complete table

8/13/2019 Complete Table

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MEDICAL DIAGNOSIS Respiratory Failure

DEFINITION

Inadequategas exchangeby therespiratory system,with the result that arterial oxygen and/or carbon dioxide

levels cannot be maintained within their normal ranges.

PATHOPHYSIOLOGY

Respiratory failure can arise from an abnormality in any of the components of the respiratory system,

including the airways, alveoli, CNS, peripheral nervous system, respiratory muscles, and chest wall.

Hypoventilation, V/Q mismatch, and shunt are the most common pathophysiologic causes of acute

respiratory failure.

Hypoventilation

Hyperventilation is usually occurs from depression of the CNS from drugs or neuromuscular diseases

affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. The

relationship between PaCO2and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6

L/min, PaCO2rises precipitously. Hypoventilation can be differentiated from other causes of hypoxemia bythe presence of a normal alveolar-arterial PO2gradient.

V/Q mismatch

V/Q mismatch is the most common cause of hypoxemia. V/Q units may vary from low to high ratios in the

presence of a disease process. The low V/Q units contribute to hypoxemia and hypercapnia in contrast to

high V/Q units, which waste ventilation but do not affect gas exchange unless quite severe. The low V/Q

ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from

overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary

embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood

flow obstruction secondary to embolism. Administration of 100% oxygen eliminates all of the low V/Q

units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor

stimulation, but the PaCO2level generally is not affected.

Shunt

Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood

(mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed

through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is

calculated by the following equation:

QS/QT = (CCO2CaO2)/CCO2CvO2)

QS/QT is the shunt fraction, CCO2(capillary oxygen content) is calculated from ideal alveolar PO2, CaO2(arterial oxygen content) is derived from PaO2using the oxygen dissociation curve, and CVO2(mixed

venous oxygen content) can be assumed or measured by drawing mixed venous blood from pulmonary

arterial catheter.

Anatomical shunt exists in normal lungs because of the bronchial and thebesian circulations, accounting for

2-3% of shunt. A normal right-to-left shunt may occur from atrial septal defect, ventricular septal defect,

patent ductus arteriosus, or arteriovenous malformation in the lung. Shunt as a cause of hypoxemia is

observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac
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origin. Hypercapnia generally does not develop unless the shunt is excessive (>60%). When compared with

V/Q mismatch, hypoxemia produced by shunt is difficult to correct by oxygen administration.

ETIOLOGY &EDPIDEMOLOGY

Almost all lung diseases including asthma, chronic obstructive pulmonary disease (COPD), AIDS-related

pneumonia, other pneumonias and lung infections, and cystic fibrosis may eventually lead to respiratoryfailure particularly if the diseases are inadequately treated. These patients find it very hard to breathe and theresult is low oxygen and high carbon dioxide blood levels.

People whose normal lungs have been injured, such as from exposure to noxious gases, steam, or heat during

a fire, can subsequently go into respiratory failure

CLINICAL MANIFESTATIONThe clinical features of respiratory failure vary widely in individual patients because so many differentconditions can lead to this disorder. There are no physical signs unique to respiratory failure. At extremelylow arterial oxygen (PaO2) levels, patients have rapid heart rates, rapid breathing rates, and they are

confused, sweaty, and cyanotic (blue). Chronically low arterial oxygen makes patients irritable, and elevatedcarbon dioxide produces headaches and sleepiness. Difficult, rapid, or labored breathing (dyspnea) is aconsistent symptom in the awake patient.

DIAGNOSTIC TESTSThe way to diagnose respiratory failure, therefore, is to measure oxygen (PaO2) and carbon dioxide (PaCO2)in the arterial blood. Depending on age, a PaO2 less than 60 mm Hg or PaCO2 greater than 45 mm Hggenerally mean that the patient is in respiratory failure.Cardiac serologic markers

Troponin, Creatine kinase- MB fraction (CK- MB) B-type natriuretic peptide (BNP)Microbiology Respiratory cultures: sputum/tracheal aspirate/broncheoalveolar lavage (BAL) Blood, urine and body fluid (e.g. pleural) cultures

Chest radiography

Identify chest wall, pleural and lung parenchymal, pathology and distinguish disorders that causeprimarily V/Q mismatch (clear lungs) vs. Shunt(intra-pulmonary shunt with opacities present)

Electrocardiogram

Identify arrhythmias, ischemia, ventricular dysfunctionEchocardiography

Identify right and/or left ventricular dysfunctionPulmonary function tests/bedside spirometry

Identify obstruction, restriction, gas diffusion abnormalities

May be difficult to perform if critically illBronchoscopy

Obtain biopsies, brushings and BAL for histology, cytology and microbiology Results may not be available quickly enough to avert respiratory failure Bronchoscopy may not be safe in the if critically ill

MEDICAL/SURGICAL

MANAGEMENT INCLUDINGPHARMACOLOGICAL

Oxygenation is the basic therapy for acute respiratory failure due to lung disease. Oxygen-enriched air isusually given to the patient by nasal prongs, oxygen mask, or by placing an air tube into the trachea

(windpipe). Since prolonged high oxygen levels can be toxic, the concentration of oxygen must be carefullycontrolled for both short- and long-term treatment. Assisted ventilation with mechanical devices may be thefirst priority for neuromuscular disease patients going into respiratory failure.

Additional treatments employ ventilation which helps to keep the lungs inflated at low lung volumes

(positive end-expiratory pressure, PEEP), and fluid and nutritional management. Bronchodilatory drugs

cause relaxation of the smooth muscles in the airways, improving airway calibre. They may be administeredusing a variety of routes, in particular inhaled in the form of aerosol sprays or nebulisers.

Inhaled bronchodilators are an essential component in the treatment of asthma and obstructive airwaysdisease. Peak expiratory flow rate measurements taken pre and post dose are usually recorded to assesseffectiveness. Other medicationsparticularly anti-inflammatory drugs such as steroidsmay be required.

Antimicrobial, antiviral or antifungal therapy is usually initiated if the cause of respiratory failure isconsidered to be of infective origin. Again, these drugs may be administered using a variety of routes andtime periods.


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NURSING MANAGEMENTPatients with acute respiratory failure should be closely observed for potential deterioration. Respiratoryassessment should occur on a frequent/continual basis. Monitoring may involve intermittent/continual pulseoximetry and regular peak expiratory flow rate measurement but should always include basic respiratory rate

monitoring and general assessment. Physiological track and trigger warning systems are widely used toidentify patients on general wards at risk of clinical deterioration. These systems provide a framework to

access higher levels of care. Patients at risk of developing acute respiratory failure are an ideal group forthese systems and their use should be encouraged. Any changes in physiological signs should be reported

promptly to the senior practitioner.

Anxiety

Patients will most likely be frightened and anxious as a result of dyspnea. While undertaking assessmentsand during subsequent care it is very important to try to alleviate these anxieties and provide reassurance.Simple techniques, such as patient positioning, may reduce symptoms by maximizing lung expansion.Patients may advise which position they feel offers some relief. Communication skills, such as asking closed

questions during assessment, may be used if patients are breathless to a point where they cannot answer insentences.

Pulmonary secretionsMany processes leading to acute respiratory failure are associated with an increase in pulmonary secretions.

Tissues or receptacles for sputum should be provided to assist patients to void secretions independently. Iftheir ability to void is limited, assistance may be required in the form of o ropharyngeal/nasopharyngealsuction. These procedures should not be undertaken without appropriate training. Sputum and other samplesmay be required for microbiological screeningthis should be performed according to local guidelines.

Pain managementPain, particularly associated with abdominal or thoracic surgery or injury, can limit chest expansion. If

patients are experiencing pain, relief should be provided and future control optimised. Expert advice may be

necessary because of the respiratory depressant effects of some analgesics. Liaison with multidisciplinaryspecialists such as acute or chronic pain specialists may be required.

