Shock states

The clinical syndrome of shock is one of the most dramatic, dynamic, and life-threatening problems faced by the physician in the critical care setting. Although untreated shock is universally lethal, mortality may be considerably reduced by rapid, proper recognition, diagnosis, monitoring, and treatment.

Definition and physiology

Shock is an acute, complex state of circulatory or metabolic dysfunction that results in failure to deliver or use sufficient amounts of oxygen and/or other nutrients to meet tissue metabolic demands. If prolonged, it leads to multiple-organ failure and death. Therefore, shock can be viewed as a state of acute cellular energy deficiency. Shock can be caused by any serious disease or injury. However, whatever the causative factors, it is always a problem of inadequate cellular sustenance. It is the final common pathway to death.

Delivery of oxygen (D o 2 ) is a direct function of cardiac output (CO) and arterial concentration of O 2 (Ca o 2 ):

Delivery of oxygen:

D o 2 = CO × Ca o 2

Cardiac output:

CO = Heart rate × Stroke volume

Oxygen content:

Ca o 2 = (Hgb × 1.34 × Sa o 2 ) + (0.003 × Pa o 2 )

where Hgb is hemoglobin, Sa o 2 is arterial oxygen saturation, and Pa o 2 is arterial partial pressure of oxygen. Stroke volume is a function of preload, afterload, contractility, and diastolic relaxation. Therefore, optimizing heart rate, contractility, diastolic relaxation, preload, and afterload improves cardiac output. Oxygen-carrying capacity can be increased by raising hemoglobin and optimizing its saturation with oxygen. Oxygen delivery can be improved by manipulation of all these factors.

Calculation of global oxygen delivery may not reflect regional hypoperfusion and localized ischemia. Inadequate oxygen delivery can result from either limitation or maldistribution of blood flow. Reduced oxygen content (anemia, low Sa o 2 ) necessitates higher cardiac output to maintain oxygen delivery. In certain situations (fever, sepsis, trauma), metabolic demands may exceed normal oxygen delivery. Impairment of the extraction or utilization of oxygen by cells and mitochondria creates a functional arteriovenous shunt and may be the harbinger of multiorgan dysfunction syndrome (MODS). ,

Functional classification and common underlying etiologies

Shock states can be classified into seven functional categories ( Box 34.1 ). Such a tidy classification implies a degree of precision that will be misleading when approaching an individual patient. Vicious cycles play a prominent role in most shock syndromes. Any given patient may display features of any functional category or features of multiple categories over time. Hemodynamic profiles of these categories are summarized in Table 34.1 . Early recognition of shock begins with a careful history and physical examination.

• BOX 34.1

Shock States

  • Hypovolemic

  • Cardiogenic

  • Obstructive

  • Distributive

  • Septic

  • Endocrine

  • Cytopathic

TABLE 34.1

Hemodynamic Patterns in Shock States and Therapeutic Receptor Targets

Hemodynamic Pattern: Blood Pressure or Systemic Vascular Resistance
Shock State Normal Decreased Elevated
Septic Shock
Stroke index ↑ ↔ None α 1 or V 1 None
Stroke index ↓ β 1 α 1 and β 1 β 1 + β 2 , or PDE
Cardiogenic Shock
Myocardial dysfunction (complicating critical illness) a β 1 and/or β 2 α 1 and β 1 β 1 + β 2 and/or PDE
Congestive heart failure β 1 and/or β 2 β 1 β 1 + β 2 , and/or PDE
Obstructive Shock
Ductal-dependent lesion PGE 1 β 1 and PGE 1 PGE 1
Distributive Shock
Neurogenic shock None α 1 None

PDE, Phosphodiesterase inhibitor; PGE1 , prostaglandin.

a For example, acute respiratory distress syndrome or anthracycline therapy.

Hypovolemic shock

Hypovolemia is the most common cause of shock in infants and children. Etiologies include hemorrhage, fluid and electrolyte loss, endocrine disease, and plasma loss ( Box 34.2 ). Acute losses of 10% to 15% of the circulatory blood volume may be well tolerated in healthy children who have intact compensatory mechanisms. However, an acute loss of 25% or more of the circulating blood volume frequently results in hypovolemic shock that requires immediate management.

