Intravenous Lines

Intravenous (IV) lines are routinely established in the superficial veins, such as those on the back of the hand, often before admission to the ICU if the patient is admitted through the emergency department or transferred from the ward. These lines provide an immediate route for fluids, electrolytes, nutrition, and medications. The choice of specific lines to use depends on the patient’s needs based on the history, laboratory tests, clinical and physical examinations, and ongoing evaluation.

Fluid and Electrolyte Balance

When the normal regulation of fluid intake, utilization, and excretion are disrupted, fluid, electrolytes, and acid-base imbalances result. Essentially, all medical and surgical conditions threaten these life-dependent mechanisms to some degree. Minor imbalances may be corrected with modification of the patient’s nutrition and fluid intake. Major imbalances can be life-threatening, necessitating immediate, highly invasive medical intervention.

Imbalances are reflected as excesses, deficits, or as an abnormal distribution of fluids within the body.² Excesses result from increased intake and decreased loss of fluid and electrolytes. Deficits result from abnormal shifts of fluid and electrolytes among the intravascular and extravascular fluid compartments of the body. Excesses can occur with kidney dysfunction, promoting fluid retention, and with respiratory dysfunction, which promotes carbon dioxide retention. Deficits are commonly associated with reduced intake of fluids and nutrition. Diaphoresis and wounds can also contribute to major fluid loss. Diarrhea and vomiting drain the gastrointestinal tract of fluid. Hemorrhage always results in fluid and electrolyte loss. Deficits may be secondary to fluid entrapment and localized edema within the body (third-spacing), making this source of fluid unavailable for regulation of homeostasis.

Moderate to severe fluid imbalance can be reflected in the systemic blood pressure and central (jugular) venous pressure (CVP). Elevated blood pressure can be indicative of fluid overload, but an intravascular fluid deficit of 15% to 25% must develop before blood pressure drops significantly. The jugular vein becomes distended with fluid overload. Normally, the jugular pulse is not visible 2 cm above the sternal angle when the individual rests at a 45-degree angle. If the jugular pulse is noted, this can be a sign of fluid overload.

Fluid replacement is based on a detailed assessment of the patient’s needs. Whole blood is preferred for replacing blood loss. Plasma, albumin, and plasma volume expanders such as Dextran can be used to substitute for blood loss and to help reestablish blood volume. Albumin and substances such as dextran increase plasma volume by increasing the osmotic pressure of the blood, hence the reabsorption of fluid from the interstitial space. Low-molecular-weight dextran has the added advantage of augmenting capillary blood flow by decreasing blood viscosity and is therefore particularly useful in treating shock.

Excesses and deficits of fluids and electrolytes can be determined on the basis of laboratory determinations of serum levels of the specific electrolytes. Electrolyte levels and hematocrit are decreased with fluid excess (hemodilution) and are increased with fluid loss (hemoconcentration).

Excess fluid can be managed by controlled fluid intake, normal diuresis, and diuretic medications. Replacement of fluid and electrolyte losses can be achieved by oral intake, tube feeding, IV infusion, and parenteral hyperalimentation.

Assessment of fluid and electrolyte balance is based on both subjective and objective findings (Table 16-1). At the bedside, the physical therapist must be alert to complaints of headache, thirst, and nausea, as well as changes in dyspnea, skin turgor, and muscle strength. More objective assessment is based on fluid intake, output, and body weight. Fluid balance is so critical to physical well-being and cardiovascular and pulmonary sufficiency that fluid input and output records are routinely maintained at bedside. These records also include fluid volume lost in urine and feces, wound drainage, and fluids aspirated from any body cavity (e.g., abdomen and pleural space).

A patient’s weight may increase by several kilograms before edema is apparent. The dependent areas of the body manifest the first signs of fluid excess. Patients on bed rest show sacral swelling; patients who can sit on the edge of the bed or in a chair for prolonged periods tend to show swelling of the feet and hands.

Decreased skin turgor can indicate fluid deficit. Tenting of the skin over the anterior chest in response to pinching may suggest fluid depletion. Wrinkled, toneless skin is more common in younger patients.

In contemporary ICU care, supplemental nutrition is a priority to maintain fluid and electrolyte balance, minimize weight loss, preserve strength and stamina, and support healing and recovery. Prescribing nutritional supplements for the patient in the ICU is a specialty in the field of nutrition and can take various forms depending on the patient’s needs.

