23.1 Shock Overview

Hemodynamic Monitoring

The study of the movement of the blood as it flows through cells, tissues, and organs is called hemodynamics. Knowledge of this field is needed to fully comprehend the pathophysiologic implications of shock. Hemodynamic monitoring of patients provides relevant data that help nurses assess tissue oxygenation, fluid balance, and the effectiveness of fluid and drug therapies. It also provides data on cardiac output (CO), which is the volume of blood the heart can pump to the vascular system in one minute; normal CO is 5 L/minute. A drop in cardiac output occurs with shock. Cardiac function is discussed in greater detail in Chapter 12 Cardiovascular System.

Hemodynamic monitoring can be performed via invasive or noninvasive methods.

• Examples of noninvasive hemodynamic monitoring include auscultation of the apical pulse and palpating the radial artery to obtain heart rate. Providers may use a sphygmomanometer, also known as a blood pressure cuff, to obtain blood pressure; they may also assess the patient’s peripheral pulses, capillary refill time, skin, and warmth and check for the presence of edema.
• Invasive methods of hemodynamic monitoring devices allow for continuous measurements and are therefore more accurate than noninvasive monitoring devices. Invasive hemodynamic monitoring devices require the insertion of a catheter into the patient’s vascular system. Examples include using a central venous catheter to measure:
  • central venous pressure (CVP), a measure of the adequacy of blood volume within the vascular system; normal range is 8–12 mmHg
  • mean arterial pressure (MAP), a measure of the average arterial pressure through one cardiac cycle; normally 70–100 mmHg
  • cardiopulmonary pressure, a measure of the pressure in the pulmonary artery, the lungs, or the right atrium and ventricle of the heart, measured by a pulmonary artery catheter (a central arterial device used to measure cardiopulmonary pressure); normal cardiopulmonary pressure is 11-–20 mmHg, and elevated ranges result in pulmonary hypertension

These methods are discussed in greater detail in Chapter 35 Nursing Care of the Critically Ill Patient.

Blood pressure readings can be impacted by the stimulation of the sympathetic nervous system seen in shock. Consequently, MAP obtained from an arterial line is recommended for monitoring patients experiencing shock. This method has been found to best reflect the state of cell perfusion. Normal MAP readings are 70–100 mmHg. Inadequate cell perfusion is suggested if the MAP falls below 65 mmHg. Table 23.1 lists hemodynamic readings that indicate shock.

Initial Stage

In the initial stage of shock, the body responds to hypotension with stimulation of the sympathetic nervous system (SNS) and the release of epinephrine and norepinephrine. Blood vessels constrict and the heart rate increases. Though overt clinical manifestations are not apparent in the initial stage, changes are taking place at the cellular level as cell metabolism converts from aerobic metabolism to anaerobic metabolism, producing an increase in lactic acid.

More subtle changes may also be detected in this stage. Decreased perfusion to the brain can result in agitation, and decreased flow to the kidneys can result in a slight decrease in urinary output. Blood pressure is usually normal or slightly elevated due to stimulation of the sympathetic nervous system.

Vital signs in the initial stage of shock include:

• normal to slightly elevated blood pressure
• normal to slightly elevated heart rate
• normal respiratory rate
• normal temperature

Compensatory Stage

If adequate cell perfusion is not restored, shock progresses to the compensatory stage. In this stage, there is a noticeable drop in blood pressure; the body responds by stimulating baroreceptors of the carotid and aortic bodies (Figure 23.2). These baroreceptors respond to changes in pressure or stretch in blood vessels within the aortic arch and carotid sinus. Decreased blood pressure causes decreased signal output from the baroreceptors, leading to disinhibition of the central sympathetic control sites and decreased parasympathetic activity with the final effect of an increase in blood pressure.

Figure 23.2 Carotid sinus baroreceptors and aortic arch baroreceptors respond to low blood pressure by decreasing parasympathetic activity, which increases vascular tone, heart rate, and blood pressure. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

In the compensatory stage, norepinephrine and epinephrine are released in response to low blood pressure, resulting in constriction of blood vessels, increased heart rate, and increased cardiac output. Serum glucose elevates in the stress response. Blood flow is diverted to the vital organs—particularly the brain and heart—to preserve life. As a result, other body systems receive even less perfusion. The kidneys respond to decreased blood flow by releasing renin and activating the renin-angiotensin-aldosterone system (RAAS), a critical regulator of blood volume, electrolyte balance, and blood vessel tone. As part of this system, the liver releases angiotensin and the lungs release angiotensin-converting enzyme (ACE). Renin and angiotensin combine to form angiotensin I, which combines with ACE to form angiotensin II. Angiotensin II then stimulates the adrenal gland to secrete aldosterone, which causes constriction of blood vessels and resorption of water and sodium in the kidney. The overall effect of RAAS is constriction of blood vessels and retention of fluid, increasing blood pressure.

