Robert J. Sigillito, MDand Peter M.C. DeBlieux, MD
Table 5.1 Classification of shock states
Hypovolemic shock Hemorrhage Fluid loss/dehydration Cardiogenic shock Pump failure Valvular disorders Cardiac dysrhythmia Distributive shock Sepsis
Anaphylaxis Intoxications Neurogenic shockb Spinal cord injury Obstructive shock Tension pneumothorax
Pericardial tamponade/constrictive pericarditisa Massive pulmonary embolus
Severe pulmonary hypertension Severe valvular stenosis
aClassified by some as cardiogenic shock.
bClassified by some as distributive shock.
Shock
Deficiencies in the historical database lead to poor treatment choices and increase patient morbidity and mortality. Unfortunately, many patients in shock states are not up to the task of providing an accurate and complete history.
Medical records, family members, and friends are invaluable resources in these situations.
Time course and progression of illness provide important information regarding the rapidity of decline and may help narrow the differential diag- nosis. Pre-existing conditions, particularly limita- tions of the cardiopulmonary system and immune deficiencies, predispose patients to poor outcomes.
Obtaining a patient’s complete medication list is vital in addressing the needs of the patient in shock. Medications that impair normal cardiac compensation in shock states, such as beta block- ers, calcium channel blockers, or digitalis, may alter patient presentations in profound shock.
Likewise, immunosuppressant agents, such as prednisone and chemotherapeutic drugs, may impair host immune response and mask serious or life-threatening infections. Lastly, social his- torical data focusing on alcohol, illicit drug use, work history, and psychosocial support systems may offer insight into these complex patients.
Physical examination
Physical examination and rapid assessment of the patient in shock follow the basic tenants of emer- gency medicine. Airway, breathing, circulation, disability, and exposure (ABCDE) are vital in the initial evaluation of the most complex patient presentations. If the impairment of shock is the inability to adequately provide O2 at the end organ, then the first critical appraisal must be airway, quickly followed by breathing and cir- culation. These first three steps comprise the crit- ical care concept of “cardiopulmonary reserve.”
Cardiopulmonary reserve refers to the interde- pendence of the heart, lungs, and O2-carrying capacity of any given patient. Those patients with an impaired cardiac pump, pre-existing pul- monary disease, or abnormalities in hemoglobin may require a more immediate intervention for possibly milder shock states when compared to patients with normal physiology. Normal lungs, heart, and hemoglobin permit a degree of physio- logic reserve that allows patients to compensate for any given cardiopulmonary insult.
One of the first steps in determining cardio- pulmonary reserve is vital sign assessment.
In evaluating and treating patients in shock, the
goal is to maintain adequate oxygenation and organ perfusion. Pulse oximetry is a rapid bedside tool that can be utilized as an initial screening tool to determine the adequacy of oxy- genation. Goal saturations during resuscitation and treatment should be maintained above 90%, although outcome data does not exist for this universally-accepted goal. The use of O2delivery devices may be required to reach the goal of 90%;
if adequate O2saturations are not obtained with 100% non-rebreather mask, then patients should be endotracheally intubated and placed on mechanical ventilation.
Once oxygenation has been addressed, the focus should be placed firmly on maintaining adequate cerebral and coronary perfusion pressures to prevent injury to these vital organs. Vital organ perfusion pressure is a function of mean arterial blood pressure (MABP). The critical nature of diastolic blood pressure (DBP) can be seen, as it is the main component of that calculation:
MABPDBP (SBPDBP) where SBPsystolic blood pressure.
Goals for resuscitation and maintenance in the majority of shock states should attempt to get MABP in the 70–80 mmHg range to offer adequate cerebral and coronary perfusion.
MABP can be better understood as it relates to preload and afterload. Physiologically, preload is defined as the left ventricular end diastolic wall tension. Clinically, several measures can be used to estimate whether the preload is low, normal, or high. The clinical situation may strongly sug- gest a patient’s volume status. Actively bleeding patients, trauma victims, or chronically dehy- drated patients are virtually certain to have a low preload. The edematous patient with congestive heart failure (CHF) is likely to be volume over- loaded. Estimation of the jugular venous pressure (JVP) on physical examination can be rapidly per- formed; however, the accuracy of this technique is not high, even in the hands of an experienced clin- ician. Auscultation of the heart and lungs is sen- sitive for detecting signs of volume overload (S3, crackles, and rales), but does not distinguish the hypovolemic state. Assessment of skin turgor, capillary refill, and the mucous membranes can likewise be misleading.