The cardiovascular and pulmonary assessments can reveal changes in fluid balance. Lung sounds are valuable in identifying fluid overload. Vesicular sounds may become more bronchovesicular. Crackles may increase in coarseness. In the presence of fluid retention involving the pleurae, breath sounds diminish to the bases. Dyspnea and orthopnea may also be symptomatic of fluid excess.

An early sign of congestive heart failure (CHF) with underlying fluid overload is an S₃ gallop (Ken-TUCK-y) caused by rapid ventricular filling.

Vigilance by the physical therapist with respect to fluid and electrolyte balance is essential in all areas of practice, not only in the ICU. Fluid imbalance is common in older people and in young children, so it needs to be watched for on the ward, in the home, and in the community.

Chest Tube Drainage and Fluid Collection Systems

Chest tubes are large catheters placed in the pleural cavity to evacuate fluid and air and to drain into a graduated collection reservoir at bedside.² A typical chest tube drainage and collection system is shown in Figure 16-4, A. The removal of thick fluids such as blood and organized exudates by chest tubes is often indicated to prevent entrapment and loculation. Chest tubes are commonly inserted in the sixth intercostal space in the mid- or posterior axillary line. Chest tubes inserted into the pleural space are used to evacuate air or exudate. Chest tubes can also be inserted into the mediastinum to evacuate blood such as after open heart surgery (Figure 16-4, B).

Any collection system is designed to seal the drainage site from the atmosphere and offer minimal resistance to the drainage of fluid and gas. This is accomplished by immersing the end of the collection tube in water. This is referred to as an underwater seal system. Additional reservoirs are included to decrease the resistance to fluid leaving the chest. This resistance is greater in a single-reservoir system in which the reservoir serves as both the collection receptacle and the underwater seal. A third reservoir can be added to the system; it is attached to the suction and serves as a pressure regulator. The more elaborate drainage systems are used for precise measurement of fluid loss in patients after thoracic and cardiovascular surgery.

The amount of exudate collected in the reservoir is measured every several hours or more often if the patient is losing considerable amounts of fluid or less than the amount predicted. This information is incorporated into the overall fluid-balance assessment. In addition, changes in the quantity and quality of exudates should be noted by the physical therapist before, during, and after changes in position and therapeutic interventions. Chest drainage systems should always be upright and below level of tube insertion. Keeping the container lower than chest level facilitates fluid drainage. It also prevents fluids from flowing back into the chest cavity. Continuous bubbling in water-seal bottle/chamber indicates an air leak. Physical therapists mobilizing patients with chest tubes should be alert to sudden severe respiratory distress and/or pain, which can indicate a tension pneumothorax. If a chest tube is accidently dislodged during physical therapy, the site needs to be immediately compressed, and the nurse must be called.

Acid-Base Balance

Control of acid-base balance in the body is achieved by regulation of the hydrogen ion concentration in the body fluids.3,4 The pH of the body is normally maintained within a narrow range of 7.35 to 7.45 or slightly alkaline. When pH of the blood drops below 7.35, a state of acidosis exists; above 7.45, a state of alkalosis exists. Regulation of pH is vital because even slight deviations from the normal range cause marked changes in the rate of cellular chemical reactions. A pH below 6.8 or above 8 is incompatible with life.

Acid-base balance is controlled by several regulatory buffer systems, primarily the carbonic acid-bicarbonate, phosphate, and protein buffer systems. These systems act very quickly to prevent moment-to-moment changes in pH. In compensation, pH is returned to normal by altering the component not primarily affected. If the primary cause is respiratory, the compensating mechanism is metabolic. If the primary cause is metabolic, the compensating mechanism is respiratory. The lungs compensate for metabolic problems over hours, whereas the kidneys compensate for respiratory problems over days (see Chapter 10).

A guide to the clinical presentation of acid-base imbalances is shown in Table 16-2. Along with the major distinguishing characteristics of acid-base imbalance described in this chapter and elsewhere in this volume, potassium excess (hyperkalemia) is associated with both respiratory and metabolic acidosis, and neuromuscular hyperexcitability is associated with both respiratory and metabolic alkalosis.

