1. Ensure the adequacy of airway, breathing, and circulation before initiating treatment.

2. Because of the many potential adverse consequences of the traditional Trendelenburg position (i.e., head lower than body), it is no longer recommended for treatment of hypotension.

3. In the obese patient, supine positioning can cause ventilatory impairment, with compression on the aorta and inferior vena cava (Babatunde & Whitten, 2006).

4. Patients who are in cardiogenic or anaphylactic shock may not be able to tolerate a supine or modified Trendelenburg position.

1. Place the patient in a supine position.

2. Raise the lower extremities to a maximum elevation of 45 degrees. This is known as the modified Trendelenburg position (Figure 48-1).

3. Do not lower the patient’s head below the level of the body, because this places pressure on the diaphragm that may result in respiratory distress. See the Contraindications and Cautions for the traditional Trendelenburg position listed earlier.

1. Explain that the position is temporary.

2. Immediately report any difficulty in breathing.

1. To measure the blood pressure, pulse, or both, when auscultation by stethoscope is unsuccessful (i.e., in the presence of hypotension, hypothermia, or shock; when the pulse is faint or weak; extremity edema; faint Korotkoff sounds; or in a noisy environment). Fetal heart tones can also be assessed by Doppler; see Procedure 108.

2. To assess peripheral blood flow when circulatory impairment or vascular trauma is suspected.

1. Use of an ultrasonic transmission gel recommended by the vendor assists in optimal sound transmission and protects the crystals, which are found in the probe. The crystals transmit and receive ultrasonic waves. In emergency situations, any surgical jelly or lubricant may be substituted for a conductive gel but ECG paste or cream should never be used as it may damage the probe (Parks Medical Electronics, 2005).

2. The probe should be checked regularly for damage to the electrode and integrity of the crystals.

3. Improper probe placement may lead to erroneous interpretations. Care should be taken to verify that the signal is coming from the intended vessel and not from a collateral vessel. This can be determined by assessing the quality of the sound, as described in the Complications section of this procedure.

4. Excess pressure on the probe may compress the artery and abolish the signal.

5. Verify sensitivity when signals are absent from a position where they would normally be expected. Sensitivity may be verified by checking one’s own pulses with the Doppler device.

6. The presence of a signal does not always indicate that circulation and perfusion are adequate to maintain viable tissue, just as absence of a signal does not always indicate that there is no blood flow through the vessel.

7. Tissue penetration varies, depending on which Doppler probe is used. A high-frequency (8 to 10 Hz) probe is usually used on the surface vessel sites; this probe is typically long and narrow. A low-frequency probe is usually used for deeper tissue sites, such as fetal heart tones; this probe is typically short and wide.

8. Falsely elevated pressures may be observed in patients with diabetes, obesity, or calcified vessels (Gorgas, 2004).

Doppler probe with a frequency of 5 to 10 MHz (for limb arteries and veins) and an amplifier (Figure 49-1)

Ultrasonic transmission gel

Blood pressure cuff

Wet towel or tissue

1. Absence of a Doppler signal may be due to any of the following:

2. The signal may be misinterpreted. Arterial sounds are loud, pulsatile, pumping sounds that are repeated with each cardiac cycle. Venous sounds are normally cyclic. They occur with respirations, and on expiration, they produce a high-pitched sound that resembles a rushing wind.

3. Static may occur. Possible causes are hair movement on the body, air bubbles in the gel popping, and radio interference.

4. The output of ultrasonic signals from diagnostic Doppler applications is very low; nevertheless, prolonged, unnecessary exposure to ultrasonic signals should be avoided to prevent tissue damage.

1. To noninvasively evaluate a patient’s symptoms of cerebral hypoperfusion or disease associated with orthostatic hypotension (hemorrhage or profound volume loss) (Bradley & Davis, 2003).

2. To assess response to a change in position in the elderly or ill.

3. To evaluate a patient with a history of known or suspected fluid loss secondary to vomiting, diarrhea, diaphoresis, bleeding, blunt abdominal or chest trauma, abdominal pain, unexplained syncope, weakness or dizziness, or autonomic dysfunction.

