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29 Cards in this Set
- Front
- Back
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Dyspnea: Common Causes and Signs
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Subjective sensation of being unable to get enough air. Breathlessness, air hunger, SOB, labored breathing, preoccupation with breathing.
Common Causes: 1) Diffuse or focal disturbances of ventilation 2) gas exchange 3) ventilation-perfusion relationship 4) increased work of breathing 5) lung parenchyma - diseases that damage lung tissue Signs: 1) flaring of the nostrils 2) use of accessory muscles of respiration, and retraction (pulling back) of the intercostal spaces. 3) Parenchymal - retractions of tissue between the ribs (subcostal and intercostal retractions) observed more often than supercostal retractions (retractions of tissues above the ribs) |
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Orthopnea and Paroxysmal Nocturnal Dyspnea
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Orthopnea - dyspnea occurs when laying down (common w/ heart failure). Recumbent position redistributes body water, causes the abdominal contents to exert pressure on diaphragm and decrease efficiency of respiratory muscles. Relieved by sitting up forward-leaning posture or supporting upper body on several pillows.
PND - individuals with heart failure or lung disease wake up at night gasping for air and must sit up or stand to relieve the dyspnea. (Left ventricular failure) |
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Kussmaul-Respiration (Hyperpnea)
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Induced by strenuous exercise or metabolic acidosis
Characterized by: - slightly increased ventilatory rate - very large tidal volume - no expiratory pause Labored Breathing - occurs w/ increased work of breathing. Airways are obstructed (ex: COPD). - When large air ways are obstructed, slow ventilatory rate, increased effort, prolonged inspiration or expiration, stridor (high pitch sound during inspiration), wheezing. - Small airway obstruction (ex: asthma and COPD) rapid ventilatory rate, small tidal volume, increased effort, prolonged expiration, wheezing. Restricted Breathing - caused by pulmonary fibrosis (stiffen lungs or chest wall) and decrease compliance. - Small tidal volumes and rapid ventilatory rate - Shock and severe cerebral hypoxia contribute to gasping respiration that consist of irregular, quick inspiration with an expiratory pause. - Anxiety |
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Cheyne-Strokes Respirations Characteristics and Causes
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Characterized by:
- alternating periods of deep and shallow breathing - Apnea lasting 15 to 60 seconds followed by ventilation that increase in volume until a peak is reached - ventilation (tidal volume) decrease again to apnea Results from any condition that slows the blood flow to the brainstem which in turn slows impulses sending info to the respiratory centers of the brainstem. |
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Manifestations and Causes of Hypoventilation and Hyperventilation
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[Hypoventilation] - inadequate alveolar ventilation in relation to metabolic demands.
- Caused by alterations in pulmonary mechanics or in the neurological control of breathing such that minute volume is reduced. - CO2 removal does not keep up with CO2 production and PaCO2 increases, causing Hypercapnia [Hyperventilation] - alveolar ventilation that exceeds metabolic demands. - Lungs remove CO2 at a faster rate than produced by cellular metabolism resulting in decreased PaCO2 or hypocapnia. - Hypocapnia results in a respiratory alkalosis that can interfere with tissue function - Overs with severe anxiety, acute head injury, and conditions that cause insufficient oxygenation of the blood |
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Hypercapnia Signs and Symptoms
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Increased CO2 in the arterial blood
Increased PaCO2 caused by Hypoventilation Causes: - decreased drive to breathe or inadequate ability to respond to ventilatory stimulation - depression of respiratory center by drugs -disease of medulla; infection of CNS or trauma - abnormalities of spinal conducting pathways as in spinal cord disruption or poliomyelitis - Disease of the NMJ or respiratory muscles themselves; myasthenia gravis or muscular dystrophy - Thoracic cage abnormalities, as in chest injury or congenital deformity - large airway obstruction; tumors or sleep apnea - increased work of breathing or physiologic dead space; emphysema CM: - electrolyte abnormalities that occur in response to low pH that may cause dysrhythmias - somnolence or in coma b/c of changes in intracranial pressure associated with high levels of arterial CO2 causing cerebral vasodilation - alveolar hypoventilation w/ increased alveolar CO2 limits the amount of oxygen available for diffusion into blood leading to secondary hypoxemia |
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Hypocapnia Signs and Symptoms
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PaCO2 less than 36 mmHg
Respiratory Alkalosis |
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Coughing Signs and Symptoms
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Important reflex that helps clear the airways of large amounts of inhaled material, excessive secretions or abnormal substances such as edema or pus.
Cough reflex - "irritant" receptor; vagus nerve |
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Hemoptysis Signs and Symptoms
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Coughing up blood or bloody secretions.
