Matrix Review

Sections H and I

Trenna Gibbs

H. Determine the Appropriateness of the Prescribed Respiratory Care Plan and Recommend Modifications When Indicated

I. - IV. Analyze available data to determine path physiological state.

A. Emphysema: permanent abnormal enlargement of the air spaces distal to the terminal bronchioles, associated with destructive changes of the alveolar walls.

1.) 3 types: pan lobular, centrilobular, and bullous

2.) causes: smoking, a1-antitypic deficiency

3.) Pathophysiology

a. decreased elastic recoil of lung, premature airway closure

b. normal inspiratory flow rates, reduced expiratory flow rates

c. air-trapping which leads to chronic hyperinflation of the lungs and an increased functional residual

capacity.

d. increased lung compliance

e. increased physiologic deadspace

4.) Clinical signs and symptoms

a. dyspnea; initially on exertion, then progressively worsens

b. digital clubbing, resulting from chronic hypoxemia

c. increase AP chest diameter (barrel chest)

d. use of accessory muscles during normal breathing

e. elevated hemoglobin level, hematocrit, and RBC count

f. ABGs: chronic CO2 retention and hypoxemia

g. reduced breath sounds and hyper resonance to percussion

h. cyanosis

i. Right-sided heart failure (cor pulmonale)

5.) Chest X-Ray and Pulmonary Function Tests

a. flattened diaphragm, hyperinflation, reduced vascular markings, bullous lesions

b. increased: residual volume, functional residual capacity; decreased: diffusion capacity, vital capacity,

FEV1, and FEV1/FVC; prolonged nitrogen washout.

6.) Treatment

a. smoking cessation programs, adequate hydration, postural drainage, Bronchodilators, prevention of

infections by immunizations, exercise, breathing exercise training (pursed lip breathing), monitor and

limit administration of oxygen.

B. Chronic Bronchitis: chronic excessive mucus production, resulting from an increase in the number and size of mucus glands and goblet cells.

1.) Causes: smoking, most commonly seen in males

2.) Pathophysiology

a. increase in the size of mucus glands

b. increase in the number of goblet cells

c. inflammation of bronchial walls

d. mucus plugs in peripheral airways

e. loss of cilia

f. emphysematous changes in advanced stages of disease

g. narrowing airways, leading to air flow obstruction

3.) Clinical Signs and Symptoms

a. cough with sputum production

b. dyspnea on exertion, progressing to dyspnea at rest

c. CO2 retention and hypoxemia in advanced stages

d. increased pulmonary vascular resistence in advanced stages

e. increased hemoglobin level, hematocrit, and RBC count in advanced stages

f. right-sided heart failure (cor pulmonale) in advanced stages

4.) Chest X-Ray and Pulmonary Function Test

a. no significance on x-ray during early disease, hyperinflation on advanced stages

b. increased residual volume; decreased FEV1, inspiratory flow rateds in obstructive bronchitis.

5.) Treatment

a. same as for emphysema

C. Asthma: a disease characterized by increased reactivity of the trachea and bronchi to various stimuli, resulting in bronchoconstriction, increased mucus production, and swelling of mucosal tissue.

1.) causes: extrinsic (allergic) or intrinsic (nonallergic)

2.) Pathophysiology:

a) mast cells in the bronchial tree are stimulated causeing release of:

1.) histamine, leukotrienes, SRS-A, ECF-A, and prostaglandins;

b) results in bronchoconstriction, muscosal edema, increased mucus production, accumulation of

eosinophils in the blood and sputum, and vasodilation.

3.) Clinical Signs and Symptoms:

a) mild wheezing and cough, which may progress to severe dyspnea if the attack isn't arrested

b) cough is nonproductive at first, then productive by end of episode.

c) secretions contain high levels of eosinophils.

d) intercostal and supraclavicular retractions

e) use of accessory muscles to breathe

f) paradoxical pulse: systolic blood press. is 10mm Hg higher on expiration than on inspiration.

g) tachycardia and tachypnea

h) ABG levels show hypoxemia and low PaCO2 initially, PaCO2 increases as attack worsens and pt.

begins to tire.

i) cyanosis

4.) Chest X-ray and PFTs

a) hyperinflation, atelectasis, infiltrates.

b) decreased: FEV1, FVC, FEV1/FVC increased: RV

5.) Treatment

a) prevention

b)medications: bronchodilators, cromolyn sodium, corticosteriods.

