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Clinician's Pocket Reference > Chapter 20. Critical Care >
Care of the Critically Ill Patient
Patients admitted to the ICU often have multisystem disease, have traumatic injuries, or are under intensive treatment regimens to avoid or manage end-organ dysfunction. The interactions between dysfunctional organ systems are complicated and can be overwhelming to students and new house officers. This chapter describes an organ-system approach to evaluating and treating critically ill patients as well as commonly encountered critical care complications. The field of critical care medicine is rapidly advancing, and evidence-based protocols and pathways are becoming an important part of clinical practice. Become familiar with unit protocols in the following major areas:
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1. Sedation and analgesia
2. Delirium and substance withdrawal
4. Intensive insulin therapy
5. Transfusion of blood products
6. DVT and stress ulcer prophylaxis
7. Weaning from mechanical ventilation
9. Management of sepsis including:
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a. Goal-directed therapy
b. Activated protein C (drotrecogin alfa)
c. Adrenal insufficiency and use of steroids
ICU Progress Note
The ICU progress note is a concise summary of the events of the past 24 h, medications, physical exam, laboratory data, and the assessment and treatment plan. Although the information can be found elsewhere in the chart, the physician 's interpretation of the data communicates the medical decision-making process. The daily progress note includes:
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1. Problem list and injury summary
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a. Active problems and major inactive problems
c. Past medical or surgical history relevant to the present illness
d. Notation of hospital day, post trauma day, postoperative day, etc
2. Events and procedures over the past 24 h
3. Current medications
4. System-specific physical exam and pertinent flow sheet data
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a. CNS: CNS functioning or other neurologic assessment and sedation level (eg, Modified Ramsay Sedation scale, Richmond AgitationSedation Scale [RASS], Confusion Assessment Method [CAM-ICU])
b. CV: Cardiovascular function, including indicators of systemic perfusion, blood pressure, heart rate, and pulmonary artery (PA) catheter data
c. Pulm: Pulmonary function, including ventilator settings and ABG values
d. GI/Nut: GI function and nutritional status
e. F/E/R: Fluids, electrolytes, and renal function
f. Heme/ID: Hematologic function, including CBC, coagulation values; infectious disease status (recent culture data, antibiotic regimen, treatment duration)
g. Prophylaxis: DVT, ethanol withdrawal, stress gastritis, etc
5. Other relevant laboratory and radiographic data
6. Assessment and plan
- 1. Continuous ECG: Computerized arrhythmia detection systems facilitate rapid detection of rhythm abnormalities and increase the likelihood of successful resuscitation.
- 2. Blood Pressure: Intermittent (sphygmomanometer) or continuous (intravascular) assessment of BP (systolic, diastolic, mean arterial, and central venous pressures). Assessment of response to treatment and titration of vasoactive drugs. Continuous intravascular methods are warranted in patients with marked hemodynamic instability.
- 3. Pulse Oximetry: Continuous, quantitative arterial O 2 saturation (Sa O 2 ); ensures adequate oxygenation of systemic arterial blood for tissue delivery.
- 4. Temperature: Critically ill patients are at high risk of thermoregulatory disorders due to their pathophysiologic condition (eg, fluid resuscitation, burns, sepsis); continuous measurements in the esophagus (esophageal probe) and central venous blood compartment (PA catheter) are accurate methods for monitoring core body temperature. ATLS definitions of hypothermia are mild, 35C; moderate 32C; and severe 28C.
- 5. Capnography: Continuous measurement of expired CO 2 . Changes imply alteration in clinical status (eg, hypoventilation, overfeeding, fever , sepsis).
Transporting Critically Ill Patients
"Whatever can go wrong, will go wrong" is especially true during the transport of critically ill patients. Adherence to common sense guidelines helps to minimize the risk of adverse events:
- 1. Maintain the patient's airway; if the airway is tenuous, intubate the patient before transport.
- 2. Transport only stable patients (unless the role of transport is to provide a life-saving intervention).
- 3. Pay attention to IV catheters and pumps and their connections.
- 4. Bring sufficient oxygen , IV fluids, medications, etc.
- 5. Adequate assistance must be available to safely transport the patient and associated equipment; the destination should be prepared to accept the patient.
- 6. Expect the unexpected; have personnel, equipment, and supplies available that can make the difference in a crisis (eg, drugs and equipment for reintubation, bag valve mask).
Central Nervous System
Severe acute illness often results in altered mental status (AMS). AMS manifests a spectrum of disability from simple, mild delirium to complex, life- threatening coma.
Critically ill patients are often intubated, and medications must be administered for sedation and analgesia. Inadequate sedation and pain control have adverse effects such as increased catabolism, tachycardia and higher myocardial O 2 consumption, immunosuppression , hypercoagulability, and severe anxiety, so great care must be taken in finding the proper balance of medications.
When acute agitation occurs, first rule out life-threatening pathology (ie, inadequate blood flow and nutrient availability to the brain). Evaluate vital signs, oxygenation and ventilation status, and serum glucose and electrolytes before administering CNS-altering medications.
Benzodiazepines are potent inducers of sedation, amnesia, muscle relaxation, and anxiolysis. These properties make this class of drug ideal for short- to intermediate- term use. Take great care to choose a drug that will not accumulate in the patient's system if end-organ dysfunction is present:
- Lorazepam: Good intermediate-duration benzodiazepine; metabolized by the liver with inactive metabolite excreted in the urine; very potent but has a long time to peak effect (ideal agent for longer-term sedation)
- Midazolam: Shorter-onset, shorter-acting benzodiazepine; metabolism altered by calcium channel blockers, erythromycin, and triazole antifungals
Titrate either agent to achieve a sedation level according to published scales (eg, RASS). The reliability and validity of the RASS for titration of sedation has been validated in numerous studies (eg, Am J Respir Crit Care Med 2002;166:13381344 and JAMA 2003;289:29832991).
The RASS ( Am J Respir Crit Care Med 2000;161:A506 and JAMA 2001;286:27032710) is scored as follows :
- +4 CombativeCombative, violent, immediate danger to staff
- +3 Very agitatedPulls or removes tubes and catheters; aggressive
- +2 AgitatedFrequent nonpurposeful movement; fights ventilator
- +1 RestlessAnxious, apprehensive but no aggressive movement
- 0 Alert and calm
- 1 DrowsySustained (> 10 s) awakening to voice
- 2 Light sedationBriefly (< 10 s) awakens to stimulation
- 3 Moderate sedationMovement or eye opening to voice
- 4 Deep sedationResponse to physical stimulation but not voice
- 5 UnarousableNo response to voice or physical stimulation
If overmedication occurs (eg, inadvertent overadministration, accumulation of metabolites), stop the medication , prepare to institute cardiopulmonary support, and use flumazenil (a benzodiazepine antagonist) to reverse the overly sedated state. Carefully review the contraindications to flumazenil use before administering the drug.
- Propofol: Nonbenzodiazepine, lipid-based sedativehypnotic; little analgesic properties; extremely short onset and half-life make accumulation unlikely ( ultra -short-term drug); expensive; longer-term use has adverse financial and infectious consequences. One approach is to initiate at 10 mcg/kg/min and adjust by increments of 1020 mcg/kg/min q515 min to achieve desired level of sedation (reconsider dosing > 50 mcg/kg/min). To discontinue, decrease infusion 25% q1015 min, then halt the infusion when the patient is conscious.
- Haloperidol: Short-term management of agitation, especially with components of delirium. Relevant considerations in the ICU setting are as follows:
- 1. Prolongation of the QT interval; discontinue if QT interval increases > 50% of baseline or exceeds 450 ms.
- 2. Lowering of the seizure threshold; be cautious with use in the presence of alcohol withdrawal, traumatic brain injury, etc
- 3. Potential CNS effects, such as extrapyramidal symptoms, tardive dyskinesia, and the uncommon but potentially devastating neuroleptic malignant syndrome
Critically ill patients may have acute pain due to recent operations or prehospital trauma. Opioid narcotic agents are best for acute pain control. (See also Chapter 14.)
- Morphine: IV opioid narcotic; commonly used (low cost, ease of use)
- Fentanyl: Synthetic opioid; more potent and shorter acting than morphine; less histamine release than morphine (ie, less potential for drug-induced hypotension)
These opioids can be administered as continuous infusions, intermittent boluses, or as part of patient-controlled analgesia (PCA) regimen. Because narcotics can cause respiratory depression, careful titration is necessary, especially when narcotics are combined with benzodiazepines. Epidural anesthesia provides good local analgesia and decreases requirements for IV narcotics.
Many critically ill patients need long-term sedation and analgesia. Current data suggest that daily interruption of sedation decreases mechanical ventilation days and ICU length of stay.
Neuromuscular paralysis is rarely indicated but may be necessary for patients with severe respiratory failure who cannot properly oxygenate or ventilate. Eliminating the muscular elastic recoil of the chest wall and ventilator dyssynchrony may improve pulmonary compliance and ventilationoxygenation ability.
Cardiovascular instability is one of the most common problems encountered in the ICU. The first step in evaluating the cardiovascular system is a thorough physical exam.
Inspection: Jugular Venous Distention (JVD)
- Neck vein visualization (with the patient sitting at a 45-degree angle) implies CVP > 1215 mm Hg
- JVD plus systemic hypotension suggests life-threatening pathology:
- 1. Tension pneumothorax
- 2. Pericardial tamponade
- 3. Severe cardiac dysfunction
Inspection: Precordial Contusion
- Associated with blunt trauma from a steering wheel; injury pattern implies possible myocardial contusion. Treatment: Continuous ECG monitoring; correction of arrhythmias (most common: sinus tachycardia). To identify anatomic heart injury and pericardial effusion, obtain an echocardiogram if arrhythmias occur.
Inspection: Extremity Perfusion
- Check extremities for perfusion (pulse, color , temperature, and capillary refill)
- Note: Pay special attention to sites distal for:
- 1. Long bone fractures
- 2. Joint dislocations
- 3. Indwelling arterial catheters
Blood Pressure (BP)
Over the short term, BP is considered adequate if renal perfusion is maintained (usually MAP > 70 mm Hg in young, previously healthy persons). Premorbid medical problems and aging, however, may mandate a higher MAP.
Note: If the cuff is too small for the arm (ie, the patient is obese), the measured systolic BP will be falsely elevated.
