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251 Cards in this Set
- Front
- Back
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What is hypoxia? |
Reduction of O2 in tissues? |
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What is hypoxemia? |
A reduction in arterial blood O2 levels (partial pressure of oxygen, PO2) |
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What causes hypoxemia? |
*Inadequate amount of O2 in air *Diseases of respiratory system *Dysfunction of neuro system *Alterations in the circulatory system |
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What do mechanisms of respiratory diseases lead to? |
*Hypoventilation *Impaired diffusion of gases *Inadequate circulation of blood through pulmonary capillaries *Mismatch of ventilation and perfusion |
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What are some clinical manifestations of mild hypoxemia? |
*Tachycardia *Tachypenia *Peripheral vasoconstriction *Diaphoresis *Cool skin *Increased BP *Slight impairment of mental performance and visual acuity *Hyperventilation may occur |
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What organs have the greatest need for O2? |
The brain and heart. |
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What happens if PO2 falls below a critical level? |
*Aerobic metabolism stops *Anaerobic metabolism takes over *Lactic acid is released which increases lactate levels and metabolic acidosis |
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What are some manifestations of pronounced hypoxemia? |
*Personality changes *Restlessness *Agitated or combative behavior *Uncoordinated muscle movements *Cyanosis (very late sign) *Euphoria *Impaired judgement *Delirium *Eventually stupor and coma |
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What are some manifestations of chronic hypoxemia? |
*May be insidious (slow) in onset *Clubbing of fingers *Body compensations: Increased ventilation, pulmonary vasoconstriction, increased production of red blood cells. |
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Describe cyanosis. |
*Bluish coloring of skin and mucous membranes *Excessive concentration of reduced or deoxygenated hemoglobin in the small blood vessels. *Mostly seen on the lips, nail beds, ears, and cheeks. |
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What are the two types of cyanosis? |
Central and peripheral. |
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Describe central cyanosis. |
*Increased amount of deoxygenated hemoglobin in ARTERIAL BLOOD. *Affects mucous membranes and skin (lips) |
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Describe peripheral cyanosis. |
*Caused by slowing of blood flow to a body area and increased extraction of oxygen. *Occurs in extremities (finger tips) and in the tip of nose or ears. |
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How is hypoxemia diagnosed? |
By... *Clinical manifestations *Diagnostic measures of PO2 levels *Pulse oximetry |
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What is the best diagnostic measure of PO2 levels? |
ABG (arterial blood gases) - blood taken from artery, usually radial or femoral. Can be painful. |
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What is a pulse oximetry? |
A non-invasive measurement of arterial O2 saturation of hemoglobin |
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How is hypoxemia treated? |
*Correct the cause of the disorder *O2 supplement by nasal cannula, face mask or mechanically ventilated |
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How can you tell you've pulled blood from an artery and not a vein? |
Look at the color of the blood. It should be bright red, not dark red. |
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What is hypercapnia? |
Increased arterial carbon dioxide content of the blood (PO2). |
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What are some contributing factors to hypercapnia? |
*Alterations in CO2 production (fever or disease) *Disturbance in gas exchange function of the lung *Abnormalities in chest wall and respiratory muscles *Changes in the neural control of respiration |
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Hypercapnia is only observed when... |
Hypoventilation causes hypoxia |
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What are the clinical manifestations of hypercapnia? |
*Effects several body systems (Acid-base balance -decreased pH; respiratory acidosis-, Kidney function, Nervous system function, Cardiovascular function) *Headache *Blood shot eyes (hyperemia) *Flushed skin *Depression of CNS function *Air hunger *Tachypnea *Tachycardia |
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What is the treatment for Hypercapnia? |
*Decrease the work of breathing *Improving the ventilation-perfusion balance at the aveolar level *Use of intermittent rest therapy *Use of respiratory muscle retraining (long-term) *Mechanical ventilation (last thing to do) |
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What is COPD and describe it? |
*2 respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways (Emphysema and Chronic bronchitis) *Usually progressive in nature, accompanied by inflammatory responses to noxious particles or gases. *Symptoms are not evident until the disease is in advanced stages. |
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What is the leading cause of mobidity and mortality world wide? |
COPD |
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What are some risk factors for COPD? |
*Smoking is the most common cause *A hereditary deficiency in alpha one antitrypsin *Asthma and airway hyper-responsiveness |
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What is the etiology and pathogenesis of COPD? |
*Inflammation and fibrosis of the bronchial wall *Hyper-secretion of mucus (bronchitis part of disease) *Loss of elastic lung fibers *Destruction of alveolar tissue *Encompasses the 2 types of obstructive airway dz - emphysema and chronic obstructive bronchitis. |
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What is emphysema and describe it. |
*Chronic disease characterized by destructive changes in the alveolar walls with an accompanying enlargement of air spaces and narrowing of small airways. *Only about 10% of patients with COPD have emphysema |
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What are the 2 recognized causes of emphysema? |
Smoking and inherited deficiency of alpha one antitrypsin |
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What are the pathological changes of emphysema? |
*Loss of elasticity *Lung hyperinflation *Formation of bullea (a large vesicle) *Airway collapse and air trapping in vessel. |
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What are the two types of emphysema?Describe each. |
*Panlobular or Panacinar - Inital invloves the peripheral alveoli; later extends to the more central bronchioles. Destruction happens from the periphery inward. *Centrolobular or centriacinar - Affects the bronchioles in the central part of the lobe initially, then the alveoli. Destruction happens from the central outward. |
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What are some clinical manifestations of emphysema? |
*Early/mid disease state able to maintain normal ABGs. *Late - chronic respiratory acidosis (hypercapnia) and ventilator drive depends on oxygen chemoreceptors instead of CO2 receptors. *"Pink puffers" - lack of cyanosis, barrel chest, pursed-lip breathing, SOB (dyspnea), decreased breath sounds, cachexia (muscle wasting), use of accessory muscles, clubbing of extremities. |
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What is chronic bronchitis? |
*Represents airway obstruction of the major and small airways resulting from exposure to infectious or non-infections irritants that produce an inflammatory response. *Chronic inflammation causes hypertrophy and hyperplasia of mucous glands and causes excess mucus production. *Airflow is impaired by thickening of bronchial walls and excess mucus production (can block smaller airways) *Mucus stasis can lead to secondary infections and mucus plugs impair gas exchange. |
