Chapter 36: Alterations of Pulmonary Function Flashcards

1
Q

s/sx of pulm dz

A

Dyspnea and cough​

Altered breathing patterns​

Hyperventilation -> resp alk. CO2 lost. ​

Hypoventilation -> resp acidosis. CO accumulates​

​Hemoptysis -> coughing up blood​

Abnormal sputum​

Cyanosis​

Chest pain​

Clubbing

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2
Q

dyspnea

A

Subjective sensation of uncomfortable breathing

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3
Q

severe dyspnea

A

Flaring of the nostrils​

Use of accessory muscles of respiration​

Retraction of the intercostal spaces

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4
Q

dyspnea on exertion

A

SOB with activity

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5
Q

orthopnea

A

Dyspnea when lying down​

Often related to left side heart failure

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6
Q

paroxysmal nocturnal dyspnea

A

Awaking at night and gasping for air; must sit up or stand up

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7
Q

cough and sputum

A

Cough​: Protective reflex that helps clear the airways by an explosive expiration​. Acute cough​m-> Resolves within 2 to 3 weeks. Chronic cough​ -> Lasts longer than 3 weeks​.

Abnormal sputum​: Changes in amount, consistency, color, and odor provide information about the progression of disease and the effectiveness of therapy.​

Hemoptysis​: Coughing up blood or bloody secretions​

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8
Q

abnormal breathing patterns

A

Adjustments made by the body to minimize the work of the respiratory muscles

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9
Q

kussmaul respirations (hyperpnea)

A

Slightly increased ventilatory rate, very large tidal volume, and no expiratory pause​

Trying to blow off acid -> metabolic acidosis.

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10
Q

labored breathing

A

increased work of breathing

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11
Q

restricted breathing

A

Disorders that stiffen the lungs or chest wall and decrease compliance​

Ex. Obesity. Weight compresses breathing

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12
Q

Cheyne-stokes respirations

A

Alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea​

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13
Q

hypoventilation

A

Alveolar ventilation is inadequate in relationship to the metabolic demands.​

Leads to respiratory acidosis from hypercapnia.​

Low RR​ and Low vT​

Result is -Increased CO2 (>40mm Hg) and Decreased pH (Resp Acidosis)

Is caused:​ Over sedation #1, airway obstruction, ​chest wall restriction​, altered neurologic control of breathing.​

Causes:​

  1. Central ​
    Drugs (narcotics), Head injury/Spinal Cord injury​
  2. Chest wall disorder: Neuromuscular Diseases, Obesity, Kyphosis/scoliosis
  3. Damaged Lung Structure: asthma, COPD​

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14
Q

hyperventilation

A

Alveolar ventilation exceeds the metabolic demands.​

Leads to respiratory alkalosis from hypocapnia.​

Is caused:​ anxiety, ​Pain​, fever

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15
Q

cyanosis

A

Bluish discoloration of the skin and mucous membranes​

Develops with five grams of desaturated hemoglobin, regardless of concentration

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16
Q

peripheral cyanosis

A

Most often caused by poor circulation​

Best observed in the nail beds

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17
Q

central cyanosis

A

Caused by decreased arterial oxygenation (low partial pressure of oxygen [Pao2]) ​

Best observed in buccal mucous membranes and lips

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18
Q

clubbing

A

Bulbous enlargement of the distal segment of a finger or toe. ​

Graded 1-5 based on nailbed changes​

Associated with diseases causing hypoxemia

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19
Q

chest pain

A

pleural and chest wall

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20
Q

pleural pain

A

Is the most common pain caused by pulmonary diseases.​

Is usually sharp or stabbing in character.​

Infection and inflammation of the parietal pleura (pleuritis or pleurisy) can cause pain when the pleura stretch during inspiration and are accompanied by a pleural friction rub.