Systolic BP > 140 mm Hg with normal diastolic BP. In the acute setting, due to:
- Increased cardiac output
- Generalized response to stress
- Pain, anxiety, or both
Diastolic BP > 90 mm Hg. Isolated diastolic hypertension may be associated with:
- Intrinsic renal disease
- Endocrine disorders
- Renovascular hypertension
- Neurologic disorders
Treatment: Hypertension is a concern after acute coronary syndromes, subarachnoid hemorrhage, and vascular anastomosis (especially carotid artery surgery). Systolic BP > 180 mm Hg usually necessitates immediate treatment. Commonly used agents include nitroprusside, nicardipine, metoprolol, labetalol, esmolol, hydralazine, and nitroglycerin. Use a rapid-acting and easily reversible beta-blocker (eg, esmolol) to manage hypertension associated with ruptured aortic aneurysm or blunt traumatic aortic injury. Emergency management of hypertension is discussed in Chapter 21, and the specific antihypertensive agents are discussed in Chapter 22.
Mean Arterial Pressure (MAP)
Calculated as DBP + [(SBP DBP)/3]
Pulse Pressure (SBP DBP)
Wide Pulse Pressure:
(> 40 mm Hg) associated with:
- Arteriovenous fistula
- Aortic insufficiency
Narrow Pulse Pressure:
(< 25 mm Hg) associated with:
- Significant tachycardia
- Early hypovolemic shock
- Pericardial effusion or tamponade
- Aortic stenosis
Systolic BP changes during the respiratory cycle as a function of changes in intrathoracic pressure (see Chapter 13 for measurement technique). Normally, systolic BP falls 610 mm Hg with inspiration. If this variation occurs over a wider range (> 10 mm Hg), the patient is said to have a paradoxical pulse (Figure 201, below). Associated conditions include:
- Pericardial tamponade
- Asthma and COPD
- Ruptured diaphragm
Auscultation: Heart Murmurs
The presence of a premorbid cardiac murmur and, more important, the interval development of a new cardiac murmur are important in the care of a critically ill patient. Characterize all new murmurs by intensity, location, and variation with position and respiration as well as whether they are systolic or diastolic. In general, diastolic murmurs are usually pathologic (see Chapter 1 for more information on heart murmurs).
Cardiac Output (Co):
Volume of blood pumped by the heart each minute; approximately 3.55.5 L/min (adult). CO is standardized to patient size by calculation of the cardiac index (CI): CI = CO/BSA; normal CI 2.83.2 L/min/m 2 . CI < 2.5 L/min/m 2 may require pharmacologic intervention if O 2 delivery is inadequate. CO is the product of heart rate and stroke volume. Stroke volume is a function of preload, afterload, and contractility.
Initial length of myocardial muscle fibers is proportional to left ventricular end-diastolic volume (LVEDV), which is governed by the volume of blood remaining in the left ventricle after systole. As LVEDV increases, the stretch on myocardial muscle fibers increases. Furthermore (Figure 202, top), as LVEDV increases (ie, stretch), the energy of contraction increases proportionally until an optimal tension develops (Starling law; Figure 202, middle). However, when the myocardial muscle fiber is overstretched, contractile strength decreases.
Resistance to ventricular ejection; measured clinically with aortic BP and calculation of systemic vascular resistance (SVR).
Ability of heart to alter its contractile force and velocity independent of fiber length (ie, the intrinsic strength of the individual muscle fiber cells ). Contractility may be increased by stimulation of beta-receptors in the heart (see following section).
Review of Sympathetic Nervous System Influence on the Cardiovascular System
CO and its determinants (preload, afterload, and contractility) are influenced by the sympathetic nervous system (SNS). The SNS releases catecholamines (predominantly epinephrine and norepinephrine), which bind to end-organ receptors and exert a physiologic response. Adrenergic receptors are divided into two major classes: alpha () and beta (). End-organ function after receptor activation is summarized in Table 201.
Table 201 Adrenergic Receptors and Their Actions on the Cardiovascular System
| Receptor || Location || Action |
| Alpha () 1 |
| Peripheral arterioles || Vasoconstriction (increased SVR) |
| Beta () 1 |
| Myocardium || Increased contractility |
| SA node || Increased heart rate |
| Beta () 2 |
| Peripheral arterioles || Vasodilatation (decreased SVR) |
| Bronchiolar smooth muscle || Bronchodilatation |
SVR = systemic vascular resistance; SA = sinoatrial.
Adrenergic receptors are important because many of the cardiovascular drugs used in the ICU act through their sympathomimetic properties. Such drugs have a specific receptor affinity (ie, versus ) and consequently differ in end-organ effects. For example, drugs that act on the 1 receptors are called vasopressors because they cause nonspecific systemic vasoconstriction. Conversely, drugs that act on 1 receptors are called inotropes because they increase myocardial contractility and heart rate.
Because each drug exerts receptor-specific effects, use of these agents provides differential activation of receptors and ultimately end-organ effects. Through tailoring pharmacologic support, physicians provide the necessary cardiovascular assistance to critically ill patients. Commonly used sympathomimetics and their relative receptor affinities are listed in Table 202. A guide to administration of these agents appears in Table 2011.
Table 202 Relative Actions of Sympathomimetic Drugs on Adrenergic Receptors
| Effect On |
| Drug || || 1 |
| 2 |
| D |
| Phenylephrine || ++++ || 0 || 0 || |
| Norepinephrine || ++++ || ++ || 0 || |
| Epinephrine || ++++ || ++++ || ++ || |
| Dobutamine || + || ++++ || ++ || |
| Isoproterenol || 0 || ++++ || +++ || |
| Dopamine (mcg/kg/min) || 1020 || 510 || || 15 |
Key: + = Relative effect; 0 = no clinically significant effect; D=dopaminergic receptors.
Central Venous Pressure (CVP)
The central venous catheter is one of two major devices used for cardiovascular instrumentation. The other, the PA catheter (also called PA catheter, SwanGanz catheter, and right-heart catheter), is discussed in the next section. For CVP monitoring, a 14-gauge IV catheter is inserted into the central venous circulation through the internal jugular or subclavian vein (see Chapter 13). A pressure transducer and monitor connected to the catheter provide the measurements. A CXR is required to confirm the position of the catheter in the superior vena cava. The zero point for the transducer is the level of the right atrium in a supine patient; this phlebostatic axis is usually 5 cm caudal to the sternal notch in the midaxillary line.
The transduced CVP reflects right atrial pressure, and by association, right ventricular filling pressure or preload. Although CVP is a relatively inaccurate indicator of preload, trends in relation to volume status and hemodynamics may be clinically useful. The general implications of CVP readings are listed in Table 203.
Table 203 Interpretation of CVP Measurements
| Reading (mm Hg) || General Description || Clinical Implications |
| < 3 || Low || Intravenous fluids may be administered |
| 310 || Midrange || Probable clinical euvolemia |
| >10 || High || Suspect fluid overload, CHF, CP, COPD, tension PTX |
CVP = central venous pressure; CHF = congestive heart failure; CP = cor pulmonale; COPD = chronic obstructive pulmonary disease; PTX = pneumothorax.
- 1. CVP does not entirely reflect total blood volume or left ventricular function. CVP is altered by:
- Changes in PA resistance
- Changes in compliance of the right ventricle
- Intrathoracic pressure (eg, mechanical ventilation)
- 2. An accurate clinical picture can be limited by conditions that radically change intrathoracic pressure:
- Positive pressure ventilation, especially when high PEEP is used
- Pneumothorax, hemothorax, hydrothorax, and tension pneumothorax
- Presence of intrathoracic tumors
- 3. CVP can be normal in the face of sepsis or hypovolemia when accompanied by compromised myocardial function
- 4. Left ventricular failure can occur in the presence of normal CVP
- 5. Patients with COPD may need an elevated CVP to optimize CO
- 6. PA catheter readings more accurately reflect fluid and cardiac status, but the technique is more invasive and expensive than use of CVP catheters.
Technical Tips Regarding CVP Measurements
- CVP readings are inaccurate if they do not fluctuate with respiration.
- If appropriate, remove the patient from the ventilator when taking a CVP reading.
- To ensure comparable readings, have the patient positioned in the same manner for each measurement.
- Flatten the bed and use the same zero point for the transducer (phlebostatic axis).
Pulmonary Artery Catheters
Used for direct measurement of central cardiovascular pressures, which are calculated circulatory values used in critical care. The catheter is placed in a central vein (usually the subclavian or internal jugular) and then passed into the right atrium, across the tricuspid valve, into the right ventricle, and through the pulmonic valve. The distal end is floated into the PA (Figure 203). The PA catheter is used to measure PA pressure (PAP), PA occlusion pressure (PAOP, also known as pulmonary capillary wedge pressure [PCWP]), and CVP. Intravascular volume status, vascular resistance (both pulmonary and systemic), and the pumping ability of the heart (CO) are calculated, mixed venous oxygen saturation (S O 2 ) is monitored , and right ventricular ejection fraction (REF) and right ventricular end-diastolic volume index (RVEDVI) are measured.
Key point: The data obtained with a PA catheter are only as good as the initial setup and the actual measurements obtained (ie, pressures). If the pressure measurements are in error or if patient data (height, weight, etc) are incorrectly entered into the system, the subsequent calculations will be incorrect.
There has been debate concerning the utility of PA catheters ( JAMA 2005;294:16641670). However, many clinicians find these catheters an essential tool in the following settings:
- Acute heart failure
- Shock states
- Complex circulatory and fluid conditions (massive resuscitation)
- Complicated MI
- Intraoperative management in high-risk cardiac patients (eg, aneurysm repair, elderly patient undergoing major operation)
The PA catheter generally consists of three (or four) lumens and a thermistor at the tip (Figure 204); markings are typically in 10-cm increments; the catheter is radiopaque.
- Balloon port: Usually a square white port; route to inflate the balloon at the tip of the catheter; inflation of the balloon requires 1.01.5 mL of air
- Proximal port: Approximately 30 cm proximal to the tip; lies in the superior vena cava; may be used for fluid administration when not used for determination of CVP and CO
- Distal port: Lies in PA beyond the balloon; this port is attached to a pressure transducer for continuous PAP tracings and intermittent PAOP measurement
Temperature sensor that provides continuous core temperature measurements as well as measurements used in thermal dilution CO techniques (see Pulmonary Artery Catheterization Technique)
Additional Functions and Measurement Capabilities
- Pacing PA catheters: Extra ports (approximately 19 cm from the tip) through which pacing wires are passed into the right ventricle; other models contain electrodes along the surface of the catheter; capable of pacing both right atrium and right ventricle
- Oximetric PA catheter: Standard PA catheter ports with fiberoptic components; emit light impulses to and from distal end of catheter; light impulses are then reflected by hemoglobin and measured; continuous O 2 saturation monitoring (see Figure 204)
- Right ventricular ejection fraction catheter: Used to measure REF, which is then used to calculate RVEDVI (best indicator of preload)
Contraindications to PA Catheter Use:
No absolute contraindications. Patients with LBBB may experience complete heart block (requiring temporary pacemaker); frequent manipulation may increase infection risk, as with any IV catheter.