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What results from the impaired gas exchange caused by mucus in chronic bronchitis? |
Hypoxemia and hypercapnia |
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How is a patient diagnosed with chronic bronchitis? |
*History of a chronic productive cough - 3 consecutive months in a least 2 consecutive years *Chronic cough with gradual increase in acute exacerbations that produce frankly purulent sputum *Earliest feature - hyper-secreation of mucus in the large airways |
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What types of infections are common with chronic bronchitis? |
Viral and bacterial (pneumonias) |
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What are the clinic manifestations of chronic bronchitis? |
*"Blue bloaters" - cyanosis and fluid retention associated with right-sided heart failure *SOB *Cyanosis *Cor pulmonale - enlarged right ventricle *Peripheral edema - due to right sided heart failure *Crackles on auscultation Polycythemia - increase in red blood cell count |
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What are the clinical manifestations of COPD? |
*Insidious onset *Fatigue, exercise intolerance, cough, sputum production, SOB, productive cough in am, dyspnea becomes more sever as the disease progresses *Frequent exacerbations of infection and respiratory insufficiency are common *Causes an absence from work and/or disability |
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What % of people with COPD have emphysema and/or chronic bronchitis? |
90% of patients with COPD have some degree of both 10% have only emphysema |
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Is it difficult to differentiate between the two types of COPD? |
Yes |
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Name some progression of s/s of COPD. |
*Expiratory phase of respiration is prolonged *Activities involving significant are work, particularly above the shoulders are difficult *Weight loss |
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How are patients with COPD diagnosed? |
*History and physical exam *Pulse ox *Pulmonary function test (PFTs) done in the respiratory dept. *Chest rads or CT scans *Labs - CBC to look at RBC and H&H, ABGs to look at PPO2 and PPCO2 |
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What is bronchial asthma? |
*Progressive respiratory disease characterized by inflammation of the respiratory tract and spasm of airway bronchiolar smooth muscle *Results in excess mucus production and accumulation, obstruction to airflow and a decrease in ventilation of the alveoli *Leading cause of chronic illness in children *Prevalence rates have increased over the past several years. |
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What is the etiology and pathogenesis of bronchial asthma? |
*Exaggerated hypersensitivity response to a variety of stimuli *Presence of inflammatory cells (eosinophils, lymphocytes and mast cells) *Damage to the bacterial epithelium contributes to the pathogenesis of the disease. |
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What are the types of bronchial asthma? Which one is typical. |
*Extrinsic (atopic) asthma (Typical) *Intrinsic asthma or bronchospastic |
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Describe extrinsic (atopic) asthma |
*Initiated by a Type I hypersensitivity reaction induced by exposure to an extrinisic antigen or allergen *Usually has onset in childhood/adholescence *Usually have other allergic disroders *Two phases - acute/late |
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Describe the acute phase of extrinsic (atopic) asthma |
*Chemical mediators from the pre-sensitized mast cells *Increased mucus production *Opening of mucosal intercellular juctions *BRONCHOSPASM |
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Describe the late-phase response |
*Develops 4-8 hours after exposure *Set in motion a vicious cycle for exacerbations *Release of inflammatory mediators *Increased vascular permeability and edema *BRONCHOSPASM |
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Describe the triggers of Intrinsic asthma or bronchospastic. |
*Respiratory tract infections
*exercise *hyperventilation *Cold air *Drugs and chemicals *Hormonal changes *Emotional upsets *Air pollutants *Gastro-esophageal reflux |
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What are the clinical manifestations of bronchoasthma? |
*Significant dyspnea *Tachypnea (rapid breathing) and shallow breathing *Coughing *Audible wheezing upon ascultation of the lungs, typically expiratory unless the condition is severe then both *Use of accessory muscles *Chest retractions *Anxiety*Air trapping*Fatigue*Skin is cool and moist*Ability to speak only 1-2 words at a time |
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How are patients with bronchoasthma diagnosed? |
*History and physical exam
*Lab tests - CBC w/diff *Pulmonary function tests (PFT) |
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How are bronchoasthma treated? |
*Control factors *Relaxation *Desensitization *Pharmacological treatments |
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What are upper airways? |
Nose to lungs |
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What are the chest and lower respiratory tract conditions? |
*Pneumonias *Tuberculosis |
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Describe pneumonias |
*Inflammation of parenchymal structures of the lung (alveoli and bronchioles) *4-5 million cases annually in the US; 6th leading cause of death in the US |
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What remains an important immediate cause of death of the elderly and persons with debilitating diseases? |
Pneumonias |
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What are some risk factors for pneumonias? |
*Chronic illness*viral respiratory infections*immunosuppression*age >65 years*impaired gag, cough or swallowing reflex = aspiration pneumonia*altered LOC (not coughing)*tracheostomy/intubation*organ transplants (immunocompromised)*AIDS*exposure to pollutants*prolonged bed rest/immobility*malnutrition*crowded living conditions (prisons, long-term care facilities) |
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What are the etiologic agents for pneumonias? |
*Infectious agents *Noninfectious agents (inhalation of irritating fumes, aspiration of gastric contents) |
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How are pneumonias classified? What are the classifications? |
*According to the setting in which it occurs (hospital or community) *According to the type of agent causing the infection (typical/infectious and atypical/noninfectious |
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Describe community - acquired pneumonias (CAP) |
*Infections from organisms found in the community *Begins outside of the hospital or diagnosed within 48 hours after admission to hosp *Most common bacterial cause - streptococcal pneumonia |
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Describe hospital-acquired pneumonias (HAP) |
*Also called nonsocomial pneumonias *Not present on incubating on admission to the hospital *Occur 48 hours or more after admission *2nd most common cause of hospital - acquired infection (1st is UTI) *Most are bacterial - S. aureus *Many have developed antibiotic resistance and are more difficult to treat. |
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Who is most at risk for HAP? |
*Patients needing intubation and/or mechanical ventilation *Patients with a compromised immune function *Chronic lung disease |
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What is Typical/infectious pneumonias? |
Result from infection by bacteria that multiply extracellularly in the alveoli and cause inflammation and exudation of fluid into the air-filled spaces of the alveoli. |