Blood Gases

Analysis of the composition of arterial and mixed venous blood provides vital information about respiratory, cardiac, and metabolic function (see Chapter 10).^5,6 For this reason, blood gases are usually analyzed in the ICU. In cases in which the patient’s condition is changing for better or worse over a short period of time or when a specific treatment response is of interest, blood gases may be analyzed several times daily. With an arterial line in place, frequent blood gas analysis is feasible and not traumatic for the patient. Should the patient be anemic, however, blood loss associated with repeated arterial blood sampling may mean that it is contraindicated. Thus requests for arterial blood gas analysis need to be particularly stringent in patients who are anemic.

Arterial saturation (SaO₂), the proportion of hemoglobin combined with oxygen, can be readily monitored noninvasively by a pulse oximeter (SpO₂). The earlobe or a finger is warmed by rubbing before the oximeter sensor is attached. Within seconds, the SpO₂ can be read directly from the monitor. Pulse oximetry is a useful adjunct for routine evaluation of the effectiveness of mechanical ventilation, the effect of anesthesia, and the treatment response. Continuous estimation of SaO₂ is particularly useful before, during, and after mobilization and exercise, position changes, and other therapeutic interventions. The SaO₂ may appear to be reduced in patients who are anemic or jaundiced or those who have reduced cardiac output. The SpO₂ reading may be inaccurate in patients with poor peripheral perfusion, who have cold extremities, or who have pigmented skin. The oxygenation of patients in the ICU varies considerably over time and even moment-to-moment, irrespective of sedation, high post end-expiratory pressure, or inverse ventilation.⁷

Mixed venous oxygen saturation () provides a useful index of oxygen delivery and utilization at the tissue level.⁸ is highly correlated to tissue oxygen extraction, and thus is a good index of the adequacy of oxygen delivery. The is particularly useful as a significant warning sign, a guide to myocardial function, and a tool to titrate positive end-expiratory pressure support. The normal value of is 75%. Concern is raised by values of less than 60% or a drop of 10% for several minutes. Excessive values above 80% are also cause for concern. High values may occur in patients with left-to-right shunts in the heart, hyperoxia, hypothermia, cyanide toxicity, sepsis, anesthesia, and drug-induced paralysis. Despite its general clinical usefulness, is a nonspecific indicator of the adequacy of oxygen transport (i.e., of the balance between oxygen supply and demand). Abnormal values do not indicate precisely where the problem lies; so other hemodynamic variables need to be considered. Further, has been reported to fluctuate as much as ±6% in patients in the ICU in response to routine activity and treatment.⁹ Maintaining normal in patients with multiple trauma improves survival rates over those in whom oxygen transport values are maintained at above normal levels.¹⁰ Enhancing cardiac output and hemoglobin as well as is essential to increase oxygen delivery (DO₂) above its critical level and avoid tissue oxygen debt.¹¹ Impaired extraction at the tissue level has been attributed to heterogeneity of oxygen delivery.¹²

ECG Monitoring

A single-channel ECG monitor with an oscilloscope, strip recorder, and digital heart rate display is typically located above the patient at bedside in the ICU (Figure 16-5). Often, the ECG can be observed at bedside and at a central monitoring console, where the ECGs of all patients in the ICU can be observed simultaneously.

The ECG monitor allows for continuous surveillance of heart rate and rhythm regardless of activity. Low and high heart rates are determined; rates below and above those rates will trigger an alarm. For routine monitoring in the coronary care unit, a modified chest lead is often used. Depending on the lead configuration desired, as few as three electrodes can be positioned on the chest to provide optimal information regarding changes in heart rate and rhythm, and thereby ensure close patient monitoring. The positive electrode is positioned at the fourth intercostal space at the right sternal border. The negative electrode is positioned at the first intercostal space in the left midclavicular line. The ground electrode, used to dissipate electrical interference, is often positioned at the first intercostal space in the right midclavicular line, although the ground electrode may be positioned wherever convenient. Other electrode placements may be required, for example, in patients with pacemakers or chest burns.

Problems with the ECG monitor usually result from faulty technique, electrical interference, or movement artifact. A thickened baseline can be caused by 60-cycle electrical interference. An erratic signal often results from coughing and movement. The cause of any irregularity must be explained and abnormal electrical activity of the myocardium ruled out. It is a dangerous practice for the physical therapist to turn off the ECG alarm system during treatment.

