Critical Care: Shock, Organ Failure, Impending Respiratory Failure

Educational Objectives

Upon completing this educational activity, participants will be better able to:
1.   Define shock and how it manifests at the clinical and biological level.

2. Discuss the main parameters used to diagnose shock.

3. Identify the minimum systolic blood pressure by age in pediatrics.

4. Explain the goals of shock therapy and management. 

Summary

Critical Care: Shock, Organ Failure, Impending Respiratory Failure

Brent Pfeiffer, MD, PhD, Assistant Professor of Clinical Medicine, Department of Pediatrics, Division of Critical Care Medicine, University of Miami, and Holtz Children’s Hospital, Miami, FL

Definition of shock: shock is a disruption of energy and a manifestation of circulatory failure; it is characterized by hypotension and poor perfusion of oxygen and blood to tissues, which impairs normal cellular metabolism; instead of oxidative phosphorylation, cells perform glycolysis and produce lactic acid; this increases the serum lactate level

Diagnosis: based upon 3 main parameters (clinical signs, hemodynamic assessment, and serum studies); not all parameters are necessary to diagnose shock; recognizing shock before hypotension occurs is critical in improving patient outcomes (especially in children)

Hemodynamic assessment: in children, definition of hypotension depends upon the age of the patient; normal systolic blood pressure in a term neonate is typically >60 mm Hg; in infants 1-12 months of age, >70 mm Hg; in children 1-10 years of age, 70 mm Hg plus 2 times age in years (eg, a 5-year-old would normally have a systolic blood pressure >80 mm Hg; children aged 10 years to adolescents and adults, >90 mm Hg

Components of blood pressure and states of shock: blood pressure — involves how much effort the heart has to exert to pump (systemic vascular resistance [SVR], or afterload) and the amount of blood the heart has pumped over a period (cardiac output); cardiac output — is determined by how fast the heart is beating (heart rate) and how much blood is pumped out with each contraction (stroke volume); stroke volume — determined by how much intravascular volume is present (preload) and how well the heart is contracting (contractility); impairment of one or more of these components — has the potential to cause hypotension and helps define the state of shock present; recognizing shock before hypotension occurs is the optimal way to lower a patient’s risk for morbidity and death by early intervention

Early signs of shock (before hypotension)

Heart rate: tachycardia not explained by fever, pain, agitation, or activity is a very sensitive marker for shock; newborns to children 3 months of age — awake heart rates are typically 85-200 beats/min; asleep, 80-160 beats/min; children aged 3-24 months — awake heart rates are 90-190 beats/min; asleep, 75-160 beats/min; children aged 2-10 years — awake heart rates are 60-140 beats/min; asleep, 60-90 beats/min; children aged 10 years to adolescents and adults — awake heart rates are 60-100 beats/min; asleep, 50-90 beats/min; sensitivity — normal infants and children have no heart disease and have a tremendous ability to increase their heart rate above normal to maintain normal cardiac output in different states of shock; therefore, their blood pressure remains normal until they exhaust the compensatory mechanism of increasing their heart rate

Urine output: in patients with poor blood flow to the kidneys associated with any cause (eg, hypovolemia, low cardiac output), reduced or absence of renal blood flow leads to production of little or no urine

Mental status: patients with poor perfusion to the brain have altered mental status (mainly agitation, confusion, lethargy, and excessive sleepiness if severe)

Poor perfusion to the skin: in patient with low cardiac output can be manifested by cold or cool extremities; if hypoxemia is present in a patient with severe pneumonia and hypoxemia, cyanosis of the lips and nail beds is present

Other clinical manifestations: delayed capillary refill (evaluate central and peripheral pulses [eg, absent, thready, bounding]); in severe shock, other organ dysfunction can occur; liver — hepatomegaly; biventricular heart failure and an increased amount of intravascular volume may impinge on the liver; in distributive or septic shock, there may be no blood flow to the liver, which causes hepatitis and “shock liver”; intestines — infants may have intolerance to, or lack of, PO intake; children and adolescents may not tolerate oral intake; gastrointestinal pain may be present in a patient with cardiomyopathy and heart failure

