Shock

Kari Santoro-Beer, Philadelphia, Pennsylvania

Deborah C. Silverstein, Philadelphia, Pennsylvania

Shock is a state of severe hemodynamic and metabolic derangements. It is characterized by poor tissue perfusion from low or unevenly distributed blood flow that leads to a critical decrease in oxygen delivery (DO₂) in relation to oxygen consumption (VO₂) (Figure 4-1) or inadequate cellular energy production. If the shock state is not promptly recognized and treated, neurohormonal compensatory mechanisms will lead to stimulation of the renin-angiotensin-aldosterone system, as well as baroreceptor- and chemoreceptor-mediated release of catecholamines and subsequent production of counterregulatory hormones (glucagon, adrenocorticotropic hormone [ACTH], and cortisol). These changes will increase cardiovascular tone, activate a variety of biochemical mediators, and stimulate inflammatory responses that contribute to the shock syndrome. This progression can cause or exacerbate uneven microcirculatory flow, poor tissue perfusion, tissue hypoxia, altered cellular metabolism, cellular death, and vital organ dysfunction or failure.

Figure 4-1 The relationship between oxygen delivery and oxygen consumption. In region B-C, the oxygen consumption remains constant as oxygen delivery is increased. The oxygen supply is in excess of consumption and VO₂ is termed supply-independent. During shock, as metabolic demand (VO₂) increases or DO₂ diminishes (C-B), OER rises to maintain aerobic metabolism so that consumption can remain independent of delivery. However, at point B, called critical DO₂ (DcO₂), the maximum OER is reached. This is believed to be 60% to 70%, and beyond this point any further increase in VO₂ or decline in DO₂ must lead to tissue hypoxia. (Data from Mellema M: Cardiac output, wedge pressure and oxygen delivery, Vet Clin North Am Small Anim Prac 31(6):1175, 2001.)

Box 4-1 lists the different types of shock, but this classification can be overly simplistic. Critically ill patients are subject to complex etiologic and pathophysiologic events and therefore may suffer from more than one type of shock simultaneously. The rationale for the functional classification of shock is the presumption that each underlying illness identified can be associated with a specific pathophysiologic process and rapid, appropriate therapy can be administered.

Box 4-1 Functional Classifications and Examples of Shock

Hypovolemic: A Decrease in Circulating Blood Volume

• Hemorrhage

• Severe dehydration

• Trauma

Cardiogenic: A Decrease in Forward Flow from the Heart

• Congestive heart failure

• Cardiac arrhythmia

• Cardiac tamponade

• Drug overdose (e.g., anesthetics, β-blockers, calcium channel blockers)

Distributive: A Loss of Systemic Vascular Resistance

• Sepsis

• Obstruction (heartworm disease, saddle thrombosis)

• Anaphylaxis

Metabolic: Deranged Cellular Metabolic Machinery

• Hypoglycemia

• Cyanide toxicity

• Mitochondrial dysfunction

• Cytopathic hypoxia of sepsis

Hypoxemic: A Decrease in Oxygen Content in Arterial Blood

• Anemia

• Severe pulmonary disease

• Carbon monoxide toxicity

• Methemoglobinemia

Clinical Presentation

Depending on the type and clinical phase of shock, the patient’s clinical signs will vary. Dogs in compensatory shock demonstrate mild-to-moderate mental depression, increased heart rate, increased respiratory rate, peripheral vasoconstriction with cold extremities as well as pale mucous membranes, and a shortened capillary refill time with normal blood pressure. As compensatory mechanisms fail, patients may develop severe mental depression, prolonged capillary refill time, increased heart rate, poor pulse quality, and decreased arterial blood pressure.

Dogs with sepsis or a systemic inflammatory response syndrome (SIRS) can show clinical signs of hyperdynamic or hypodynamic shock. The initial hyperdynamic phase of sepsis is characterized by tachycardia, fever, bounding peripheral pulse quality, and hyperemic mucous membranes secondary to peripheral vasodilation. If septic shock or SIRS progresses unchecked, a decreased cardiac output and signs of hypoperfusion may ensue as a result of cytokine effects on the myocardium or myocardial ischemia. Clinical alterations may then include tachycardia, pale (and possibly icteric) mucous membranes with a prolonged capillary refill time, hypothermia, poor pulse quality, and dull mentation. Hypodynamic septic shock is the decompensatory stage of sepsis and without intervention results in organ damage and death. Finally, the gastrointestinal (GI) tract is considered the shock organ in dogs and often leads to ileus, diarrhea, hematochezia, or melena.

