrinolysis. Despite widespread use, there is limited evidence regarding the use of graduated compression stockings, venous foot pumps, or combined medical and mechanical prophylaxis.
-Vital signs & O2 Sat
-Hypotension, tachycardia, and decreased oxygen saturation could indicate the presence of a PE or bleeding, especially if the patient is anticoagulated.
-Assess extremity for pain, tenderness, warmth, redness or swelling
-Common symptoms of DVT that occur because of obstruction of blood flow and may indicate location of the clot
-Compare right and left calf, thigh or arm circumferences
-Localized edema due to obstruction to blood flow in one extremity may suggest a DVT.
-Gentle palpation to inspect for induration
-Induration (hardening) helps to locate the placement of the clot in the blood vessels
-Measures fibrin degradation products produced from clot breakdown.
-A positive result stratifies the patient into a high-risk category for DVT
-Laboratory values: INR, PT/aPTT, hemoglobin and hematocrit
-The INR and PT/aPTT should be prolonged
-The hemoglobin and hematocrit should be within normal limits. The PT/INR evaluates the extrinsic coagulation cascade and is used to evaluate the effectiveness of warfarin. The aPTT evaluates the intrinsic coagulation cascade and is used to evaluate the effectiveness of heparin.
-Assess for signs of bleeding such as bruising, petechiae, hematuria, bloody stools.
-Signs of bleeding may indicate a need to modify or decrease anticoagulation therapy.
Nursing interventions - Actions
-Viruses invade upper respiratory tract
-Airborne droplet infection
-Frequency increases in winter months
-Tickling irritation, dry nose and throat - copious nasal secretions, nasal obstruction, fever, watery eyes, malaise, headache
-Antibiotics have no effect (viral infection)
-Patinet's with chronic illnesses should avoid crowded places
-Pharyngitis, otitis media, sinusitis, tonsillitis, chest infections
-Inflammed sinuses filled with excess mucus
-Inflammation and swelling of the sinuses
-Perfect environment for bacterial, viral or fungal growth
-May be acute or chronic
-Pain over affected sinus, purulent nasal drainage, nasal obstruction, congestion, fever, malaise, headache, tenderness, bad breath, facial or dental pain
-Upper airways narrow or collapse > increased resistance to airflow
-Sleep > muscle tone relaxes > normal work of breathing unable to overcome increased resistance > airway collapse
-Periods of apnea > no tidal volume or air movement
-Hypoxemia and hypercapnia
-Obstructive sleep apnea occurs during sleep as the upper airways narrow or collapse, increasing resistance to airflow. Narrowing can occur in the redropalatal region, retroglossal region, or nose. With the onset of sleep, the body muscle tone relaxes, which includes the muscles of the upper airway. With OSA, the normal work of breathing is unable to overcome the increased resistance in the upper airway, causing airway collapse. Narrowing of the upper airways increases inspiratory pressure and intrathoracic pressure, resulting in decreased minute ventilation and gas exchange.
-Ultimately, there are periods of apnea. During apnea, there is no tidal volume, or movement of air in or out; thus, no gas exchange occurs in the alveoli. Hypoxemia (decreased concentration of oxygen in the blood), hypercapnia (increased concentration of carbon dioxide in the blood), acidosis, and increased sympathetic vasoconstrictive activity occur as a result of the decreased tidal volume and apnea.
-Polysomnography (sleep study)
-Continuous positive airway pressure
-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.
Unpredictable and variable
-Increased respiratory rate
Wheezing, coughing, dyspnea, chest tightness after exposure to a trigger.
Expiration may be prolonged - 1;3, 1;4
-Air takes longer to move out because of bronchospasms, edema and excess mucous (characteristic wheezing)
-Difficulty with air movement can create a feeling of suffocation
-Signs of hypoxemia, restlessness, anxiety, inappropriate behavior, increase pulse & BP
-Respiratory rate greater than 30 bpm
-As condition worsens, difficult to speak in complete sentences.
-Unresponsive to typical rescue treatment with bronchodilators
-Bronchospasm, inflammation, increased mucus or mucus plugging
-Chest tightness, wheezing, dry cough, shortness of breath, severe respiratory distress
-Can be life threatening
-If wheezing decreases, with severely diminished breath sounds - respiratory failure
-Status asthmaticus describing when an asthma attack is unresponsive to typical rescue treatment with bronchodilators. It is caused by bronchospasm, inflammation, increased mucus, or mucus plugging which presents as chest tightness, wheezing, dry cough, shortness of breath, and severe respiratory distress. If not treated early, it can be life threatening.
-Detailed history and physical exam
-Pulmonary function tests (PFTs)
-Peak expiratory flow rate (PEFR)
-use of peak flow meter
-Underdiagnosis of asthma is common. A detailed history is important to determine if a person has had similar attacks, which are often precipitated by a known trigger
-The peak expiratory flow rate (PEFR) measured by the peak flow meter (at home or in a health care setting) is an aid to diagnose and monitor asthma.
-Spirometry (measured in a health care setting) is usually normal between asthma attacks if the patient has no other underlying pulmonary disease. However, the patient with asthma may show an obstructive pattern including a decrease in forced vital capacity (FVC), FEV1, PEFR, and FEV1 to FVC ratio (FEV1/FVC). Spirometry can be done before and after the administration of a bronchodilator to determine the degree of the response.
-The patient with asthma may show an obstructive pattern with asthma including a decrease in forced vital capacity (FVC), FEV1, PEFR, and FEV1 to FVC ratio (FEV1/FVC). (the normal values for pulmonary function tests are discussed in ch 25)
-Chest x-ray is usually normal for asymptomatic patients, but can tell if something else (pneumonia, foreign body in the airway) could be causing symptoms similar to asthma
2nd EditionLawrence Scanlon, Renee H. Shea, Robin Dissin Aufses
3rd EditionDarlene Smith-Worthington, Sue Jefferson
1st EditionCarol Jago, Lawrence Scanlon, Renee H. Shea, Robin Dissin Aufses
3rd EditionDarlene Smith-Worthington, Sue Jefferson