Impending respiratory failure: patients who present with impending respiratory failure may have signs of tachypnea and respiratory distress and need aggressive support in oxygenation and ventilation; patients in any type of shock develop acidosis, which drives their respiratory response to correct the acidosis and causes tachypnea; depending on the cause of the shock (eg, severe sepsis due to pneumonia, pulmonary edema due to acute heart failure), the respiratory system can become severely compromised; treatment depends on the classification of respiratory failure (eg, hypoxemia, hypercarbia)

Hypoxic respiratory failure: defined as O2 saturation <90% or Pao2 <60 mm Hg; typically, a hypoxic patient presents with tachycardia, tachypnea, nasal flaring, accessory muscle use, and diaphoresis; late findings in hypoxic respiratory failure are cyanosis and altered mental status (eg, agitation, which can be severe)

Hypercarbic respiratory failure: defined as PCO2 >50 mm Hg; patients often present with tachypnea and increased depth of breathing (they are trying to increase ventilation to decrease carbon dioxide); late finding in patient with extreme hypercarbia is altered mental status (usually somnolence [CO2 narcosis])

Supporting a patient’s respiratory system: potentially life-saving; determine patient’s work of breathing using a pulse oximeter or (ideally) arterial blood gas testing; mild to moderate hypoxia — supplemental oxygen (eg, nasal cannula, face mask, nonrebreather, noninvasive ventilation) may be sufficient while supporting the patient through the shock state; moderate to severe hypoxemia with very high or inadequate work of breathing (eg, apnea) — bag-mask ventilation and securing the airway are likely necessary; supporting a patient’s respiratory efforts is the key step in initial resuscitation in the setting of shock, regardless of the shock state

Biochemical signs of shock

High serum lactate level (lactic acidosis): is a marker of anaerobic respiration; oxygen delivery is impaired, so the cell is forced to use glycolysis to produce energy; a byproduct is lactate; as the lactate level increases, the acidosis worsens; this is revealed on arterial blood gas testing as lower or persistent acidosis (acidemia); start therapies for shock; obtain serial measurements of serum lactate levels to guide the treatment of shock

Low mixed venous oxygen saturation: mixed venous oxygen saturation is the amount of hemoglobin saturated in all the venous blood pooled together in the body; typically measured from a sample of pulmonary artery blood (eg, in a patient with a Swan-Ganz catheter, blood drawn from the pulmonary artery port and sent for CO-oximetry); blood drawn from central venous catheters may also be used (superior vena cava or inferior vena cava arterial sampling); normal mixed venous oxygen saturation is ≈75% (of the 4 hemoglobin sites to bind oxygen, 3 sites are bound with oxygen, and 1 is not); if it is assumed that the 4 hemoglobin sites of the arterial blood sample are completely bound with oxygen (100% saturation), 1 oxygen molecule is released from the hemoglobin to the tissue and then returned to the heart; all together, throughout the body when mixed, saturation is ≈75%; the extraction of oxygen from arterial to venous has a ratio of ≈25%; a low mixed venous saturation (eg, 65%, 60%, 55%) represents increased oxygen extraction; this can occur in severe anemia, fever, or state of low cardiac output; measuring mixed venous saturation or CO-oximetry can help guide use of vasopressor drugs to support the contraction of the heart or even blood-transfusing therapies; in a patient with severe anemia, hemoglobin level <7 g/dL

Distributive shock: the most frequent shock state in pediatrics; septic shock is by far the most common type; distributive shock is characterized by the maldistribution of regional blood flow; arterioles have different tones to provide blood flow according to the needs of various tissues; in a patient with low SVR (decreased afterload), cardiac output must be sufficient provide blood to the entire body at the same time; this can be difficult, as it is an abnormal situation; loss of arterial tone often leads to hypotension

Causes: sepsis, anaphylaxis (typically severe), injury to the spinal cord (sympathetic nervous system), and drug intoxications; the majority of cases of distributive shock are caused by sepsis; guidelines of the Surviving Sepsis Campaign are updated every 5-7 years

