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AACN CCRN Review
Pulmonary System
Presenter:
Suzanne M. Burns, RN, MSN, RRT, CCRN, ACNP, FAAN, FCCM, FAANP
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Adult CCRN Certification Review Course: Pulmonary
Objectives This CCRN pulmonary review session will cover pulmonary diseases/conditions, pharmacology, and diagnostics common in critical care. Specific content consists of:
Basic acid-base abnormalities
Traditional mechanical ventilation modes and methods
Pathophysiology and management of selected restrictive and obstructive pulmonary disease conditions, pulmonary hypertension, pulmonary embolus, and traumatic injuries
Pulmonary Adult Program
Pulmonary clinical judgment questions make up 18% of the examination
Covers diseases/conditions, pharmacology, and diagnostics common in critical care
These content areas are covered today
Some extra content is included, but may not be covered in-depth
Good luck!
Arterial and Venous Blood Gases Arterial Norms
pH: 7.35‒7.45 o <7.35 = acid; >7.35 = alkaline
PaCo2: 35‒45 mm Hg o <35 = alkaline; >45 = acid
PaO2: 80‒100mm Hg o <60 = severe, 60‒80 = moderate hypoxemia
Venous Norms
Mixed venous O2: 40 mm Hg o Lower: too much being extracted (ie, cardiogenic shock) o Higher: not enough being extracted (eg, sepsis)
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Uncompensated Acid‒Base Abnormalities (In these, the pH is abnormal. Look to the respiratory or metabolic component to determine primary mechanism)
Compensated Acid‒Base Abnormalities (pH is normal. The primary mechanism—respiratory or metabolic—can be determined by looking at the DIRECTION of the pH)
Partial compensation is present when the pH is not fully corrected but there is evidence that the buffering system is at work to compensate
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Base Excess The base excess indicates the amount of excess or insufficient level of bicarbonate in the system (a negative base excess indicates a base deficit in the blood) This is a calculated number and is helpful in determining presence of metabolic acidosis and degree of acidosis Compensated vs Uncompensated
First, interpret the ABGs
Second, check the pH; to be fully compensated, the pH must be within normal range (7.35‒7.45)
Third, check the respiratory and metabolic components to see which is going in the direction of acidosis or alkalosis. The one that matches the pH direction (acidotic or alkalotic) is the primary mechanism
The body tries to restore a normal pH by altering the buffer system component not involved in the imbalance, either HCO3 or CO2. The kidneys take longer than the lungs!
So, you may have a partially compensated picture, as well (this is when the pH is not normal but there is compensation from another system)
A Few Examples of Conditions and Associated Treatments
Respiratory acidosis o Conditions: hypoventilation, oversedation, drug overdose, neuromuscular disease,
inappropriate vent settings o Treatments: naloxone (Narcan), adjust vent settings, etc.
Respiratory alkalosis o Conditions: inappropriate vent settings, pulmonary embolus, pregnancy, hysterical reaction,
anxiety o Treatments: decrease vent rate, decrease Vt, sedation etc.
Metabolic acidosis o Conditions: DKA, Hypoperfusion, aspirin OD, renal failure, shock, sepsis, diarrhea o Treatments: bicarb, increase perfusion, dialysis, etc.
Metabolic alkalosis o Conditions: antacid OD, NGT suctioning, vomiting, K+-wasting diuretics o Treatments: stop offending drugs, acetazolamide (Diamox, a diuretic that eliminates bicarb ions
from blood), etc. Mechanical Ventilation A brief review of traditional volume and pressure modes… Volume Modes
Principle o Delivers preset volume with every breath
Disadvantage o Volume is delivered regardless of the pressure required
Normal tidal volume (Vt) o 8‒12 mL/kg (6 mL/kg in ARDS). Lower volumes may need to be used in any sick patient. We’ll
come back to this! Volume Modes—Monitoring
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Monitor pressure!
