General Principles

  • A process in which blood flow and oxygen delivery to tissues are deranged, leading to tissue hypoxia and resultant compromise of cellular metabolic activity and organ function.
  • Main goal of therapy is rapid cardiovascular resuscitation to reestablish tissue perfusion.
  • Definitive treatment requires reversal of underlying processes.

Classifications of Shock

Hemodynamic patterns associated with the different shock states are listed in Table 8-5.

Table 8-5: Hemodynamic Patterns Associated With Specific Shock States

aEqualization of RAP, PAOP, diastolic PAP, and diastolic RVP establishes a diagnosis of cardiac tamponade.

CI, cardiac index; N, normal; PAOP, pulmonary artery occlusion pressure; PAP, pulmonary artery pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation; SVR, systemic vascular resistance.

  • Distributive: Shock caused by massive vasodilation and impaired distribution of blood flow, resulting in tissue hypoxia. Usually associated with hyperdynamic cardiac function, unless cardiac function is somehow impaired (see later discussion of cardiogenic shock).
    • Primary etiologies are septic shock and anaphylactic shock. Septic shock is most commonly seen in medical ICUs and will be further discussed in the next section. Anaphylaxis is discussed in Chapter 11, Allergy and Immunology. Other less common types include neurogenic shock and adrenal shock.
    • Hemodynamic parameters will generally demonstrate increased cardiac output (CO), decreased systemic vascular resistance (SVR) due to vasodilation, and elevated central venous oxygen saturation (ScvO2) due to ineffective oxygen extraction by tissue.
    • Primary goals of therapy
      • Volume resuscitation: Owing to massive peripheral vasodilation, patients have a functionally decreased oxygen-carrying capacity, requiring volume resuscitation. IV crystalloid fluids are primarily used.
      • Treatment of underlying infection: Inadequate initial antimicrobial therapy is an independent risk factor for in-hospital mortality in patients with septic shock, so timely, effective antimicrobial therapy is a cornerstone of treatment.
      • Removal of the offending agent in anaphylactic shock.
      • Cardiovascular support with vasoactive agents (e.g., norepinephrine). Vasoactive agents will be discussed in more detail in a later section.
  • Hypovolemic: Shock caused by a decrease in effective intravascular volume and decreased oxygen-carrying capacity.
    • Primary etiologies are hemorrhagic (e.g., trauma, gastrointestinal bleeding) or fluid depletion (e.g., diarrhea, vomiting).
    • Hemodynamic parameters will generally demonstrate a decreased CO, increased SVR, and decreased ScvO2 due to increased oxygen extraction by peripheral tissue.
    • Primary goals of therapy
      • Volume resuscitation: IV blood product and crystalloid are used for resuscitation of hemorrhagic and fluid depletion shock, respectively, with goal mean arterial pressure (MAP) of 60–65 mm Hg. Overresuscitation may be detrimental in hemorrhagic shock and patients without significant comorbidities may tolerate lower hemoglobin levels (7 g/dL) than previously believed.
      • Definitive treatment of underlying etiology of volume loss: For hemorrhagic shock, surgical intervention may be necessary.
  • Obstructive: Shock caused by obstruction of the heart or great vessels, resulting in decreased left ventricular filling and cardiovascular collapse.
    • Primary etiologies are pulmonary embolism, cardiac tamponade, and tension pneumothorax.
    • Hemodynamic parameters will generally demonstrate decreased CO, normal to increased SVR, and normal to decreased ScvO2.
    • Primary goals of therapy
      • Supportive: Although patients are preload dependent, excessive fluid administration can lead to right ventricular overload and impairment of LV filling, thereby worsening shock.
      • Definitive therapy involves relieving the obstruction (e.g., thoracostomy in the case of a pneumothorax, and pericardiocentesis in tamponade).
      • In a carefully selected group of patients, thrombolytic therapy may be beneficial in patients with pulmonary emboli.
  • Cardiogenic: Shock caused by left ventricular systolic failure, resulting in decreased CO and subsequent insufficient oxygen distribution.
    • Primary etiologies are myocardial infarction, acute mitral regurgitation, and myocarditis.
    • Hemodynamic parameters will demonstrate decreased CO, increased SVR, and decreased ScvO2.
    • Primary goals of therapy
      • Mitigation of pulmonary edema: NPPV or endotracheal intubation with mechanical ventilation reduces afterload, thereby encouraging forward flow, as well as preload. Additionally, the application of positive pressure to the alveolar space causes pulmonary edema fluid to move to the interstitial space.
      • Careful fluid management: Adequate preload to optimize ventricular function is important, but volume overload will worsen respiratory status, so careful fluid management is necessary. Volume removal (whether via diuresis or hemodialysis) is often a critical component of early management.
      • Definitive therapy for underlying cardiac disease: In the event of myocardial infarction, percutaneous revascularization should be performed in a timely fashion.
      • Supportive: Inotropic agents such as dobutamine may be used to augment CO. Other inotropes are discussed in “Pharmacologic Therapies.” Mechanical circulatory assist devices, including left ventricular assist devices and intra-aortic balloon pumps, may be necessary in patients who do not respond to medical therapy.