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21
Q

chest wall pain

A

may be from the airways
may be from muscle or rib pain

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22
Q

conditions caused by pulm dz or injury

A

Hypercapnia​: Increased carbon dioxide (CO2) in the arterial blood​, Occurs from hypoventilation​

Hypoxemia​: Hypoxemia (blood) versus hypoxia (tissue)​, Reduced oxygenation of arterial blood

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23
Q

caises of hypoxemia

A

in order of most to least common
1. V:Q Mismatch**​ Ventilation and perfusion are different than what it should be​

  1. Hypoventilation​
  2. Shunt​
  3. Thickened diffusion barrier​
  4. Low inspired O2 (Altitude)​
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24
Q

most common cause of hypoxemia in pt with pneumonia, atelectasis, PE

A

V:Q mismatch
* does improve with O2

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25
alveolar shunt
Alveoli blocked from ventilation​ Entry of blood into the systemic arterial system without going through ventilated areas of lung​ causes: Severe pneumonia​, Pulmonary Edema​, Atelectasis​, ARDS*​ -> diseased alveoli and inflamed caps, need put on a ventilator Does not improve with oxygen
26
thicken diffusion barrier
Diffusion Capacity is reduced by diseases in which the thickness is increased.​ Causes​: pulmonary fibrosis, asbestosis, sarcoidosis, ​ILD
27
low V/Q
ventilation problem. Perfusion is fine. 
28
shunt (very low) V/Q
blocked vent -> collapse alveolus –any cap passing will not get any O2
29
high V/Q
no problem with ventilation, problem with perfusion. Ex. PE. Dead space: any O2 that gets into alveoli and not used for perfusion 
30
low inspired ppO2
Low PaO2​. Pressure pushes O2 in from high level to low level  Normal or Decreased PaCO2 (hyperventilation)​ Causes:​ 1. FiO2 decreases at higher altitude​. hyperventilate. May have normal or deceased PaCO2. People who live high alt accumulates and they have normal PaCO2. Alt sickness is from hyperventilation an low CO2 -> get medicine ​ 2. Decrease in FiO2 (accidental ex.) COPD pt who needs 3L O2 at all time has NC fall off and now they have decrease Fi02 
31
pulmonary vascular resistance
Amount of right ventricular force required to pump blood into lungs depends on resistance to flow present in the pulmonary vascular system​ This resistance to flow is PVR Hypoxemic -> vasoconstriction​ Emphasema is common cause for pulm HTN ​ COPD. -> right vent. Hypertrophy -> death
32
cor pulmonale
Right ventricular hypertrophy secondary to pulmonary disease​ Can cause right sided heart failure​ Major cause of death in COPD patients​ Increased PVR makes it harder for right side of the heart to pump blood into pulmonary circulation
33
acute resp. failure
Hypoxia (Gas exchange is inadequate)​ Pao2 is ≤50 mm Hg.​ Hypercapnia (ventilation is inadequate)​ Paco2 is ≥50 mm Hg with a pH of ≤7.25.​ Requires ventilatory support, oxygen, or both. emergency condition, can affect all ages, major cause of death, successful outcome depends on prompt recognition and immediate initiation of supportive rx
34
chest wall restriction
Chest wall is deformed, traumatized, immobilized, or made heavy by fat; work of breathing is increased, and ventilation may be compromised because of a decrease in tidal volume.​ Impaired respiratory muscle function is caused by neuromuscular disease. can be caused by amiodarone and nitrofurantoin
35
restrictive lung diseases: parenchymal
interstitial pulm fibrosis: 1ry (idiopathic) occupational, collagenic, granulomatous, irradiation, resection, drug-induced (bleomycin, methotrexate, cyclophosphamide)
36
restrictive lung diseases: extra parenchymal pleura
pleural effusion, pneumothorax, pleural fibrosis, pleural tumors, pleural thickening.
37
restrictive lung diseases: extra parenchymal abdomen
severe distension
38
restrictive lung diseases: chest wall