Afterload is the force that the heart must generate in order to eject blood into the arterial compartment. Since MABP is proportional to the product of systemic vascular resistance (SVR) and the cardiac output (CO), SVR is one of the
1–3
main determinants of afterload. A comprehensive review of the technique for insertion, calibration, and collection of data from a pulmonary artery (PA) catheter is beyond the scope of this chapter.
It is essential to note that excessive heart rate (HR) increases myocardial O2consumption and may further compromise at-risk myocardium.
Additionally, patients with normal vital signs can be in profound shock states despite calcu- lated MABP, central venous pressure (CVP), HR, and O2 saturation that are considered within normal ranges.
After the assessment of the cardiopulmonary reserve, a rapid neurological assessment is per- formed followed by complete exposure of the patient. Next, a comprehensive head-to-toe phys- ical examination is performed to identify evi- dence of decreased organ perfusion and to search for the etiology of the presenting complaint.
Altered mental status, cyanosis, delayed capillary refill, and skin mottling may be early signs of decreased oxygenation and perfusion.
Differential diagnosis
Physical examination and right heart catheteriza- tion are useful in the determination of the etiology of the various shock states, but the latter is rarely immediately available in the emergency depart- ment (ED). Table 5.2 outlines the physiologic parameters that characterize each shock state.
Hypovolemic shock
Hypovolemic shock is defined by the loss of intravascular volume. CVP, pulmonary artery occlusion pressure (PAOP), and cardiac output are low, while SVR is elevated. In the early com- pensated stages, the pulse pressure is narrowed due to vasoconstriction, but ultimately hypoten- sion occurs with decompensation. The initial treatment of hypovolemic shock is aggressive volume expansion with crystalloid solution.
Transfusion of blood products may be required if hemorrhage is the cause of hypovolemia.
Cardiogenic shock
The most common cause of cardiogenic shock is acute myocardial infarction, accounting for nearly half the cases. Low cardiac output and high SVR characterize cardiogenic shock. CVP and PAOP are most often elevated during acute exacerbations of CHF, but may be normal if the patient has
received adequate diuresis. Suggested cardiac parameters for the diagnosis of cardiogenic shock include cardiac index (CI)1.8 L/min/m2, SBP80 mmHg, and PAOP18 cmH2O. The initial treatment of CHF includes preload and afterload reduction. When shock is present, add- ition of a cardiotonic vasopressor is required.
Strong evidence supporting selection of one vaso- pressor over another does not exist. Consensus committee (ACC/AHA) has recommended the use of dobutamine if SBP is greater than 90, dopamine if SBP is less than 90, and norepin- ephrine if hypotension is severe or refractory to dopamine infusion. An intra-aortic balloon pump (IABP) should be considered for patients who do not respond to vasopressor therapy. This tech- nique employs placing an intra-aortic balloon that inflates during diastole, augmenting MABP and systemic perfusion, and deflates during systole, effectively diminishing afterload and improving cardiac output. Percutaneous coronary angioplasty and/or coronary artery bypass grafting should be strongly considered in patients with acute coro- nary ischemia complicated by shock.
Shock
Table 5.2 Physiologic parameters in shock states
CVP PAOP SVR/ CO/
SVRI CI
Hypovolemic ↓ ↓ ↑ ↓
Cardiogenic ↑ ↑ ↑ ↓
Distributive
Sepsis ↔↓ ↔↓ ↓ ↕
Anaphylaxis ↔↓ ↔↓ ↓ ↑
Neurogenic ↔ ↔ ↓ ↔↑
Obstructive
Tamponade ↑ ↑ ↑ ↓
Tension PTX ↕a ↕a ↑ ↓
Massive PE ↑ ↕b ↑ ↓
CVP: central venous pressure
PAOP: pulmonary artery occlusion pressure SVR: systemic vascular resistance SVRI: systemic vascular resistance index CO/CI: cardiac output/cardiac index PTX: pneumothorax
PE: pulmonary embolism.
aTrue CVP and PAOP are diminished due to impaired venous return. Measured pressure is falsely elevated, reflecting pleural pressure rather than vascular pressure.
bTrue left atrial pressure is low due to obstruction of flow through the pulmonary vasculature. Measured pressure may be falsely elevated, reflecting pulmonary vascular resistance rather than left heart filling pressure.