Case example 1: patient presents to the ED with a history of solid organ transplantation and 1 or 2 days of fever; patient has tachycardia, hypotension, and no or little output over the past day; presumptive diagnosis is septic shock because of the presentation and known history of immunosuppression; Surviving Sepsis Campaign guidelines instituted

Hypovolemic shock: the next most common type in pediatrics; a state of shock characterized by severely reduced intravascular volume; blood volume is very low, and the amount of blood returning to the heart is minimal; essentially, patients have low preload

Causes: loss of blood (internal or external hemorrhage); loss of plasma (eg, due to diarrhea, emesis); loss from kidneys (eg, DKA in diabetes mellitus or diabetes insipidus, use of diuretics); losses from the skin (eg, burns, increased insensible losses); pancreatitis; intestinal ischemia; peritonitis; severe capillary leak; in children — diarrhea, emesis, and insensible losses from burns are most prevalent causes

Case example 2: infant with diarrhea and emesis has tachycardia (not hypotension) and reduced number of wet diapers; diagnosis is mild to moderate hypovolemic shock; patient receives fluid resuscitation to improve preload

Assessment of hypovolemia: in the pediatric ICU, one method is to use a central venous catheter and measure the pressure in the central venous system; if that pressure is low (<5 mm Hg), the patient has hypovolemia; indirect tests include palpation of the liver or leg raise test to increase temporarily the return of blood flow to the heart

Cardiogenic shock: less common than hypovolemic shock; characterized by decreased myocardial contraction; the heart is unable to pump enough blood to meet the metabolic demands of the body (poor contractility)

Causes: myocardial disease the most common cause in pediatrics; tachyarrhythmias, bradyarrhythmias, myocarditis, cardiomyopathies, coronary ischemia, drug intoxications, or intracardiac disease (eg, incompetent valves, critical valvular stenosis); in pediatrics, the most common causes arrhythmias, myocarditis, and typical cardiomyopathies; cyanotic patients with a VSD are common in the cardiac ICU setting; as they get older, chronic heart failure becomes acute-on-chronic heart failure, causing cardiogenic shock; patients have poor weight gain and diaphoresis with eating; surgical repair of the VSD may be required

Obstructive shock: relatively uncommon in the pediatric population; the mechanical obstruction of blood going into or out of the heart; blood is unable to enter or leave the heart, which severely and rapidly decreases the stroke volume and rapidly reduces the ability of the ventricle to contract

Causes: pericardial tamponade, tension pneumothorax, massive pulmonary embolism, and intracardiac tumors

Dissociative shock: uncommon; an inappropriate binding of oxygen or release of oxygen by the hemoglobin molecule; found in carbon monoxide poisoning or methemoglobinemia induced by medical therapies

Determining states of shock: in patients with signs and symptoms of shock, more than one shock state may be present at the same time

Case example 1 (continued): patient found to be bacteremic because of an infected tunneled catheter; bacteremia stimulates the immune system, resulting in high volume of cytokines in the serum; antibiotics given to treat the bacteremia; more cytokines released in response to bacterial components in the bloodstream; the cytokine release causes distributive septic shock and can affect the endothelial cells of the vascular system; they start leaking fluid, causing hypovolemia; large cytokine response can cause myocardial dysfunction, which can cause cardiogenic shock; patient who presented with distributive septic shock progressed to hypovolemic and cardiogenic shock; understanding different shock states can help guide therapy

Classifying the severity of shock: a patient with normal blood pressure, who is tachycardic and vasoconstricted, and who has normal cardiac output and normal blood pressure is in a compensated shock state; patient has impending shock but is not hypotensive yet; if the same patient is tachycardic and vasoconstricted but is hypotensive for age, those compensatory mechanisms that maintain a normal blood pressure have been depleted (uncompensated shock); more aggressive support is needed for this patient; prolonged hypotension and prolonged poor tissue perfusion lead to severe acidosis and multiple organ dysfunction (potentially irreversible shock, “shock liver,” hepatitis, disseminated intravascular coagulation defects, and persistent thrombocytopenia because the bone marrow is not functioning well); patient requires aggressive respiratory support (eg, intubation); try to intervene before patient is in uncompensated and irreversible shock state; correct respiratory and cardiac problems to prevent further tissue injury as shock progresses

