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Tintinalli's Emergency Medicine > Section 4: Shock > Chapter 30. Approach to the Patient in Shock >
Epidemiology
More than 1 million cases of shock are estimated to present to U.S. hospital EDs each year.1 The presentation may be cryptic, as in the patient with compensated heart failure, or obvious as in the ultimate shock state of cardiac arrest. Despite aggressive treatment, mortality from shock remains high. Approximately 30 to 45 percent of patients in septic shock, and 60 to 90 percent for those with cardiogenic shock, die within 1 month of presentation.2,3 The definition and treatment of shock continues to evolve. With a contemporary understanding of the disease and new evolving technology, the emergency physician can recognize shock at an earlier stage and initiate expert, timely intervention. The general approach to a patient in the initial stages of shock follows similar principles regardless of the inciting factors or etiology.
Pathophysiology
Shock is defined as circulatory insufficiency that creates an imbalance between tissue oxygen supply and oxygen demand. The result of shock is global tissue hypoperfusion and is associated with a decreased venous oxygen content and metabolic acidosis (lactic acidosis). Shock is classified into four categories by etiology: (1) hypovolemic (caused by inadequate circulating volume), (2) cardiogenic (caused by inadequate cardiac pump function), (3) distributive (caused by peripheral vasodilatation and maldistribution of blood flow), and (4) obstructive (caused by extra cardiac obstruction to blood flow). Clinically, shock may have a predominant cause, but as the shock state persists or progresses to irreversible end organ damage, other pathophysiologic mechanisms become operative.
Knowledge of the principles of oxygen delivery and consumption is important to the understanding of shock. A maximum of four molecules of oxygen is loaded onto each molecule of hemoglobin as it passes through the lungs. If all available oxygen sites are occupied (four per molecule of hemoglobin), arterial oxygen saturation (SaO2) is 100 percent (Table 30-1). Arterial oxygen content (CaO2) is the amount of oxygen bound to hemoglobin plus the amount dissolved in plasma (Table 30-2). Oxygen is delivered to the tissues by the pumping function (cardiac output) of the heart.
Table 30-1 Definitions of Abbreviations
(a-v)CO2
Arterial-central venous carbon dioxide difference
CaO2
Arterial oxygen content
CmvO2
Mixed venous oxygen content
CI Cardiac index (cardiac output/body surface area)
CO Cardiac output
CPP Coronary perfusion pressure
CVP Central venous pressure
DO2
Systemic oxygen delivery
DBP Diastolic blood pressure
Hb Hemoglobin
MAP Mean arterial pressure
MODS Multiorgan dysfunction syndrome
OER Oxygen extraction ratio
PaCO2
Arterial carbon dioxide pressure
PaO2
Arterial oxygen pressure
PAOP Pulmonary artery occlusion (wedge) pressure
SaO2
Arterial oxygen saturation
ScvO2
Central venous oxygen saturation
SmvO2
Mixed venous oxygen saturation (pulmonary artery)
SrvO2
Retinal venous oxygen saturation
SIRS Systemic inflammatory response syndrome
SVR Systemic vascular resistance
VO2
Systemic oxygen consumption
Table 30-2 Oxygen Transport and Utilization Components
Arterial oxygen content CaO2= 0.0031 x PaO2+ 1.38 x Hb x Sao2
CaO2 is the amount of O2 within 100 mL blood. Oxygen is contained within blood in two forms: dissolved in plasma and chemically combined with hemoglobin. Assuming 15 g hemoglobin per 100 mL blood and an oxygen saturation of 97%, the representative normal value of CaO2 is 20.1 mL/100 mL blood (vol%).
Central venous/mixed venous oxygen saturation ScvO2 or SmvO2
SmvO2 reflects physiologic efforts to meet tissue O2 demands. Normal SmvO2 is 65 to 75%. When the SmvO2 falls below 50%, the body's limits to compensate have been reached and O2 availability for tissue metabolism will be compromised, leading to lactic acidosis.
Central venous/mixed venous oxygen content CmvO2= 0.0031 x PmvO2+ 1.38 x Hb x SmvO2
CmvO2 is the amount of oxygen content returning to the heart. Normal CmvO2 is 15 mL/100 mL blood (vol%).
