Treatment requires both manual and intellectual dexterity. The history must be identified and vital organ function assessed clinically while therapy and essential monitoring are initiated simultaneously. The first goal in resuscitation is restoration of arterial perfusing pressures to levels consistent with reversing the numerical and clinical signs of shock, i.e. increasing systolic blood pressure to at least 90 mmHg in previously normotensive patients, and to levels not less than 10 to 15 per cent below pre-illness pressures in previously hypertensive patients. Achieving acceptable perfusing pressures is often accompanied by reversal of the signs of shock—improved peripheral skin temperatures and urine output, and conscious state.
A successful approach to ebb phase resuscitation is best ensured by following a pragmatic regimen, namely the ABC (airway, breathing, circulation) of resuscitation, as developed for adult cardiac life support (Tab!").
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Table 4 Emergency approach to ebb phase resuscitation
1. Secure the airway: most hypotensive patients will benefit from early intubation to protect against aspiration of gastric contents or blood and to facilitate appropriate ventilation and oxygenation.
2. Breathing: an elevated respiratory workload is common in hypotensive patients, increasing O 2 needs of the respiratory muscles at the very time that O2 delivery is impaired. Controlled ventilation will discount the work of breathing, thereby allowing a redistribution of any limited systemic O 2 delivery to other core organs. To maximize diffusive O2 transport in the lungs, we recommend starting with an inspiratory O2 fraction (FiO2) of 1.0 which can later be adjusted to maintain PaO2 values above 70 mmHg (9.3 kPa) or an SpO2 above 98 per cent. Without intubation in spontaneously breathing patients, most high-flow O 2 devices fail to provide an FiO2 above 0.5. In contrast, an FiO2 of 0.9 to 1.0 is easily obtained in the intubated patient.
3. Circulation: hypotension often signals a fall in O 2 delivery that may lead to irreversible dysfunction of vital organs. Long resuscitation times increase the risk of developing multiple organ dysfunction syndrome and reduce the likelihood of survival. Thus timely restoration of the arterial perfusing pressures is crucial. Once blood pressure has been restored to levels consistent with goals previously defined (i.e. systolic blood pressure above 90 mmHg and return of peripheral perfusion and urine output), time can be more carefully apportioned to further diagnostic evaluation to manage the cause of the hypotension, repay any O 2 debt that occurred during the ebb phase, and optimize O2 delivery to match ongoing needs.
Two general approaches are used for restoring arterial perfusing pressures during ebb phase resuscitation: increasing cardiac preload; increasing arterial tone and cardiac contractility. Fluid restores intravascular volume in the volume-depleted patient, optimizing left ventricular preload and thereby elevating cardiac output according to the Starling hypothesis. As fluid therapy is potentially less injurious than exogenous sympathomimetics for improving cardiac output and blood pressure, an important first question is to determine whether fluids can be used. When history and clinical signs suggest intravascular volume contraction, a fluid challenge is appropriate while clinical signs (blood pressure, heart rate, etc.) are closely monitored. If the patient has cardiogenic pulmonary edema or hypotension does not respond quickly to fluid challenges, exogenous sympathomimetics are recommended (Table.5). As the initial therapeutic objective in ebb phase resuscitation is blood pressure elevation, a-agonists such as norepinephrine (noradrenaline) and epinephrine (adrenaline) are preferable. Sympathomimetics with predominately b or dopaminergic effects are not recommended, as the vasodilation that they induce may be greater than can be compensated for by an increase in cardiac output, in which case hypotension will be accentuated.
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Table 5 Specific pharmacological agents commonly used in the hypotensive patient
The use of bicarbonate in the hypotensive acidotic patient is controversial. CO 2 excretion may be impaired (e.g. due to respiratory failure) and tissue CO 2 increased due to tissue hypoperfusion. Under such circumstances bicarbonate therapy may cause an additional load of CO 2, resulting in further intracellular acidosis. Alternatively, a pH below 7.15 to 7.2 may limit the response to pharmacological treatment, particularly on b-receptors. Our practice is to use bicarbonate therapy when the arterial pH is below 7.2 and hypotension persists despite adequate fluid therapy.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...