6.) Status Asthmaticus: severe asthmatic attack not responding to tx with an adequate amt. of routine

medications within a few hours.

D. Bronchiectasis: a dilation of the bronchi and bronchioles, chronic in nature, that results in inflammation and damage to the walls of these airways.

1.) causes:

a)chronic resp. infections

b) TB lesion

c) secondary to pt. with cystic fibrosis

d)bronchial obstruction

2.) Pathophysiology

a) chronic dilation is a result of destructive changes in the bronchial walls caused by inflammation and

infection, or it may to caused by a congenital defect of the airways.

b) bronchial obstruction may render the mucociliary transport system ineffective, leading to an

accumulation of thick secretions.

c) the bronchial wall is destroyed, with a resultant atrophy of the mucosal layer.

d) because of the decresed values in both flows and volumes this disease may be either obstructive or

restrictive in nature.

3.) Clinical signs and symptoms:

a) productive cough, large amts. of thick, purulent secretions (possibly foul-smelling)

b) tachypnea and tachycardia

c) hemoptysis

d) recurrent pulmonary infections

e) digital clubbing

f) cyanosis

g) respiratory alkalosis with hypoxemia ( in early stage)

h) chronic respiratory acidosis with hypoxemia ( in late stage)

i) barrel chest

4.) Chest x-ray and PFTs:

a) increased lung markings, flattened diaphragm, segmental atelectasis

b) decreased: FVC, FRC, FEV1, FEF 25-75%.

5.) Treatment:

a) CPT, aerosol therapy, bronchodilator therapy, Mucolytics, antibiotics, O2 therapy, expectorants.

E.) Pneumonia: acute inflammation of the gas exchange units of the lungs.

1.) causes:

a) variety of organisms

b) decreased airway defense mechanisms

1) ineffective cough, obtunded airway reflexes, impaired mucocilary transport system,

obstructed airways.

c) Various conditions resulting in a predisposition to pneumonia:

1) COPD, alcoholism, malnutrition, seizure disorders, chronic debilitating illness, major surgical

procedures, old age.

2.) Pathophysiology:

a) pathogenic microorganisms that reach the alveolus, cause inflammation

b) WBCs phagocytize the invading organisms, further inflammation.

c)consolidation of the lungs with inflammatory exudates and cells.

d) if tissue necrosis is not present, the lung heals and returns to normal function; if necrosis occurs,

healing is slow, with production of fibrous scar tissue (pulmonary fibrosis and loss of normal lung

function).

3.) Clinical Signs and Symptoms:

a)infection, malaise, fever, chest pain, dyspnea, tachycardia, inspiratory crackles.

4.) Chest x-ray: consolidation, air brochogram.

5.) Types of Pneumonia:

a) Bacterial

1.) most common: Streptococcus pneumoniae (pneumococcal).

2) Haemophilus influenzae, Klebsialla pneumoniae, Legionella pneumoniae,

Pseudomonas aeruginosa.

b)Mycoplasma pneumoniae: smaller than bacteria, more common in children.

c)Viral

1.) influenza viruses, adenoviruses, chickenpox (varicella-zoster virus)

d) Protozoan

1.) Pneumocystis carinii pneumonia (PCP) ; seen in 60% of AIDS cases. Diagnosis with

culture of lung secretions and tissue. Tx with antiprotozoal drug pentamidine via aerosolization.

6.) Treatment

a) antibiotics, supplemental O2, CPT, adequate hydration and nutrition, tracheal suctioning (if poor

removal occurs because of ineffective cough).

F.) Lung Abscess: an infection of the lung that is characterized by a localized accumulation of pus with destruction of the surrounding tissue.

1.) causes:

a.) most causative organisms are anaerobic bacteria.

b.) aerobic bacteria (staphylococci, streptococci, some gram-negative bacteria).

c.) may occur after aspiration

d.) seen in conjunction with lung cancer.