Oxygen therapyThe majority of patients in acute respiratory failure will need oxygen supplementation. Before startingoxygen therapy, it is important to explain the reasons for this to them, their relatives and carers, and check

their understanding (Jevon and Ewens, 2001). Unless in a medical emergency situation, the oxygen flow rateor percentage and duration of therapy should be prescribed. Nurses are best placed to select the mostappropriate delivery system for a particular patient.

The system chosen should aim to deliver therapy with maximum effectiveness and optimise patientindependence. The detrimental effects of oxygen therapy, such as the dehydration of mucosa, should beobserved for and appropriate therapies such as gas humidification introduced where necessary. Tissue

damage from a delivery device may occurin particular, oxygen masks cause soreness behind the ears afterlonger-term use and nasal cannulas cause irritation to the nostrils. Small adaptations to the device, such asadding gauze padding, may prevent or alleviate this.

Other medicationIf aerosol-inhaled medications are prescribed, effective delivery will only occur through patient compliance.

Therapeutic effectiveness can be improved by providing education on inhaler technique. It is imperative that

appropriate devices are chosen and patients technique is adequate (Bennett, 2003). When administeringnebulizers, patients should be sat upright (as tolerated), be encouraged to take normal breaths and avoidtalking in order to maximize drug delivery (Bennett, 2003). Nebulised medication may be administered usingair flow or oxygen and nurses should ensure the type of gas used to deliver the drug is prescribed. Certain

concentrations of oxygen may be contraindicated in certain patients. Practitioners should also bear in mindthat patients may be dependent on a certain oxygen flow before nebulisation and interrupting this may becontraindicated.

Attempts should be made to minimize oxygen consumption (Smyth, 2005). This can be achieved byminimizing patient exertion. They should be assisted with activities of daily living such as meeting hygiene


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needs, and all essential items, such as sputum pots, drinks and nurse call bells, should be within easy reach.Patients will also require time to catch their breath following exertion, so activities should be planned withthis in mind.

NURSING DIAGNOSISKnowledge deficit related to condition evidenced by verbalization.

COMPLICATIONSHypoxemia, pulmonary hypertension

MEDICAL DIAGNOSIS ADULT RESPIRATORY DISTRESS SYNDROME

DEFINITIONAlso referred to as acute respiratory distress syndrome, is a form of acute respiratory failure caused byextensive lung injury following a variety of catastrophic events such as shock, severe infection, and burns.

ARDS can occur in individuals with or without previous lung disease.

PATHOPHYSIOLOGY ARDS is a massive inflammatory response by the ling that increases permeability of the alveolar membrane,with resultant fluid movement into the interstitial and alveolar space. This leads to the development ofnoncardiogenic pulmonary edema, which decreases lung complicance and impairs oxygen transport. There

are three phases:

1. Phase oneExudative : happens about 24 hours after the initial insult and consist of damage to thecapillary endothelium and leakage of fluid into the pulmonary interstitium. Microemboli also

develop and cause a futher increase in pulmonary artery pressure. Inflammatory stage responseaccompany the pulmonary parenchymal damage , leading to the release of toxic mediators , theactivation of compliment , the mobilization of macrophages and the release of vasoactivesubstances from mast cells. There is future damage to the basal membrane, interstitial space,

around the alveoli and increase the distance around the capillary membrane.2. Phase Twoproliferative: begins about 7-10 days later. At this time type one and type 2 alveolar

cells are damaged. As a result there is decreased surfactant production, alveolar collapse, andatelectasis, leading to future impairment in gas exchange. Hypoxemia is present because of

decreased surfactant production, intrapulmonary shunting and V/Q mismatch.3. Phase 3- Fibrotic: 2-3 weeks. There is irreversible decomposition of fibrin into the lungs, resulting

in pulmonary fibrosis , future decrease in lung compliance and worsening hypoxemia . the endresult is significant V/Q imbalance and profound arterial hypoxemia.


Oxygen toxicity Breathing in (aspiration) of the stomach contents when regurgitated, or salt water or fresh water

from nearly drowning.

Inhaling smoke, as in a fire; toxic materials in the air, such as ammonia or hydrocarbons; or toomuch oxygen, which itself can injure the lungs.

Infection by a virus or bacterium, orsepsis,a widespread infection that gets into the blood.
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Massive trauma, with severe injury to any part of the body. Shock with persistently low blood pressure may not in itself cause ARDS, but it can be an

important factor.

A blood clotting disorder called disseminated intravascular coagulation, in which blood clots formin vessels throughout the body, including the lungs.

A large amount of fat entering the circulation and traveling to the lungs, where it lodges in smallblood vessels, injuring the cells lining the vessel walls.

An overdose of a narcotic drug, a sedative, or, rarely,aspirin. Inflammation of the pancreas (pancreatitis), when blood proteins, called enzymes, pass to the lungs

and injure lung cells.

Severe burn injury. Injury of the brain, or bleeding into the brain, from any cause may be a factor in ARDS for reasons

that are not clear. Convulsions also may cause some cases.

CLINICAL MANIFESTATIONIncreased respiratory rate, cough, respiratory acidosis, crackles, tachypnea, , hypoxemia, refractoryhypoxemia, defused bilateral infiltrates, severe dyspnea, thick frothy sputum, hemoptysis, decreased

compliance.

DIAGNOSTIC TESTS Chest x ray (interstitial edema), ABG analysis (resp. acidosis)

MEDICAL/SURGICALMANAGEMENT INCLUDING

PHARMACOLOGICAL

Administer O2, antioxidants to reverse O2 toxicity, homodynamic agents, to improve cardiac out put, highfowlers position,prophylactic antibiotics, anti-inflammatory agents, surfactant, and mechanical ventilation.

NURSING MANAGEMENT

Place client in high fowlers position, give emotional support, educate client about progression of disease,

adequate perfusion, monitor and record VS, I/O, lad studies, pulse oximetry, allow rest periods.

NURSING DIAGNOSIS Anxiety related to implications of condition and critical care settingPowerlessness related to condition and treatments (ventilator, monitoring)

COMPLICATIONSLung fibrosis, cardiac dysrhythmias caused by hypoxemia, oxygen toxicity , renal failure, thrombocytopenia,gastrointestinal bleeding secondary to stress ulcer, sepsis from invasive line , and disseminated intravascularcoagulation.

MEDICAL DIAGNOSISCystic fibrosis

DEFINITIONCystic fibrosis (CF) is an inherited disease characterized by an abnormality in the glands that produce sweatand mucus. It is a chronic and progressive disease. Cystic fibrosis is life-threatening and causes severe lungdamage and nutritional deficiencies.

PATHOPHYSIOLOGY The protein created by this gene is anchored to theouter membrane ofcells in thesweat glands,lungs,pancreas, and other affectedorgans.The protein spans this membrane and acts as achannel connecting theinner part of the cell (cytoplasm)to thesurrounding fluid.This channel is primarily responsible forcontrolling the movement of chloride from inside to outside of the cell; however, in the sweat ducts it

facilitates the movement of chloride from the sweat into the cytoplasm. When the CFTR protein does notwork, chloride is trapped inside the cells in the airway and outside in the skin. Because chloride isnegativelycharged,positively chargedions cross into the cell because they are affected by theelectrical attraction of the
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chloride ions. Sodium is the most common ion in the extracellular space and the combination of sodium andchloride creates thesalt,which is lost in high amounts in the sweat of individuals with CF. This lost salt

forms the basis for the sweat test

ETIOLOGY &

EDPIDEMOLOGY

An inherited condition, cystic fibrosis affects the cells that produce mucus, sweat, saliva and digestive juices.Normally, these secretions are thin and slippery, but in cystic fibrosis, a defective gene causes them to

become thick and sticky. Instead of acting as a lubricant, the secretions plug up tubes, ducts and

passageways, especially in the pancreas and lungs.

