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intubation can allow for increased airway pressures to be provided that reduce intrapulmonary shunt and improve oxygenation. Patients with acute arterial oxygen saturations less than 92% should be considered for supplemental oxygen or intubation to improve their oxygenation status.

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Impending airway obstruction is an indication for intubation to prevent complete obstruction and loss of the airway. Anatomical changes as a result of trauma, tumors, edema, or vocal cord abnormalities can interfere with airway patency, as can functional changes as a result of depressed neurologic status from head trauma, drugs, anesthesia, or stroke. If concern for impending airway obstruction is present, it is preferable to intubate early rather than later to allow easier passage of the endotracheal tube in a controlled manner.

C Ventilator support

Once the decision has been made to intubate, the next decision is how to manage the patient on the ventilator. Ventilator support should address two basic issues: ventilation and oxygenation. Ventilation determines CO2

elimination and is dependent on alveolar minute ventilation. Alveolar minute ventilation is total minute ventilation minus dead space ventilation. Total minute ventilation is the product of respiratory rate times tidal volume and is expressed as liters per minute. To alter PCO 2 , adjustments in rate and tidal volume should be made with

increases in minute ventilation, resulting in decreases in PCO 2 . Oxygenation or PO 2 is determined by the partial pressure of alveolar oxygen and the intrapulmonary shunt. Increasing the FiO 2 will increase alveolar oxygen while

increasing mean airway pressure, such as by increasing positive end expiratory pressure (PEEP), will decrease shunt and increase PO 2 . The mode of ventilation will alter how ventilation and oxygenation are achieved;

however, more commonly, the mode influences patient tolerance of mechanical ventilation. For any patient receiving ventilatory support, ventilator-associated lung injury is an inherent risk to mechanical ventilation. This risk is increased with larger tidal volumes (volutrauma), higher airway pressures (barotrauma), or higher inhaled oxygen concentrations (oxygen toxicity).

Modes of ventilation. The modes of ventilation determine how the ventilator will provide a mechanical breath to the patient and are based on pressure or volume. There are more modes than are discussed here, but these will suffice in the vast majority of patients.

Synchronized intermittent mandatory ventilation (SIMV). A preset rate and tidal volume are provided by the ventilator. Additional spontaneous breathing by the patient can occur that provides additional minute ventilation (tidal volume and rate) dependent on the patient's work of breathing capability. The work of breathing is shared between the machine's minute ventilation and the patient's spontaneous minute ventilation. This is the usual mode of ventilation when weaning a patient: By turning down the ventilator rate, the patient assumes more work of breathing until the ventilator is no longer needed. Pressure support (see below) can be added to this mode to facilitate the spontaneous breaths.

Assist or volume control (AC/VC). A preset rate and tidal volume are provided by the ventilator, and all additional breaths by the patient are assisted by the ventilator, providing a full preset tidal volume. Minute ventilation becomes the result of the preset tidal volume times the preset ventilator's plus patient's rates. This allows the patient to receive full ventilatory support without expending extra energy on the work of breathing. Weaning cannot occur in this mode, and pressure support cannot be added to this mode.

Pressure support (PS). Rather than providing a preset tidal volume or rate, the pressure support mode pressurizes the ventilator circuit to a preset level above the baseline pressure when the patient initiates a breath and maintains that level until the patient stops inhaling. The patient is able to initiate and terminate the respiratory cycle in this mode. Inspired tidal volume is determined by the amount of pressure support and the patient's intrinsic work of breathing capacity. Increasing the amount of pressure support reduces the work of breathing for the same tidal volume or allows a larger tidal volume for the same amount of work. The pressure support mode facilitates the patient's comfort and aids in weaning from the ventilator. The usual starting point of pressure support is 5–10

mm Hg above the baseline pressure (CPAP/PEEP) and can be used alone or in combination with SIMV.

Continuous positive airway pressure (CPAP) and PEEP. For a basic understanding, these modes are considered similar, as both modes result in the ventilator circuit being pressurized to a specified level above atmospheric at all times, during inspiration and expiration. This increases mean airway pressure and the number of alveoli that are inflated, which increases the surface area of the lung that is available for gas exchange. This results in a decrease in intrapulmonary shunt and is considered a primary way to increase oxygenation. Usually, CPAP/PEEP of 5 mm Hg above atmospheric pressure is used and is increased as necessary to

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improve oxygenation. Because these modes increase intrathoracic pressure at higher levels, they can decrease venous return to the heart and therefore cardiac output. PEEP is used with SIMV and AC, while CPAP is used with PS.

Rate. After the mode, the next parameter to set is rate, with a normal rate about 10–12 bpm. Higher rates may be necessary to decrease the PCO 2 if higher minute ventilation or lower tidal volumes are required.