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What are the two patterns of distributions of typical/infectious pneumonias and describe them. |
*(A) Lobular pneumonia - consolidation of a part or all of a lung lobe * (B) Bronchopneumonia - a patchy consolidation involving more than one lobe |
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What are some risk factors for typical/infectious pneumonia? |
*People unknowingly aspirate small amounts of organisms *Loss of the cough reflex and damage to ciliated endothelium *impaired immune defenses *bacterial adherence plays a role in colonization of the lower airways *Antibiotic therapy that alters the normal bacterial flora *Diabetes *Smoking *Chronic bronchitis |
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What are the two types of typical/infectious pneumonia? |
*Pneumococcal pneumonia *Legionnaire disease |
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What is type one typical/infectious pneumonia (pneumococcal pneumonia)? |
*Most common cause of bacterial pneumonia (s. pneumonia) *A gram-positive diplococcus; possesses a capsule of polysaccharide which is hard to phagotosize *Prevents or delays digestion by phagocytes *Pathogenesis of pheumococcal pneumonia is four stages (Edema, Red hepatization, Gray hepatization, and resolution) |
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Describe the Edema stage (early stage) of pneumococcal pneumonia? |
*Alveoli become filled with protein-rich edema fluid *Productive cough (serous exudates) *Fever *Malaise *Inflammatory response starts |
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Describe the Red hepatization stage of pneumococcal pneumonia? |
*Capillary congestion *Massive outpouring of poly-morphonuclear leukocytes and red blood cells *Pleuritic pain *Bloody sputum (RBCs in there) |
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Describe the gray hepatization stage of pneumococcal pneumonia? |
*Arrival of WBC macrophages that phagocytose *Purulent sputum (WBC) *Pleuritic pain |
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Describe the Resolution stage of pneumococcal pneumonia? |
*Alveolar exudates are removed *Fever decreases *Lung gradually returns to normal |
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What are s/s of pneumococcal pneumonia? |
Depends on the age and health status of the patient. Healthy people: *Onset usually sudden*malaise*shaking and chills*fever*cough (initially-watery sputum, later-blood tinged or rust colored to purulent)*breath sounds are limited (crackles)*pleuritic pain Elderly Persons: *Less likely to get fever *Only sign may be a loss of appetite and deterioration in mental status*less likely to see s/s of healthy person. |
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How is pneumococcal pneumonia treated? Can it be prevented? |
Antibiotics. |
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Can pneumococcal pneumonia be prevented? |
Yes, by the 23-valent pneumococcal vaccine. *Given by IM injection in the deltoid *Recommended for 65yrs or age or older *Single dose allows some lifetime immunity *Antibody levels decline after 5-10 years *A 2nd dose is recommended for immunocompromised people and 65+ every 5 years |
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What is type two typical/infectious pneumonia (Legionnaire Disease)? |
*Form of bronchopneumonia *Caused by a gram-negative rod, Legionella pneumophila *Infection normally occurs by acquiring the organism from the environment (standing water) *Water that contains the pathogen is aerosolized into droplets and is inhaled or aspirated by a susceptible host *Healthy people can get it but most at risk are: smokers, chronic diseases, impaired cell-mediated immunity |
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How was Legionnaire disease discovered? |
*1st recognized after an epidemic of severe and some fatal pneumonias developed among delegates to the 1976 American Legion convention in a PA hotel - it was traced to a water-cooled air-conditioning system. |
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What are the s/s of Legionnaire disease? |
*Abrupt onset (2-10 days after infections) *Malaise, weakness and lethargy *Dry cough *CNS disturbances - confusion, somulent, coma *Hyponatremia *GI involvement *Arthralgias *Fever *Consolidation of lung tissue which impairs gas exchange |
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What are the characteristic signs of Legionnaire disease that are different than pneumococcal pneumonia? |
*Presence of pneumonia w/ diarrhea, hyponatremia, and confusion. |
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How is legionnaire disease diagnosed? |
*Clinical manifestations *Rad studies *Special lab tests to detect organism *Legionella urinary antigen test (quick and cheap) |
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Is Legionnaire disease contagious? |
Nope. |
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How is legionnaire treated? What happens if a person waits to be treated? |
With antibiotics. Delay in treatment significantly increases the mortality rate. |
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Describe atypical/noninfectious pneumonias. |
*Caused by viral and mycoplasma infection that involve the alveolar septum and the interstitium of the lungs. *Less striking symptoms and physical findings *Most common organism is mycoplasma pneumonia *Common among children and young adults *patchy involvment of lungs, confined to alveolar septum and pulmonary interstitium *Sporadic form is usually mild with a low mortality rate |
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What does atypical refer to in atypical/noninfectious pneumonia? |
*Atypical refers to the lack of lung consolidation, production of moderate amounts of sputum, moderate elevation of WBC and lack of alveolar exudate |
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What are the s/s of atypical/noninfectious pneumonias? |
*Varies widely from mild to severe *Fever *Headache *muscle aches and pains |
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How are atypical/noninfectious pneumonias diagnosed? |
*History and physical exam *Chest rads |
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Name some statistics of Tuberculosis. |
*World's foremost cause of death from a single infectious agent *1953-1984 reported cases when down each year 6% b/c of introduction of antibiotics *1985-1995 reported cases have gone up by 14% b/c of HIV |
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Which populations are at risk for TB? |
*Foreign-born persons from countries of high incidence of TB *Residence of high-risk congregate settings (prisons, homeless shelters, etc) *Long-term care facilities *HIV positive persons |
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What is the pathogenesis of TB? |
*10% of infected persons will develop active TB disease at some point in their lives *Certain conditions increase the risk that TB infection will progress to TB disease *Caused by mycobacterium M. tuberculosis |
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What conditions increase the risk that TB infection will progress to TB disease |
*HIV *Substance abuse *recent TB infection *ESRD -erythrocyte sedamentation rate disease *immunosuppressive therapy |
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Describe the mycobacterium responsible for TB |
*M. tuberculosis *slender, rod shaped, aerobic bacteria that do not form spores *similar to other bacteria except for the outer waxy capsule *more resistant to destruction *organism can persist in old necrotic and calcified lesions *remain capable to reinitiating growth *waxy coat causes organism to retain red dye when treated with acid in acid-fast staining |
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Where are the body sites of TB disease? |
*Lungs 85% of all cases *Pleura (sac around lungs) *CNS *Lymphatic system *GU system *Bone and joints *disseminated - tiny lesions all over body (resembles millet seed) |