Bright red, alkaline pH, mixed with frothy sputum. Common cause: bronchiectasis, lung cancer, bronchitis, pneumonia. TB Results from damage to the lung parenchyma with rupture of pulmonary vessels or from inflammation, injury, or cancer of bronchial tree. |
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Cyanosis Signs and Symptoms
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Bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin.
Evident with severe hypoxia |
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Pain Signs and Symptoms
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Caused by pulmonary disorders originating in pleurae, airways, or chest walls
Pleural pain - pulmonary disease, sharp or stabbing, infection and inflammation of parietal pleura, cause pain when pleura stretch during inspiration. Pain localized to portion of chest wall. Common with pulmonary infarction (tissue death), pulmonary embolism. Chest pain - after coughing, occurs w/ infection and inflammation of trachea or bronchi. Muscle pain or rib pain. Excessive coughing. Costochondritis; pressing on sternum or ribs. |
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Clubbing Signs and Symptoms
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Selective bulbous enlargment of the end of a digit.
Commonly associated w/ diseases that interfere with oxygenation such as bronchiectasis, CF, pulmonary fibrosis, lung abscess, Congenital heart disease. Lunger cancer is sometimes associated w/ clubbing |
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Sputum Signs and Symptoms
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- distinctive color, consistency, odor
- Changes in amount and consistency provide info about progression of disease and effectiveness of therapy |
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Acute Cough Vs Chronic Cough
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Acute - resolves within 2 to 3 weeks of the onset of illness or resolves with treatment of the underlying condition. Result of URI, allergic rhinitis, acute bronchitis, pneumonia, CHF, pulmonary embolus, or aspiration.
Chronic - >3 weeks; 7 or 8 weeks. Caused by postnasal drainage syndrome, non-asthmatic eosinophilic bronchitis, asthma, or gastro-esophageal reflux disease. Chronic bronchitis , lung cancer. |
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Five Causes Hypoxemia
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1) Decrease in inspired oxygen
- high altitude - low O2 content of gas mixture - enclosed breathing spaces (suffocation) 2) Hypoventilation of the alveoli - lack of neurologic stimulation of respiratory center (drug overdose, neuro damage) - Defects in chest wall mechanics (neuromuscular disease, trauma, chest deformity, air trapping) - Large airway obstruction (laryngospasm, foreign body aspiration, neoplasm) - Increased work of breathing (emphysema, severe asthma) 3) Ventilation-perfusion Mismatch - Asthma - Chronic bronchitis - Pneumonia - ARDS - Atelectasis - Pulmonary Embolism 4) Alveolocapillary diffusion abnormality - Edema - Fibrosis - Emphysema 5) Decreased pulmonary capillary perfusion - Intra-cardiac defects - Intrapulmonary arteriovenous malformations |
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Pulmonary Edema: Causes, Signs and Symptoms
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Excess Water in the lungs
Predisposing factors: heart disease, ARDS, inhalation of toxic gases (ammonium). Common cause: - heart disease; left ventricle fails, filling pressures on left side of the hart increase and cause a concomitant increase in pulmonary capillary hydrostatic pressure. - Hydrostatic pressure exceeds oncotic pressure, fluid moves out into interstitium or interstitial space - fluid is picked back up by lymphatic vessels and removed from the lung. When flow of fluid out of the capillarities exceeds lymphatic system's ability to remove it, pulmonary edema develops Edema Begins to Develop: at pulmonary capillary wedge pressure or left atrial pressure of 20 mmHg. If capillary oncotic pressure is decreased for any reason, PE develops at a lower hydrostatic pressure - Capillary injury that INC capillary permeability - Capillary injury causes water and plasma proteins to leak out of capillary and move into interstitium. When plasma proteins move into lung interstitium, they increase the interstitial oncotic pressure, which is usually very low. Interstitial oncotic pressure begins to equal capillary oncotic pressure, water moves out of capillary and into lung. Results from obstruction of lymphatic system: drainage can be blocked by compression of lymphatic vessels caused by edema, tumors, and fibrotic tissue or by increased systemic venous pressure that elevates hydrostatic pressure of the lung pulmonary veins into which pulmonary lymphatic system drains. Left-sided heart failure Clinical Manifestation: 1) Dyspnea, orthopnea, hypoxemia, INC work of breathing 2) Pink, frothy sputum is expectorated, hypoxemia worsens, hypoventilation w/ hypercapnia may develop 3) Ventricular dilation (S3 gallop and cardiomegaly) 4) Inspiratory crackles (rales), dullness to percussion over lung bases |
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Opening (Communicating) Pneumothorax
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When there is air or gas in the chest because of injury or trauma
- air pressure in pleural space equals barometric pressure because air is drawn into the pleural space during inspiration is forced back out during expiration |
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Tension Pneumothorax
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When spontaneous air gets into the chest and pressure builds up
- site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing up during expiration - As more and more air enters the pleural space, air pressure in pneumothorax begins to exceed barometric pressure - Air pressure in pleural space pushes against already recoiled lung, causing compression atelectasis, and against the mediastinum, compressing and displacing the heart and great vessels |
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Spontaneous Pneumothorax
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Occurs unexpectedly in healthy individuals caused by spontaneous rupture of blebs on visceral pleura.
