Hemodynamic Terminology Cardiac Output and Cardiac Index Cardiac output is the volume of blood in liters pumped by the

heart in 1 minute. Cardiac index is the measurement of the CO adjusted for body surface area (BSA). It is a more precise measurement of the efficiency of the pumping action of the heart. Although minor beat-to-beat changes may occur, generally the left and right ventricles pump the same volume. The volume ejected with each heartbeat is the stroke volume. Like CI, stroke volume index is the measurement of SV adjusted for BSA. CO and the forces opposing blood flow determine BP. Systemic vascular resistance (SVR) (opposition encountered by the left ventricle) or pulmonary vascular resistance (PVR) (opposition encountered by the right ventricle) is the resistance to blood flow offered by the vessels. Preload, afterload, and contractility (see Chapter 32) determine SV (and thus CO and BP). It is essential that you understand these concepts and relationships. In addition, you must understand the effects of manipulation of each of these variables. Table 66-1 presents the formulas and normal values for common hemodynamic parameters. Preload Preload is the volume within the ventricle at the end of diastole. Unfortunately, chamber volume measurements are difficult to obtain. Instead, various pressures are used to estimate volume. Left ventricular preload is called left ventricular end-diastolic pressure. PAWP, a measurement of pulmonary capillary pressure, reflects left ventricular end-diastolic pressure under normal conditions (i.e., when there is no mitral valve dysfunction, intracardiac defect, or dysrhythmia). CVP, measured in the right atrium or in the vena cava close to the heart, is the right ventricular preload or right ventricular end-diastolic pressure when there is no tricuspid valve dysfunction, intracardiac defect, or dysrhythmia. Frank-Starling's law explains the effects of preload and states that the more a myocardial fiber is stretched during filling, the more it shortens during systole and the greater the force of the contraction. As preload increases, force generated in the subsequent contraction increases, thus SV and CO increase. The greater the preload, the greater the myocardial stretch and the greater the O2 requirement of the myocardium. Hence, increases in CO via increased preload require increased delivery of O2 to the myocardium. Remember that the change in SV with preload comes about because of stretching and recoil of the heart muscle. However, the clinical measurement made is not a direct measurement of the muscle length. The measurement made is of the pressure at the time of the peak stretch (end diastole) (see Table 66-1).

This pressure indirectly indicates the amount of stretch and the volume. This pressure is also important because it indicates pressure in the blood vessels of the lung or in the blood returning to the heart. Diuresis and vasodilation decrease preload and fluid administration increases preload. Afterload Afterload refers to the forces opposing ventricular ejection. These forces include systemic arterial pressure, the resistance offered by the aortic valve, and the mass and density of the blood to be moved. Clinically, although the measures fail to include all the components of afterload, SVR and arterial pressure are indices of left ventricular afterload. Similarly, PVR and pulmonary arterial pressure are indices of right ventricular afterload. Increased afterload often results in a decreased CO. CO can be restored and myocardial O2 needs reduced by decreasing afterload (i.e., decreasing forces opposing contraction). Vasodilator drug therapy (e.g., milrinone [Primacor]) can reduce afterload.Vascular Resistance Systemic vascular resistance is the resistance of the systemic vascular bed. Pulmonary vascular resistance is the resistance of the pulmonary vascular bed. Both of these measures reflect afterload as described earlier and can be adjusted for body size (see Table 66-1). Contractility Contractility describes the strength of contraction. Contractility is said to increase when preload is unchanged yet the heart contracts more forcefully. Epinephrine, norepinephrine [Levophed], isoproterenol (Isuprel), dopamine (Intropin), dobutamine (Dobutrex), digitalis-like drugs, calcium, and milrinone increase or improve contractility. These agents are termed positive inotropes. Contractility is reduced by negative inotropes. Examples include certain drugs (e.g., alcohol, calcium channel blockers, -adrenergic blockers) and clinical conditions (e.g., acidosis). Increased contractility results in increased SV and increased myocardial O2 requirements. There are no direct clinical measures of cardiac contractility. Measuring the patient's preload (PAWP) and CO and graphing the results assesses contractility indirectly. If preload, heart rate, and afterload remain constant yet CO changes, contractility is changed. Contractility is reduced in the failing heart.