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What is the pathophysiology of TB? |
*Transmitted by airborne droplets *Highly contagious *Four phases of disease (transmission, immune response, tubercle formation, dissemination) |
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What happens during the transmission phase of TB? |
*infected person coughs or sneezes speading infected droplets *a person inhales droplets and the bacilli are deposited in the alveoli *The bacilli are phagocytosed by alveloar macrophages but resist killing. |
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What happens during the immune response phase of TB? |
*Macrophages initiate a cell-mediated immune response that contains the infection *As the tubercle bacilli multiply, the infected macrophages degrade the mycobacteria and present their antigens to T lymphocytes which then stimulate the macrophages to increase their concentration of lytic enzymes and ability to kill the mycobacteria *The cell-mediated response plays a dominant role in walling off the tubercle bacilli and preventing the development of active TB *DISEASE ENDS HERE IN HEALTHY PEOPLE* |
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What happens during the tubercle formation phase of TB? |
*In immunocompramised patients the infection continues *macrophages that ingest the bacilli fuse to form epithelioid cell tubercules (tiny nodules surrounded by lymphocytes called a Ghon focus) *Caseous necrosis develops and scar tissue encapsulated the tubercle |
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What happens during the Dissemination phase of TB? |
*If the tubercles and inflamed nodes rupture, the infection contaminates the surrounding tissue and may spread through the blood and lymphatic circulation to distant sites |
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What is primary TB? |
*Previously unexposed& unsensitized persons *Initiated from inhaling droplet nuclei that contain the tubercle bacillus *T-lymphocytes & macrophages surround the organism in granulomas the limit their spread *DO NOT have active TB, cannot transmit it *In 5% of newly infected people the immune system is inadequate and they go on to develop progressive primary TB *As dz progresses organism gains access to sputum which is how others are infected |
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What is secondary (reactivated) TB? |
*Either reinfection from inhaled droplet nuclei or reactivation of a previously healed primary lesion *Occurs in situations of impaired body defense mechanisms *Cell-mediated hypersensitivity reaction can be an aggravating factor *Cavitation - spreads to other parts of system *Pleural effusions and empyema(pus formation) are common |
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What are the s/s of Primary TB? |
Insidious/non-specific *Fever*Weight loss*fatigue*night sweats Acute *High fever*pleuritis (pain in lung)*lymphadenitis (inflamed lymph nodes) |
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What are the s/s of secondary (reactivated) TB? |
*low-grade fever*night sweats*easy fatigability*anorexia and weight loss* *cough is initially dry then becomes productive with purulence |
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How is TB diagnosed? |
*Most frequent is TB skin test *chest rad *sputum test for organism |
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Describe the PPD test for TB |
*Mantoux Tuberculin skin test *0.1 ml of five tuberculine units PPD is administered intradermally into dorsal surface of forearm *A 6-10mm wheal should develop *measures the delayed hypersensitivity that follows exposure *Reactions are read 48-72 hours later *Measures induration by inspection and palpation. Redness is NOT significant |
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What would a chest rad show if positive for TB? |
Nodular lesions, patchy infiltrates, cavity formation, scar tissue, calcium deposits. |
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Describe sputum test for organism of TB. |
*Definitive diagnosis of active TB either from culture or ID from DNA or RNA *GOLD STANDARD cultures of solid media take up to 12 weeks *liquid medium culture systems allow for detection in several days. |
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What are the treatments for TB? |
*eliminate all tubercle bacilli from infected person while avoiding significant drug resistance *Isoniazid (INH) daily for 6-12 months Active TB: *4 drugs at once *six-month regimen |
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Is TB reportable? |
Yes and the public health department has the power to come in, take over, and confine infectious patient. |
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What is the leading cause of cancer death in both men and women in the US? |
Lung cancer |
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What accounts for the majority of cases of lung cancer that can be prevented? |
Smoking |
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What are the risk factors for lung cancer? |
*Smoking (80%) of all cases *industrial hazards (asbestos, coal mines, pesticides) *familial predisposition |
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What is the pathogenesis of lung cancer? |
*95% arise in the lung tissue *5% are misc group *It is generally aggressive, locally invasive, and widely metastatic *Divided into four major categories |
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What are the four categories of lung cancer? |
1 - small cell lung cancer *not surgical candidate *see next card for more info 2 - Non-small cell squamous cell carcinoma *surgical candidate 3- non-small cell adenocarcinoma *most common type in women *Surgical candidate 4 - non-small cell large cell carcinoma *surgical candidate |
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Describe small cell lung cancer |
*Extremely aggressive *strongest association with smoking *Highly malignant *tend to infiltrate widely *metastasis early (70% of people have mets when they are diagnosed) *NOT SX CANDIDATE b/c of mets at time of diagnosis |
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What are the clinical manifestations of lung cancer caused by? |
*involvement of the lung and adjacent structures *Local irritation and obstruction of airways *paraneoplastic manifestations |
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What are the non-specific s/s of lung cancer? |
*Anorexia *weight loss |
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What is a good prognosticator of whether or not the patient will do well with treatment? |
*Anorexia*weight loss |
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What are the s/s involving the lungs and adjacent structures? |
*Chronic cough *SOB *Wheezing *Hemoptysis (blood in sputum) *Pain |
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What are the s/s involving metastasis of lung cancer? |
*Hoarseness - invasion of the mediastinum and the invasion of the laryngeal nerve *Dysphagia - due to compression of the esophagus *Superior cava syndrome *Pleural effusions - compresses lung *Paraneoplastic disorders - hormones or secretions *Hematologic disorders - bleeding issues |
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What is superior vena cava syndromeand what are the s/s of ? |
Interruption of blood flow in the superior vena cava from compression by tumor which interferes with venous drainage from head, neck, and chest wall. *edema of face, neck, arms, hands, and breasts. *Redness and edema of conjuctivae and around eyes *neck and thoracic vein distention *cyanosis of upper torso *nasal stuffiness *LATE SIGNS: sever headache, irritability, visual disturbances, dissiness, change in mental status, stridor, tachycardia |
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What are some paraneoplastic disorders? |
*Hypercalcemia *Cushing syndrome - ACTH secretion *SIADH (syndrome of inappropriate antidiuretic hormone) - water intoxication *Neuromuscular syndromes |