Respiratory failure is the most dangerous consequence of cystic fibrosis. Also, the secretions block

pancreatic enzymes that help digest fats and proteins, and they prevent your body from absorbing keyvitamins. In cystic fibrosis, a defective gene alters a protein that regulates the normal movement of salt(sodium chloride) in and out of cells. This results in thick, sticky secretions in the respiratory and digestivetracts, as well as in the reproductive system. It also causes increased salt in sweat.

The affected gene, which is inherited from a child's parents, is a recessive gene. With recessive genes,

children need to inherit two copies of the gene, one from each parent, in order to have the disease. If childreninherit only one copy, they won't develop cystic fibrosis, but will be carriers and possibly pass the gene totheir own children.

If two people who carry the defective gene conceive a child, there's a 25 percent chance the child will have

cystic fibrosis, a 50 percent chance the child will be a carrier of the cystic fibrosis gene, and a 25 percentchance the child will neither have the disease nor be a carrier.

People who carry the cystic fibrosis gene are healthy and have no symptomsthey may be carriers and not

know it.

The greatest risk factor for cystic fibrosis is a family history of the disease. If both you and your partner

come from families with cystic fibrosis, then each of your children has a one in four chance of having cysticfibrosis.

Your risk is also greater if you're of Northern European ancestry. In that case, you have a one in 29 chance ofcarrying the gene. Among other ethnic groups in the United States, Hispanics have a one in 46 chance of

carrying the gene, blacks have a one in 65 chance and Asian-Americans a one in 90 chance.

CLINICAL MANIFESTATIONThe following are the most common symptoms for cystic fibrosis. However, individuals may experience

symptoms differently. Symptoms may include:

Abnormalities in the glands that produce sweat and mucus

This may cause a loss of salt. A loss of salt may cause an upset in the balance of minerals in the blood,

abnormal heart rhythms, and, possibly, shock.

Thick mucus that accumulates in the lungs and intestinesThis may cause malnutrition, poor growth, frequent respiratory infections, breathing difficulties, and/or lung

disease.

Other medical problems, such as: sinusitis, nasal polyps, clubbing of fingers and toes - a condition marked

by the ends of the fingers and toes become enlarged; more prevalent in the fingers, pneumothorax - the

presence of air or gas in the pleural cavity causing the lung to collapse, hemoptysis - coughing blood, cor

pulmonale - enlargement of right side of heart, abdominal pain, gas in the intestines, rectal prolapsed, liver
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disease, diabetes, pancreatitis, gallstones.

Infants born with CF usually show symptoms within the first year. Some children, though, may not show

symptoms until later in life. The following signs are suspicious of CF, and infants having these signs may be

tested for CF: diarrhea that does not go away, foul-smelling stools, greasy stools, frequent episodes of

wheezing, frequent episodes of pneumonia, persistent cough, skin tastes like salt, poor growth

DIAGNOSTIC TESTS Prenatal and genetic tests are performed to identify fetal disease and carrier status. Failure to thrive andfrequent upper respiratory infections often leadto diagnostic testing to confirm the CF diagnosis.

Quantitative sweat electrolyte test.Genotyping, Serum electrolytes, chest x-ray, arterial blood gases, pulmonary functiontests, semen analysis, nasal potential difference measurement of the nasal mucosa, pulmonary function tests,

bronchoalveolar lavage, and sputum microbiology.

MEDICAL/SURGICALMANAGEMENT INCLUDINGPHARMACOLOGICAL

The major goals of treatment are to improve pulmonary, GI, and pancreatic status. These goals are achievedthrough a combination of medications, nutrition, and exercise regimens. If antibiotics are given to preventand treat pneumonia, the physician and pharmacist monitor therapeutic blood levels of the antibiotics todetermine the peak and trough levels. To help prevent the recurrence of pneumonia, chest physiotherapy

(CPT) is performed in the home or hospital four

times a day before meals to avoid emesis or after an aerosol treatment. A ThAIRapy vest, a device thatprovides high-frequency chest wall oscillations to loosen secretions, may also be used to maintain caloriecounts on daily meal plans; supplement nutritional needs with high-calorie feedings. A patient may also have

nasogastric feedings to which pancreatic enzymes are added to ensure the digestion and absorption of fats,protein, and carbohydrates. The physician may also prescribe total parenteral nutrition and fat-solublevitamins (A, D, E, and K).Regular exercise, including mobility and muscle-strengthening exercises should be encouraged on a regular

basis. Exercises help maintain physical wellness and supplement the patients airway clearance strategies byhelping to loosen pulmonary secretions. Some patients develop right-sided heart failure, and if this occurs,most of them die within a year. They may require the use of home portable oxygen therapy and receivedioxin and/or diuretics. As the disease progresses toward the terminal phase, hemoptysis is present and

cyanosis is markedly apparent.

NURSING MANAGEMENT

Educate to reinforce the importance of regular CPT and expectoration of the mucus. Encourage increased

fluid intake to loosen the secretions, and provide frequent mouth care before meals.Teach the parents not to offer cough suppressants, which can lead to obstruction, lung collapse, andinfection.Support the childs or adolescents body image concerns; compliment the patient on her or his strengths.

Encourage the child to develop in as many areas as possible. Very often, other CF patients become asignificant support group as the child matures. The child is always dramatically affected when another peerwith CF dies. Plan group discussions with the patients and have a psychiatric nurse clinical specialist serveas facilitator of this grief work for both patients and staff. In addition, siblings often worry that they maycontract the disease or they may exhibit feelings of jealousy of the attention given to the sibling with CF. A

referral to a social worker or the Cystic Fibrosis Foundation may be needed.Counsel couples on the risk that subsequent pregnancies may result in a child with CF, since there is a one infour chance with any pregnancy that a child could have CF if both parents are carriers. Discuss the role ofamniocentesis and the difficult issues surrounding terminating a pregnancy if CF is confirmed prenatally.

NURSING MANAGEMENT

(Nursing Diagnoses)

Ineffective airway clearance related to excess tenacious mucus.

Altered nutrition less than body requirement related to impaired digestive process and absorption ofnutrients.

COMPLICATIONS Respiratory complicationsFrequent complications of cystic fibrosis are chronic respiratory infections, including pneumonia, bronchitis,chronic sinusitis and bronchiectasisan abnormal dilation of the walls of the bronchial tubes that makes it

more difficult to clear your airways. Asthma can result from chronic inflammation of the bronchial lining.

Nutritional complicationsCystic fibrosis makes you prone to chronic diarrhea and severe nutritional deficiencies. That's because thicksecretions obstruct the ducts in your pancreas, preventing enzymes that digest fats and proteins from


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reaching your intestines. These secretions also prevent your body from absorbing the fat-soluble vitamins A,D, E and K.

Reproductive complications

Cystic fibrosis also affects the reproductive system. Because thick secretions often block the tube connecting

the testes and prostate gland (vas deferens), many men with cystic fibrosis are infertile. Although womenwith cystic fibrosis may be less fertile than other women, it's possible for them to conceive and to havesuccessful pregnancies.

MEDICAL DIAGNOSIS Bronchiectasis

DEFINITIONAn extreme form of onstructive bronchitis, causes permanent, abnormal dilation and distortion of bronchiand bronchioles

PATHOPHYSIOLOGY All the causative conditions impair airway clearance mechanisms and host defenses, resulting in an inabilityto clear secretions, which, in turn, predisposes patients to chronic infection and inflammation. As a result offrequent infections, most commonly withHaemophilus influenzae(35%),Pseudomonas aeruginosa(31%),

Moraxella catarrhalis(20%), Staphylococcus aureus(14%), and Streptococcus pneumoniae(13%), airwaysbecome inspissated with viscous mucous containing inflammatory mediators and pathogens and slowly

become dilated, scarred, and distorted. Histologically, bronchial walls are thickened by edema,inflammation, and neovascularization. Destruction of surrounding interstitium and alveoli causes fibrosis,

emphysema, or both.Superinfection with multidrug-resistant organisms, includingMycobacterium tuberculosis, and mycobacteriaother thanM. tuberculosiscan cause recurrent exacerbations and worsen airflow limitation on pulmonaryfunction tests. Pulmonary hypertension and right-sided heart failure may ensue because functional lung

tissue decreases.