Septic Shock

  • Definition of sepsis: Sepsis is defined as a life-threatening organ dysfunction caused by dysregulation of the host response to an infection.
    • Sepsis was previously identified based on the presence of at least two systemic inflammatory response syndrome (SIRS) criteria:
      • Tachypnea: Respiratory rate >20 breaths/min or PaCO2 <32 mm Hg
      • White blood cell count <4000 cells/μL or >12,000 cells/μL
      • Tachycardia: Pulse >90 bpm
      • Hypo- or hyperthermia: Temperature >38°C or <36°C
    • The new sepsis guidelines now identify organ dysregulation in sepsis as an increase in the Sequential Organ Failure Assessment (SOFA) score of ≥2.1
    • Septic shock is a subset of sepsis identified by persistent hypotension requiring vasopressors to maintain a mean arterial blood pressure ≥65 mm after adequate volume resuscitation. Mortality in these patients is ∼40%.
  • Management of septic shock: Management of septic shock involves early aggressive volume resuscitation and attempting to achieve hemodynamic stability quickly.2
    • Volume resuscitation: Patients should begin to receive at least 30 mL/kg IBW IV crystalloid fluid within the first hour of presentation.3 Smaller amounts of fluid may be needed if there is concomitant heart failure or pulmonary edema, whereas additional volume may be required if the patient remains volume responsive after the initial 30 mL/kg bolus. Parameters to determine volume responsiveness (discussed in “Hemodynamic Measurements”) should be closely monitored during volume resuscitation to prevent volume overload.
      • A recent RCT found that balanced crystalloids (i.e., lactated Ringer solution) may be associated with lower rates of renal dysfunction and even improved mortality when used as compared with normal saline.4
      • Several trials have not found significant benefit in albumin administration when compared with crystalloid in septic patients.5
    • Cardiovascular support: Vasoactive medications may be necessary if volume resuscitation is insufficient to maintain MAP ≥65 mm Hg. Norepinephrine has become the first-line agent after it was demonstrated that dopamine had more adverse events.6 Vasopressin is frequently used as a second-line agent. Mechanisms of action and other agents are discussed in “Pharmacologic Therapies.”
    • Timely, effective antimicrobial administration: Delays in starting appropriate antimicrobials are associated with increased mortality.7 The Surviving Sepsis Guidelines recommend starting antibiotics immediately after obtaining blood cultures, if possible.3
    • Source control: If a specific anatomical source of infection is identified (e.g., necrotizing soft tissue infection), intervention for source control should be performed as soon as reasonably possible.8
    • Early goal-directed therapy: Protocol for management of the first 6 hours of sepsis proposed by Rivers et al. in 2001.2 Widely adapted in practice before recent multicenter, prospective, RCTs called its effectiveness into question.9,10 However, these studies were limited by practice changes in control group (Figure 8-3).
    • Lactate clearance: Lactate clearance is associated with improved mortality in septic patients.11 The most recent Surviving Sepsis Guidelines recommend targeting resuscitation to normalize lactate in patients with elevated lactate levels.3
    • Procalcitonin (PCT): PCT is a biomarker that may aid in diagnosing sepsis, assessing treatment response, and determining antibiotic duration. An elevated PCT >0.5 ng/mL is suggestive of a bacterial infection while a PCT <0.1 ng/mL makes bacterial infection less likely.12 Some studies have shown that use of PCT may reduce the unnecessary usage of antibiotics.13 However, caution must be used, as a low PCT does not exclude the possibility of a severe bacterial infection.
Figure 8-3 Early goal-directed therapy protocol.
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(Adapted from Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-1377.)  [PMID:11794169]
*Although included in the original early goal-directed therapy protocol, more recent trials have demonstrated a trend toward increased harm in patients who receive more transfusions; current Surviving Sepsis Guidelines do not recommend transfusing to achieve Hct of 30%. CVP, central venous pressure; Hct, hematocrit; IBW, ideal body weight; MAP, mean arterial pressure; ScvO2, central venous oxygen saturation.

