Page 163 - Cardiac Nursing

LWBK340-c06_p132-152.qxd 09/09/2009 08:25 AM Page 139 Aptara

C HAP TE R 6 / Hematopoiesis, Coagulation, and Bleeding 139

may also be linked to inflammation because angiotensin II not each case, bleeding is the primary manifestation. The bleeding may
only may be a vasoconstrictor but also may cause intimal inflam- be minor, such as petechiae and easy bruising of the skin, or ma-
mation by stimulating the smooth muscle and endothelial cells to jor, with massive hemorrhage.
express proinflammatory cytokines such as IL-6 and monocyte The focus of cardiac interventions today emphasizes main-
3
chemoattractant protein-1. Hyperglycemia associated with dia- taining blood flow with percutaneous interventions (vascular in-
betes can lead to the formation of advance glycation end products jury) and anticoagulation to prevent thrombus formation. This
that may augment the secretion of proinflammatory cytokines. 3 intentional disruption of the coagulation system can potentially
Even chronic extravascular infections such as gingivitis, prostati- lead to bleeding disorders or even shock with excessive blood loss
tis, bronchitis, etc., can augment extravascular production of in- from percutaneous interventions and/or thrombolysis. Shock can
flammatory cytokines, which can accelerate the evolution of ath- lead to hypoperfusion and decreased oxygen delivery, which can
3
erosclerotic lesions. This new scientific insight into the role of trigger the intrinsic and extrinsic pathways simultaneously. Dis-
inflammation in the development of atherosclerosis has led to us- seminated intravascular coagulation (DIC) is a complication of
ing new markers to determine the degree of inflammation. Find- shock. Although DIC is actually a disorder of coagulation, it is
ings of a relationship between increased C-reactive protein levels discussed as a bleeding disorder because its major manifestation
and unfavorable cardiovascular outcomes have led to new thera- is bleeding.
peutic considerations for acute coronary syndrome. 3

Disseminated Intravascular
BLEEDING DISORDERS
Coagulation
Bleeding can occur when the intricate relationship between the DIC is a pathological syndrome resulting in the indiscriminate
various elements of the hemostatic system is disturbed. Bleeding formation of fibrin clots throughout all or most of the microvas-
defects in the hemostatic system can be categorized into three ar- culature. Paradoxically, diffuse bleeding occurs as a result of the
eas: vascular issues, platelet dysfunction, or coagulation dysfunc- consumption of clotting factors and is usually the hallmark sign of
tion. Vascular issues generally cause endothelial damage by an au- the syndrome. It is a disorder in which the coagulation cascade has
toimmune process (allergy induced), endotoxins from infections, been “pathologically activated” either by the extrinsic pathway re-
or abnormal vascular structure. Platelet dysfunction can present as leasing tissue factor or by the intrinsic pathway with endothelial
1
thrombocytopenia (low platelet count) or thrombocytosis (high injury. It is considered a complication of many different diseases
platelet count). Thrombocytopenia can result from decreased pro- and is known as a consumptive coagulopathy or defibrination syn-
5
duction, decreased distribution, or increased destruction of drome. Successful treatment of DIC must include treatment of
platelets. Thrombocytosis can result from either a primary or a sec- the primary cause of the disorder as well as the hematologic con-
ondary cause. Coagulation dysfunction can be either congenital or sequences. (See Display 6-2 for diseases associated with dissemi-
acquired deficiencies in the coagulation factors (Display 6-1). In nated intravascular coagulation.)

DISPLAY 6-1 Conceptual Etiology of Bleeding Disorders

Autoimmune

Vascular issues Infections

Structural

Production

Thrombocytopenia Destruction

Distribution
Platelet dysfunction
Primary (genetic)

Thrombocytosis
Secondary (reactive)