2.) Pathophysiology:

a.) looks much like pneumonia in acute phase

b.) necrosis is evident in later phase, which may spread to adjacent lung tissue.

3.) Clinical Signs and Symptoms:

a.) fever, cough (purulent, foul-smelling secretions), chest pain, weight loss, hemoptysis, digital

clubbing, tachycardia, tachypnea

4.) Chest x-ray and Lab findings:

a.) localized area of consolidation, most common sites: superior segments of lower lobes and posterior

segments of upper lobes

b.) increased WBC count, anemia (decreased RBC), sputum culure reveals purulence and necrosis.

5.) Treatment

a.) antibiotics, postural drainage, adequate nutrition.

G.) Tuberculosis (TB): a granulomatous bacterial infection, chronic, affecting the lungs and other organs.

1.) cause: inhalation or ingestion of the bacterium, Mycobacterium tuberculosis; spread by coughing and sneezing; diagnosis based on skin tests, chest x-ray, and sputum culture (acid-fast).

2.) Pathophysiology:

a.)bacilus is inhaled and enters the alveoli resulting in an inflammatory reaction similar to that seen in

pneumonia. Macrophages enter area, engulf bacilli but do no fully kill them. Surrounding lung tissue

capsulates the bacilli (granuloma). Cheese-like granuloma forms (necrotic material fills granuloma).

b.) Fibrotic tiisue forms as healing occurs. Bacillus can remain dormant in the lungs for many years.

c.) Chronic dilation of the bronchi may result during healing process of TB.

d.) Uncontrolled cases may lead to larger granulomas that may burst and lead to pneumothorax.

3.) Clinical Signs and Symptoms

a.) cough, sputum production that tests positive for acid-fast bacilli

b.) tachycardia, increased cardiac output,

c.) chest pain

d.) hemoptysis

e.) dull percussion note

f.) crackles and rhonchi

g.) hyperventilation and hypoxemia

h.) chronic respiratory acidosis with hypoxemia

i.) cyanosis

4.) Chest x--ray and PFTs

a.) enlarged lymph nodes in hilar region; pleural effusion; cavitation; Ghon's complex, fibrosis, infiltrates

b.) decreased: VC, FRC, RV, TLC

5.) Treatment

a.) Supplemental O2

b.) Antituberculosis drugs: used in combination for 2 to 4 months

1.) Rifampin, Isonaizid (INH), Ethambutol, Streptomycin

c.) Placement in respiratory isolation

d.) Routine airway maintenance.

H.) Pulmonary Edema: an excessive amt. of fluid in the lung tissues or alveoli, caused by an increase in pulmonary capillary pressure resulting from hydrostatic left-sided abnormal heart function.

1.) Causes: left-sided heart failure, aortic stenosis, mitral valve stenosis, systemic hypertension, alveolar

capillary membrane leak

2.) Pathophysiology:

a.) abnormal level of plasma oncotic pressure or capillary hydrostatic pressure.

b.) decreased lung compliance, increased Raw, widened A-a gradient as a result of intrapulmonary

shunting and V/Q mismatch.

3.) Clinical signs and symptoms

a.) dyspnea: orthopnea and paroxysmal nocturnal dyspnea

b.) thin, pink frothy secretions; productive cough

c.) crackles in bases of lung

d.) tachypnea, cyanosis, tachycardia

e.) diaphoresis, distended neck veins.

4.) Chest x-ray

a.) increased vascular markings, interstitial edema, enlarged heart shadow

5.) Treatment

a.) O2, cardiac glycosides, ventilatory support with PEEP, maintain adequate airway, morphine, IPPB

with ethyl alcohol, diuretics

I.) Pulmonary Embolism (PE): obstruction of the pulmonary artery or one of its branches by a blood clot.

1.) causes: blood clot originates in deep veins of legs, dislodges, and lodges in the pulmonary artery.

2.) Pathophysiology:

a.) blood flow is obstructed to areas of the involved lung (deadspace ventilation)

b.) compliance decreases as atelectasis occures ( lungs response to decreased perfusion) c.) widened A-a gradient

3.) Clinical signs and Symptoms

a.)dyspnea, chest pain, tachypnea, cough, pleuritic pain

b.) hemoptysis, tenderness and swelling in lower extremities due to thrombophlebitis

c.)tachycardia, cyanosis, decreased BS over affected area. Possible wheezes and crackles heard.