ETIOLOGY &

EDPIDEMOLOGY

Develops when bronchial wall are weakened by chronic inflammatory changes in the bronchial mucosa andoccurs most often recurrent inflammatory conditions .conditions which cause the narrowing of the lumen of

the bronchioles i.e tuberculosis, adenoviral infections, & pneumonia.

CLINICAL MANIFESTATION

May vary according to etiologic agent.main manifestation including, coughing, and purulent sputum

production in large amount. Fever , Hemoptysis, nasal stuffiness, and drainage from sinusitis. Client

complains of fatigue. Clubbing of nails present.

DIAGNOSTIC TESTSDiagnosis may be confirmed by performing chest radiograph, bronchogram, or computer tomography (CT)scan.

MEDICAL/SURGICAL


Antibiotics, chest therapy, hydration, bronchodilators, and oxygen are prescribed.

In severe cases surgical resection in the pathologic process is well localized in one lobe or two adjacent

lobes & when no contraindications exist.

NURSING MANAGEMENTNote signs of dyspnea, orthopnea, decreased breath sounds, evaluate mental status for confusion andrestlessness due to hypoxia, and hypercapnea record baseline oximetry and level of inspired O2. note color


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of sputum or hemoptysis.

(Nursing Diagnoses)

Imbalanced Nutrition: Less than body requirements, related to malnutrition caused by bronchiectasis

Impaired gas exchange related to damage to the bronchial walls caused by bronchiectasisIneffective airway clearance related to abnormal mucosa clearance and stagnated sputum in bronchi

COMPLICATIONSAdvanced bronchiectasis may produce chronic malnutrition and amyloidosis, right ventricular failure, andcor pulonale

Dypnea, nasal flaring, pursed lip breathing, use of accessory muscles, wheezing cyanosis,

MEDICAL DIAGNOSISBronchial asthma

DEFINITION

Bronchial asthma is a chronic relapsing inflammatory disorder with increased responsiveness oftracheobroncheal tree to various stimuli, resulting in paroxysmal contraction of bronchial airways.


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PATHOPHYSIOLOGY During an asthma episode, inflamedairways react to environmental triggers such as smoke, dust, or pollen.The airways narrow and produce excessmucus,making it difficult to breathe. In essence, asthma is the resultof animmune response in thebronchial airways.

The airways of asthma patients are "hypersensitive"to certain triggers, also known asstimuli. In response toexposure to these triggers, thebronchi (large airways) contract intospasm (an "asthma attack").Inflammation soon follows, leading to a further narrowing of the airways and excessivemucusproduction,

which leads to coughing and other breathing difficulties. Bronchospasm may resolve spontaneously in 12hours, or in about 50% of subjects, may become part of a 'late' response, where this initial insult is followed312 hours later with further bronchoconstriction and inflammation.

The normal caliber of the bronchus is maintained by a balanced functioning of these systems, which bothoperate reflexively. Theparasympathetic reflex loop consists of afferent nerve endings which originate underthe inner lining of the bronchus. Whenever these afferent nerve endings are stimulated (for example, by dust,cold air or fumes) impulses travel to the brain-stem vagal center, then down the vagal efferent pathway to

again reach the bronchial small airways. Acetylcholine is released from the efferent nerve endings. Thisacetylcholine results in the excessive formation of inositol 1,4,5-trisphosphate (IP3) in bronchial smoothmuscle cells which leads to muscle shortening and this initiates bronchoconstriction.


Inherited disorder. Environmental factors interact with inherited factors to produce disease. Symptoms can

occur spontaneously or can be triggered by respiratory infections, exercise, cold air, tobacco smoke or otherpollutants, stress or anxiety, or by food allergies or drug allergies.


Dypnea, nasal flaring, pursed lip breathing, use of accessory muscles, wheezing cyanosis,

DIAGNOSTIC TESTSSpirometery, pulse oximetry, ABG, chest x ray


PHARMACOLOGICAL

Prevention of chronic asthma, maintain patent airway, administer beta2- agonists, nebulize atropine, IVcorticosteroids, supplemental oxygen, end tracheal intubation,. bronchodilators such as inhaled Alupent orVanceril. Acute severe asthma may require hospitalization, oxygen, and intravenous medications.

NURSING MANAGEMENTReinforce pursed lip breathing, monitor and record color, amt, and consistency of sputum, high fowlers

position.Ineffective breathing pattern related to impaired exhalation evidenced by dyspnea use of accessory muscles

and wheezing.

NURSING MANAGEMENT(Nursing Diagnoses)

Ineffective airway clearance related to increased production of secretions.

COMPLICATIONS

Apart from chronicity, usually no complications. Pneumothorax, emphysema, or areas of consolidation or pulmonary collapse may occur in very

advanced cases.
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MEDICAL DIAGNOSIS Atelectasis

DEFINITIONAtelectasis is a medical condition in which the lungs are not fully inflated. It may affect part or all of onelung. It is a condition where thealveoli are deflated, as distinct from pulmonaryconsolidation.There is acollapse of lung tissue, preventing the respiratory exchange of carbon dioxide and oxygen.

PATHOPHYSIOLOGY Obstructive atelectasisFollowing obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading

to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airlesslung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A filling of the alveolar spaceswith secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. Theuninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart andmediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.

Nonobstructive atelectasisThe loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructiveatelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusionsaffect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleural-

based lung mass may cause compression atelectasis by decreasing lung volumes.Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl

phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of

production or inactivation of surfactant, which may occur in ARDS, radiation pneumonitis, and blunt trauma

to the lung, cause alveolar instability and collapse.Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobe and/orlingula) has recently been reported as the pulmonary manifestation of primary Sjgren syndrome.Scarring of the lung parenchyma leads to cicatrization atelectasis.

Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma.Platelike atelectasisAlso called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs.Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of

hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occurbecause of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia,hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because ofventilation-perfusion mismatch and intrapulmonary shunt.

Postoperative atelectasisAtelectasis is a common pulmonary complication in patients following thoracic and upper abdominal

procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic

dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental indistribution.

ETIOLOGY &

EDPIDEMOLOGY

The most common cause is post-surgical atelectasis, characterized by splinting, restricted breathing afterabdominal surgery.Smokers and theelderly are at an increased risk. Outside of this context, atelectasis

implies some blockage of abronchiole orbronchus,which can be within the airway (foreign body, mucusplug), from the wall (tumor, usuallysquamous cell carcinoma)or compressing from the outside (tumor,lymph node,tubercle). Another cause is poorsurfactant spreading duringinspiration,causing an increase insurface tension which tends to collapse smaller alveoli. Atelectasis may also occur during suction, as along
http://en.wikipedia.org/wiki/Alveolihttp://en.wikipedia.org/wiki/Consolidation_(medicine)http://en.wikipedia.org/wiki/Tobaccohttp://en.wikipedia.org/wiki/Elderlyhttp://en.wikipedia.org/wiki/Bronchiolehttp://en.wikipedia.org/wiki/Bronchushttp://en.wikipedia.org/wiki/Squamous_cell_carcinomahttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Lymph_nodehttp://en.wikipedia.org/wiki/Tuberculosishttp://en.wikipedia.org/wiki/Pulmonary_surfactanthttp://en.wikipedia.org/wiki/Inhalationhttp://en.wikipedia.org/wiki/Surface_tensionhttp://en.wikipedia.org/wiki/Surface_tensionhttp://en.wikipedia.org/wiki/Inhalationhttp://en.wikipedia.org/wiki/Pulmonary_surfactanthttp://en.wikipedia.org/wiki/Tuberculosishttp://en.wikipedia.org/wiki/Lymph_nodehttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Squamous_cell_carcinomahttp://en.wikipedia.org/wiki/Bronchushttp://en.wikipedia.org/wiki/Bronchiolehttp://en.wikipedia.org/wiki/Elderlyhttp://en.wikipedia.org/wiki/Tobaccohttp://en.wikipedia.org/wiki/Consolidation_(medicine)http://en.wikipedia.org/wiki/Alveoli


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with sputum, air is withdrawn from the lungs. Another cause of Atelectasis is aPulmonary embolism (PE).

