Page 171 - Cardiac Nursing

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C HAPTER 6 / Hematopoiesis, Coagulation, and Bleeding 147
sites, with special attention to the abdomen and flank areas where same outcome as a patient with poor cardiopulmonary function
large amounts of blood can sequester before the patient becomes and a partial obstruction. Cardiac failure with a massive PE is
symptomatic. Gastrointestinal bleeding is also another mecha- caused by increased wall stress and ischemia that comprises the
nism for blood loss. Assessing for symptoms of abdominal discom- right ventricular (RV) function quickly and eventually impacts
fort as well as guiac testing of excretions of patients on anticoagula- left ventricular (LV) function. 17 Increased afterload develops due
tion should be routine nursing interventions. Patient education to obstruction of blood flow out of the right ventricle. Additional
regarding PT monitoring, anticoagulant medications and their side factors that increase afterload are neural reflexes, the release of hu-
effects, and interactions with other drugs should be reviewed. Leg moral factors, mediators that are released by platelets (platelet ac-
elevation while sitting should be emphasized and the importance of tivating factor and serotonin), and systemic arterial hypoxemia. 17
physical activity when discharged should be emphasized. Risk fac- The CO is initially maintained by increased catecholamine release
tors such as obesity, smoking, and estrogen therapy should be iden- resulting in an increased heart rate and contractility. The RV will
tified and interventions designed to assist the patient to modify attempt to contract against the resistance presented by the em-
24
them as appropriate. Because embolization is always a threat, spe- bolism, but will eventually decompensate leading to an increase in
cial attention to the assessment of cardiopulmonary indicators is RV volume. This increased RV preload leads to increased wall
paramount. PE may present with sudden onset of dyspnea, chest stress and compromised RV coronary blood flow and ischemia.
pain, and tachypnea, accompanied by other symptoms that will be Increased RV volume will also cause a septal shift that will de-
discussed in the next section. crease LV distensibility and decrease LV preload. This alteration in
preload will lead to a decrease in CO and mean arterial pressure
Pulmonary Embolism (MAP). RV coronary perfusion pressure is dependent on the gradi-
17
ent between the MAP and the RV subendocardial pressure. The
Although diagnostic and therapeutic modalities have improved decrease in MAP will aggravate the compromised RV oxygen sup-
over the years, PE remains a challenging clinical entity. The inci- ply. Further RV ischemia will perpetuate decreased RV performance
dence of symptomatic PE is estimated to occur in more than and the cycle will continue until complete decompensation occurs.
600,000 patients annually in the United States and contributes to This pathophysiological cycle is summarized in Figure 6-5.
50,000 to 200,000 deaths. 17 Two thirds of patients with fatal The emboli itself can lead to a local aggregation of platelets and
cases will die within 1 hour of presentation. The mortality rate for the release of vasoactive substances, which increase vasoconstric-
hospitalized patients with PE has remained at approximately 15% tion. Gas exchange abnormalities are related to the size and type of
over the past 40 years. 17 Similar information has been gleaned embolic material, the extent of the occlusion and the underlying
from the International Cooperative Pulmonary Embolism Reg- cardiopulmonary status and length of time since embolization. 17
istry (ICOPER), which is a collaborative study developed to With PE, there is initial adequate ventilation coupled with inade-
gather worldwide data about PE. The overall 3-month mortality quate perfusion (i.e., alveolar deadspace). The persistent obstruc-
rate for all PE patients in the ICOPER was 17.4%. 25 An interest- tion and associated vasoconstriction can lead to bronchoconstric-
ing finding of the ICOPER is that postoperative prophylaxis is tion, which produce shunting, another ventilation–perfusion (VQ)
not instituted in more than half the patients in that database. imbalance. Any sustained VQ mismatch results in arterial hypox-
Concern regarding lack of prophylaxis was echoed in the ACCP emia. The hemodynamic and gas exchange consequences of a mas-
Consensus Conference report, 20 which recommended that every sive PE can lead to a dramatic clinical presentation.
hospital develop a formal strategy that addresses the prevention of
thromboembolic complications with a written thromboprophy- Clinical Manifestations
laxis policy, especially for high-risk groups. PE may occur with a sudden, abrupt onset, or have an insidious
PE may be the result of either arterial or venous thrombi. onset that mimics other cardiopulmonary disorders. Dyspnea is
Common sources of PE include deep venous thrombi from the the most common symptom associated with PE and tachypnea is
lower legs, right atrial thrombi, septic foci (often related to IV the most frequent sign. 26 Other signs such as pleuritic pain,
drug abuse or infected vascular access sites), and tumors. Other cough, or hemoptysis can be present and may indicate a small PE
26
sources of emboli are amniotic fluid, fat, air, bone marrow, and located near the pleura. Classic cardiac signs such as tachycardia,
other foreign bodies. These latter sources have a pathophysiology low-grade fever, and neck vein distention can also be observed on
that is different from the usual venous source and occur less fre- presentation but may also be the function of age, the size of the
quently. Many factors predispose patients to PE and are similar to PE, and the underlying cardiopulmonary status. Younger patients
those risk factors for development of DVT discussed earlier. One may not have any of these signs whereas older patients may pres-
unique factor that predisposes patients to PE is an inherited pre- ent with several or all of these signs. 26 There may also be vague
disposition to hypercoagulability caused by a resistance to APC. complaints of chest discomfort, which can also be associated with
This inherited predisposition manifests itself as a gene mutation acute coronary ischemic syndromes.
known as factor V Leiden in the factor V gene. Factor V Leiden is The presentation of a patient with a massive PE can be very
the most common of all the other inherited hypercoaguable similar to the signs and symptoms mentioned above. The only
states. 25 difference is that the signs and symptoms are a more extreme and
exaggerated response to the embolic event. The classic clinical
Pathophysiology presentation of a massive PE can include syncope, cyanosis,
A PE is a mechanical complete or partial obstruction to blood tachycardia (heart rate 120 beats/min), tachypnea (respiratory
flow from the right to left heart. The physiological response of the rate 30 breaths/min), and hepatomegaly. 17 Because symptoms
patient is dependent on the degree of obstruction and the under- of a massive PE can be so vague, it is important to gather data
lying cardiopulmonary function. 17 A patient with good car- about patients and continually consider what their risk factors are
diopulmonary function and a complete obstruction may have the for having a PE.