Chapter 9

Hemorrhagic Shock

When global tissue perfusion is inadequate to meet the body’s metabolic demand, a state of shock exists. Conceptually, shock can be divided into three distinct but overlapping categories: cardiogenic shock, distributive shock, and hypovolemic shock. Although the late stages of shock are easily recognized by the presence of tachycardia and hypotension, its presentation may be insidious and manifest only as multiple end organ dysfunction secondary to hypoperfusion. Furthermore, because individual organs may be variably affected, a patient with only subtle hemodynamic perturbations may present with nonspecific signs, such as oliguria, skin pallor, coolness of extremities, and altered mental status.

Cardiogenic shock (see Chapter 8) results from an inability of the heart to effectively pump blood to surrounding tissues. Compensatory activation of the sympathetic nervous system increases systemic vascular resistance in an attempt to restore perfusion pressure that in some patients is manifested by cool extremities with a netlike pattern of bluish skin mottling known as livedo reticularis.

Distributive shock (Chapter 10) is characterized by a loss of vasomotor tone in capacitance and resistance vessels. Therefore, circulating blood volume is effectively insufficient (“relative hypovolemia”). In addition, it results in a low afterload state as a result of low systemic vascular resistance.

Hypovolemic shock results from a decrease in actual intravascular volume, the etiology of which may be myriad (Box 9.1). Hemorrhagic shock, the most common form of hypovolemic shock, is classically divided into four stages of severity (Table 9.1). These four stages correspond to the progression of blood loss and the associated physiologic responses in otherwise healthy individuals with normal cardiopulmonary systems.

BOX 9.1 Causes of Shock Resulting from Hypovolemia or Decreased Venous Return

Decreased Intravascular Volume

Hemorrhage

Gastrointestinal tract losses

— Vomiting or elevated nasogastric tube outputs

— Diarrhea

— Enterocutaneous fistula

Renal losses

— Polyuria in diabetic ketoacidosis

— Postobstructive diuresis

— Neurogenic diabetes insipidus in head trauma

Inflammatory “third spacing”: extravasation of intravascular volume into the interstitium

— Pancreatitis

— Thermal or chemical burns

— Abdominal surgery

Decreased Venous Return to the Heart ^∗

Abdominal compartment syndrome (Chapters 90 and 97)

Elevated intrathoracic pressures

— Tension pneumothorax

— Positive pressure ventilation

— Excessive positive end-expiratory pressure (PEEP) or auto-PEEP (Chapter 2)

Cardiac (pericardial) tamponade (Chapter 54)

Venodilation

Anaphylaxis

Cervical spinal cord injuries

Spinal and epidural anesthesia

^∗With normal global blood volume.

TABLE 9.1

Estimated Blood Loss Based on Patient’s Initial Presentation

The guidelines in this table are based on the 3-for-1 (3:1) rule, which derives from the empiric observation that most patients in hemorrhagic shock require as much as 300 mL of electrolyte solution for each 100 mL blood loss. Applied blindly, these guidelines may result in excessive or inadequate fluid administration. For example, a patient with a crush injury to an extremity may have hypotension that is out of proportion to his or her blood loss and may require fluids in excess of the 3:1 guidelines. In contrast, a patient whose ongoing blood loss is being replaced by blood transfusion requires less than 3:1. The use of bolus therapy with careful monitoring of the patient’s response may moderate these extremes.

^∗Values are based on an adult with a predicted body weight (PBW) of 70 kg in which total intravascular blood volume is estimated at 70 mL per kg PBW or, in this example, 70 mL x 70 kg PBW = 4900 mL or ~5000 mL.

From American College of Surgeons: Advanced Trauma Life Support Student Course Manual, 8th Ed. Chicago: American College of Surgeons, 2008, with permission.

Although conceptually useful, the distinction between cardiogenic, distributive, and hypovolemic shock is somewhat artificial as shock is frequently multifactorial. For instance, a patient who has sustained severe thermal burns will almost certainly manifest hypovolemia as intravascular volume migrates into the interstitial space secondary to capillary leak. The same patient may also have attenuated vasomotor tone secondary to the systemic inflammatory response syndrome (SIRS; see Chapter 10) causing a distributive shock. Finally, a fraction of patients with distributive shock caused by sepsis may also have an element of cardiogenic shock resulting from the depression of myocardial function from circulating inflammatory mediators or from preexisting disease or other factors.