Atelectasis may be an acute or chronic condition.

Acute atelectasis is a common postoperative complication, especially after chest or abdominal surgery. Acuteatelectasis may also occur with an injury, usually to the chest (such as that caused by a car accident, a fall, ora stabbing). Atelectasis following surgery or injury, sometimes described as massive, involves most alveoliin one or more regions of the lungs.

Chronic atelectasis may take one of two formsmiddle lobe syndrome or rounded atelectasis. In middlelobe syndrome, the middle lobe of the right lung contracts, usually because of pressure on the bronchus from

enlargedlymph glands and occasionally atumor.The blocked, contractedlung may developpneumonia thatfails to resolve completely and leads tochronic inflammation,scarring, andbronchiectasis.

CLINICAL MANIFESTATIONSome client is asymptomatic. If significant, hypoxia is present; however dyspnea, tachycardia, and cyanosisIn severe cases the following is present over the affected area: -A dull percussion note-A decrease in tactile fremitus.-decrease chest movement on the involved side

-A tracheal shift toward the side of the atelectasis may occur. Symptoms may not be present if the atelectasisis minor and the patient has previously healthy lungs. Dyspnea is common when the atelectasis is severe,cough, but not prominent, chest pain, breathing difficulty, low oxygen saturation, pleural effusion (transdatetype), cyanosis (late sign), increased heart rate.

DIAGNOSTIC TESTS

ABG, chest radiography (airless area over region of atelectisis area.) Diagnosed through physical

examination when auscultation of the lungs reveal bronchial or diminished breathe sounds and crackles overthe involved area. Generally its detected on a chest radiograph.


Chest physiotherapy, lung expansion therapy, artificial surfactant, analgesics, bronchodilators, antieffective

agents, surgical excision or insertion of drainage tube, bronchoscopy.

NURSING MANAGEMENT

Elevate for dyspnea, decreased chest wall expansion, diaphoresis, tachypnea, tachycardia and pleuritic chest

pain. Auscultate for abnormal breath sounds. Pulse oximetry and hypoxemia, instruct & monitor the use ofincentive spirometry.

Localized airway obstruction related to mucus plugging.


Nursing care focuses on preventing atelectasis, especially when the client is at risk because of failure toaerate the lungs properly. Postoperative deep breathing and coughing can prevent atelectasis. If atelectasis

occurs, the nurse encourages the client to take deep breaths and coughs at frequent intervals and instructs theclient in the use of an incentive spiromter.

COMPLICATIONSComplications arising from underlying disorderHypoxemiaSecondary infection of the atelectatic lungBronchiectasis in the atelectatic of the chronically infected lung
http://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Lymphhttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Chronic_inflammationhttp://en.wikipedia.org/wiki/Bronchiectasishttp://en.wikipedia.org/wiki/Bronchiectasishttp://en.wikipedia.org/wiki/Chronic_inflammationhttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Lymphhttp://en.wikipedia.org/wiki/Pulmonary_embolism


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MEDICAL DIAGNOSIS

Pleural effusion

DEFINITIONIs an accumulation of fluid in the pleural spaces. Two types transcudate and exudate

PATHOPHYSIOLOGY Pleural effusion is an indicator of a pathologic process that may be of primary pulmonary origin or of

an origin related to another organ system or to systemic disease. It may occur in the setting of acute orchronic disease and is not a diagnosis in itself.

Normal pleural fluid has the following characteristics: clear ultrafiltrate of plasma, pH 7.60-7.64,

protein content less than 2% (1-2 g/dL), fewer than 1000 WBCs per cubic millimeter, glucose contentsimilar to that of plasma, lactate dehydrogenase (LDH) level less than 50% of plasma and sodium, and

potassium and calcium concentration similar to that of the interstitial fluid.

The principal function of pleural fluid is to provide a frictionless surface between the two pleurae inresponse to changes in lung volume with respiration. The following mechanisms play a role in the

formation of pleural effusion:

Altered permeability of the pleural membranes (eg, inflammatory process, neoplastic disease,pulmonary embolus)

Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, hepatic cirrhosis) Increased capillary permeability or vascular disruption (eg, trauma, neoplastic disease,

inflammatory process, infection, pulmonary infarction, drug hypersensitivity, uremia,

pancreatitis)

Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg,congestive heart failure, superior vena caval syndrome)

Reduction of pressure in pleural space; lung unable to expand (eg, extensive atelectasis,mesothelioma)

Inability of the lung to expand (eg, extensive atelectasis, mesothelioma) Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or

rupture (eg, malignancy, trauma)

Increased fluid in peritoneal cavity, with migration across the diaphragm via the lymphatics(eg, hepatic cirrhosis, peritoneal dialysis)

Movement of fluid from pulmonary edema across the visceral pleura Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing

accumulation of further fluid

Iatrogenic causes (eg, central line misplacement)

ETIOLOGY &

EDPIDEMOLOGY

Transcudate: congestive heart failure, cirrhosis, peritoneal dialysis, pericarditis.Exudates;TB, trauma, lung cancer, respiratory infection, heart surgery complications, pneumonia,

metastatic disease.OrConditions that interferes with either secretion or drainage of pleural fluid leads to effusion. It can be

grouped into 4 groups: Increased systemic hydrostatic pressure.(e.g., heart failure.)Reduced capillary oncotic pressure ( e.g. Liver or renal failure.)

Increased capillary permeability ( e.g. Infections of trauma)Impaired lymphatic function ( e.g. Lymphatic obstruction caused by tumor)

CLINICALDepends on the amount of fluid present& severity of lung compression. There may be dyspnea ,

primarily on exertion, and a dry non productie cough cause by bronchial irritation or mediastinal shift.


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MANIFESTATION Tactile fremitus may be decreased or absent , percussion note dull or flat

DIAGNOSTIC TESTSThoractcentesis is used to remove excess pleural fluid.the removed fluid is assess to determine weatherwhether it is transudate or exudates. Differenciating the fliud type helps extablish a specificdiagnosis.other test include white blood cell, malignant cells, bacteria, Glucose, ph, LDH.

MEDICAL/SURGICAL

MANAGEMENTINCLUDING

PHARMACOLOGICAL

Two features of human parietal pleura explain its role in the formation and removal of pleural

liquid and protein in the normal state: the proximity of the microvessels to the pleural surfaceand the presence of stomata situated between mesothelial cells. For pleural fluid to

accumulate in disease, there must be increased production from increased hydrostatic

pressure, decreased oncotic or pleural pressure, increased microvascular permeability, or

peritoneal-pleural movement. The rate of formation must overwhelm lymphatic clearance,

which may be decreased by hydrostatic forces or blocked by malignant infiltration.

NURSING MANAGEMENT

Assess patient for respiratory changes and chest pain during inspiration. Auscultate lungs for decreased

breath sounds or a pleural rub. Perform chest percussion and assess for alterations in tactile fremitus.Monitor pulse oximetry.