trauma, kyphoscoliosis, ankylosing spondylitis, NM dz (MG, GB), morbid obesity, scleroderma
39
flail chest
Is the instability of a portion of the chest wall from rib or sternal fractures.​ Causes paradoxical movement of the chest with breathing.​ ​
40
pneumothorax
Pneumothorax refers to air in the intrapleural space
41
hemothorax
hemothorax refers to blood in the intrapleural space around the lung.
42
s/sx of pneumotorax
Signs of chest trauma​ Tachypnea, tachycardia​ Shortness of breath​ Unequal Lung Excursion​ Diminished or absent breath sounds on one side or one area of lung​ ABG: decreased PaO2 and SaO2, respiratory alkalosis​ Patient might complain of sharp chest pain on one side of chest​ Positive chest x-ray for pneumothorax
43
spontaneous pneumothorax patho
rupture of a bleb on the lung surface allows air to enter pleural space from airways. primary affects prev. healthy people. common for a young, tall, thin man. secondary affects people with preexisting lung dz (COPD)
44
spontaneous pneumothorax s/sx
abrupt onset, pleuritic chest pain, dyspnea, SOB, tachypnea, tachycardia, unequal lung excursion, decreased breath sound and hyperresonant percussion tone on affected side.
45
traumatic pneumo patho
trauma to the chest wall or pleura disrupts the pleural membrane. open occurs with penetrating chest trauma that allows air from the environment to enter the pleural space. closed occurs with blunt trauma that allows air from the lung to enter the pleural space. iatrogenic involves laceration of visceral pleura during a procedure such as thoracentesis or central line insertion.
46
traumatic pneumo s/sx
pain, dyspnea, tachypnea, tachycardia, decreased resp. excursion, absent breath sounds in affected area, air movement thru an open wound
47
tension pneumo patho
air enters pleural space thru chest wall or from airways but is unable to escape, resulting in rapid accumulation. lung on affected side collapses. as intrapleural pressure increases, heart, great vessels, trachea, and eso shift toward unaffected side.
48
tension pneumo s/sx
hypotension, shock, distended neck veins, severe dyspnea, tachypnea, tachycardia, decreased resp. excursion, absent breath sounds on affected side, tracheal deviation toward unaffected side.
49
dx of tension pneumo
CXR ex. left side tension pneumo. sides of push to right, trachea and mediastinum are pushes to right side, not the density bw 2 sides, right side is normal, left side hyperlucent signs of push: 1. collapse left lung 2. air under tension in left pleural cavity. no bronchovascular markings 3. tracheal shift to right side 4. mediastinal shift to right side tension pneumo left side
50
tension penumo tx
needle decompression: 2nd rib space in the mid-clavicular line, immediate rush of air, concerts a tension pneumo to a simple pneumo, asso with complications
51
penumo tx: chest drainage management
Removal of air or fluids from intrapleural space of the lungs or from the mediastinal compartment.​ May be short term or long term​ Used to treat large pleural effusions and pneumothorax
52
plural effusions
Build up of excess fluid between the layers of the pleura
53
causes of pleural effusions
Transudative (watery and diffuses out of the caps)​. HF​ and Pulmonary edema​ Exudative (protein rich and high concentrations of WBC, less watery). Pneumonia (para pneumonic)​ and Cancer
54
tx pf pleural effusoins
Diuretic​ Thoracentesis​ Chest Tube * take sample of fluid to dx
55
empyema
Infected pleural effusion​ Pus in the pleural space​
56
causes of empyema
chest trauma, pneumonia, or tb
57
s/sx of empyema
Cyanosis, fever, tachycardia​, cough, and pleural pain
58
tx of empyema
Administration of antimicrobial medications​ Drainage of the pleural space with a chest tube​ Severe cases: Ultrasound-guided pleural drainage, instillation of fibrinolytic agents TPA, or deoxyribonuclease (DNase) injected into the pleural space
59