Principles of Invasive Pressure Monitoring Invasive lines are used in the ICU to measure systemic and pulmonary BPs. Figure 663 shows the components of a typical invasive arterial BP monitoring system. The catheter, pressure tubing, flush system, and transducer are disposable. Pressure monitoring equipment is referenced and zero balanced to the environment and dynamic response characteristics optimized for accuracy. Referencing means positioning the transducer so that the zero reference point is at the level of the atria of the heart. The stopcock nearest the transducer is usually the zero reference for the transducer. To place this level with the atria, you use an external landmark, the phlebostatic axis. To identify the phlebostatic axis, you draw two imaginary lines with the patient supine (Fig. 66-4, A). Draw the first line, a horizontal line, through the midchest, halfway between the outermost anterior and posterior surfaces. Draw the second line, a vertical line, through the fourth intercostal space at the sternum. The phlebostatic axis is the intersection of the two imaginary lines. Once you identify the phlebostatic axis, mark it on the patient's chest with a permanent marker. Position the port of the stopcock nearest the transducer level with the phlebostatic axis. Tape the transducer to the patient's chest at the phlebostatic axis or mount it on a bedside pole. Zeroing confirms that when pressure within the system is zero, the monitor reads zero. To do this, open the reference stopcock to room air (off to the patient) and observe the monitor for a reading of zero. This allows the monitor to use the atmospheric pressure as a reference for zero. Zero the transducer during the initial setup, immediately after insertion of the arterial line when the transducer has been disconnected from the pressure cable or the pressure cable has been disconnected from the monitor, and when the accuracy of the measurements is questioned. Always follow the manufacturer's guidelines. Optimizing dynamic response characteristics involves checking that the equipment reproduces, without distortion, a signal that changes rapidly. Perform a dynamic response test (square wave test) every 8 to 12 hours and when the system is opened to air or the accuracy of the measurements is questioned. It involves activating the fast flush and checking that the equipment reproduces a distortion-free signal (Fig. 66-5). Table 66-2 outlines the steps in obtaining BP measurements with an invasive line. Obtain measurements from both digital and printed analog outputs. Readings from a printed pressure tracing at the end of expiration (to limit the effect of the respiratory cycle on arterial BP) are most accurate.25 Position the patient supine for initial readings. Unless the patient's BP is extremely sensitive to orthostatic changes, values with head-of-bed elevation (up to 45 degrees) are generally equal to measurements

with the patient supine. Most studies do not support the accuracy of readings for patients in the lateral position but do support the accuracy of readings for patients in the prone position.26 It is not necessary to reposition the patient for each pressure reading. However, it is necessary to move the zero reference stopcock to keep it positioned at the phlebostatic axis Arterial Blood Pressure Continuous arterial BP monitoring is indicated for patients in many situations, including acute hypertension and hypotension, respiratory failure, shock, neurologic injury, coronary interventional procedures, continuous infusion of vasoactive drugs (e.g., sodium nitroprusside [Nipride]), and frequent arterial blood gas (ABG) sampling. A 20-gauge, 2-inch (5.1-cm) nontapered Teflon catheter is typically used to cannulate a peripheral artery (e.g., radial, femoral) using a percutaneous approach. After insertion, the catheter is usually sutured in place.25 You must immobilize the insertion site to prevent dislodging or kinking the catheter line. Measurements Use the arterial line to obtain systolic, diastolic, and mean BPs (Fig. 66-6). The highand low-pressure alarms are set based on the patient's current status and activated. Various patient conditions will alter the pressure tracings. In heart failure, the systolic upstroke may be slower. In volume depletion, systolic pressure varies greatly with mechanical ventilation, decreasing during inspiration. Observe simultaneous ECG and pressure tracings with dysrhythmias. Dysrhythmias that significantly diminish arterial BP are more urgent than those that cause only a slight decrease in systolic amplitude. Complications Arterial lines carry the risk of hemorrhage, infection, thrombus formation, neurovascular impairment, and loss of limb. Hemorrhage is most likely to occur when the catheter dislodges or the line disconnects. To avoid this serious complication, use Luer-Lok connections, always check the arterial waveform, and activate alarms. If the pressure in the line falls (e.g., when the line is disconnected), the low-pressure alarm sounds immediately, allowing you to promptly correct the problem. Infection is a risk with any invasive line. To limit the risk of contamination and catheter-related infection, inspect the insertion site for local signs of inflammation and monitor the patient for signs of systemic infection. Change the pressure tubing, flush bag, and transducer every 96 hours. When infection is suspected, remove the catheter and replace the equipment.