Systemic oxygen extraction ratio (OER) OER = C(a – v)O2/CaO2
The amount of O2 taken out of the blood by the tissues is the systemic OER. It is described as a percentage. Normal OER is about 25%. Lactic acid production, an indicator of anaerobic metabolism, usually accompanies an OER of greater than 50%.
Oxygen delivery DO2= CO x CaO2x 10
DO2 is the amount of O2 delivered to the tissues per minute. Assuming a normal cardiac output of 5 L per min and a CaO2 of 20.1 vol%; a normal value for O2 delivery would be 1000 mL O2 per min.
Oxygen consumption VO2= CO x Hb x 1.38 x (SaO2– SmvO2) x 10
The amount of O2 consumed by tissues each minute and is equal to the difference in O2 delivered to tissues and the O2 returning from tissues. The normal value is about 250 mL O2 per min. Note that this formula ignores the small contribution from dissolved oxygen.
Oxygen affinity
Shifts in the oxyhemoglobin dissociation curve affect the release of O2 in the peripheral circulation. Increased pH, decreased temperature, decreased carbon dioxide concentration (PcO2) and decreases in 2,3-DPG levels all result in a shift of the oxyhemoglobin curve to the left. Thus, for any particular value of PaO2, the O2 saturation will be higher. This increased affinity of hemoglobin for O2 makes O2 loading easier, but release of O2 in the peripheral tissues is impaired. The reverse is true with a decreased pH, increased temperature, increased PcO2, and increased 2,3-DPG: there is a shift of the oxyhemoglobin dissociation curve to the right resulting in a decreased affinity of hemoglobin for O2.
Note: See Table 30-1 for abbreviation definitions.
Systemic oxygen delivery (DO2) is the product of the CaO2 and cardiac output (CO). Systemic oxygen consumption (VO2) comprises a sensitive balance between supply and demand. Normally, the tissues consume approximately 25 percent of the oxygen carried on hemoglobin, and venous blood returning to the right heart is approximately 75 percent saturated [mixed venous oxygen saturation (pulmonary artery) (SmvO2)]. When oxygen supply is insufficient to meet demand, the first compensatory mechanism is an increase in CO. If the increase in CO is inadequate, the amount of oxygen extracted from hemoglobin by the tissues increases, which decreases SmvO2.
When compensatory mechanisms fail to correct the imbalance between tissue supply and demand, anaerobic metabolism occurs, resulting in the formation of lactic acid. Lactic acid is rapidly buffered, resulting in the formation of measured lactate; normally between 0.5 and 1.5 mM/L. An elevated lactate level is associated with an SmvO2 1.0) indicates an impaired left ventricular function (as a result of blood loss and/or cardiac depression) and carries a high mortality rate.15
Central nervous system Acute delirium or brain failure; restlessness, disorientation, confusion, and coma secondary to decrease in cerebral perfusion pressure (mean arterial pressure – intracranial pressure). Patients with chronic hypertension may be symptomatic at normal blood pressures.
Skin Pallor, pale, dusky, clammy, cyanosis, sweating, altered temperature, and decreased capillary refill.
Cardiovascular Neck vein distention or flattening, tachycardia, and arrhythmias. An S3 may result from high-output states. Decreased coronary perfusion pressures can lead to ischemia, decreased ventricular compliance, increased left ventricular diastolic pressure, and pulmonary edema.
Respiratory Tachypnea, increased minute ventilation, increased dead space, bronchospasm, hypocapnia with progression to respiratory failure, and adult respiratory distress syndrome.
Splanchnic organs Ileus, gastrointestinal bleeding, pancreatitis, acalculous cholecystitis, and mesenteric ischemia can occur from low flow states.
Renal Reduced glomerular filtration rate, renal blood flow redistributes from the renal cortex toward the renal medulla leading to oliguria. Paradoxical polyuria can occur in sepsis, which may be confused with adequate hydration status.
Metabolic Respiratory alkalosis is the first acid–base abnormality, as shock progresses metabolic acidosis occurs. Hyperglycemia, hypoglycemia, and hyperkalemia.