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How is lung cancer diagnosed? |
*Careful history and exam *Chest rads and CT *Labs: Na, Ca levels *Bronchoscopy with needle biopsy of lung tissue and sputum specimen |
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What is the treatment for non-small cell lung cancers? |
*Surgery (wedge resection, lobectomy, pneumonectomy) *Radiation *Chemo and targeted therapy |
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What is the treatment for small cell lung cancer? |
*Chemo and targeted therapies *Radiation |
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What is atelectasis and what is it caused by? |
*Collapse of the alveolus or larger unit. Caused by: *Airway obstruction *lung compression *increased recoil of the lung due to loss of pulmonary surfactant (infants) |
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What is the difference between primary and acquired/secondary atelectasis? |
Primary is present at birth (lungs never inflated), acquired/secondary develops during neonatal period or later in life (newborn established respiration but then had an issue). |
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Who does acquired atelectasis affect? |
Mainly adults caused by airway obstruction or lung compression (by fluid or mass). |
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What are the manifestations of atelectasis? |
Depends on the amount of lung collapsed *Tachypnea *Dyspnea *Decreased check expansion *Shallow breaths *Absence of breath sounds *Intercostal retractions *Fever *Mediastinum and trachea shift to the affected side if collapse is large *In compression mediastinum shifts away from the affected lung. |
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What is the treatment for atelectasis? |
*Reduce airway obstruction or lung compression *Ambulation *Deep breathing *Administration of O2 therapy *Bronchoscopy |
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What is pleural effusion? |
Abnormal collection of fluid in the pleural cavity |
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What are the types of fluid in pleural effusion? |
*Transudate serous exudates or hydrothorax (clear) - CHF *Exudates - pneumonia, empyema (infection in pleural cavity) *Purulent - pus |
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What are the manifestations of pleural effusion? |
Varies with the cause *Empyema - fever, increased WBC, inflammation Characteristic signs: *Dullness or flatness to percussion *Diminished breath sounds *Hypoxemia *DYSPNEA - most common sign *pleuritic pain |
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How is pleural effusion diagnosed and treated? |
*Chest rads and CT *Thoracentesis - aspiration of fluid from space *Chest tube drainage needed with continued effusion. |
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What is a hemothroax? |
A specific type of pleural effusion where blood accumulates in the pleural cavity |
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What is the cause of a hemothorax? |
*Chest injury *Complication of chest sx *malignancies *Rupture of a great vessel |
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Pneumothorax? Cause? |
Presence of air in the pleural space. Can occur with no obvious cause (spontaneous pneumothorax) or from the rupture of an air-filled bleb or blister on the surface of the lung. |
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What is primary pneumothorax? |
Occurs in healthy people |
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What is secondary pneumothorax? |
Occurs in person with underlying lung dz. |
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What is traumatic pneumothorax? |
Occurs due to injury to chest or major airway. |
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What is Tension pneumothorax? |
LIFE THREATENING! increased pressure within the pleural cavity impairs both respiratory and cardiac functions. *Air enters but cannot leave the space *Rapid increase of pressure in chest, causes compression atelectasis of the unaffected lung and a shift of mediastinum to the unaffected side *Decrease in venous return to the heart and reduced cardiac output. |
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What are the manifestations of spontaneous and traumatic pneumothorax? |
*Ipsilateral (one sided) chest pain *immediate increase of resp rate *Dyspnea *Asymmetry of chest *Lag in movement on affected side during inspiration *Hyperresonant sound on percussion *Decreased or absent breath sounds over affected area |
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What are the manifestations of Tension pneumothorax? |
*Mediastinal shift to opposite side of chest *Trachea deviates with the mediastinum *Stroke volume impaired so cardiac output is decreased *Increase in HR *Distention of neck veins *SubQ emphysema *Clinical signs of shock |
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What is the diagnosis of a pneumothorax? |
*Confirmed by chest rads or CT *Pulse Ox and ABGs |
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What is the treatment of a pneumothorax? |
Depends on cause and extent Spontaneous or traumatic *Air usually reabsorbs spontaneously *Needle aspiration of closed drainage if large Tension *PROMPT insertion of a large bore needle or chest tube. |
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What is HTN? |
An abnormally high blood pressure measured on at least three different occasions from a person who has been at rest at least 5 minutes. |
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Which number is more significant if it's high and why? |
Diastolic because this is when the left ventricle is supposed to be relaxing. |
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What are the incidences of HTN? |
*Affects approx 50 million people in the US *Leading risk factor for cardiovascular dzs *Nearly 1/3 of hypertensive americans don't know they have HTN |
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What is the etiology of HTN? |
Measurement of two things: *Cardiac output (CO)- the volume of blood, in liters, ejected by the heart each min (regulated by metabolic needs of body) *Peripheral vascular resistance (PVR) - sum of all resistance that the body has within the vascular system. *BP=CO x PVR |
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What is the cardiac output of a normal adult? |
4-8L/min |
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How is BP regulated? |
By arterioles, heart, and kidneys |
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What happens if the diameter of a vessel gets smaller? |
It will change the vascular resistance and cause BP to rise. |
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What can cause increases in PVR? |
*Increased activity of SNS *Angiotensin and catecholamines (neurohormones) *Thickening of blood vessel walls from atherosclerosis |
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What are some neuro-hormonal mediators that help control BP? |
*Baroreceptors located in carotid sinus and wall of aortic bodies - monitor arterial pressure *chemoreceptors located in the medulla, carotid bodies, and aortic bodies |
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How can body fluid volume affect BP? |
Excessive concentration of NA+ and water. |
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What does increased activity of the RAA system cause? |
Retain Na+ and water and increases BP |
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How does blood viscosity affect BP? |
Blood flow resistance increases as blood gets thicker and this increases BP. |
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What are some risk factors for HTN? |
*Age *Gender - greater in men than women until age 65 *Race - AA are at greater risk *Family history of HTN *Weight - obesity *Habit - smoking, alcohol *Diet - high in Na+ and calorie intake *Lifestyle - exercise habits *Oral contraceptives - especially if there is a family history of HTN |
