Shock

Description #

Learning Objectives #

Upon completion of this module the learner should be able to:

1.Demonstrate the pathophysiological features related to, and identify patients at risk for the following types of shock:

I) hypovolemic shock

II) cardiac shock

III) anaphylactic shock

IV) septic shock.

2.For the following, explain the risk factors and identify the early indications of impending and developing;

I) hypovolemic shock

II) cardiac shock

III) anaphylactic shock

IV) septic shock.

3. Associate the following clinical indicators and associated laboratory findings related to shock:

I) neurological indicators

II) perfusion indicators

III) respiratory indicators

IV) blood pressure and pulse changes.

4. Indicate and implement appropriate early interventions, notifying appropriate personnel clearly and promptly to minimize further deterioration of the patient experiencing shock using the following systematic approaches:

I) ABC: Airway, Breathing, Circulation

II) SBAR Communication Tool: Situation, Background, Assessment, Recommendations.

5. Implement appropriate emergency responses and contribute effectively to the resuscitation of a patient experiencing shock as a member of the health care team

What is Shock? #

• A state of inadequate perfusion, occurring when there is inadequate circulation. 
• Tissues are deprived of oxygen. 
• Results in waste accumulation in cells.
• Generally there are 3 physiological classifications of shock (see etiology) but in some classifications you may see diabetic shock or adrenal shock included.

Shock Syndrome #

Shock is a multifaceted pathophysiologic process that usually causes multiple organ dysfunction syndrome (MODS) and death. Regardless of the type of shock, if not treated promptly will result in ineffective tissue perfusion and the development of acute circulatory failure. There are four stages to shock syndrome, which includes initial, compensatory, progressive, and refractory.

Etiology of Shock #

Shock is classified as:

• Hypovolemic
• Cardiogenic
• Distributive (septic, neurogenic, and anaphylactic shock). 

Specifically, hypovolemic shock occurs when there is a loss of intravascular volume. Cardiogenic shock occurs when the heart pumps ineffectively. Finally, distributed shock occurs there is sufficient volume but a decrease in vascular tone. Anaphylactic shock occurs when the body has a severe antibody-antigen reaction. Septic shock results when microorganisms invade the body. Whereas, neurogenic shock is caused by loss of sympathetic tone.

Pathophysiology of Shock #

In the initial Stage of shock the cardiac output (CO) is diminished and tissue perfusion is compromised. As soon as this occurs the compensatory stage starts as the bodies homeostatic mechanisms try to sustain CO, blood pressure (BP), and tissue perfusion. 

The compensatory mechanisms are mediated by the sympathetic nervous system (SNS). Specifically, the neural response causes an increase in heart rate and contractility, vasoconstriction, and the shunting of blood to the vital organs. Whereas, hormonal compensation results in the activation of the renin response which causes the production of angiotensin II resulting in vasoconstriction and the release of aldosterone and antidiuretic hormone (ADH) causing Na+ and water retention. The stimulation of the anterior pituitary causes the secretion of adrenocorticotropic hormone (ACTH), which stimulates the adrenal medulla to create glucocorticoids, resulting in an increase in blood glucose. This stimulation of the adrenal medulla results in the release of epinephrine and norepinephrine that further promotes these compensatory mechanisms. 

It is during the progressive stage of shock that the compensatory mechanisms start to fall short in meeting the tissues metabolic needs. Basically, as tissue perfusion becomes unsuccessful, the cells change from aerobic to anaerobic metabolism as a resource of energy. It is with anaerobic metabolism that the body produces little amounts of energy but large amounts of lactic acid, resulting in lactic academia. Subsequently, rising vascular permeability from endothelial and epithelial hypoxia and inflammatory mediators causes intravascular hypovolemia, tissue edema, and advanced worsening of tissue perfusion. At the bodies cellular level the amount of energy produced by anaerobic metabolism is inadequate to maintain cellular functioning and irreparable injury starts to occur. Some of the cells die due to apoptosis, whereas others die as the result of failure of the sodium-potassium pump, causing the cells to engorge. The cells energy production stops because the mitochondria (the power plant of the cell) engorge and rupture. The concern at the point is O2 utilization rather then O2 delivery. This is because the mitochondria is injured so even if the cells could get more O2 they would not be able to utilize it. The digestive organelles of the cells start to engorge causing the seepage of harsh enzymes into the cell, which hastens death of cell.