Diagnosis
Ancillary Studies
The clinical presentation and the presumptive etiology of shock will dictate the use of ancillary studies. A battery of standard hematologic, coagulation, and biochemical tests usually provides an assessment of the patient's general physiologic condition and occasionally detects an abnormality that requires specific treatment (Table 30-4). A wide range of laboratory abnormalities may be encountered in shock, but most abnormal values merely point to the particular organ system that is either contributing to or being affected by the shock state. No single laboratory value is sensitive or specific for shock.
Table 30-4 Ancillary Studies
Basic evaluation
Hemogram: white blood cell count and differential, hemoglobin and hematocrit, platelet count
Electrolytes, glucose, calcium, magnesium, phosphorus
Blood urea nitrogen, creatinine
Prothrombin time, partial thromboplastin time
Urinalysis
Chest radiograph
Electrocardiogram
Moderate physiologic assessment
Arterial blood gas (measured oxygen saturation)
Serum lactate
Fibrinogen, fibrin split products, d-dimer
Hepatic function panel
Noninvasive hemodynamic assessment
End-tidal carbon dioxide
Noninvasive cardiac output measurement
Echocardiogram
Invasive hemodynamic assessment
Filling pressures: CVP or PAOP
Cardiac output
Central venous oxygen saturation: SmvO2
Calculation of hemodynamic values: SVR, CO, DO2, VO2
As clinically indicated to define etiology or detect complications
Blood, sputum, urine, and pelvic cultures
CT of head and sinuses
Lumbar puncture
Culture suspicious wounds
Cortisol level
Pregnancy test
Acute abdominal series
Abdominal or pelvic ultrasound
Abdominal or pelvic CT
Note: See Table 30-1 for abbreviation definitions.
Hemodynamic monitoring is important in the assessment of patients in shock and evaluation of response to treatment. Monitoring capabilities will vary from institution to institution, but should include pulse oximetry, electrocardiographic monitoring, continuous noninvasive but preferably intraarterial blood pressure monitoring, end-tidal CO2 monitoring, and central venous pressure (CVP) monitoring.7 Because hemodynamic measurements are physiologic values, they should be used to answer specific physiologic questions rather than to serve as therapeutic end points.
Treatment
The Rationale for Early Intervention
The tenet of trauma resuscitation is to initiate care within the "golden hour" of disease presentation. A similar principle applies to patients with nonsurgical causes of shock. Current national increases in ED patient acuity and overcrowding have resulted in extending the golden hour into hours and even days, consequently requiring the provision of critical care in the ED. The benefit of timely ED intervention in nontraumatic critical illness is significant; standard ED care can significantly decrease the predicted mortality of critically ill patients in as little as 6 h of treatment.8 Application of an algorithmic approach to optimize hemodynamic endpoints with early goal-directed therapy in the ED reduces mortality by 16 percent in patients with severe sepsis or septic shock.9 The ABCDE tenets of shock resuscitation are establishing Airway, controlling the work of Breathing, optimizing the Circulation, assuring adequate oxygen Delivery, and achieving End points of resuscitation.
Establishing Airway
Airway control is best obtained through endotracheal intubation for airway protection, positive pressure ventilation (oxygenation), and pulmonary toilet. Sedatives, which are frequently used to facilitate intubation, can exacerbate hypotension through arterial vasodilatation, venodilation, and myocardial suppression. Furthermore, positive pressure ventilation reduces preload and cardiac output. The combination of these interventions can lead to hemodynamic collapse. Volume resuscitation or application of vasoactive agents may be required prior to intubation and positive pressure ventilation.
Controlling the Work of Breathing
Control of breathing is required when tachypnea accompanies shock. Respiratory muscles are significant consumers of oxygen during shock and contribute to lactate production. Mechanical ventilation and sedation decrease the work of breathing and have been shown to improve survival. SaO2 should be restored to greater than 93 percent and ventilation controlled to maintain a PaCO2 35 to 40 mm Hg. Attempts to normalize pH above 7.3 by hyperventilation are not beneficial. Mechanical ventilation not only provides oxygenation and corrects hypercapnia but assists, controls, and synchronizes ventilation, which ultimately decreases the work of breathing. Neuromuscular blocking agents are used as adjuncts to further decrease respiratory muscle, oxygen consumption and preserve DO2 to vital organs.
