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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.