Pharmacologic Therapies

Vasoconstrictive and Inotropic Agents

  • Norepinephrine: Causes potent vasoconstriction via α1- and β1-adrenergic activity. Preferred agent in septic shock.
  • Vasopressin: Causes vasoconstriction via three different G-peptide receptors. Primarily used as an adjunct to norepinephrine. Weak evidence that it may have mortality benefit over norepinephrine in less severe septic shock (defined as requiring treatment with norepinephrine 5–14 μg/min to maintain MAP ≥65 mm Hg).14
  • Epinephrine: Has inotropic and vasoconstrictive properties in a dose-dependent fashion owing to α1- and β-adrenergic activity. At low doses (≤0.05 μg/kg/min), it increases CO and slightly reduces SVR owing to predominant β activity. At higher doses (>0.05 μg/kg/min), vasoconstriction predominates owing to increased α1 activity. Preferred agent for anaphylactic shock, and is also frequently used in cardiogenic shock.
  • Phenylephrine: Selective α1-receptor agonist causing vasoconstriction of larger arterioles. Few studies supporting its use in septic shock.
  • Angiotensin II: Recent studies have investigated angiotensin II which engages the renin–angiotensin–aldosterone system. These studies showed that angiotensin II increased blood pressure in patients with vasodilatory shock.15
  • Dobutamine: Inotropic agent that reduces afterload and increases stroke volume and heart rate via β1-agonist activity. Good agent for cardiogenic shock but increases risk of cardiac arrhythmias.
  • Dopamine: Has inotropic, vasodilatory, and vasoconstrictive properties in a dose-dependent fashion due to action on peripheral α1-receptors, cardiac β1-receptors, and renal and splanchnic dopaminergic receptors. At doses <5 μg/kg/min, primarily behaves as a vasodilator, increasing renal blood flow. At doses of 5–10 μg/kg/min, behaves as an inotrope. At doses >10 μg/kg/min, behaves as a vasopressor. Is associated with a higher rate of cardiac arrhythmias than norepinephrine.6
  • Milrinone: Phosphodiesterase III inhibitor that has positive inotropic effect, causing increase in CO. Also causes systemic vasodilation, which decreases afterload, making it an alternative option for cardiogenic shock.
  • Regarding venous access, low-dose norepinephrine, phenylephrine, and epinephrine may be infused peripherally for a limited period of time. However, central access is preferred as medication extravasation can lead to local ischemia.
    • If extravasation occurs, phentolamine (an α-antagonist) can be injected into the area of extravasation to reduce ischemic injury.
    • Peripheral administration of vasopressin and angiotensin II is not recommended.