Optimizing the Circulation
Circulatory or hemodynamic stabilization begins with intravascular access through large-bore peripheral venous lines. Trendelenburg positioning, historically considered necessary for maintaining perfusion in the hypotensive patient, does not improve cardiopulmonary performance compared with the supine position. It may worsen pulmonary gas exchange and predispose to aspiration. If a volume challenge is urgently required, rather than using the Trendelenburg position, an alternative is to raise the patient's legs above the level of the heart with the patient supine. Central venous access will aid in assessing volume status (preload) and monitoring ScvO2. It is the preferred route for the long-term administration of vasopressor therapy, and provides rapid access to the heart if pacemaker placement is required.
Fluid resuscitation begins with isotonic crystalloid; the amount and rate are determined by an estimate of the hemodynamic abnormality. Most patients in shock have either an absolute or relative volume deficit, except the patient in cardiogenic shock with pulmonary edema. Fluid is given rapidly, in set quantities (e.g., 500 or 1000 mL), with reassessment of the patient after each amount. Patients with modest degree of hypovolemia usually require an initial 20 mL/kg of isotonic crystalloid. More fluids may be necessary with profound volume deficits.
The colloid-versus-crystalloid resuscitation controversy remains despite evidence that there is a slight increase in mortality when colloids are used for volume replacement in critically ill patients.10 Some studies have found a lower incidence of pulmonary edema, and possibly greater benefit, in elderly patients with colloid resuscitation, although survival is not statistically improved. In the acute situation with severe shock, colloids may be considered to achieve rapid plasma expansion using less volume compared to crystalloids.
Without invasive hemodynamic monitoring, noncardiogenic pulmonary edema may be difficult to differentiate from cardiogenic pulmonary edema in the ED. Even though the former may respond to fluids, fluids should be minimized in a patient with clinical or radiographic evidence of pulmonary edema until appropriate monitoring is established.
Vasopressor agents are used when there has been an inadequate response to volume resuscitation or when a patient has contraindications to volume infusion.11 They are most effective when the vascular space is "full" and least effective when the vascular space is depleted. However, vasopressors may be necessary early in the treatment of shock, before volume resuscitation is complete, in order to prevent potentially lethal consequences of prolonged systemic arterial hypotension. This is especially important in elderly patients with significant coronary and cerebrovascular disease. Rapidly restoring the MAP to 60 mm Hg or systolic pressure to 90 mm Hg may avoid the coronary and cerebral complications of decreased blood flow. Vasopressor agents are based on the catecholamine molecule and have variable effects on the -adrenergic, -adrenergic, and dopaminergic receptors (Table 30-5).11,12
Table 30-5 Commonly Used Vasoactive Agents
Drug Dose/Mixture* Action Cardiac Stimulation Vasoconstriction Vasodilation Cardiac Output Side Effects and Comments
Dopamine 0.5–25 g/kg per min
400 mg/250 mL , , and dopaminergic ++ at 2–10 g/kg per min ++ at 7 g/kg per min + at 0.5–5.0 g/kg per min Usually increases Tachydysrhythmias, increases myocardial O2 consumption, a cerebral, mesenteric, coronary and renal vasodilator at low doses
Norepinephrine 0.01–0.5 g/kg per min
4 mg/250 mL Primarily 1, some 1
++ ++++ 0 Slight decrease Dose related, reflex bradycardia; useful when loss of venous tone predominates, spares the coronary circulation
Phenylephrine 0.15–0.75 g/kg per min
10 mg/250 mL Pure 0 ++++ 0 Decrease Reflex bradycardia, headache, restlessness, excitability, rarely arrhythmias; ideal for patients in shock with tachycardia or supraventricular arrhythmias
Ephedrine 5–25 mg and +++ ++ + Increases Causes palpitations, hypertension, cardiac arrhythmias, an indirect-acting CNS stimulant; limited long-term value as therapy for shock.