Distributive shock
In early sepsis, SVR is elevated. However, as septic shock progresses, SVR drops precipitously.
Cardiac output is increased in most cases, but a cytokine known as myocardial depressant factor is believed to be released from the pancreas, and may impair systolic function in later stages. Impaired cardiac perfusion will also adversely affect cardiac output. Vascular permeability is increased. Fluid shifts and increased insensible losses may lead to intravascular volume depletion and low CVP and PAOP. Early broad-spectrum antibiotic therapy and emergent surgical drainage or debride- ment, when indicated, are the cornerstones of treatment. Volume replacement should be guided by invasive monitoring of either CVP or PAOP.
Norepinephrine is the vasoactive agent of choice.
Recently introduced to the US, activated protein C complex (Xigris®) may improve survival.
Anaphylactic shock is accompanied by the massive release of cytokines in an inflammatory cascade, with loss of vasomotor tone and increased vascular permeability. Epinephrine, steroids, and antihistamines are initial therapies. Persistent hypotension requires infusion of an agent that supports vasomotor tone. Again, norepinephrine makes the most sense physiologically.
Neurogenic shock
Neurogenic shock, classified by some as a type of distributive shock, is a consequence of injury to the sympathetic ganglion chain. Neurogenic shock characteristically manifests as hypotension and bradycardia. Since spinal cord injury is most preva- lent in the young population, this entity usually occurs in patients with normal cardiac function.
It is of the utmost importance to rule out occult hemorrhage, and to use signs of organ perfusion to guide the initiation of pharmacologic therapy.
Many of these patients perfuse their organs well at below-normal MABP. If signs of hypoperfu- sion develop, then selection of an agent that sup- ports SVR (norepinephrine or neosynephrine) makes the most sense physiologically.
Obstructive shock
Two causes of obstructive shock, tension pneumo- thorax and cardiac tamponade, are reversible by surgical intervention. Support of the patient by volume loading is temporizing at best. Massive pulmonary embolus causes the release of vaso- active cytokines from the pulmonary vascular bed,
obstruction of flow, and acute right ventricular dysfunction, collectively impairing left ventricu- lar filling. Thrombectomy or thrombolysis can be life-saving interventions. Support of cardiac func- tion with volume infusions and dobutamine may be a bridge to these interventions. Chronic pul- monary hypertension may also limit flow through the pulmonary vascular bed. The onset of shock is an end-stage, pre-terminal event. Treatment with potent pulmonary vasodilators is hazardous in this shock state since hypotension from peripheral arterial dilation is a frequent side effect, mandat- ing use of a pulmonary artery catheter.
Diagnostic testing
Rapid bedside screening is the hallmark of the initial approach to screening and assessment of the undifferentiated patient in shock. Vital signs, pulse oximetry, and continuous monitoring are the standard testing. Following a head-to-toe assessment, a Foley catheter should be placed with an urometer to assess adequate hourly uri- nary output (0.5ml/kg/hour). Initial screening studies for the undifferentiated patient include:
bedside blood sugar analysis, arterial blood gas analysis, chest radiography, and an electrocar- diogram. A comprehensive metabolic profile, uri- nalysis, and complete blood count are required on each patient. Consideration for toxicologic stud- ies, blood and urine cultures, cardiac profiles, and endocrinologic screening should be made on a case-by-case basis. Serum lactate levels can be used to guide therapy, and may have prognostic value. An argument can be made to perform a quick, bedside echocardiogram to exclude cases of cardiac tamponade and global cardiac hypoki- nesis, but controlled trials supporting this approach have not been published. Additional radiographic studies of the head, chest, abdomen, pelvis, and extremities are second-tier studies and should only be obtained once the patient has been clinically stabilized.
General treatment principles
Oxygenation
Whenever a shock state is present, O2supplemen- tation is required. O2may be delivered via facial delivery devices, non-invasive mechanical venti- lation, or by conventional mechanical ventilation.