Cardiac dysrhythmias can be broadly categorized into tachydysrhythmias and bradydysrhythmias. Tachydysrhythmias are subdivided into supraventricular and subjunctional tachycardias. Bradydysrhythmias are subdivided into sinus bradycardia and those related to heart block and conduction abnormalities. The subjunctional tachycardias and ventricular dysrhythmias are particularly life-threatening. Ventricular tachycardia and ventricular fibrillation are medical emergencies requiring immediate recognition and treatment.

The characteristic features of common dysrhythmias are illustrated in Chapter 12. Physical therapists specializing in ICU management should be thoroughly familiar with ECG interpretation and the implications of the various dysrhythmias on patient management. For further elaboration of ECG application and interpretation, refer to Kinney and Packa¹⁶ and Dubin.¹⁷

The clinical picture associated with cardiac dysrhythmias depends on the nature of the dysrhythmia, the age and condition of the patient, the medications, and specifically, the absence or presence of underlying heart disease. The distinguishing clinical features of common atrial and ventricular dysrhythmias are outlined in Table 16-4.

The subjunctional or ventricular dysrhythmias are typically associated with severe illness. Cyanosis and duskiness of the mucosal linings and periphery may be apparent. The patient is unresponsive, the pulse is ineffective, and spontaneous respirations are likely to be absent. In this case, defibrillation is initiated by the nursing and medical staff to restore an effective, more normal rhythm. The high incidence of myocardial conduction irregularities warrants a defibrillator being present in the ICU for rapid implementation of this common cardioversion procedure by the medical and nursing staff. Ventricular dysrhythmias may be better tolerated if ventricular rate is low, thereby improving cardiac output. Even in this circumstance, however, these dysrhythmias present an emergency.

The ECG of a patient with a pacemaker reflects either an imposed fixed or intermittent rhythm and rate, depending on whether a fixed rate or a demand pacemaker has been inserted. The electrical impulse from the pacemaker has a unique ECG wave form.

Hemodynamic Monitoring

Hemodynamic status reflects the adequacy of blood volume and electromechanical coupling of the myocardium to effect adequate cardiac output and peripheral perfusion commensurate with changing metabolic demand. In individuals who are not critically ill, monitoring fluid input and output, heart rate, and blood pressure may suffice in providing a profile. To monitor a patient’s hemodynamics more closely in the ICU, however, the insertion of various invasive lines may be indicated in addition to the lines and leads needed to monitor basic fluid and electrolyte balance and ECG. These require invasive arterial and venous lines.

Intraarterial Lines

An arterial line is established by direct arterial puncture. It is usually in the radial artery; however, it can be seen in the femoral, axillary, or brachial artery (Figure 16-6, A, B). Blood pressure can be measured directly from this line. A digital monitor displays systolic and diastolic blood pressures above the patient at bedside. High and low blood pressure levels are set, above and below which the alarm will sound. Blood gas analysis can be performed routinely with an intraarterial line in place without repeating the puncture of a blood vessel.

Pulmonary Artery Balloon Flotation Catheter

The pulmonary artery balloon flotation (Swan-Ganz) catheter is designed to provide an accurate and convenient means of hemodynamic assessment in the ICU by monitoring intracardiac pressures and, in combination with other measures, assessing cardiac reserve, an important determinant of outcome following critical illness.¹⁸ The catheter is usually inserted into the internal jugular vein, the subclavian vein, or a large peripheral arm vein and is directed by the flow of blood into the right ventricle and pulmonary artery (see Figure 16-3, A). The catheter is carefully secured to prevent dislodging. Some of the complications that have been associated with pulmonary artery catheterization, however, include infection, venous thrombosis, myocardial irritation, air embolism, and pulmonary ischemia or infarct to segmental lung tissue.¹⁹

Complex catheters are available for monitoring a variety of parameters. In a two-lumen catheter, the first lumen is used to measure pulmonary artery pressure (PAP) and obtain mixed venous blood samples. The second lumen terminates in a balloon with a volume of less than 1 mL, which is inflated and deflated to obtain pulmonary artery occlusion or wedge pressure (PAOP or PAWP, respectively). The normal range of the systolic PAP is 20 to 30 mm Hg, and it normally reflects right ventricular pressure (RVP). The diastolic PAP ranges from 7 to 12 mm Hg and reflects left ventricular pressure in the absence of pulmonary disease. The average range of PAWP is 8 to 12 mm Hg and gives an estimation of mean left atrial pressure (LAP) and the pressure in the left ventricle (LVP). Figure 16-7 shows the normal cardiac pressures in each heart chamber. More elaborate catheters have pacing wires, thermistors for cardiac output determination, and sensors for arterial saturation.

