Shock

Published on 14/03/2015 by admin

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4 Shock

Haney A. Mallemat, Michael E. Winters

Key Points

• Circulatory dysfunction can occur at three levels—the central circulation, the peripheral circulation, and the microcirculation—sometimes with subtle clinical findings.

• The initial history and physical examination should focus on identifying signs of hypoperfusion and detecting any immediately life-threatening circulatory disorders.

• Bedside ultrasonography can be helpful in assessing intravascular volume status and cardiac function and in detecting vascular catastrophes.

• Circulatory support is aimed at restoring adequate oxygen delivery.

• End points of circulatory resuscitation include clinical signs, mean arterial blood pressure, serum lactate level, and central venous oxygenation.

Perspective

The circulatory system is a complex vascular network that stretches more than 60,000 miles and circulates an average of 8000 L of blood each day. When circulatory dysfunction occurs, oxygen delivery is impaired, which leads to progressive cellular dysfunction. If not identified and treated, organ failure and death can ensue rapidly. This chapter discusses important elements of the history and physical examination along with invasive and noninvasive monitoring modalities used by the emergency physician (EP) to assess and support the circulatory system.

Anatomy

Figure 4.1 illustrates the anatomy of the circulatory system.

Fig. 4.1 Anatomy of the circulatory system.

Pathophysiology of Circulatory Dysfunction

Normal organ function requires adequate perfusion and delivery of oxygen. Oxygen delivery is determined by arterial oxygen content and cardiac output. Arterial oxygen content is a function of hemoglobin concentration and arterial oxygen saturation. Cardiac output is governed by heart rate, contractility, and loading conditions. Any process that adversely affects cardiac output or arterial oxygen saturation can decrease oxygen delivery and result in circulatory dysfunction.

Cardiac output can be affected by the heart rate, arrhythmias, and alterations in ventricular loading. Preload, afterload, and contractility each affect ventricular loading. The Frank-Starling law (Fig. 4.2) states that the principal force governing the strength of ventricular contraction is the length of muscle fibers.¹ In a normal heart, muscle fiber length is determined by intravascular volume, often termed preload. As preload increases, myocardial fibers increase in length, which results in increased force of contraction. Increased force of ventricular contraction increases stroke volume and cardiac output. In contrast, depletion of intravascular volume results in muscle fiber shortening, less forceful cardiac contractions, lower stroke volume, and decreased cardiac output.

Fig. 4.2 Frank-Starling curve demonstrating the relationship between end-diastolic pressure (preload) and systolic performance (stroke volume).

Increasing ventricular preload improves myocardial contractility only to a point, beyond which myocardial fibers become overstretched. Overstretched fibers can lead to worsening myocardial contractility and, eventually, increased hydrostatic pressure and interstitial edema (e.g., pulmonary edema).

Changes in afterload can also affect ventricular function. For example, severe hypertension impedes ventricular function by reducing cardiac emptying and flow while increasing myocardial workload. Similarly, reducing afterload increases cardiac emptying and flow while decreasing myocardial workload.

Contractility, a measure of ventricular function, is altered by a variety of factors. Medications such as dobutamine can increase the force of contraction for a given preload. In contrast, diseases such as congestive heart failure can reduce contractility and worsen stroke volume and cardiac output.

Circulatory dysfunction can also occur with alterations in regional or microcirculatory blood flow. Disorders that affect arteriolar tone, such as sepsis, cause maldistribution of blood flow between organs and a mismatch of oxygen delivery with demand. Capillary obstruction and endothelial impairment interrupt intraorgan oxygen delivery, thereby potentially resulting in organ failure.

Circulatory dysfunction exists as a spectrum ranging from mild impairment to shock with overt circulatory collapse. Shock is defined as the inability of the circulatory system to provide adequate tissue perfusion, which potentially leads to cellular dysfunction.¹ Four categories of shock have been differentiated and defined by the underlying patho-physiology of the circulatory dysfunction: hypovolemic, cardiogenic, distributive, and obstructive (Box 4.1).² Because each category requires specialized management, every attempt must be made to determine the exact cause of the shock.

Presenting Signs and Symptoms

Circulatory insufficiency can be accompanied by myriad clinical findings. The signs and symptoms primarily reflect organ dysfunction secondary to hypoperfusion and decreased oxygen delivery. Classic signs of circulatory dysfunction include reduced blood pressure, abnormal heart rate, tachypnea, hypoxemia, mottled extremities, and decreased urine output. The most dramatic manifestation is cardiac arrest with complete circulatory failure. Unfortunately, many emergency department (ED) patients with circulatory dysfunction have vague, nonspecific symptoms. Common nonspecific symptoms of circulatory insufficiency include fatigue, malaise, weakness, lightheadedness, dizziness, altered mental status, diaphoresis, dyspnea, and syncope. Circulatory dysfunction should be considered in every patient with vague, undifferentiated symptoms.