There are many versions of the flow-directed, balloon-tipped PA catheter; a generic representation is in Figure 204. A PA catheter introducer insertion kit contains an introducer sheath (cordis catheter), flexible J-tip guidewire, vessel dilator, catheter contamination shield, and other items needed to insert the catheter (Figure 205). The monitoring system ( transducers , tubing, and stopcocks) and pressurized flush system are usually set up by the nursing staff and should be operational before catheter insertion.
Pulmonary Artery Catheterization Procedure
- 1. Obtain informed consent from the patient or the patient's medical decision maker.
- 2. Make sure that emergency resuscitation medications are on hand in the event of refractory arrhythmia.
- 3. Choose a site. In a patient who may receive thrombolytic therapy or who has a coagulopathy, femoral and internal jugular veins may be preferred because of their compressibility if a complication occurs. The easiest sites for floating the PA catheter are the right internal jugular and the left subclavian veins. Rationale: The PA catheter is packaged in a coiled position; these sites tend to the natural curve of the catheter as it assists in placement.
- 4. Widely prep the insertion site with a topical antiinfective agent such as chlorhexidine gluconate. Important: Antiinfective agents must fully dry on the skin to be effective.
- 5. Fully drape the patient (not just the immediate site) because of the length of the tubing and guidewire. Use aseptic technique with gown, gloves, and mask to decrease the rate of line infection.
- 6. With the patient in Trendelenburg position, cannulate the chosen central vein (see Central Venous Catheterization, Chapter 13). Pass the flexible end of the J-wire (standard length, 45 cm) into the vein through the needle. Never force a guidewire, and always keep one hand on the guidewire while it is in the patient. The flexible tip end is passed first because the stiff end can perforate the blood vessel.
- 7. Mount the introducer sheath on the vessel dilator. Pass the dilatorsheath unit over the wire. Make a full- thickness skin nick at the wire entry site with a no. 11 blade scalpel.
- 8. Pass the vessel dilatorsheath unit into the vessel over the guidewire (Figure 206). A gentle, slight twisting motion may be necessary. Remove the guidewire and the vessel dilator. Catheter sheaths have a hemostatic valve mechanism to prevent air from entering the central system and blood from escaping. The side port does not have a valve, so cap it or clamp it. Mount a syringe on the side port and aspirate blood to confirm intravascular positioning of the sheath; flush with sterile saline solution after confirmation.
- 9. Prepare the PA catheter (attach to the monitor, flush lumens with sterile saline). Zero the transducer at the phlebostatic axis; ask the ICU nursing staff for help with the setup. Check balloon function and gently wave the catheter to ensure that an appropriate waveform is present on the monitor. Note: Never fill the balloon with fluid; use only air. The volume is typically 1.5 mL. After placing the catheter through the contamination shield, check balloon function by insufflating with 1.5 mL of air.
- 10. Insert the prepared catheter (flushed, transduced, contamination shield in place) into the sheath (Figure 207). Once you have advanced approximately 1520 cm and a CVP tracing is visible on the monitor, gently inflate the balloon with 1.01.5 mL of air using the volume-limiting syringe provided with the set. There should be no resistance to balloon inflation.
- 11. Once the balloon is inflated, advance the catheter to the level of the right atrium under the guidance of the pressure waveform and the ECG. Monitor the waveform and ECG at all times while advancing the balloon catheter. Figure 208B shows the normal pressures encountered as the catheter is advanced. Important: Never advance the catheter with the balloon deflated. Conversely, always withdraw the PA catheter with the balloon deflated.
- 12. Positioning of the PA catheter in the right atrium is probably best determined by watching for the characteristic waveform on the monitor (Figure 208B). The right atrium is generally approximately 30 cm from the right internal jugular or subclavian vein insertion site and approximately 3540 cm from the left subclavian vein insertion site.
- 13. An abrupt change in the pressure tracing occurs as the catheter enters the right ventricle (Figure 208B). There is generally little ectopy on entry into the right ventricle; however, as the catheter advances into the right ventricular outflow tract , PVCs may occur.
- 14. Steadily advance the catheter until ectopy disappears and the PA tracing (heralded by a rise in diastolic pressure) is obtained (Figure 208). If this does not occur by the time 60 cm is reached, deflate the balloon, withdraw the catheter to 20 cm, and make another attempt with the balloon inflated after slightly rotating the catheter.
- 15. Once the catheter is in the PA, obtain the PAOP after advancing the catheter another 1015 cm. The final position of the catheter should be such that PAOP is obtained with no less than full balloon inflation and the PAP tracing is present with the balloon deflated. In the ideal position, transition from PAP to PAOP (and vice versa) occurs within three or fewer heartbeats. In an adult, the typical length to the PA position is 4560 cm. Table 204 shows normal PA catheter measurements important for patient evaluation and treatment.
- 16. Once the position is acceptable, lock the contamination shield onto the sheath. The catheter can be readjusted after the sterile field is taken down. Suture the sheath to the skin, secure the catheter in place and dress the surgical site according to unit protocol. Connect catheters to the ports on the sheath. The inflow port on the sheath can be used for IV fluid and medication administration.
- 17. Obtain a CXR to document the catheter position and to rule out pneumothorax or other complications. A properly positioned catheter should lie just beyond the vertebral bodies in the nonwedged position.
- 18. Common problems: Catheter placement is more difficult if severe PA hypertension is present. If there is significant cardiac enlargement , particularly dilatation of the right-heart structures, the catheter may coil in its path to the right ventricular outflow tract; fluoroscopy may be needed for correct positioning. Furthermore, under these conditions, the PA catheter may have difficulty holding its proper position. Because the balloon-tipped catheter depends on flow to carry it through the right-heart chambers, placement in the PA may be difficult if the patient has low CO.
- 19. CO can be measured by thermal dilution (Fick equation). Connect the thermistor to the CO computer and then rapidly inject fluid (usually 10 mL of ice-cooled NS) through the right atrial port. The computer displays a curve, and CO is calculated from the area under the thermal dilution curve. Do this two more times. If all of these values are approximately the same, average the readings and record. Continuous CO-monitoring PA catheters are used in some hospitals . Normal values for CO and CI are listed in Table 204.
Table 204 Normal Pulmonary Artery and Cardiac Performance Measurements
| Parameter || Range |
| Right atrial pressure || 17 mm Hg |
| Right ventricular pressure || |
| Systolic || 1525 mm Hg |
| Diastolic || 08 mm Hg |
| PAP || |
| Systolic || 1525 mm Hg |
| Diastolic || 815 mm Hg |
| Mean || 1020 mm Hg |
| PAOP ("wedge pressure") || 612 mm Hg |
| Cardiac output || 3.55.5 L/min |
| Cardiac index || 2.83.2 L/min/m 2 |
| Mixed venous O 2 saturation |
| 6585% |
PAP = pulmonary artery pressure; PAOP = pulmonary artery occlusion pressure.
Complications of PA Catheters
- 1. Most complications due to PA catheterization are related to central vein cannulation: Arterial puncture, extravascular placement, pneumothorax, hemothorax
- 2. Arrhythmias are common. Transient PVCs are most common and occur when the catheter is advanced into the right ventricular outflow tract. If a patient with a PA catheter suddenly develops frequent PVCs, deflate the balloon and pull back the catheter to prepare for another attempt.
- 3. Ventricular tachycardia and fibrillation are rare . If they continue after the catheter has been withdrawn, treat the patient with standard ACLS protocols (see Chapter 21).
- 4. Transient RBBB occurs occasionally as the catheter passes through the right ventricular outflow tract. In a patient with preexisting LBBB, complete heart block can occur. In this setting, have backup pacing readily available.
- 5. Pulmonary infarction and PA rupture are serious but infrequent complications of PA catheters and are usually secondary to "over wedge" or peripheral placement of the catheter. Place the patient affected-lung-down, and intubate (if not already done). Insert the ET tube into the unaffected mainstem bronchus to protect the airway. Obtain an emergency thoracic surgery consultation.
- 6. Complications tend to increase with the length of time the catheter is in place. The risk of bacteremia and spontaneous bacterial endocarditis (SBE) are high in severely ill patients undergoing long-term instrumentation. In the setting of unexplained fever, always remove and culture the PA catheter and sheath. Replace the catheter and sheath at a different site if a pulmonary catheter is still indicated.
PA Catheter Measurements
Measured when the PA catheter is in its resting position (balloon deflated). Measurements include pulmonary systolic arterial pressure (PAS), mean pulmonary arterial pressure (MPAP), and diastolic (PAD) arterial pressure.
Pulmonary Artery Occlusion Pressure (PAOP):
Estimate of left atrial pressure (LAP). Measured while the inflated balloon at the tip of the PA catheter occludes a branch of the PA. Important: To avoid pulmonary infarction, fully deflate the balloon when it is not in use.
In the absence of mitral valvular disease, PAOP correlates closely with LAP and with the left ventricular end-diastolic pressure (LVEDP). This correlation exists because of the unobstructed continuity between the PA and the left side of the heart. As a result of this continuity, PAOP may never be greater than the PAD. Increased LVEDP is reflected in an increase in PAOP, which increases PAD. Therefore if a PA catheter monitor shows a wedge pressure higher than PAD pressure, a technical error exists.
Left Ventricular End-Diastolic Pressure:
A measure of preload used to optimize fluid resuscitation and CO. For optimal stroke volume on the Starling curve, the preload must be adequate to stretch the wall of the left ventricle (see Figure 202). Hypovolemia results in too little tension on the muscle fibers and therefore decreased stroke volume and CO. Too much preload stretches beyond the point of maximum tension and decreases CO. Clinically, LVEDP and PAOP are used to keep preload in an optimum range. The normal PAOP varies between 6 and 12 mm Hg but may be higher for different disease states and for preexisting cardiac disease leading to decreased chamber compliance.
Right Ventricular Ejection Fraction (REF)/Right Ventricular End-Diastolic Volume Index (RVEDVI):
RVEDVI, the most accurate assessment of preload, is most helpful in patients with high intrathoracic pressure. A rapid-response thermistor and CO computer are used to calculate REF. Once REF and CO are known, RVEDVI can be calculated. RVEDVI is a more accurate assessment of volume status than PAOP. For example, a patient with severe ARDS may have markedly elevated peak inspiratory pressure. Although the CVP and PAOP may be falsely elevated, RVEDVI is a calculation of a volume, not pressure, so volume status can be determined across a variety of clinical situations. The normal range for EDVI is 80120 mL/m 2 .