Remember that if the patient is severely acidotic, he or she may have been compensating with the respiratory system and may require a much higher respiratory rate.

Tidal volume. Normal tidal volume is 5 mL/kg, but ventilated patients are usually set between 8–10 mL/kg. The higher volumes are needed to overcome dead space and to ensure alveolar filling. However, as compliance of the lungs decreases, especially in patients with ARDS, smaller tidal volumes of 6 mL/kg are beneficial. This volume will need to be adjusted as the patient's condition requires. Occasionally, permissive hypercapnia is beneficial to avoid barotrauma in particularly diseased lungs.

With the ventilator settings described previously, one should be able to handle the majority of ventilatory problems. Depending on the patient's condition, there are many other modes used to ventilate patients, but the basic ones that have been listed should suffice for routine ventilatory management. The starting point for most routine ventilator support involves the following:

Mode: SIMV; however, if no work of breathing is desired, then use the AC mode

Rate: 10–12 bpm

Tidal volume: 8–10 mL/kg

Pressure support: 5–10 mm Hg

PEEP/CPAP: 5 mm Hg

Fraction of inspired oxygen (FiO2 ): 0.4

The settings described need to be modified for the patient's condition: higher FiO 2 and/or higher PEEP if the patient is hypoxic, lower PEEP if hypotensive, faster rate if acidotic, etc.

Extubation. Ventilator weaning is the progressive transfer of the responsibility for work of breathing from the ventilator to the patient, eventually leading to the patient being extubated from the ventilator. After a patient is intubated, placed on a ventilator, and stabilized, one should start to think about weaning from the ventilator. Patients placed on a ventilator are usually in a catabolic state and as a result are breaking down muscle protein for fuel and for repair of other damaged proteins elsewhere. If a patient in such a state is placed on complete ventilator support without any work of breathing, the respiratory muscles will rapidly atrophy. Therefore, once the patient is stabilized on the ventilator, the amount of ventilatory support should

be adjusted to allow the patient to continue to do a normal amount of the work of breathing in order to keep the respiratory muscles intact. As the patient's condition improves, the respiratory rate delivered by the ventilator is decreased until the patient adequately assumes the work of breathing on an SIMV less than 4 bpm and PS less than 10 mm Hg, have acceptable oxygenation on an FiO 2 of 0.4 and PEEP less than 8 mm

Hg, have acceptable weaning parameters as described below, be awake enough to control airway, and have acceptable acid–base balance. When these conditions have been met, the patient is ready for extubation.

Respiratory rate less than 30.

Spontaneous tidal volume greater than 5 mL/kg.

Rapid shallow breathing index (respiratory rate bpm divided by tidal volume in liters) less than 100.

Vital capacity or the maximum amount of air that can be moved in and out of the lungs voluntarily of greater than 20 mL/kg. The normal amount is 60–80 mL/kg and represents the reserve ventilation that the patient has to increase his or her minute ventilation.

Negative inspiratory force (NIF) , or the amount of negative pressure created during a forced inspiration against a closed glottis, of greater than 20 mm Hg. The normal value is 60–80 mm Hg below atmospheric and is a measure of the strength of the patient's respiratory muscles, and as well is another measure of how much reserve the patient has to increase ventilation as needed.

Arterial blood gases. In addition to having acceptable spirometry values, the patient must also have acceptable blood gases. The oxygen saturation should be greater than 90% due to the limitations of providing high concentrations of oxygen via a face mask. The PCO 2 should

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be between 35 and 45 mm Hg with a corresponding pH between 7.35 and 7.45. Patients with a significant metabolic or respiratory acidosis with or without compensation should not be extubated without careful consideration of the underlying cause and potential future issues.

D Invasive monitoring

The mainstay of invasive monitoring in modern ICUs is the arterial line for blood pressure, the pulmonary artery catheter for cardiac outputs, pulmonary artery wedge pressures, and mixed venous oxygen saturation and the intracranial catheter for intracranial pressure monitoring.

Arterial catheter

An arterial catheter is usually placed in one of the radial arteries, as these are the most accessible sites. If a radial artery cannot be cannulated, other common sites are femoral, axillary, and brachial arteries. These catheters are slowly flushed with a dilute heparin solution to keep them from clotting. In addition to providing continuous arterial blood pressure monitoring, the arterial line can be used as a simple, nonpainful source for blood sampling.

There are three pressure measurements obtained from an arterial line: systolic, diastolic, and mean. The systolic is the highest pressure recorded during a cardiac cycle, the diastolic is the lowest measured during a cardiac cycle, and the mean is measured by integrating the area under the curve of the cardiac pressure wave. The mean pressure can be indirectly determined as (BP systolic - 2 × BP diastolic )/3 and represents the pressure that is available to perfuse the organs.