Initial Assessment

An initial circulatory assessment should be performed for every ED patient within the first minutes after arrival. This assessment consists of a review of triage vital signs, a focused history, physical examination, and possibly bedside ultrasonography. The goal of the initial circulatory assessment is to detect signs of organ hypoperfusion and identify any immediately life-threatening disorders. Life-threatening disorders requiring rapid diagnosis and treatment include pulmonary embolism, acute myocardial infarction, cardiac tamponade, tension pneumothorax, aortic dissection, and ruptured abdominal aortic aneurysm.

Vital Signs

For nearly all ED patients, circulatory assessment begins with the noninvasive measurement of vital signs. Although blood pressure and heart rate are central to the initial assessment, it is important to note the respiratory rate and oxygen saturation. Any abnormality in the respiratory rate or oxygen saturation may affect arterial oxygen content and impair oxygen delivery. Noninvasive measurement of vital signs correlates poorly with organ perfusion in critically ill patients but serves as an important component of the initial ED assessment of the circulatory system.³

Blood Pressure

Blood pressure, the driving force for organ perfusion, is determined by cardiac output and arterial tone.¹ It is important to understand that no blood pressure value is considered normal for every patient. Normal blood pressure values do not always indicate sufficient oxygen delivery. Blood pressure values should be interpreted in the context of the patient’s clinical findings, medical history, and treatment received.

Blood pressure is one of the most common measurements in all of clinical medicine, yet it is often measured incorrectly.⁴ In the ED, blood pressure is initially obtained during triage with automated blood pressure devices that apply the oscillometric method. These devices can be adversely affected by ambient noise and cuff position. In addition, automated devices typically overestimate true arterial blood pressure in patients with low-flow states. These limitations, combined with activity in the triage environment and patient anxiety, often result in inaccurate measurements of blood pressure. Understandably, triage values can be an unreliable indicator of true blood pressure. Blood pressure measurements should be repeated serially at the bedside in patients demonstrating any evidence of circulatory insufficiency.

The auscultatory method has long been considered the “gold standard” for noninvasive blood pressure measurement. It determines systolic and diastolic pressure on the basis of detection of Korotkoff sounds. The ideal location is the upper part of the arm. The procedure is performed as follows:

1. Remove all clothing from the arm and place the blood pressure cuff so that the middle of the cuff is approximately at the level of the right atrium. The lower edge of the cuff should be 2 to 3 cm above the antecubital fossa to allow easy palpation and auscultation of the brachial artery.

2. Locate the radial artery and inflate the blood pressure cuff to approximately 30 mm Hg above the point at which the radial arterial pulse disappears.

3. Place the bell of the stethoscope over the brachial artery and deflate the cuff at a rate of 2 to 3 mm Hg per second. The appearance of faint, repetitive sounds for at least two consecutive beats is phase I of the Korotkoff sounds. Phase I is systolic blood pressure. The point at which all sounds disappear is phase V, or diastolic blood pressure.

Measure blood pressure bilaterally during the initial circulatory examination. A difference of more than 10 mm Hg is significant and may indicate an aortic emergency. Unfortunately, up to 20% of individuals have significant blood pressure differences between their arms.⁵ Nevertheless, an aortic emergency must be ruled out in any patient with evidence of circulatory insufficiency and blood pressure discrepancies.

Though considered the gold standard, the auscultatory method has several pitfalls. Box 4.2 lists errors commonly made during measurement of blood pressure with the auscultatory method.

Heart Rate

The heart rate is an integral component of cardiac output. Tachycardia or bradycardia can impair circulatory function. As with blood pressure, triage measurements of the heart rate can be inaccurate and unreliable. Therefore, heart rate measurement should be repeated in every patient on initial examination. In addition to the rate, irregularities in rhythm should be noted. Arrhythmias can severely compromise circulatory function and organ perfusion. Furthermore, heart rate variability may be an early indication of circulatory dysfunction.⁶ Methods to determine heart rate variability remain investi-gational and require additional research before clinical application.

Orthostatic Blood Pressure

Depletion of intravascular volume can impair oxygen delivery by decreasing venous return and cardiac output. Symptoms of volume depletion are attributable to reduced cerebral blood flow and include weakness, lightheadedness, unsteadiness, impaired cognition, tremulousness, and syncope. Orthostatic blood pressure measurements can occasionally aid the EP in detecting otherwise unsuspected intravascular volume depletion, but they must be integrated with specific clinical findings. They are not obtained routinely because they have significant limitations.