The PAP increases as a result of elevated pulmonary blood flow, increased pulmonary arteriolar resistance secondary to primary pulmonary hypertension or mitral stenosis, and left ventricular failure. Measurement of PAP and PAWP, in particular, allows for more prudent management of heart failure and cardiogenic shock.

The PAP, PAWP, and end-diastolic LVP are directly related. Impaired left ventricular contractility that compromises normal emptying (e.g., left ventricular failure, mitral stenosis, or mitral insufficiency) results in an elevated end-diastolic LVP, which in turn, elevates PAWP and PAP. An end-diastolic PAP greater than 20 mm Hg or a PAWP greater than 12 mm Hg is considered abnormal.

The PAP and PAWP are low during hypotension secondary to hypovolemia. Infusion of normal saline, whole blood, or low-molecular-weight dextran elevates the blood volume and blood pressure. Restoration of blood volume returns end-diastolic PAP and PAWP to normal.

Elevation of the end-diastolic PAP secondary to heart failure with pulmonary edema can typically be reduced with appropriate medication. The effectiveness of a drug and its prescription parameters can be assessed by the observed changes in the end-diastolic PAP.

Deterioration of cardiovascular status and worsening of the clinical signs and symptoms of heart failure elevate end-diastolic PAP and PAWP, decrease cardiac output, decrease arterial and right atrial oxygen tension, and increase the oxygen difference between arterial and venous blood. As the heart pump continues to fail, arterial oxygen tension decreases, suggesting abnormal lung function and probably elevated LAP. Pulmonary dysfunction at this stage includes diffusion abnormalities, redistribution of pulmonary blood flow into the less well-ventilated upper lobes, and right-to-left shunting, which causes deoxygenated blood to bypass well-ventilated regions of the lungs. All patients with acute infarction or shock have reduced arterial oxygen tension. When the failing heart is unable to effectively eject blood through the aorta to the systemic circulation, fluid may back up into the lungs. Pulmonary congestion must be cleared before the patient can appropriately respond to oxygen administration.

Despite the enormous benefits of direct invasive hemodynamic monitoring to patient assessment and management, the benefits of basic hemodynamic assessment are a fundamental part of the cardiovascular and pulmonary assessment, regardless of whether the patient has an invasive line inserted.²⁰ Basic hemodynamic monitoring includes heart rate, ECG, blood pressure, and peripheral tissue perfusion. These are fundamental to the physical therapy assessment of all patients across settings. Even though ECG may not necessarily be monitored by the physical therapist directly in non-ICU settings, knowledge of its status is imperative in order to establish whether an individual is safe to treat and, if so, how treatment should be modified and what precautions should be taken.

Intraaortic Balloon Counterpulsation Device

Intraaortic balloon counterpulsation (Figure 16-8, A) provides mechanical circulatory assistance by using an intraaortic balloon. The balloon is inserted into the femoral artery (see Figure 16-8, B). To maintain proper placement and good circulation, the patient’s leg must be extended. The presence of an intraaortic balloon must be taken into consideration whenever the patient is being treated and positioned. Inflation and deflation of the balloon with helium is correlated with the ECG. The intraaortic balloon is deflated during ventricular systole and assists the emptying of the aorta. Stroke volume is potentiated, afterload is reduced (hence reducing ventricular pressure), and myocardial oxygen delivery enhanced. The balloon is inflated during diastole, thereby restoring arterial pressure and coronary perfusion. Counterpulsation improves cardiac output, reduces evidence of myocardial ischemia, and reduces ST-segment elevation. Intraaortic balloon counterpulsation is commonly used after open-heart surgery and for CHF, medically refractory myocardial ischemia, ventricular septal defects, and left main coronary stenosis in patients who are in shock. The intraaortic balloon pump provides protection for the myocardium in many instances until surgery can be performed. Limb ischemia, the most common complication, occurs in 10% to 15% of patients.

