Oxygenation and perfusion depend on how much oxygen from arterial blood perfuses the tissue. Tissue and organ perfusion is related to mean arterial pressure (MAP). Because the cardiovascular system is a closed but continuous circuit, the factors that influence MAP include:

The size of the vascular bed is inversely (negatively) related to MAP. This means that increases in the size of the vascular bed lower MAP and decreases raise MAP (Fig. 39-2). The small arteries and veins connected to capillaries can increase in diameter by relaxing the smooth muscle in vessel walls (dilation) or decrease in diameter by contracting the muscle (vasoconstriction). When blood vessels dilate and total blood volume remains the same, blood pressure decreases and blood flow is slower. When blood vessels constrict and total blood volume remains the same, blood pressure increases and blood flow is faster.

Types of shock and their causes vary because shock is a manifestation of a pathologic condition rather than a disease state (see Table 39-1). More than one type of shock can be present at the same time. For example, trauma caused by a car crash may trigger hemorrhage (leading to hypovolemic shock) and a myocardial infarction (leading to cardiogenic shock).

Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease, resulting in inadequate total body oxygenation. Common problems leading to hypovolemic shock are hemorrhage and dehydration. A complete discussion of the pathophysiology and management of hypovolemic shock begins on p. 812.

Cardiogenic shock occurs when the actual heart muscle is unhealthy and pumping is directly impaired. Myocardial infarction is the most common cause of direct pump failure (Held & Sturtz, 2009). Other causes are listed in Table 39-1. Any type of pump failure decreases cardiac output and MAP. Chapter 40 discusses the pathophysiology and care for the person with cardiogenic shock from myocardial infarction.

Distributive shock occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot circulate and deliver oxygen. It can be caused by a loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak. All these factors can decrease mean arterial pressure (MAP) and may be started by nerve changes (neural-induced) or the presence of some chemicals (chemical-induced).

Neural-induced distributive shock is a loss of MAP that occurs when sympathetic nerve impulses controlling blood vessel smooth muscle are decreased and the smooth muscles relax, causing vasodilation. This blood vessel dilation can be a normal local response to injury, but shock results when vasodilation is widespread (King & Olson, 2007). Problems leading to loss of sympathetic tone are listed in Table 39-1.

Chemical-induced distributive shock has three common origins: anaphylaxis, sepsis, and capillary leak syndrome. It occurs when certain body chemicals or foreign substances in the blood and vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock also can be induced by substances normally found in the body (endogenous), such as excessive amounts of the mediator histamine.

Anaphylaxis is one result of type I allergic reactions. It begins within seconds to minutes after exposure to a specific allergen in a susceptible person. The result is widespread loss of blood vessel tone and decreased cardiac output. Table 22-2 (in Chapter 22) lists common allergens that can cause anaphylaxis. Chapter 22 describes the pathophysiology, prevention, and care of the patient with anaphylactic shock.

Sepsis is a widespread infection that triggers a whole-body inflammatory response. It leads to distributive shock when infectious microorganisms are present in the blood. This form of shock is most commonly called septic shock. A complete discussion of the pathophysiology, prevention, and collaborative care for the patient with sepsis and septic shock begins on p. 819.

Capillary leak syndrome is the response of capillaries to the presence of biologic mediators that change blood vessel integrity and allow fluid to shift from the blood vessels into the interstitial tissues. Once in the interstitial tissue, these fluids are stagnant and cannot deliver oxygen or remove tissue waste products. Fluid shifts result from increased size of capillary pores, loss of plasma osmolarity, and increased hydrostatic pressure in the blood. Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, paralytic ileus, severe malnutrition, large wounds, hyperglycemia, kidney disease, hypoproteinemia, and trauma.

Obstructive shock is caused by problems that impair the ability of the normal heart muscle to pump effectively. The heart itself remains normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. The most common causes of obstructive shock are pericarditis and cardiac tamponade (see Table 39-1). Care of the person with cardiac tamponade is presented in detail in Chapter 37 (pericarditis) and Chapter 40 (as a complication after cardiac bypass graft surgery).

Although the causes and initial manifestations associated with the different types of shock vary, eventually the effects of hypotension and anaerobic cellular metabolism (metabolism without oxygen) result in the common key features of shock listed in Chart 39-1. The origin of these features is explained below in the discussion of Pathophysiology in the Hypovolemic Shock section.

The basic problem of hypovolemic shock is a loss of blood volume from the vascular space, resulting in a decreased mean arterial pressure (MAP) (see Fig. 39-2) and a loss of oxygen-carrying capacity from the loss of circulating red blood cells (RBCs). The reduced MAP slows blood flow, resulting in decreased tissue perfusion. The loss of RBCs decreases the ability of the blood to oxygenate the tissue it does reach. These oxygenation and perfusion problems lead to cellular anaerobic (without oxygen) conditions and abnormal cellular metabolism.

The main trigger leading to hypovolemic shock is a sustained decrease in MAP that results from decreased circulating blood volume. A decrease in MAP of 5 to 10 mm Hg below the patient’s normal baseline value is detected by pressure-sensitive nerve receptors (baroreceptors) in the aortic arch and carotid sinus. This information is transmitted to brain centers, which stimulate adjustments (compensatory mechanisms) that help ensure continued blood flow and oxygen delivery to vital organs while limiting blood flow to less vital areas. The movement of oxygenated blood into selected areas while bypassing others (“shunting”) results in some shock manifestations.

If the events that caused the initial decrease in MAP are halted now, compensatory mechanisms provide adequate oxygenation and perfusion without outside intervention. If the initiating events continue and MAP decreases further, some tissues function under anaerobic conditions. This condition increases lactic acid levels and other harmful metabolites (e.g., protein-destroying enzymes, oxygen free radicals). These substances cause electrolyte and acid-base imbalances with tissue-damaging effects and depressed heart muscle activity. These effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. When shock conditions continue for longer periods without help, the resulting acid-base imbalance, electrolyte imbalances, and increased metabolites cause so much cell damage in vital organs that multiple organ dysfunction syndrome (MODS) occurs and recovery from shock is no longer possible. Table 39-2 summarizes the responses during the progression of shock.

The Concept Map on p. 815 addresses assessment and nursing care issues related to hypovolemic shock.