Pulmonary artery catheter

The pulmonary artery catheter is a flow -directed catheter designed to be inserted into a subclavian

or jugular vein, and because of an inflatable balloon on the tip, it can be floated through the heart and into the pulmonary artery. The catheter has an opening (port) in the tip distal to the balloon, another opening in the side of the catheter at a position that rests in the vena cava or right atrium, and a thermistor (a temperature-measuring device) near the distal port; there may also be extra ports for infusion of medications. When the catheter is in position in a distal pulmonary artery, the balloon is inflated and occludes antegrade blood flow, thereby allowing the distal port to measure retrograde pressure from the left atrium. This is referred to as the pulmonary capillary wedge pressure (PCWP) or occlusion pressure (PCOP) and is an indirect measure of left ventricular preload. By assessing ventricular preload, alteration fluid therapy can be made to maximize cardiac output.

Using thermodilution methodology, the pulmonary artery catheter is able to determine cardiac output by accurately measuring changes in blood temperature after introduction of a known thermal challenge. This is accomplished intermittently by injecting a small (10 mL) amount of cold IV fluid in the right atrium or continuously by warming a heating probe and then measuring the temperature change in the pulmonary artery. The less change in temperature, the higher the cardiac output. By using known calibrations, the actual cardiac output can be determined.

By either aspirating blood from the distal port or by using oximetry located on the distal tip, the mixed venous oxygen saturation (SvO 2 ) can be assessed. The SvO 2 provides a means to determine if the

amount of oxygen being pumped by the heart (oxygen delivery) is adequate for the amount of oxygen the body needs (oxygen consumption). The normal mixed venous oxygen saturation is about 70%, and if oxygen consumption is elevated or oxygen delivery is decreased, the saturation will be lower than 70%. The SvO 2 , therefore, is one of the best measures readily available to determine if shock is

present. If the SvO 2 is persistently low (60% or less), the body is being deprived of sufficient oxygen,

and organ dysfunction will begin to appear. Using similar technology, a less invasive but not as accurate method for determining SvO 2 can be obtained from the end of a central venous catheter.

By knowing the cardiac output, the mean arterial pressure, and the central venous pressure, the systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) can be calculated:

SVR = [(MAP – CVP)/CO] × 80 normal: 800–1200 dynes .second/cm 5 PVR = [(MPAP – PCWP)/CO] × 80 normal: 20–120 dynes .second/cm 5 P.29

Where MAP is mean airway pressure, CVP is central venous pressure, MPAP is mean pulmonary artery pressure, CO is cardiac output, and 80 is a conversion factor. Low SVR is an indication of systemic inflammation such as in sepsis, and high SVR is an indication of inadequate cardiac output.

In summary, the information gathered from the pulmonary artery catheter is as follows:

Left atrial and left ventricle preload pressures

Cardiac output (CO)

Mixed venous oxygen saturation (SvO 2 )

Systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR)

E Vasoactive medications

In the ICU, many patients are on vasoactive medications to affect their hemodynamic parameters; most of the time, this is to increase blood pressure (vasoconstrictors) and cardiac output (inotropes), but there are also times when these parameters need to be decreased. The following medications are the most frequently used, and are all administered in a continuous IV drip.

Dopamine has different effects, depending on the concentration used. At a low dose of 1–3 µg/kg/minute, it primarily affects dopamine receptors in the kidneys and intestine, leading to increased blood flow. At doses of 3–10 µg/kg/minute, it is primarily a beta receptor agonist and leads to an increase in cardiac contractility with resulting increase in cardiac output. At doses above 10 µg/kg/minute, it acts primarily as an alpha agonist and vasoconstrictor. Its limiting effect is tachycardia.

Dobutamine primarily affects both the beta -1 and beta -2 receptors. As a result, it leads to an increase in cardiac output as well as vasodilatation. This can be beneficial in cases of cardiogenic shock, where an increase in cardiac output and decrease in SVR would be beneficial. The doses are similar to dopamine, but dobutamine does not have the variable dosing effects, and the limiting factor is tachycardia.

Norepinephrine is a strong alpha agonist that primarily causes vasoconstriction with mild beta agonist activity that causes some increase in contractility of the heart. Norepinephrine is begun at a concentration of 1–2 µg/kg/minute, and the dose is increased in 1–2 µg/kg/minute increments until the desired effect is reached. The major limiting effect of the medication is the tachycardia that it causes; otherwise, there is really no upper limit.

Epinephrine is primarily an alpha agonist but has some beta agonist effect. It is useful for vasoconstriction and increasing cardiac output. It is dosed similar to norepinephrine but causes more tachycardia.