Shock
Simple means of delivering supplemental O2 include the use of a nasal cannula, venturi mask, or O2-reservoir non-rebreathing apparatus. O2 delivered via nasal cannula is appropriate only when low O2 flow is required. It is impossible to determine the fraction of inspired O2 (FiO2) delivered to any given patient because it varies with respiratory rate, the degree of nasal versus mouth breathing, and the O2flow rate. In general, if more than 5 L/min of O2flow is required with a nasal cannula, then an alternative device should be employed.
A venturi mask uses various O2 flow rates combined with various venturi apertures to pro- duce increasing O2 supplementation, generally higher than can be delivered by nasal cannula.
Although each mask lists specific FiO2 ratings from 0.28 to 0.50, these are rough estimates at best. If the listed flow rate with the smallest aper- ture does not provide enough supplemental O2, then an alternative device is required.
A non-rebreathing apparatus combines a col- lapsible bag reservoir with high-flow O2 and an exhalation valve so that high FiO2 can be delivered. When used optimally, the FiO2range may approach 0.6–0.8.
The current literature supports the use of non- invasive positive pressure ventilation (NPPV) in patients without hemodynamic compromise, cardiac dysrhythmias, or altered mental status.
Therefore, NPPV use in the management of shock should be limited to patients with respira- tory failure without hemodynamic instability.
This literature strongly supports the use of NPPV in patients with hypercapneic hypoxemic respiratory failure, such as those with exacerba- tion of chronic obstructive pulmonary disease (COPD). Data from descriptive studies regarding its use in selected cases of hypoxemic respiratory failure, such as acute respiratory distress syn- drome (ARDS), is available, but prospective ran- domized trials are lacking. Prospective trials investigating NPPV use in CHF with pulmonary edema suggest that continuous positive airway pressure (CPAP) is beneficial. Studies utilizing bilevel positive airway pressure (BiPAP) have been small and did not demonstrate benefit.
Early generations of non-invasive ventilators bled O2 into the ventilator tubing, so FiO2 was not tightly controlled. O2 flow was increased until the patient’s arterial O2 saturation (SaO2) was optimized. In newer models, the FiO2 can be more precisely set with a mixture valve, and adjusted as needed based on saturation monitoring.
Invasive mechanical ventilation should be considered for any patient who does not achieve adequate SaO2despite maximal non-invasive O2 supplementation. All patients who are placed on invasive ventilation should initially receive an FiO2of 1.0 because the switch from spontaneous breathing (negative pressure) to assisted ventila- tion (positive pressure) causes unpredictable alterations in pulmonary blood flow and ventila- tion–perfusion mismatch. FiO2 can then be decreased as the patient’s SaO2allows. Patients with pulmonary edema, particularly those with ARDS, may require the addition of positive end- expiratory pressure (PEEP) to optimize oxygen- ation. Although many factors must be considered in determining the optimal level of PEEP, most authors recommend starting at 3–5 cmH2O.
Thereafter, PEEP is incrementally increased by 2–3 cmH2O, allowing 15–30 minutes after each increase for alveolar recruitment. PEEP is increased until SaO2reaches a minimum 88–90%.
Further increases in PEEP may then be required to allow the FiO2to be decreased to 0.6. As PEEP is increased, the mean intrathoracic pressure increases. A critical point is reached when venous return to the heart is compromised due to increased intrathoracic pressure, impairing cardiac output. PEEP should not be increased beyond the point where hemodynamic compromise occurs.
Cardiac intervention
Pathologic rhythms may be a cause or conse- quence of a shock state. In either scenario, the goal of therapy should be to convert this to a perfu- sing rhythm. Bradycardic rhythms should be sped up either pharmacologically or with electrical transthoracic or transvenous pacing. Atropine is considered the first-line agent in patients with a pulse. It should be considered a temporary meas- ure, and preparation for pacing should be rapidly accomplished. In contrast, a bradycardiac patient without a pulse should receive CPR and alternat- ing doses of epinephrine and atropine while preparing to initiate electrical pacing.
The principles for electrically pacing the heart are the same for transthoracic and transvenous techniques. In both modes, the initial HR is set between 80 and 100 beats per minute. In the pulseless patient, the output is set at maximum, and dialed downward after the heart demon- strates capture. In contrast, the output is set at a minimum in the patient with a pulse, and dialed upward until capture is achieved.