Continuous CO Measurement
The specially designed PA catheter emits small pulses of energy that heat the surrounding blood for continuous CO measurement. CO is then calculated on the basis of the magnitude and rate of temperature change. This continuous measurement, along with calculated derivatives, is intermittently updated and displayed on the device.
Differential Diagnosis of PA Catheter Abnormalities
Table 204 and Figure 208 show normal PA pressures and cardiovascular measurements. Perturbations of these values indicate a disease process with the differential diagnoses shown in Table 205.
Table 205 Differential Diagnosis by Category Based on Perturbations in Hemodynamic Parameters a
a These are the trends usually seen with the conditions noted. Clinical variables (medications, secondary conditions, etc) may vary these trends somewhat. Highlighted areas denote major differences between subgroups.
CVP = central venous pressure; CO = cardiac output; PAOP = pulmonary artery occlusion pressure; LVEDP = left ventricular end-diastolic pressure; PAP = pulmonary artery pressure; PVR = peripheral vascular resistance; SVR = systemic vascular resistance.
= usually increased; = usually decreased; = usually unchanged.
Estimation of volume status and myocardial performance: CO is a function of heart rate and stroke volume. Stroke volume depends on preload, afterload, and contractility.
Heart rate is increased to maintain or increase CO in the face of inadequate tissue perfusion. Hence, tachycardia is an additional indicator of O 2 debt (ie, deliverydemand deficit). Tachycardia > 120 beats/min increases myocardial O 2 demand significantly and should be promptly treated. The PA catheter is used to establish adequate myocardial filling pressures such that heart rate may be clinically manipulated to maximize CO. In a patient with adequate filling pressures, slow heart rate (< 80 beats/min), and low CO, drugs that accelerate heart rate (chronotropes) can be used to increase CO. Alternatively, tachycardia > 120 beats/min with an adequate PAOP can be pharmacologically slowed to decrease strain on the heart.
Preload (Stroke Volume):
Indicated by PAOP or EDVI, a reflection of LVEDV. In simple terms, preload is the amount of blood in the heart before contraction. Consequently, preload represents the stretch placed on an individual myocardial cell . When PAOP is optimized, myocardial performance is optimized according to the Starling curve.
- 1. Clinical implications in a healthy heart. Low PAOP or EDVI means suboptimal myocardial muscle stretch. CO can be increased first by administration of fluids. The result is an increase in LVEDV, an increase in myocardial muscle tension, and improved myocardial performance.
- 2. Clinical implications in a failing heart. Long-standing myocardial disease can shift the Starling curve to the right. Consequently, a markedly elevated PAOP may be needed to optimize myocardial performance. It is common for patients who have just undergone heart valve replacement to need a PAOP of 2025 mm Hg to optimize CO (because of decreased compliance of the postoperative heart muscle). Patients with a recent MI may similarly need a PAOP of 1618 mm Hg to optimize output.
Resistance to ventricular ejection; measured clinically by calculation of SVR. Normal SVR = 900 1200 dynes/s/cm 3 .
- 1. Indications for afterload reduction.
- Significant mitral regurgitation
- An increased PAOP coincident with elevated SVR/decreased CI
- 2. Treatment. Vasodilators (eg, nitroprusside, nitrates, ACE inhibitors , hydralazine)
The ability of the heart to alter its contractile force and velocity independent of fiber length. This aspect is difficult to measure directly but can be estimated with surrogate markers. Correctable metabolic causes of depressed contractility include:
- Acidosis (pH < 7.3)
- Adrenal insufficiency
Improve contractility with inotropic agents such as dobutamine or milrinone.
Continuous S O 2 Monitoring
Oximetric PA catheters are used for direct measurement of mixed venous Hgb saturation (S O 2 ). A microprocessor then displays a continuous graph of S O 2 measurements. Calibration is periodically confirmed with ABG measured from heparinized blood drawn from the distal port of the oximetric catheter.
- Follow trends in O 2 supplydemand balance.
- Because it is the best indicator of decreased peripheral O 2 delivery, a decrease in S O 2 is an early sign of organ dysfunction. Correct the problem before hemodynamic compromise occurs.
- Fix the underlying cause. The effect of interventions (eg, transfusions, fluid administration, inotropic agents) can be assessed by following S O 2 before changes are apparent in other hemodynamic variables.
- Clinically, S O 2 values between 65% and 85% represent adequate tissue O 2 delivery and extraction. This generally implies appropriate perfusion of peripheral tissues.
- If S O 2 drops to < 60%, immediately assess O 2 delivery. As O 2 delivery falls, S O 2 falls proportionally because there is less O 2 for the tissues to extract.
- If S O 2 is < 60% and O 2 delivery is unchanged, identify unrecognized conditions causing increased O 2 demand.
In summary, a decline of S O 2 must prompt a review of the parameters of O 2 delivery (ie, CO, [Hgb], Sa O 2 ) and consumption (Sa O 2 S O 2 ). Potential treatments include:
- Correction of hypoxia
- Optimization of myocardial performance for decreased CO
- RBC transfusion for symptomatic anemia
- Identification and management of conditions leading to increased metabolic demands (eg, unrecognized seizures, shivering, and large tissue defects) because these conditions markedly increase in O 2 demand (Figure 209, above)
Continuous Sp O 2 Monitoring (Pulse Oximetry)
The same fiberoptic technology used to measure S O 2 is used to measure Sa O 2 . A light-emitting external probe is placed around a well-perfused appendage such as a digit, earlobe, lip, or bridge of the nose. The light is transmitted through the appendage and reflected by hemoglobin according to its O 2 saturation (the hemoglobin molecule absorbs different wavelengths of light at different O 2 saturations). The oximeter, in addition to calculating oxyhemoglobin saturation, measures the pulse rate and is thus referred to as the pulse oximeter. The reading obtained is the Sp O 2 .
Sp O 2 < 90% implies inadequate oxygenation and under most circumstances necessitates immediate intervention. One exception would be a patient with severe COPD who may have a normal O 2 saturation in the upper 80% range. Conversely, Sp O 2 > 90% does not necessarily imply adequate O 2 delivery (see Clinical Pulmonary Physiology). Pulse oximetry is not useful in the setting of smoke inhalation and carbon monoxide poisoning because of the higher affinity of the hemoglobin molecule for carbon monoxide.
Clinical Pulmonary Physiology
The key to understanding pulmonary physiology and mechanical ventilation in the ICU is to know the difference between oxygenation and ventilation (Figure 2010).
Ventilation is the mechanical movement of air into and out of the respiratory system. The result is the exchange of CO 2 . Several parameters, such as volumes and capacities, are important in assessing the adequacy of ventilation. Spirometry gives both dynamic information (ie, ability to move air into and out of the lungs) and static volume measurements. The lung volume subdivisions and capacities are shown on a spirometric graph in Figure 2011, below.
Total lung capacity (TLC), or the amount of gas in the lung at full inspiration, comprises four basic lung volumes:
- 1. Inspiratory reserve volume (IRV): The volume of gas that can be maximally inspired beyond a normal tidal volume inspiration
- 2. Tidal volume (TV): The volume of inspired gas during a normal breath ; approximately 68 mL/kg in resting, healthy adults
- 3. Expiratory reserve volume (ERV): The volume of gas that can be maximally expired beyond a normal tidal volume expiration
- 4. Residual volume (RV): The volume of gas that remains in the lung after a maximal expiratory effort
The sum of two or more of these lung volumes makes up four divisions called lung capacities (see Figure 2011).
- 1. Vital capacity (VC): The volume of gas expired after a maximal inspiration followed by maximal expiration (VC = ERV + TV + IRV)
- 2. Inspiratory capacity (IC): The volume of gas expired from maximal inspiration to the end of a normal, resting TV (IC = TV + IRV)
- 3. Functional residual capacity (FRC): The amount of gas remaining in the lung after a normal tidal volume expiration (FRC = ERV + RV); acts as a buffer against extreme changes in alveolar P O 2 and consequent dramatic changes in arterial P O 2 with each breath
These volumes and capacities are important factors in assessing ventilation because they can change under different conditions (eg, atelectasis, obstruction, consolidation, small airway collapse). For example, as ERV decreases with small airway collapse, FRC decreases (Figure 2012). These alterations in lung volume affect respiratory reserve as well as oxygenation and ventilation.
Critical Closing Volume (CCV):
CCV is the minimum volume and pressure of gas necessary to prevent small airways from collapsing during expiration. When collapse occurs, blood is shunted around nonventilated alveoli. This phenomenon decreases the surface area available for gas exchange. CCV can vary as compliance changes. If CCV > FRC (air in the lung after tidal expiration), collapse tends to occur in a higher proportion of airways (see Figure 2012).
One method of overcoming CCV is to increase the amount of positive end-expiratory pressure (PEEP) in the lung (see Ventilator Management). The effect of PEEP is to increase FRC by minimizing small airway collapse at the end of expiration. This maneuver improves alveolar ventilation, decreases shunting, and ultimately improves oxygenation (Figure 2013).
Compliance is the change in lung volume (V) as a function of change in pressure (P) (Figure 2014):
This value can be measured at the bedside and is a reflection of FRC and CCV.
Measure tidal volume (TV) and divide it by peak inspiratory pressure (PIP):
Normal: 80100 mL/cm water
Similar to dynamic compliance, except that static PIP is substituted for PIP. Measure static peak pressure (also called plateau pressure) by occluding the exhalation port at the beginning of exhalation (no flow = static pressure).
Comparing dynamic with static compliance may indicate the type of processes causing changes in the elasticity of the lung. Dynamic compliance is affected by both elasticity and airway resistance. Static compliance reflects elasticity and is not affected by airway resistance because there is no flow.
- 1. Reduction in dynamic compliance without a change in static compliance indicates an airway resistance problem (obstruction, bronchospasm, or collapse of the small airways)
- 2. Reduction in both static and dynamic compliance indicates a decrease in lung elasticity (pulmonary edema, atelectasis, or excessive PEEP)
Oxygenation is the process of transporting O 2 from the alveolus across the capillary membrane into the pulmonary circulation and subsequently distributing that O 2 to the body's tissues. O 2 delivery is a function of arterial O 2 content and CO.
Arterial Oxygen Content (Ca O 2 ):
The ability of the blood to carry O 2 to the periphery depends on the O 2 content. Ca O 2 is directly influenced by Hgb concentration ([Hgb]) and the saturation of Hgb with O 2 (Sa O 2 ) (ie, Ca O 2 = Sa O 2 x 1.39 [Hgb])
Oxygen Delivery (D O 2 ):
Normal D O 2 600 mL of O 2 /min with an average normal O 2 uptake of 250 mL of O 2 /min. Calculate D O 2 with PA catheter data by multiplying measured CO by calculated (Ca O 2 ).
