Shock

Oxygen delivery to tissues is one of the primary functions of the cardiopulmonary system and of primary importance to the patient manifesting signs of circulatory failure. Oxygen delivery is a function of cardiac output and oxygen content of arterial blood (Fig. 2.1). In health, blood flow (cardiac output) is adjusted to meet the oxygen demands of the individual. This occurs primarily through changes in heart rate and vasomotor control of perfusion to maintain oxygenation of active tissues. Many acute disease states result in inadequate oxygen delivery to the tissues and tissue hypoxia. Initially, this drop in oxygen delivery can be overcome by compensatory increases in oxygen delivery variables and increases in oxygen extraction. When these mechanisms fail to restore oxygen homeostasis, global tissue hypoxia (shock) results [1]. If the defect in the transport of oxygen to the vital tissues can be identified and corrected while the patient is undergoing supportive care, recovery is possible. Failure to correct poor perfusion will lead to decreased oxygen consumption in the tissues, organ dysfunction, and death.

Classification of Shock

Shock may be classified in many ways, including by common pathway or specific cause. It is helpful to think of shock in terms of broad categories before further defining the type of shock within each category. The broadest classification system includes three major and exceedingly different causes of shock: cardiogenic shock, hypovolemic shock, and distributive shock [2]. Each results in reduced oxygen delivery to tissues through low blood flow or uneven distribution of flow. In practice, each primary event can lead to a cascade of complex physiologic problems, neurohormonal compensations, and activation of various biochemical mediators and inflammatory responses integral to the shock syndromes. A single patient may have several pathologic processes simultaneously resulting in reduced perfusion of tissues.

Hypovolemic Shock

The primary defect in hypovolemic shock is an inadequate circulating volume. This can be from sudden massive blood loss as in surgery or trauma, or fluid loss from vomiting, diarrhea, or renal disease. Neurohormonal pathways detecting a drop in blood pressure will stimulate the renin-angiotensin-aldosterone system to conserve water through the action of antidiuretic hormone. Stimulation of the sympathetic nervous system leads to epinephrine and norepinephrine release from the adrenal gland. These hormones increase vascular tone in an attempt to shunt circulation from the periphery to vital tissue beds and result in cool extremities and prolonged capillary refill time. Myocardial contractility is also increased through their action. As the patient begins to decompensate, tachycardia is a common finding, allowing maintenance of oxygen delivery in the face of diminished stroke volume. Concurrently, fluid shifts from interstitial fluid reserves in an attempt to preserve vital perfusion of the brain, heart, and kidneys while stealing supplies from other organs and tissues such as skeletal muscle and the gastrointestinal tract [3].

Cardiogenic Shock

Cardiogenic shock occurs when the pumping function of the heart is severely impaired, leading to circulatory failure. As with hypovolemic shock, the patient will be tachycardic, weak, oliguric, have cool extremities and weak pulses. The patient with cardiac failure may also have evidence of primary cardiac disease such as an auscultable murmur, ascites, jugular venous distention, pulmonary edema, or cardiac arrhythmias. The primary defect in oxygen delivery is a reduced cardiac output [4].

CO = Heart Rate x Stroke Volume

Stroke volume is determined by preload, afterload, and contractility. Within limits, cardiac output increases as heart rate increases. High heart rates will eventually decrease cardiac output by impairing cardiac filling and subsequent stroke volume. Tachycardia may be the result of cardiac arrhythmia or simply a physiologic response to low volume. Specific antiarrhythmic therapy and correction of underlying causes of tachycardia should be used to normalize heart rate. Clinically significant bradyarrhythmias are less common. Hyperkalemia or decompensated shock (especially in the feline) can result in clinical bradycardia. Specific arrhythmias include sick sinus syndrome, second- and third-degree atrioventricular block. It is uncommon for these slow heart rates to require emergency treatment. Often these patients have already compensated with increased stroke volume and can be referred for pacemaker treatment [5].

Stroke volume is dependent on three determinants of cardiac function: preload, afterload, and contractility. With congestive heart failure, the pump is failing because of decreased contractility. The body attempts to compensate by increasing preload (sodium and fluid retention). Normally, the heart is able to pump the fluid presented to it through increased stretch of myocardial muscle fiber, resulting in increased contractility. Therefore, by increasing preload, the heart will increase stroke volume. In cardiac failure, the excess fluid cannot be moved and it accumulates downstream of the failing ventricle. This results in pulmonary edema in left-ventricular failure and ascites, pleural effusion, and hepatic congestion in right-ventricular failure [6].