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What are the classifications of BP/HTN? |
Normal <120 and <80 Pre HTN 120-139 or 80-89 Stage 1 140-159 or 90-99 Stage 2 >159 or >99 |
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What are the types of HTN? |
Primary (essential HTN) and secondary |
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Describe primary HTN |
*occurs without evidence of other dz *accounts for 90-95% of all HTN *result of genetics, environment, mediated by neurohormonal effects *Caused by an increase in PVR *Begins as intermittent in late 30s to early 50s and gradually becomes permanent *Two types are Benign HTN and malignant HTN |
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What is benign HTN? |
*Slow onset and initially is asymptomatic *Called the silent killer |
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What is malignant HTN? |
*A severe HTN *Develops abruptly *Acute elevation in Diastolic pressure usually over 130mm/Hg *Also called "hypertensive crisis" *Can rapidly produce irreversible neurologic, cardiac, and renal damage |
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What are some complications of primary HTN? |
*Long-term ear and tear on the heart and blood vessels *HTN accelerates atherosclerosis |
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What is secondary HTN? |
*Related to an identifiable medical diagnosis (side effect of some other dz) Examples: *Renal issues *Vascular disorders *Alterations in endocrine function or hormone levels (thyroid dz) *Acute brain lesion *Sleep apnea *Drug induced (cocaine) or related *Chronic stress |
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What is the target organ damage of HTN? |
*heart dz - left vent hypertrophy, angina or MI, heart failure *Stroke - hemorrhagic *Nephropathy - Kidney dz *Peripheral arterail dz *Retinopathy |
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How is HTN managed? |
Non pharmacological measures *Reduction in sodium intake *Weight reduction *Regular aerobic physical activity *Modification of alcohol intake *reduction in dietary saturated fats and cholesterol *Smoking cessation Pharm treatments: *Based on severity of HTN but usually more than one drug. |
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What is Coronary Artery dz (CAD)? |
An insidious, progressive disease of the vessels of the heart (coronary arteries). They narrow or are completely occluded (decrease in lumen) which leads to decreased blood flow through those arteries. |
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What are the coronary artery wall layers? |
*Tunica externa - outer most *Tunica media - middle coat, smooth muscle layer *Tunica intima - inner coat - endothelial layer |
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What is the patho of CAD? |
Two things happen in CAD *Atherosclerosis - accumulation of fatty deposits, platelets, neutrophils, monocytes, and macrophages throughout the tunica intima and eventually into the tunica media (lumen narrows over time) *Arteriosclerosis - abnormal thickening and hardening of arterial walls by atherosclerotic plaques. |
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When does Atherosclerosis begin? |
*Process begins in our 20s but effects are not usually evident for 20-40 years. |
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What vessels are affected by atherosclerosis? |
Most often the arteries *Coronary arteries *the aorta *cerebral arteries |
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What is the leading cause of CAD? |
Atherosclerosis |
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Describe the atherosclerosis process. PART 1 |
*Injury to the endothelial cells lining the lumen of the artery results in increased permeability of endothelial cells which allows components of plasma to enter (including fatty acids and triglycerides). *Oxidation of fatty acids causes further damage *Inflammatory and immune react to injury which attracts WBC (neuts, monos, platelets) to area. once there they get stuck. *Once attached to the endothelial layer, monocytes and neuts begin to emigrate between endothelial layer and interstitial space *SEE NEXT CARD* |
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Describe the atherosclerosis process. PART 2 |
*In interstitium the monocytes mature into macrophages and release cytokines *Additional plasma cholesterol and fats gain access to the tunica intima *Blood clot can form (thrombus) *Results are cholesterol and fat build up, scar tissue deposits, platelet -derived clots and smooth muscle proliferation *Progressive narrowind of lumen by plaque enlargement results in ischemia. *EKG changes *Chest pain |
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What is an early indication of damage to the vessel in atherosclerosis? |
A fatty streak in the artery |
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What is the end result for an artery that is affected by atherosclerosis? |
Decrease in the diameter of the artery and an increase in it's stiffness. |
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What are some non-modifiable risk factors for the development of CAD? |
*Age - over 50% are > 65 *Gender - males until women are 65 *Heredity - AA at greater risk b/c of HTN *Genetics - HTN, dyslipidemia, diabetes, obesity |
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What are some modifiable risk factors for the development of CAD? |
*Elevated serum cholesterol *Smoking *HTN *Physical inactivity *Obesity *diabetes *Homosysteine levels *Stress *Menopause |
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What is the role of cholesterol in atheroma (plaque) formation of CAD? |
*Hypercholesteremia - .200mg/dL *lipids are insoluble in plasma - encapsulated by fat carrying proteins *Five classes of cholesterol - very low density lipoproteins (VLDL), low density lipoproteins (LDL), High density lipoproteins (HDL) |
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Describe the five classes of cholesterol. |
1 don't need to know 2 VLDL - carry triglycerides which are fatty acids and should be below 150 3 LDL - major carrier of cholesterol and promotes atherosclerosis by depositing cholesterol on the artery walls. Less than 130mg/dL 4 HDL - synthesized in liver HDL removes excess cholesterol. Also inhibits cellular uptake of LDL and provides protection against CAS. >35mg/dL |
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How does smoking cause increase risk of CAD? |
*Nicotine increases release of epi and norepi which causes vasoconstriction, elevated BP, and elevated HR |
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What happens to risk for CAD if a person quits smoking? |
*Risk decreases in 3-5 years |
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How does HTN cause increase risk of CAD? |
*2-3 fold increase risk of CAD with HTN because it contributes to endothelial injury. |
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How does physical inactivity cause increase risk of CAD? |
*25% of adults report no aerobic activity *There is an inverse relationship between exercise and CAD *Exercise promotes higher HDL levels, lower BG levels, decreased BP, decreased weight |
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How does obesity cause increase risk of CAD? |
*Body weight greater than 30% of ideal body wt increase risk because it increases cardiac workload *Is associated with increased serum cholesterol, high BP, Diabetes *Central obesity is associated in increase risk as well (apple shaped body) |
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How does diabetes cause increase risk of CAD? |
*Affects blood vessels and PVR |
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How do homocysteine levels cause increase risk of CAD? |
*Amino acids that are associated with endothelium dysfunction *elevated levels can be reduced with folic acid, Vit B6, and Vit B12 |
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How does stress cause increase risk of CAD? |