aspiration
Passage of fluid and solid particles into the lungs​ Right lower lobe: Is the most frequent site. notice after eat or drink
60
aspiration s/sx
Both choking and intractable cough have a sudden onset.
61
aspiration tx
Supplemental oxygen; may require mechanical ventilation with positive end-expiratory pressure (PEEP).​ May need steroids and antibiotics
62
atelectasis
Collapse of lung tissue. loss of lung vol caused by inadequate expansion of the airspaces
63
types of atelectasis
Compression atelectasis​: External compression on the lung​ Absorption atelectasis​: Gradual absorption of air from obstructed or hypoventilated alveoli​. closed pore of Kohn Surfactant impairment​: Decreased production or inactivation of surfactant
64
atelectasis s/sx
Dyspnea, cough, fever, and leukocytosis
65
tx of atelectasis
prevention and deep breathing
66
bronchiectasis
Persistent abnormal dilation of the bronchi​ Dilated with filled with mucous. Can’t cough mucous out -> frequent infections. Pseudomonas. Sx doesn’t work well Cylindrical, saccular, and varicose​
67
bronchiectasis s/sx
Chronic productive cough
68
bronchiectasis tx
Sputum culture antibiotics​ Bronchodilators, antiinflammatory drugs​ Chest physiotherapy​ Supplemental oxygen​ Surgery
69
pulmonary fibrosis
Excessive amount of fibrous or connective tissue in the lung​ scarred tissue impairs gas exchange Idiopathic pulmonary fibrosis: No specific cause
70
pulmonary fibrosis s/sx
Increasing dyspnea on exertion
71
pulmonary firosis tx
Corticosteroids​ antifibrotic drugs ​ lung transplantation
72
O2 toxicity
Prolonged exposure to high concentrations of supplemental oxygen​ Severe inflammatory response mediated primarily by oxygen radicals​ Causes damage to alveolocapillary membranes, disruption of surfactant production, interstitial and alveolar edema, and decrease in compliance
73
O2 toxicity tx
Ventilatory support and reduction of inspired oxygen concentration to less than 60% as soon as tolerated​ ​
74
factors on which O2 toxicity depends
pressure: normobaric hypoxia and hyperbaric hypoxia time of exposure and O2 concentration: FiO2 > 60% longer than 36 hr. FiO2 >80% longer than 24 hr and FiO2 >100 % longer than 12 hr
75
pneumoconiosis
any change in lung caused by the inhalation of inorganic dust particles, usually from the workplace​
76
pneumoconiosis
Silica (concrete workers), asbestos (steel workers), and coal: Most common causes
77
pneumoconiosis s/sx
Cough, sputum production, dyspnea, decreased lung volumes, and hypoxemia​, large nodules on lungs, stiff lungs -cant fully expand, progressive masive fibrosis
78
pneumoconiosis tx
Palliative and prevention of further exposure ​ Improved working conditions​ Pulmonary rehabilitation and management of associated hypoxemia and bronchospasm
79
pulmonary edema
Excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability​ Most common cause of pulmonary edema: Left-sided heart disease
80
s/sx of pulm edema
Dyspnea, orthopnea, hypoxemia, and increased work of breathing​
81
pulm edema tx
Increased hydrostatic pressure caused by heart failure​: Improve cardiac output and volume status with diuretics, vasodilators, and drugs that improve the contraction of the heart muscle.​ Increased capillary permeability resulting from injury​ (ARDS) : Remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation.​ Any type of pulmonary edema​: Provide supplemental oxygen and/or mechanical ventilation.​
82
ARDS
Most severe expression of Acute lung injury ARDS is a devastating often fatal, inflammatory disease of the lung characterized by the sudden onset of pulmonary edema and respiratory failure.​ Involves both capillary and alveoli
83
causes of direct ARDS
pneumonia, gastric aspiration, near drowning, inhalation injury, direct chest injury
84
causes of indirect ARDS
sepsis, trauma, pancreatitis, drug overdose
85
s/sx of ARDS