Left ventricular assist devices are used when patients develop cardiogenic shock and are unresponsive to conventional management. These devices take over the pumping action of the left ventricle and decrease myocardial workload and oxygen consumption. These types of assistive devices may have considerable potential in the management of refractory heart failure.

Intracranial Pressure Monitoring

Increased ICP results from neurological insults such as head injury, hypoxic brain damage, aneurysm, hemorrhage, and cerebral tumor. If severe and unrelenting, the pressure may need to be decompressed with surgery; otherwise, brain tissue may be irreversibly damaged, leading to permanent neurological deficits. In the adult, the cranial vault is rigid and noncompliant. Increases in the volume of the cranial contents from tissue edema result in an elevated ICP and decreased cerebral perfusion pressure.

Changes in consciousness are the earliest and most sensitive indicators of increased ICP.²¹ Altered consciousness reflects herniation of the brainstem and compression of the midbrain. Compression of the oculomotor nerve and the pupilloconstrictor fibers results in abnormal pupillary reactions that are associated with brain damage.

The effects of ICP on blood pressure and pulse are variable. Blood pressure may be elevated secondary to elevated ICP and hypoxia of the vasomotor center. A reflex decrease in pulse occurs as blood pressure rises.

Compression of upper motor neuron pathways interrupts the transmission of impulses to lower motor neurons; progressive muscle weakness results. A contralateral weakened hand grasp, for example, may progress to hemiparesis or hemiplegia. The Babinski sign, hyperreflexia, and rigidity are additional motor signs that provide evidence of decreasing motor function as a result of upper motor neuron involvement.

Herniation can produce incoordinate respirations that are correlated with the level of brainstem compression. Cerebrate rigidity results from tentorial herniation of the upper brainstem. This results in the blocking of the motor inhibitory fibers and the familiar extended body posture. Seizures may be present. These neuromuscular changes may further compound existing cardiovascular and pulmonary complications in the patient in the ICU.

Clinically, increased ICP is best detected by altered consciousness, blood pressure, pulse, pupillary responses, movement, temperature, and respiration. The ICP monitor provides direct measurement of ICP. A hollow screw is positioned through the skull into the subarachnoid space. The screw is attached to a Luer-Lok, which is connected to a transducer and oscilloscope for continuous monitoring.

The prevention of further increase in ICP and a corresponding reduction in cerebral perfusion pressure is a treatment priority. High ICP and low cerebral perfusion pressure are highly correlated with brain injury. Measures to reduce venous volume are maintained until ICP has stabilized within normal range. Prudent body positioning is used to enhance venous drainage by elevating the bed 15 to 30 degrees and maintaining the head above heart level. Neck flexion is avoided by the placement of a neck support or sand bags. Fluid intake and output are carefully regulated and monitored; the patient may need to be fluid restricted. Stimulation of the Valsalva maneuver is avoided because intrathoracic pressure and ICP may increase correspondingly.

The normal range of the ICP is 0 to 10 mm Hg for adults and 0 to 5 mm Hg for patients under 6 years of age. The ICP may reach 50 mm Hg in the normal brain; typically, however, this pressure returns to baseline levels instantaneously. In patients with high levels of ICP and low cerebral compliance, extra care must be exercised during routine management and therapy. An ICP up to 30 mm Hg that is elicited by turning or suctioning may be acceptable, provided the pressure drops immediately following removal of the pressure-potentiating stimulus. Patients may be mechanically hyperventilated to keep arterial PCO₂ at low levels, because hypercapnia dilates cerebral vessels and hypocapnia constricts them.

To establish whether a patient will tolerate a treatment that requires movement or body positioning, an indication of cerebral compliance is needed. This can be obtained by observing changes in ICP during routine nursing procedures or by titrating small degrees of movement or position change and observing the rate at which the ICP returns to baseline following the challenge. Rapid return to baseline minimizes the risk for reduced cerebral perfusion pressure secondary to the increased ICP. A slow return to baseline or sustained elevation of ICP is consistent with poor cerebral compliance and indicates that treatment should be modified or possibly not performed at all, depending on the absolute level of the ICP. Physical therapy assessment only may be indicated until compliance improves.