Help client into a position that maximizes ventilation, typically high Fowler's position. Teach clientdeep-breathing and effective coughing techniques. Show client how to splint his chest during coughing

and how to perform incentive spirometry.

Provide supplemental oxygen, as ordered.

If client requires thoracentesis or insertion of a chest tube, gather the equipment and explain theprocedure. Provide emotional support; administer analgesics, as ordered; and assist with positioning.Prepare to receive specimen tubes as the physician removes fluid.

If your patient has a chest tube inserted, monitor the amount and type of fluid drained. Maintain thefluid level in the suction control chamber and watch for bubbling in the water seal chamber. If the

bubbling stops, evaluate whether the lung has completely reexpanded or if the drainage tube hasbecome occluded.

Complete a respiratory assessment after each procedure and as needed. Increased dyspnea, decreased orabsent breath sounds, and increased pain on inspiration could indicate further effusion or developmentof a pneumothorax.


Ineffective breathing pattern related to decreased lung expansion.

COMPLICATIONSDelaying antimicrobial therapy for parapneumonic and other effusions, when antimicrobial therapy isindicated, potentially increases the risk of developing empyema, pulmonary fibrosis, and sepsis.


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MEDICAL DIAGNOSISPleuritis

DEFINITION

Pleurisy is inflammation of the linings around the lungs thepleura.There are two layers of pleura: one

covering the lung termed thevisceralpleura and the other covering the inner wall of the chest theparietalpleura. These two layers are lubricated by pleural fluid.

PATHOPHYSIOLOGY The pleural space normally contains 0.10.2 ml/kg bodyweight of fluid, filtered from systemic capillariesdown a smallpressure gradient. Fluid drains into the systemic circulationvia a delicate network oflymphatics and eventually enters themediastinal lymph nodes. Fluid may accumulate in the pleuralspace by

a number of mechanisms: increased pulmonary capillarypressure, decreased (more negative) intrapleuralpressure (e.g.atelectasis), decreased plasma oncotic pressure (e.g. hypoalbuminaemia),increased pleuralmembrane permeability and obstructed lymphaticflow (e.g. pleural malignancy or infection).


Pleurisy can be caused by any of the following conditions

Infections:bacterial (including those that causetuberculosis), fungus, parasites, or viruses

Inhaled chemicals or toxic substances: exposure to some cleaning agents like ammonia

Collagen vascular diseases:lupus,rheumatoid arthritis

Cancers:for example, the spread oflung cancer orbreast cancer to the pleura

Tumors of the pleura:mesothelioma orsarcoma

Congestion:heart failure

Pulmonary embolism:blood clot inside the blood vessels to the lungs. These clots sometimes severelyreduce blood and oxygen to portions of the lung and can result in death to that portion of lung tissue (termedlung infarction). This, too, can cause pleurisy.

Obstruction of lymph channels:as a result of centrally located lung tumors

Trauma:rib fractures or irritation from chest tubes used to drain air or fluid from the pleural cavity in thechest

Certain drugs:drugs that can cause lupus-like syndromes (such asHydralazine,Procan,Dilantin, and others)

Abdominal processes:such aspancreatitis,cirrhosis of the liver

Lung infarction:lung tissue death due to lack of oxygen from poor blood supply


Pain in the chest that is aggravated by breathing

Shortness of breath"Stabbing" sensationThe most common symptom of pleurisy is pain that is generally aggravated by inspiration (breathing in).Although the lungs themselves do not contain any pain nerves, the pleura contains abundant nerve endings.

When extra fluid accumulates in the space between the layers of pleura, the pain usually is a less severe formof pleurisy. With very large amounts of fluid accumulation, the expansion of the lungs can be limited, andshortness of breath can worsen.

DIAGNOSTIC TESTSChest x-rayAchest x-ray takes a picture of the heart and lungs. It may show air or fluid in the pleural space.It also may show what's causing the pleurisyfor example, pneumonia, a fractured rib, or a lung tumor.
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Sometimes an x-ray is taken while lying on the painful side. This may show fluid that did not appear on thestandard x-ray taken while standing.

UltrasoundUltrasonography uses sound waves to create pictures of the lungs. It may show where fluid islocated in the chest. It also can show some tumors.

Magnetic resonance imaging (MRI)Magnetic resonance imaging (MRI), also called nuclear magnetic

resonance (NMR) scanning, uses powerful magnets and radio waves to show pleural effusions and tumors.

Blood tests:Blood tests can detect bacterial or viral infection, pneumonia,rheumatic fever,a pulmonary

embolism, or lupus.

Arterial blood gasInarterial blood gas sampling,a small amount of blood is taken from anartery,usually inthe wrist. The blood is then checked foroxygen andcarbon dioxide levels. This test shows how well the

lungs are taking in oxygen


Treatment has several goals:

Remove the fluid, air, or blood from the pleural space Relieve symptoms Treat the underlying condition

Procedures: If large amounts of fluid, air, or blood are not removed from the pleural space, they may putpressure on the lung and cause it to collapse. The surgical procedures used to drain fluid, air, or blood fromthe pleural space are as follows:

During thoracentesis, a needle or a thin, hollow, plastic tube is inserted through the ribs in the backof the chest into the chest wall. A syringe is attached to draw fluid out of the chest. This procedure

can remove more than 6 cups (1.5 liters) of fluid at a time.

When larger amounts of fluid must be removed, a chest tube may be inserted through the chestwall. The doctor injects a local painkiller into the area of the chest wall outside where the fluid is.A plastic tube is then inserted into the chest between two ribs. The tube is connected to a box thatsuctions the fluid out. A chest x-ray is taken to check the tube's position.

A chest tube also is used to drain blood and air from the pleural space. This can take several days.The tube is left in place, and the patient usually stays in the hospital during this time.

Sometimes the fluid contains thick pus or blood clots, or it may have formed a hard skin or peel.This makes it harder to drain the fluid. To help break up the pus or blood clots, the doctor may usethe chest tube to put certain medicines into the pleural space. These medicines are calledfibrinolytics.If the pus or blood clots still don't drain out, surgery may be necessary.

Medications

A couple of medications are used to relieve pleurisy symptoms:

Paracetamol (acetaminophen) oranti-inflammatory agents to control pain and decreaseinflammation. Onlyindomethacin (brand name Indocin) has been studied with respect to relief of

pleurisy.

Codeine-basedcough syrups to control a coughThere may be a role for the use ofcorticosteroids (for tuberculous pleurisy),tacrolimus (Prograf) and

methotrexate (Trexall, Rheumatrex) in the treatment of pleurisy. Further studies are needed before theyare used routinely.
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Empyema in the pleural cavity is sometimes called empyema thoracis, or empyema of the chest.

PATHOPHYSIOLOGY In normal breathing, air is drawn in through thebronchi and into thealveoli,which are tiny sacs surrounded

by capillaries. Alveoli absorboxygen and then transfer it into theblood.When toxicants, such as cigarettesmoke, are breathed into the lungs, the harmful particles become trapped in the alveoli, causing a localizedinflammatory response. Chemicals released during the inflammatory response (e.g.,elastase)can eventually

cause thealveolar septum to disintegrate. This condition, known as septal rupture, leads to significantdeformation of the lung architecture. These deformations result in a large decrease of alveoli surface areaused for gas exchange. To accommodate the decreased surface area, thoracic cage expansion (barrel chest)and diaphragm contraction (flattening) take place. Expiration increasingly depends on the thoracic cage andabdominal muscle action, particularly in the end expiratory phase. Due to decreased ventilation, the ability toexude carbon dioxide is significantly impaired. In the more serious cases, oxygen uptake is also impaired.