Pressure changes along with changes in compliance (lung and chest wall) and resistance (airways) Volume Ventilation Parameters
Fraction of inspired O2 (FiO2): 21‒100%
Vt: 8‒12 (with lung protective strategies a lower volume is used; ie, 6 mL/kg)
Rate (fx) o 10‒20; adjusted after ABG
Inspiratory time (Ti) o Speed (flow rate) of the gas (L/M)
Average adult Ti time: 7-1.0 second o I:E ratio usually 1:2 or 1:3
Sensitivity: either pressure or flow setting
PEEP Positive End-expiratory Pressure (PEEP)
Maintains continuous positive pressure throughout exhalation
“Recruits” alveoli and holds them open. Restores FRC PEEP
Restores FRC (used to “recruit” alveoli)
Redistributes lung water?
5 cm PEEP “physiologic”?
Allows for decrease in FiO2 (decreases shunt)
Increased in 5‒10 cm increments in adult
Weaned slowly (rapid loss of effect) PEEP
When set PEEP >10 cm, avoid breaking the circuit
Clinical implications of PEEP o Hypotension and barotrauma
What is auto-PEEP?
Inadequate expiratory time (“waiting to exhale”)
Common in patients with asthma, COPD, those with high minute ventilation requirements, and those with long inspiratory times. Can also be caused by mechanical factors (ie, water in the tubing, small endotracheal tubes)
Can be measured at bedside. If found… o Shorten inspiratory time, lower rate, decrease tidal volume, give bronchodilators, etc.
Continuous Positive Airway Pressure (CPAP) Definition
PEEP in spontaneously breathing patient, no positive pressure breaths
Intubated/non-intubated patients o Weaning method (intubated) o Nocturnal ventilation in OSA (non-intubated)
Nasal pillows/nasal mask
Prevents upper airway obstruction by keeping tongue and soft palate away from posterior
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pharyngeal wall Traditional Modes of Ventilation: Volume How the parameters are configured to deliver breaths to the patient. Synchronized Intermittent Mandatory Ventilation (SIMV)
Delivers set number of volume breaths
Allows patient to breathe spontaneously between set breaths at own volume (in synchrony with machine breaths)
Advantages o “Weaning mode”—gradual decrease in the rate of set breaths o Often used in conjunction with PSV
SIMV
Disadvantages o Risk of increased WOB at low rates, especially if inadequate flow or slow ventilator response time
(this is the main reason we mix PSV with SIMV)
Parameters set by clinician
Vt
Ti
RR (fx)
Sensitivity
FiO2
PEEP Assist/Control (A/C) aka, Assist Mandatory
Delivers mandatory (set) number of volume breaths
Allows the patient to breathe between set breaths but… o Upon sensing patient effort, ventilator delivers full preset tidal volume
Disadvantages o Excessive patient work if inspiratory time not matched to patient (ie, inadequate flow) or not
sensitive enough o Potential for patient/ventilator dysynchrony
A/C
Not for weaning
Parameters o Vt o Ti o Sensitivity o RR (fx) o PEEP o FiO2
Traditional Pressure Modes
Principle o Preselected pressure o Vt varies with each breath
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o Decelerating flow pattern may improve gas distribution
Disadvantages o Sensitive to changes in patient condition
Compliance (lung)
Resistance (airway) Pressure Modes—Monitoring
The tidal volume will change with changes in lung or airway
Monitor tidal volume!
In spontaneously breathing patients…must also monitor rate! Pressure Support Ventilation (PSV)
A mode of ventilation that augments or supports a spontaneous inspiration with a clinician-selected pressure level
Patient selection o Stable? o Reliable ventilatory drive o Ready to wean
PSV: Parameters
To set o FiO2 o Inspiratory pressure level (PS level) o PEEP o Sensitivity
To monitor HOURLY o RR (fx) o Vt
PSV: Advantages o Patient comfort
Patient controls Ti, I:E, RR, Vt o Provides gradual respiratory muscle work
o Endurance o WOB less than with SIMV (depending on the level of PSV) PSV: Disadvantages
o RR and Vt dependent on patient condition (lung compliance/airway resistance)
PSV
High pressure levels provide nearly total ventilatory support!