Adjunctive Therapies

  • Corticosteroids: Relative adrenal insufficiency may contribute to refractory hypotension during septic shock. Data do not support the use of corticosteroids in mild septic shock. However, corticosteroids should be considered on an individual basis in patients with more severe shock, particularly in patients chronically on steroids. Generally, hydrocortisone 200–300 mg daily divided on a q6–8h basis is given. Previous trials have shown faster resolution of shock when administering hydrocortisone, but no difference in mortality.16,17 Another recent trial showed a benefit in 90-day mortality when hydrocortisone (50 mg every 6 hours) and fludricortisone (50 µg daily) were administered in conjunction.18
  • Sodium bicarbonate: No evidence supports the use of bicarbonate therapy in lactic acidemia from sepsis with a pH ≥7.15. Effect of bicarbonate on hemodynamics and vasopressor requirements with more severe acidemia is unknown, but bicarbonate is often recommended in patients with severe lactic acidemia (pH <7.1) who are hemodynamically unstable.
  • Methylene blue: Selective guanylate cyclase inhibitor, thereby mitigating nitric oxide–mediated vasodilation. Observational studies have demonstrated beneficial effects on hemodynamic parameters, but effects on morbidity and mortality are unknown.19

Hemodynamic Measurements

Although CVP, MAP, and SvO2/ScvO2 are used as therapeutic end points in treating shock, there is evidence that these parameters do not reflect intravascular volume. There is a growing body of evidence that dynamic parameters, including pulse pressure variation and inferior vena cava (IVC) diameters, may better reflect intravascular volume, but it is unclear that the use of these leads to improved outcomes.

  • Static parameters
    • CVP: An approximation of right atrial pressure and, therefore, preload. Should be measured from an internal jugular or subclavian venous catheter because readings from femoral catheters are influenced by intra-abdominal pressures and thus inaccurate. There is a poor relationship between CVP and blood volume,20 but low values (<4 mm Hg) should generally lead to fluid resuscitation with careful monitoring.21
    • ScvO2/SvO2: ScvO2 is a surrogate that is often used to reflect SvO2, which is the percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart. ScvO2 is measured from an internal jugular or subclavian venous catheter, while a true SvO2 must be measured with a pulmonary artery catheter (PAC). Normal values are 65%–75%. A high value often represents decreased oxygen consumption (commonly seen in mitochondrial dysfunction with sepsis), whereas low values indicate inadequate oxygen delivery (often due to low CO states such as cardiogenic shock). Previous guidelines recommended targeting an ScvO2 >70% with dobutamine administration if needed, though more recent trials have shown that using lactate clearance as a resuscitation goal is noninferior.22
    • PACs: A PAC catheter provides direct measurements of pressures in the right atrium, right ventricle, and pulmonary artery, as well as a pulmonary capillary wedge pressure. Previously commonly used in the management of septic shock and ARDS but did not affect mortality or morbidity.23
  • Dynamic parameters
    • Esophageal Doppler: A Doppler probe is placed into the esophagus and rotated to measure blood flow through the descending aorta. System can be used to calculate CO and stroke volume, and correlates well with CO as measured by PAC.24 Predicts volume responsiveness in critically ill ventilated patients without spontaneous breathing.25
    • Pulse pressure variation (ΔPp): Requires arterial line placement. Calculated as the difference between maximal and minimal systolic blood pressures measured over one respiratory cycle divided by the mean of those values. ΔPp of 13% was an accurate predictor of fluid responsiveness in mechanically ventilated patients without spontaneous breathing.26
    • IVC distensibility index (dIVC): Calculated as the difference between maximal and minimal IVC diameter measured over one respiratory cycle divided by the minimal IVC diameter. dIVC of 18% discriminated between volume responders and nonresponders with 90% sensitivity and specificity in mechanically ventilated patients without spontaneous breathing in one study,27 but more recent studies have shown this method to be a poor predictor of fluid responsiveness.28
    • Thoracic bioreactance: A noninvasive device is applied to the chest and measures bioreactance across the thorax using sensor pads placed on a patient’s thorax surrounding their heart. Blood flow (which is predominately in the aorta in the thorax) causes phase shifts in impedance, which is detected by the sensors. From these measurements, stroke volume and CO can be estimated. There are conflicting data on the ability of thoracic bioreactance devices to reliably determine fluid responsiveness.29,30