• BOX 34.2

Etiologies of Hypovolemic Shock

Whole blood loss

  • Absolute loss: hemorrhage

    • External bleeding

    • Internal bleeding

      • Gastrointestinal

      • Intraabdominal (spleen, liver)

      • Major vessel injury

      • Intracranial (in infants)

      • Fractures

  • Relative loss

    • Pharmacologic (barbiturates, vasodilators)

    • Positive-pressure ventilation

    • Spinal cord injury

    • Sepsis

    • Anaphylaxis

Plasma loss

  • Burns

  • Capillary leak syndromes

    • Inflammation, sepsis

    • Anaphylaxis

  • Protein-losing syndromes

Fluid and electrolyte loss

  • Vomiting and diarrhea

  • Excessive diuretic use

  • Endocrine

    • Adrenal insufficiency

    • Diabetes insipidus

    • Diabetes mellitus

Cardiogenic shock or congestive heart failure

Cardiogenic shock or congestive heart failure (CHF) during infancy and childhood is a diagnostic and therapeutic challenge because of its myriad etiologies ( Box 34.3 ). The common denominator in all forms of cardiogenic shock is depressed cardiac output. In many instances, the underlying mechanism is systolic dysfunction or “pump failure.” Cardiogenic shock can also be caused by diastolic dysfunction, as seen in postoperative patients, ischemic heart disease (anomalous left coronary artery from pulmonary artery [ALCAPA]), or disorders associated with ventricular hypertrophy. , Lack of myocardial relaxation increases ventricular end-diastolic pressure and eventually reduces end-diastolic volume. Elevated right ventricular (RV) end-diastolic pressures can cause hepatic and systemic venous congestion and may reduce end-organ perfusion pressures. Elevated left ventricular (LV) end-diastolic pressures result in pulmonary edema and decreased myocardial perfusion pressure leads to subendocardial ischemia. Abnormalities of the heart rate and rhythm can also cause cardiogenic shock. While bradyarrhythmias cause low cardiac output due to decreased heart rate, atrioventricular dyssynchrony and tachyarrhythmias cause low cardiac output owing to inadequate diastolic filling. Tachyarrhythmias also increase myocardial oxygen consumption and compromise myocardial perfusion. Finally, myocardial dysfunction is frequently a late manifestation of shock of any etiology. It is important to understand the underlying pathophysiology of cardiogenic shock, as therapy designed to improve certain conditions may also adversely affect prognosis in other conditions.

• BOX 34.3

ALCAPA, Anomalous left coronary artery from pulmonary artery; AS, aortic stenosis; CoA, acetylcoenzyme A; HLHS, hypoplastic left heart syndrome; IAA, i nterrupted aortic arch; L-TGA, looped transposition of the great arteries.

Etiologies of Cardiogenic Shock

Heart rate abnormalities

  • Supraventricular tachycardia

  • Ventricular dysrhythmias

  • Bradycardia

Congenital heart defects

  • Lesions with ductal-dependent systemic blood flow in neonates (CoA, critical AS, IAA, HLHS)

  • Left-to-right shunt lesions

  • Single-ventricle dysfunction

  • Systemic ventricular dysfunction (L-TGA)

  • Ischemic cardiomyopathies (ALCAPA)

Cardiomyopathy, carditis

  • Hypoxic-ischemic events

    • Postcardiac arrest

    • Prolonged shock

    • Head injury

    • Anomalous coronary artery

    • Excessive catecholamine state

    • Cardiopulmonary bypass

  • Infectious

    • Viral

    • Bacterial

    • Fungal

    • Protozoal

    • Rickettsial

    • Sepsis

  • Metabolic

    • Hypothyroid, hyperthyroid

    • Hypoglycemia

    • Pheochromocytoma

    • Glycogen storage disease

    • Mucopolysaccharidoses

    • Carnitine deficiency

    • Disorders of fatty acid metabolism

    • Acidosis

    • Hypothermia

    • Hypocalcemia

  • Connective tissue disorders

    • Systemic lupus erythematosus

    • Juvenile rheumatoid arthritis

    • Polyarteritis nodosa

    • Kawasaki disease

    • Acute rheumatic fever

  • Neuromuscular disorders

    • Duchenne muscular dystrophy

    • Myotonic dystrophy

    • Limb girdle (Erb)

