Monitoring Systems, Catheters, and Devices in the Intensive Care Unit

Elizabeth Dean and Christiane Perme

The primary goal of the intensive care unit (ICU) team is to achieve hemodynamic stability and optimal oxygen transport for each patient who is critically ill, keeping a view toward the patient’s eventual return to maximal functional participation in life and activity. This chapter introduces monitoring systems used in the evaluation of cardiovascular and pulmonary status in patients in the ICU and describes some related elements of cardiovascular and pulmonary regulation and control that are relevant to the assessment of risk and oxygen transport status, and to physical therapy intervention.

ICUs are highly specialized. Medical advances now preserve lives that would have been lost in the past. Patients admitted to the ICU require intense and often invasive yet life-preserving medical management. ICUs can be categorized as either general or specific. In major hospital centers, units are often designed and staffed for the exclusive management of specific types of conditions such as medical, surgical, trauma, burns, coronary care, and neonatal care. Although monitoring priorities may differ among specialized ICUs, the principles are similar and relate either directly or indirectly to the foremost goal of preserving life by maximizing oxygen transport and minimizing threat to it and by preventing the risks associated with recumbency and restricted mobility. In recent years, attention has focused on long-term outcomes of people who have had ICU stays—that is, the emphasis is on patients thriving after, rather than simply surviving, a course of ICU care.

The cardiovascular and pulmonary status of the patient in the ICU is often jeopardized by fluid and electrolyte disturbances and acid-base imbalance. This chapter describes the regulation of these systems and the clinical implications of imbalance relevant to the physical therapist. The principal monitoring systems used in assessing cardiovascular and pulmonary sufficiency in the ICU are highlighted. These include the electrocardiogram (ECG), arterial and venous lines, intracardiac monitoring, and the intracranial pressure (ICP) monitor. Although not monitoring systems per se, ventricular-assist devices (e.g., the intraaortic counterpulsation technique) are used to augment myocardial efficiency. These warrant special attention by the physical therapist with respect to determining the patient’s readiness for treatment, establishing treatment parameters, and assessing safety.

Familiarity with the extensive monitoring facilities in the ICU relieves some of the apprehensions the physical therapist may have about practicing in this setting. Such monitoring is central to the standard of physical therapy care in the ICU to guide progressive mobilization and management overall.¹ On introduction to the unit, the physical therapist is immediately struck by the high-tech environment. Quality care in this setting depends on harnessing the potential of high-tech monitoring equipment to optimize assessment, evaluate treatment parameters, and establish anticipated and actual effectiveness of intervention, as well as to reduce untoward risk for the patient.

Figure 16-1 illustrates a general view of a typical ICU. A view of a patient’s bedside area in the ICU shows life-support equipment and the various lines and catheters that are in place (Figure 16-2). A closer view of the patient demonstrates precisely where the various lines and catheters are positioned and identifies where caution must be observed. Treatments are modified according to the types and positions of the lines and catheters for each patient (Figure 16-3).

Fig. 16-1 General view of an intensive care unit.

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).

Table 16-1

Assessment of Fluid and Electrolyte Imbalance

Area	Fluid Excess/Electrolyte Imbalance	Fluid Loss/Electrolyte Imbalance
Head and neck	Distended neck veins, facial edema	Thirst, dry mucous membranes
Extremities	Dependent edema “pitting,” discomfort from weight of bed covers	Muscle weakness, tingling, tetany
Skin	Warm, moist, taut, cool feeling when edematous	Dry, decreased turgor
Respiration	Dyspnea, orthopnea, productive cough, moist breath sounds	Changes in rate and depth of breathing
Circulation	Hypertension, jugular pulse visible at 45-degree sitting angle, atrial dysrhythmias	Pulse rate irregularities, dysrhythmia, postural hypotension, sinus tachycardia
Abdomen	Increased girth, fluid wave	Abdominal cramps

Modified from Phipps WJ, Long BC, Woods NF, editors: Medical-surgical nursing: Concepts and clinical practice, ed 6, Philadelphia, 1999, Elsevier.

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).

Fig. 16-4 A, Chest tube drainage. B, Anterior view; mediastinal drains.

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.

Table 16-2

Signs and Symptoms of Common Acid-Base Disturbances

	Respiratory Disturbances	Metabolic Disturbances
Acidosis	Hypercapnia Hypoventilation Headache Visual disturbances Confusion Drowsiness Coma Hyperkalemia Ventricular fibrillation (secondary to hyperkalemia) Depressed tendon reflexes	Bicarbonate deficit Hyperventilation Headache Mental dullness Deep respirations Stupor Coma Hyperkalemia Cardiac dysrhythmias (secondary to hyperkalemia)
Alkalosis	Hypocapnia Lightheadedness Numbness/tingling of digits Tetany Convulsions Hypokalemia Cardiac dysrhythmias (secondary to hypokalemia)	Bicarbonate excess Depressed respirations Mental confusion Dizziness Numbness/tingling of digits Muscle twitching Tetany Convulsions Hypokalemia Cardiac dysrhythmias (secondary to hypokalemia)

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