A positive orthostatic blood pressure response is defined as a reduction in systolic blood pressure of at least 20 mm Hg or a reduction in diastolic blood pressure of at least 10 mm Hg within 3 minutes after standing in a patient with symptoms of volume depletion.⁷ Orthostatic blood pressure should be measured with the patient in the supine and standing positions. For patients who are unable to stand or who are markedly unsteady, a sitting position may be used. Wait at least 2 minutes before obtaining a standing blood pressure measurement because nearly all patients have a brief orthostatic response immediately on standing. Always measure the heart rate with orthostatic blood pressure. In normal patients, the heart rate increases from 5 to 12 beats/min with standing. Increases greater than 30 beats/min are abnormal and indicate significant volume depletion.

Orthostatic blood pressure measurements have several limitations. Numerous conditions in addition to volume depletion impair the postural hemodynamic response and result in orthostatic hypotension. Most notable are the effects of aging and medications. Up to 30% of elderly patients demonstrate an orthostatic response in the absence of volume depletion.⁸ Many elderly patients take medications that alter the postural response to changes in position; such medications include antiadrenergics, antidepressants, antihypertensives, neuroleptics, anticholinergics, and antiparkinsonian drugs. In addition, any disorder causing primary or secondary autonomic dysfunction can lead to orthostatic hypotension.

Pulse Pressure

Increasing evidence demonstrates that abnormal pulse pressure—the difference between systolic and diastolic blood pressure—is an independent risk factor for cardiovascular morbidity and mortality. To date, studies have focused on outpatients with established hypertension. Nevertheless, it is important to determine pulse pressure in the initial circulatory assessment of an ED patient. Acute disorders that alter circulatory function are often manifested as abnormalities in pulse pressure. A narrow pulse pressure (<40 mm Hg) indicates reduced stroke volume and thus reduced cardiac output. Life-threatening conditions resulting in a narrow pulse pressure include tension pneumothorax, cardiac tamponade, pulmonary embolism, acute myocardial infarction with cardiogenic shock, and severe volume depletion. A widened pulse pressure (>40 mm Hg) results from processes that lower systemic vascular resistance. Diseases that can be accompanied by widened pulse pressure include sepsis, anaphylaxis, acute aortic insufficiency, adrenal insufficiency, and neurogenic shock.

History

A focused history is essential during the initial circulatory assessment. Key elements are a history of the present illness, previous medical history, medication history, family history, and social history. With respect to the history of the present illness, determine the onset and duration of symptoms, the context in which the symptoms developed, any associated symptoms, and any aggravating or alleviating factors. Important associated symptoms include chest pain, dyspnea, palpitations, syncope, and altered mental status. Review the patient’s medical history and direct attention to disorders that may impair cardiac output or arterial oxygen content.

Medications can result in circulatory abnormalities through direct effects or side effects. Two important classes of medications are antiarrhythmic agents and antihypertensive agents. It is crucial to note whether the patient is taking a beta-blocker or calcium channel blocker because both agents can alter the compensatory response to circulatory insufficiency. Always interpret vital signs in the context of the medical history and medication regimen.

Additional key components of the history are the family and social histories. Directly question patients about their family history of sudden death, premature coronary artery disease, venous thromboembolism, and connective tissue disorders (e.g., Marfan syndrome). Similarly, question patients about their use of illicit substances known to have circulatory effects, namely, cocaine.

Physical Examination

Physical examination of the circulatory system begins with the general appearance of the patient. Observe the patient’s positioning, mental status, skin color, and respiratory pattern. Suspect circulatory abnormalities in restless, diaphoretic, delirious, pale, mottled, or tachypneic patients. In addition, note any distinct clinical features implying an underlying medical condition. Table 4.1 lists the characteristic features of disorders that can affect the circulatory system.

Table 4.1 Characteristics of Conditions That Affect the Circulatory System

CONDITION	CLINICAL APPEARANCE	POTENTIAL CIRCULATORY IMPLICATIONS
Marfan syndrome	Arachnodactyly Arm span greater than height Longer pubis-to-foot length than pubis-to-head length	Aortic dissection
Osteogenesis imperfecta	Blue sclera	Aortic dissection Aortic aneurysm Aortic valve insufficiency Mitral valve prolapse
Hyperthyroidism	Exophthalmos	Congestive heart failure
Hypothyroidism	Expressionless face Periorbital edema Loss of lateral third of the eyebrows Dry, sparse hair	Congestive heart failure Pericardial effusion
Hemochromatosis	Bronze pigmentation of skin Loss of axillary and pubic hair	Cardiomyopathy
Turner syndrome	Short stature Webbed neck “Shield” chest Medial deviation of the extended forearm	Aortic coarctation
Aortic insufficiency	Bobbing of the head with heartbeat Systolic flushing of the nail beds	—

Examine the head and neck for abnormalities suggesting circulatory disease. Facial edema implies impaired venous return resulting from conditions such as superior vena cava thrombosis and constrictive pericarditis. Examination of the jugular venous pulse provides important information about central venous pressure (CVP) and the dynamics of the right side of the heart.⁹ Place the patient in a 45-degree recumbent position and shine a light tangentially across the neck. The right side is preferred because of its anatomic alignment with the superior vena cava and right atrium. Beginning at the sternal notch, measure the height (in centimeters) of the internal jugular vein pulsations. Pulsations more than 4 cm above the sternal notch are abnormal and a sign of elevated CVP.⁹ Figure 4.3 illustrates jugular venous distention in a young woman with pericardial effusion.