Maximize stroke volume (and cardiac output) by recognizing and treating the primary defect. In congestive failure, preload can be optimized by monitoring central venous pressure, administering diuretics such as furosemide, and venodilators such as nitroglycerine. With obstructive failure, as is seen with pericardial effusion, removal of even a small amount of pericardial fluid will relieve the pressure on the right ventricle and allow more normal filling [7]. Cardiac output can also be enhanced by decreasing afterload with calcium channel blockers or ACE inhibitors. These are especially useful in treating failure caused by mitral insufficiency where contractility may be normal to increased but a portion of the cardiac output is going backwards into the left atrium instead of out and into systemic circulation. In documented myocardial failure, contractility can be enhanced with positive inotropic drugs such as dobutamine, digoxin, or pimobendan [8].

Distributive Shock

Distributive shock is probably the most challenging of the shock syndromes and one of the most difficult to reverse. The primary defect with distributive shock is an abnormal systemic vasomotor response leading to peripheral vasodilation and maldistribution of blood flow [9]. Increases in vascular permeability can further exacerbate this shock syndrome. Both peripheral vasodilation and increased vascular permeability result in decreased perfusion of vital tissues. The many causes of distributive shock are summarized in Table 2-1.

Components of other forms of shock may contribute to poor tissue oxygenation in distributive shock. Fluid loss into body cavities and interstitial spaces results in relative hypovolemia. The release of inflammatory mediators in septic shock can depress the myocardium, resulting in a cardiogenic component. Therapy must be directed at the underlying systemic defect. In sepsis, therapy consists of drainage and control of the infected focus. Because systemic inflammation resulting from sepsis and other inflammatory disease can affect oxygen delivery in many vital tissues, serial monitoring of many. variables becomes necessary to treat the variety of problems an individual may face [10].

Treatment and Monitoring

Treatment of shock should be directed at the primary problem(s) while correcting the fluid deficit. Crystalloid fluids can be used initially to restore circulating volume. Crystalloids improve cardiac output and should not be withheld for fear of diluting the red blood cell mass [11]. Oxygen delivery is a function not only of oxygen content, but also of cardiac output. Improved stroke volume should offset the initial drop in packed cell volume as the patient's true level of anemia becomes apparent. If signs of shock persist as the patient becomes more anemic, a hemoglobin-containing fluid (whole blood, packed red blood cells, or Oxyglobin®) should be administered [12,13].

With a treatment goal of improving oxygen delivery to the tissues, we can increase cardiac output by increasing stroke volume (appropriate fluids). Oxygen content can be increased by increasing the hemoglobin concentration (hemoglobin transfusion) and by increasing oxygen saturation (oxygen supplementation).

Volumes of fluid for resuscitation should be tailored to the individual patient. It has long been recommended that the initial goal with crystalloid fluids is to give a blood volume (approximately 90 ml/kg dog, 60 ml/kg cat) in an hour [14]. This is often more than enough fluid, and in extremely debilitated patients may lead to fluid overload (pulmonary and cerebral edema) [15]. Patients with systemic inflammatory conditions may also be prone to vascular leakage. Excessive fluids can affect electrolytes, dilute clotting factors, and lead to accumulations of fluid in interstitial spaces and body cavities. It may be more practical to titrate this dose in smaller increments. Smaller boluses of 22 ml/kg in dogs or 10 ml/kg in cats (approximately 25% of the total shock volume) of crystalloid fluids should be given intravenously followed by repeated doses if the patient's clinical signs fail to improve [16]. Endpoints of resuscitation should be evaluated closely and the rapid administration of fluids should be discontinued when the patient is improving [17]. Questions to ask: Are the pulses stronger? Slower? Is the patient more alert? If the answer is "no", more fluids are administered while alternate mechanisms of shock are investigated.