Note: This calculation simplifies D O 2 to three parameters: CO, Sa O 2 , and [Hgb]. Pa O 2 has been omitted because of the extremely small role it plays with regard to Ca O 2 (Remember: its contribution is 0.0031 x Pa O 2 ).
Alveolar-to-Arterial ( A a) Gradient:
Assessment of alveolarcapillary gas exchange used to indirectly quantify ventilationperfusion abnormalities. The calculation is occasionally useful as a tool to help determine the cause of hypoxemia (eg, hypoventilation).
Normal < 5%. Reflects the portion of CO that traverses the heart from right to left without increasing Ca O 2 ( 5% of pulmonary capillary blood leaves the lung without being oxygenated). In an ideal state, the volume of lung ventilation equals the volume of pulmonary capillary blood flow (Figure 2015, below). Alterations in these ventilationperfusion relationships have two causes:
- Relative obstruction of alveolar ventilation
- Relative obstruction of pulmonary blood flow
- 1. Perfusion greater than ventilation: A common scenario is pulmonary consolidation due to infection or secretions (Figure 2016). An alveolus receives no ventilation because of bronchiolar obstruction, yet normal pulmonary capillary perfusion continues (ie, complete pulmonary AV shunt exists with respect to that alveolus).
- 2. Ventilation greater than perfusion: Impairment of pulmonary blood flow to the alveolar level occurs after lung surgery and after pulmonary embolism (Figure 2017, below). Uniform ventilation continues to the alveoli, but no blood flow passes some of them. This situation increases the ventilated physiologic dead space and increases the shunt fraction.
- 3. Compensation mechanism: Figure 2018 represents the compensatory changes that occur when an alveolus is partially occluded. Local vasoconstriction results in diversion of blood flow to better ventilated alveoli. This mechanism is called hypoxic pulmonary vasoconstriction.
Principle: Recognize that at any given time, combinations of these situations exist simultaneously within the lung (remember that the normal shunt fraction is 5%). Therefore alterations in either ventilation or perfusion can seriously affect oxygenation.
- 1. Decreased lung-to-blood transfer. Associated factors include:
- Pulmonary edema
- Bronchial secretions
- 2. Decreased perfusion. Associated factors include:
- Massive PE
- Continued micropulmonary embolization
- Postoperative changes
Calculation of A a Gradient and Shunt Fraction:
The equations for determining A a gradient and shunt fraction are in comprehensive textbooks on critical care. Online (eg, http://medcalc3000.com) and PDA-based resources are available to assist in the calculations.
Indications for Intubation
The decision to intubate is often a stress-provoking process. The primary objective of mechanical ventilation is to decrease the work of breathing and reverse life-threatening hypoxia and hypercapnia. A point-prevalence study has shown that the most common indications for intubation and mechanical ventilation are respiratory failure (66%), coma (15%), acute exacerbation of COPD (13%), and neuromuscular disorders (5%). Common indications for mechanical ventilation include:
- Inability to adequately ventilate (eg, airway obstruction, severe chest trauma, excessive sedation, neuromuscular disease, paralyzed or fatigued respiratory muscles )
- Inability to adequately oxygenate (eg, pneumonia, pulmonary embolism [PE], pulmonary edema, ARDS)
- Excessive work of breathing (eg, severe bronchospasm, airway obstruction)
- Airway protection (eg, unconsciousness, altered mental status, massive resuscitation, facial or head trauma)
A timely decision to intubate a decompensating patient can turn an otherwise chaotic intubation into a controlled, elective procedure. Diagnostic factors that help predict impending respiratory failure are listed in Table 206.
Table 206 Indicators of Impending Respiratory Failure Necessitating Intubation and Mechanical Ventilation
| Condition || Normal Range (adults) |
| Respiratory impairment || |
| Tachypnea > 30 breaths/min || 1020 breaths/min |
| Dyspnea || |
| Neurologic impairment || |
| Loss of gag reflex || |
| Altered mental status (ie, patient is unable to protect airway against aspiration) || |
| Gas exchange impairment || |
| Pa CO 2 > 60 mm Hg |
| 3545 mm Hg |
| Pa O 2 < 70 mm Hg (on 50% mask) |
| 80100 mm Hg (on room air) |
| Sa O 2 < 90% |
Securing the Airway
An essential treatment component of respiratory failure is securing and maintaining a patent airway (see Chapter 21). Briefly, the airway is kept open with the chin-lift or the jaw- thrust maneuver. Perform the maneuver with great care if there is a possible cervical spine injury. Use a nasopharyngeal or oropharyngeal airway to keep the patient's tongue from obstructing the oropharynx. Definitive airway management includes oral or nasal endotracheal intubation. Use a laryngeal mask airway (LMA) as a temporary measure if attempts at endotracheal intubation fail. Use the Difficult Airway Algorithm established by the American Association of Anesthesiologists (Figure 2019) as a framework for managing a difficult airway. (See also Chapter 21, Emergency Airway and Ventilatory Support.)
Confirmation of Endotracheal Tube Placement:
Confirm tube placement with a colorimetric end-tidal CO 2 detector and auscultation of bilateral breath sounds.
- Tracheostomy. Used when long-term intubation is anticipated and for patients with severe maxillofacial injuries. This procedure is elective, unlike cricothyroidotomy. The benefits of tracheostomy are improved patient comfort and oral hygiene, ease of secretion removal, and a more secure airway.
- Cricothyroidotomy. Emergency procedure used when nonsurgical attempts to secure the airway have failed:
| || |
1. Extend the neck (if possible).
2. Make a midline incision with a no. 11 blade.
3. Puncture the cricothyroid membrane with the scalpel and rotate 90 degrees.
4. Keeping a finger in the cricothyroidotomy site, place a 6-0 ETT or cricoid tube into cricothyroidotomy site, and confirm placement.
5. Establish a definitive airway as soon as possible.
Esophageal intubation; pneumothorax; pneumomediastinum; recurrent laryngeal nerve injury; hemorrhage; tracheal stenosis (can be avoided by keeping cuff pressures < 25 mm Hg); ET tube dislodgement/self-extubation
Mechanical Ventilation Modes
See Figure 2020.
Controlled Mechanical Ventilation (CMV):
The patient receives only ventilator-delivered breaths at a set rate (ie, patient cannot initiate a breath without the ventilator). This mode once was used in the care of patients who were intentionally paralyzed by drugs because of extreme illness or trauma.
Assist-Control Ventilation (AC):
The ventilator delivers a full tidal volume with each inspiratory effort. The respiratory rate can be determined by the patient, although a set rate ensures adequate minute ventilation.
- Advantages: The patient can easily increase minute ventilation even with poor inspiratory effort. The result is a marked decrease in the work of breathing.
- Disadvantages: Can produce overventilation and respiratory alkalosis in tachypneic patients. Agitation can also result in breath-stacking and auto-PEEP. The reduced work of breathing with this mode comes at the expense of predisposition to diaphragmatic and intercostal muscle atrophy.
Synchronous Intermittent Mandatory Ventilation (SIMV):
The ventilator delivers set tidal volume at a minimum set rate (synchronized to patient inspiratory effort) during spontaneous breathing between mandatory tidal volumes. The spontaneous tidal volumes can be augmented with pressure support (PS). As the ventilator rate is decreased, the patient assumes more and more work of breathing. This mode can either provide full support (with a high mandatory rate) or be used as a weaning mode by decreasing the rate over time.
Maximal inspiratory pressure is defined. The delivered tidal volume is then a function of specified pressures and lung compliance. With volume- targeted modes, airway pressure varies with changing lung compliance. This mode requires careful monitoring because minute ventilation can decline with worsening lung compliance. Pressure control is often used in conjunction with inverse-ratio ventilation (ie, longer inspiratory times with shorter expiratory times) as another means of increasing mean airway pressure to improve oxygenation in hypoxic patients.
Pressure Support Ventilation (PSV):
Flow-cycled; patient determines tidal volume and cycle length. A preset level of positive pressure boost is turned on during inspiration and is off during expiration. The higher the PS, the less work the patient expends to take a breath. Because the patient is able to control the duration of lung inflation and tidal volume, PSV tends to be comfortable for most patients. PSV is useful for weaning because the PS can be turned down slowly, with changes as small as 1 cm water. Patient assumes additional work of breathing in small increments.
Pressure-Regulated Volume Control (PRVC):
Used in the setting of increased airway pressures (eg, acute lung injury, ARDS). A microprocessor in the ventilator minimizes the pressure needed to deliver the specified tidal volume by using decelerating flow during inspiration. PRVC can be thought of as dynamic pressure-controlled ventilation without the variation in tidal volumes associated with changing lung compliance.
The following is a sample of typical initial ventilator settings for an adult:
- Mode (eg, AC, SIMV)
- F IO 2 30100%
- Rate 1018 breaths/min
- Tidal volume 46 mL/kg
- PS (520 cm water)
- PEEP (5 cm water or higher, if needed)
Ventilator Setting Changes
Five basic respiratory parameters (F IO 2 , minute ventilation, PS, PEEP, I/E ratio) can be changed to improve ventilation, oxygenation, and compliance.
- 1. F IO 2 : Choose an initial F IO 2 that ensures adequate arterial O 2 saturation (Sa O 2 > 90%). Increasing the level of PEEP is often a helpful means of decreasing the F IO 2 requirement while maintaining adequate oxygenation. Once adequate oxygenation is established, decrease the F IO 2 to avoid O 2 toxicity (avoid F IO 2 > 60%).
- O 2 toxicity: Damage to lungs occurs if the intraalveolar O 2 concentration is > 60% (injury actually occurs after a few hours if F IO 2 = 1.0). The mechanism probably involves generation of reactive O 2 species that oxidize the cell membranes. O 2 toxicity has not been documented if F IO 2 is maintained < 60%.
- 2. Minute ventilation: Adjust to maintain P CO 2 within a normal range (3545 mm Hg). Because minute ventilation is the product of rate and tidal volume, make this adjustment by varying either of these values. Once a tidal volume is chosen, set the respiratory rate ( 816 breaths/min) for adequate minute ventilation. For a spontaneously breathing patient, PS can be increased to achieve a target minute ventilation.
- 3. Pressure support: After the patient's respiratory pattern is established on SIMV, add PS at an initial level of 510 cm water. Increase PS to the level at which the patient can achieve reasonable tidal volume and breathe at a comfortable rate (< 30 breaths/min). Depending on the overall stability and mental status of the patient, turn down the number of SIMV backup breaths so that the patient assumes more control of ventilation. PS rarely has to exceed 20 cm water.