Vasopressin 0.01–0.04 units per min
200 units/250 mL ++++ Primarily vasoconstriction, outcome data from its use is lacking; infusions of 0.04 units per min may lead to adverse, vasoconstriction-mediated events
Epinephrine 0.01–0.75 g/kg per min
1 mg/250 mL and ++++ at 0.03–0.15 g/kg per min ++++ at 0.15–0.30 g/kg per min +++ Increases Causes tachydysrhythmia, leukocytosis, increases myocardial oxygen consumption
Dobutamine 2.0–20 g/kg per min
250 mg/250 mL 1, some 2 and 1 in large dosages
++++ + ++ Increase Causes tachydysrhythmia, occasional GI distress, increases myocardial oxygen consumption, hypotension in volume depleted patient; has less peripheral vasoconstriction than dopamine, can cause fewer arrhythmias than isoproterenol
Isoproterenol 0.01–0.05 g/kg per min
1 mg/250 mL 1 and some 2
++++ 0 ++++ Increases Causes tachydysrhythmia, facial flushing, hypotension in hypovolemic patients; increases myocardial oxygen consumption; never use alone in shock.
Note: 0 = no effect, += mild effect, ++= moderate effect, +++= marked effect, ++++= very marked effect.
Abbreviations: CNS = central nervous system; GI = gastrointestinal.
*Individual drugs may be diluted in D5W or NS, and may be diluted in larger volumes or concentrated into smaller volumes according to the fluid needs of the individual patient.
The use of vasopressors is accompanied with potential pitfalls. While improving perfusion pressure in the large vessels, they may decrease capillary blood flow in certain tissue beds, especially the bowel. Vasopressors also may alter the relationship between volume and pressure measurements through their effect on the pulmonary and peripheral vascular beds. In other words, vasopressors will falsely elevate intracardiac filling pressures (i.e., CVP). They should be used judiciously, generally only after volume resuscitation. When multiple vasopressors are used, they should be simplified as soon as the best therapeutic agent is identified.
Assuring Adequate Oxygen Delivery
Once blood pressure is stabilized through optimization of preload and afterload, DO2 can be assessed and further manipulated. Arterial oxygen saturation should be returned to physiologic levels (93 to 95 percent) and hemoglobin maintained above 10 g/dL.13 If cardiac output can be assessed, it should be increased by using volume infusion and inotropic agents in incremental amounts until venous oxygen saturation (SmvO2 or ScvO2) and lactate are normalized.
The control of VO2 is important in restoring the balance of oxygen supply and demand to tissues. A hyperadrenergic state results from the compensatory response to shock, physiologic stress, pain, and anxiety. Shivering frequently results when a patient is unclothed for examination and then left inadequately covered in a cold resuscitation room. The combination of these variables increases systemic oxygen consumption. Pain further suppresses myocardial function, thus impairing DO2 and VO2. Providing analgesia, muscle relaxation, warm covering, anxiolytics, and even paralytic agents, when appropriate, decreases this inappropriate VO2.
Tissue oxygen extraction assesses adequacy of the resuscitation in meeting the oxygen needs of the tissues. Sequential examination of lactate and SmvO2 or ScvO2 is a method to assess adequacy of tissue oxygen extraction. Continuous measurement of SmvO2 or ScvO2 through fiberoptic technology can be used in the ED.4 A variety of other technologies have potential to assess tissue perfusion during resuscitation (Table 30-6).14–17
Table 30-6 Adjuncts in Assessing Tissue Perfusion
Base deficit Base deficit is an indicator of metabolic acidosis and is an index of hemodynamic and tissue perfusion changes in shock. Predicts illness severity in intraabdominal hemorrhage and blunt trauma.
Invasive blood pressure monitoring Intensive vasoconstriction caused by sympathetic activity or vasopressors given will cause the cuff pressure to underestimate true blood pressure. A Doppler may be used in conjunction with a sphygmomanometer may enable more accurate measure of systolic blood pressure once Korotkoff sound are no longer audible. Intra-arterial pressure measurement is preferable because vasoactive drugs may cause rapid swings in blood pressure and multiple blood samplings will typically be required.