Following the administration of a bolus of 25% shock dose of crystalloid fluids, the packed cell volume and total solids should be compared to pre-fluid values. If a patient receiving large quantities of crystalloids becomes anemic or hypoproteinemic, the fluid should be switched to an appropriate colloid such as whole blood, packed red blood cells, plasma, or a synthetic colloid. If the total solids drop to less than 50% of pretreatment values, a colloid should be considered for further resuscitation. If the PCV has dropped precipitously, administer whole blood and search for the source of blood loss. Often, in traumatic hemorrhage, correction of blood loss volume and pressure facilitates repeated hemorrhage in areas of vascular trauma, while simultaneously diluting available clotting factors. Therefore, close attention during initial fluid resuscitation is important.

Heart and respiratory rates are useful objective variables to monitor in critical patients. Capillary refill, peripheral pulse quality, and mentation are subjective but still valuable parameters to help assess perfusion when used by experienced professionals. Blood pressure and pulse oximetry are gaining wider use in veterinary medicine and may provide additional information on cardiopulmonary function so long as limitations of the equipment are understood.

Blood pressure is the lateral force per unit area of vascular wall. Blood flow is the amount of motion provided by blood pressure working against vascular resistance. Throughout the cardiac cycle, the blood pressure oscillates about a mean pressure. Pulse pressure, which determines pulse quality or strength, is the difference between systolic and diastolic pressure. Systolic pressure is determined by stroke volume, peak rate of ejection, and arterial compliance. Diastolic pressure is a function of end-systolic arterial pressure, diastolic duration, peripheral vascular resistance, and blood volume [18].

Indirect blood pressure measurement involves the occlusion of a peripheral artery by inflation of a pneumatic cuff. The closing and opening of the artery is detected through palpation, auscultation, or oscillometric or ultrasonic means. Diastolic pressure, which is much more important in the critically ill animal, unfortunately is much more difficult to establish. Limitations to the use of indirect blood pressure monitoring include the expense of the equipment and the inability to reliably detect blood pressure in smaller animals or those critically ill patients with low-pressure readings.

Oscillometric indirect blood pressure measurement senses amplitude of oscillations in a pressurized cuff. These oscillations are produced by changes in arterial diameter caused by changes in pulse pressure. A sudden increase in the amplitude of oscillations corresponds to systolic pressure and a low point of maximum oscillations corresponds to the diastolic pressure. The mean arterial pressure is measured directly as the lowest cuff pressure at which the oscillations are at their highest amplitude. Appropriate cuff size should be 40% of limb circumference. If the cuff is too narrow it may lead to a falsely high blood pressure. If it is too wide the blood pressure will be falsely low [18, 19].

Ultrasonic pulse detectors use ultrasound kinetoarteriography to detect arterial wall motion using ultrasonic waves to amplify the sound of pulsating blood. Gradual deflation of cuff pressure allows blood flow as pressures drop below systolic blood pressure. Systolic pressure is recorded as the first audible sound as blood begins to flow through the artery [18]. Diastolic pressure is much more subjective and is recorded when the sound quality changes dramatically and becomes muffled. The advantage of ultrasonic sphygmomanometry is its adaptability to many animals. Also, the equipment is relatively inexpensive. Disadvantages and limitations are similar to those of the oscillometric devices. Because determination of actual pressure cutoff points is operator dependent, fluctuation in reported values can be greater. Mean arterial pressure cannot be determined directly by this method but can be calculated if systolic and diastolic pressures are recorded.

Pulse oximetry allows the estimation of arterial oxyhemoglobin saturation by transmitting light through a skin fold and sensing the difference between light absorption during pulsation (arterial flow) and background absorption. Although oxyhemoglobin (SaO2) saturation is not directly related to arterial PO2, it provides information about tissue delivery of oxygen. The advantage of measuring SaO2 is the continuous, immediate noninvasive estimate of oxygenation. Disadvantages include the difficulty in maintaining the transducer in small conscious patients, interference in pigmented skin, and the inability to detect adequate signals with certain diseases (low cardiac output states, icterus, anemia, and hypothermia) [20].

An important clinical question is how to determine when the shock state is controlled. With goal-directed therapy, fluid rates can be lowered to deficit replacement, maintenance volumes, and ongoing losses when clinical signs of shock resolve. It is important to note that traditional endpoints of resuscitation (capillary refill time, heart rate, peripheral pulse quality, blood pressure, level of mentation, and urine output) may be normal in early, compensated shock and altered only when the patient decompensates. However, the opposite is also a problem: In animals in which the above endpoints are successfully corrected but that still have ongoing evidence of tissue hypoxia, more sensitive markers of oxygen transport must be evaluated [17].