As the alveoli continue to break down, hyperventilation is unable to compensate for the progressivelyshrinking surface area, and the body is not able to maintain high enough oxygen levels in the blood. The

body's last resort is vasoconstricting appropriate vessels. This leads to pulmonary hypertension, which placesincreased strain on the right side of the heart, the side responsible for pumping deoxygenated blood to the

lungs. The heart muscle thickens in order to pump more blood. This condition is often accompanied by theappearance of jugular venous distension. Eventually, as the heart continues to fail, it becomes larger and

blood backs up in the liver


Empyema results as a complication of bacterial infections such as pneumonia and lung abscess.

Empyema may be caused by bacteria such as Streptococcus pneumonia, Staphylococcus aureus, orHaemophilus influenza type b. The infected fluid may be build up to a quantity of a pint or more, which puts

pressure on the lungs, causing shortness of breath and pain. The infected fluid can build up to a quantity of apint or more.

Empyema thoracis may be caused by a number of different organisms, fungi, and amebas, in connection with

pneumonia, chest wounds, chest surgery, lung abscesses, or a ruptured esophagus. Pelvic empyema inwomen is most often caused byBacteroides strains or Pseudomonas aeruginosa.

CLINICAL MANIFESTATIONPhysical findings include tachypnea, and decreased breath sounds; percussion over the effused area, detectsdullness, which doesn't change with breathing. The signs and symptoms of empyema vary somewhat

according to the location of the infection and its severity. Ultrasound confirms the size and location of thepocket of pus and the presence of fibrin aggregates.

The symptoms of the empyema may be included: fever & cough, coma, malaise, fatigue, sweating, weightloss, chest pain, general discomfort, shortness of breath.

DIAGNOSTIC TESTSChest x ray, arterial blood gas, sputum specimen, pulmonary function test

The goal of treatment is to cure the infection and remove the collection of pus from the lung. A chest tube is
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PHARMACOLOGICAL

inserted to drain the pus from the pleural space. Ultrasound has been used to evaluate empyema. Someevidence suggests that intrapleural fibrinolytic drugs may be useful, especially in children. Intravenous

antibiotics may be given. If this is insufficient, surgical decortication of the pleura may be required.Mechanical ventilation, bronchodilators, corticosteroids, beta agonists, methylxanthines H.F position.

NURSING MANAGEMENTGive O2 at 2L because with emphysema excessive exogenous O2diminishes the respiratory drive and results in breathing and CO2retention (CO2 narcosis). Normally CO2 stimulates breathing. With

emphysema there is chronic CO2 and as a result low O2 stimulatesbreathing Teach diaphragmatic and pursed-lip breathing to extend exhalation andkeep alveoli open


Impaired gas exchange related to decreased ventilation and mucus plugs.

COMPLICATIONS The list of complications that have been mentioned in various sources for Emphysema includes:

Finger clubbing

Recurrent chest infections

Heart failure

Right-sided heart failure

Often individuals who are unfortunate enough to contract this disease have a very short life expectancy often

0-3 years at most
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MEDICAL DIAGNOSIS

Acute Bronchitis

DEFINITION

Bronchitis is a respiratory disease in which the mucous membrane in the lungs' bronchial passages becomes

inflamed. As the irritated membrane swells and grows thicker, it narrows or shuts off the tiny airways in thelungs, resulting in coughing spells accompanied by thick phlegm and breathlessness. The disease comes in

two forms: acute (lasting less than 6 weeks) and chronic (reoccurring frequently for more than two years). Inaddition, people withasthma also experience an inflammation of the lining of the bronchial tubes calledasthmatic bronchitis.

Acute bronchitis is responsible for the hacking cough and phlegm production that sometimes accompanyanupper respiratory infection. In most cases the infection is viral in origin, but sometimes it's caused by

bacteria.

PATHOPHYSIOLOGY Respiratory viruses are the most common causes of acute bronchitis. The most common viruses includeinfluenza A and B, parainfluenza, respiratory syncytial virus, and coronavirus, although an etiologic agent isidentified only in a minority of cases.

During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous

membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently,the air passages become clogged by debris and irritation increases. In response, copious secretion of mucusdevelops, which causes the characteristic cough of bronchitis. For instance, with mycoplasmal pneumonia,

bronchial irritation results from the attachment of the organism (Mycoplasma pneumoniae) to the respiratorymucosa, with eventual sloughing of affected cells. Acute bronchitis usually lasts approximately 10 days. Ifthe inflammation extends downward to the ends of the bronchial tree, into the small bronchi (bronchioles),

and then into the air sacs, bronchopneumonia results.Chronic bronchitis is a condition associated with excessive tracheobronchial mucus production sufficient tocause cough with expectoration for at least 3 months for more than 2 consecutive years. The alveolarepithelium is both the target and the initiator of inflammation in chronic bronchitis.


Acute bronchitis is generally caused by lung infections; approximately 90% of these infections are viralinorigin, 10% bacterial. Chronic bronchitis may be caused by one or several factors. Repeated attacks ofacute bronchitis, which weaken and irritate bronchial airways over time, can result in chronic bronchitis,

Industrial pollution is another culprit

CLINICAL MANIFESTATIONA cough that is frequent and produces mucus

A lack of energy

A wheezing sound when breathing, which may or may not be present

A fever, which may or may not be present

DIAGNOSTIC TESTScultures of respiratory secretions for influenza virus,M pneumoniae,andBordetella pertussiswhen theseorganisms are suspected.

Obtain a throat swab. Obtain a CBC count with differential. Blood culture may sometimes be helpful if bacterial superinfection is suspected. Sputum cytology may be helpful if the cough is persistent Culture and Gram stain of sputum is often performed Chest radiography should be performed in those patients whose physical examination findings

suggest pneumonia.

Bronchoscopy may be needed to exclude foreign body aspiration, tuberculosis, tumors, and other
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chronic diseases of the tracheobronchial tree and lungs.


Medical therapy generally targets symptoms and includes use of analgesics and antipyretics. These agents

are used to control fever, myalgias, and arthralgias.

Acetaminophen (Tylenol, Aspirin-Free Anacin, Feverall)

Treatment of choice for pain in patients who are unable to take aspirin or NSAIDs.

Ibuprofen (Ibuprin, Advil, Motrin)

Usual treatment of choice for mild-to-moderate pain if no contraindications exist. Inhibits inflammatory

reactions and pain, probably by decreasing activity of cyclooxygenase, which inhibits prostaglandinsynthesis.

Corticosteroids, systemic

These agents are used for short courses (3-10 d) to gain prompt control of inadequately controlled acute

asthmatic episodes. Systemic corticosteroids also are used for long-term prevention of symptoms in severe

persistent asthma, as well as for suppression, control, and reversal of inflammation.

NURSING MANAGEMENT1. Encourage mobilization of secretion through ambulation, coughing, and deep breathing.2. Ensure adequate fluid intake to liquefy secretions and prevent dehydration caused by fever and

tachypnea.3. Encourage rest, avoidance of bronchial irritant, and a good diet to facilitate recovery.4. Instruct the patient to complete the full course of prescribed antibiotics and explain the effect of

meals on drug absorption.

5. Caution the patient on using over-the-counter cough suppressants, antihistamines, anddecongestants, which may cause drying and retention of secretions. However, cough preparations

containing the mucolytic guaifenesin may be appropriate.6. Advise the patient that a dry cough may persist after bronchitis because of irritation of airways.

Suggest avoiding dry environments and using a humidifier at bedside. Encourage smoking

cessation.7. Teach the patient to recognize and immediately report early signs and symptoms of acute

bronchitis.


