IV Troubleshooting: AIR EMBOLISM

-by Torregosa, Cyrus Dan A.

Nursing care plan for air embolism with a primary nursing diagnosis of Decreased
cardiac output related to blocked left ventricular filling.

An embolism happens when an object or substance travels through the bloodstream

and becomes lodged in a blood vessel. The trapped material is called an embolus.
An air embolism, is an obstruction in a vein or artery caused by a bubble of gas. Air
enters the circulatory system when the pressure gradient favors movement of air or gas
from the environment into the blood. A venous air embolism is the most common form
of air embolism. It occurs when air enters the venous circulation, passes through the
right side of the heart, and then proceeds to the lungs. In relatively small amounts, the
lungs can filter the air; it is absorbed without complications. When large amounts of air
(80 to 100 mL) are introduced into the body, however, the lungs no longer have the
capacity to filter the air, and the patient has serious or even lethal complications. One of
the most serious complications is when the large air bubble blocks the outflow of blood
from the right ventricle into the lungs, preventing the blood from moving forward.

The patient develops cardiogenic shock because of insufficient cardiac output.

Experts have found that the risk from air embolism, increases as both the volume and
the speed of air injection increase. An arterial embolism occurs when air gains entry into
the pulmonary venous circulation and then passes through the heart and into the
systemic arterial circulation. An arterial embolism can also form in the patient who has a
venous embolism and a right-to-left shunt (often caused by a septal defect in the heart)
so that the air bubble moves into the left ventricle without passing through the lungs.
Pulmonary capillary shunts can produce the same effect. The arterial embolism may
cause serious or even lethal complications in the brain and heart. Scientists have found
that as little as 0.05 mL of air in the coronary arteries can cause death.

Causes of Air Embolism

The two major causes of air

embolism are iatrogenic and
environmental. Iatrogenic
complications are those that occur as a
result of a diagnostic or therapeutic
procedure. Situations in which
iatrogenic injury is a possibility include
insertion, maintenance, or removal of
the central line. The risk is highest
during catheter insertion because the
large-bore needle, which is in the vein,
is at the hub while the catheter is threaded into the vein. Air can be pulled into the
circulation whenever the catheter is disconnected for a tubing change or the catheter-
tubing system is accidentally disconnected or broken. When the catheter is removed, air
can also enter the fibrin tract that was caused by the catheter during the brief period
between removal and sealing of the tract. Other procedures that can lead to air
embolism are cardiac catheterization, coronary arteriography, transcutaneous
angioplasty, embolectomy, and hemodialysis. Some surgical procedures also place the
patient at particular risk, including orthopedic, urologic, gynecologic, open heart, and
brain surgery, particularly when the procedure is performed with the patient in an upright
position. Conditions such as multiple trauma, placenta previa, and pneumoperitoneum
have also been associated with air embolism.

Environmental causes occur when a person is exposed to atmospheric pressures

that are markedly different from atmospheric pressure at sea level. Two such examples
are deep-sea diving (scuba diving) and high-altitude flying. Excessive pressures force
nitrogen, which is not absorbable, into body tissues and the circulation. Nitrogen
accumulates in the extracellular spaces, forms bubbles, and enters into the bloodstream
as emboli.

Physical Assessment and Examination

The patient may have been scuba diving or flying at the onset of symptoms. Usually
patients who develop an iatrogenic air embolism are under the care of the healthcare
team, who assesses the signs and symptoms of air embolism as a complication of
treatment. Some patients have a gasp or cough when the initial infusion of air moves
into the pulmonary circulation. Suspect an air embolism immediately when a patient
becomes symptomatic following insertion, maintenance, or removal of a central access
catheter. Patients suddenly become dyspneic, dizzy, nauseated, confused, and
anxious, and they may complain of substernal chest pain. Some patients describe the
feeling of “impending doom.”

On inspection, the patient may appear in acute distress with cyanosis, jugular neck
vein distension, or even seizures and unresponsiveness. Some reports explain that
more than 40% of patients with an air embolism have central nervous system effects
such as altered mental status or coma. When auscultating the patient’s heart, listen for
a “millwheel murmur” produced by air bubbles in the right ventricle and heard
throughout the cardiac cycle. The murmur may be loud enough to be heard without a
stethoscope but is only temporarily audible and is usually a late sign. More common
than the mill-wheel murmur is a harsh systolic murmur or normal heart sounds. Most
patients have a rapid apical pulse and low blood pressure. You may also hear wheezing
from acute bronchospasm. The patient may have increased central venous pressure,
pulmonary artery pressures, increased systemic vascular resistance, and decreased
cardiac output.

Most patients respond with fear, confusion, and anxiety. The family or significant
others are understandably upset as well. Evaluate the patient’s and family’s ability to
cope with the crisis and provide the appropriate support.