PSV may be added to SIMV to offset the WOB on spontaneous breaths
Pressure Control Ventilation (PCV)
Purpose o To lower airway pressures o To optimize gas exchange
Application
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o ARDS PCV
Set parameters o Pressure limit (IPL)
Initially set at 25‒35 cm H2O or at plateau pressure
RR o 20‒40
Initial FiO2 usually 1.00
Set Ti PC‒Inverse Ratio (PC‒IRV)
Reverses normal I:E o Start at 1:1; up to 4:1
Improves oxygenation o Expands stiff alveoli with longer distending times
MONITOR FOR AUTO-PEEP
Sedation/NMBA often required! Non-invasive Ventilation Bi-level Positive Airway Pressure (Bi-PAP )
Noninvasive via mask
Two distinct levels of positive pressure o I-PAP (PSV) o E-PAP (PEEP)
Modes’ names vary with vent manufacturer: spontaneous (PS), spontaneous/timed (A/C), timed (control)
Patient selection o Patients with chronic respiratory failure o ‘Bridging’ o CHF
Bilevel (Bi-PAP)
Application o Set E, then I o Rate (if a control mode) o FiO2 o Creativity and mask selection o Huge time component
Assessment o RR and pattern o Patient comfort o Skin integrity o Patient safety
Emesis
Secretions
ABGs
Abdominal distension
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Traditional Ventilator Settings and Relationship to ABGs
PaO2 or O2 saturation: FiO2 and PEEP
PaCO2: rate and volume (minute ventilation)
pH: can be affected by ventilation (too much/not enough) or lack of oxygenation (ie, lactic acidosis) The New Pressure Modes
Application of microprocessor technology has resulted in sophisticated mode options that are very responsive to patient initiated efforts!
Spontaneous breathing is encouraged. However, no data have demonstrated that they improve outcomes!
Volume-assured Pressure Modes
Combine pressure supported ventilation with a decelerating flow pattern and a guaranteed volume
Settings vary with ventilator
All require a “selected volume”
Spontaneous versus control modes determined by selection of fx, Ti, etc. Examples
VS—Spontaneous mode that adjusts pressure to attain volume
PRVC—Adjusts pressure to attain volume, but other parameters set Airway Pressure Release and Bilevel/Biphasic Positive Airway Pressure
APRV: Allows spontaneous breathing on a preset CPAP level which is interrupted by a short (1 sec) release for further expiration. Similar to PC/IRV
BiPAP: Similar to pressure-controlled ventilation, during which unrestricted spontaneous breathing is possible in each phase of the respiratory cycle
Patient Selection
ARDS
Noncompliant lungs
Those who otherwise may require muscle relaxants Weaning from Mechanical Ventilation
Protocols work! Use short duration, spontaneous breathing trials—SBTs (CPAP or t-piece) or decrease ventilatory support (eg, PSV) over time
SBTs range from ½ hour to 2 hours. More than that may tire the patient, and longer trials are not associated with better outcomes
Assure rest between trials
Attention to nonpulmonary factors as well as pulmonary factors (eg, nutrition, mobility, psychological support)
With tracheostomy…more prolonged trials
Note: Many of the new pressure modes are ventilator-specific! While many of the modes are similar, the names differ.
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Signs of Intolerance (When to Stop!)
Symptoms: Dyspnea, anxiety, etc.
Signs: tachypnea, chest‒abdominal asynchrony, drop in saturation, tachycardia, BP changes, diaphoresis, etc.
Trial is terminated with these signs and symptoms
Rest is necessary and generally means a return to full ventilation for 12‒24 hours Prior to wean trials
WAKE THEM UP!