Circulatory impairment can result from formation of a thrombus around the catheter, release of an embolus, spasm, or occlusion of the circulation by the catheter. Before inserting a line into the radial artery, perform an Allen test to confirm that ulnar circulation to the hand is adequate. In this test, apply pressure to the radial and ulnar arteries simultaneously. Ask the patient to open and close the hand repeatedly. The hand should blanch. Release the pressure on the ulnar artery while maintaining pressure on the radial artery. If pinkness fails to return within 6 seconds, the ulnar artery is inadequate and you should not use the radial artery for line insertion. To maintain line patency and limit thrombus formation, assess the continuous flush system every 1 to 4 hours to determine that the (1) pressure bag is inflated to 300 mm Hg, (2) flush bag contains fluid, and (3) system is delivering 3 to 6 mL per hour. Due to the risk of heparin-induced thrombocytopenia, heparinized saline should not be routinely used for the flush solution.26 Once the catheter is inserted, evaluate the neurovascular status distal to the arterial insertion site hourly. The limb with compromised arterial flow will be cool and pale, with capillary refill time longer than 3 seconds. There may be symptoms of neurologic impairment (e.g., paresthesia, pain, paralysis). Neurovascular impairment can result in loss of a limb and is an emergency. Pulmonary Artery Flow-Directed Catheter Pulmonary artery (PA) pressure monitoring guides the acute-phase management of patients with complicated cardiac, pulmonary, and intravascular volume problems (Table 66-3). PA diastolic (PAD) pressure and PAWP are sensitive indicators of cardiac function and fluid volume status. PAD pressure and PAWP increase in heart failure and fluid volume overload. They decrease with volume depletion. Fluid therapy based on PA pressure can restore fluid balance while avoiding overcorrection or undercorrection of the problem. Monitoring PA pressures permits precise therapeutic manipulation of preload. This allows CO to be maintained without placing the patient at risk for pulmonary edema.A PA flow-directed catheter (e.g., Swan-Ganz) is used to measure PA pressures, including PAWP. The standard PA catheter is number 7.5 Fr, 43 inches (110 cm) long, with four or five lumens (Fig. 66-7). When properly positioned, the distal lumen port (catheter tip) is within the PA. This port is used to monitor PA pressures and sample mixed venous blood specimens (e.g., to evaluate O2 saturation). A balloon connected to an external valve surrounds the distal lumen port. Balloon inflation has two purposes: (1) to allow moving blood to float the catheter forward and (2) to allow PAWP measurement. There will be one or two proximal lumens, with exit ports in the right atrium or right atrium and right ventricle (if two). The right atrium port is used for measurement of CVP, injection of fluid for CO

determination, and withdrawal of blood specimens. If a second proximal port is available, it is used for infusion of fluids and drugs or blood sampling. A thermistor (temperature sensor) is located near the distal tip and is wired to an external connector. This is used to monitor blood or core temperature and for the thermodilution method of measuring CO. In addition to these standard features, PA catheters with specialized features are available. One modification is the inclusion of an atrial electrode, useful in recording the atrial ECG or pacing the heart. Another common modification is inclusion of a fiberoptic sensor in the distal tip that detects mixed venous O2 saturation. Another type of PA catheter provides continuous measurement of right ventricular volume and EF, and some catheters provide continuous CO monitoring. The PA catheter sheath (introducer) usually has a side port that serves as a large-bore IV line. Most catheters have a plastic sleeve connected to the sheath. This allows the catheter to be advanced or pulled back while maintaining sterility. The physician or other qualified health care provider (e.g., ACNP) usually manipulates the PA catheter, but this practice varies by institution. Pulmonary Artery Catheter Insertion Before PA catheter insertion, note the patient's electrolyte, acid-base, oxygenation, and coagulation status. Imbalances such as hypokalemia, hypomagnesemia, hypoxemia, or acidosis can make the heart more irritable and increase the risk of ventricular dysrhythmia during catheter insertion. Coagulopathy increases the risk of hemorrhage. Preparation for the procedure includes arranging the monitor, cables, and infusion and pressurized flush solutions. The system is zero referenced to the phlebostatic axis. The physician or other health care provider explains the procedure to the patient and obtains informed consent. The patient is positioned supine and flat. The PA catheter is inserted through a sheath percutaneously into the internal jugular, subclavian, antecubital, or femoral vein using surgical asepsis. Venous cut-down is rarely required. The catheter is advanced through the venous system to the right side of the heart. Continuously observe the characteristic waveforms on the monitor as the catheter is moved through the heart to the PA (Fig. 66-8). When the tip reaches the right atrium, the balloon is inflated. Inflation of the balloon should not exceed the balloon's capacity (usually 1 to 1.5 mL of air). The catheter is then floated through the tricuspid valve into the right ventricle and then through the pulmonic valve to the PA. It is necessary to monitor the ECG continuously during insertion because of the risk for dysrhythmias, particularly when the catheter reaches the right ventricle. Once a typical PAWP tracing is observed, the balloon is deflated, and the PA waveform should return on the monitor. Following insertion, a chest x-ray confirms the catheter's position. To

