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Adv. Patho > Chapter 36: Alterations of Pulmonary Function > Flashcards

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
Q

alveolar shunt

A

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

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26
Q

thicken diffusion barrier

A

Diffusion Capacity is reduced by diseases in which the thickness is increased.​

Causes​: pulmonary fibrosis, asbestosis, sarcoidosis, ​ILD

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27
Q

low V/Q

A

ventilation problem. Perfusion is fine.

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28
Q

shunt (very low) V/Q

A

blocked vent -> collapse alveolus –any cap passing will not get any O2

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29
Q

high V/Q

A

no problem with ventilation, problem with perfusion. Ex. PE. Dead space: any O2 that gets into alveoli and not used for perfusion

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30
Q

low inspired ppO2

A

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

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31
Q

pulmonary vascular resistance

A

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

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32
Q

cor pulmonale

A

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

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33
Q

acute resp. failure

A

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

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34
Q

chest wall restriction

A

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

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35
Q

restrictive lung diseases: parenchymal

A

interstitial pulm fibrosis: 1ry (idiopathic) occupational, collagenic, granulomatous, irradiation, resection, drug-induced (bleomycin, methotrexate, cyclophosphamide)

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36
Q

restrictive lung diseases: extra parenchymal pleura

A

pleural effusion, pneumothorax, pleural fibrosis, pleural tumors, pleural thickening.

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37
Q

restrictive lung diseases: extra parenchymal abdomen

A

severe distension

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38
Q

restrictive lung diseases: chest wall

A

trauma, kyphoscoliosis, ankylosing spondylitis, NM dz (MG, GB), morbid obesity, scleroderma

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39
Q

flail chest

A

Is the instability of a portion of the chest wall from rib or sternal fractures.​

Causes paradoxical movement of the chest with breathing.​

​

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40
Q

pneumothorax

A

Pneumothorax refers to air in the intrapleural space

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41
Q

hemothorax

A

hemothorax refers to blood in the intrapleural space around the lung.

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42
Q

s/sx of pneumotorax

A

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

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43
Q

spontaneous pneumothorax patho

A

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)

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44
Q

spontaneous pneumothorax s/sx

A

abrupt onset, pleuritic chest pain, dyspnea, SOB, tachypnea, tachycardia, unequal lung excursion, decreased breath sound and hyperresonant percussion tone on affected side.

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45
Q

traumatic pneumo patho

A

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.

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46
Q

traumatic pneumo s/sx

A

pain, dyspnea, tachypnea, tachycardia, decreased resp. excursion, absent breath sounds in affected area, air movement thru an open wound

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47
Q

tension pneumo patho

A

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.

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48
Q

tension pneumo s/sx

A

hypotension, shock, distended neck veins, severe dyspnea, tachypnea, tachycardia, decreased resp. excursion, absent breath sounds on affected side, tracheal deviation toward unaffected side.

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49
Q

dx of tension pneumo

A

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

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50
Q

tension penumo tx

A

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

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51
Q

penumo tx: chest drainage management

A

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
Q

plural effusions

A

Build up of excess fluid between the layers of the pleura

53
Q

causes of pleural effusions

A

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
Q

tx pf pleural effusoins

A

Diuretic​

Thoracentesis​

Chest Tube

  • take sample of fluid to dx
55
Q

empyema

A

Infected pleural effusion​

Pus in the pleural space​

56
Q

causes of empyema

A

chest trauma, pneumonia, or tb

57
Q

s/sx of empyema

A

Cyanosis, fever, tachycardia​, cough, and pleural pain

58
Q

tx of empyema

A

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
Q

aspiration

A

Passage of fluid and solid particles into the lungs​

Right lower lobe: Is the most frequent site.

notice after eat or drink

60
Q

aspiration s/sx

A

Both choking and intractable cough have a sudden onset.

61
Q

aspiration tx

A

Supplemental oxygen; may require mechanical ventilation with positive end-expiratory pressure (PEEP).​

May need steroids and antibiotics

62
Q

atelectasis

A

Collapse of lung tissue. loss of lung vol caused by inadequate expansion of the airspaces

63
Q

types of atelectasis

A

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
Q

atelectasis s/sx

A

Dyspnea, cough, fever, and leukocytosis

65
Q

tx of atelectasis

A

prevention and deep breathing

66
Q

bronchiectasis

A

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
Q

bronchiectasis s/sx

A

Chronic productive cough

68
Q

bronchiectasis tx

A

Sputum culture antibiotics​

Bronchodilators, antiinflammatory drugs​

Chest physiotherapy​

Supplemental oxygen​

Surgery

69
Q

pulmonary fibrosis

A

Excessive amount of fibrous or connective tissue in the lung​

scarred tissue impairs gas exchange

Idiopathic pulmonary fibrosis: No specific cause

70
Q

pulmonary fibrosis s/sx

A

Increasing dyspnea on exertion

71
Q

pulmonary firosis tx

A

Corticosteroids​

antifibrotic drugs ​

lung transplantation

72
Q

O2 toxicity

A

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
Q

O2 toxicity tx

A

Ventilatory support and reduction of inspired oxygen concentration to less than 60% as soon as tolerated​

​

74
Q

factors on which O2 toxicity depends

A

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
Q

pneumoconiosis

A

any change in lung caused by the inhalation of inorganic dust particles, usually from the workplace​

76
Q

pneumoconiosis

A

Silica (concrete workers), asbestos (steel workers), and coal: Most common causes

77
Q

pneumoconiosis s/sx

A

Cough, sputum production, dyspnea, decreased lung volumes, and hypoxemia​, large nodules on lungs, stiff lungs -cant fully expand, progressive masive fibrosis