    • Spinal muscular dystrophy

    • Friedreich ataxia

    • Multiple lentiginosis

  • Toxic reactions

    • Sulfonamides

    • Penicillins

    • Anthracyclines

  • Other

    • Idiopathic dilated cardiomyopathy

Obstructive shock

Obstructive shock is caused by the inability to produce adequate cardiac output despite normal intravascular volume and myocardial function. Causative factors may be located within the pulmonary or systemic circulation or may be associated with the heart itself. Examples of obstructive shock include acute pericardial tamponade, tension pneumothorax, pulmonary or systemic hypertension, and congenital or acquired outflow obstructions. Recognition of the characteristic features of these syndromes is essential because most of the causes can be treated provided that the diagnosis is made early.

Cardiac tamponade is defined as hemodynamically significant cardiac compression resulting from accumulating pericardial contents that evoke and defeat compensatory mechanisms. The pericardial space may contain effusion fluid, purulent fluid, blood, or gas. Clinical manifestations of tamponade may be insidious, especially when it occurs in conditions such as malignancy, connective tissue disorders, renal failure, or pericarditis. As cardiac output becomes restricted, the overall picture resembles CHF; however, the lungs are usually clear. Findings on physical examination that suggest cardiac tamponade include pulsus paradoxus, narrowed pulse pressure, pericardial rub, and jugular venous distension. Echocardiography is of particular value in detecting the presence of pericardial effusion and can provide clues about the presence of tamponade physiology before a patient is symptomatic. The normal effects of respiration are accentuated in cardiac tamponade. Echocardiography is useful in demonstrating the exaggerated phasic variation in cardiac volumes and flows caused by tamponade. Respiratory variation in tricuspid and pulmonary flow is more dramatic than mitral and aortic flow: with inspiration, RV early diastolic filling is augmented (>25%), while LV diastolic filling diminishes (>15%). The stroke volume in the pulmonary artery increases with inspiration, while the aortic stroke volume decreases (>10%). The free walls of the right atrium and/or right ventricle collapse in diastole due to compression of these relatively low-pressure chambers by the higher-pressure pericardial effusion. This collapse is exaggerated during expiration when right heart filling is reduced.

Distributive shock

Distributive shock results from maldistribution of blood flow to the tissues and can be considered relative hypovolemia. Abnormalities in distribution of blood flow may result in profound inadequacies in tissue oxygenation even in the face of a normal or high cardiac output. Such maldistribution of flow generally results from widespread abnormalities in vasomotor tone. Distributive shock may be seen with anaphylaxis, spinal or epidural anesthesia, disruption of the spinal cord, or inappropriate administration of vasodilatory medication. Treatment generally includes reversal of the underlying etiology and vigorous fluid administration. In severe cases of distributive shock that is unresponsive to fluids, vasopressor infusions may be necessary.

Septic shock

Septic shock is often a combination of multiple problems, including infection; relative or absolute hypovolemia; maldistribution of blood flow; myocardial depression; and various metabolic, endocrine, and hematologic problems. The most common presentation (80%) in children is low cardiac index with or without abnormalities of vascular tone. These children have tachycardia, mental status changes, diminished peripheral pulses, mottled cold extremities, and prolonged capillary refill (>2 seconds). In many pediatric patients with septic shock, oxygen consumption is dependent on oxygen delivery. This is similar to the physiologic relationship seen in pediatric patients with cardiogenic shock, suggesting that these two groups could be resuscitated with the same physiologic principles. Adults and some children (20%) present in a hyperdynamic state characterized by an elevated (or normal) cardiac output and decreased systemic vascular resistance. , These patients appear plethoric with warm extremities. They have tachycardia, bounding (or collapsing) pulses, a widened pulse pressure, high fever, mental confusion, and hyperventilation. There may be a rapid progression from high to low cardiac output state. As tissue perfusion worsens, anaerobic metabolism ensues and lactic acid accumulates. The hemodynamic profile changes over time owing to evolution of the shock state and response to therapies.