maintain the catheter in its proper position, it is secured at the point of entry into the skin. Note and record the measurement at the exit point. Finally, apply an occlusive dressing, and then change it according to institution policy. Pulmonary Artery Pressure Measurements Systolic, diastolic, and mean PA pressures are routinely monitored. PA systolic is the peak pressure and PA diastolic is the lowest pressure point on the PA waveform. Mean PA pressure is the time-weighted average. Because PA ports are in the chest, intrathoracic pressures alter PA pressure. For accurate data, obtain PA measurements at the end of expiration. Measure PAWP by slowly inflating the balloon with air (not to exceed balloon capacity) until the PA waveform changes to a PAWP waveform (Fig. 66-9). Before inflation the PA pressure tracing on the monitor looks similar to an arterial tracing. There is a distinct systolic peak, dicrotic notch, and a diastolic low point. As the waveform becomes wedged, the tracing changes shape and amplitude. Generally, the PAWP waveform is characterized by two small positive waves, the a and v waves. The a wave indicates atrial contraction. It is followed by the x descent, indicating atrial relaxation. At times, a c wave may be seen following the a wave and indicates closure of the mitral valve. The v wave is seen during the interval between the T and P waves of the ECG. The v wave indicates inflow into the left atrium when the mitral valve is closed and the ventricle is contracting. The y descent follows the v wave and indicates the emptying of the left atrium when the mitral valve opens and the ventricle fills. When measuring the PAWP, do not inflate the balloon for more than four respiratory cycles or 8 to 15 seconds. There is danger of rupture of the PA if the catheter moves distally into a smaller vessel or if the balloon is overinflated. This is suspected when the waveform looks wedged spontaneously, when less than 1 mL is needed to wedge the tracing, or an overwedge tracing is obtained (Fig. 66-10). When obtaining readings from an analog strip pressure recording, place the strip in the patient's record. If a printout of the tracing is not available, you can take readings from the monitor. Central Venous or Right Atrial Pressure Measurement CVP is a measurement of right ventricular preload. It is measured with a PA catheter using the proximal lumen located in the right atrium. It is also measured with a central venous catheter placed in the internal jugular or subclavian vein. CVP is measured as a mean pressure at the end of expiration. CVP waveforms (Fig. 66-11) are similar to PAWP waveforms. Although the PA diastolic pressure and PAWP are more sensitive indicators of fluid volume status, CVP also reflects fluid volume problems. An

elevated CVP indicates right ventricular failure or volume overload. A low CVP indicates hypovolemia. Invasive Cardiac Output Measurement Techniques CO is frequently monitored in patients with hemodynamic instability. Normal resting CO is 4 to 8 L per minute. CI accounts for variations in body size and is normally 2.2 to 4 L/min/m2. CO and CI are decreased in conditions such as shock states (e.g., cardiogenic, hypovolemic) and heart failure. Under normal conditions, CO increases with exercise. Increases in CO at rest indicate a hyperdynamic state often seen with fever or early sepsis. The PA catheter is used to measure CO via the intermittent bolus thermodilution CO (TDCO) method or the continuous CO (CCO) method. With the TDCO method, a fixed volume (5 to 10 mL) of room temperature (64.4 to 77 F [18 to 25 C]) or cold (32 to 53.6 F [0 to 12 C]) solution of normal saline or 5% dextrose in water is injected rapidly (less than or equal to 4 seconds) and smoothly into the proximal lumen port of the PA catheter.26 The thermistor sensor detects the differences in blood temperature. The computer calculates the CO from the area under the temperature curve. The larger the area under the curve, the lower the CO, and, conversely, the smaller the area under the curve, the higher the CO (Fig. 66-12). Repeat this procedure three times, with each measurement 1 to 2 minutes apart. Discard any CO measurement that does not have a normal curve. The average of three acceptable measurements (within 0.5 L of each other) is used to determine the CO. The CCO method uses a heat-exchange CO catheter. This PA catheter contains a thermal filament that is located in the right atrium. This filament emits a pulsed signal every 30 to 60 seconds that allows for the mixing of blood with heat as it passes through the right ventricle. The thermistor sensor detects the change in temperature. A bedside computer displays digital measurements every 30 to 60 seconds that reflect the average CO for the past 3 to 6 minutes. The CCO method eliminates the need for fluid boluses, reduces the risk of contamination, and permits ongoing evaluation (or trending) of the CO. Comparisons of the TDCO method with the CCO method have shown the CCO method to be reliable.26 SVR, SVR index (SVRI), SV, and SVI can be calculated each time that CO is measured. Table 66-1 presents the formulas for calculating these parameters. Increased SVR (more than 1200 dynes/sec/cm5) indicates vasoconstriction from shock, hypertension, increased release or administration of epinephrine and other vasoactive agents, or left ventricular failure. A low SVR (less than 800 dynes/sec/cm5) indicates