Critical Care Ultrasound

The use of bedside ultrasonography has greatly expanded recently and is rapidly becoming standard of care in ICUs. Courses in critical care ultrasonography are becoming more readily available and are necessary for complete proficiency. This section is intended to serve as an overview of basic concepts only. Critical care ultrasound should be used as an adjunct to other clinical data.

  • Basic concepts: Air and calcified structures transmit sound waves poorly. Free-flowing fluids transmit sound waves well.
  • Basic definitions
    • Echogenicity: The ability of an object to reflect sound waves.
    • Hyperechoic: Structures that reflect sound waves well; shows as white on ultrasound (e.g., bone, pleura, lung).
    • Hypoechoic: Structures that reflect sound waves poorly; shows as gray on ultrasound. Deeper structures are also more hypoechoic owing to attenuation with distance (e.g., lymph nodes, adipose tissue, muscle).
    • Anechoic: Containing structures that allow sound waves to pass through freely; shows as black on ultrasound (e.g., blood vessels, transudative pleural effusion).
  • Ultrasound to facilitate vascular access: More detailed instructions are available in the Washington Manual of Critical Care, Section XIX. Use of ultrasound to guide central venous access results in increased success and reduced complication rates.
    • Location: Ultrasound guidance is most commonly used for internal jugular and femoral venous access.
    • Before starting the procedure: Both internal jugular and femoral veins should be scanned to evaluate for aberrant anatomy or venous thrombosis.
    • After applying the sterile field: The probe is positioned so that the needle is visualized for the entire duration of accessing the vessel.
    • During the procedure: Following insertion of the guidewire, the length of the vessel is scanned to ensure that the guidewire did not inadvertently enter any adjacent arteries.
    • After the procedure: Lung ultrasound can be used to rule out a pneumothorax.
  • Cardiac ultrasound: Includes five standard views, reviewed below. Uses body transducer. Intended to facilitate assessment of volume responsiveness, global left and right ventricular systolic function, and valvular function.
    • Parasternal long-axis view: Probe is placed adjacent to the sternum in the left third to fifth intercostal space with the orientation marker pointing toward the patient’s right shoulder. The right ventricular outflow tract, left ventricular cavity, ascending aorta, mitral valve, and left atrium should be visualized. Assesses for pericardial effusion, left and right ventricular dysfunction, and valvular pathologies.
    • Parasternal short-axis view: Probe remains adjacent to the sternum in the left third to fifth intercostal space, but orientation marker is rotated 90 degrees clockwise to point at the patient’s left shoulder. Cross-sectional view of the left and right ventricles at the level of the papillary muscles should be visualized. Assesses for pericardial effusion and left and right ventricular dysfunction.
    • Apical four-chamber view: Probe is placed between the midclavicular and midaxillary lines of the left lateral chest between the fifth and seventh intercostal spaces, underneath the left nipple, with the orientation marker pointed at 3 o’clock. The left and right ventricles and atria, as well as the tricuspid and mitral valves, should be visualized. Assesses left and right ventricular size and function. See Figure 8-4.
    • Subcostal long-axis view: Probe is placed below the xiphoid process with the orientation marker pointed at 3 o’clock. The left and right ventricles and atria should be visualized. Assesses for pericardial effusion and left and right ventricular dysfunction. May be used for rapid assessment of cardiac function during performance of cardiopulmonary resuscitation.
    • IVC longitudinal view: Probe remains below the xiphoid process, but orientation marker is rotated 90 degrees counterclockwise to point at 12 o’clock. IVC in the longitudinal axis should be visualized. Assesses IVC diameter during the respiratory cycle to determine volume responsiveness.