1. The value of orthostatic vital signs is disputed as there is no universal definition of how to perform them or what blood pressure and heart rate changes constitute “positive orthostatics.” Euvolemic patients may have orthostatic changes, whereas hypovolemic patients may not. Therefore, the vital signs should be interpreted in the context of the patient’s other signs and symptoms such as dizziness and visual dimming.

2. An assistant may be necessary because a patient with orthostatic hypotension may experience dizziness, lightheadedness, or syncope when moving from a lying to a standing position for postural vital sign measurement. Do not leave the patient alone during this procedure.

3. Orthostatic vital signs are contraindicated in patients with supine hypotension, shock, or a severe alteration in mental status, as well as in those who may have spinal, pelvic, or lower-extremity injuries (Gorgas, 2004).

4. Certain medications, such as sympatholytic drugs, diuretics, nitrates, narcotics, antihistamines, psychotropic agents, barbiturates, antihypertensives, and anticholergenics, can predispose a patient to orthostatic hypotension in the absence of hypovolemia. Studies have demonstrated a significant incidence of orthostatic hypotension, even in euvolemic patients (Irvin & White, 2004).

5. Paradoxical bradycardia may be observed in hypovolemic patients who have rapid and massive bleeding; this may be interpreted as orthostasis (Gorgas, 2004).

6. Prevent unreliable results by avoiding invasive or painful procedures during the measurement of postural vital signs.

1. Measure the blood pressure and heart rate measurements after the patient has been in supine position for 2 to 3 minutes. Taking two sets of measurements and using the second set as baseline helps prevent false-positive results that are based on patient’s sympathetic response (Bradley & Davis, 2003).

2. Have the patient move from the supine to the sitting position (if three measurements are taken) or from supine to standing. If the patient is unable to stand for blood pressure measurement, try the high Fowler’s position, although the results may be less credible. A supine-to-standing measurement is more accurate than a supine-to-sitting measurement (Gorgas, 2004).

3. Question the patient about weakness, dizziness, or visual dimming associated with a change of position. Note any pallor or diaphoresis. These symptoms are as important as the measurement of vital signs. If the patient becomes extremely dizzy and needs to lie down or becomes syncopal, the measurement should be terminated.

4. Take the standing or sitting blood pressure (in the same arm as the initial readings) and the heart rate measurement within 1 minute. Support the patient’s forearm at heart level when taking the blood pressure to prevent an inaccurate measurement.

5. If an intermediate sitting measurement was taken, have the patient move into the standing position and repeat steps 3 and 4.

6. Return patient to supine or sitting position.

7. Note all measurements on the patient record, including the position in which they were taken (i.e., with the patient lying, sitting, or standing). Positive findings in adults are usually considered to be a heart rate increase of 30 beats/min, a decrease in systolic blood pressure of 20 mm Hg, a diastolic blood pressure decrease of 10 mm Hg, or symptoms of cerebral hypofusion, such as dizziness and syncope (Bradley & Davis, 2003). Other authors state that changes in blood pressure are too variable to be considered a reliable indicator of blood loss (Gorgas, 2004). The results of one study indicate that the two most valuable predictors for hypovolemia are a pulse increase of 30 beats/min or severe dizziness on standing (McGee, Abernethy, & Simel, 1999).

1. The usefulness of orthostatic vital signs in children is not clear. Postural near-syncope or an increase in heart rate of 25 beats/min or more may be a predictor of dehydration in children (Gorgas, 2004). Assessment of dehydration in children should be based on preillness and postillness weight, capillary refill, and clinical assessment (Gorelick, Shaw, & Murphy, 1997).

2. Patients with nondemand pacemakers or those taking beta-blocking medications may not have significant changes in heart rate.

1. Decompensated shock

2. Stabilization of pelvic fractures with hypotension (ACS, 2004; McSwain Frame, & Salomone 2003)

3. Significant trauma (see 1 and 2 above) with a transport time of 20 to 40 minutes (Salomone, Ustin, McSwain, & Feliciano, 2005)

1. Absolute contraindications to the application of a PASG include the following:

2. Relative contraindications to the use of a PASG include the following:

3. The application of PASG for isolated lower-extremity fractures is not recommended because of the risk of the development of compartment syndrome (McSwain, Frame, & Salomone, 2003). A traction splint provides a better method of stabilizing femur fractures.