All patients with septic shock present with an absolute or functional hypovolemia. Increased microvascular permeability, arteriolar and venular dilation with peripheral pooling of intravascular volume, inappropriate polyuria, and poor oral intake all combine to result in reduced effective blood volume. Volume loss secondary to fever, diarrhea, vomiting, or sequestered third-space fluid also contributes to hypovolemia.

Progressive deterioration in oxygen consumption and oxygen extraction portends a poor prognosis. Prior to the onset of cellular hypoxia, , , changes in glycolysis and gluconeogenesis are early metabolic manifestations of sepsis. Insulin responsiveness, intracellular calcium stores, glucose distribution, and adrenergic effects have all been implicated.


Endocrinologic causes of shock are often omitted as a formal category because they manifest as cardiac or distributive shock. However, since the underlying pathobiology is due to dysfunction of the endocrine system, it is addressed specifically here. Severe hypothyroidism results in bradycardia and hypotension, whereas thyrotoxicosis is a cause of tachydysrhythmias and cardiomyopathy. Hypothyroidism has long been associated with other causes of shock and critical illness. Although this “sick euthyroid syndrome” has been thought to be adaptive rather than pathologic, recent data associating low circulating thyroid hormones with worse clinical outcomes suggests that this conventional belief should be reconsidered. Adrenal insufficiency may be congenital or acquired and results in a life-threatening inability to mount a stress response. Relative adrenal insufficiency associated with critically ill patients has been well described. However, diagnosis and treatment of critical illness–related corticosteroid insufficiency remain controversial, and there is a current clinical trial to determine the risks and benefits of adjunctive hydrocortisone in septic children. ,


Resolution of all of the shock states discussed earlier depend on intact mitochondrial function to restore oxidative phosphorylation of adenosine diphosphate. However, inherited and acquired mitochondrial dysfunction result in an inability to use nutrients delivered to tissues and cells. Cytopathic hypoxia is an acquired mitochondrial failure observed in some septic patients. , These patients characteristically present with normal to high cardiac output, high arterial and venous oxygen content, and persistent organ dysfunction and lactic acidosis. Diagnosis and treatment of inherited inborn errors of metabolism and mitochondriopathies require genetic and metabolic subspecialty collaboration.

Multisystem effects of shock

Management of the multisystem deterioration that occurs in shock states is as important as treating the underlying condition. Respiratory, gastrointestinal, central nervous system, renal, and hematologic abnormalities must be anticipated. Multiple organ dysfunction syndrome (MODS) is the derangement of two or more organs after an insult. The severity of MODS has been associated with increased mortality in pediatric intensive care unit (PICU) patients.


Respiratory failure frequently accompanies shock states. It may result from failure of the ventilator pump (i.e., respiratory muscle fatigue) and/or deterioration of lung function (i.e., acute respiratory distress syndrome). Therefore, providing supplemental oxygen is essential in all children with shock. Early tracheal intubation protects the airway, provides relief from respiratory muscle fatigue, facilitates provision of positive airway pressure, redistributes blood flow from the muscles of respiration to core organs, afterload-reduces the left ventricle, and reduces oxygen demands of respiratory muscles. Patients should be ventilated with a lung-protective strategy (see Chapter 48 ).