vasodilation, which may occur in shock states (e.g., septic, neurogenic) or with drugs that reduce afterload. In clinical practice, changes in SV are becoming more important indicators of the pumping status of the heart than other parameters. A high SV is seen with bradycardia and exercise, and with the use of positive inotropes (e.g., dopamine). Low SV is seen with tachydysrhythmias, extreme vasodilation, and cardiac tamponade. Complications with PA Catheters Infection and sepsis are serious problems associated with PA catheters. Careful surgical asepsis for insertion and maintenance of the catheter and attached tubing is essential to prevent infection. Cleanse the skin according to institution policy, usually with a chlorhexidine preparation. Cover the insertion site with a sterile occlusive dressing. Monitor the patient for local and systemic signs of infection (e.g., redness and exudate at the insertion site, fever, increased white blood cell count). The PA catheter must be removed if there are any signs of infection. To reduce the risk of infection, change the flush bag, pressure tubing, transducer, and stopcock every 96 hours, and remove the PA catheter once hemodynamic monitoring is no longer needed. Air embolus is another risk associated with PA catheters. Always check the catheter for balloon integrity before insertion and discard any defective catheters. After insertion, balloon rupture or injection of air into any of the lumens, including the lumen of a ruptured balloon, can cause an air embolus. You can decrease the risk of air embolus by first aspirating to check for the absence or presence of blood and by injecting only the prescribed volume of air into the balloon before obtaining the PAWP. If you aspirate blood from the balloon port or observe that injected air does not passively flow back into the syringe, label the catheter (e.g., do not use) and notify the physician. Air can also be introduced into the system if connections are not tight. Always use Luer-Lok connections on all pressure lines. In addition, activate the lowpressure alarm for all pressure lines to signal any substantial drop in the pressure. The patient with a PA catheter is at risk for pulmonary infarction or PA rupture from the following causes: (1) the balloon may rupture, releasing air and fragments that could embolize; (2) prolonged balloon inflation may obstruct blood flow; (3) the catheter may advance into a wedge position, obstructing blood flow; and (4) a thrombus could form and embolize. To reduce these risks, never inflate the balloon beyond the balloon's capacity (usually 1 to 1.5 mL of air). Monitor PA pressure waveforms continuously for evidence of catheter occlusion, dislocation, or spontaneous wedging. The pressure tracing will be blunted if the catheter starts to be occluded. The pressure tracing will appear wedged if the PA catheter advances and becomes spontaneously wedged. In each of these cases, the physician or other qualified health care provider must reposition the catheter immediately. To reduce the risk of