Fig. 4.3 Jugular venous distention in a young woman with pericardial effusion.

The cardiopulmonary examination is a quintessential component of circulatory assessment. Observe the rate, depth, and effort of respirations. Tachypnea accompanied by shallow respirations or the use of accessory muscles indicates impending respiratory failure. Auscultate the lungs for asymmetric breath sounds, rhonchi, rales, and wheezing. Recall that any pulmonary process can adversely affect arterial oxygen content and thereby impair oxygen delivery. Auscultate the heart over the right and left upper sternal edges, the lower left sternal edge, and the cardiac apex. Determine the rate and listen for rhythm irregularities, the intensity of heart sounds, murmurs, gallop rhythms, and pericardial rubs. Though difficult with the ambient noise in the ED, attempt to determine whether cardiac murmurs are systolic or diastolic, which can potentially provide valuable information in patients with acute cardiopulmonary dysfunction. Gallop rhythms are low-frequency heart sounds that are heard best with the bell of the stethoscope.

The extremities must be examined as part of the initial circulatory assessment. It is important to observe their color and temperature. Signs of poor perfusion include cold, pale, clammy, mottled skin associated with delayed capillary refill (normal capillary refill is less than 2 seconds). Inspect for symmetric or asymmetric edema and clubbing of the fingers and toes. Finally, palpate the carotid, radial, femoral, dorsalis pedis, and posterior tibial pulses for rate, amplitude, and regularity.

Emergency Ultrasonography

Even after the most careful evaluation of the history, vital signs, and physical examination, the pathophysiology of the circulatory dysfunction may not be completely clear. In this situation, further diagnostic testing is needed to confirm a diagnosis or initiate treatment. Unfortunately, diagnostic testing may require transfer of the patient from the ED to areas in the hospital with significantly less monitoring (e.g., the radiology suite).

Over the past 3 decades, ultrasonography has become essential in the initial assessment of patients with circulatory dysfunction. Ultrasonography is easily performed at the bedside and provides a noninvasive, real-time assessment of causes of circulatory dysfunction. Because ultrasonography may identify the cause of circulatory dysfunction faster than traditional diagnostic testing can, definitive interventions can be initiated rapidly, thereby potentially minimizing end-organ damage.¹⁰

Many ultrasonography algorithms and approaches for assessing circulatory dysfunction have been published. For the purposes of this discussion, we will use the RUSH (Rapid Ultrasound in SHock) protocol to illustrate the utility of ultrasonography in evaluating circulatory dysfunction.¹¹ In three systematic steps, the RUSH protocol evaluates circulatory dysfunction as follows:

Step 1: Evaluate the heart (the “pump”).

Step 2: Assess intravascular volume status (the “tank”).

Step 3: Evaluate the major vascular structures (the “pipes”).

Procedures and Circulatory Monitoring

Procedures pertinent to circulatory assessment and support center on obtaining vascular access and placing invasive circulatory monitors. Rapid attainment of intravenous access is required for patients exhibiting signs and symptoms of hypoperfusion. Invasive circulatory monitoring is used to ensure adequate tissue perfusion and oxygen delivery. Invasive monitoring is indicated for patients who continue to exhibit signs of hypoperfusion despite initial resuscitative measures. Common invasive modalities include arterial blood pressure monitoring, CVP monitoring, and pulmonary artery catheterization. A number of new monitoring modalities have been developed to evaluate the adequacy of circulation. These new modalities include esophageal Doppler analysis, pulse contour analysis, thoracic bioreactance, near-infrared retinal spectroscopy, transcutaneous tissue oxygen monitors, central venous oxygen saturation monitoring, and sublingual capnometry.

Intravenous Access

Despite the physician’s desire to perform central venous catheterization during initial resuscitation, peripheral venous cannulation is preferred. As stated by Poiseuille’s law, the rate at which intravenous fluids can be infused depends on the radius and length of the catheter. Greater volume can be infused over a shorter time with short peripheral catheters than with a central venous line. Peripheral catheters should be 18 gauge or larger. The external jugular veins and the veins of the antecubital fossa provide rapid and safe access for peripheral venous cannulation.

