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56 Cards in this Set
- Front
- Back
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What is Dyspnea?
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is subjective, difficult breathing, need for O2 exceeds supply, may manifest as breathlessness or SOB, w/exertion or @ rest, if severe may be accompanied by flaring nostrils, & accessory muscle use.
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What is Orthopnea?
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Dyspnea while pt is supine, pulmonary congestion develops as blood pools in the lungs & abdominal contents push upward against the lungs.
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What is Paroxysmal Nocturnal Dyspnea (PND)?
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Sudden acute type of dyspnea common in pts w/left-sided CHF, during sleep the body fluid is redistributed → pulmonary edema, → pt wake up gasping for air & coughing (fluid collected in lungs)
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What is the normal breathing pattern?
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regular; inhalation/exhalation cycle occurs w/in the same time period between one inhalation & the next.
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What is Cheyne-Stokes?
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Ventilation rate & volume gradually ↑, peak, then gradually ↓, w/interspersed periods of apnea. (brains stem injury, neurologic impairment above the brain stem)
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What is Kussmaul's respirations?
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Deep gasping respirations, very lg tidal volumes, no expiratory pause. (diabetic coma, COPD, pulmonary fibrosis, & anxiety)
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What is Biot's respirations?
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Irregular pattern, rate, volume w/ intermittent periods of apnea (↑ ICP, space occupying lesions)
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What are Agonal Respirations?
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"dying breath", slow, shallow, irregular & sometimes gasping respirations, (from brain anoxia) are terminal respiration unless aggressive intervention is performed.
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What is Central Neurologic Hyperventilation?
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Similar to Kussmaul's, associated w/ICP
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What is Hypoventilation?
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Tidal volume ↓ normal range, ↑ blood CO2 level, (overdoses, head injury)
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What is Hyperventilation?
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Tidal volume ↑ normal range, ↓ blood CO2 level, (infection, fever, or fear)
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What can cause cough?
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Irritation (nasal discharge dripping into the oropharynx), Inflammation, Foreign material, Inhaled irritants, Aspiration of food or fluid.
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Explain the physiology of cough;
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Cough reflex is controlled by a center in the medulla, is coordinated actions that inspire air & then close the glottis & vocal cords, forceful expiration follows, opening the glottis.
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What are some causes of Haemoptysis?
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Pneumonia, Bronchogenic carcinoma, Bronchiectasis, Lung abscess, TB.
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If a pt does not have cyanosis, does that mean he has normal oxygenation?
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No, in adults cyanosis is not evident until severe hyposemia is present. Severe anemia & carbon monoxide poisoning can cause inadequate oxygenation of tissues w/out cyanosis.
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What is the most characteristic pain of lung dz?
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That resulting from inflammation of the pleura. Pulmonary pain is central CP that is pronounced after coughing
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What are the characteristics of chest pain?
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Sharp & cutting, aggravated by coughing, sneezing & breathing (pt usually develops a pattern of rapid shallow breathing & avoids any unnecessary movement.
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What are the most common causes of pleuritic pain?
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Pulmonary infection or infarction, pts w/infection & inflammation of the trachea or bronchi.
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What is the most common cause of digital clubbing?
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Pulmonary dz; bronchogenic CA, bronchiectasis, lungabscess, or TB.
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What are other causes of digital clubbing?
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CV dz; Congenital intracardial shunting or Subacute endocarditis.
5-10% associated w/dz of the GI tract (including liver) |
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What is a rusty or dark-colored sputum usually a sign of?
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Pneumococcal pneumonia
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What is very large amounts of purulent sputum w/a foul odor associated with?
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Bronchiectasis
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What can a thick, tenacious muccous be associated with?
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Asthma or Cystic Fibrosis
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What can blood-tinged muccous be a result of?
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Chronic cough & irritation → rupture of superficial capillaries. (also could be a sign of a Tumor or TB)
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What is sneezing?
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Reflex response to irritation in the upper resp. tract, assists w/removal of irritant, associated w/inflammation or foreign material in the nasal passages.
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What is atelectasis?
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Nonaeration or collapse of a lung or part of a lung leading to ↓ gas exchange & hypoxia, occurs as a complication of many primary conditions.
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What are the 2 major causes of collapse due to atelectasis?
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Obstrutive or resorption atelectasis,
Compression atelectasis. |
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What is Obstrutive or resorption atelectasis?
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Develops when total obstruction of the airway due to muccous or tumor leads to diffusion of air into the tissue distal to the obstruction (air is not replaced)
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What is Compression atelectasis?
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Results when a mass (tumor), exerts pressure on a part of the lung & prevents air from entering that section of the lung.
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What situations can prevent lung expansion?
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↑ pressure in the pleural cavity, ↑ surface tension in the alveoli, Fibrotic tissue in the lungs or pleura.
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What is postoperative atelectasis?
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Commonly occurs 24-72h following surgery. Factors are; restricted ventilation, slow, shallow resps, ↑ secretions, & ↓ cough effort.
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What is the pathophysiology of atelectasis?
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When aveoli become airless, the shrivel up as the natural elasticity of the tissues dominates, interferring w/blood flow through the lung, vent & perfusion are altered, → O2 diffusion, ↑ RR can control CO2 levels, None quick reinflation of lungs → lung tissue necrosis & infection → permanent lung damage.