Goals of therapy in patient with shock: early detection is critical in preventing organ dysfunction; if early intervention was not possible, increase the oxygen content of the blood (give supplemental oxygen); try to improve mean arterial pressure and enhance systolic blood pressure to improve cardiac output; reduce oxygen demand (take away work of breathing, especially in the uncompensated and irreversible shock state); correct any electrolyte abnormalities (serum electrolytes and low glucose levels); goal is to improve the regional microvascular blood flow and prevent further end-organ dysfunction as therapy is started; overaggressive administration of fluids and fluid overload are potentially harmful in patients being treated for shock

Ventilatory support: administer supplemental oxygen to increase oxygen delivery; treat hypoxemia by nasal cannula, face mask, or temporary nonrebreathing mask; in patients with severe hypoxemia, severe dyspnea, or persistent acidosis, endotracheal intubation must be instituted early to reduce the work of breathing and improve the cardiac output (supports the left ventricle and may reduce the afterload of the LV)

Fluid resuscitation: mainstay of management of shock; the goal is improving microvascular blood flow and increasing cardiac output; administer fluids; stable IV access required (eg, effective peripheral IV access); if prolonged management is needed because the patient is in an uncompensated or irreversible shock state, central venous catheters required; reassess and monitor the response to fluids; excess fluids cause edema, which increases risk; in patients with cardiogenic shock, giving too much fluid can worsen heart failure; in patients with distributive shock, excessive fluids may lead to increase in leakage of fluid outside the intravascular system due to capillary leak; this can lead to acute pulmonary edema and impending respiratory failure; fluid therapy can be challenging, and thoughtful reassessment of the patient’s response is necessary

Fluid challenge: first-line fluid is usually crystalloids (eg, normal saline, lactated Ringer solution); they are well-tolerated, widely available, and inexpensive; second-line fluids are colloids; 5% albumin is appropriate when trying to correct severe hypoalbuminemia; platelets to treat thrombocytopenia; packed red blood cells for the treatment of anemia

Dosage and main goals: for pediatric patients (Surviving Sepsis Campaign guidelines), administer 10-20 mL/kg over 5-10 minutes, and observe patient for a response; give fluids quickly enough to observe a response, but without putting undue strain on the heart; goal is an improvement in blood pressure, decrease in heart rate, improvement in mental status (if patient is awake and alert and not intubated), and eventually increased urine output; assessment of fluid status is aided by a central venous catheter to measure the intravascular venous volume; the goal is a few millimeters of mercury above the baseline (eg, if the original level was 3 mm Hg, aim for 5-6 mm Hg); trying to get a normal cardiac output (or at least the minimal cardiac output for normal systolic blood pressure) can help prevent fluid overload and excessive administration of fluids; the other goal is achieving normal blood pressure; if fluid administration is insufficient, consider vasoactive medication therapy (eg, for severe hypotension, persistent hypertension, severe acidosis); as a general rule, start vasoactive medications after 20-60 mL/kg of fluid has been given over 1-3 hours with some or very little improvement in blood pressure

Vasoactive agents: vasopressors are short-acting agents that improve vascular tone or cardiac output; inotropic agents improve cardiac output by affecting contractility; vasodilatory agents help lower the afterload (SVR) so that the heart can pump more effectively

Vasopressor agents: short-acting agents that are adrenergic, dopaminergic, or agonists (positively affect vasopressin receptors); the common adrenergic agents are norepinephrine, epinephrine, and dopamine; these agents, at different concentrations, have either an α- or β-adrenergic effect; dopamine has an additional dopaminergic effect at the very lowest dose; according to the Surviving Sepsis Campaign guidelines, norepinephrine is the preferred agent; low SVR (afterload) is causing the distributive shock, and norepinephrine is mainly an α-adrenergic present on the blood vessels (arterioles); this causes vasoconstriction; however, as the dose increases, there is also a β-adrenergic effect (can affect the heart)