- 4. PEEP: With the addition of PEEP, the ventilator maintains positive airway pressure at the end of expiration even though net airflow is zero. PEEP increases alveolar ventilation by preventing small-airway collapse, thereby improving lung compliance and FRC. Increasing levels of PEEP are typically used in the care of hypoxemic patients who need F IO 2 > 50%. With PEEP, F IO 2 can be reduced and O 2 toxicity limited. PEEP 5 cm water is considered physiologic. If oxygenation remains marginal, PEEP is added in 2- to 3-cm increments until oxygenation is improved. In acute lung injury, the PEEP at which lung compliance is optimized can be determined by observation of pressure-volume loops .
- High-Dose PEEP: The elevated intrathoracic pressure associated with high PEEP can compromise venous return and thus decrease stroke volume and CO, particularly in hypovolemic patients. The result is decreased oxygen delivery. Consider placement of a PA catheter. Because ICP can become elevated, titrate PEEP upward with caution in patients with intracranial hypertension.
- 5. Inspiratory to expiratory (I/E) ratio: The normal I/E ratio is 1/2 or 1/3. Inverse-ratio ventilation (eg, 2/1) results in progressive recruitment of alveoli and elevation of mean airway pressure, which improves oxygenation. This beneficial effect on oxygenation is lost if "breath stacking" or auto-PEEP occurs. Note: This technique may be inappropriate in the care of patients with obstructive lung disease, in which longer expiratory times are required. Inverse-ratio ventilation is poorly tolerated by awake patients and typically requires heavy sedation. Shorter expiratory times can result in hypercapnia; this "permissive hypercapnia" is sometimes accepted to improve oxygenation. Balance F IO 2 and peak pressure to keep peak pressure < 35 cm water. If unable to do so, move to pressure support ventilation.
Before weaning the patient from the ventilator, assess pulmonary mechanics and oxygenation (Table 207).
Table 207 Criteria for Extubation from Mechanical Ventilation
| Parameter || Value |
| Pulmonary mechanics || |
| Vital capacity || > 1015 mL/kg |
| Resting minute ventilation || > 10 L/min |
| (tidal volume x rate) || |
| Spontaneous respiratory rate || < 33 breaths/min |
| Lung compliance || > 100 mL/cm water |
| Negative Inspiratory force (NIF) || > 25 cm water |
| Oxygenation || |
| A a gradient || < 300500 mm Hg |
| Shunt fraction || < 15% |
| P O 2 (on 40% F IO 2 ) |
| > 70 mm Hg |
| P CO 2 |
| < 45 mm Hg |
Information about the patient's ability to perform the work of respiration. Routine pulmonary mechanics consist of:
- Vital capacity
- Tidal volume
- Spontaneous respiratory rate
- Lung compliance
The maximum negative pressure that can be exerted against a completely closed airway (a function of respiratory muscle strength). An inspiratory force between 0 and 25 cm water suggests that the patient may be incapable of generating adequate inspiratory effort for successful extubation.
Ventilators are designed to facilitate weaning. Once the preceding criteria have been met, select a ventilator mode appropriate to the clinical situation. SIMV and PSV are considered weaning modes because the patient assumes more of the workload of breathing as mechanical support is reduced.
Order of Weaning:
Take the following steps to wean the patient from the ventilator:
- 1. Reduce F IO 2 to 40% while monitoring Sp O 2 .
- 2. Sequentially reduce the IMV rate to a level of 48 breaths/min. Add PS to maintain adequate minute ventilation. Closely monitor minute ventilation (on ventilator display).
- 3. Sequentially reduce PEEP in increments of 2- to 3-cm water while maintaining Sp O 2 > 90% until a level of 5 cm water is achieved.
- 4. Sequentially reduce PS by increments of 23 cm water while maintaining minute ventilation (goal: 510 cm water); monitor respiratory rate, work of breathing, and minute ventilation.
Checklist for Extubation
- Correction of primary problem that prompted intubation and mechanical ventilation (eg, successfully treated pneumonia, returned hemodynamic stability)
- Level of consciousness stable or improved
- Stable vital signs
- Pulmonary mechanics and oxygenation meet acceptable criteria (see Table 207)
Once weaning has been achieved, attempt trials with minimal mechanical support while the patient is still intubated. CPAP trials (with 5 cm water positive pressure) is the most commonly used method. A CPAP trial with an F IO 2 of 40% should result in a Pa O 2 of > 70 mm Hg, and a respiratory rate < 25 breaths/min. One of the best predictors of successful extubation is the ratio of respiratory rate to tidal volume (f/Vt, or Tobin index). Extubation frequently is unsuccessful in patients with a rapid shallow breathing pattern. A ratio > 100 has been shown in some studies to be predictive of extubation failure ( N Engl J Med 1991;324:14451450). These trials may vary in duration from 30 min to several hours and are used primarily as the last test before extubation.
A patient who is able to maintain a P O 2 > 70 mm Hg, a P CO 2 < 45 mm Hg, and a respiratory rate < 25 breaths/min for 12 h on a CPAP trial is ready for extubation.
- 1. Disconnect the ET tube from the ventilator or T-piece.
- 2. Suction the ET tube and oropharynx.
- 3. Have the patient take a deep breath.
- 4. As the patient expires forcefully , deflate the cuff and remove the tube.
- 5. Suction any secretions and administer O 2 through a nasal cannula at 24 L/min.
- 6. Check postextubation ABG if adequate ventilation and oxygenation are in doubt.
Nutrition in the ICU
The nutritional support of critically ill patients is crucial to their survival. Restoring an anabolic state hastens recovery and avoids complications. Protocols for nutritional support are covered in Chapters 11 and 12. Remember the following two rules:
- 1. The "2-day" rule applies to most patients. If you believe the critically ill patient will not be able to take nutrition for 2 days because of conditions such as postoperative ileus and intubation, make arrangements for nutritional support.
- 2. "If the gut works, use it." Use enteral nutrition (oral, NG tube, jejunostomy tube) in all patients with a functioning intestinal tract (see Chapter 11).
Complications in Critical Care
Acute Respiratory Distress Syndrome (ARDS)
ARDS is acute pulmonary injury manifested by marked respiratory distress and hypoxia. Pulmonary capillaries become more permeable, resulting in noncardiogenic pulmonary edema. ARDS has been defined by the AmericanEuropean Consensus Conference as:
- Acute onset
- P/F ratio (Pa O 2 /F IO 2 ) 200 regardless of PEEP level
- Bilateral infiltrates on CXR
- PAOP < 18 if measured, or no clinical evidence of left atrial hypertension
Acute lung injury is similarly defined; it differs only in the degree of hypoxemia (P/F ratio 300).
The causes of ARDS are multifactorial and include but are not limited to:
- Severe pancreatitis
- Severe burns
- Transfusion-related acute lung injury
- Chemical pneumonitis or inhalational injury
Management of ARDS is generally supportive. Focus efforts on preventing secondary insults and avoiding ventilator-associated lung injury. The ARDS Network low tidal volume approach entails use of a tidal volume of 6 mL/kg of predicted body weight with respiratory rate adjusted to achieve adequate minute ventilation. The goal is to achieve plateau pressures of 30 cm water. The PEEP ladder in Table 208 guides PEEP settings according to F IO 2 .
| F IO 2 |
| 0.30 || 0.40 || 0.50 || 0.60 || 0.70 || 0.80 || 0.90 || 1.0 |
| PEEP || 5 || 58 || 810 || 10 || 1014 || 14 || 1418 || 1822 |
Based on data in: The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:13011308.
Upper Gastrointestinal Hemorrhage
Critically ill patients are at increased risk of GI hemorrhage secondary to stress-induced mucosal ulceration. Head injury (Cushing ulcers); mechanical ventilation; NSAID use; shock, trauma, and burns (Curling ulcers); coagulopathy; and a history of peptic ulcer disease or portal hypertension are a few of the risk factors.
- Enteral feedings: method of choice to protect the gastric mucosa
- Cardiovascular support of visceral perfusion
- Acid suppression: prophylaxis with H 2 -blockers (eg, ranitidine, famotidine). Proton-pump inhibitors (eg, lansoprazole, omeprazole) for refractory bleeding or in patients with adverse reaction to histamine blockade.
Management of Ulceration
- 1. Early endoscopy for upper GI bleeding
- 2. Endoscopic or surgical intervention for visible bleeding vessel
- 3. Aggressive acid suppression for diffuse gastritis; empiric therapy for Helicobacter pylori infection
- 4. Possible surgical intervention for persistent bleeding from gastritis
Shock can be defined simply as tissue hypoperfusion. Uncorrected shock leads to cellular dysfunction, organ failure, and death. Direct the management of shock at correcting the underlying problem. Endogenous compensatory mechanisms directed at reversing hypotension and shock include the release of catecholamines, cortisol, and activation of the reninangiotensinaldosterone axis.
The morbidity and mortality of shock are related to the cause but probably more to the degree and time of circulatory compromise. When the causes are identified and corrected, the patient is resuscitated to restore tissue perfusion and reverse the effects of shock.
Inadequate circulating blood volume (at least 20% loss) is caused by dehydration or acute hemorrhage. Hemodynamic parameters show decreased CVP, PAOP, and EDVI with a consequent decrease in CO and increase in SVR. Table 209 lists the current classification and physiologic changes associated with hypovolemic shock.
- 1. Control the source of intravascular volume loss.
- 2. Rapidly replace intravascular volume with isotonic crystalloid, colloid, or blood products as appropriate.
Cardiogenic shock is caused by pump failure either from intrinsic cardiac abnormalities (eg, severe valvular disease, AMI, coronary ischemia, arrhythmias) or extrinsic processes (eg, tension pneumothorax, pericardial tamponade, PE).
Directed at improving cardiac performance
- 1. Resolve extrinsic processes if present.
- 2. Optimize preload for CO.
- 3. Decrease afterload (ACE inhibitors, nitrates, etc).
- 4. Improve cardiac contractility with inotropic support.
- 5. Consider mechanical support (intraaortic balloon pump).
- 6. Consider aspirin and heparin therapy.
Septic shock is a clinical syndrome associated with severe infection and is characterized by a systemic inflammatory response with resultant tissue injury. The following definitions have been established by a consensus conference convened by the American College of Chest Physicians and the Society of Critical Care Medicine ( Crit Care Med 2003;31, no. 4).
- Systemic inflammatory response syndrome (two or more of the following):
- Temperature > 38C or < 36C
- Heart rate > 90 beats/min
- Respiratory rate > 20 breaths/min or P CO 2 < 32 mmHg
- WBC > 12,000/ L or < 4000/ L
- Sepsis: Infection with a systemic inflammatory response
- Severe sepsis: Sepsis with organ dysfunction
- Septic Shock: Acute circulatory failure with persistent unexplained hypotension
Surviving Sepsis Campaign Guidelines:
Evidence-based recommendations for the management of sepsis and septic shock published in 2004 ( Crit Care Med 2004;32, no. 3) call for early goal-directed therapy.