thrombus and embolus formation, the PA catheter is continuously flushed with a slow infusion of normal saline solution (similar to an arterial line) to prevent thrombus formation. Ventricular dysrhythmias can occur during PA catheter insertion or removal or if the tip moves from the PA to the right ventricle and irritates the ventricular wall. In this case, you will note that the PA catheter cannot be wedged. It will need to be repositioned by a physician or other qualified health care provider. Following this, an x-ray is used to confirm the catheter location. Nursing Management Hemodynamic Monitoring Assessment of hemodynamic status requires integration of data from many sources and trending these data over time. Thorough, basic nursing observations provide important clues about the patient's hemodynamic status. Begin by obtaining baseline data regarding the patient's general appearance, level of consciousness, skin color and temperature, vital signs, peripheral pulses, capillary refill, and urine output. Does the patient appear tired, weak, exhausted? There may be too little cardiac reserve to sustain even minimum activity. Pallor, cool skin, and diminished pulses may indicate decreased CO. Changes in mental clarity may reflect problems with cerebral perfusion or oxygenation. Monitoring urine output reflects the adequacy of perfusion to the kidneys. The patient with diminished perfusion to the GI tract may develop hypoactive or absent bowel sounds. If the patient is bleeding and developing shock, BP might initially be relatively stable, yet the patient may become increasingly pale and cool from peripheral vasoconstriction. Conversely, the patient experiencing septic shock may remain warm and pink yet develops tachycardia and BP instability. Elevated heart rates are common in stressed, compromised, critically ill patients. However, sustained tachycardia increases myocardial O2 demand and can result in decreased CO. Always correlate observational data with data obtained from biotechnology (e.g., ECG, arterial and PA pressures, SvO2/ScvO2). Single hemodynamic values are rarely helpful. You must monitor trends in these values and evaluate the whole clinical picture with the goals of recognizing early clues and intervening before problems escalate.

Mechanical Ventilation Mechanical ventilation is the process by which the FIO2 is at 21% (room air) or greater and is moved in and out of the lungs by a mechanical ventilator. Mechanical ventilation is not curative. It is a means of supporting patients until they recover the ability to breathe independently. It can also serve as a bridge to long-term mechanical ventilation, or until a decision is made to withdraw ventilatory support. Indications for mechanical ventilation include (1) apnea or impending inability to breathe, (2) acute respiratory failure (see Chapter 68), (3) severe hypoxia, and (4) respiratory muscle fatique.44,45 Patients with chronic pulmonary disease and their caregivers should be given the opportunity to discuss the issue of mechanical ventilation before terminal respiratory disease develops. All patients, particularly those with grave or chronic illnesses, should be encouraged to discuss the subject with their families and health care providers and place the results of that discussion in an advance directive. The decision to use, withhold, or withdraw mechanical ventilation must be made carefully, respecting the wishes of the patient and caregiver. When there is disagreement among the health care team, the patient, and/or the caregiver over the plan of care, consult the institution's ethics committee for assistance. Types of Mechanical Ventilation The two major types of mechanical ventilation are negative pressure and positive pressure ventilation. Negative Pressure Ventilation Negative pressure ventilation involves the use of chambers that encase the chest or body and surround it with intermittent subatmospheric or negativ e pressure. The iron lung was the first form of negative pressure ventilation that developed during the polio epidemic. Intermittent negative pressure around the chest wall causes the chest to be pulled outward. This reduces intrathoracic pressure. Air rushes in via the upper airway, which is outside the sealed chamber. Expiration is passive; the machine cycles off, allowing chest retraction. This type of ventilation is similar to normal ventilation in that decreased intrathoracic pressures produce inspiration and expiration is passive. Negative pressure ventilation delivers noninvasive ventilation and does not require an artificial airway. Several portable negative pressure ventilators are available for home use for patients with neuromuscular diseases, central nervous system disorders, diseases and injuries of the spinal cord, and severe COPD (Fig. 66-20). Negative pressure ventilators are not used extensively for acutely ill patients.

Positive Pressure Ventilation Positive pressure ventilation (PPV) is the primary method used with acutely ill patients (Fig. 66-21). During inspiration the ventilator pushes air into the lungs under positive pressure. Unlike spontaneous ventilation, intrathoracic pressure is raised during lung inflation rather than lowered. Expiration occurs passively as in normal expiration. Modes of PPV are categorized into two groups: volume and pressure ventilation. Volume Ventilation With volume ventilation, a predetermined tidal volume (VT) is delivered with each inspiration, and the amount of pressure needed to deliver the breath varies based on the compliance and resistance factors of the patient-ventilator system. Consequently, the VT is consistent from breath to breath, but airway pressures will vary. Pressure Ventilation With pressure ventilation, the peak inspiratory pressure is predetermined, and the VT delivered to the patient varies based on the selected pressure and the compliance and resistance factors of the patient-ventilator system. With this understanding, careful attention must be given to the VT to prevent unplanned hyperventilation or hypoventilation. For example, when the patient breathes out of synchrony with the ventilator, the pressure limit may be reached quickly, and the volume of gas delivered may be small. Initially, pressure ventilation was used only in stable patients being weaned from the ventilator. Today, pressure ventilation is frequently used to treat critically ill patients.44,45 Settings of Mechanical Ventilators Mechanical ventilator settings regulate the rate, depth, and other characteristics of ventilation (Table 66-10). Settings are based on the patient's status (e.g., ABGs, body weight, level of consciousness, muscle strength). The ventilator is tuned as finely as possible to match the patient's ventilatory pattern. Settings are evaluated and adjusted frequently until the patient achieves optimal ventilation. Some settings serve as a failsafe mechanism, alerting staff to problems with ventilation. It is important that you ensure that all ventilator alarms are always on. Alarms alert the staff of potentially dangerous situations such as mechanical malfunction, apnea, unplanned extubation, or patient asynchrony with the ventilator (Table 66-11). On many ventilators the alarms can be temporarily suspended or silenced for up to 2 minutes for suctioning or testing while a staff member is in the room. After that period of time, the alarm system automatically becomes functional again.

