A nurse is caring for a client who is at risk for shock. which of the following findings

Tips to improve patient education

Preventing re-hospitalization is a huge responsibility, especially in consideration of costly penalties that are levied for early readmissions. To accomplish this, nurses need to constantly improve patient teaching and education prior to discharge. Some of the things nurses can do to advance patient education include:

• Delegate more responsibilities to support staff and be more focused on patient education.
• Begin educating patients with every encounter from admission.
• Find out what the patient already knows. Correct any misinformation.
• Feed patients information in layman’s terms. Utilize visual aids as often as possible.
• Question their understanding of the care, and plan for the next lesson.
• Use return demonstration when administering care. Involve the patient from the very first treatment.
• Ask the patient to tell you how they would explain (step-by-step) their disease or treatment to their loved one.
• Make sure the patient understands the medications as you administer them. Make sure they understand how and when to refill medications.
• Provide patients with information about signs and symptoms of their condition that will require immediate attention.

Five strategies for patient education success

Teaching patients is an important aspect of nursing care. Whether teaching a new mom how to bathe a newborn baby or instructing an adult who is living with a chronic heart disease, a successful outcome depends on the quality of the nurse’s instruction and support. Consider these five strategies.

1. Take advantage of educational technology

Technology has made patient education materials more accessible. Educational resources can be customized and printed out for patients with the touch of a button. Make sure the patient’s individualized needs are addressed. Don't simply hand the patient a stack of papers to read, review them with patients to ensure they understand the instructions and answer questions that arise. Some resources are available in several languages.

2. Determine the patient’s learning style

Similar information may be provided by a range of techniques. In fact, providing education using different modalities reinforces teaching. Patients have different learning styles so ask if your patient learns best by watching a DVD or by reading. A hands on approach where the patient gets to perform a procedure with your guidance is often the best method.

3. Stimulate the patient’s interest

It's essential that patients understand why this is important. Establish rapport, ask and answer questions, and consider specific patient concerns. Some patients may want detailed information about every aspect of their health condition while others may want just the facts, and do better with a simple checklist.

4. Consider the patient’s limitations and strengths

Does the patient have physical, mental, or emotional impairments that impact the ability to learn? Some patients may need large print materials and if the patient is hearing impaired, use visual materials and hands on methods instead of simply providing verbal instruction. Always have patients explain what you taught them. Often people will nod “yes” or say that they comprehend what is taught even if they have not really heard or understood. Consider factors such as fatigue and the shock of learning a critical diagnosis when educating patients.

5. Include family members in health care management

Involving family members in patient teaching improves the chances that your instructions will be followed. In many cases, you will be providing most of the instruction to family members. Families play a critical role in health care management.

Teaching patients and their families can be one of the most challenging, yet also rewarding elements of providing nursing care. First-rate instruction improves patient outcomes dramatically.

The value of patient education resources

For further resources that will strength your organization’s patient-teaching, let Lippincott Advisor help. Our best-in-class, evidence-based decision support software for institutions includes over 16,000 customizable patient teaching handouts and content entries.

Continuing Education Activity

Shock is a life-threatening manifestation of circulatory failure. Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes including multiorgan failure (MOF) and death. This activity reviews the evaluation and management of shock, and explains the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

• Identify the etiology and epidemiology of shock and describe the types of shock.

• Outline the evaluation of a patient potentially in shock.

• Summarize the treatment and management options available for shock.

• Review the importance of improving care coordination among the interprofessional team to improve outcomes for patients in shock.

Access free multiple choice questions on this topic.

Introduction

Shock is a life-threatening manifestation of circulatory failure.  Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages, and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes, including multiorgan failure (MOF) and death.

Etiology

Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive.[1] The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying etiology has not been uncovered.

1. Distributive Shock

Characterized by peripheral vasodilatation. 

Types of distributive shock include:

Septic Shock

Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated host response to infection.[2] Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)

The most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus.

Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of the vigorous inflammatory response caused by either infectious or noninfectious causes. Infectious causes include pathogens such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid embolism

Anaphylactic Shock

Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after the presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex.

Neurogenic Shock

Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain. The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.

Endocrine Shock

Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

2. Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension. Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic.

Common causes of hemorrhagic hypovolemic shock include

• Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma

• Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor eroding into a major blood vessel)

• Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic INR from drug interactions)

Common causes of non-hemorrhagic hypovolemic shock include:

• GI losses - the setting of vomiting, diarrhea, NG suction, or drains.

• Renal losses - medication-induced diuresis, endocrine disorders such as hypoaldosteronism.

• Skin losses/insensible losses - burns, Stevens-Johnson syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.

• Third-space loss - in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.

3. Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different subtypes of etiologies contributing to cardiogenic shock include:

• Cardiomyopathies - include acute myocardial infarction affecting more than 40% of the left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due to myocardial stunning), myocarditis.

• Arrhythmias - both tachy- and bradyarrhythmias

• Mechanical - severe aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.

4. Obstructive Shock

Mostly due to extracardiac causes leading to a decrease in the left ventricular cardiac output

• Pulmonary vascular - due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.[3]

• Mechanical - impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Epidemiology

Distributive shock is the most common type of shock, followed by hypovolemic and cardiogenic shock. Obstructive shock is relatively less common. The most common type of distributive shock is septic shock and has a mortality rate between 40 to 50%.

Pathophysiology

Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in acidosis and a decrease in regional blood flow, which further worsens the tissue hypoxia.[4] In hypovolemic, obstructive, and cardiogenic shock, there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages, which are reversible to the final stages, which are irreversible with multiorgan failure and death. Generally, shock has the following three stages:

1. Pre-shock or compensated shock - As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressure

2. Shock - During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from the progression of the pre-shock stage as the compensatory mechanisms become insufficient.

3. End-organ dysfunction - This is the final stage, leading to irreversible organ dysfunction, multiorgan failure, and death

History and Physical

A focused history should be obtained from the patient (if feasible) and/or patient's relatives. Also, a review of the patient’s outpatient medical records (information regarding risk factors, medications, and trend of baseline vital signs including blood pressure), as well as hospital medical records, could give valuable clues regarding the patient's risk for shock and potential etiology. Clinical features and symptoms can vary according to the type and stage of shock. The most common clinical features/labs which are suggestive of shock include hypotension, tachycardia, tachypnea, obtundation or abnormal mental status, cold, clammy extremities, mottled skin, oliguria, metabolic acidosis, and hyperlactatemia.[5][6] Also, features pertaining to the underlying cause of the shock can be present.

Patients with hypovolemic shock can have general features as mentioned above as well as evidence of orthostatic hypotension, pallor, flattened jugular venous pulsations, may have sequelae of chronic liver disease (in case of variceal bleeding).

Patients with septic shock may present with symptoms suggestive of the source of infection (example-skin manifestations of primary infection such as erysipelas, cellulitis, necrotizing soft-tissue infections), and cutaneous manifestations of infective endocarditis.

Patients with anaphylactic shock can have hypotension, flushing, urticaria, tachypnea, hoarseness of voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of exposure to common allergens such as medications or food items the patient is allergic to or insect stings.

Tension pneumothorax should be suspected in a patient with undifferentiated shock who has tachypnea, unilateral pleuritic chest pain, absent or diminished breath sounds, tracheal deviation to the normal side, distended neck veins and also has pertinent risk factors for tension pneumothorax such as recent trauma, mechanical ventilation, underlying cystic lung disease).

In a patient with undifferentiated shock, diagnostic clues to pericardial tamponade as the etiology include dyspnea, the Beck triad (elevated jugular venous pressure, muffled heart sounds, hypotension), pulses paradoxus, and known risk factors such as trauma, the recent history of pericardial effusion, and thoracic procedures. 

