Cardiovascular

The signs and symptoms of deconditioning and immobility

include tachycardia, hypotension, hypertension, lower extremity
edema, and deep venous thrombosis. These signs
and symptoms can influence how the person with a brain
injury feels, sleeps, participates in therapy, tolerates therapy,
and even breathes. Hypotension can be managed through
the usual means of applying compression stockings, perhaps
an abdominal binder, managing fluid status, nutrition, anemia,
and reassessing the need for medications. Some patients
will be hypotensive because of medications that were started
early in the course of their event which, in itself, may more
acutely have caused hypertension and tachycardia. These
may no longer be needed. Beta-blockers are frequently used
in the acute medical setting but can often be weaned as the
acute TBI is more remote. Although some may find this class
useful in neurobehavioral situations, the cognitive and hypotensive
side effects may be exacerbated in this population.
The effect of anemia on endurance should also be factored
into someones rate of progress. Although the acute care facility
may be comfortablewith the patient who is asymptomatic
in bed with hemoglobin of 8, the rehabilitation setting
demands more. It is best to avoid the use of as needed antihypertensives
that can result in rebound hypertension (e.g.,
clonidine). Ideally, practitioners should look at what other
events or changes present before or simultaneously with the
tachycardia, hypotension, or hypertension to be able to pinpoint
the possible triggers.

Cardiovascular System
Research on cardiovascular effects of immobility is drawn
both from microgravity experiments during space flight and
from experiments using a head-down tilt position to mimic
weightlessness. Obviously, these studies seek to maximize
the effects of bed rest. Normal positioning of patients in bed
after TBI will mitigate the severity of cardiovascular effects.

Reduction of Cardiopulmonary Functional Capacity

and Postural Hypotension

Functional efficiency of the heart depends on both intravascular

volume (hydrostatic forces) and coordinated filling and
emptying of the ventricles (hydrodynamic forces). Normally,
arterial pressures and certain levels of intravascular volume
interact to maintain adequate body and cerebral perfusion
in the face of gravity. However, when the body is placed
horizontally for a prolonged period, about a liter of fluid is
relocated from the legs to the chest area. Initially, this increases
diastolic filling and increases the stroke volume of
each cardiac contraction (i.e., the Frank-Starling mechanism).
However, baroreceptor responses eventually result in a diuresis
and loss of plasma volume within 2448 hours (75).
When a normal upright position is resumed, there is a sudden
decrease in both ventricular filling and stroke volume
that results in orthostatic symptoms (76). Cardiovascular
baroreflex responses become attenuated without the challenges

of baroreceptor unloading that comes from upright

standing (77). Other factors may include disordered sympathetic
activation in combination with hypovolemia and diminished
baroreceptor reflexes (78). Particularly interesting
in the context of TBI is the involvement of brain autonomic
nuclei such as the paraventricular nucleus of the hypothalamus
that includes basal and reflex control of the SNS vasopressin
and oxytocin release and secretion of corticotrophinreleasing
factor (79).
Other changes in cardiac function have been noted.
After immobilization, the maximal oxygen uptake (V o2max)
is reduced and the heart rate is increased in response to submaximal
exercise (80). This equates to a loss in aerobic capacity
of 0.9% per day over 30 days of bed rest (3). The heart
rate during prolonged bed rest is higher for the same oxygen
requirement (81) (see Figure 49-1). Part of this is related to
the fluid changes noted previously; these effects are much
less during supine submaximal exercise (80). The heart rate
is probably increased because of increased beta-adrenergic
receptor sensitivity (81).
Simple replacement of volume does not abolish the
orthostatic response (82). It appears that there are some alterations
to the ventricles themselves during a period of prolonged
bed rest leaving them less distensible (83). This
appears to be an effect on cardiac muscle similar to the loss
of muscle volume seen in skeletal muscle during prolonged
immobilization (76). Actual muscle contractile properties
seem to be preserved (84). The effects on stroke volume
and cardiac output after prolonged bed rest will persist for
at least a month (84). These effects are partially masked by

an increase in peripheral volume and retention of sodium

and, at least initially, an increase in sympathetic nerve activity
(85).

Hematological System
Deconditioning causes a reduction in red blood cell mass
by 5%25% that may compromise blood oxygen-carrying
capacity. However, the hematocrit generally remains stable
during bed rest. Therefore, the effect of reduced blood cell
mass is still unclear (81). As noted elsewhere in this chapter,
there is a significant decrease in resting blood flow to the leg
muscles and a reduction in capillarization. This is correlated
with fatigability in calf muscles (81,86,87). Reversing these
effects requires not only the upright position and adequate
fluid volume but also the exercise that induces arterial baroreceptor
loading (77). In animals, daily standing for only 1
hour per day prevented depression of myocardial contractility
(88).

