Hypotension

The above approach to fluid management may seem reasonable in the "well" ELBW
infant, however, the majority of preterm births result in an infant who is not "well."
Normal blood pressure limits for the ELBW infant have not been validated. "Normal"
blood pressure values currently are gestational and postnatal age-dependent blood
pressure values between the 10th and 90th percentile and have no proven physiologic
relevance.[38] Acceptable mean arterial blood pressure during the first 12 to 24 hours of
life is typically equivalent to the infant's gestational age. By day three of life most ELBW
infants have attained a mean blood pressure of 30 mm Hg. [39] If one considers that a
normal physiologic blood pressure is one that supports perfusion (oxygen delivery) to
the major organs, it is possible that "hypotension" in a nonacidotic and
nonhypoxemic baby need not be treated immediately, especially in an infant who
appears to be well perfused and whose mean arterial pressure continues to rise.
[40,41]
 Cautious observation and monitoring of this infant may result in the establishment of
urine output (postnatal diuresis), assuming that the blood pressure values continue to
rise over time. A recent retrospective analysis of serial mean arterial pressure values
during the first three days of life in the ELBW infant population suggests that it is
important for blood pressure to continue to increase and that between three and six
hours of age may be a critical time period to aggressively treat hypotension. [42] The
hypotensive ELBW infant of most concern may be the infant
demonstrating fluctuations in blood pressure. A recent trial is the first to demonstrate
direct evidence that blood pressure fluctuations increase the incidence of IVH and
periventricular leukomalacia (PVL) in preterm infants with low or absent cerebral blood
flow autoregulation and that cerebral oxygenation is dependent on systemic blood
pressure.[43] In addition, infants who developed severe IVH had significantly lower early
right ventricular outputs, which was associated with left to right shunts through larger
diameter patent ductus arteriosus and higher mean airway pressures. [44] Blood pressure
is a function of blood flow and systemic vascular resistance. [45] Due to the dynamic
changes in blood flow (ductal and atrial shunts) and systemic vascular resistance after
birth, blood pressure may not be a good measure of cardiovascular status.
[44,45,46]
 Superior vena cava (SVC) flow may be a marker of systemic blood flow. [46] SVC
flow represents flow to the upper body of which 80% goes to the brain and is not
affected by ductal and atrial shunting.[46,47] Kluckow and Evans[46] measured SVC flow in
infants 26 to 29 weeks during the first 48 hours of life to determine reproducibility and
establish normal ranges. They found that an increase in SVC flow occurred during the
first 48 hours of life, possibly as a result of improved myocardial function. A follow up
study measured SVC flow and the association between hypoperfusion and development
of IVH during the first 48 hours of life.[44] Their hypothesis was that the incidence of IVH
relates to systemic and cerebral hypoperfusion-reperfusion cycle resulting from slow
postnatal adaptation of the immature cardiovascular system. SVC flow was measured at
5, 12, 24, and 48 hours of age. Measurement of lowest SVC flow occurred at 5 and 12
hours of age in 80% of the studied infants (n = 126) but improved spontaneously over
time. Low SVC flow was poorly predicted by mean arterial pressure (MAP). There was a
strong association between low flow rates and subsequent IVH as the flow improved.
The grade of IVH related significantly to severity and duration of low SVC flow. Low flow
rates were significantly associated with lower gestation, higher upper body vascular
resistance, larger diameter ductal shunts, and higher mean airway pressures. [44,46] At the
5-hour echocardiogram, 50% of the ducts had constricted, but the other 50% were still
hemodynamically significant. A recent randomized trial studied the effects of high
frequency ventilation (HFOV) compared with conventional ventilation on SVC flow
during the first 24 hours of life.[48] There were no significant effects on SVC flow
associated with HFOV (higher MAP), however, there was a trend toward increased
incidence of borderline SVC flows (<50 mL/kg/min) in the infants on HFOV with an
increasing trend toward increased use of cardiovascular support. As a part of the study
design, any infant with an SVC flow <50 mL/kg/min received dobutamine and, if that
failed to increase the SVC flow, dopamine was added to therapy. The use of inotropes
in this study does not duplicate current clinical practice, as SVC flow is not routinely
measured. The previous studies highlight interesting observations and intriguing
possibilities into the accurate assessment of systemic organ perfusion and as well as
subsequent therapies to maximize organ perfusion in a timely manner after birth to
minimize neurologic morbidity.