4.) Chest X-ray and Diagnostic procedures

a.) decreased lung volumes, linear densities of atelectasis, pleural effusion, elevated hemidiaphragm, (May be normal)

b.) CT scan is most popular at this time but V/Q scan and Pulmonary angiography are also used.

5.) Treatment

a.) Prevention

b.) Anticoagulation therapy

c.) supplemental O2

d.) Vasopressors and fluids if hypotension is present.

J.) Acute Respiratory Distress Syndrome (ARDS): a group of symptoms causing acute, catastrophic,

respiratory failure, resulting from pulmonry injury. Three criteria: infiltrates on chest x-ray, normal heart function, P02/FiO2 ratio of less than 200.

1.) causes

a.) diffuse lung injury ( sepsis, aspiration, near-drowning, O2 toxicity, shock, thoracic trauma, extensive

burns, inhalation of toxic gases, fluid overload, fat embolism, narcotic overdose.

b.) Most patients have no previous pulmonary problems.

2.) Pathophysiology:

a.) lung injury occurs followed by an inflammatory process.

b.) alveolar capillary membrane leakage, fluid builds up in interstitial spaces, alveoli, and distal airways.

c.) surfactant production decreases, atelectasis, and decreased lung compliance.

3.) Clinical signs and symptoms

a.) hypoxemia, refractory in severe cases

b.) cyanosis, severe dyspnea and cough, tachypnea

c.) decreased lung compliance

d.) suprasternal and intercostal retractions

e.) widened A-a gradient on 100% O2.

4.) Chest x-ray

a.) interstitial edema, alveolar edema (fluffy infiltration)

5.) Treatment

a.) mechanical ventation with PEEP (elevated PIP is seen)

b.) monitor heart pressures

c.) diuretics

d.) routine airway maintenance

e.) surfactant replacement (most commonly used in infants, beginning to see its use in adults)

K.)Pneumothorax: the presence of air in the pleural space.

1.) causes: spontaneous ( tall, thin, young males; COPD pts.; previous trauma) and traumatic (broken ribs,

puncture wound, chest or neck surgery)

2.) Pathophysiology

a.)air enters the pleural space, lung begins to collapse because of its' natural recoil and because of lack

of negative pressure when the pleural space becomes atmospheric.

b.) tension pneumothorax: occurs if the opening to the pleural spce in the lung acts as a one-way valve,

permitting air to enter the space but not allowing the air to exit.

3.) Clinical Signs and Symptoms

a.) chest pain, dyspnea, decreased BS over affected lung,

b.) hyperresonant percussion note over affected lung.

c.) asymmetric chest excursion

d.) tachypnea, cyanosis

4.) Chest x-ray

a.) hyperlucency, deviation of the heart, trachea, and mediastinum to the opposite side ( if tension

pneumothorax is present)

b.) Chest x-ray provides definitive diagnosis, but transillumination has been succesful in diagnosis in

infants.

5.) Treatment

a.) Needle aspiration immediately in tension pneumothorax

b.) placement of chest tube

c.) supplemental O2 as needed

L.)Atelectasis: partial or complete collapse of alveoli, may involve localized area, a lobe, or the entire lung.

1.) casues: obstructed airways (absorption), high O2 levels (wash out), loss of negative pleural pressure, right mainstem bronchus intubation, left mainstem bronchus intubation, deficiency or loss of surfactant, hypoventilation, decreased pulmonary blood flow.

2.) Pathophysiology

a.) FRC and VC decrease, intrapulmonary shunting occurs as capillary blood passes by collapsed

alveoli.