Renal failure may develop in association with any of the shock syndromes. Shock-related renal failure is a continuum of acute prerenal azotemia through classic acute tubular necrosis to cortical necrosis. Although low-dose dopamine (3–5 μg/kg per minute) improves renal blood flow, , it also impairs renal oxygen kinetics, inhibits protective feedback loops with the kidney, may worsen tubular injury, and has failed to show benefit in preventing or altering the course of acute renal failure in adults. , Acute anuric renal failure may require treatment with peritoneal dialysis, ultrafiltration, continuous hemofiltration or hemodiafiltration, or hemodialysis (see Chapter 75 ). Populations for whom early renal replacement therapies result in decreased mortality have not been consistently identified, but there is evidence that fluid overload is associated with mortality in critically ill children with renal dysfunction. If renal dysfunction exists, all medications and therapies should be adjusted for creatinine clearance. High-output renal failure may occur in shock states without previous oliguria. The polyuria associated with this condition may falsely suggest adequate renal perfusion and adequate vascular volume at a time when the patient’s intravascular volume is, in fact, depleted. Restoration of renal perfusion pressure remains the standard of care.


Coagulation abnormalities (e.g., disseminated intravascular coagulation) probably occur to some extent in all forms of shock. Monitoring of prothrombin time, partial thromboplastin time, and platelet count and observation for abnormal bleeding are essential. Replacement therapies of absent clotting factors seem to be the most advantageous treatments. Use of vitamin K, fresh-frozen plasma, cryoprecipitate, and platelet transfusions should correct most coagulopathies. If general replacement therapy is ineffective and the patient is at risk for complications, specific factor therapy may be indicated (see section on septic shock).


The degree of hepatic dysfunction may determine a patient’s ultimate outcome in severe shock states. Maintaining adequate circulation helps maintain liver function and prevents further hepatocellular damage. Liver function tests should be performed early and followed frequently. If dysfunction exists, drugs requiring hepatic metabolism must be carefully titrated.


Acute nonocclusive mesenteric ischemia is a devastating condition characterized by intense, prolonged splanchnic vasoconstriction, intestinal mucosal hypoxia, and acidosis. Mesenteric ischemia eventually leads to transmural necrosis of the bowel, bacterial translocation, sepsis, and multisystem organ dysfunction. Morbidity and mortality for this condition are high because the signs and symptoms are nonspecific. Prevention of gut ischemia through adequate oxygen delivery may prevent bacterial translocation. Some clinicians advocate the use of selective gut decontamination and early enteral nutrition. , Most children with shock will tolerate postpyloric enteral feeding, although gastrointestinal feeding complications are more common than in critically ill patients without shock. , Other gastrointestinal disturbances after hypoperfusion and stress include bleeding, ileus, and bacterial translocation. Ileus may result from electrolyte abnormalities, administration of narcotic medications, or from shock itself. Abdominal distension from ileus or ascites may cause respiratory compromise, especially in infants. The substantial morbidity and mortality of upper gastrointestinal bleeding due to “stress-related mucosal damage” has led to widespread prophylactic use of medications to suppress gastric acid production, but the benefit of this practice remains unproven. ,


Multiple endocrine problems involving fluid, electrolytes, and mineral balance may arise and complicate the management of children in shock. Severe abnormalities of calcium homeostasis can occur during the course of acute hemodynamic deterioration. Patients who have been administered corticosteroids within 6 months preceding the onset of shock should be considered for stress doses of glucocorticoids. Patients in shock because of head or abdominal trauma may have disruption of the hypothalamic-anterior pituitary-adrenal axis. Adrenal hemorrhage has been demonstrated as a manifestation of severe sepsis; however, more commonly, patients may develop a relative or functional adrenal insufficiency. Dopamine may also inhibit secretion of prolactin, growth hormone, and thyrotropin in critically ill children.


Consumption of oxygen or any other nutrient can be calculated or measured in a variety of ways. Direct calorimetry is used to measure metabolic activity and was first used in the 18th century by Antoine Lavoisier and Pierre-Simon Laplace to measure the heat generated by an animal. Direct calorimetry is a measure of all metabolic activity (aerobic + anaerobic). Early studies led to understanding the relationships between oxygen consumption, carbon dioxide production, and metabolic activity. Indirect calorimetry involves the measurement of oxygen consumption and carbon dioxide production to estimate a heat equivalent. These early direct and indirect calorimetry studies led Adolf Fick to determine a relationship between cardiac output, oxygen consumption, and the arterial and venous concentrations of oxygen (Cv o 2 ).

