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56 Cards in this Set

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  • Back
What is Dyspnea?
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.
What is Orthopnea?
Dyspnea while pt is supine, pulmonary congestion develops as blood pools in the lungs & abdominal contents push upward against the lungs.
What is Paroxysmal Nocturnal Dyspnea (PND)?
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)
What is the normal breathing pattern?
regular; inhalation/exhalation cycle occurs w/in the same time period between one inhalation & the next.
What is Cheyne-Stokes?
Ventilation rate & volume gradually ↑, peak, then gradually ↓, w/interspersed periods of apnea. (brains stem injury, neurologic impairment above the brain stem)
What is Kussmaul's respirations?
Deep gasping respirations, very lg tidal volumes, no expiratory pause. (diabetic coma, COPD, pulmonary fibrosis, & anxiety)
What is Biot's respirations?
Irregular pattern, rate, volume w/ intermittent periods of apnea (↑ ICP, space occupying lesions)
What are Agonal Respirations?
"dying breath", slow, shallow, irregular & sometimes gasping respirations, (from brain anoxia) are terminal respiration unless aggressive intervention is performed.
What is Central Neurologic Hyperventilation?
Similar to Kussmaul's, associated w/ICP
What is Hypoventilation?
Tidal volume ↓ normal range, ↑ blood CO2 level, (overdoses, head injury)
What is Hyperventilation?
Tidal volume ↑ normal range, ↓ blood CO2 level, (infection, fever, or fear)
What can cause cough?
Irritation (nasal discharge dripping into the oropharynx), Inflammation, Foreign material, Inhaled irritants, Aspiration of food or fluid.
Explain the physiology of cough;
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.
What are some causes of Haemoptysis?
Pneumonia, Bronchogenic carcinoma, Bronchiectasis, Lung abscess, TB.
If a pt does not have cyanosis, does that mean he has normal oxygenation?
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.
What is the most characteristic pain of lung dz?
That resulting from inflammation of the pleura. Pulmonary pain is central CP that is pronounced after coughing
What are the characteristics of chest pain?
Sharp & cutting, aggravated by coughing, sneezing & breathing (pt usually develops a pattern of rapid shallow breathing & avoids any unnecessary movement.
What are the most common causes of pleuritic pain?
Pulmonary infection or infarction, pts w/infection & inflammation of the trachea or bronchi.
What is the most common cause of digital clubbing?
Pulmonary dz; bronchogenic CA, bronchiectasis, lungabscess, or TB.
What are other causes of digital clubbing?
CV dz; Congenital intracardial shunting or Subacute endocarditis.
5-10% associated w/dz of the GI tract (including liver)
What is a rusty or dark-colored sputum usually a sign of?
Pneumococcal pneumonia
What is very large amounts of purulent sputum w/a foul odor associated with?
What can a thick, tenacious muccous be associated with?
Asthma or Cystic Fibrosis
What can blood-tinged muccous be a result of?
Chronic cough & irritation → rupture of superficial capillaries. (also could be a sign of a Tumor or TB)
What is sneezing?
Reflex response to irritation in the upper resp. tract, assists w/removal of irritant, associated w/inflammation or foreign material in the nasal passages.
What is atelectasis?
Nonaeration or collapse of a lung or part of a lung leading to ↓ gas exchange & hypoxia, occurs as a complication of many primary conditions.
What are the 2 major causes of collapse due to atelectasis?
Obstrutive or resorption atelectasis,
Compression atelectasis.
What is Obstrutive or resorption atelectasis?
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)
What is Compression atelectasis?
Results when a mass (tumor), exerts pressure on a part of the lung & prevents air from entering that section of the lung.
What situations can prevent lung expansion?
↑ pressure in the pleural cavity, ↑ surface tension in the alveoli, Fibrotic tissue in the lungs or pleura.
What is postoperative atelectasis?
Commonly occurs 24-72h following surgery. Factors are; restricted ventilation, slow, shallow resps, ↑ secretions, & ↓ cough effort.
What is the pathophysiology of atelectasis?
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.
What are the clinical manifestations of atelectasis?
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.
What is the managemnet of atelectasis?
Deep breathing, Incentive spirometry,Adequate hydration, O2, ABX if indicated.
What is acute respiratory failure?
Dz sequeala, which occurs when the lungs are unable to adequately oxygenate the blood or prevent CO2 retention.
What can cause respiratory failure?
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.
What is the pathophysiologic process of acute respiratory failure?
Impaired gas exchange, pt loses the ability to ventilate or perfuse @ the alveolar-cap level, O2 absorption & CO2 elimination will not occur.
When a dz that affects gas exchange is the primary cause of acute respiratory failure what is the result?
Impaired O2 perfusion & CO2 removal result in hypoxaemia & hypercapnia
What do ABG studies usually reveal for a pt in acute respiratory failure?
PaO2 <55-60mmHg (O2 partial pressure),
PCO2 > 40mmHg
What is the result of the hypoxia?
Tissue hypoxia → anaerobic metabolism & lactic acidosis; stupor, coma, bradycardia, vasoconstriction, hypotension & cyanosis occur.
What is the result of the hypercapnia?
Respiratory acidosis, vasodilation, may sedate the CNS, hypotension, circulatory failure, & ↑ HR & CO.
What are the clinical manifestations of acute respiratory failure?
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.
What complications can occur w/Acute respiratory failure?
Tissue hypoxia, Metabolic acidosis, Cardiac arrest.
What tests should be ran to dx Acute respiratory failure?
ABG, CXR, EKG, Pulse ox, WBC, RBC, Electrolytes, Blood cultures, Pulmonary artery cath.
What is the tx for Acute respiratory failure?
O2 therapy, Mech vent, High-freq vent, ABX, bronchodialtors, corticosteroids, fluid restrictions, positive inotropic agents (digoxin), vasopressors, diuretics, deep breathing, incentive spirometry.
What is pulmonary edema?
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.
What are the causes/predisposing factors of pulmonary edema?
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.
What is the pathophysiology of pulmonary edema?
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.
Excess fluid in the alveolar tissue may develop when?
There is inflammation in the lungs, ↑ cap permeability, or when plasma proteins are low, ↓ plasma osmotic pressure. (a common cause is pulmonary HTN)
What causes a shift of fluid out of the capillaries into the aveoli?
When hydrostatic pressure in the pulmonary capillaries become high.
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)
What are the early S/Sx of Pulmonary edema?
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).
What complications may occur with pulmonary edema?
Respiratory failure
Respiratory acidosis
Cardiac arrest
What are the late S/Sx of Pulmonary edema?
Labored resp, Cold, clammy skin, Arrhythmia, Hypotension, Tachycardia, ↑ Crackles, Diaphraseis, Thready pulse, Productive cought w/hemoptysis.
What tests should be ordered to dx pulmonary edema?
ABG (hypoxia & resp acidosis), CXR, Pulse ox, Pulmonary cath, EKG
How is Pulmonary Edema managed?
High O2, Assisted vent, diuretics, pressor agents, antiarrhythmics, arterial vasodilators, morphine.