3.) Clinical Signs and Symptoms

a.) asymptomatic in mild cases

b) hypoxemia, dyspnea, cough

c.) dullness to percussion

d.) elevated diaphragm, crackles in lung bases

e.) diminished or absent BS

f.) tracheal deviation toward the affected lung

4.) Chest X-ray

a.) increased density , elevated diaphragm, displaced interlobar fissures, mediastinal shift, altered

bronchial and carinal angles

5.) Treatment

a.) prevention ( incentive spirometry)

b.) Adequate pulmonary hydration to prevent mucus plugs

c.) treatment of underlying atelectasis with deep-breathing evercises (IS or IPPB)

d.) placement on CPAP if pt is hypoxemic on 60% O2 or more

e.) use of PEEP is on ventilator

V. Respiratory Quality Assurance

A) quality assurance plan: used to provide a system for controlling quality; required by JCAHO in order for a hospital to receive accreditation; assures public that hospital maintains high standards.

1.) Nine steps for a quality assurance plan

a.) Identify problems

b.) Determine cause(s) of problems

c.) Rank problems

d.) Develop a strategy for resolving problem

e.) Develop appropriate measurement techniques

f.) Implement problem resolution strategy

g.) Analyze and compile results of the intervention

h.) Report results to appropriate personnel

i.) Evaluate intervention outcome.

2.) The Goals of a Respiratory Care Continuous Quality Impovement Plan (at least one of following):

a.) provide a method for ongoing monitoring of both quality and appropriateness of respiratory care

b.) ensure that respiratory care methods and procedures are cost-effective.

c.) ensure that respiratory care methods and procedures are effective.

d.) identify, rank, and resolve patient care-related problems.

VI. - VIII. Respiratory Care Protocols

1.) Respiratory Care protocols are guidelines for delivering appropriate respiratory care treatments and services by the correct method.

2.) Protocols may be written in outline form or algorithms. May be constructed for individual therapies such as aerosol therapy, bronchopulmonary hygiene, oxygen therapy, hyperinflation techniques, suctioning, pulse oximetry, etc. Can also be written for a specific purpose such as ABG sampling, weaning from mechanical ventilation, decannulating a tracheostomy, titrating oxygen therapy, etc.

3.) Key elements of a protocol program:

a.) strong and committed medical direction

b.) capable therapists

c.) active quality monitoring.

d.) collaborative environment among respiratory therapists, physicians, and nurses.

e.) responsiveness of all elements to address and correct problems.

4.) Elements of a Respiratory Care Protocol (as described by the ACCP)

a.) clearly stated objectives

b.) outline that includes an algorithm

c.) description of alternative choices to decision and action points

d.) description of potential complications and corrections

e.) description of end points and decision points where the physician must be contacted

f.) protocol program

5.) Sequence of Events:

a.) A physician writes an order for a respiratory care protocol or consult.

b.) The nursing unit secretary notifies a respiratory therapist evaluator

c.) The evaluator assesses the patient using specific guidelines.

d.) The evaluator writes a care plan using designated indications and algorithms and documents the care plan in

the patient's chart for review by the physician.

e.) The respiratory therapist covering the nursing unit delivers the care.

f.) The patient is assessed on a shift-by-shift basis for changes in status and indicated modifications for the care

plan, which are also documented.

g.) The physician is notified of any deterioration in the patient's status.

h.) When indications for respiratory care no longer exist, respiratory care treatment is discontinued, and

notification is placed in the patient's chart.

IX. Disease Management Education.

A.) Goals:

1.) to delay disability and death

2.) to maximize quality of life

B.) Examples of ways Respiratory Therapist impact health education

1.) nicotine intervention and cessation

2.) asthma education

3.) community health screening

4.) patient disease education and support.

I. Initiate, Conduct, or Modify Respiratory Care Techniques in an Emergency Setting.

I. BCLS, ACLS, PALS, NRP

A.) CPR

1.) Obstructed Airway in a Conscious Adult

a.) Ask if patient can speak to determine airway obstruction

b.) Perform Abdominal thrusts until foreign body is expelled or the patient loses consciousness ( if this

occurs place patient on back and call for help).

c.) Use tongue/jaw lift to open the mouth and perform finger sweep with head turned to side.

d.) Open the airway by using the head tilt/chin lift method.

e.) Give two breaths. If ventilation attempts fail reposition the airway and ventilate again.

f.) If there is no airmovement straddle the patient and perform abdominal thrust and then finger sweep

again.

g.) repeat until airway is cleared.