Cardiogenic shock should be considered as the etiology if the patient with undifferentiated shock had chest pain suggestive of cardiac origin, narrow pulse pressure, elevated jugular venous pulsations or lung crackles, and significant arrhythmias on telemetry or EKG.

Evaluation

Resuscitation should not delay while investigating the etiology of undifferentiated shock. Physicians should have a high clinical suspicion for the presence of shock, and an attempt to stratify the severity of the shock should also take place to assess the need for emergent or early interventions. Evaluation of undifferentiated shock should begin with a thorough history and physical examination.

Besides telemetry monitoring, a 12-lead electrocardiogram should be obtained. ECGs might show evidence of acute coronary syndrome, arrhythmias, or provide diagnostic clues suggestive of pericardial effusion or pulmonary embolism.

Laboratory tests in a patient with undifferentiated shock should include a CBC and differential, renal and liver function tests, serum lactate level, cardiac biomarkers, D-dimer level, coagulation profile, type and screen for a possible blood transfusion if appropriate (if concern for hemorrhagic shock), blood and urine cultures, and blood gas analysis. Initial imaging studies recommended in patients with undifferentiated shock and hypotension include chest x-rays to look for the source of infection such as pneumonia, complications of shock such as ARDS, clinical findings supporting the diagnosis of pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection. CT scans can also assist in unmasking the etiology of shock in appropriate clinical scenarios. Point of care ultrasonography or focused cardiac ultrasound is also a useful bedside diagnostic tool.[7]

Treatment / Management

The initial approach to management is the stabilization of the airway and breathing with oxygen and oral mechanical ventilation when needed. Peripheral IV or intraosseous infusion (IO) access should be obtained. Central venous access may be required in the setting of shock if there is difficulty securing peripheral venous access, or the patient needs prolonged vasopressor therapy or large-volume resuscitation. Immediate treatment with intravenous (IV) fluid should be initiated, followed by vasopressor therapy, if needed, to maintain tissue perfusion. Depending on the underlying etiology of shock, specific therapies might also be needed.

Septic shock - initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within 3 hrs with additional fluid based on frequent reassessment, empiric antibiotic therapy within one hr. [8] For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of 65 mmHg. The first choice of a vasopressor is norepinephrine, with the addition of vasopressin if refractory.[9]

Anaphylactic shock - aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids. Stop the offending agent, intramuscular epinephrine, antihistamines, corticosteroids, nebulized albuterol.

In adrenal crisis - judicious fluid resuscitation, IV dexamethasone.

Hypovolemic shock - obtain two large-bore IVs or central line. Place the patient in the Trendelenburg position. Aggressive IV fluid resuscitation with 2 to 4 L of isotonic crystalloids. PRBC transfusion if ongoing bleed. Appropriate medical or interventional strategies to treat the underlying etiology. Continue with isotonic crystalloids and use vasopressors if needed

Obstructive shock - the judicious use of IV crystalloids. If shock persists, early initiation of vasopressors-norepinephrine is the first choice and add vasopressin if refractory. Continue IV fluids but monitor very closely. 

If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has a paradoxical worsening of hypotension; it may develop due to severe right ventricular dilatation and septal bowing compromising left ventricle filling. 

If tension pneumothorax - needle thoracotomy followed by tube thoracotomy. If cardiac tamponade-pericardiocentesis, significant clinical improvement is possible, even with minimal fluid removal).

Cardiogenic shock - if unstable tachyarrhythmia or bradyarrhythmias, initiate ACLS protocol and cardioversion. Judicious use of IV fluids in the absence of pulmonary edema. Consider inotropes (dobutamine is the most commonly used agent) or intra-aortic balloon pump (IABP), if refractory shock, and vasopressor (norepinephrine) with inotropes.

If STEMI - consider thrombolysis or coronary revascularization procedures and or IABP.