Central venous catheterization has become a common bedside procedure in emergency medicine. In the United States, more than 5 million central venous catheters are placed each year. Table 4.3 lists several indications for and contraindications to establishing central venous access. The procedure presents a risk for a number of complications (see the Red Flags box), but their occurrence can be minimized by following the basic rules of good practice (see the Tips and Tricks box). For catheterization of the internal jugular vein, the ultrasonography probe should be positioned on the anterior aspect of the neck, as demonstrated in Figure 4.7. Identification of the vein can be facilitated by asking the patient to perform the Valsalva maneuver, which causes engorgement of the neck veins (Fig. 4.8, A and B).

Table 4.3 Central Line Placement: Indications and Contraindications

Indications

Failed peripheral venous access

Cardiopulmonary arrest

Central venous pressure monitoring

Transvenous pacemaker insertion

Emergency hemodialysis

Administration of medications known to irritate the peripheral veins

Contraindications Absolute None Relative

Cutaneous infection at the site of puncture

Existing venous thrombosis

Existing arteriovenous fistula

Coagulopathy—subclavian and internal jugular sites

Thrombocytopenia—subclavian and internal jugular sites

Fig. 4.7 Proper positioning of the ultrasonography probe for catheterization of the internal jugular vein.

Fig. 4.8 Ultrasonographic appearance of the internal jugular vein (IJ) at baseline (A) and when the patient performs a Valsalva maneuver (B).

CA, Carotid artery.

Tips and Tricks

Tips for Decreasing the Rate of Complications with Central Venous Catheterization

Use maximal sterile barrier precautions—cap, mask, gown, gloves, and sterile drapes.

Use chlorhexidine-based solutions if available.

Do not allow inexperienced operators (<50 catheterizations) more than three attempts.

Whenever possible, place a subclavian central venous catheter, which is associated with the lowest rate of mechanical, infectious, and thrombotic complications.

Use ultrasonographic guidance routinely for internal jugular venous catheterization.

Do not use topical antibiotic ointments; they have not been shown to decrease the risk for catheter-related infections.

Arterial Blood Pressure Monitoring

Invasive arterial blood pressure monitoring is required for patients with persistent circulatory dysfunction despite initial resuscitative measures. Primary indications for placement of an arterial line include continuous blood pressure monitoring, the need for frequent blood sampling, and serial measurements of PaO₂. When possible, the radial artery should be used for this purpose. It offers the advantages of a peripheral position and easy compressibility in the event of unsuccessful cannulation. Additionally, the nearby ulnar artery supplies collateral blood flow to the hand while the radial artery is cannulated. If the radial artery cannot be used, a line can be placed in other arteries, as listed in Box 4.3.

Box 4.3 Arterial Cannulation

Insertion Sites, Possible Complications, Procedure Tips

Sites of Insertion

Radial artery (most common and preferred)

Dorsalis pedis artery

Complications

Thrombosis with arterial occlusion

Hematoma

Infection (catheter-related bloodstream infections)

Heparin-induced thrombocytopenia

Anemia (frequent blood sampling)

Catheter placement is guided by palpation of the artery. When the pulse is difficult to detect, ultrasound becomes an important aid for visualization of the target artery. Cannulation of the radial artery under ultrasound guidance is faster, requires fewer attempts, and is associated with fewer complications than the palpation method is.¹⁵ Proper patient positioning for radial artery cannulation is illustrated in Figure 4.9.

Fig. 4.9 Proper patient positioning for cannulation of the radial artery.

Central Venous Pressure

CVP is intravascular pressure in the central vena cava system, near its junction with the right atrium. Clinically, CVP is used as a marker of volume status and cardiac preload. Normal values for CVP range from 8 to 12 mm Hg. CVP can be estimated noninvasively by examining the internal jugular vein (as described in the physical examination section of this chapter), but bedside determinations have been shown to be inaccurate and unreliable.¹⁶ Direct measurements, through a subclavian or internal jugular vein catheter, provide more reliable results. CVP can be measured via a femoral central venous catheter; however, values typically differ by 0.5 to 3 mm Hg from those obtained from the superior vena cava. In a patient who is not mechanically ventilated, CVP can be estimated noninvasively by visualizing the IVC with ultrasound (Table 4.4). For example, a normally sized IVC that collapses more than 50% correlates with a CVP between 0 and 5 mm Hg.¹⁷

Table 4.4 Estimation of Right Atrial Pressure from Measurement of the Inferior Vena Cava

SIZE OF IVC	IVC SIZE ON INSPIRATION	RA PRESSURE (mm Hg)
<1.5 cm (small)	Nearly total collapse	0-5
1.5-2.5 cm (normal)	Decrease >50%	5-10
1.5-2.5 cm	Decrease <50%	10-15
>2.5 cm	Decrease <50%	15-20
IVC and hepatic vein dilation	No change	>20

IVC, Inferior vena cava; RA, right atrial.