Refractory Hypoxemia is a HALLMARK SX**** Etiologic Factors​: Worsening respiratory symptoms​ Bilateral opacities on CXRay ​ Hypoxic Respiratory failure​ pul. edema
86
tx of ARDS
Treat the Cause! Mechanical Ventilation -> Increased PEEP Patient positioning strategies -> Include prone positioning
87
Prognosis/mortality rate of ARDS
Varies widely: 30% to more than 85% Quality of life key for survivors -survivors may not have good quality of life Predictors associated with high mortality: Severity of illness Non pulmonary organ dysfunction Comorbidities Sepsis Increased Age
88
Phases of ARDS
Inflammatory/exudative, proliferative, fibrotic
89
Inflammatory phase of ARDS
Within 72 hr Alveolocapilary membrane damage, increased cap membrane permeability, pulmonary edema, surfactant inactivated
90
Proliferative phase of ARDS
4-21 days Resolution of pulm edema and proliferation of type II pnemocytes, fibroblasts, myofibroblasts hyaline membranes hypoxia
91
Fibrotic phase of ARDs
14-21 days Remodeling and fibrous Alveoli destruction Severe right to left shunting Acute resp. Failure
92
Obstructive pulm dz
Asthma COPD -> chronic bronchitis and emphysema
93
Asthma
Chronic inflam disorder of bronchial mucosa Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible. One half of all cases develop during childhood. Episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucous production
94
Asthma s/sx
Asymptomatic between attacks Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea, sleep prob, fatigue, allergies, common cold, chest pain Pulsus paradoxus -> drop in BP on inspiration
95
Status asthematicus
Bronchospasm not reversed by usual measures Life threatening
96
Ominous signs of impending death in asthma
Silent chest (no audible air movement) and a Paco2 greater than 70 mm Hg
97
Causes of triggers of asthma
Pollution, smoking, household chemicals, genetics, fat foods, dust, pets, bacteria, viruses
98
Asthma tx
Administration of oxygen and inhaled beta-agonist bronchodilators, HFA or nebulizers Oral corticosteroids administration early in the course of management Antibiotics are not indicated for acute asthma unless a bacterial infection is documented Education over allergens and irritants
99
COPD
Airflow limitation that is not fully reversible Inadequate exhalation Usually progressive Third leading cause of death in the United States and the sixth leading cause of death worldwide COPD: Chronic bronchitis plus emphysema
100
RF of COPD
obacco smoke Environmental -> ETS, indoor and outdoor air pollution, occupational dust and chemicals Aging Infections Socio-economic status Genetic susceptibilities Inherited mutation in the alpha-1 antitrypsin gene results in the development of emphysema even in nonsmokers.
101
Chronic bronchitis
Hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years -Inspired irritants increase mucous production, size and number of mucous glands, and bronchial edema; mucus is thicker than normal -Hypoxemia and hypercapnia -Airways collapse early in expiration, trapping gas in the lung -hyperinflation of alveoli
102
Chronic bronchitis s/sx
Decreased exercise tolerance Wheezing and shortness of breath Productive cough (“smoker’s cough”) becomes copious Polycythemia Barrel Chest
103
Emphysema
Abnormal permanent enlargement and destruction of the alveolar walls Loss of elastic recoil Alveolar destruction also produces large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs).
104
S/sx of emphysema
Later progresses to marked dyspnea, even at rest Little coughing and very little sputum Thin Tachypnea with prolonged expiration; use of accessory muscles for ventilation; pursed lips Increased anteroposterior diameter of the chest (barrel chest) To increase lung capacity: Leans forward with arms extended and braced on knees when sitting
105
COPD tx