2.) Obstructed Airway in a Unconscious Adult

a.) Determine unresponsiveness. Call for Help.

b.) Position the patient on their back.

c.) Open the airway using the head tilt/chin lift method.

d.) Determine breathlessnesss by placing ear over the patient's mouth and look, listen, and feel for

air movement.

e.) Attempt to ventilate. If no airmovement, perform abdominal thrust times five, then perform finger

sweep.

f.) Attempt to ventilate. Repeat process until airway is cleared.

3.) One-Rescuer CPR (Adult Patient)

a.) Perform Steps A through D. (as explained above)

b.) Give two breaths while observing chest rise.

c.) Determine pulselessness by palpating the carotid artery. (brachial artery in infants).

d.) Begin chest compressions at a rate of 80 to 100 per min. ( 15 compressions to 2 breaths).

e.) Continue until patient responds, help arrives, or you can't physically continue.

4.) Two Rescuer CPR (Adult Patient)

a.) When second rescuer arrives, he or she should take over as the new compressor, while the first

resceur gets into position to be the breather. Palpate for a spontaneous pulse at this time.

b.) If no pulse is present give one breath and then 5 compressions.

c.) Patient should be intubated as soon as possible to provide more effective airway and to prevent air

from entering the stomach.

d.) Compressor and breather should alternate as compressor tires.

5.) Neonatal Resuscitation (Immediately after Delivery).

a.) Dry and warm infant.

b.) Suction the nose and mouth with a bulb syringe or DeLee suction catheter.

c.) If meconium stained, intubate and suction trachea.

d.) Provide tactile stimulation to stimulate breathing.

e.) If infant is not breathing or the heart rate is less than 100/min. begin positive pressure ventilation with

100% oxygen with a bag and mask. (40 bpm. Ventilation pressure should be 30 to 40 cm H2O

and then 15 to 20 cm H2O for following breaths.

f.) Reassess pulse after 15 to 30 sec. If heart rate is less than 60/min or 60 to 80/min and not

increasing, then ventilation should be continued and chest compressions should be started.

(Compressions 120/min; DC compressions when heart rate is 80/min or higher. If heart rate stays

below 80/min then the infant should be intubated and positive pressure ventilation should be started

along with continued compressions. Reasess infant periodically.

II. Drugs used during CPR

1.) Epinephrine

a.) Indications: Asystole, Sinus Arrest, Ventricular fibrillation.

b.) Administration: IV bolus, ET tube, intracardiac

c.) Dosage: 0.1 mL/kg IV every 5 min ( 10 ml max); 10 ml down ET tube; 0.1 mL/kg intracardiac

dose every 5 min (10 ml max).

d.) Increases HR, increases force of contraction, increase coronary perfusion pressure,

vasoconstruction.

2.) Lidocaine

a.) Indications: ventricular fibrillation, ventricular tachycardia, PVCs

b.) Administration: IV bolus, IV drip, ET tube

c.) Dosage: 1 mg/kg IV bolus followed by additional boluses of 0.5 to 1.5 mg/kg every 3-5 min. up to

3 mg/kg; Drip may be started at a rate of 2.0 to 4.0 mg/min when perfusion is restored.

d.) Decreases ventricular activity.

3.) Atropine sulfate

a.) Indications: sinus bradycardia, asystole, nodal bradycardia

b.) Administration: IV bolus, ET tube

c.) Dosage: 1.0 mg IV every 5 min for asystole; 0.5 mg IV every 5 min for bradycardia.

d.) increased heart rate, increased force of contraction of the heart.

4.) Procainamide

a.)Indications: V-trach, V-fib, PVCs

b.) Administration: IV bolus or drip

c.) Dosage: 50 mg IV bolus every 5 min; 1 to 4 mg/min IV drip of a 100 mg/ml preparation.

d.) may cause hypotension, increases electrical stimulation threshold, decreases electrical activity of the

ventricles.

5.) Bretylium tosylate

a.) Indications: V-tach, V- fib, PVCs

b.) Administration: IV bolus

c.) Dosage: 5 mg/kg in 50 ml diluent over 5 to 10 min.

d.) same as Procainamide.