78
Q

pneumoconiosis tx

A

Palliative and prevention of further exposure ​

Improved working conditions​

Pulmonary rehabilitation and management of associated hypoxemia and bronchospasm

79
Q

pulmonary edema

A

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
Q

s/sx of pulm edema

A

Dyspnea, orthopnea, hypoxemia, and increased work of breathing​

81
Q

pulm edema tx

A

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
Q

ARDS

A

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
Q

causes of direct ARDS

A

pneumonia, gastric aspiration, near drowning, inhalation injury, direct chest injury

84
Q

causes of indirect ARDS

A

sepsis, trauma, pancreatitis, drug overdose

85
Q

s/sx of ARDS

A

Refractory Hypoxemia is a HALLMARK SX**

Etiologic Factors​:
Worsening respiratory symptoms​
Bilateral opacities on CXRay ​
Hypoxic Respiratory failure​
pul. edema

86
Q

tx of ARDS

A

Treat the Cause!
Mechanical Ventilation -> Increased PEEP
Patient positioning strategies -> Include prone positioning

87
Q

Prognosis/mortality rate of ARDS

A

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
Q

Phases of ARDS

A

Inflammatory/exudative, proliferative, fibrotic

89
Q

Inflammatory phase of ARDS

A

Within 72 hr
Alveolocapilary membrane damage, increased cap membrane permeability, pulmonary edema, surfactant inactivated

90
Q

Proliferative phase of ARDS

A

4-21 days
Resolution of pulm edema and proliferation of type II pnemocytes, fibroblasts, myofibroblasts
hyaline membranes
hypoxia

91
Q

Fibrotic phase of ARDs

A

14-21 days
Remodeling and fibrous
Alveoli destruction
Severe right to left shunting
Acute resp. Failure

92
Q

Obstructive pulm dz

A

Asthma
COPD -> chronic bronchitis and emphysema

93
Q

Asthma

A

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
Q

Asthma s/sx

A

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
Q

Status asthematicus

A

Bronchospasm not reversed by usual measures
Life threatening

96
Q

Ominous signs of impending death in asthma

A

Silent chest (no audible air movement) and a Paco2greater than 70 mm Hg

97
Q

Causes of triggers of asthma

A

Pollution, smoking, household chemicals, genetics, fat foods, dust, pets, bacteria, viruses

98
Q

Asthma tx

A

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
Q

COPD

A

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
Q

RF of COPD

A

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
Q

Chronic bronchitis

A

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
Q

Chronic bronchitis s/sx

A

Decreased exercise tolerance
Wheezing and shortness of breath
Productive cough (“smoker’s cough”) becomes copious
Polycythemia
Barrel Chest

103
Q

Emphysema

A

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
Q

S/sx of emphysema

A

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
Q

COPD tx

A

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
Q

Pneumonia

A

Infection of the lower respiratory tract
Responsible for more disease and death than any other infection

107
Q

Community-acquired pneumonia

A

Streptococcus pneumoniae

108
Q

Health care-associated pneumonia

A

More virulent bacteria

109
Q

Hospital-acquired (nosocomial) pneumonia

A

More virulent bacteria
Ventilator-associated pneumonia

110
Q

Routes of infection for pneumonia

A

Aspiration
Inhalation
Endotracheal tubes and suctioning
Respiratory defenses cannot destroy the microorganism

111
Q

Viral pneumonia

A

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
Q

Viral pneumonia s/sx

A

Preceded by an upper respiratory infection
Cough, dyspnea, and mild fever
Chills, malaise, and pleuritic chest pain

113
Q

Prevention of viral pneumonia

A

Vaccination for appropriate populations

114
Q

Pneumonia tx

A

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
Q

TB

A

Infection caused by Mycobacterium tuberculosis, an acid-fast bacillus

Leading cause of death from a curable infectious disease throughout the world

116
Q

TB patho

A

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
Q

TB s/sx

A

Latent: Asymptomatic
Active: Fatigue, weight loss, lethargy, anorexia , a low-grade fever, and night sweats; purulent cough

118
Q

Dx of TB

A

Positive tuberculin skin test: a purified protein derivative (PPD): Does not differentiate past, latent, or active disease
Sputum culture
Chest radiographs

119
Q

Tx of TB

A

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
Q

Acute bronchitis

A

Is an acute infection or inflammation of airways or bronchi; commonly follows a viral illness.

121
Q

Acute bronchitis s/sx

A

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
Q

Acute bronchitis s/sx

A

Rest, aspirin, humidity, and cough suppressant (codeine).

123
Q

PE

A

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
Q

PE s/sx

A

Dyspnea*
Tachypnea*
Pleuritic pain*
(often sudden onset)
Cough
Unilateral leg pain and swelling
Wheezing
Crackles (rales)

125
Q

PE Dx

A

Clinical probability assessment
D-dimer (< 200)
95% negative predictability
Ventilation-perfusion scan
CT angiogram
Compression ultrasound

126
Q

PE Tx

A

Anticoagulant therapy!!
Heparin IV, Enoxaparin SQ, Oral Warfarin, oral Factor Xa inhibitors -> Xarelto (rivaroxaban) & Eliquis (apixiban)

Vena cava filter

Embolectomy

127
Q

PE prevention

A

DVT prophylaxis

Early ambulation

Compression Stockings

Elevation of injured leg

Assess for DVT
Asymptomatic OR Swelling, pain, redness, tenderness, cramping

Adv. Patho (5 decks)

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