Intensive oxygen transport monitoring gives greater importance to detecting oxygen delivery. Researchers in the 1980s hypothesized that oxygen delivery and oxygen consumption were the best means of assessing adequate tissue oxygenation. Their research led to the idea that supranormal oxygen delivery in acute perioperative shock would lead to reduced mortality [21].

This led to the routine use of pulmonary artery catheters and measurement of variables such as cardiac index (cardiac output standardized to body weight), central venous pressure, and pulmonary capillary wedge pressure. By sampling mixed venous (pulmonary arterial) blood and comparing it with arterial blood, oxygen extraction and utilization could be measured and monitored. Unfortunately many studies performed since have led to conflicting results and routine placement of pulmonary artery catheters has been associated with technical problems and catastrophic complications [22]. Even so, decreases in oxygen utilization have been shown to negatively affect prognosis in patients that fail to achieve normal oxygen utilization within 12 hours of resuscitation [23]. For this reason, alternative means to assess patients' relative oxygen debt continue to be investigated. Blood lactate, serum base excess (or deficit), gastric tonometry, and organ-specific cellular oxygen utilization techniques have provided new means to assess oxygen debt [17].

Lactate is produced from pyruvate (via lactate dehydrogenase) during periods of tissue hypoxia. Normally less than 2 mmol/L, arterial lactate climbs with anaerobic metabolism. Tissue hypoxia causes lactate levels to climb beyond the ability of normal clearance mechanisms [24]. While it can indicate poor perfusion, tissue hypoxia, and lactic acidosis, lactate can be normal during periods of deranged cardiac output (before clearance mechanisms have become saturated). Hemorrhagic shock in a canine model found lactic acidosis more predictive of the severity of oxygen debt than blood pressure or cardiac output [25]. Lactate can be used to monitor resuscitative efforts, as levels should drop quickly with improved perfusion. Lactate measurement has limitations because other forms of lactic acidosis exist that are not specific for global oxygen debt. An example of this occurs with sepsis and catecholamine administration in which altered lactate metabolism can overestimate the severity of tissue hypoxia [24].

Determination of base deficit has been favored over that of blood lactate in human critical care. Base deficit is calculated by most blood gas analysis equipment as the amount of a base required to titrate a set volume of the patient's blood to a normal pH (7.40). Base deficit is a measure of the amount of excess fixed acid (metabolic acidosis) in the patient. Clinical and experimental studies have shown that high base deficit is inversely related to outcome [26, 27]. Compared with lactate, mean arterial blood pressure, and cardiac output in another canine model of hemorrhagic shock, base deficit correlated the most closely with oxygen debt and mortality [27].

Although technically demanding, direct analysis of organ-specific oxygenation is becoming available. Gastric tonometry allows the measurement of gastric pH and with it, evaluation of gastric perfusion [28]. Transcellular probes applied to skin, inserted into muscle, or attached directly to the surface of organs can evaluate tissue oxygenation of specific vascular beds. These newer techniques may take some of the subjective guesswork out of treating shock. Each deserves objective evaluation and further research in evaluation of the ability to monitor the effectiveness of shock therapy.

Conclusions

New technology is providing interesting new choices in the diagnosis and management of shock. Each intervention deserves investigation and, if proven practical and effective, will help clinicians manage this devastating syndrome. In the meantime, circulatory shock needs multimodal treatment with a basic goal: to improve oxygen delivery (DO2) (Table 2-2). Improved oxygen delivery is achieved by optimizing oxygen content (CaO2) and increasing oxygen saturation (SaO2). If the packed cell volume is limiting DO2, we can increase hemoglobin concentration with whole blood transfusion, packed red blood cell transfusion, or hemoglobin-based oxygen-carrying fluids (HBOC). We may also improve DO2 by optimizing cardiac output (CO). This is done by optimizing heart rate (monitor pulse rate, quality, electrocardiogram), treating specific arrhythmias, and optimizing stroke volume. The goal of shock stabilization is to give the clinician time to treat the primary problem and improve the chance of a successful outcome.