Symptoms (awake patients)

 Acute dyspnea
 Continuous cough
 "Gasp" reflex (a classic gasp at times reported when a bolus of air enters the
pulmonary circulation and causes acute hypoxemia)
 Dizziness/lightheadedness/vertigo
 Nausea
 Substernal chest pain
 Agitation/disorientation/sense of "impending doom"

Signs
Cardiovascular
 Dysrhythmias (tachyarrhythmias/bradycardias)
 "Mill wheel" murmur - A temporary loud, machinerylike, churning sound due to
blood mixing with air in the right ventricle, best heard over the precordium (a late sign)
 JVD
 Hypotension
 Myocardial ischemia
 Nonspecific ST-segment and T-wave changes and/or evidence of right heart
strain
 Pulmonary artery hypertension
 Increased CVP
 Circulatory shock/cardiovascular collapse

Pulmonary
 Adventitious sounds (rales, wheezing)
 Tachypnea
 Hemoptysis
 Cyanosis
 Decreased end-tidal carbon dioxide, arterial oxygen saturation, and tension
 Hypercapnia
 Increased pulmonary vascular resistance and airway pressures
 Pulmonary edema
 Apnea

Neurological
 Acute altered mental status
 Seizures
 Transient/permanent focal deficits (weakness, paresthesias, paralysis of
extremities)
 Loss of consciousness, collapse
 Coma (secondary to cerebral edema)

Ophthalmologic
 Funduscopic examination may reveal air bubbles in the retinal vessels.

Skin
 Crepitus over superficial vessels (rarely seen in setting of massive air embolus)
 Livedo reticularis

The above hemodynamic, pulmonary, and neurologic complications primarily result

from gas gaining entry into the systemic circulation, occluding the microcirculation and
causing ischemic damage to these end organs. Animal studies have also suggested the
presence of secondary tissue damage resulting from the release of inflammatory
mediators and oxygen free radicals that occur in response to air embolism.

Nursing care plan Intervention and Treatment

Several strategies can help prevent development of air embolism. First, maintain the
patient’s level of hydration because dehydration predisposes the patient to decreased
venous pressures. Second, some clinicians recommend that you position the patient in
Trendelenburg’s position during central line insertion because the position increases
central venous pressure. Third, instruct the patient to perform Valsalva’s maneuver on
exhalation during central line insertion or removal to increase intrathoracic pressure and
thereby to increase central venous pressure.

Prime all tubings with intravenous fluid prior to connecting the system to the catheter.
Immediately apply an occlusive pressure dressing after catheter removal, and maintain
the site with an occlusive dressing for at least 24 hours. To prevent air embolism during
surgical procedures, the surgeon floods the surgical field with liquid in some situations
so that liquid rather than air enters the circulation.

If an air embolus occurs, the first efforts are focused on preventing more air from
entering the circulation. Any central line procedure that is in progress should be
immediately terminated with the line clamped. The catheter should not be removed
unless it cannot be clamped. Place the patient on 100% oxygen immediately to facilitate
the washout of nitrogen from the bubble of atmospheric gas. Place the patient in the left
lateral decubitus position. This position allows the obstructing air bubble in the
pulmonary outflow tract to float toward the apex of the right ventricle, which relieves the
obstruction. Use Trendelenburg’s position to relieve the obstruction caused by air
bubbles. Other suggested strategies are to aspirate the air from the right atrium, to use
closed-chest cardiac compressions, and to administer fluids to maintain vascular
volume. Hyperbaric oxygen therapy may improve the patient’s condition as well: This
therapy increases nitrogen washout in the air bubble, thereby reducing the bubble’s size
and the absorption of air. Note that if the patient has to be transferred to a hyperbaric
facility, the decrease in atmospheric pressure that occurs at high altitudes during fixed-
wing or helicopter transport may worsen the patient’s condition because of bubble
enlargement or “bubble explosion.” Ground transport or transport in a low-flying
helicopter is recommended, along with administering 100% oxygen and adequate
hydration during transport.
Independent

If the patient suddenly develops the symptoms of an air embolism, place the patient
on the left side with the head of the bed down to allow the air to float out of the outflow
track. Notify the physician immediately, and position the resuscitation cart in close
proximity. Initiate 100% oxygen via a nonrebreather mask immediately before the
physician arrives, according to unit policy.

Be prepared for a sudden deterioration in cardiopulmonary status and potential for

cardiac arrest. The patient and family need a great deal of support. Remain in the
patient’s room at all times, and if the patient finds touch reassuring, hold the patient’s
hand. Provide an ongoing summary of the patient’s condition to the family. Expect the
patient to be extremely frightened and the family to be anxious or even angry. Ask the
chaplain, clinical nurse specialist, nursing supervisor, or social worker to remain with the
family during the period of crisis.