In cats the hyperdynamic phase of shock is rarely recognized. Also, in contrast to dogs, cats with shock have unpredictable changes in heart rate; they may exhibit tachycardia or bradycardia. In general, cats typically present with pale mucous membranes (and possibly icterus), weak pulses, cool extremities, hypothermia, and generalized weakness or collapse. In cats the lungs seem to be the organ most vulnerable to damage during shock or sepsis, and signs of respiratory dysfunction are common (Schutzer et al, 1993; Brady et al, 2000; Costello et al, 2004).

Patient Monitoring

General Diagnostics

Basic diagnostic tests, including venous or arterial blood gases, a complete blood cell count, blood chemistry panel, coagulation panel, blood typing, and urinalysis, should be completed for all patients in shock to assess the extent of organ injury and identify the cause of the shock state. Thoracic and abdominal radiographs, abdominal ultrasound, and echocardiography may be indicated once the patient is stabilized. Thoracic imaging can help distinguish cardiogenic from other forms of shock.

Monitoring Perfusion and Oxygen Delivery

The magnitude of oxygen deficit is a key predictor in determining outcome in patients with shock. Therefore optimizing tissue perfusion and DO₂ are goals of effective therapy, and thorough monitoring is necessary to achieve this objective. An optimally perfused patient maintains the following characteristics: central venous pressure between 5 and 10 cm H₂O (2 to 5 cm H₂O in cats); urine production of at least 1 ml/kg/hr; a mean arterial pressure (MAP) between 70 and 120 mm Hg and diastolic pressure above 40 mm Hg; normal body temperature, heart rate, heart rhythm, and respiratory rate; and moist, pink mucous membranes with a capillary refill time of less than 2 seconds. Monitoring these parameters creates the baseline for patient assessment. Additional monitoring elements that may prove beneficial include measurements of blood lactate, indices of systemic oxygenation transport, and mixed venous oxygen saturation.

Blood Lactate Levels

Critically ill patients with inadequate tissue perfusion, DO₂, or oxygen uptake often develop a hyperlactatemia and acidemia that reflect the severity of tissue hypoxia. Human patients with lactic acidosis are at greater risk of developing multiple organ failure and demonstrate a higher mortality rate (Nguyen et al, 2004). High blood lactate levels may also help to predict mortality in dogs (Boag and Hughes, 2005; de Papp et al, 1999; Nel et al, 2004; Lagutchik et al, 1998). The normal lactate level in adult dogs and cats is reported to be less than 2.5 mmol/L; lactate concentrations greater than 7 mmol/L are considered severely elevated (Boag et al, 2005). However, normal neonatal and pediatric patients may have higher lactate concentrations (McMichael et al, 2005). In addition, sample collection and handling techniques can affect lactate concentration (Hughes et al, 1999). Serial lactate measurements can be taken during the resuscitation period to gauge response to treatment and evaluate the resuscitation end points; the trends in lactate concentrations are a better predictor of outcome than are single measurements in both human and veterinary patients (Husain et al, 2003; Zacher et al, 2010; Green et al, 2011; Conti-Patara et al, 2012). The ability of the body to correct an elevated lactate concentration is directly correlated to survival.

Cardiac Output Monitoring and Indices of Oxygen Transport

The most direct way to assess the progress of resuscitation in shock patients is to measure indices of systemic oxygen transport. Measurement and monitoring of these values requires right-sided cardiac catheterization, which is performed using a specialized pulmonary artery catheter (PAC), also termed Swan-Ganz catheter or balloon-directed thermodilution catheter. When connected to appropriate electronic monitoring systems, the PAC allows access for the measurement of central venous and pulmonary arterial pressure, mixed venous blood gases (PvO₂ and SvO₂), pulmonary capillary wedge pressure (PCWP), and cardiac output. With these data additional information regarding the function of the circulatory and respiratory systems can be derived (i.e., stroke volume, end-diastolic volume numbers, systemic vascular resistance index, pulmonary vascular resistance index, arterial oxygen content, mixed venous oxygen content, DO₂ index, VO₂ index, and oxygen extraction ratio). The cardiac output is most commonly determined using thermodilution methods, although other techniques are available, including noninvasive Doppler-based methods.