Shock
In both scenarios, the final output should be set at 10–20% above the threshold for capture.
The causes of failure to capture include malposi- tion of the pacing leads, hypothermia, hypo- glycemia, hypoxemia, acidosis, and electrolyte disturbance.
Sinus tachycardia in the shock state is compen- satory. Except in some types of intoxication (sym- pathomimetic or anticholinergic overdose), acute ischemic coronary syndromes, and other unusual circumstances, measures directed at slowing the HR should be limited to correcting the underlying cause. All other tachycardias are pathologic, and may be the etiology for the shock state. These should be converted to a perfusing rhythm by the most rapid means, usually electrical cardiover- sion. The exception to this rule is atrial fibrillation (Afib). Acute Afib, defined as Afib of less than 48 hours duration, may be treated with cardiover- sion. Patients with chronic Afib, defined as Afib of greater than 48 hours duration, have an increased risk of systemic embolization of an atrial throm- bus. Such patients, or those in whom the duration of Afib is unknown, should receive anticoa- gulation or undergo transesophageal echocar- diography before attempts at cardioversion are undertaken. The decision to cardiovert such a patient should be made in consultation with a cardiologist.
Volume intervention
Following initial assessment of the preload, either fluid or diuretic therapy should be insti- tuted. The size of an initial fluid bolus is a matter of clinical judgment. A previously healthy young adult with acute hemorrhage may safely receive rapid infusion of several liters of a crystalloid solution. In contrast, a frail, elderly patient with a history of CHF may require boluses of only a few hundred milliliters at a time. The crucial step is reassessment after each intervention to decide whether further volume expansion is indicated.
A patient who is volume overloaded requires diuresis. Loop diuretics, such as furosemide, torsemide, and bumetadine, are the most com- monly used first-line agents. Frequent reassess- ment of the response in urinary output is mandatory to guide subsequent therapy. Other interventions that may be employed to lower preload include the administration of B-type natriuretic peptide (nesiritide), nitrates, opiates, rotating tourniquets, and dialysis. Opiates should be used with caution as they are associated with worse outcomes in acute CHF.
Blood transfusion intervention
The effect of raising the hemoglobin (Hgb) on O2 delivery is profound. The administration of 2 units of packed red blood cells (RBCs) to increase the Hgb by 25% (e.g., an increase of hematocrit from 20% to 25%) will also increase the calcu- lated O2delivery by 25%. For this reason, admin- istration of blood should be considered in patients with shock and anemia. Rapid estimation of Hgb is available in most centers by commercially- available analyzers, blood gas machines, or cen- trifuge techniques.
The threshold for administration of blood has been dictated by practice habit, and not by the evidence in the medical literature. It is generally recommended that adult trauma victims unre- sponsive to initial volume expansion with 2 L of crystalloid receive blood transfusion. Patients with coronary artery disease or CHF should be transfused with a goal of keeping the hematocrit above 30%. Other patients may benefit from blood therapy if the hematocrit falls below 20–24%. Of note, blood therapy has not been demonstrated to improve survival, decrease the duration of mechanical ventilation, or decrease the need for vasopressors. Controversy also exists because transfused allogenic RBCs may impair host immune response, and are less effi- cient at carrying O2than native RBCs.
Vasoactive agent intervention
Treatment of abnormalities in contractility and afterload should follow correction of preload, par- ticularly in hypovolemic states. Use of vasocon- stricting agents in the setting of volume depletion will further compromise organ perfusion, causing organ ischemia and infarction. Many of the vasoactive medications used to treat shock affect both myocardial contractility and SVR. A thor- ough knowledge of the action of adrenergic recep- tor physiology and the action of the vasoactive agents on these receptors is necessary to guide selection of a vasoactive agent.
Alpha-1 (-1) receptors are found in arterial smooth muscle and in the conduction system of the heart. The physiologic effect of -1 stimulation is increased cardiac excitation/conduction and arterial vasoconstriction (including coronary, cere- bral, renal, and splanchnic arterial beds). Beta-1 (-1) receptors are found in the myocardium and the conduction system. -1 stimulation results in increased contractility and cardiac excitation.
Beta-2 (-2) receptors are found in arterial and
Shock