Modes of Volume Ventilation The variable methods by which the patient and the ventilator interact to deliver effective ventilation are called ventilator modes. The selected ventilator mode is based on how much WOB the patient should or can perform. WOB refers to inspiratory effort needed to overcome the elasticity and viscosity of the lungs along with the airway resistance. The mode is determined by the patient's ventilatory status, respiratory drive, and ABGs. Generally, ventilator modes are controlled or assisted. With controlled ventilatory support, the ventilator does all of the WOB, and with assisted ventilatory support, the ventilator and the patient share the WOB. Historically, volume modes such as controlled mandatory ventilation (CMV), assist-control ventilation (ACV), and synchronized intermittent mandatory ventilation (SIMV) have been used to treat critically ill patients. More recently, pressure modes such as pressure support ventilation (PSV) and pressure-controlled inverse ratio ventilation (PC-IRV) have become more widespread. Assist-Control Mechanical Ventilation With assist-control ventilation, the ventilator delivers a preset VT at a preset frequency. When the patient initiates a spontaneous breath, the preset VT is delivered. The ventilator senses a decrease in intrathoracic pressure and then delivers the preset VT. The patient can breathe faster than the preset rate but not slower. This mode has the advantage of allowing the patient some control over ventilation while providing some assistance. ACV is used in patients with a variety of conditions, including neuromuscular disorders (e.g., Guillain-Barr syndrome), pulmonary edema, and acute respiratory failure. In the ACV mode, the patient has the potential for hypoventilation and hyperventilation. The spontaneously breathing patient can easily be overventilated, resulting in hyperventilation. If the volume or minimum rate is set low and the patient is apneic or weak, the patient will be hypoventilated. Thus these patients require vigilant assessment and monitoring of ventilatory status, including respiratory rate, ABGs, SpO2, and SvO2/ScvO2. It is also important that the sensitivity or amount of negative pressure required to initiate a breath is appropriate to the patient's condition. For example, if it is too difficult for the patient to initiate a breath, the WOB is increased and the patient may tire and/or develop ventilator asynchrony (i.e., the patient fights the ventilator).

Synchronized Intermittent Mandatory Ventilation

With synchronized intermittent mandatory ventilation, the ventilator delivers a preset VT at a preset frequency in synchrony with the patient's spontaneous breathing. Between ventilator-delivered breaths, the patient is able to breathe spontaneously through the ventilator circuit. Thus the patient receives the preset FIO2 during the spontaneous breaths but self-regulates the rate and volume of those breaths. This mode of ventilation differs from ACV, in which all breaths are of the same preset volume. It is used during continuous ventilation and during weaning from the ventilator. SIMV may also be combined with PSV (described below). Potential benefits of SIMV include improved patient-ventilator synchrony, lower mean airway pressure, and prevention of muscle atrophy as the patient takes on more of the WOB. Modes of Pressure Ventilation Pressure Support Ventilation With pressure support ventilation (PSV), positive pressure is applied to the airway only during inspiration and is used in conjunction with the patient's spontaneous respirations. The patient must be able to initiate a breath in this modality. A preset level of positive airway pressure is selected so that the gas flow rate is greater than the patient's inspiratory flow rate. As the patient initiates a breath, the machine senses the spontaneous effort and supplies a rapid flow of gas at the initiation of the breath and variable flow throughout the breath. With PSV the patient determines inspiratory length, VT, and respiratory rate. VT depends on the pressure level and airway compliance. PSV is used with continuous ventilation and during weaning. PSV may also be used with SIMV during weaning. PSV is not used as a sole ventilatory support during acute respiratory failure because of the risk of hypoventilation. Advantages to PSV include increased patient comfort, decreased WOB (because inspiratory efforts are augmented), decreased O2 consumption (because inspiratory work is reduced), and increased endurance conditioning (because the patient is exercising respiratory muscles). Pressure-Control Inverse Ratio Ventilation Pressure-control inverse ratio ventilation (PC-IRV) combines pressure-limited ventilation with an inverse ratio of inspiration (I) to expiration (E). Some clinicians use PC without IRV. The I/E ratio is the ratio of duration of inspiration to the duration of expiration. This value is normally a ratio of 1:2. With IRV, the I/E ratio begins at 1:1 and may progress to 4:1. With IRV, a prolonged positive pressure is applied, increasing inspiratory time. IRV progressively expands collapsed alveoli. The short expiratory time has a PEEP-like effect, preventing alveolar collapse. Because IRV imposes a nonphysiologic breathing pattern, the patient requires sedation with or