Assessment of Arousal and Brain Activity

Patients in the ICU tend to have low arousal directly or indirectly related to underlying pathology, as well as from induced sedation and antianxiety medications.²² Although medication is often indicated to reduce arousal, a balance must be maintained by the medical staff to avoid under- or oversedating the patient. To benefit maximally from physical therapy and actively participate in treatment, patients need to be as consciously aware as possible. Tools such as the Richmond Agitation-Sedation Scale²³ have been developed to quantify arousal state, which can be helpful in directing the course of treatment.

The Glasgow Coma Scale is a common tool for the clinical assessment and evaluation of the adequacy of basic brain function; it includes review of motor, sensory, pain, arousal, and cognitive status. An electroencephalogram (EEG), provides useful information about gross cerebral functioning and changes in level of consciousness. A single-channel EEG monitor can be readily used in the ICU to reveal evidence of posttraumatic epilepsy when the clinical signs may be inhibited by muscle relaxants. An EEG assessment may be of benefit in assessing arousal, prognosis, the response to treatment of cerebral function, and the planning and prescribing of treatment.

Neuromuscular Assessment

The neuromuscular assessment is a fundamental component of the assessment of the patient in the ICU. The patient may have been admitted for a primary neuromuscular condition with risk for respiratory failure. In addition, all patients in the ICU are at risk for ICU-acquired weakness. ICU-acquired weakness is defined as weakness developing in a patient who is critically ill with no identifiable cause other than nonspecific inflammation.²⁴ It has been associated with the administration of steroids, neuromuscular blockade, hyperglycemia, sepsis, multiple organ failure, bedrest (recumbency), and restricted mobility. The terms critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are commonly used in the ICU. The neuromuscular manifestations of CIP and CIM are difficult to assess in a valid manner. Despite this, their early identification is essential in order to avoid significant weakness, irreversible deterioration, delayed recovery, and prolonged dependence on mechanical ventilation.²⁵ Other causes need to be ruled out. Prognosis is good if ICU-acquired weakness is detected early and rehabilitation is instituted.

Because many patients in the ICU are administered sedatives and muscle relaxants, placing them at increased risk for ICU-acquired weakness, the physical therapist needs to monitor level of arousal and sedation. The use of agitation and sedation scales can be useful in monitoring arousal and the patient’s capacity to cooperate with treatment.23,26 The physical therapist has an important role in minimizing the need for pharmacological sedation by optimizing pain control, relaxation, comfort, and the individual’s perception of control.

Peripheral-nerve electrical stimulation (e.g., of the median nerve) is used to monitor potential neuropathies in a patient in a coma or under neuromuscular blockade. Such stimulation is sufficient to activate the pathways of the ascending reticular activating system associated with consciousness and to hasten awaking from coma.²⁷ In addition, patients score better on repeated assessment with the Glasgow Coma Scale initially and at 1 month after injury, and they have shorter ICU stays.

There is no specific treatment for ICU-acquired weakness. It is prudent to consider reducing patients’ exposure to the risk factors. Recent studies have demonstrated that the most promising management of ICU-acquired weakness is physical therapy, even while the patient is receiving life-and-organ support interventions.28,29

Cognitive Assessment

The ICU experience can contribute to cognitive impairment or worsen it in patients who are already impaired.30,31 These effects can extend for several months beyond the ICU stay.³² Risk factors include functional dependence and low body mass, as well as previous cognitive impairment.³³ Preexisting cognitive impairment must be identified and changes in cognition should be monitored so they can be detected early. Strategies can be implemented to avoid cognitive impairment, including frequent orientation of the patient to time and place, surrounding the individual with familiar objects and family and friends, using familiar tape recordings (voices or music), taking time to talk to the patient, and being reassuring. Further, strategies to reduce anxiety, stress, restlessness, and negative mood states can reduce the duration of hospitalization in patients in the ICU.³⁴

Acute distress disorder comparable to traumatic stress syndrome has been described recently in individuals after accidental injuries. In addition to the nature of the accident itself and the associated threat to life, factors contributing to an individual’s overall stress include hospitalization, length of the ICU stay, the ICU experience, and pain management.35,36 Thus optimizing the patient’s perception of care is important in preventing and offsetting symptoms of acute distress.