4. In conditions that require long inflation times (20 to 40 minutes or greater), significant alterations in fluid and electrolyte balance may occur and may complicate management and recovery. The patient is also at greater risk of developing pressure sores as well as compartment syndrome the longer the pants remain inflated.

5. PASG application should always be used in combination with oxygen administration and intravenous (IV) fluid resuscitation.

6. If the patient is transported to a higher altitude (air transport or over mountain passes), the air in the PASG expands and the pressure inside the garment increases. Monitor the PASG pressures carefully in these situations.

Pneumatic antishock garment (Figure 51-1)

Long spine board or scoop stretcher

Foot pump or inflation device that comes with the pants

Board straps or cravats

1. If the mechanism of injury warrants immobilization, place the patient on a long spine board or a scoop stretcher (see Procedure 111). Position the garment on the board or the scoop stretcher before the patient. The patient may be log rolled onto the garment and the garment slid up under the patient (technique A), or, alternatively, the garment may be placed on the patient like trousers (technique B).

2. Remove all clothing and anything else below the waist to prevent compression injuries from objects such as belts when the pants are inflated.

1. Use of the PASG for children is not recommended in the prehospital setting (NHTSA, 1998).

2. Pediatric and toddler-sized PASGs are available.

3. If an adult-sized PASG must be used for a child, inflate the leg compartments only (Eichelberger et al., 1998).

1. Sudden and severe hypotension may ensue after sudden removal of the garment.

2. Metabolic acidosis may develop after prolonged use of the garment as a result of a release of lactic acid from peripheral tissues.

3. Respiratory compromise may occur as a result of decreased vital capacity or pulmonary congestion (see Contraindications and Cautions).

4. Decreases in renal blood flow may result in a decline in renal perfusion, glomerular filtration rate, and urine output.

5. Inflation of the abdominal compartment may aggravate lumbar instability because of the circumferential compartment expansion.

6. Bleeding from extremity wounds may increase with increased blood pressure.

7. Skin breakdown and decubitus ulcer formation may occur.

8. Compartmental syndrome may develop in the lower extremities.

1. The PASG is a temporary measure to help increase blood pressure or splint pelvic fractures.

2. Report any increases in pain in areas under the PASG.

1. To decrease iron stores in iron overload syndromes, such as hemochromatosis, porphyria cutanea tarda, and African dietary iron overload (previously known as African siderosis). For every 500 ml of blood withdrawn, 200 to 250 mg of iron is removed (Heaney & Andrews, 2004). Iron is then mobilized from tissue stores by the bone marrow as it replaces the lost hemoglobin.

2. To decrease red blood cell mass in the presence of high blood viscosity (e.g., polycythemia vera). In patients with severe polycythemia (hematocrit greater than 55%), phlebotomy provides a means to reduce mean pulmonary artery pressure and pulmonary vascular resistance and enhance exercise performance (Wiedemann, 2004).

3. Rarely, therapeutic phlebotomy is advised in the patient with acute decompensation of cor pulmonale with marked polycythemia or for the rare patient who continues to have significant polycythemia despite appropriate long-term oxygen therapy (Wiedemann, 2004).

1. A physician from transfusion medicine should be involved in the decision to perform therapeutic phlebotomy (AABB, 2006).

2. Monitor patients who have bleeding disorders and those who are taking anticoagulant medications closely.

3. Generally, less than 500 ml of blood is removed slowly; the volume can be replaced with normal saline (Hamilton & Janz, 2006).

4. For patients with known cardiovascular disease, take care to prevent a large reduction in blood volume at one time (Means, 2004).

5. Prompt initiation of phlebotomy is critical following the diagnosis of iron overload because accumulation of iron can lead to cardiac arrhythmias, cardiomyopathy, and sudden death (Tavill, 2001).