During the compensatory stage, all body systems experience hypoxia, which initiates further disruption to each body system. Inadequate perfusion to the lungs causes disruption to the endothelial lining of the alveolar capillary membrane, increasing permeability. The result is fluid accumulation in the alveoli, leading to the development of pulmonary edema, respiratory failure, and possibly acute respiratory distress syndrome (ARDS), as shown in Figure 23.3.

Figure 23.3 Shock can cause the development of acute respiratory distress syndrome (ARDS), as alveoli in the lungs fill with fluid. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Vital signs in the compensatory stage of shock include:

• low blood pressure
• high heart rate
• normal to slightly elevated respiratory rate
• normal temperature
• cool skin
• decreased urine output

If the cause of shock is identified and appropriate interventions are implemented, the situation is reversible with no permanent damage to cells and tissues. If the cause of shock is not corrected, the next stage of shock begins.

Progressive Stage

In the progressive stage of shock, profoundly decreased cellular perfusion results in a significant increase of capillary permeability, causing protein and fluid to leak out of the vascular system into the interstitial space. This massive shift of fluid further disrupts cell perfusion. To fully understand this process, it is helpful to review the three spaces where fluid exists in the body (Figure 23.4):

• The intracellular space consists of fluid in the cells.
• The intravascular space consists of fluid within the blood vessels.
• The interstitial space consists of fluid in the space between tissues.

Figure 23.4 Fluids exist in three distinct spaces in the body. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

A balance in these three spaces is needed for homeostasis. Loss of fluid or an overabundance of fluid in any of these spaces impairs cell function. In the progressive stage of shock, substantial capillary permeability results in dramatic shifts in fluid from the vascular space into the interstitial space, causing hypotension and electrolyte imbalance that further impair cell perfusion. All systems experience cellular hypoxia, resulting in the development of metabolic acidosis. The patient experiences pallor and cool clammy skin, as well as altered levels of consciousness because of poor perfusion to the brain. The hypoxic heart may develop irregular tachydysrhythmias, myocardial ischemia, or myocardial infarction. Complete deterioration of the cardiovascular system is possible. Additionally, the significant increase of capillary permeability results in fluid movement from the capillaries of the lung into the alveolar space, causing impaired diffusion of oxygen and carbon dioxide as well as pulmonary edema, bronchoconstriction, decreased lung capacity, tachypnea, increased crackles, increased work of breathing, respiratory acidosis, and ARDS.

Insufficient perfusion to the gastrointestinal system can result in disruption of the protective barrier of the stomach, resulting in ulceration, possible mitigation of bacteria from the gastrointestinal track, and inadequate absorption of nutrients. The renal system undergoes changes due to cellular hypoxia and further deteriorates if treatment includes the use of nephrotoxic drugs. Urine output decreases to a rate of less than 30 mL/hour, and blood urea nitrogen (BUN) and creatinine (Cr) increase. Metabolic acidosis develops due to the buildup of waste products. Hypoperfusion of the liver results in the development of jaundice, elevated liver markers, decreased immune function, and impaired homeostasis. However, if treatment is initiated in a timely manner and the body responds, there is still a chance of recovery.

Changes by body system or organ in the progressive stage of shock are summarized in Table 23.2.

Vital signs in the progressive stage of shock include:

• increased heart rate
• decreased blood pressure
• increased respiratory rate
• hypothermia
• cool skin and weak distal pulses
• decreased urine output

Refractory Stage

The refractory stage of shock is characterized by extreme dysfunction of cellular processes in multiple body systems. The significant increase in capillary permeability, anaerobic metabolism, lactic acid buildup, metabolic acidosis, tachycardia, and profound hypotension continues despite treatment. Cells, tissues, and organ systems shut down because of irreversible cell and organ damage, and recovery is unlikely.

Vital signs in the refractory stage of shock include mottled skin, characterized by a bluish-red lace pattern under the skin, caused by the pooling of deoxygenated blood. Other manifestations include:

• continued low blood pressure despite treatment
• increased tachycardia
• increased respiratory rate
• low to no urine output
• cool skin
• weak to absent peripheral pulses
• low temperature

Table 23.3 summarizes vital sign changes in each stage of shock.

Multiorgan Failure

Multiorgan dysfunction syndrome (MODS), or multiorgan failure (MOF), results from prolonged cellular hypoperfusion. Figure 23.5 illustrates the organ systems that may be affected. It is most often a result of hypovolemic and septic shock. The prognosis for MOF/MODS is dependent upon the number of organs affected and the body’s response to treatment. Older patients and patients with multiple comorbidities are at a higher risk for MOF/MODS.

Figure 23.5 Multiorgan failure can manifest in many body systems. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

A normal inflammatory response to decrease cell perfusion and cellular injury facilitates healing. Part of the normal inflammatory response includes the release of cytokines, which are protein substances that regulate the inflammatory response. MOF and MODS results when the inflammatory response extends beyond the area of injury throughout the body for a prolonged period of time. The development of MOF/MODS in sepsis has been linked to the release of cytokines. This causes an exaggerated inflammatory response throughout the body, leading to a cascade of events that can ultimately result in cell hypoxia, cell death, and organ failure.