  • Thoracic ultrasound: Includes four standard positions, performed bilaterally. Uses the body transducer on the abdominal setting to examine lung parenchyma; vascular transducer may be used for detailed examination of the pleura. Intended to facilitate the diagnosis of pleural effusion, pulmonary edema, pulmonary consolidation, and pneumothorax. Also used to guide a safe thoracentesis.
    • Probe placement: Bedside lung ultrasound in emergency (BLUE)s protocol, intended for immediate diagnosis of acute respiratory failure, defines four areas for investigation.31 The orientation marker should be pointed toward the patient’s head.
      • Upper BLUE point: Midclavicular line, second intercostal space
      • Lower BLUE point: Anterior axillary line, fourth or fifth intercostal space
      • Phrenic point: Midaxillary line, sixth or seventh intercostal space; location of the diaphragm
      • Posterolateral alveolar and/or pleural syndrome point: Posterior to the posterior axillary line, fourth or fifth intercostal space
    • Anatomic landmarks and ultrasound appearance: Knowledge of the normal sonographic appearance of thoracic anatomy is paramount to identifying key structures.
      • Chest wall: Hypoechoic, linear shadows of soft tissue density.
      • Ribs: Hyperechoic, curvilinear structures with a deep, hypoechoic, posterior acoustic shadow.
      • Pleura: Bright, hyperechoic, roughly horizontal line located approximately 0.5 cm below rib shadows.
      • Diaphragm: Curvilinear, hyperechoic line that moves caudally with inspiration. In a seated patient, it is located caudad to the ninth rib.
      • Splenorenal and hepatorenal recesses: Should be confirmed before any procedure because its curvilinear appearance is similar to that of the diaphragm. Identified by visualization of the liver or spleen and the kidney caudally.
      • Lung: Air-filled lung appears hyperechoic due to the poor echogenicity of air. Atelectatic or consolidated lung appears hypoechoic relative to normal lung.
    • Sonographic artifacts and terminology: A number of sonographic artifacts are caused by air–tissue interfaces, and presence or absence of these artifacts is indicative of disease.32
      • Pleural line: Brightly echogenic, roughly horizontal line; caused by parietopulmonary interface and indicating the lung surface.
      • A-lines: Brightly echogenic horizontal lines roughly parallel to the chest wall; caused by reverberations of the pleural line.
      • B-lines: Also called “comet tails”; a grouping within one intercostal space is called “lung rockets.” Hyperechoic line arising perpendicularly from the pleural line that extends across the whole screen without fading, erasing A-lines; moves with lung slide. Caused by thickened interlobular septa or ground-glass areas; isolated B-lines are a normal variant. See Figure 8-5.
      • Lung slide: “Twinkling” movement of the pleural line that occurs with the respiratory cycle; caused by movement of the lung along the craniocaudal axis during respiration. In M-mode, lung slide is visualized as the “seashore sign,” with the chest wall generating the “waves,” the aerated lung forming the “sand,” and the pleural line as the interface.
      • Lung pulse: Pulsation of the pleural line due to transmission of the heartbeat through noninflated lung.
    • Ultrasonography of lung pathology
      • Pleural effusion: A fluid collection bordered by the diaphragm, chest wall, and lung surface. Transudative effusions are typically anechoic; exudative effusions may have some echogenicity. If the effusion is loculated, septations—visualized as hyperechoic, weblike structures—may be seen. Atelectatic lung may be seen in the effusion.
      • Pneumothorax: Owing to air’s poor echogenicity, diagnosis of pneumothorax on ultrasound is made by artifact analysis.
        • The presence of lung slide or lung pulse effectively rules out pneumothorax in the location being investigated.
        • Abolishment of lung slide has a characteristic stratosphere sign in M-mode, with loss of the “sand,” but is neither sufficient nor specific for diagnosis of pneumothorax.