For any infant with hypotension, the cause needs to be determined so that the
appropriate treatment may be initiated. The development of persistent hypotension may
be the first physiologic indicator that an infant may be infected or entering into the
uncompensated phase of shock.[49] The birth history can give us additional information
as to the etiology of the hypotension (birth asphyxia and/or maternal infection). Birth
asphyxia can result in hypoxemia and metabolic acidosis resulting in peripheral
vasodilatation and myocardial dysfunction (poor contractility). These events, which may
be coupled with an inflammatory response due to infection, can result in fluid
accumulation in the periphery (tissue edema). [25,49] Management approaches should be
centered around efforts to minimize further development of tissue edema without
excessive fluid administration, correct metabolic acidosis, minimize peripheral
vasodilatation, and augment cardiac contractility with the administration of pressors.
Within the first few hours of birth, the most common causes of hypotension are related
to immature vasoregulation and myocardial dysfunction, sometimes referred to as
"distributive shock."[49,50] Hypovolemia does not appear to be a common cause of
hypotension in the newly born and yet most infants receive at least one course of
volume administration to treat hypotension. [49] There appears to be no relationship
between blood pressure and blood volume and dopamine is at least twice as effective
as volume administration in treating hypotension in the first hours after birth. [49,51] One
may argue that, since objective assessment of intravascular volume is not practical at
the bedside, and there is evidence that up to 23% of preterm infants may be
hypovolemic, administration of a single bolus of 10 to 20 mL/kg of volume may not be
unreasonable in a hypotensive patient without evidence of acute volume loss.
[40]
 However, in view of recent evidence that the severity and duration of low SVC flow
correlates with more severe grades of IVH, it may be prudent to initiate pressor support
as a first line therapy for hypotension in patients in high-risk categories for IVH or to
begin volume support and pressor support at the same time to augment cardiovascular
function. In older infants (28 to 29 weeks' gestational age) at lesser risk without other
IVH risk factors, if normal blood pressure is not achieved after a single volume bolus,
then dopamine should be initiated. [40,41,49] The type of volume, colloid versus crystalloid,
 can also be of some controversy. However, it has been demonstrated that it is the
volume infused, not the protein content of the fluid that is important in sustaining blood
pressure.[45,49] Normal saline (0.9% sodium chloride) is as effective as 5% albumin in
increasing blood pressure and causes less fluid retention after its administration.
[49,52,53]
 The administration of 5% albumin can impair gas exchange due to leaking of
protein in patients with increased capillary permeability such as the infected or
asphyxiated infant.[21,49,53] Due to this permeability, albumin is not preferentially retained in
the intravascular space and could cause a shift of fluid out of the intravascular space.
[49,54]
 The sudden shift in fluid could potentiate brain injury or lead to IVH. In a patient in
whom there is an identifiable volume loss (preload), the volume should be replaced with
the type of fluid that was lost, such as blood with packed red blood cells, platelets, or
fresh frozen plasma (fibrinogen). The circulatory capacity for preload is estimated to be
between 30 to 50 mL/kg in the premature infant and can guide the total volume of fluid
administered for volume expansion.[25] A common mistake in fluid management is to
increase the maintenance fluids to facilitate urine output. However, it is likely that fluids
should remain restricted until kidney function and circulation are established to prevent
further tissue edema from occurring.[25] Birth is associated with renal innervation
stimulation that can increase renal vascular resistance (sympathetic stimulation), which
results in a suppressed glomerular filtration rate (GFR) and urine output (prediuretic
phase first 12 hours of life). As the ECF volume expands, there is an inhibition of
sympathetic activity and subsequent decreased renal vascular resistance resulting in
increased urine output (diuretic phase).[10]
One study has retrospectively evaluated the relationship between mean blood pressure
and neonatal death and morbidity in infants <1,500 g and found no relationship between
mean blood pressure, death, and PVL. However, there was a relationship between IVH
and MAP lows, highs, and extremes in mean blood pressure variability. [39,55] Early and
effective treatment of hypotension to obtain a stable cardiovascular status may increase
the chance of improved neurological outcome and survival. [49]
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