Stress causes us to *Overeat *Smoke *increase BP |
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How does menopause cause increase risk of CAD? |
*Estrogen offers cario-protective effects by increasing HDL and decreasing LDL |
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What are the clinical manifestations of CAD? |
*Usually occur late in the course of the dz Extremities *intermittent claudication (pain in periphery) *aching, cramping feelings in lower extremities *pain during or after exercise *cold sensitivity *skin color changes Central - more common *Angina |
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What are the diagnostics for CAD? |
*HDL, LDL, VLDL, cholesterol, and triglyceride levels *Areteriogram - light up arteries around heart *EKG |
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What is angina pectoris? |
Chest pain caused by *reduced blood flow *reduced O2 supply compared to demand by myocardium *Temporary or reversible cause |
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What is the patho of angina pectoris? |
*Body's way of communicating that there is not enough oxygenated blood *Forewarning of MI *Reduced oxygen supply causes a switch from areobic metabolism to anaerobic which causes build up of lactic acid and pain |
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What is silent ischemia? |
Caused by decrease O2 supply without warning signs of pain. |
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What is coronary artery spasm? |
Another form of occlusion that causes ischemia |
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What are the types of angina? |
*Stable angina - most common *Prinzmetal's (variant) angina *Unstable angina |
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Describe stable angina. |
*aka classic angina *Predictable *Coronary arteries cannot dilate to increase blood flow *no change in cause, amount, or duration of pain over time *Relieved with rest and nitrates |
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Describe Prinzmetal's (varient) angina. |
*Occurs without any obvious increase in work load of the heart *Coronary artery undergoes spasm *frequently occurs during rest or sleep *Dysrhythmias are common with this type |
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Describe unstable angina |
*Combo of classic and variant angina *worsening coronary artery dz and increased frequency of chest pain *accompanies an increase workload of the heart *results from coronary atherosclerosis *Acute Coronary Syndrome (ACS) = unstable angina and MI |
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What is the etiology of Angina pectoris? |
*Atherosclerotic dz (CAD) *HTN *Aortic valve dz *anemia *dysrhythmias *Thyrotoxicosis *Shock *CHF *Aortitis *Coronary artery spasm |
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What are the s/s of angina pectoris? |
*constriction or squeezing pain in the pericardial or substernal area *may radiate to arms, jaw or throax *Pain of short duration *often precipitated with excursion and relieved with rest *Dyspnea *Anxiety *Sweating *Hypotension *Relief also obtained with nitro within 2-3 min |
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What is a classic sign of angina? |
Levine sign - grabbing chest |
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What is ST-segment Elevation Myocardial Infarction (Acute STEMI) |
*Death of myocardial cells which begin to die after about 20 min of oxygen deprivation. |
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What is the patho of STEMI? PART 1 |
Injury - ischemia - infarction CAD Angina cell death *Cell injury occurs because of a lack of O2 over time (ischemia) *Prolonged (20-45min) ischemia can lead to cell death *after 20-45min the ability of the cell to produce ATP aerobically is exhauseted and cells fail to meet their energy demands |
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What is the patho of STEMI? PART 2 |
*Without ATP, Na/K pump quits and the cells fill with Na ions and water which causes them to burst *When cell lyse they release intracellular Na stores and enzymes which injure neighboring cells *accumulation of lactic acid and the electrical conduction pathways are altered (dysrhythmias) *Can result in interruption of arterial or ventricular depolarization or in dysrhythmias |
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How are MIs described? |
*Location *Myocardial surface affected |
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What are the locations of possible MIs? |
*Anterior - usually occuring in area supplied by left anterior descending (LAD) coronary artery (widow maker) *Posterior - area supplied by the right coronary artery (RCA) *Lateral - area supplied by left circumflex artery |
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What are they myocardial surfaces in an MI? |
Transmural infarct Subendocardial Intramural infarct |
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What are the causes of STEMI? |
*Long-standing coronary artery dz (CAD) *Rupture and dislodgement of an atherosclerotic plaque from one of the coronary arteries *Thrombotic lesion adhering to a damaged artery becomes large enough to obstruct flow *heart chamber becomes hyperatrophied |
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What are some risk factors of STEMI? |
*Family history of CAD or HTN *HTN *Hypercholesterolemia *Obesity *Smoking *Diabetes *Particular genotype patterns (mutations in a gene, MEF2A) *Chronically stressed |
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What are the clinical manifestations of STEMI? |
*Abrupt onset of pain, pressure, tightness, Squeezing *Substernal, radiating to neck, arm, jaw *Pain is prolonged, persistent, and not relieved with rest or nitro. *SOB/dyspnea *Diaphoresis *Pale, dusky, or cyanotic skin *weakness *Nausea *Restlessness and apprehension *Tachycardia, bradycardia, or other dysrhythmias *EKG changes *increase in serum cardiac isoenzymes |
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What are the diagnostic studies for STEMI? |
*EKG or ECG *Labs |
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What kinds of EKG/ECGs are done for STEMIs? |
*Resting - ER patient - a single recorded picture of the electrical activity of the heart *Dynamic - Ambulatory Holter Monitor (continuous picture of electrical activity over time) and exercise stress test |
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What are some lab blood test done for STEMI diagnosis? |
*Serum electrolytes - build up lactic acid *CBC *Serum enzyme studies - cardiac markers *Troponin |
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Describe the Serum enzyme studies (cardiac markers) as a diagnostic tool for STEMI |
Creatine Kinase CK/creatine phosphokinase CPK *CPK II (MB) present in heart muscle and is specific to myocadial muscle *Rises w/I 6hr of injury, peaks at 18hr, returns to normal in 2-3 days Lactic dehydrogenase (LDH) *Consist of 5 isoenzymes (LD1 - LD5) *Found in many body tissues *Normal ratio is L2>L1 but if flipped = MI *ratio detected w/i 24h, peaks in 3-4 days, returns to normal in 2 weeks. |
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What is the procedure for isoenzyme test of LDH? |
Three blood samples are drawn 1 - on admission 2 - 8 hours later 3 - 8 hours after #2 |
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Describe the Troponin blood test for STEMI |
*Two markers Troponin T and Troponin I *Very specific and sensitive *Begins to rise 3-9 hours after MI *T remains elevated for 10-14 days *I remains elevated for 7-10 days *Good for diagnosing an MI in a patient who did not receive treatment for one. |
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What is the gold standard, best definitive marker to diagnose an MI? |
Troponin levels |
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What is an acid? What is a base? |
-A substance that releases H+ ions when dissolved in water -A substance that binds to H+ ions when dissolved in water |