Initial Resuscitation: Begin as soon as the syndrome is recognized. Do not wait for ICU admission. Goals for the first 6 h of resuscitation include:
- CVP 812 mm Hg
- MAP 65 mm Hg
- Urine output 0.5 mL/kg/h
- Central venous or S O 2 70%
- If the S V O 2 goal is not achieved with fluid resuscitation to the target CVP within the first 6 h, add transfusion of PRBC to a hematocrit of 30%, infusion of dobutamine, or both.
Diagnosis: Obtain cultures before initiating antibiotic therapy. Draw blood cultures peripherally, and from each vascular access device. Obtain appropriate imaging studies to evaluate for possible sources when possible. Remember: transport of a critically ill patient can be dangerous.
Antibiotic Therapy: Obtain cultures and initiate IV antibiotics within the first hour after recognizing severe sepsis. Consider broad-spectrum antibiotics on the basis of susceptibility patterns at the hospital. Alter antibiotics as dictated by culture results, or discontinue them if a noninfectious cause of cardiovascular collapse is identified.
Source Control: Evaluate for possible source control measures (eg, abscess drainage, debridement, removal of infected devices). Expedite source control after initial resuscitation.
Fluid Therapy: No evidence-based support exists to guide choice of resuscitation fluid (natural or artificial colloid vs isotonic crystalloid). Give fluid challenges as a bolus with careful monitoring so that hemodynamic response can be observed . Large volumes may be needed during the first 24 h of management.
Vasopressors: If fluid resuscitation does not restore adequate blood pressure and perfusion, initiate vasopressor support with dopamine or norepinephrine via a central venous catheter. Do not use "renal dose" dopamine as a protective strategy because it has no demonstrated outcome benefit. Direct measure of arterial blood pressure with arterial catheters is preferred over cuff measurements in the setting of shock. Add low-dose vasopressin (0.010.04 units/min) if shock is refractory to fluid resuscitation and usual vasopressor support.
Inotropic Therapy: If CO stays low despite fluid resuscitation, add dobutamine with the goal of achieving adequate O 2 delivery to peripheral tissues. If hypotension is present, use dobutamine in conjunction with vasopressors (ie, norepinephrine).
Steroids: Hydrocortisone is recommended for patients with septic shock necessitating vasopressor support (200300 mg/d in divided doses or by continuous infusion). Higher doses are not effective and are potentially harmful . Relative adrenal insufficiency has been defined as a post-ACTH (250 mcg stimulation test) cortisol increase < 9 mcg/dL at 3060 min. Some clinicians would discontinue steroid therapy in patients who respond appropriately to the stimulation test.
Recombinant Human Activated Protein C: Consider rhAPC (Xigris) for patients at high risk of death (APACHE II score 25, multiple organ system dysfunction, septic shock, sepsis-induced ARDS). Carefully review contraindications before starting this therapy.
Blood Product Administration: After resolution of the shock state (and in the absence of ongoing hemorrhage, coronary artery disease, etc), decrease the transfusion threshold to 7 g/dL for most patients with a target hemoglobin of 79 g/dL. Erythropoietin is not recommended for management of anemia associated with sepsis in the absence of other indications (eg, renal failure). FFP is not recommended for the correction of abnormal clotting times unless bleeding is present or an invasive procedure anticipated. Administration of antithrombin is not recommended. Transfuse platelets when the platelet count decreases to < 5000/ L, and consider transfusion for platelet counts of 500030,000/ L if there is high risk of hemorrhage.
Mechanical Ventilation of Sepsis-Induced Acute Lung Injury: The Surviving Sepsis Guidelines support the low tidal volume (6 mL/kg) strategy (ie, ARDSNet) with goal plateau pressures < 30 cm water. Permissive hypercapnia is allowed if needed; PEEP is adjusted on the basis of F IO 2 requirement or is titrated to achieve optimal compliance. Consider prone positioning of patients who need high F IO 2 . Elevate the head of bed to 45 degrees to reduce pneumonia risk.
Sedation, Analgesia, and Neuromuscular Blockade in Sepsis: Sedation protocols (with scales such as the RASS) and daily interruption of sedation have been shown to decrease duration of mechanical ventilation and hospital length of stay. Avoid neuromuscular blockade unless absolutely necessary.
Glucose Control: Recommended upper limit for glucose control is 150 mg/dL. (The range used in the landmark study [ N Engl J Med 2001;345:13591367] of intensive insulin therapy in critically ill patients was 80110 mg/dL). Extending the upper range of glucose control reduces hypoglycemic episodes . Tight glucose control is achieved through infusion of insulin. Assure a glucose source (eg, D 5 or D 10 infusion). Enteral feeding is the preferred source of glucose.
Renal Replacement: If the patient is in hemodynamically stable condition, continuous venovenous hemofiltration (CVVH) and intermittent hemodialysis are equivalent therapies. CVVH is more appropriate for hemodynamically unstable patients.
Bicarbonate Therapy: Bicarbonate therapy is not recommended for the management of sepsis-related lactic acidemia for pH 7.15.
Deep Vein Thrombosis Prophylaxis: Administer DVT prophylaxis in the form of subcutaneous heparin or low-molecular-weight heparin. If contraindications are present, consider mechanical prophylaxis sequential compression devices).
Stress Ulcer Prophylaxis: H 2 -receptor inhibitors are preferred.
Consideration for Limitation of Support: Communication between caregivers and families is vital, particularly with respect to end of life care and patient wishes.
Pediatric Considerations: In general, the aforementioned guidelines apply to adult patients. Refer to the Surviving Sepsis Campaign guidelines for special issues related to the care of pediatric patients ( Crit Care Med 2004;32[11 suppl]).
Caused by loss of sympathetic vascular tone (eg, high thoracic or cervical spinal cord injury) producing an increase in vascular capacitance .
- 1. Optimize filling pressures by IV fluid administration.
- 2. Provide vasopressor support as necessary.
- 3. Keep fluids and room temperature warm because these patients lose the ability to thermoregulate.
Acute Renal Failure (ARF)
Sudden development of renal insufficiency resulting in retention of nitrogenous wastes (BUN, creatinine), variable effects on fluid balance, oliguria and anuria, and progressive azotemia. ARF is usually divided into prerenal, renal, and postrenal causes (see Chapter 6). Once ARF is recognized, the primary objective is to correct the underlying cause. The most common causes of renal failure in the ICU are acute tubular necrosis (ATN) and prerenal disease. Among the many causes of ATN are nephrotoxic medications, ischemia, and hypotension. Prerenal causes include intravascular volume depletion and CHF. Indications for hemodialysis include:
- Refractory fluid overload
- Severe metabolic acidosis
- Severe uremia
- Toxic accumulation of drugs
Iatrogenic cause of ARF. If use of contrast agents is unavoidable in high-risk patients (eg, diabetic patients with chronic renal insufficiency) the following strategies may reduce the risk:
- Avoiding volume depletion and NSAIDs
- Acetylcysteine (600 mg PO bid the day before and the day of contrast administration) and prehydration ( N Engl J Med 2000;343:180184)
- Bicarbonate infusion (154 mEq/L at 3 mL/kg/h for 1 h) before exposure, then 1 mL/kg/h during exposure and for 6 h after exposure ( JAMA 2004;291:23282334)
Abdominal Compartment Syndrome
Consequence of intraabdominal hypertension resulting in symptomatic organ dysfunction. Caused by resuscitation-related bowel edema and fluid sequestration or retroperitoneal hemorrhage causing a mass effect. Increased intraabdominal pressure directly decreases visceral perfusion and results in organ dysfunction and respiratory compromise.
Consider the diagnosis in the setting of worsening lung compliance, abdominal distention, and oliguria. Hypotension is a late finding. Measurement of bladder pressure confirms the diagnosis. Although the clinical scenarios can be highly variable, organ dysfunction may be present with pressures as low as 10 mm Hg. Consider abdominal decompression when abdominal pressure exceeds 2025 mm Hg.
Early decompressive celiotomy. Close the abdominal fascia when edema and organ dysfunction resolve.
Cholecystitis in the absence of gallstones is common among ICU patients. Although the precise cause is not known, it is probably related to diminished blood flow to the gallbladder and to bacterial overgrowth.
Signs are similar to those in noncritical patients with cholecystitis and include right upper quadrant pain, fever, and leukocytosis. Perform right upper quadrant ultrasonography. Add a HIDA scan if the sonographic findings are nondiagnostic (nonvisualization of the gallbladder is highly suggestive of acalculous cholecystitis).
Treatment is open surgical removal of the gallbladder (cholecystectomy). Percutaneous cholecystostomy is an alternative in the care of critically ill patients who may not tolerate operative intervention. Interval cholecystectomy is performed when the patient's condition improves.
Acute Adrenal Insufficiency
Adrenal crisis may be precipitated in patients with primary adrenal insufficiency in the setting of severe infection or surgical stress. It may also arise as a consequence of bilateral adrenal infarction or hemorrhage. Clinical manifestations include cardiovascular collapse, hyponatremia, hyperkalemia, fever, abdominal pain, and nonspecific findings such as malaise, anorexia , nausea, and decreased mental status. Initial treatment is directed at correcting hypotension and electrolyte abnormalities, as well as cortisol replacement. Initiate resuscitation with normal saline solution; large volumes may be required. Administer IV dexamethasone (4 mg) or hydrocortisone (100 mg) first. Dexamethasone may be preferable initially because it is longer acting than hydrocortisone and does not interfere with ACTH stimulation tests. Determine the factor that precipitated the adrenal crisis (eg, infection) and correct it promptly. Once the crisis resolves, administer oral glucocorticoids and taper them over several days. Consider adding mineralocorticoid (eg, fludrocortisone) replacement.
Clinical pneumonia that develops after 48 h of mechanical ventilation. Occurs in approximately 25% of intubated ICU patients; overall mortality, 2050%. The strongest risk factor for ICU pneumonia is mechanical ventilation (6- to 15-fold increase); others are age > 70 y, chronic lung disease, nasoenteric tubes, altered mental status, chest trauma or surgery, and frequent transportation of the patient.
Diagnosis: A positive airway culture (preferably of a bronchoalveolar lavage (BAL) specimen with quantitative cultures showing > 10 4 CFU/mL) plus three of the four following:
- New, persistent, or progressive CXR infiltrate
- Purulent tracheobronchial secretions
Treatment: Empiric therapy customized according to the institution's antibiogram for the particular ICU and adjusted when C&S data are available. Continue therapy for 812 d. Repeat BAL with cultures and special stains as needed if standard antibiotic therapy fails.