6.) Propranolol hydrochloride

a.) Indications: MI, angina pectoris, supraventricular arrhythmias, V-tach.

b.) Administration: IV bolus

c.) Dosage: 1 to 5 mg of a 1 mg/ml preparation (max of 1 mg/min)

d.) decreased HR, decreased Stroke volume, increased left ventricular end-diastolic pressure.

7.) Dobutamine hydrochloride

a.) Indications: depressed myocardial contractility

b.) Administration: IV drip

c.) Dosage: 2.5 to 10 ug/kg/min

d.) increased cardiac output, enhanced atrioventricular conductionl.

8.) Isoproteronol hydrochloride

a.) Indications: bradycardia, heart block, hypotension

b.) Administration: IV drip

c.) Dosage: 1 mg/500ml of 5 % dextrose

d.) increased HR, increased force of contraction.

9.) Dopamine hydrochloride

a.) indications: hypotension

b.) Administration: IV drip

c.) Dosage: 2 to 30 ug/kg/min

d.) increased cardiac output, increased blood pressure

10.) Sodium nitroprusside ( Nipride)

a.) Indications: Hypertension

b.) Administration: IV drip

c.) Dosage: 0.5 to 8.0 ug/kg/min

d.) peripheral vasodialtion, decreased blood pressure
11.) Calcium chloride

a.) Indications: hypocalcemia, hyperkalemia

b.) Administration: IV ( do not mix with other medication)

c.) Dosage: 0.2 ml/kg

d.) increased force of contraction of the heart.

III. Defibrillation and Cardioversion

1.) Defibrillation: a nonsynchronized current of electricity delivered to the heart during V-fib.

a.) administered by paddles placed on the anterior chest.

b.) initial current delivered should be 200 joules for adults, no more than 360 joules, ( 2 joules/kg in

infants and children, no more than 4 joules/kg)

2.) Cardioversion: a synchronized current of electricity delivered to the heart during ventricular

depolarizaiton.

a.) used to terminate: atrial flutter, atrial fibrillation, V-tach, paroxysmal supraventricular tachycardia, V

fib.

b.) delivers a lower energy level than defib. ( 25 to 100 joules, 0.2 to 1.0 joules/kg in infants)

c.) Respiratory duties during cardioversion: monitor HR, RR, O2 saturation; have O2 delivery device

readily available; have manual resuscuitator and intubation equipment readily available.

II. Treatment of a tension pneumothorax

1.) A tension pneumothorax occurs if the opening to the pleural space in the lung acts as a one-way valve, permitting air to enter the space but not allowing the air to exit. The immedicate action to take is to relieve the pressure in the pleural space by inserting a needle in the second or third intercostal space (trapped air rises to the upper most part of the pleural space, where as trapped fluid (pleural effusion) settles in the lowest point and must be drained).

III. Patient Transport

1.) Land/Air transport outside the hospital

a.)Unstable pts. must be transported with great care to avoid worsening of their condition.

b.) The practitioner should hold the ET tube with one hand and bag with the other this better stabilizes

the tube and helps avoid inadvertent extubation.

c.) Suddent changes in speed or direction may cause a drop in the patient's blood pressure.

d.) Special atttention must be given to monitoring lines that could become dislodged in transport.

e.) Ventilators used for transport should have demand valves to conserve gas.

f.) Patients should be adequately sedated to help prevent anxiety and allow safer transport.

g.) During transport in an unpressurized aircraft, rapid increases in altitude result in decreased

atmospheric pressure and PO2. This may be managed by increasing delivered O2 concentrations.

h.) Higher altitudes (lower atmospheric pressure) may increase the size of an untreated pneumothorax

and increase ET tube cuff pressure, which may decrease capillary perfusion to the trachea.

i.)Lightweight equipment (such as transport ventilators) is necessary for air transportation.

j.) Patient monitoring is more difficult in aircraft, expecially helicopters.

k.) Heated humidity or aerosol for ventilators or masks during transport is not necessary for such short

term use.

l.) Needed respiratory equipment:

1.) O2 system (cylinders or liquid)

2.) Portable suction machine and appropriate sized catheters.

3.) Portable ventilator

4.) Portable ECG unit

5.) Arterial pressure monitor

6.) Pulse oximeter

7.) Intubation equipment

8.) Manual resuscitator.