Abnormal breathing sounds related to ineffective cough

COMPLICATIONS Complications occur in approximately 10% of patients with acute bronchitis and include the

following:o Bacterial superinfectiono Lower respiratory tract infection and pneumonia: Less than 5% of patients with

bronchitis develop pneumonia. The incidence of subsequent pneumonia, however,

remains unaffected by the use of antibiotics.o Chronic bronchitis: Repeated episodes of acute bronchitis may lead to chronic bronchitis.o Reactive airway disease: Acute bronchitis may lead to reactive airway disease.o Hemoptysis


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MEDICAL DIAGNOSIS

Lung abscess

DEFINITIONLung abscessisnecrosis of thepulmonary tissue and formation of cavities (more than 2 cm) containingnecrotic debris or fluid caused bymicrobial infection.

This pus-filled cavity is often caused by aspiration, which may occur during altered consciousness.Alcoholism is the most common condition predisposing to lung abscesses

PATHOPHYSIOLOGY Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouthanaerobes. The patients who develop lung abscess are predisposed to aspiration and commonly have

periodontal disease. A bacterial inoculum from the gingival crevice reaches the lower airways, and infection

is initiated because the bacteria are not cleared by the patient's host defense mechanism. This results inaspiration pneumonitis and progression to tissue necrosis 7-14 days later, resulting in formation of lung

abscess.

Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, causing

septic emboli (usually multiple) to the lung. Lemierre syndrome, an acute oropharyngeal infection followedbyseptic thrombophlebitis of the internal jugular vein, is a rare cause of lung abscesses. The oral anaerobeFnecrophorumis the most common pathogen.


Conditions contributing to lung abscessAspiration oforopharyngeal orgastric secretionSeptic emboli

NecrotizingpneumoniaVasculitis:Wegener's granulomatosis

Necrotizingtumors:8% to 18% are due toneoplasms across all age groups, higher in older people; primarysquamous carcinoma of the lung is the commonest.

OrganismsIn the post-antibiotic era pattern of frequency is changing. In older studies anaerobes were found in up to90% cases but they are much less frequent now.

Anaerobic bacteria:Peptostreptococcus,Bacteroides,Fusobacterium species,Microaerophilicstreptococcus :Streptococcus milleri

Aerobic bacteria:Staphylococcus,Klebsiella,Haemophilus,Pseudomonas,Nocardia,Escheria coli,Streptococcus,MycobacteriaFungi:Candida,AspergillusParasites:Entamoeba histolytica

CLINICAL MANIFESTATIONOnset of symptoms is often gradual, but in necrotizing staphylococcal or gram-negative bacillary

pneumonias patients can be acutely ill.Cough,fever with shivering andnight sweats are often present.Cough can be productive with foul smellingpurulentsputum (70%) or less frequently with blood (i.e.

hemoptysis in one third cases). Affected individuals may also complain of chest pain, shortness of breath,lethargy and other features of chronic illness.

Patients are generallycachectic at presentation. Fingerclubbing is present in one third of patients. Dentaldecay is common especially in alcoholics and children. On examination of chest there will be features of

consolidation such as localised dullness onpercussion,bronchial breath sound etc.

DIAGNOSTIC TESTSChest Xray and other imaging studies

Abscess is oftenunilateral and single involving posterior segments of the upper lobes and the apical

segments of the lower lobes as these areas are gravity dependent when lying down. Presence of air-fluidlevels implies rupture into thebronchial tree or rarely growth of gas forming organism.

Laboratory studies
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Raised inflammatory markers (highESR,CRP)are usual but not specific. Examination of sputum is

important in any pulmonary infections and here often reveals mixed flora.Transtracheal ofTransbronchial(via bronchoscopy) aspirates can also be cultured. Fibre opticbronchoscopy is often performed to excludeobstructive lesion; it also helps in bronchial drainage of pus.

MEDICAL/SURGICAL


Antibiotic therapy

Standard treatment of an anaerobic lung infection is clindamycin (600 mg IV q8h followed by 150-300 mg PO qid). This regimen has been shown to be superior over parenteral penicillin in

published trials. Several anaerobes may produce beta-lactamase (eg, various species ofBacteroidesandFusobacterium) and therefore develop resistance to penicillin.

Although metronidazole is an effective drug against anaerobic bacteria, the experience withmetronidazole in treating lung abscess has been rather disappointing because these infections aregenerally polymicrobial. A failure rate of 50% has been reported.

In hospitalized patients who have aspirated and developed a lung abscess, antibiotic therapy shouldinclude coverage against S aureusandEnterobacterandPseudomonasspecies.

Ampicillin plus sulbactam is well tolerated and as effective as clindamycin with or without acephalosporin in the treatment of aspiration pneumonia and lung abscess.

Moxifloxacin is clinically effective and as safe as ampicillin plus sulbactam in the treatment ofaspiration pneumonia and lung abscess.Duration of therapy

Although the duration of therapy is not well established, most clinicians generally prescribeantibiotic therapy for 4-6 weeks.

Expert opinion suggests that antibiotic treatment should be continued until the chest radiograph hasshown either the resolution of lung abscess or the presence of a small stable lesion.

The rationale for extended treatment maintains that risk of relapse exists with a shorter antibioticregimen.

NURSING MANAGEMENT Antibiotic administration as indicatedChest physiotherapy

Ensure proper nutritional intakeEmotional support


Impaired gas exchange related to mismatch between ventilation and perfusion as a result of a thoracotomy

COMPLICATIONS Complications of pulmonary abscess

o Rupture into pleural space causing empyemao Pleural fibrosiso Trapped lungo Respiratory failureo Bronchopleural fistulao Pleural cutaneous fistula

In a patient with coexisting empyema and lung abscess, draining the empyema while continuingprolonged antibiotic therapy is often necessary.
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MEDICAL DIAGNOSIS

Pneumothorax

DEFINITION

Presence of air in pleural cavity:the presence of air or gas in the pleural cavity surrounding the lungs,

causing pain and difficulty in breathing. This creates positive intrapleural pressure and prevents proper lunginflation. If this accumulation is of a sufficient size, the lung parenchyma may collapse.

PATHOPHYSIOLOGY Thelungs are located inside the chest cavity, which is a hollow space. Air is drawn into the lungs by the

diaphragm (a powerfulabdominalmuscle). Thepleural cavity is the region between the chest wall and thelungs. If air enters the pleural cavity, either from the outside (open pneumothorax) or from the lung (closed

pneumothorax), the lung collapses and it becomes mechanically impossible for the injured person to breathe,even with an openairway.If a piece of tissue forms a one-way valve that allows air to enter the pleural

cavity from the lung but not to escape, overpressure can build up with every breath; this is known astensionpneumothorax.It may lead to severe shortness of breath as well as circulatory collapse, both life-threateningconditions. This condition requires urgent intervention.


It most commonly arises:

Spontaneously (most commonly in tall slim young males and inMarfan syndrome) Following a penetrating chest wound FollowingBarotrauma to the lungs

It may also be due to:

Chroniclung pathologies includingemphysema,asthma Acuteinfections Chronic infections, such astuberculosis Lung damage caused bycystic fibrosis Cancer Rare diseases that are unique to women such asCatamenial pneumothorax (due toendometriosis in

the chest cavity) andlymphangioleiomyomatosis (LAM).

Pneumothoraces are divided into tension and non-tension pneumathoraces. Atension pneumothorax is amedical emergency as air accumulates in the pleural space with each breath. The increase inintrathoracic

pressure results in massive shifts of themediastinum away from the affected lung compressingintrathoracic

vessels.A non-tension pneumothorax by contrast is of lesser concern because there is no ongoingaccumulation of air and hence no increasing pressure on the organs within the chest.

The accumulation ofblood in thethoracic cavity (hemothorax)exacerbates the problem, creating ahemopneumothorax.


Signs and symptoms of a pneumothorax usually include:

Sudden, sharp chest pain on the same side as the affected lungthis pain doesn't occur in the center of

your chest under the breast bone

Shortness of breath, which may be more or less severe, depending on how much of your lung is collapsed

A feeling of tightness in your chest
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