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Surgeries Resulting in PostOperative Respiratory Failure
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Cause:
- Smokers esp. if preexisting lung disease - Limited cardiac reserve - Chronic renal failure - Chronic hepatic disease - Infection - Atelectasis - Pneumonia - Pulmonary Edema - Pulmonary Emboli Common Surgeries - CNS - Thorax - upper abdomen |
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Prevention Measures for Postoperative Respiratory Failure
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-Frequent turning
- Deep breathing - Early ambulation to prevent atelectasis and accumulation of secretions - Humidification of inspired air help loosen secretions - Incentive spirometry - immediate feedback about tidal volumes encouraging them to breath deeply - Supplemental oxygen - hypoxemia - antibiotics only to treat infection |
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Obstructive Pulmonary Disease: Clinical Manifestation
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Airway obstruction that is worse with expiration
1) more force (use of accessory muscles of expiration) 2) more time required to expire a given volume of air 3) BOTH Unifying symptom - dyspnea - wheezing - increased work of breathing - ventilation-perfusion mismatching - decreased forced expiratory volume in one second |
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Asthma
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Chronic Inflammatory Disorder of the Airways
Causes Recurrent episodes of wheezing, breathlessness, chest tightness, and coughing Short lived attacks Bronchial Muscles Contract and cause Bronchospasm Familial Disorder Acute and Intermittent Risk factors: Family history, allergen exposure, urban residence, pollution, smoke, recurrent respiratory viral infections, and other allergic diseases Inflammation results in hyper-responsiveness |
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Asthma
Causes of airway obstruction - Precipitating Causes - CM |
Airway obstruction:
- Thick mucus - Mucosal Edema - Smooth Muscle spasm Precipitating Causes - Hyper-responsiveness to inflammatory mediators - Bronchoconstriction -TNF and IL-1 cause mucus secretion - Familial CM: - Dyspnea - Wheezing - Nonproductive cough early, but later mucoid - Prolonged expiration - Tachycardia - Tachypnea |
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Emphysema
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Abnormal permanent enlargement of gas exchange airways
Accompanied by destruction of alveolar walls w/o obvious fibrosis Precipitated by alpha-1-antitrypsin deficiency Alveoli are less able to recoil and expel air Due to loss of elastic recoil in the lungs Obstructions result from changes in lung tissue rather than mucus production and inflammation (bronchitis) |
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Emphysema
- Causes of airway obstruction - Precipitating Causes - CM |
Airway obstruction:
- Enlargement and destruction of alveoli - Loss of elasticity - Trapping of air Precipitating Causes: - Alpha-1-antitrypsin deficiency - Cigarette smoke CM: - Marked dyspnea - Nonproductive cough early but develops later - Tachypnea w/ prolonged expiration - Accessory muscles used for ventilation - Barrell chest - Normal or elevated hematocrit - Late cor pulmonale |
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Chronic Bronchitis
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Hyper-secretion of mucus and chronic productive cough that continues for 3 months, for at least 2 years
Smokers, air pollution, and elderly Irritants increase mucus production and increase the size and number of mucous glands and goblet cells in airway epithelium. Mucus becomes thicker and more tenacious, this sticky mucus coating makes it more likely that bacteria will become embedded in the airway secretions, where they produce. As infection and injury increase the bronchial walls inflame and thicken and swell Cilia become impaired Bronchial walls become inflamed and thicken from the edema and accumulation of inflammatory cells Leads to bronchospasm and permanent narrowing of airway |
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Chronic Bronchitis
- Causes of airway obstruction - Precipitating Causes - CM |
Airway obstruction
- Inflammation and thickening of mucous membrane - Ciliary impairment - Accumulation of mucus and pus Precipitating Causes - Cigarette smoke - Air pollutants - Infection CM: - Exercise intolerance - Late dyspnea - Wheezing -Productive cough - Marked hypoxemia leading to polycythemia and cyanosis - Early cor pulmonale |
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Pneumonia: Clinical Manifestations
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Preceded by an URI; usually viral
- onset of cough, dyspnea, and fever - cough may be productive/nonproductive - Symptoms: chills, malaise, pleuritic chest pain. Physical Examination will show: - pulmonary consolidation - inspiratory crackles - INC tactile fremitus - egophony -whispered pectoriloquy Individuals may demonstrate symptoms ands signs of underlying systemic disease or sepsis |