Pulmonary Artery Catheterization

First described by Swan and colleagues in the early 1970s, pulmonary artery catheterization is considered the gold standard for circulatory monitoring in the critically ill. Circulatory measurements obtained with pulmonary artery catheterization include cardiac output, right ventricular ejection fraction, mixed venous oxygen saturation, and intrapulmonary vascular pressure. From these measurements, oxygen delivery, oxygen consumption, systemic vascular resistance, and left ventricular stroke index can be calculated. Because a pulmonary artery catheter gives clinicians the ability to measure oxygen delivery directly, it would seem to be an invaluable tool for circulatory monitoring. Unfortunately, routine use of this type of catheter remains controversial. Use of a pulmonary artery catheter has not been shown to decrease patient morbidity or mortality rates.¹⁸ In fact, use of a pulmonary artery catheter may be detrimental. Complications of insertion include pneumothorax, ventricular arrhythmias, ventricular perforation, and pulmonary artery rupture. Until further evidence is published, pulmonary artery catheters should not be used in the ED for assessment and support of the circulatory system.

Additional Circulatory Monitoring Modalities

The circulatory system can also be assessed with global, or tissue, markers of hypoperfusion. Methods of assessing global hypoperfusion in the ED include central venous oxygen saturation and serum lactate values. Under normal circumstances, cells extract 25% to 30% of the oxygen from the circulation. Therefore, blood returning to the central circulation has an oxygen saturation ranging from 70% to 75%. When the circulation fails to deliver adequate oxygen, cellular oxygen extraction is increased. This increase is reflected as decreased mixed venous oxygen saturation, measured via a pulmonary artery catheter. Mixed venous oxygen saturation values of less than 65% are associated with decreased perfusion and oxidative impairment of some vascular beds. Central venous oxygen saturation of less than 70%, measured intermittently or continuously via a central venous catheter, is a reliable surrogate for mixed venous oxygen saturation. Central venous oxygen saturation, as a global marker of hypoperfusion, was used in a landmark study that demonstrated a significant decrease in mortality rate in ED patients with sepsis in whom that marker was used.¹⁹ Central venous oxygen saturation values should be obtained from either subclavian or internal jugular central venous catheters.

Serum lactate values are also used as global markers of hypoperfusion. With persistently impaired oxygen delivery, cells convert to anaerobic metabolism, which results in the accumulation of lactic acid. A lactate level higher than 2 mmol/L is considered an indicator of inadequate oxygenation. Abnormal lactate levels have numerous causes, but the clinician should always regard impaired tissue perfusion as the primary cause in an ED patient.

The trend in lactate values is the most clinically useful information. Increasing serial lactate levels portend a worse prognosis and indicate a persistent circulatory dysfunction. A 10% reduction in lactate concentration in serial samples may be a more clinically useful marker of resuscitation than central venous oxygen concentration.²⁰

Tissue-specific monitors of hypoperfusion include gastric tonometry, sublingual capnometry, near-infrared spectroscopy, and tissue oxygen tension. These circulatory monitoring modalities detect hypoperfusion and impaired oxygen delivery in specific vascular beds. These promising modalities require further prospective investigation and are not used in the daily practice of emergency medicine. Available noninvasive methods for measuring cardiac output include esophageal Doppler ultrasonography, impedance plethysmography, and pulse-contour analysis. As with tissue-specific monitors of hypoperfusion, these noninvasive methods require further prospective analysis before widespread clinical application.

Treatment of Circulatory Dysfunction

Treatment goals for circulatory support are based on restoring adequate oxygen delivery. Methods of restoration consist of improving cardiac output, arterial oxygen content, and peripheral perfusion pressure. General ED therapies include supplemental oxygen, endotracheal intubation, intravenous fluids, vasoactive medications, and the use of mechanical support devices such as cardiac pacemakers. Regardless of the therapy chosen, it is important to recognize established end points of circulatory resuscitation. First and foremost, patients should exhibit clinical signs of improvement, such as improving mental status, increasing urine output, and normalization of vital signs. Additional end points of resuscitation are mean arterial blood pressure, serum lactate level, and central venous oxygen saturation. Mean arterial pressure represents true perfusion pressure; its measurement is superior to systolic blood pressure monitoring. Mean arterial pressure in patients with sepsis should be at least 65 mm Hg. There is no survival benefit to raising it beyond that level. As discussed earlier, serum lactate values should show a decreasing trend over serial measurements. Persistently elevated lactate values indicate inadequate and incomplete circulatory resuscitation. For patients with a central venous catheter, CVP and central venous oxygen saturation can be monitored. CVP should range from 8 to 12 mm Hg, whereas central venous oxygen saturation values should exceed 70%. The goals of resuscitation are summarized in Box 4.4.