500-ml vacuum bottle or blood collection bag if available

Phlebotomy tubing with needles on both ends

or

Saf-T donor set (36-inch tubing with a 17-G needle on one end and a 15-G stopper-piercing needle on the other end) (anticoagulant is not required)

Blood pressure cuff or tourniquet

Antiseptic solution

Local anesthesia (optional)

Occlusive dressing

Gauze dressing

Hemostat

1. Obtain an order including the diagnosis, most recent hemoglobin or hematocrit value, and the amount of blood to be removed.

2. Apply the tourniquet or blood pressure cuff and locate the most suitable antecubital vein. Remove the tourniquet or deflate the blood pressure cuff.

3. Cleanse the site with antiseptic solution.

4. Clamp the tubing with the hemostat at the patient’s end and insert the other end into the vacuum bottle. If using the Saf-T donor set, clamp the tubing to maintain the vacuum in the bottle and connect the 15-G stopper-piercing needle to the bottle.

5. Reapply the tourniquet or inflate the blood pressure cuff to a pressure between the patient’s systolic and diastolic readings.

6. Inject 1 to 2 ml of local anesthetic intradermally at the venipuncture site (optional).

7. Perform the venipuncture with the needle on the proximal end of the tubing.

8. Tape the needle in place and cover the site with an occlusive dressing.

9. Unclamp the hemostat and collect the desired amount of blood, usually 250 to 500 ml, in the collection bottle or bag.

10. Reclamp the tubing with the hemostat.

11. Release the tourniquet or deflate the cuff.

12. Withdraw the needle and apply pressure with a gauze dressing until the bleeding stops.

13. Assess and document the patient’s vital signs.

1. Adverse effects include fainting, weakness, chills, nausea, vomiting, and muscular twitching. If adverse effects occur, clamp the tubing and notify the physician.

2. Hematoma, bruising, and tenderness at the IV insertion site may occur.

1. Rest for 15 minutes before moving to a sitting or standing position.

2. Eat and drink before the procedure, and drink after the procedure if not contraindicated.

3. Avoid vigorous exercise within 24 hours of therapeutic phlebotomy.

4. Do not take iron supplements if you have iron overload problems. Vitamin C supplements, which increase the absorption of iron, should also be avoided.

5. Avoid alcohol if you have iron overload problems; alcohol is toxic to the liver.

6. Patients with porphyria can contact the American Porphyria Foundation (http://www.porphyriafoundation.com/) for additional information. For patients with hemochromatosis, information on treatment with therapeutic phlebotomy is available at:http://www.cdc.gov/ncbddd/hemochromatosis/training/pdf/phlebotomy_info.pdf

1. To assist in the diagnosis of pericardial tamponade in patients with decreased cardiac output, elevated central venous pressure with jugular vein distention, muffled heart tones, and hypotension (also known as Beck’s triad) who have sustained blunt or penetrating trauma to the chest. Ultrasound is the preferred diagnostic technique as it is noninvasive and easily performed at the bedside.

2. To relieve pericardial tamponade secondary to infection, tumor, bleeding diathesis, or recent intracardiac instrumentation, such as pacemaker insertion.

3. To assist in the diagnosis and treatment of patients in pulseless electrical activity.

4. Placement of an indwelling “pigtail catheter” may be considered for serial drainage if effusion is likely to recur.

1. Ideally, pericardiocentesis is performed in the cardiac catheterization laboratory using fluoroscopic or echocardiac guidance. In the emergency department, ultrasound or echocardiography may be useful adjunctive techniques for this procedure (Ciccone, 2004; Tang, 2005; Tibbles & Porcaro, 2004). The electrocardiogram (ECG)-assisted “blind” technique for pericardiocentesis is associated with significant morbidity, and therefore, it is only recommended when there may be a considerable delay in obtaining an ultrasound or a fluoroscope (Harper, 2004). If the patient is stable and ultrasound is not available, a computed tomography (CT) scan can provide definitive diagnosis of pericardial effusion (Harper, 2004).

2. Extreme caution is necessary when performing pericardiocentesis on patients who are taking anticoagulant medication.

3. All equipment must be secured and properly grounded to prevent small current leaks, which may result in arrhythmias.

4. Pericardiocentesis may be inadequate for traumatic pericardial tamponade; a pericardial window or other operative intervention may be necessary to remove clots in the pericardium.