Sedation off! Acute Respiratory Failure Oxygenation and ventilation abnormalities
PaO2 <60 and/or PaCO2 >50 at rest Etiology
Obstructive, restrictive, neuromuscular, V/Q (ie, PE) Restrictive Diseases Definition and Concepts Expansion of the lung is restricted or decreased Restrictive Diseases
Acute respiratory distress syndrome
Pneumonia
Atelectasis (volume loss)
Pulmonary edema
Others (eg, pneumothorax) Restrictive Disorders
Lung volumes decreased
Loss of functional residual capacity
Compliance decreased
Increased WOB.
Abnormal v/q (ie, shunt)
Oxygenation problems Functional Residual Capacity
Volume that remains in the lungs at the end of a resting exhalation
Helps keep the alveoli open
Reduces shunt Compliance
How easy the lungs distend
Takes less pressure to get big volume Clinical Features
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Dyspnea
Tachypnea
Hypoxemia
Increased WOB.
Weakness and fatigue Hypoxemia
Hypoventilation
Diffusion defect
Shunt
V/Q mismatch Clinical Indices of Oxygenation
Alveolar‒arterial (A‒a) gradient: 10‒15 on RA, 50‒75 on 100%
a/A ratio: N = ≥0.8
PaO2/FiO2 (P/F) ratio:
<300 = ARDS. ARDS scored as mild, moderate, or severe.
Blood flow shunted/blood flow total (Qs/Qt): ≥15% is significant in ventilated patient Treatment (General)
Treat precipitating causes
Support oxygenation and ventilation
Mechanical ventilation Acute Respiratory Distress Syndrome (ARDS)
Pathogenesis: noncardiogenic pulmonary edema, pulmonary capillary leak, bilateral diffuse infiltrates, P/F ratio <200
Etiology is indirect or direct injury. High mortality
Acute lung injury terminology eliminated in favor of “mild,” “moderate,” and “severe” ARDS
Berlin definition of ARDS
o Timing of condition
o Chest imaging criteria
o Origin of lung edema
o Oxygenation status
Pathology
Increased capillary leak
V/Q abnormalities
Decreased lung compliance (and atelectasis)
Shunt
Hypoxemia
Dyspnea
3 phases (diffuse alveolar damage) Phases of ARDS
Exudative (0‒4 days)
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Proliferative (3‒10 days)
Fibrotic (7‒14 days) Clinical Features
Dyspnea
Tachypnea
Hyperventilation (initially)
Increased work of breathing (respiratory distress) Diagnosis
X-ray o Bilateral diffuse infiltrates
ABGs o PaO2 low despite FiO2, increased A-a gradient, P/F ratio <200, “refractory hypoxemia”
PCW o <18 (or other evidence that it is not due to a cardiac condition)
Therapy for ARDS
Treat etiology
Infection, trauma, hypotension, etc.
Supportive
Oxygenation, ventilation, cardiac output
Optimize lung recovery prevent volu-press trauma “Volu-Press” Trauma
Large Vt’s create high pressures
Injury to the stiff lung at “distending pressures” >35 cm H2O for >72 hours
Alveolar fractures and edema: non-ARDS, ARDS PEEP
PEEP—protects against ventilator-induced injury by preventing shear stress injury from repeated opening/closing of alveoli; protects from tidal stress!