General Treatment Principles

Patients with circulatory dysfunction require rapid assessment and simultaneous treatment:

1. Begin cardiac monitoring immediately to determine the patient’s heart rate and rhythm regularity.

2. Provide supplemental oxygen to improve arterial oxygen saturation.

3. Maintain a low threshold for intubation. The respiratory muscles are avid consumers of oxygen, thereby limiting oxygen delivery to other vital organs. Early intubation and paralysis of respiratory muscles may be required in patients with ongoing circulatory compromise.

4. Establish peripheral intravenous access rapidly.

5. Obtain an electrocardiogram and a portable chest radiograph within the first minutes to evaluate for acute myocardial infarction and pneumothorax.

6. Perform ultrasonography early to look for myocardial dysfunction, pericardial effusion, hemoperitoneum, and abdominal aortic aneurysm in patients with persistent hypotension.

Trendelenburg Position

Hypotensive patients are often placed in the Trendelenburg position while resuscitative efforts, such as establishing intravenous access and administering fluids, are initiated. The Trendelenburg position was thought to increase venous return and thereby augment cardiac output. This assumption is incorrect because of the capacitance of the venous circulation. The Trendelenburg position does not promote venous return or increase cardiac output. Hypotensive patients should not be put in the Trendelenburg position. This position serves only to increase the risk for aspiration.

Intravenous Fluid Administration

Acute circulatory failure should be treated initially with intravenous fluids. In the absence of left ventricular failure, rapid fluid therapy is provided to improve preload and augment cardiac output. For patients without preexisting cardiopulmonary disease, a 20- to 40-mL/kg bolus should be infused over a 10-minute period. In patients with existing cardiac disease, smaller volumes of fluid are infused (e.g., 250 to 500 mL over a 15-minute period). Regardless of the volume chosen, patients must be reassessed after every fluid bolus to determine whether additional treatment is needed.

The administration of colloid fluids during the initial circulatory resuscitation confers no mortality benefit.²¹ An isotonic crystalloid solution should be the first-line intravenous fluid. Fluid therapy is continued until the end points of resuscitation are achieved or the patient demonstrates pulmonary edema or evidence of right heart dysfunction.

Preload Responsiveness

Before volume resuscitation is initiated in a critically ill patient, preload responsiveness should be assessed; that is, whether cardiac output is likely to improve with the administration of fluids. Depending on the underlying disease, cardiac output might not increase with volume infusion. Additionally, inappropriate administration of volume may be harmful (e.g., exacerbation of pulmonary edema leading to hypoxemia). Several techniques are available for assessment of preload responsiveness.

Static Versus Dynamic Measurements

Static and dynamic measurements are the two general methods for assessing preload responsiveness. Static measures are used as absolute cutoffs, and examples are CVP and PAOP.

Proponents of the use of CVP to assess preload responsiveness state that blood pressure will probably increase in a hypotensive patient with low CVP when a fluid bolus is given; that is, the patient will be preload responsive. Conversely, blood pressure will not increase after volume infusion in a hypotensive patient with elevated CVP. These assumptions may be true for hypotensive patients, but the clinical utility of CVP is limited by several factors. CVP is affected by venous compliance, arrhythmias, right-sided heart disease, and alterations in intrathoracic pressure (e.g., as induced by mechanical ventilation). In addition, CVP depends on an appropriately selected reference point, and false results can be obtained if that point is zeroed incorrectly. The same limitations exist when considering PAOP to assess for preload responsiveness, and thus it should be used with caution.

Several studies have demonstrated that static measures are inaccurate in predicting preload responsiveness.^22,²³ Nonetheless, the most recent Surviving Sepsis Campaign consensus guidelines recommend using static measurements such as CVP and PAOP to assess preload responsiveness and guide fluid resuscitation in septic patients.²⁴

Given the controversies surrounding the use of CVP for assessment of preload responsiveness, we recommend the following:

• Patients with low CVP who are given a fluid challenge and show at least a 2–mm Hg increase in pressure probably have intravascular depletion and are preload responsive. Such patients require additional fluid administration to optimize preload and cardiac output.

• Normal or elevated CVP should not be interpreted as indicating adequate circulatory volume and cardiac preload. A method other than measurement of CVP should be used to assess preload responsiveness.

Dynamic assessments of preload responsiveness are believed to be more accurate than static assessments. Dynamic measures are derived from the interaction between the respiratory and cardiac systems during mechanical ventilation. Mechanical ventilation elevates intrathoracic pressure, which affects left ventricular preload and changes stroke volume in patients who are preload responsive. Patients who are not preload responsive do not have variations in stroke volume with mechanical ventilation. Stroke volume can be assessed with an arterial catheter or noninvasively by pulse oximeter plethysmographic waveform amplitude.²⁵

Dynamic measures predict preload responsiveness as a percentage of change throughout the respiratory cycle. Examples of dynamic measurements for preload responsiveness include stroke volume variation, esophageal Doppler analysis, pulse pressure variation (PPV), the IVC distensibility index (DI), and the passive leg-raise maneuver. Dynamic assessment requires the patient to be mechanically ventilated (except for the passive leg-raise maneuver), to have ventilation at a set tidal volume (6 to 8 mL/kg), to have no spontaneous breaths, and to be in sinus rhythm. The most useful dynamic measures of preload responsiveness for the EP are the DI and PPV.