Differential Diagnosis

Uncovering the etiology of undifferentiated shock is very important. In a patient presenting with undifferentiated shock, the differential diagnosis includes a wide variety of etiologies that falls under the four major categories of shock, as outlined above. Also, sometimes patients can have a combination of shock syndromes. Another differential is "pharmacological shock," which results from vasodilatation or myocardial depression from medications (e.g., benzodiazepines, beta-blockers, calcium channel blockers, opiates, anticholinergics, and sildenafil).

Prognosis

Sepsis and septic shock, in general, are associated with long-term morbidity and mortality, with many of the survivors requiring placement into long-term acute care facilities or post-acute care centers.[10][11] Septic shock has a mortality rate between 40% and 50%. Cardiogenic shock has a mortality rate ranging from 50% to 75%, an improvement over prior mortality rates. Hypovolemic and obstructive shock generally have much lower mortality and respond better to timely treatment. 

Pearls and Other Issues

• Shock is a clinical manifestation of circulatory failure and is associated with high morbidity and mortality.

• There are broadly four types of shock: distributive, cardiogenic, hypovolemic, and obstructive.

• An accurate diagnosis requires a good understanding of underlying pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock.

• Serum lactate level is a useful risk stratification tool in managing undifferentiated shock.

• Timely diagnosis and initiation of appropriate therapy are of paramount importance as it can prevent progression to the reversible shock, multiorgan failure, and death.

• Treatment includes hemodynamic stabilization and correction of underlying etiology of shock.

Enhancing Healthcare Team Outcomes

The management of patients with shock calls for a collaborative, interprofessional approach. Clinicians must react promptly to the emergency and determine the precise cause of shock. Nursing will be on hand to assist at every step of the way, assisting with measures such as intubation and administering medications. Pharmacists must rapidly prepare and deliver the needed drugs and yet still verify that dosing and interactions do not present a problem. Depending on the etiology, various specialists may also be called in on the case. Each area will need to act and react as the situation dictates. WIth interprofessional cooperation, these patients will stand a better chance of recovery from shock with minimal deleterious effects. [Level 5]

Review Questions

References

Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2014 Feb 06;370(6):583. [PubMed: 24499231]

Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013 Aug 29;369(9):840-51. [PubMed: 23984731]

Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000 Oct;48(1):23-33. [PubMed: 11033105]

Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May;4(2):161-7. [PubMed: 8774792]

Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):762-74. [PMC free article: PMC5433435] [PubMed: 26903335]

Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2015 Mar 12;372(11):1078-9. [PubMed: 25760366]

Shokoohi H, Boniface KS, Pourmand A, Liu YT, Davison DL, Hawkins KD, Buhumaid RE, Salimian M, Yadav K. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit Care Med. 2015 Dec;43(12):2562-9. [PubMed: 26575653]

Howell MD, Davis AM. Management of Sepsis and Septic Shock. JAMA. 2017 Feb 28;317(8):847-848. [PubMed: 28114603]

Hylands M, Moller MH, Asfar P, Toma A, Frenette AJ, Beaudoin N, Belley-Côté É, D'Aragon F, Laake JH, Siemieniuk RA, Charbonney E, Lauzier F, Kwong J, Rochwerg B, Vandvik PO, Guyatt G, Lamontagne F. A systematic review of vasopressor blood pressure targets in critically ill adults with hypotension. Can J Anaesth. 2017 Jul;64(7):703-715. [PubMed: 28497426]

Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M., Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. [PMC free article: PMC4910392] [PubMed: 26903336]

Cecconi M, Evans L, Levy M, Rhodes A. Sepsis and septic shock. Lancet. 2018 Jul 07;392(10141):75-87. [PubMed: 29937192]

What is the earliest indicator of shock?

What are the symptoms of compensated shock?

What are the metabolic findings on a client experiencing shock?

Which of the following manifestations would indicate a client is in the compensatory stage of shock?