With improvement in the management of acute respiratory distress syndrome (ARDS), long-term studies have examined the relationship between cognitive performance, employability, and return to work in survivors. These patients may exhibit long-term cognitive deficits and impaired health status, which contribute to disability and marked reduction in health-related quality of life.³⁷ An understanding of these potential consequences will help their prevention and the comprehensive management of ARDS.

Pain Assessment

Pain has been described as one of the vital signs. Assessing pain in the ICU is particularly challenging, given that patients cannot readily communicate their discomfort and pain. Physical therapists need to monitor discomfort and pain as part of the ongoing assessment to ensure not only that the patient is comfortable but also that therapeutic interventions do not contribute to compromised oxygen transport by increasing distress and that they do not interfere with sleep and recovery. Further, noninvasive interventions should be used as much as possible to reduce the necessity of pharmacological agents that can compromise the patient’s capacity to cooperate with treatment. Optimal management can be achieved only with accurate assessment and ongoing evaluation as the basis for progressing treatment. Pain assessment tools include the McGill Pain Questionnaire, a pain analog scale, the Wong-Baker FACES pain scale, and others.³⁸ The therapist should choose the format to which the patient can most readily respond.

Long-Term Outcomes Related to ICU Care

The study of outcomes of patients who have experienced ICU stays has become a focus of research. In previous decades, if a patient survived the ICU stay, this was viewed as the primary outcome. These days, most patients survive the ICU; however, outcomes related to their return to a full and active life may be less favorable.³⁹ Focusing on long-term outcomes can be integrated into the physical therapy care in the ICU. This includes assessment and evaluation of some aspects of functional status, as well as a premorbid evaluation based on the patient’s self-report, if possible, or that of family members. In addition, the practice of physical therapy needs to extend from the ICU to the ward and then to the home, with judicious follow up after the patient has returned to the community. Depending on the age of the patient, the reason for ICU admission, and comorbidity, return to a maximal level of functioning could take a year or more.

Summary

The capacity of patients in the ICU to participate in life and perform the requisite activities is severely compromised because of life-threatening illness or injury (i.e., involving the oxygen transport system). The immediate goal of the ICU is to provide intense life-preserving, specialized care with the view of ultimately returning the individual to a healthy and productive life. Monitoring cardiovascular and pulmonary functions and oxygen transport is an essential component of management. Regulation of homeostasis is disrupted in disease or following highly invasive medical and surgical interventions. Physical therapists practicing in the ICU need to have a thorough understanding of homeostatic regulation and the monitoring of fluid and electrolyte balance, acid-base balance, and blood gases. Physical therapy has an essential role in restoring homeostasis in patients requiring intensive care by using conservative, noninvasive approaches, in addition to averting the musculoskeletal, neuromuscular, and multisystem complications associated with recumbency and restricted mobility. The selection of treatment and the assessment of treatment response are based on quantitative evaluation of the parameters affecting oxygen transport and cardiovascular and pulmonary functions, as well as the patient’s subjective sense of well-being. Detailed monitoring is necessary to provide well reasoned and informed management of the patient in the ICU, as well as to prevent deterioration and detect complications early. In the ICU, where a patient’s status may change from moment to moment, the information gathered from monitoring is essential to maximize physical therapy effectiveness and minimize deleterious effects. This information is critical in establishing the indications for physical therapy, prescribing treatment parameters, and determining when to progress, withhold, or discontinue treatment. The windows of opportunity for intervention are often narrow, so the physical therapist must be able to identify these expeditiously on the basis of frequent serial assessment and to intervene appropriately.

Further, psychosocial assessment is fundamental to eliciting the most favorable outcomes. Other anticipated outcomes include reduced requirement for invasive care (i.e., drugs and surgery) and shorter length of stay in the ICU and in hospital afterwards. Physical therapists have a major role in employing noninvasive, ethical interventions in the ICU and in helping to minimize the costs of this expensive, high-tech, labor-intense area of care. Databases and longitudinal studies of the profiles and long-term outcomes of patients following various critical illnesses after return to the community are needed. Such prognostic information would help to refine the assessment of patients by physical therapists, as well as the short- and long-term management of patients in the ICU. Finally, the physical therapist has a primary role in ensuring that the patient has returned as fully as possible to life in the community in the following months after discharge. ICU outcomes have now extended from merely surviving an ICU stay to thriving afterwards—even if this outcome takes a year or more to achieve.