Distensbility Index

The IVC is measured easily and reliably with ultrasound via the subcostal view. In mechanically ventilated patients, variations in intrathoracic pressure cause changes in IVC diameter; that is, increased diameter with a positive pressure breath and decreased diameter with expiration (Fig. 4.10, A and B). This variability in diameter (the DI) is most pronounced when a patient is preload responsive. DI is defined as the difference between the maximum and minimum diameters divided by the minimum diameter × 100. A DI greater than 18% has 90% sensitivity and specificity for predicting preload responsiveness.²⁶ Because the IVC is easy to visualize and measure, the DI can be assessed following each fluid bolus. By continuously reassessing the DI, volume can be given up to the point at which a patient is no longer preload responsive.

Fig. 4.10 Sonographic demonstration of the inferior vena cava in a preload-responsive patient maintained on mechanical ventilation.

Notice the variation in diameter between a positive pressure breath (A) and expiration (B).

Limitations of the DI include its unreliability in nonintubated patients and uncertainty about the optimal tidal volume and positive end-expiratory pressure during measurements. Nonetheless, because the DI is easy to measure and is reproducible, it remains a clinically valuable tool.

Pulse Pressure Variation

PPV is another dynamic measure of preload responsiveness. PPV can be calculated with an arterial catheter or via pulse oximeter plethysmographic waveform analysis. PPV is calculated by taking the difference between the maximum and minimum pulse pressures during one respiratory cycle, dividing by the average of the two values (maximum and minimum), and then multiplying by 100 (Fig. 4.11). Values higher than 18% predict a hypotensive patient to be preload responsive; a volume challenge would probably increase stroke volume and cardiac output.²⁷ As mentioned previously, PPV has limitations when used to predict preload responsiveness (e.g., ventilation must be at a set tidal volume [6 to 8 m L/kg], no spontaneous breaths, sinus rhythm).

Fig. 4.11 Determining pulse pressure variation as an index of preload responsiveness.

Arterial waveform tracings are used to detect pulse pressure variation.

Vasoactive Therapy

Vasoactive medications are indicated when mean arterial pressure remains below 65 mm Hg despite a fluid challenge of 20 to 40 mL/kg and there is evidence that a patient is not preload responsive. Vasopressor agents help restore perfusion pressure and maintain cardiac output. These agents typically exert their effects through stimulation of α- and β-adrenergic receptors. The degree to which these receptors are stimulated depends on the agent. Common vasopressor agents used in emergency medicine are norepinephrine, dopamine, and vasopressin. Less commonly used agents are phenylephrine, epinephrine, and milrinone. The hemodynamic dose responses and dosage ranges of these agents are listed in Table 4.5. An important caveat is that a rise in blood pressure after administration of one of these drugs may not correlate with clinical improvement. Additional markers of hypoperfusion, such as the serum lactate level and central venous oxygen saturation, must be considered in the overall circulatory assessment. No studies have clearly supported the superiority of any vasopressor agent. The choice depends on the acute disease process and underlying comorbid conditions.

Table 4.5 Vasopressor Agents

Patients with poor cardiac contractility may require inotropic support. Inotropic agents increase cardiac contractility through stimulation of α₁ receptors, which results in rises in the intracellular calcium concentration. Dobutamine is the prototypic inotropic agent, but any vasopressor that stimulates β₁ receptors increases cardiac contractility. Dopamine, milrinone, and epinephrine are potent inotropic medications. Dobutamine can also cause peripheral vasodilation in hypovolemic patients. An additional vasopressor medication, such as norepinephrine, should be used in hypotensive patients requiring dobutamine for inotropic support.

Mechanical Circulatory Support

Support of the circulatory system may require cardiac pacing (Box 4.5), which can be performed transcutaneously or transvenously. Transcutaneous pacing is noninvasive and more commonly used in the ED. Proper pacer pad placement is crucial in this modality. The anterior pacer pad is placed close to the heart, typically at the location of the V₃ lead on an electrocardiogram; the posterior pad is placed between the spine and the inferior border of the left or right scapula. The subsequent steps in transcutaneous pacing are listed in Box 4.6.

Box 4.5 Indications for Temporary Cardiac Pacing

Witnessed asystole

Hemodynamically significant bradycardia

Symptomatic second- or third-degree atrioventricular block

Complete atrioventricular dissociation with a ventricular rate lower than 50 beats/min

Termination of supraventricular or ventricular tachyarrhythmias