Prevent Lung Injury (aka Volu-trauma)
Avoid O2 toxicity (FiO2 <50%‒60%)
Low tidal volumes—6 mL/kg (low volumes may result in >CO2 and lower pH—called permissive hypercarbia)
Maintain lung recruitment: PEEP Pneumonia
Definition o An inflammatory process (usually due to infection; may be chemical pneumonitis)
Pathophysiology o Alveolar filling with exudate (or other), tissue necrosis, ischemia
Classification of Pneumonias
Community-acquired
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Hospital-acquired (within 3‒5 days of being in the hospital, recent hospitalization, nursing home, etc.). Often an aspiration pneumonia
Ventilator-associated (after 3‒5 days of mechanical ventilation)
Treatment varies: nosocomial organisms include gram-negative organisms and are treated differently Ventilator-associated Events
Ventilator-associated condition (VAC): PEEP (>3 cm H2O and FiO2 (>20%) following period of stability
Infection-related ventilator--associated condition (IVAC): elevated temperature (>38 or <36) OR WBC (≥12 or ≤4) AND start of antimicrobials and continued for ≥4 days
Possible ventilator-associated pneumonia: purulent secretions and positive culture
Probable ventilator-associated pneumonia: purulent secretions and defined for possible VAP AND specific diagnostics such as histopathology, pleural fluid cultures, etc.
Clinical Presentation
Symptoms o Dyspnea, tachypnea, pleuritic chest pain, fever, chills, rigors, etc.
Signs o Evidence of consolidation, pleural effusions, wheezing, fever, cough (with or without purulent
sputum) Diagnostic Findings
Chest x-ray: infiltrates (especially gravity dependent)
Purulent sputum (or change in quality/quantity)
Hypoxemia and hypercapnia
Decreased compliance and/or obstruction to flow Sputum Characteristics Appearance
Rust
Brick red
Salmon colored
Yellow/green
Thick purulent, foul
Frothy
Watery
Organism
Pneumococcal
Klebsiella
Staphylococcus
Bacterial
Lung abscess
Pulmonary edema
Cold/allergy
Tenacious, white
Mucoid, gray
Brown
Anchovy chocolate
Red
Asthma
Bronchitis
Aspergillosis
Amoebic abscess
Rifampin Diagnosis
Sputum gram stains
Sputum cultures
CBC with diff
Chest x-ray
Bronchoscopy
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Treatment
Antibiotics o Hospital-acquired organisms include gram-negative and other opportunistic organisms o Treated with broad coverage, as are pneumonias in immunocompromised patients
Fluids
Oxygen
Mechanical ventilation Pulmonary Aspiration Pathophysiology and etiology
Aspiration of particulate or fluid matter causing generalized tissue reaction and/or airway obstruction. Widespread chemical pneumonitis within 12‒36 hours
Compliance is decreased Clinical Presentation
Solid objects o Cough, dyspnea, wheezing, respiratory distress, cyanosis, aphonia (café coronary)
Gastric acid o Abrupt onset of respiratory distress, hypotension, bronchospasm, increased secretions,
tachypnea, fever, crackles, and rhonchi
Bacterial o Infection fever
Diagnostic Findings
Chest x-ray: infiltrates (especially gravity-dependent)
Purulent sputum (or change in quality/quantity)
Hypoxemia and hypercapnia
Decreased compliance and/or flow Therapy/Prevention
HOB >30⁰!
Suctioning and cuff management (CASS-continuous aspiration subglottic suction)
Oxygenation
Chest PT
Bronchoscopic removal
Antibiotics, oral decontamination
Ventilatory support Obstructive Diseases
Definition—A group of diseases including asthma, chronic bronchitis, and emphysema in which the common denominator is airflow obstruction
Chronic Bronchitis
Chronic or recurrent excess mucus production in bronchial tree
Occurs 3 months in a year for 2 consecutive years
Common to have repeated respiratory infections (RSV: respiratory syncytial virus, strep pneumonia,
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Hflu) Emphysema
Abnormal permanent enlargement of airspaces distal to terminal bronchiole
Accompanied by destruction of the walls
Centrilobular proximal most common Resistance
How easy, or hard, it is for gases to flow down the airways
Affected by small airways (eg, bronchospasm, small-diameter tubes)
Takes more pressure to maintain flow Concepts Obstructive Diseases Concepts
Lung volumes are increased (TLC, FRC, RV)
Expiratory flow rates decreased (FEV1 and peak flow)
Airways resistance is increased
Gas trapping common-dynamic hyperinflation and auto-PEEP (if on the ventilator)
Increased WOB
Increased drive
Mechanical disadvantage and fatigue
Precipitating events: infection (and other) Clinical Features
Signs of precipitating event
Hypoxemia
Hypercarbia
Pattern of breathing Treatment Goals
Treat cause
Improve O2 saturation!