A PAC can provide the clinician with useful information to assess and monitor the cardiovascular and pulmonary function of shock patients. It may also help the clinician evaluate the response to therapeutic interventions and allow titration of fluid therapy, vasopressors, and inotropic agents. Cardiac output and systemic DO₂ should be optimized by intravascular volume loading until the PCWP approaches 18 to 20 mm Hg. A higher PCWP (>18 to 20 mm Hg) promotes the formation of pulmonary edema, further impairing oxygenation and overall oxygen transport. Higher cardiac index (CI), DO₂, and VO₂ measurements have been linked with improved survival in critically ill human patients. Finally, the use of a PAC does not necessarily translate into reduced mortality in the critically ill shock patient; it is an invasive monitoring technique that is not without risk.

Although much information can be obtained from it, the PAC has a number of limitations. The accuracy of its measurements relies on catheter placement, calibration of transducers, coexisting cardiac or pericardial disease, and interpretation of waveforms and measurements or calculations. Thus PAC placement should be performed by experienced individuals, and interpretation of the data should be systematic. In veterinary practice today, PAC catheters and monitoring systems are largely confined to academic centers and to specialty referral practices. In humans the most common complications that occur during or after PAC insertion include arrhythmias, pulmonary injuries, thromboembolism, and sepsis.

Mixed Venous Oxygen Saturation and Central Venous Oxygen Saturation

Mixed venous oxygen saturation (SvO₂) can be used to assess changes in the global tissue oxygenation (oxygen supply-to-demand). If VO₂ is constant, SvO₂ is determined by cardiac output, hemoglobin concentration, and systemic arterial oxygen tension. The SvO₂ decreases if DO₂ is reduced by low cardiac output, hypoxia, or severe anemia, or if the VO₂ is increased (as with fever). SvO₂ is increased in hyperdynamic stages of sepsis and cytotoxic tissue hypoxia (e.g., cyanide poisoning). A reduction in SvO₂ may be an early sign that the patient’s clinical condition is deteriorating. Also, SvO₂ may be a surrogate for measuring the CI during resuscitative efforts.

Ideally SvO₂ is measured in a blood sample derived from a PAC because this represents a true mixed venous oxygen sample. However, in cases in which the insertion of a PAC is not possible or desirable, SvO₂ can be determined within the central circulation using a central venous catheter in the cranial vena cava. SvO₂ is then termed central venous oxygen saturation (ScvO₂). In critically ill patients with circulatory failure of any origin, ScvO₂ values generally are higher than SvO₂, but the two measurements closely parallel one another. Therefore the presence of a low ScvO₂ likely indicates an even lower SvO₂. The difference between the two values is usually about 5% and can be explained by blood flow redistribution and differences in VO₂ across the hepatosplanchnic, coronary, and cerebral circulations during shock states. The potential value of this monitoring was shown in a study comparing two algorithms for early goal-directed therapy in human patients with severe sepsis and septic shock (Rivers et al, 2001). In this study maintenance of a continuously measured ScvO₂ above 70% (in addition to maintaining central venous pressure above 8 to 12 mm Hg, MAP above 65 mm Hg, and urine output above 0.5 ml/kg/hr) resulted in a 15% absolute reduction in mortality compared with the same treatment without ScvO₂ monitoring (see Early Goal-Directed Therapy section later in the chapter for further details). ScvO₂ measurement in small animals has not gained widespread use, but clinical research in critically ill and septic dogs suggests that it may prove useful as a diagnostic, prognostic, and monitoring tool in the future (Conti-Patara et al, 2012; Hayes et al, 2011).

Therapy of Shock

Optimal therapy of the shock state involves careful patient monitoring, as discussed in the previous section, and specific treatments that include oxygen and various forms of fluid therapy tailored to the clinical situation. Additional treatment often involves vasopressors, inotropic agents, antimicrobials, gastrointestinal protectants, and nutritional support.

Oxygen

If the animal is not breathing or displays signs of impending respiratory fatigue, immediate intubation and positive-pressure ventilation should be instituted. If the animal is breathing spontaneously, oxygen is administered (see Chapters 10 and 11). This can involve flow-by methods (50 to 150 ml/kg/min) such as simply holding the oxygen tubing to the nose or administering oxygen into a mask, hood, or bag. Nasal or nasopharyngeal catheter(s) are effective methods of oxygen administration (using rates of 50 to 100 ml/kg/min per catheter). Once the vital signs are obtained, vascular access is established and fluid administration is initiated if indicated. Preliminary diagnostics and appropriate treatment should be rapidly initiated to maximize DO₂ to the tissues and prevent irreversible shock.