Page 173 - Cardiac Nursing

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C HAPTER 6 / Hematopoiesis, Coagulation, and Bleeding 149
the Greenfield filter, which is placed suprarenally. 26 In rare in- Heparin-Induced Thrombocytopenia
stances, pulmonary embolectomy may be performed in con-
junction with cardiopulmonary bypass. Mortality rates with this Anticoagulation is a key intervention in treating cardiovascular
procedure can exceed 50% and should be performed only in in- disease. The primary agent that has been used for years is heparin
stitutions that can quickly mobilize a cardiac surgery team. 17 and with an increased use of heparin, a new syndrome has been
With prompt identification and treatment, prognosis is good for identified. Heparin-induced thrombocytopenia (HIT) is a chal-
patients with PE. Successful treatment results in little long-term lenging immunohematologic issue that was originally described in
morbidity. Sequelae such as pulmonary hypertension and cor the early 1960s. Key elements of the syndrome were discovered in
pulmonale may be seen in patients with underlying cardiopul- the mid 1970s, and the antigen target of the HIT antibody was
29
monary disease or those with massive emboli. identified in 1992. However, knowledge about this disease is still
in the developmental stages. With more patients being exposed to
Nursing Interventions heparin or related drugs, the occurrence of HIT is increasing. One
Because PE can be a life-threatening event, the emphasis of nurs- issue with the disease is that it is difficult to diagnose and unpre-
ing management is on prevention. As discussed previously, preven- dictable in incidence but can have some devastating outcomes. Un-
tion of thrombus formation and early detection of PE is essential. like other clotting disorders, HIT is the result of an immunohe-
Fifty percent of those patients who die of PE do so within the first matologic reaction.
hour. Any patient experiencing a sudden onset of dyspnea, tachyp-
nea, and possible chest pain must be evaluated for the possibility of Pathophysiology
PE. Assessing the character of the patient’s chest pain is important The development of the pathogenic IgG is the key to this disor-
because most patients describe their pain as pleuritic. A 12-lead der. The heparin binds with PF4, which leads to the development
ECG and an ABG also provide useful data. Explaining all proce- of a highly reactive antigenic complex. Pathogenic IgG is formed
30
dures and tests helps reassure patients during a time of discomfort and activates the platelets. The major target antigen is a macro-
and anxiety about the sudden change of their condition. Once the molecular complex comprising heparin or other high-sulfated
30
diagnosis of PE has been established, continued nursing manage- oligosaccharides and PF4, which binds to the platelet surface.
ment of the patient’s cardiopulmonary function is essential. HIT is an immune-mediated adverse drug reaction that is
Because profound arterial hypoxemia can accompany PE, the caused by heparin-dependent, platelet-activating IgG antibodies
31(p589)
primary goal is to normalize gas exchange. By normalizing the ex- that recognize complexes of PF4 bound to “heparin.”
change of gases and minimizing the VQ mismatch, other systemic These antibodies are known as HIT antibodies because once they
effects of impaired gas exchange can also be ameliorated. Inter- “see” heparin, the autoimmune response is triggered and they be-
ventions to support respiratory function by patient positioning come anti PF4/heparin, platelet-activating IgG antibodies. The
and the use of supplemental oxygen may help decrease the degree activated platelets release procoagulant and PF4 neutralizes he-
31
of hypoxemia accompanying PE. Supplemental oxygen may be parin that leads to increased thrombin generation. With more
administered by face mask or, if necessary, by endotracheal intu- thrombin available, a hypercoagulable state develops and can lead
bation and mechanical ventilation. Positioning the patient with to the formation of thrombi (arterial and venous). The HIT anti-
the head of the bed elevated allows for better chest expansion with bodies are also thought to activate the endothelium and mono-
respiration. Coaching of the patient to promote the best respira- cytes leading to the expression of tissue factor at cell surfaces,
tory pattern can be very important and maintaining a calm envi- which can also lead to thrombin formation (see Fig. 6-6). With
ronment and approach to the patient can make the difference in this immunologic cascade of events, HIT is a potentially devas-
the patient’s course. The administration of prescribed analgesics tating thrombotic disorder.
and sedatives may help relieve the patient’s discomfort and anxi-
ety. By reducing discomfort and anxiety, respiratory rate may also Etiology
decrease, thus reducing the additional vasoconstriction and bron- The cause of HIT is the exposure to heparin leading to the devel-
choconstriction caused by lower Pa CO2 levels. Anticoagulants and opment of anti-PF4/heparin platelet-activating IgG antibodies,
thrombolytic agents, as described earlier, are usually ordered by which leads to thrombocytopenia. Patients generally experience a
the physician. These agents help decrease the recurrence of emboli 50% decrease in platelet count, but it is important to note that the
and may help lyse the embolus; thus, restoring normal blood flow postoperative patient’s “baseline” platelet count is the highest
through the pulmonary vasculature. postoperative count prior to the decrease suspected with HIT. 31
Frequent assessment of cardiopulmonary function is also im- An immune response requires time for the reaction to develop.
portant. Vital signs, particularly respiratory rate, heart rate, and Because of this aspect of the disease, HIT can have varying time
blood pressure should be assessed and documented hourly and as onsets and is important in diagnosing HIT. The usual onset for
needed. Normal vital signs may indicate improved gas exchange. 70% of patients is a decrease in platelet count 5 to 10 days after
ABG analysis offers a quantitative assessment of gas exchange. starting heparin (first day of heparin use day 0). 31 If patients
Because of the prolonged duration of anticoagulant therapy, pa- have an exposure to heparin within the past few weeks or months
tients require extensive teaching about the administration and leading to HIT antibody development, a “rapid onset” HIT pres-
follow-up schedules of oral anticoagulants, a medication identifi- entation can occur within 24 hours of subsequent heparin ad-
31
cation card or band, potential hazards associated with therapy, ministration. When the platelet count decreases after all heparin
and the signs and symptoms of bleeding and recurrent VTE. Di- has been stopped, this is a “delayed presentation” HIT and
etary restrictions and foods that contain large amounts of vitamin thought to be due to high levels of circulating antibodies. 31 Al-
K should be reviewed. This is a disease with long-term implica- though HIT can develop in any patient who has exposure to he-
tions that can be successfully managed with patient participation parin, there are certain patient populations that seem to have a
and education. higher incidence. These risk factors include: (1) duration of