Phenylephrine is an alpha agonist that causes pure arterial constriction. It is useful in cases of low SVR with a high cardiac output associated with systemic inflammatory response syndrome (SIRS), as in sepsis. Care must be taken not to use this medication in cases of hypotension associated with low cardiac output, as this would decrease oxygen delivery even more. Phenylephrine is not a very potent medication, and drips are usually begun at about 50 µg/minute and increased in increments of 50 µg/minute until a total dose of 300 µg/minute is reached, and then a more potent vasoconstrictor is needed.

While there are more pressors available, thorough knowledge of the indications, actions, and side effects of those discussed previously will suffice in most circumstances. Occasionally, patients will be hypertensive and need their blood pressure lowered, or their SVR will be excessively high and need vasodilation. The following medications are the most commonly used vasodilators:

Nitroprusside is primarily an arterial vasodilator. The initial dose of this medication is 0.3 µg/kg/minute, with a maximum dose of 3 µg/kg/minute. Nitroprusside can result in reflex tachycardia, and one of its metabolites is cyanide. If used in large doses for a prolonged period, it can cause cyanide poisoning and acidosis.

Nitroglycerin is primarily a venodilator as well as a coronary artery dilator. It is useful in decreasing venous preload to decrease diastolic wall tension and to allow better contraction of the heart if it has been overstretched. Nitroglycerin will also allow better diastolic blood flow to the heart itself and may lead to an increase in cardiac output. Its dosing is begun at

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5 µg/minute and increased in 5–20 µg/minute increments until the desired effect is obtained.

VIII Shock

A Definition

Shock is the clinical syndrome resulting from inadequate tissue perfusion to maintain normal cellular metabolism. The definition implies that the normal balance between perfusion and cellular needs becomes disrupted, leading to pathophysiologic changes. Most often, inadequate perfusion is related to decreased oxygen delivery to mitochondria but may also be related to the provision of other nutrients or even the removal of toxins or carbon

dioxide from cells.

B Types of shock

Shock can result from derangement in various fundamental physiologic processes related to volume status, cardiac performance, vascular tone, and cellular metabolism. The physiologic presentation differs depending on the cause of the derangement (Table 1-5).

Hypovolemic shock. Inadequate blood volume, or hypovolemia, is the most common type of shock, and hemorrhage is the most common reason for hypovolemia. Loss of plasma volume such as with major burns or third spacing can also result in hypovolemia. The perfusion defect is the result of blood volume loss (decreased preload) leading to decreased cardiac output and oxygen delivery to cells. Furthermore, loss of red cell volume reduces hemoglobin levels and oxygen-carrying capacity, worsening oxygen delivery as well. Although hypotension occurs with

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hypovolemia, the important concept is loss of perfusion, not decreased pressure. The clinical presentation and mortality are dependent on the magnitude and duration of volume loss. As blood volume loss increases, peripheral tissue perfusion is decreased to maintain perfusion to key central organs such as the brain, heart, and liver. This is achieved by peripheral vasoconstriction, but as volume loss continues, eventually inadequate perfusion and decreased oxygen delivery affects all organs, leading to cellular damage despite maximal oxygen extraction from hemoglobin. Increased lactate production occurs as normal aerobic cellular metabolism progresses to less energy efficient (fewer ATP produced) anaerobic metabolism, resulting in cellular damage and death. If allowed to progress untreated or if the initial magnitude of volume loss is large, then multisystem organ failure, and eventually death, occurs.

TABLE 1-5 Types of Shock Based on Hemodynamic Profile Analysis

aMixed venous saturation (SvO2).

bArteriovenous oxygen content difference (CaO2 – CvO2). cOxygen consumption (VO2).

dBlood pressure changes are dependent on percentage of blood volume lost. eThe specific change is dependent on the type of obstructive shock.

Cardiogenic shock. Inadequate perfusion can result from inadequate cardiac performance, leading to decreased cardiac output. Most commonly, this is related to myocardial ischemia, but congestive heart failure and valvular diseases can also cause cardiogenic shock. Blood volume remains normal or increased, but loss of adequate pump function results in decreased perfusion. Similar to hypovolemic shock, cardiogenic shock results in decreased oxygen delivery, peripheral vasoconstriction, hypotension, and multisystem organ failure. However, unlike in hypovolemia, the central venous pressures are increased in cardiogenic shock.

Neurogenic shock. Loss of sympathetic tone leading to peripheral vasodilatation can result in both relative hypovolemia and decreased cardiac performance. This can be a result of vasovagal response, cervicothoracic spinal cord injury, or spinal anesthesia. Hypotension and vasodilatation leading to maldistributive perfusion results in deranged cellular metabolism.

Septic shock. Toxins released by microbes result in profound hyperinflammatory physiologic derangements, including hypovolemia, cardiac dysfunction, and vasodilatation. The complex nature of this form of shock results in progressive maldistributive hypoperfusion associated with hypovolemia due to decreased blood volume and increased vascular space. Cardiac output may be decreased, normal, or increased, depending