Thrombogenesis

Thromboembolic disease is a well-described risk in the setting

of immobilization. In the patient with brain injury, this
risk remains present with significant complicating factors for
diagnosis and treatment. Often after significant trauma, each
of the factors of Virchow triad (stasis, endothelial damage,
and hypercoagulable state) is present on admission to the
emergency department. In the patient with TBI, one sequelae

of the injury may be hemiparesis, which contributes to stasis

in a more discrete and prolonged manner. Patients with TBI
may also present with bleeding in the subdural or subarachnoid
space, limiting the choice of treatment modalities. The
patient with TBI may also be impulsive and have considerable
fall risk, which may limit pharmacologic prophylaxis and
treatment options. Identification and treatment of venous
thromboembolism is therefore of increased complexity but
of great necessity in the population with TBI (89).
Initial traumatic injury inherently carries with it risk for
hypercoagulability when multiple organ systems are involved
and bleeding present at one or more sites. When
bleeding occurs, the body initiates the coagulation cascade,
a response that may be prolonged when blood remains present
acting as a nidus for continued production of coagulation
factors. With TBI, bleeding may occur at any site in the body
because of concomitant trauma but is of particular concern
intracranially. The patient may require prolonged monitoring
to ensure resorption or neurosurgical intervention to reduce
mass effect because of bleeding, contributing to further
stasis. A functional limitation of TBI may be hemiparesis or
bilateral weakness, which may persist following the acute
period of immobility after trauma. Thrombi are noted to
occur most frequently in the paralyzed limb of hemiparetic
patients and more likely to occur in the proximal segment
of the limb, placing them at higher risk for propagation (90).
In a similar setting, deep vein thrombosis (DVT) risk has
been found to be comparable following brain tumor surgery
as in the orthopedic hip replacement population (91). The
patient with TBI is also likely to have suffered endothelial
damage with the initial inciting injury.
Identification of thromboembolism may be suspected
clinically by the presence of a warm, edematous, and painful
limb. Unfortunately, the affected limb often exhibits no signs
at all of thrombophlebitis; therefore, physical exam is unreliable
for venous thrombosis diagnosis (92). The venous duplex
exam is the mainstay of diagnosis. Testing carries high
accuracy, is noninvasive, and often readily available at the
bedside (93). If pulmonary embolism (PE) is suspected by
clinical findings of decreased oxygen saturation, tachypnea,
and pleuritic chest pain, studies to assist in diagnosis for PE
should be employed as well as the previously mentioned
venous duplex to identify potential source of the embolus.
The D-dimer assay, spiral computed tomography (CT), and
ventilation-perfusion studies are all well-accepted means to
assist in diagnosis of PE. In the patient with TBI, there are
noted limitations to the use of these means of diagnosis. Following
trauma, it is anticipated that D-dimer levels will be
unspecifically high and therefore are noncontributory to assisting
in diagnosis. Using D-dimer levels has not been
shown to be useful in predicting DVT after acute TBI (94).
However, a low D-dimer may assist to rule out a PE if this
be the goal. A ventilation-perfusion scan may be limited by
any other concomitant pulmonary conditions such as pneumonia,
secretions, or atelectasis. The spiral CT is the most
readily available tool for reliable diagnosis, albeit at a higher
initial cost.
Treatment for identified thromboembolism is primarily

pharmacologic by using unfractionated or regular heparin.

Heparin acts initially by enhancing antithrombin III activity.
In high doses, heparin also acts to inhibit prothrombin and
platelet aggregation. This constitutes its efficacy in meeting
the key treatment goals for PE and thromboembolism by
inducing a hypocoagulable state and decreased potential for
clot propagation (92). However, the patient with TBI may
have comorbidities limiting the use of anticoagulation in his
pharmacologic regimen. Anticoagulation with heparin prophylaxis
has been noted to be safe in patients with intracranial
bleeds who had stable or improved head imaging at

24 hours (95). Early anticoagulation resulted in a stastically

significant lower rate of thromboembolism. A 2010 observational
study examined screening, prophylaxis, and treatment
in patients with TBI in the rehabilitation setting (96). No
definitive proof of prevention of venous thromboembolism
was observed in those treated with propyhylactic medications.
For those individuals who are not candidates for anticoagulation,
the use of retrievable inferior vena cava filters
provide an alternative to disrupt the clot pathway to decrease
risk of PE. These filters are generally used in patients
in whom recurrent PE has occurred despite treatment with
anticoagulants or those in whom anticoagulant therapy is
contraindicated (97). A review of case series has indicated
that these filters are successfully removed in 91% of cases;
9% of filters could not be removed because of large trapped
thrombus (98). It is important to note that these filters are
associated with a twofold increase in the incidence of recurrent
DVT. If it is safe to anticoagulate a patient, they should
remain on therapeutic anticoagulation even with a filter in
place for the recommended length of time (99).