Central venous pressure (CVP) Aids in assessing volume status. Preferred for the long-term administration of vasopressor therapy and provides rapid access to the heart if pacemaker placement is required. May not reliably reflect the left ventricular filling pressure in clinical states such as pulmonary embolus, obstructive airway disease, right ventricular infarction, and pericardial effusion. Common iliac venous pressure can approximate CVP.
Central venous oximetry (ScvO2)
ScvO2 closely approximates mixed venous O2 saturation (SmVO2) and can be monitored continuously using infrared oximetry. This technology enables the clinician to detect clinically unrecognized tissue global tissue hypoperfusion in the treatment of myocardial infarction, general medical shock, trauma, hemorrhage, septic, hypovolemic, end-stage heart failure, and cardiogenic shock during and after cardiopulmonary arrest.
Arterial-central venous CO2 difference
Increased arterial-mixed venous carbon dioxide gradients or (a-v)CO2 are seen in acute circulatory failure, and inversely correlate with the cardiac index (CI).
Pulmonary artery catheterization The standard of care for assessing cardiac status. Valuable in determining left-sided heart filling, pulmonary artery pressure, and assessing the cause of pulmonary edema. Can obtain cardiac output and mixed venous oxygen saturation. Will be able to calculate hemodynamic (i.e., SVR) and oxygen transport variables (VO2 and DO2). The effectiveness of this monitoring technique on improving outcome is challenged.
Noninvasive cardiac output Cardiac output can be measured by transesophageal Doppler, cutaneous bioimpedance, and lithium dilution.
Gastric tonometry and sublingual capnography Serial measurements of gastric and sublingual mucosal blood flow are based on hydrogen ion diffusion and carbon dioxide elimination. Inadequate visceral perfusion as evidenced by persistently low intramucosal pH or increased sublingual carbon dioxide concentration after resuscitation is associated with subsequent organ dysfunction and death.
Retinal venous O2 saturation
Retinal venous O2 saturation (SrvO2) correlates with blood volume, central venous O2 saturation and arterial O2 saturation.
Metabolic cart Directly measured VO2 without a pulmonary artery catheter. A reduction in VO2 (after acute myocardial infarction) predicts cardiogenic shock and mortality after human cardiac arrest.
Achieving End Points of Resuscitation
Traditional end points have been normalization of blood pressure, heart rate, and urine output. Because these underestimate the degree of remaining hypoperfusion and oxygen debt, more physiologic end points have been investigated (Tables 30-7 and 30-8).18 No therapeutic end point is universally effective, and only a few have been tested in prospective trials, with mixed results.18 The goal of resuscitation is to maximize survival and minimize morbidity using objective hemodynamic and physiologic values to guide therapy. A goal-directed approach at achieving urine output >0.5 mL/kg per h, CVP 8 to12 mm Hg, MAP 65 to 90 mm Hg, and ScvO2 >70 percent during ED resuscitation of septic shock significantly decreases mortality.9
Table 30-7 End Points of Resuscitation
Traditional: normalization of blood pressure, pulse, and urine output
Restoration of circulating volume
Restoration of all fluid compartments
Vascular space is "full"
Hemodynamic parameters are "normalized"
Tissue oxygen delivery is maximized
Restoration of aerobic metabolism, elimination of tissue acidosis, and repayment of oxygen debt
Table 30-8 Hemodynamic Resuscitation End Points
Modality Goals
Preload CVP 10–12 mm Hg
PAOP 12–18 mm Hg
Afterload MAP 90–100 mm Hg
SVR = (MAP – CVP/CO)(80) 800–1400 dyne s/cm5
Contractility CO 5.0 L/min
CI 2.5–4.5 L per min m2
SV = CO/heart rate 50–60 mL per min
Heart rate 60–100 bpm Avoid >100 bpm; this will decrease SV and increase myocardial oxygen consumption
Coronary perfusion pressure CPP = DBP – CVP (or PAOP) >60 mm Hg
Tissue oxygenation ScvO2 or SmvO2
>70%
Serum lactate ................
................
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