Pathophysiology of Decreased Preload

Cardiac output is the product of heart rate and stroke volume. Stroke volume, in turn, is determined by ventricular preload, contractility, and afterload (Figures 8.1–8.4, Chapter 8). Preload corresponds to the stretch placed on cardiac muscle immediately prior to contraction. There is a direct relationship between sarcomere length (or stretch) and contractile force. As illustrated by the Starling curves, increasing preload increases the force of muscle fiber contraction and cardiac stroke volume up to a maximum after which the output plateaus (see Figure 8.1). The term preload is most accurately reflected by left ventricular end-diastolic volume (LVEDV) rather than the left ventricular end-diastolic pressure (LVEDP), which is commonly estimated in the intensive care unit (ICU) using the pulmonary artery catheter. For clinical purposes, the LVEDP is often assumed to be proportional to the LVEDV, although this relationship may become nonlinear, particularly in the noncompliant myocardium because of preexisting diastolic dysfunction (such as that caused by chronic hypertension) or ischemia. Preload is a function of the global circulating blood volume as well as venous return to the heart (see Box 9.1).

Physiologic and Pathophysiologic Changes in Hypovolemic Shock

Hypovolemic shock is characterized by a decreased cardiac preload, which results in a decreased stroke volume. Compensatory mechanisms for low cardiac output or hypotension are mediated by means of a sympathetic adrenergic response. In an attempt to maintain cardiac output, the force of cardiac contraction (inotropy) and the rate of contractility (chronotropy) both increase (see Figure 8.2). As hypovolemia progresses, in an effort to maintain an adequate perfusion pressure to organs, systemic vascular resistance and left ventricular afterload increase, redirecting blood flow from the periphery (skin, skeletal muscles, and fat in extremities) and from the splanchnic bed to the central circulation. For example, blood flow to the kidneys may decrease to only 5% to 10% of normal during acute hypovolemia, supporting the utility of monitoring urine output per hour as a gauge of adequate renal blood flow.

During hypovolemic shock the venous capacitance beds constrict as well, enhancing blood return to the heart. The renin-angiotensin system is activated, causing a release of aldosterone from the adrenal cortex and arginine vasopressin (antidiuretic hormone) from the posterior pituitary. These enhance renal reabsorption of sodium and water, which act to preserve the circulating blood volume. In addition to its antidiuretic effects, arginine vasopressin is a potent vasoconstrictor. Other endocrine responses include increased levels of plasma glucagon, cortisol, and growth hormone. Along with an increase in endogenous catecholamine release, these hormones all tend to increase the plasma glucose level.

Blood pressure within vascular beds influences microcirculatory flow, which is further regulated by precapillary and postcapillary sphincters. Sphincter tone is controlled by autoregulation of the capillary bed and by the autonomic nervous system. The former is mediated both by endothelial stretch receptors, which modulate microcirculatory tone at varying perfusion pressures, and by the concentration of various metabolites mediating local vasodilatation (e.g., nitric oxide). In contrast, the sympathetic nervous system primarily results in vasoconstriction through an increase in precapillary tone. In the early phases of shock, this may serve to shunt blood away from the skin and skeletal muscle toward organs necessary for immediate survival.

When all these compensatory mechanisms are active, the patient may tolerate even severe fluid loss with minimal or no tissue dysfunction (“compensated shock”) or with some reversible tissue dysfunction (“progressive shock”). In these states, resuscitation alone will restore the intravascular volume and is likely to reverse inadequate tissue perfusion. As both the volume of blood lost and length of time in shock increase, the degree of reversibility in response to intravascular volume resuscitation decreases and eventually it reaches an irreversible state in which survival is unlikely.

From a macrocirculatory standpoint, circulatory shock can be described as an imbalance between tissue oxygen supply and demand. Systemic oxygen delivery (o₂) is equal to the product of arterial oxygen content and cardiac output (Box 9.2). Oxygen consumption per minute (o₂) is dependent on the body’s total metabolic activity, distribution of blood flow, and the ability of tissues to extract and utilize oxygen. The mixed venous oxygen saturation (So₂) is measured in the pulmonary artery and is dependent on the relationship between o₂ and o₂. The oxygen extraction ratio (o₂/o₂) represents the proportion of delivered oxygen to the oxygen consumed by the tissues. Under normal conditions, the o₂/o₂ is approximately 1/4, which corresponds to an So₂ of ~75%. Under normal conditions, the amount of oxygen delivered to the tissues (o₂) is far in excess of oxygen consumption (o₂), and this explains why o₂ typically varies independent of o₂ (Figure 9.1).