Indwelling catheters are essential, but they also act as a portal of entry for bacteria. Consider catheter-related sepsis if a fever develops in an ICU patient. The most common mechanism is entry of skin flora along the catheter track. Because prolonged use of polyurethane dressings increases the risk of infection, avoid these dressings. Some ICUs have a policy of routine line changes over a guidewire every 34 d. This policy, however, is not supported by evidence in the literature, and the infection rate may increase with this approach. Prevent line sepsis with meticulous aseptic technique during line placement (including full gowning, gloving, and draping) and meticulous care of the line once it is in place.
Diagnosis: If the site does not appear infected, the catheter may be exchanged over a guidewire and the intracutaneous segment and tip sent for culture. A new IV site is chosen if the catheter culture result is positive. Erythema is suggestive of catheter site infection; however, coagulase-negative staphylococci can elicit minimal inflammation .
Treatment: Remove short-term central venous catheters suspected of being infected and culture them. Start empiric antimicrobial therapy pending culture results. A catheter colony count > 15 CFU suggests catheter infection.
Deep Venous Thrombosis (DVT) and Pulmonary Embolism (PE)
PE causes 150,000 deaths annually in the United States. DVT causes most cases of PE in hospitalized patients. About 90% of cases of PE originate in the femoraliliacpelvic veins. DVT is promoted by the presence of the Virchow triad : endothelial injury, hypercoagulability, and blood stasis.
Prevention of DVT:
Risk factors include malignant disease, obesity, history of DVT, age > 40 y, extensive abdominal or pelvic surgery, long bone or pelvic fractures, and prolonged immobilization. For surgical patients, initiate prophylaxis in the OR before induction of anesthesia. Use of sequential compression devices and selected heparinoids has reduced the incidence of DVT.
Physical Methods: Leg elevation, sequential compression devices, and early postoperative ambulation (most important).
- Heparin 5000 units SQ q8h. Monitor platelet count ( = q3d) for heparin-induced thrombocytopenia.
- Coumadin for chronic therapy
- Low-molecular-weight heparin (LMWH) (eg, Enoxaparin) is the drug of choice for high-risk patients.
Diagnosis of PE
- Signs and symptoms: None is diagnostic; dyspnea, tachypnea, tachycardia, chest pain (usually pleuritic), and hypoxia.
- CXRs are not sensitive enough to be useful in the diagnosis of PE but help may rule out other causes of the symptoms (eg, pneumonia, pneumothorax).
- Spiral CT: The clinical validity of CT in ruling out PE equals that of pulmonary angiography ( JAMA 2005;293:20122017).
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1. Support oxygenation. Monitor Sp O 2. Intubation may be needed.
2. Anticoagulate with unfractionated or LMWH to prevent clot propagation, decrease inflammation, and allow intrinsic fibrinolysis to lyse the clot.
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a. Evidence-based guidelines suggest body weightadjusted subcutaneous LMWH is the preferred initial therapy for acute nonmassive PE ( Chest 2004;126:401s428s). If unfractionated heparin is chosen (eg, patient with severe renal failure), administer bolus with 80 units/kg IV and start an infusion at 18 units/kg/h. Titrate the infusion to maintain the PTT at 22.5 x control value. Check the PTT 6 h after rate adjustments.
b. Monitor the platelet count for heparin-induced thrombocytopenia.
c. Start oral warfarin (Coumadin) by day 3 of heparin therapy to achieve and maintain an INR of 23 (see Chapter 22).
3. In massive PE, administer thrombolytic therapy (TPA) if not contraindicated.
4. Consider pulmonary embolectomy for hemodynamically unstable patients with massive PE if medical therapy is not successful.
5. If anticoagulation is contraindicated (eg, recent surgery, stroke, GI bleeding) or if PE recur despite anticoagulation, consider placement of a vena caval filter placement.
Quick Reference for Critical Care Formulas
Table 2010 provides a summary of commonly used formulas in the critical care setting.
Guidelines for Adult Critical Care Infusions
Table 2011 provides key information on the use of infusions in the ICU setting.
Table 2011 Guidelines for Adult Critical Care Drug Infusions
| Drug || Use/Mechanism || Dose Range || Side Effects/Cautions |
| Amrinone (Inocor) || Inotrope and vasodilator (systemic, pulmonary coronary); used in CHF-resistant to diuretics and afterload reduction || Load: 0.75 mg/kg over 3 min || Adverse effects to catecholamines and digoxin; hypotension (dose-dependent); thrombocytopenia (12%); increase AV and ventricular conduction; nausea/vomiting/abdominal pain |
| Dose: 520 mcg/kg/min (max 10 mg/kg/d) |
| Diltiazem (Cardizem) || Slow calcium channel blocker; negative inotrope; prolongs AV node refractory time; vasodilates to lower BP without reflex tachycardia || Bolus=0.25 mg/kg over 2 min (may give second bolus 0.35 mg/kg 15 min after initial dose) || Hypotension: AV block; drug-induced hepatitis; flushing |
| Dose 515 mg/hr || Contraindications : Wide-complex tachycardia; WolffeParkinsonWhite syndrome; existing 2nd or 3rd degree AV block; concurrent -blockade |
| Dobutamine (Dobutrex) || Racemic mixture ( L -isomer: -agonist/ D -isomer; -agonist); positive inotrope/afterload reduction for circulatory failure after AMI, CHF, etc || Dose: 220 mcg/kg/min || May exacerbate ventricular arrhythmias |
| Max: 40 mcg/kg/min || Contraindications : hypertrophic cardiomyopathy |
| Dopamine (Inotropin) || Dopaminergic (0.52.0 mcg/kg/min): renal, cerebral, mesenteric vasodilation || -agonist (1020 mcg/kg/min); predominantly vasopressor || Enhances AV conduction, especially with atrial fibrillation; may exacerbate psychosis and arrhythmias |
| -/ -agonist (2.010 g/kg/min): positive inotrope and vasopressor || Max: 40 mcg/kg/min || Caution : Urgently treat extravasated drug with phentolamine to prevent skin necrosis |
| Epinephrine (Adrenalin) || Nonspecific adrenergic agonist ( > ); potent bronchodilator ( 2 , agonist) |
| Shock: 2 mcg/min, then titrate || Increases myocardial oxygen consumption; protachyarrhythmia; splanchnic vasoconstrictor (if dose < 4 mcg/min); diabetogenic; promotes hypokalemia |
| Cardiac arrest: 1 mg IV q35 min |
| Esmolol (Brevibloc) || 1 -selective; very short half-life (9 min); slows AV node conduction; useful to test blockade in patients with potential contraindications |
| Load: 500 mcg/kg over 1 min || Bronchospasm; pallor; nausea; flushing; bradycardia; pulmonary edema (if heart failure occurs); asystole |
| Dose: 50 mcg/kg min; titrate by 50 mcg/kg min to target HR (may need to repeat load) |
| Isoproterenol (Isuprel) || Nonspecific -agonist; potent inotrope/chronotrope for bradycardic states || Initially: 14 mcg/min || Hypotension; tachycardia; myocardial ischemia |
| Titrate up to 20 mcg/min based on target HR || Contraindications : Angina/myocardial ischemia; tachycardia; digitalis-induced bradycardia |
| Milrinone (Primacor) || Inotrope and vasodilator (systemic, pulmonary, coronary); used in CHF || Load: 50 mcg/kg over 10 min || Renal elimination ; hypotension; tachycardia; aggravates atrial, ventricular arrhythmias; headache |
| Dose: 0.3775 mcg/kg/min |
| Nicardipine (Cardene) || Calcium channel blocker; vasodilator >> negative inotrope; short half-life and rapid hepatic elimination || Dose 5 mg/h; titrate to BP goal (increase rate by 2.5 mg/h q515min) || Delayed clearance with hepatic and renal insufficiency; may worsen portal hypertension; may cause reflex tachycardia |
| Max: 15 mg/h || Contraindications : Critical aortic stenosis; will alter cyclosporine levels |
| Nitroglycerin (Tridil) || Arterial/venous vasodilator (dose-dependent); coronary vasodilator; combined with dobutamine with acute coronary syndrome || Dose: 510 mcg/min; titrate by 1020 mcg/min q5 min based on current dose and patient condition; hypotension at 200 mg/min || Headache, nausea, vomiting, dizziness |
| Contraindications : Increased ICP; narrow-angle glaucoma; pericardial tamponade |
| Nitroprusside (Nipride) || Arterial/venous vasodilator; donates nitric oxide to interact with vascular smooth muscle >> visceral smooth muscle || Dose: 0.510 mcg/kg/min; titrate to goal BP every few min || Reacts with Hgb to form met-Hgb cyanide accumulation; detoxified to thiocyanate by liver and kidney; keep met-Hgb < 10%; may shunt blood away from renal/splanchnic beds |
| Max: 10 mcg/kg/min |
| Norepinephrine (Levophed) || Potent 1 / -agonist (low-dose: > ) (high-dose: > ); use for cardiogenic/septic/neurogenic shock after volume repletion |
| Initial: 2 mcg/min || Peripheral A-lines may be dampened by vasoconstriction; suspect volume depletion with hypotension; treat extravasation with phentolamine |
| Dose: 220 mg/min; titrate to response |
| Max: 40 mg/min || May decrease splanchnic blood flow; spares cerebral, coronary blood flow |
| Phenylephrine (Neo-Synephrine) || Postsynaptic -agonist; use for hypotension shock, spinal anesthesia, or drug-induced hypotension || Bolus: 0.10.5 mcg IV q15min || May cause reflex brachycardia (blocked by atropine); constricts coronary, cerebral, and pulmonary vessels |
| Initial: 100 mcg/min; titrate to 40200 mcg/min || Contraindications : Use reduced doses in patients taking MAO inhibitors |
| Vasopressin (Pitressin) || Potent vasoconstrictor; anti-diuretic; procoagulant; used for variceal hemorrhage to reduce portal pressures; emerging indications in septic shock || Dose: 0.040.1 units/min || Myocardial ischemia due to coronary vasoconstriction; may need to combine with nitroglycerin; hepatic/renal metabolism with renal excretion |
| SIADH/water intoxication; abdominal cramps |
a Note : These agents must be administered in the appropriately monitored clinical setting.
CHF = congestive heart failure; AV = atrioventricular; BP = blood pressure; AMI = acute myocardial infarction; HR = heart rate; Hgb = hemoglobin; MAO = monoamine oxidase; SIADH = syndrome of inappropriate antidiuretic hormone.