Administration: norepinephrine is given through a central venous catheter; if a patient is resuscitated in the ED and has only peripheral IV access initially, starting dopamine is acceptable (this pressor can be given peripherally until central venous access is obtained); dopamine at a low dose has a mainly dopaminergic and β-adrenergic effect; at 10-15 μg/kg/min, its effect is also α-adrenergic, and it can cause some vasoconstriction

Vasopressin: does not affect adrenergic receptors; works on vasopressin receptors themselves; is purely a vasoconstrictive agent; is given through central venous access; would be appropriate in a patient who develops arrhythmia and needs a higher SVR for supportive management; a patient in cardiogenic shock may need more inotropic support (more support for the contractility of the heart); epinephrine or dopamine at lower doses would be appropriate, as would dobutamine (has more of a β-adrenergic effect on the heart and improves contractility) or milrinone (a phosphodiesterase inhibitor, which also enhances contractility); dobutamine, epinephrine, and dopamine are much shorter-acting; milrinone has a much longer half-life and must be administered by an experienced clinician; in a patient in cardiogenic shock (low-output state) who has elevated SVR, the use of both inotropic support and a vasodilator is effective to help relax the arterioles but still allow the heart to pump better; this improves the contractility of the heart and reduces the work of the heart to pump against resistance

Summary of treatment of shock: treatment includes ventilatory support, fluid administration, and potentially vasoactive medication; the phases of treatment depend on the severity at presentation; salvage the patient; restore an acceptable minimal blood pressure; try to optimize oxygen delivery using different measures (eg, serum lactate over time, mixed venous saturation over time) to improve cardiac output and oxygen use; continue that support until the patient stabilized; patient may have renal dysfunction for a period, have excess fluid overload, become dialysis-dependent, or have delay in enteral feeding; once the patient is stabilized and some of the multiorgan dysfunction is reversed, start to deescalate some of the agents; try to discontinue the vasoactive agents; try to improve the fluid balance to eliminate edema

Surviving Sepsis Campaign guidelines (Bundles): the majority of pediatric patients with shock have distributive shock due to sepsis (eg, bacteremia, pneumonia, pyelonephritis); it is important to recognize shock early, institute IV access, obtain cultures from the appropriate source, and give antibiotics within the first 60 minutes of presentation; recognition of shock has been shown to improve outcomes in patients in septic shock; fluid resuscitation in patients with septic shock is 10-20 mL/kg (usually crystalloids given over 5-10 minutes); assess patient for improvement of hypotension, heart rate, and urine output; fluid challenges continue; if those fluid challenges are insufficient and the hypotension is severe, starting peripheral inotropic support is necessary until central venous access can be obtained; in the ED, this may mean starting dopamine; patients who have cardiogenic shock may require additional treatment determined over time; patients who present with refractory shock may require extracorporeal membrane oxygenation (ECMO), if available

Case example 1 (continued): the patient has been taking steroids for a prolonged period after organ transplantation; stress has brought on adrenal insufficiency; therapy using stress doses of hydrocortisone is necessary because the shock remains refractory and resistant to vasoactive medication (consider also in patients in septic shock); support hemoglobin targets; attempt to maintain hemoglobin levels ≈10 g/dL (≥7 g/dL)

Other guidelines: children who present with DIC due to severe sepsis may be thrombocytopenic or have intravascular coagulation defects that need FFP support

Suggested Reading

Angus DC, van der Poll T: Severe sepsis and septic shock. N Engl J Med 2013 Aug 29;369(9):840-51; Dellinger RP et al: A Users’ Guide to the 2016 Surviving Sepsis Guidelines. Crit Care Med 2017 Mar;45(3):381-385; Marcdante KJ, Kliegman, RM: Nelson’s Essential Pediatrics 2015; Seventh Edition; Ch 39,40; Elsevier; Vincent JL, De Backer D: Circulatory shock. N Engl J Med 2013 Oct 31;369(18):1726-34.

Readings

Disclosures

For this activity, members of the faculty and planning committee reported nothing to disclose.

Acknowledgements

CME/CE INFO

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The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

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Lecture ID:

PDBR180125

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.