Oxygen; may require noninvasive positive pressure ventilation or mechanical ventilation Inhaled bronchodilators by either an inhaler or a nebulizer Immediate administration of oral corticosteroids and antibiotics Inhaled anticholinergic agents and beta agonists -> bronchodilators Inhaled corticosteroids can be added Smoking cessation Pulmonary rehabilitation Improved nutrition Breathing techniques
106
Pneumonia
Infection of the lower respiratory tract Responsible for more disease and death than any other infection
107
Community-acquired pneumonia
Streptococcus pneumoniae
108
Health care-associated pneumonia
More virulent bacteria
109
Hospital-acquired (nosocomial) pneumonia
More virulent bacteria Ventilator-associated pneumonia
110
Routes of infection for pneumonia
Aspiration Inhalation Endotracheal tubes and suctioning Respiratory defenses cannot destroy the microorganism
111
Viral pneumonia
Is seasonal; usually mild and self-limiting. Can set the stage for a secondary bacterial infection. Provides an ideal environment for bacterial growth and by damaging ciliated epithelial cells, which normally prevent pathogens from reaching the lower airways. Most common form: Influenza
112
Viral pneumonia s/sx
Preceded by an upper respiratory infection Cough, dyspnea, and mild fever Chills, malaise, and pleuritic chest pain
113
Prevention of viral pneumonia
Vaccination for appropriate populations
114
Pneumonia tx
Establishment of adequate ventilation and oxygenation May require mechanical ventilation Adequate hydration Good pulmonary hygiene (e.g., deep breathing, coughing, chest physical therapy) Bacterial pneumonia: Antibiotics Viral pneumonia: Supportive therapy alone, unless secondary bacterial infection is present. Severe cases: Antiviral medications and/or antifungal, multiple drugs
115
TB
Infection caused by Mycobacterium tuberculosis, an acid-fast bacillus Leading cause of death from a curable infectious disease throughout the world
116
TB patho
Airborne droplet transmission Tubercle formation: Granulomatous lesion Caseous necrosis: Cheeselike material May remain dormant for life or cause active disease Isolation of bacilli by enclosing them in tubercles and surrounding the tubercles with scar tissue
117
TB s/sx
Latent: Asymptomatic Active: Fatigue, weight loss, lethargy, anorexia , a low-grade fever, and night sweats; purulent cough
118
Dx of TB
Positive tuberculin skin test: a purified protein derivative (PPD): Does not differentiate past, latent, or active disease Sputum culture Chest radiographs
119
Tx of TB
Rifampin, Isoniazid, pyrazinamide, and ethambutol Drug-resistant bacilli: Combination of at least four drugs to which the microorganism is susceptible, administering for 6-9 months. Latent TB get over length of tx just rifampin for ~4month
120
Acute bronchitis
Is an acute infection or inflammation of airways or bronchi; commonly follows a viral illness.
121
Acute bronchitis s/sx
Causes symptoms similar to pneumonia but does not demonstrate pulmonary consolidation and chest infiltrates. Nonproductive cough occurs in paroxysms and is aggravated by cold, dry, or dusty air.
122
Acute bronchitis s/sx
Rest, aspirin, humidity, and cough suppressant (codeine).
123
PE
Is the occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or air bubble. Pulmonary emboli commonly arise from the deep veins in the calf. Virchow triad: Venous stasis, hypercoagulability, endothelial damage
124
PE s/sx
Dyspnea* Tachypnea* Pleuritic pain* (often sudden onset) Cough Unilateral leg pain and swelling Wheezing Crackles (rales)
125
PE Dx
Clinical probability assessment D-dimer (< 200) 95% negative predictability Ventilation-perfusion scan CT angiogram Compression ultrasound
126
PE Tx
Anticoagulant therapy!! Heparin IV, Enoxaparin SQ, Oral Warfarin, oral Factor Xa inhibitors -> Xarelto (rivaroxaban) & Eliquis (apixiban) Vena cava filter Embolectomy
127
PE prevention
DVT prophylaxis Early ambulation Compression Stockings Elevation of injured leg Assess for DVT Asymptomatic OR Swelling, pain, redness, tenderness, cramping