without paralysis. PC-IRV is indicated for patients with acute respiratory distress syndrome (ARDS) who continue to have refractory hypoxemia despite high levels of PEEP. Not all patients with poor oxygenation respond to PC-IRV. Airway Pressure Release Ventilation Airway pressure release ventilation (APRV) permits spontaneous breathing at any point during the respiratory cycle with a preset continuous positive airway pressure (CPAP) with short timed pressure releases. The CPAP level (pressure high, pressure low) is adjusted to maintain oxygenation goals while the timed releases (time high, time low) are increased or decreased to meet ventilation goals. VT is not a set variable and is dependent on the CPAP level, the patient's compliance and resistance, and spontaneous breathing effort. The mode is designed for patients with ARDS who require high pressure levels for alveolar recruitment. One advantage of this mode is the ability to permit spontaneous respirations. This may reduce the need for deep sedation or paralytics. Other Ventilatory Maneuvers Positive End-Expiratory Pressure Positive end-expiratory pressure (PEEP) is a ventilatory maneuver in which positive pressure is applied to the airway during exhalation. Normally during exhalation, airway pressure drops to zero, and exhalation occurs passively. With PEEP, exhalation remains passive, but pressure falls to a preset level, often 3 to 20 cm H2O. Lung volume during expiration and between breaths is greater than normal with PEEP. This increases functional residual capacity (FRC), and often improves oxygenation with restoration of lung volume that normally remains at the end of passive exhalation. The mechanisms by which PEEP increases FRC and oxygenation include increased aeration of patent alveoli, aeration of previously collapsed alveoli, and prevention of alveolar collapse throughout the respiratory cycle. PEEP is titrated to the point that oxygenation improves without compromising hemodynamics. This is termed best or optimal PEEP. Often 5 cm H2O PEEP (referred to as physiologic PEEP) is used prophylactically to replace the glottic mechanism, help maintain a normal FRC, and prevent alveolar collapse. PEEP of 5 cm H2O is also used for patients with a history of alveolar collapse during weaning. PEEP improves gas exchange, vital capacity, and inspiratory force when used during weaning. In general, the major purpose of PEEP is to maintain or improve oxygenation while limiting risk of O2 toxicity. FIO2 can often be reduced when PEEP is used. PEEP is indicated in lungs with diffuse disease, severe hypoxemia unresponsive to FIO2 greater than 50%, and loss of compliance or stiffness. It is used in pulmonary edema to

provide a counterpressure opposing fluid extravasation. The classic indication for PEEP therapy is ARDS (see Chapter 68). PEEP is contraindicated or used with extreme caution in patients with highly compliant lungs (e.g., COPD), unilateral or nonuniform disease, hypovolemia, and low CO. In these cases the adverse effects of PEEP may outweigh any benefits.

Continuous Positive Airway Pressure Continuous positive airway pressure (CPAP) restores FRC and is similar to PEEP. However, the pressure in CPAP is delivered continuously during spontaneous breathing, thus preventing the patient's airway pressure from falling to zero. For example, if CPAP is 5 cm H2O, airway pressure during expiration is 5 cm H2O. During inspiration, 1 to 2 cm H2O of negative pressure is generated, thus reducing airway pressure to 3 or 4 cm H2O. The patient receiving SIMV with PEEP receives CPAP when breathing spontaneously. CPAP is commonly used in the treatment of obstructive sleep apnea. CPAP can be administered noninvasively by a tight-fitting mask or an ET or tracheal tube. CPAP increases WOB because the patient must forcibly exhale against the CPAP and so must be used with caution in patients with myocardial compromise.