Consequently, this process affects all systems of the body. Problems with normal cardiac function develop as an outcome of myocardial hypoperfusion and the freeing of myocardial depressant substances. Eventually ventricular failure occurs, causing continuation of the entire process. Problems with normal function of the central nervous system (CNS) are the result of cerebral hypoperfusion, causing breakdown of the SNS, cardiac and respiratory depression, and thermoregulatory collapse. Hypoxia, inflammatory cytokines, and impaired blood flow produces microvascular thrombosis, which causes endothelial damage. Hematologic problems occur because of consumption of clotting factors, freeing of inflammatory cytokines, and dilutional thrombocytopenia. Eventually, disseminated intravascular coagulation (DIC) may occur. Problems with pulmonary function occur due to rising pulmonary capillary membrane permeability, microemboli, and vasoconstriction. In time ventilatory failure and acute lung injury (ALI) develop. In addition, problems with renal function occur due to vasoconstriction and hypoperfusion causing acute tubular necrosis (ATN). Dysfunction of the gastrointestinal system arises due to splanchnic vasoconstriction and hypoperfusion that causes failure of gut organs. Disturbance of the intestinal epithelium allows gram-negative bacteria into the system causing further perpetuation of the entire shock syndrome. 

In the refractory stage, shock does not respond to therapy and permanent tissue damage occurs despite etiologic characteristics due to inadequate tissue perfusion because the circulation does not met the O2 needs of the cells. This damage is irreversible. This is because each organ system dies and MODS, which is the failure of two or more body systems, takes place. Death is the resulting outcome

Hypovolemic Shock #

Hypovolemic shock is the most common form of shock and is the result of inadequate fluid volume in the intravascular space. As a result of inadequate circulating volume, there is a decrease in tissue perfusion and activation of the shock response.  

Statistics

80% of trauma-related fatalities that happen immediately or early, with the majority a result of rapid exsanguinations

27% The preventable death rate for failure to recognize and adequately treat patients at risk for acute hemorrhage

30% is the amount of circulating blood volume a health adult may loose before becoming hypotensive

Risk Factors for Hypovolemia #

Table 1 highlights risk factors associated with developing hypovolemic shock.

Etilogical Factors of Hypovolemic Shock-Table 2 #

Pathophysiology of Hypovolemic Shock #

Table 3 illustrates the pathophysiology of Hypovolemic shock (Thelans, 2006).

Treatment and Monitoring of Hypovolemic Shock #

Treatment of Hypovolemic Shock – Table 5

Treatment and Monitoring of Hypovolemic Shock-Table 7

Complications of Hypovolemia #

Complications of Hypovolemia-Table 6

Cardiogenic Shock #

Cardiogenic shock occurs when the heart fails to adequately pump blood forward. It may occur with dysfunction of either the right, left or both ventricles. When the heart is unable to pump effectively the result is reduced tissue perfusion and circulatory failure. The most frequent reason is MI resulting in the loss of 40% or more of the functional myocardium. In addition, structural difficulties of the cardiopulmonary system and arrhythmias can also cause cardiogenic shock. For a comprehensive review of cardiogenic shock please refer to the Cardiac Unit.

Etilogical Factors of Cardiogenic Shock-Table 8 #

Pathophysiology of Cardiogenic Shock-Table 9 (Thelans, 2006) #

Clinical Manifestations of Cardiogenic Shock-Table 10 #

Treatment and Monitoring of Cardiogenic Shock-Table 11 #

Anaphylactic Shock #

Anaphylactic shock is a type of distributive shock that occurs as a result of an instantaneous hypersensitivity reaction. It is a life-threatening situation that demands timely intervention. A severe antibody-antigen response causes inadequate tissue perfusion and activation of the general shock response.

Etiological Factors in Anaphylactic Shock-Table 12 #

Pathophysiology of Anaphylactic Shock-Table 13 (Thelans, 2006) #

Clinical Manifestations of Anaphylactic Shock-Table 14 #

Anaphylactic shock is a severe systemic reaction that may affect multiple organ systems. As such an array of clinical manifestations can occur in the patient in anaphylactic shock, depending on the extent of system involvement. The symptoms generally begin to appear within minutes of exposure to the antigen, however, that may not occur for up to 1 hour.

Treatment and Monitoring of Anaphylactic Shock-Table 15 #

Septic Shock #

Sepsis happens when microorganisms infect the body and activate a systemic inflammatory response. This response usually results in perfusion irregularities with organ dysfunction (severe sepsis), which leads to hypotension (septic shock). The key mechanism of this form of shock is the inadequate distribution of blood flow to tissues.

Definitions for Sepsis

 Infection: characterized by an inflammatory response to the presence of microorganisms or the invasion of a usual sterile host tissue by such microorganisms.  

Bacteremia: bacteria in the blood. 