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What are the clinical manifestations of atelectasis?
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Sm areas are asymptomatic, lg area cause ↑ hrt & resp rates & CP, Chest expansion appears abn or asymmetrical, affected side lags behind unaffected side, mediastinum shifts toward the other side in compression atelectasis.
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What is the managemnet of atelectasis?
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Deep breathing, Incentive spirometry,Adequate hydration, O2, ABX if indicated.
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What is acute respiratory failure?
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Dz sequeala, which occurs when the lungs are unable to adequately oxygenate the blood or prevent CO2 retention.
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What can cause respiratory failure?
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Conditions that can result in alveolar hypoventilation, V/Q mismatch or R-to-L shunting, COPD, Bronchitis, pneumonia, vent failure, CNS dz, Trauma, Depressant drugs, neuromuscular dz, pneumothorax, atelectasis, cor pulmonale, pulmonary edema, bronchospasm.
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What is the pathophysiologic process of acute respiratory failure?
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Impaired gas exchange, pt loses the ability to ventilate or perfuse @ the alveolar-cap level, O2 absorption & CO2 elimination will not occur.
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When a dz that affects gas exchange is the primary cause of acute respiratory failure what is the result?
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Impaired O2 perfusion & CO2 removal result in hypoxaemia & hypercapnia
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What do ABG studies usually reveal for a pt in acute respiratory failure?
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PaO2 <55-60mmHg (O2 partial pressure),
PCO2 > 40mmHg |
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What is the result of the hypoxia?
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Tissue hypoxia → anaerobic metabolism & lactic acidosis; stupor, coma, bradycardia, vasoconstriction, hypotension & cyanosis occur.
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What is the result of the hypercapnia?
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Respiratory acidosis, vasodilation, may sedate the CNS, hypotension, circulatory failure, & ↑ HR & CO.
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What are the clinical manifestations of acute respiratory failure?
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Cyanosis or oral mucosa, lips & nail beds, Nasal flaring, Ashen skin, Use of accessory muscles, Restlessness, Anxiety, Agitation, Confusion, Tachypnea, Cold, clammy skin, Dull or flat sound on percussion, Diminished BS.
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What complications can occur w/Acute respiratory failure?
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Tissue hypoxia, Metabolic acidosis, Cardiac arrest.
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What tests should be ran to dx Acute respiratory failure?
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ABG, CXR, EKG, Pulse ox, WBC, RBC, Electrolytes, Blood cultures, Pulmonary artery cath.
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What is the tx for Acute respiratory failure?
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O2 therapy, Mech vent, High-freq vent, ABX, bronchodialtors, corticosteroids, fluid restrictions, positive inotropic agents (digoxin), vasopressors, diuretics, deep breathing, incentive spirometry.
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What is pulmonary edema?
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Accumulation of fluid in the extravascular spaces of the lungs, a common complictation of cardiac disorders & may occur as chronic condition or may develop quickly & rapidly become fatal, it is a medical emergancy.
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What are the causes/predisposing factors of pulmonary edema?
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Barbituate or opiate poisoning, Cardiac failure, Infusion of excessive volume of IV fluids or overly rapid infusion, Impaired pulmonary hymphatic drainage, Inhalation of irritating gases, Mitral stenosis & L atrial myxoma, Pneumonia, Pulmonary venocclusive dz.
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What is the pathophysiology of pulmonary edema?
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When the balance of pulmonary cap hydrostatic pressure, cap oncotic pressure, Cap permeability & Lymphatic drainage ▲, or lympatic drainage is obstructed, fluid infiltrates into the lung → pulmonary edema.
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Excess fluid in the alveolar tissue may develop when?
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There is inflammation in the lungs, ↑ cap permeability, or when plasma proteins are low, ↓ plasma osmotic pressure. (a common cause is pulmonary HTN)
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What causes a shift of fluid out of the capillaries into the aveoli?
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When hydrostatic pressure in the pulmonary capillaries become high.
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Excessive amounts of fluid in the interstitial areas & alveoli interfere with the diffusion of what?
& what does this lead to? |
O2 → severe hypoxaemia & interferes w/the action of surfactant → difficulty in lung expansion w/ultimate collapse (caps may rupture → hemoptysis)
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What are the early S/Sx of Pulmonary edema?
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Dyspnea on exertion, Tachycardia, PND (fluid), Orthopnea (diaphram unable to expand), Cough, ↑BP (↑ vasoconstriction), Dependent crackles (fluid accumilation w/air), Neck vein distention (↑ pulmonary pressure, ↑ cardiac output, ↑ afterload).
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What complications may occur with pulmonary edema?
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Respiratory failure
Respiratory acidosis Cardiac arrest |
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What are the late S/Sx of Pulmonary edema?
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Labored resp, Cold, clammy skin, Arrhythmia, Hypotension, Tachycardia, ↑ Crackles, Diaphraseis, Thready pulse, Productive cought w/hemoptysis.
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What tests should be ordered to dx pulmonary edema?
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ABG (hypoxia & resp acidosis), CXR, Pulse ox, Pulmonary cath, EKG
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How is Pulmonary Edema managed?
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High O2, Assisted vent, diuretics, pressor agents, antiarrhythmics, arterial vasodilators, morphine.
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