Secretion clearance
Decrease ventilatory demand and load
Improve respiratory muscle force and endurance
Correct electrolytes and fluid deficits
Avoid complications Therapeutics
Provide oxygen (check CO2 levels)
Beta 2 agonists (eg, albuterol)
Anticholinergics (eg, ipratropium)
Methylxanthines (eg, aminophylline)
Steroids
Antibiotics
Hydration
Nutrition
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Mechanical Ventilation
Provide respiratory muscle rest first 12‒24 hours
Prevent hyperinflation (small volumes, short inspiratory times, and adequate exhalation times)—check for auto-PEEP!
Status Asthmaticus: Acute Severe Asthma Severe acute bronchoconstriction that is intense, unrelenting, and unresponsive to usual therapy. A clinical emergency! Asthma Pathophysiology
Inflammation
Bronchoconstriction
Mucus production Precipitating Events (“Triggers”): Pathophysiology
Gas exchange o Predominately high V/Q (dead space ventilation)
Increased WOB
Precipitating events o History is essential!
Clinical Features History
Recurrent frequent episodes
Change in pattern of symptoms
Increased dyspnea
Cough with sputum
Change in sputum color
Refractory to drugs
Personality changes Physical Exam
Mental status
Anxiety
Tachypnea and tachycardia
Accessory muscle use
Wheezing
Prolonged expiration
Pulsus paradox Laboratory Data
Flow measurements decreased (peak flow, etc.)
Hypoxemia
Eucapnia or hypercapnia
Chest x-ray (hyperinflation)
Eosinophils in sputum
Purulent sputum
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Therapy (General)
Bronchodilators o Beta 2 agonists (first-line) o Anticholinergics (second-line, but often given in combination with beta agonists) o Methylxanthines, magnesium
Steroids (always a first-line drug)
Oxygen
Hydration
Antibiotics if infection suspected Asthma—Mechanical Ventilation
Avoid pressure-limiting modes (hard to control volumes with bronchospasm)
Prevent dynamic hyperinflation (small volumes and low rates)
May require heavy sedation and paralytics
Permissive hypercarbia
Check for auto-PEEP Acute Pulmonary Embolus
Pathogenesis o A complication of deep vein thrombosis. Migration of a clot to the pulmonary vasculature
DVT—Clinical Features
Pain, increased girth, tenderness, warmth, redness, swelling, edema, venous cord
Virchow's triad: hypercoagulability (acquired or congenital/inborn resistance to activated protein C-genetic mutation in factor V known as "Factor V Leiden”), stasis and injury (most common is hospitalization and lack of prophylaxis)
More common in left leg (compression of the left common iliac vein by the overlying right common iliac artery [May-Thurner syndrome])
DVT: Diagnosis and Therapy
D-dimer
Duplex ultrasonography, due to its high sensitivity, specificity and reproducibility, has replaced venography as the most widely used test in the evaluation of the disease
DVT prophylaxis: unfractionated heparin, LMWH, warfarin, SCDs PE: Clinical Features
Chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, hemoptysis, shortness of breath, painful respiration, new onset of wheezing, any new cardiac arrhythmia, or any other unexplained symptom referable to the thorax o Of those who die from PE, only 60% have dyspnea
Hemodynamic: increased PA pressures, right ventricular failure
Pulmonary: V/Q abnormalities, hypoxemia, hyperventilation, atelectasis, infarction
X-ray: possible wedge
ABGs: hypoxemia with hyperventilation (at least initially) Diagnosis and Therapy PE
Diagnosis: estimate risk, search for source, V/Q scan (when CTPA not available), CTPA, pulmonary
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angiogram (gold standard—but being replaced with CTPA)
Therapy: heparin, thrombolytics, vena cava interruption (filters—removable are popular now), embolectomy, oxygenation, and ventilation
Fat Embolism
Often caused by physical trauma such as fracture of long bone, soft tissue trauma, and burns
Fat Embolism
Signs and symptoms: otherwise unexplained dyspnea; tachypnea; arterial hypoxemia with cyanosis and diffuse alveolar infiltrates on chest X-ray; otherwise unexplained signs of cerebral dysfunction, such as confusion, delirium or coma; petechiae over the upper half of the body; conjunctive, oral mucosa, and retinae
Prevention: Prompt surgical stabilization of long-bone fractures and correcting or preventing decreased systemic perfusion reduce the risk of the syndrome
Treatment: supportive (O2, ventilation etc.)