        • Lung point is pathognomonic for pneumothorax but has poor sensitivity. Occurs at the interface of the pneumothorax and aerated lung. Characterized by alternation between absent lung slide and present lung slide or B-lines in one location with respirations. In M-mode, will transition between seashore sign and stratosphere sign.
      • Pneumonia: Can only be visualized when the consolidation abuts the pleura. A heterogeneous, hypoechoic area with irregular margins where aerated lung abuts the consolidated area. Air bronchograms should be seen to make the diagnosis of pneumonia.
      • Pulmonary edema: Presence of multiple B-lines within one intercostal space (“lung rockets”) may indicate cardiogenic or noncardiogenic pulmonary edema. Corresponds to the Kerley B-lines seen on chest radiograph. Isolated B-lines are a normal variant.
  • Abdominal ultrasound: Abdominal ultrasound in critical care is limited and intended to evaluate for intra-abdominal fluid and assess the urinary tract and abdominal aorta.
    • Evaluating for intra-abdominal fluid: Standard evaluation of the trauma patient who may have intra-abdominal bleeding includes the focused assessment with sonography for trauma (FAST) examination. The patient is in the supine position, and four views are obtained:
      • Hepatorenal space: The probe is placed on the right in the 10th or 11th intercostal space at the posterior axillary line with the orientation mark pointed cephalad.
      • Pelvis: The probe is placed in the suprapubic area with the orientation mark in the 3-o’clock position.
      • Perisplenic space: The probe is placed on the left in the 10th or 11th space at or slightly posterior to the posterior axillary line with the orientation mark pointed cephalad.
      • Pericardial space: The probe is placed in the subxiphoid position with the orientation marker in the 3-o’clock position.
    • Paracentesis: Paracentesis should be performed under ultrasound guidance because there is evidence supporting a decrease in complications. More details can be found in the Washington Manual for Critical Care, Section XIX.
    • Assessment of the urinary tract: Bedside ultrasonography can identify bladder distention or hydronephrosis.
      • Bladder distention: The probe is placed in the suprapubic position with the orientation marker pointed cephalad for longitudinal dimensions and in the 3-o’clock position for transverse dimensions.
      • Hydronephrosis: The probe should be placed slightly caudad to the locations used for examination of the hepatorenal and perisplenic spaces in the FAST examination. Hydronephrosis is characterized by thinning of the renal cortex as the collecting system dilates.
    • Assessment of the abdominal aorta: The goal is to visualize the entire abdominal aorta to ensure that its diameter from outer wall to outer wall is <3 cm. The examination begins caudad to the xiphoid process, with the probe perpendicular to the abdominal wall and the orientation marker in the 3-o’clock position.
  • Vascular diagnostic ultrasound: Bedside ultrasonography may be performed to evaluate for deep vein thrombosis when clinically indicated. The target vein is visualized in the transverse plane. A vessel with normal blood flow should appear internally anechoic and should be easily compressible. Organized thrombus appears as a discrete, echogenic structure within the venous lumen. A very recently formed thrombus may be anechoic, but the vessel will be incompressible.
Figure 8-4 Cardiac ultrasound.
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Left (A): normal apical four-chamber view. A, apex; RV, right ventricle; RA, right atrium; LV, left ventricle; LA, left atrium. Right (B): demonstrates same view in a patient with right ventricular hypertrophy and dilation.
Figure 8-5 Lung ultrasound.
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A-lines demonstrated on left are equidistant horizontal lines created by reflections of the pleural line. B-lines demonstrated on the right are bright vertical lines that move with the pleura and extend to the bottom of the screen representing thickened fluid-filled interlobular septae.

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