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What is an indicator of H+ concentration? |
Plasma pH - inverse |
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What is the normal rage for: pH pCO2 pO2 HCO3 SaO2 |
*7.35-7.45 *35-45 mm Hg *80-100 mm Hg *22-26 mEq/L *>95% |
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How does the body maintain a normal pH? |
H+ must be neutralized or excreted by the bones, lungs, and kidneys |
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What is the acid/base buffer system? |
Buffers acids or bases to maintain homeostasis |
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What are the two types of buffer mechanisms to correct altered pH? |
Chemical and physiological |
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Describe the Chemical buffer system |
*OCCURS IMMEDIATELY *neutralizes acids and bases which keeps pH in narrow, normal range *Prevents major changes in the ECF by releasing or accepting H+ *Buffers are found in all tissues of the body *Four major chemical buffers - 1 carbonic acid-bicarb, 2 phosphate buffer system, 3 protein buffer system, 4 Hemoglobin-oxyhemoglobin buffer system |
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Describe the Carbonic acid-bicarbonate buffer system. |
*MOST IMPORTANT SYSTEM *Major extracellular system *Consists of a water solution that contains a weak acid and a bicarbonate salt *The ratio of bicarbonate to carbonic acid is 20:1 *This ratio changes if pH is changed *Compensation occurs and then the ratio becomes stable again *The system is linked to the respiratory and renal systems. |
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What are the physiological buffers? |
*Pulmonary regulation *Renal regulation |
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Describe pulmonary regulation |
*Lungs control the respiratory carbonic acid buffer system *Lungs compensate for acid-base disturbances that are primarily metabolic in nature *The respiratory system is extremely sensitive to changes in pH & compensates with in sec to min *Not as efficient as renal |
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Describe Renal regulation |
*Kidneys control the metabolic buffer by excreting an acidic urine or an alkaline urine *The system works within several hours to days but is powerfully effective. *Control the HCO3 in ECF by either reabsorbing or excreting the H+ *Excrete the weak acids into the urine *Body depends on the kidneys to excrete acids from cellular metabolism (urine is normally acidic pH=6) |
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What is the problem with the elderly and pulmonary regulation? |
*Elderly have reduced amount of gas exchange during breathing and loss alveolar membrane so CO2 retention and an increase in H+ is a problem |
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What is the problem with the elderly and renal regulation? |
Renal function decreases with age so elderly DO NOT excrete H+ or synthesize HCO3 as efficiently. Their acid-base balances are more difficult to correct. |
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What is compensation in the acid-base buffering systems |
*Occurs when the body uses regulatory mechanisms to return the pH to its normal level *pH is normal but there are abnormal amounts of CO2 and/or HCO3 *Metabolic alterations have resp compensation *Respiratory disturbances have metabolic compensation *Three types of compensation - Complete, partial, or decompensation. |
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Define the three types of compensation |
Complete compensation - the buffers have achieved homeostasis and the pH is fully corrected Partial compensation - the buffers are in the process of restoring homeostasis Decompensation - worsening state of acid-base imbalance |
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What are the main indicators that compensation for an acid-base imbalance is occurring in the body? |
pH, pCO2, HCO3 |
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What are the four main acid-base imbalances? |
*Respiratory acidosis *Respiratory alkalosis *Metabolic acidosis *Metabolic alkalosis |
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What is respiratory acidosis? |
*pH is decreased & CO2 is retained (increased) *ALWAYS due to hypoventilation and CO2 retention (COPD patients) |
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What are the causes of respiratory acidosis? |
*CNS depression *Obstruction of resp passages *Weakness of resp muscles *Restriction of resp *Neruomuscular disorders |
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What are some s/s of respiratory acidosis? |
*Rapid, shallow resp *Tachycardia *Dizziness, headache, mental confusion *Weakness, irritability, anxiety, apprehension *Warm, flushed skin, diaphoresis *Nausea, vomiting |
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How does the body compensate for respiratory acidosis? |
*Increased rate and depth of resp to blow off CO2 *Kidneys eliminate H+ and retain HCO3 *HCO3 levels rise |
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What is the compensating organ in respiratory acidosis? |
Kidneys |
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What is respiratory alkalosis? |
pH is elevated and CO2 is decreased ALWAYS due to hyperventilation |
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What are some causes of respiratory alkalosis? |
*Hyperventilation *Resp center stimulation *Infection *Anxiety *Inappropriate ventilator settings |
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What are some s/s of respiratory alkalosis? |
*Lightheadedness *tingling/numbness of extremities *restlessness, agitation, confusion, headache *Dizziness, chest tightness *Seziures |
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How does the body compensate for respiratory alkalosis? |
*Kidneys conserve H+ and excrete HCO3 |
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What do low levels of HCO3 indicate? |
The body is trying to compensate for respiratory alkalosis. |
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What is metabolic acidosis? |
*pH decreases and HCO3 decreases *Occurs when other acids accumulate in the ECF or when there is a loss of HCO3 *Hyperkalemia is seen *Rarely occurs spontaneously, usually accompanied by other conditions or problems |
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What are some causes of metabolic acidosis? |
*Diabetic ketoacidosis *GI (malnutrition, starvation, chronic diarrhea) *Kidney failure *Hyperthyroidism *Trauma, shock *Increased exercise *Sever infection or fever |
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What are some s/s of metabolic acidosis? |
*Headache, confusion, drowsiness, lethargy *Increased resp rate and depth - Kussmaul's resp *Fruity breath *N/V/D, ab pain *Cold, clammy skin, shock *Dysrhythmias, hypotension |
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How does the body compensate for metabolic acidosis? |
*Lungs eliminate CO2 *Kidneys conserve HCO3 *pCO2 decreases |
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What is metabolic alkalosis? |
*pH increases and HCO3 increases *Occurs when there is a loss of H+ or an increase in HCO3 |
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What are the causes of metabolic alkalosis? |
*Severe vomiting *Excessive NG suctioning *Diuretic therapy *Hypokalemia *Eating large amounts of licorice *Excessive NaHCO3 use *Excessive mineral corticosteroids |
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What are some s/s of metabolic alkalosis? |
*Tingling in fingers and toes *Dizziness, irritability, nervousness, confusion, tremors *Tachycardia, hypertension *Dysrhythmias due to lack of K+ *Hypoventilation, resp failure *Anorexia, N/V *Paralytic ileus if hypokalemia occurs |
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How does the body compensate for metabolic alkalosis? |
*Lungs retain CO2 *Kidneys conserve H+ and excrete HCO3 *pCO2 increases |