Pulmonary Hypertension
Definition—primary pulmonary hypertension (PPH) is a rare disease of unknown etiology; occurs in young adults (twice as common in women as in men)
Known causes o Use of the appetite suppressant “fen-phen” (dexfenfluramine and phentermine); chronic liver
disease; some rheumatologic disorders; congenital heart malformations; illicit drug use
Symptoms: often undetected until the patient gets sick with a virus
Diagnosis: supported by an abnormal echocardiogram of the heart and confirmed with right heart catheterization (increased PA pressures)
Treatment: difficult to treat, although intravenous prostacyclin has proven effective in many patients. Only cure is lung transplantation
Pneumothorax Definition—air in the pleural space Etiology
Spontaneous, traumatic, tension Pneumothorax: Clinical Features
Depends on size
Symptoms: dyspnea, pleuritic chest pain
Signs: tachycardia, tachypnea, hypotension, decreased respiratory excursion, elevated chest on affected side, widened costal spaces, absent or reduced breath sounds, hyper-resonant to percussion, tracheal shift
ABGs o Hypoxemia +/hypercapnia
Ventilator o Increased peak airway pressure (plateau pressure will increase)
Cardiac tamponade! Diagnosis and Treatment
Chest x-ray
Large-bore catheter in second intercostal space if unstable
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Chest tube Other Air-leak Syndromes
Pneumopericardium
Pneumomediastinum
Treatment depends on how it is affecting the patient Chest Trauma Definition
Penetrating or blunt injury to the chest and/or lungs that interferes with any of the components of respiration
Clinical Presentation
Tachypnea, dyspnea, ecchymosis, shock, pain, history of injury
Pneumothorax, hemothorax, and tension pneumothorax
Flail chest: unstable chest wall sinks with inspiration (three consecutive ribs)
Trauma to lung (contusions): hemoptysis, respiratory distress Presentation Open sucking wounds
During inspiration the affected lung collapses, resulting in ineffective gas exchange. Patient is dyspneic and sucking sounds on inspiration are noted from wound
Hemothorax
Limited motion of affected side, dull to percussion, absent breath sounds Therapies
ABGs and clinical assessment to follow and intervene
Pain control, fluids, blood, prepare for surgery
Flail: Intubation, PEEP and mechanical ventilation
Emergency decompression of tension pneumo, chest tubes for hemo, and other Thoracic Surgery
Tracheal perforation and surgery
Lung reduction
Pneumonectomy, lobectomy Selected References
Burns SM, ed. AACN Protocols for Practice. Caring for Mechanically Ventilated Patients. 2nd ed. Sudbury, MA: Jones and Bartlett Publishers; 2007.
Chulay M, Burns SM, eds. AACN Essentials of Critical Care Nursing. 2nd ed. New York, NY: McGraw Hill Publishers; 2010.
Pierce LBN, ed. Management of the Mechanically Ventilated Patient. 2nd ed. St. Louis, MO: Saunders Elsevier; 2007.