Systemic Inflammatory Response Syndrome (SIRS): a response to an array of severe clinical insults. Two or more of the following must be evident for SIRS: T >38o C or < 36o C; HR > 90 beats/min; RR >20 breaths/min or PaCO2 < 32 mm Hg; and WBC count >12,000/mm3, < 4,000/mm3, or 10% immature (band) forms.     

Severe Sepsis: related with organ dysfunction, hypoperfusion (i.e. lactic acidosis, oliguria, acute alteration in mental state), or hypotension.  

Septic Shock Sepsis: induced shock with hypotension regardless of adequate fluid resuscitation, coupled with perfusion abnormalities (i.e. lactic acidosis, oliguria, acute alteration in mental state). 

Sepsis Induced Hypotension: a SBP of < 90 mm Hg or a reduction of >40 mm Hg from baseline in the absence of other causes for hypotension.   

Multiple Organ Dysfunction Syndrome (MODS): incidence of altered organ function in an acutely ill patient in which homeostasis cannot be maintained without intervention.  

Risk Factors Associated with Septic Shock-Table 16 #

Etiological Factors in Septic Shock-Table 17 #

The source of the microorganisms may be either:

The most common site of infection resulting in severe sepsis and septic shock is the lungs. In recent years the prevalence of chest-related infections has increased dramatically. Gram-negative bacteria are to blame for more then half of the cases of septic shock. 

Pathophysiology of Septic Shock-Table 18 (Thelans, 2006) #

Clinical Manifestations of Septic Shock-Table 19 #

The success of treatment of severe sepsis and septic shock is reliant on prompt recognition. The diagnosis of sepsis is dependent upon the recognition of three conditions: known or assumed infection, evidence of two or more of the clinical indicators of SIRS, and indication of at least one organ dysfunction. The 2 most common organs to exhibit dysfunction are the cardiovascular and lungs. 

Treatment and Monitoring of Septic Shock-Table 20 #

Treatment of septic shock necessitates a multifaceted approach. The ultimate aim of treatment is to reverse the pathophysiololgic responses, manage infection, and sustain metabolic support. The patient in severe sepsis or septic shock needs immediate resuscitation of the hypoperfused state. Interventions are intended to increase cellular O2 supply and decrease cellular O2 demand.

Establish a Systemic Approach to Report Shock to Appropriate HCT #

In order to communicate effectively to the resident or the staff man, one must use a systematic approach to report changes in a patient’s condition. The SBAR is one such system. Table 21 demonstrates an example of the SBAR system using a patient exhibiting signs and symptoms of shock. Remember to act promptly; time is crucial with shock patients

Participate in the emergency response to the resuscitation #

Participate in the emergency response to the resuscitation of a ARF patient as a member of the health care team

When the patient progresses to a code situation, the role of the primary nurse is to activate the code button at the bedside, get other staff to bring the ward code cart to the bedside and stay with the patient to ensure A, B, and C is maintained. 

Airway (A)         

• Maintain patient’s airway with oral airway

Breathing (B)         

• Use ambu bag with 100% oxygen to assist ventilation if patient is not breathing or having difficulty breathing or the rate is too slow

Circulation (C)        

• Check BP and HR and if no palpable pulses check carotid pulses before starting CPR. 
• Ensure a running IV line exist to administer medications.
• Delegate duties to other staff such as recording the code, gathering supplies and calling the admitting service/doctor.
• Prepare the patient’s chart to be available to the code team. 
• Provide the code team with a brief overview of the patient’s history and the event that led to the code and any interventions rendered.
• Assist the code team to get supplies and send laboratory specimens.
• Prepare and assist the code team to move the patient to ICU. 
• Notify the family of the event and/or the transfer to ICU.

Simulation of a Pre-code Event with a Patient in Shock #

Cyber Patient Module

Current Orders:

• Dx: Uterine Fibroids
• NPO for the OR
• VSR
• IV NS 100 / hr
• Strict I / 0Follow current Bipap protocols.

Meds:

• Premarin 2.5 mg PO OD
• Tylenol 325mg PO Q4h prn
• Tylenol #3 ii PO Q4h PRN
• Morphine 5 – 10 mg S / C q 4 hr
• Morphine 1 – 2 mg IV q 1 hr pm for breakthrough pain
• Blood cultures X 2 for Temp > 38.5
• Gravol 25 to 50 mg PO / 1V q 4 hr prn

References #

Boutin, J. L. (1987). Shock: a self-learning module. Vancouver General Hospital.    

Rice, V. (1991). Shock, a clinical syndrome: an update. Part 2: the stages of shock.

          Critical Care Nurse, (11)5, 74-85.

Thelans, (2006). Critical Care Nursing Diagnosis & Management (5th ed.). New York:

         Mosby.