Fick equation for oxygen consumption

V o 2 = (CO × Ca o 2 ) – (CO × Cv o 2 )

Since the first description of lactate as a prognostic tool in 1964, serum lactate levels have been used as a surrogate for illness severity and to monitor response to therapeutic interventions. Although elevated lactate levels are best described in the context of septic shock, all forms of shock or tissue hypoperfusion will result in elevated serum lactate. In aerobic conditions, oxidation of glucose generates pyruvate that undergoes oxidative decarboxylation and is transformed into carbon dioxide and water. Conversely, in anaerobic conditions, there is an accumulation of pyruvate that is associated with an elevated lactate/pyruvate ratio, higher glucose utilization, and low energy production, resulting in elevated serum lactate. Conditions that are associated with an elevation of lactate include trauma, hypoxemia, severe anemia, and shock. In critically ill children, elevated serum lactate concentration (>2 mmol/L) on admission is associated with higher mortality risk. Elevated lactate in pediatric trauma patients is strongly correlated with the severity of the injury, length of stay, and mortality.

Similarly, elevated blood lactate levels at admission in pediatric septic shock patients are predictive of death. , Owing to the technical challenges of obtaining an arterial blood sample in children, venous lactate levels have been demonstrated to be a surrogate for arterial lactate levels (≤2 mmol/L). However, the agreement between arterial and venous lactate levels in septic patients is poor for venous lactate levels ≥2 mmol/L. Therefore, an arterial sample must be drawn to confirm an initial measurement for serum lactate ≥2.0 mmol/L.

In response to a decrease in cardiac output and the subsequent reduction in oxygen delivery, there is a compensatory increase in oxygen extraction to prevent anaerobic metabolism.

The Fick equation states that

CO = V o 2 /(Ca o 2 − Cv o 2 )

where V o 2 is oxygen consumption and Cv o 2 is venous oxygen content. The equation can be rearranged and simplified:

CO × Ca o 2 − V o 2 = CO × Cv o 2

Dividing both sides by D o 2 (which equals CO × Ca o 2 ) yields:

1− ERO 2 = (CO × Cv o 2 )/(CO × Ca o 2 )


Sv o 2 = (1− ERO 2 ) × Sa o 2 , where ERO 2 = V o 2 /D o 2

where ERO2 is the oxygen extraction ratio, Sv o 2 is systemic mixed venous oxygen saturation, and Scv o 2 is central venous oxygen saturation.

In clinical practice, Sa o 2 is often kept quite constant and often greater than 0.9; therefore :

Sv o 2 = 1− ERO 2

Scv o 2 greater than or equal to 70% remains a target in the American College of Critical Care Medicine Clinical Guidelines for Hemodynamic Support of Neonates and Children with Septic Shock. Examination of the correlation between CO and Sv o 2 measurement reveals that Sv o 2 measurement performs poorly in high cardiac output states but typically performs well in clinically relevant situations when oxygen delivery is inadequate. At present, when pulmonary artery catheters are not being placed, the Scv o 2 is used as a surrogate for Sv o 2 . It is noteworthy that the Scv o 2 can be 2% to 8% higher than the Sv o 2 , and the relationship between these two variables changes with catheter placement, flow states, and relative changes in the flow in the venae cavae and coronary sinus. Brierley and Peters reported that children with community-acquired septic shock were more likely to have low cardiac output shock. In contrast, children with hospital-acquired (catheter) sepsis were more likely to manifest high cardiac output shock. Furthermore, they noted that low Scv o 2 occurred in children with a low cardiac index (CI), but they also found that children with a high CI could have a low Scv o 2 . Similar findings of low Scv o 2 in shock have been reported by other investigators. , It is important to emphasize that the clinical context should always be considered when Scv o 2 measurements are interpreted—patients in extreme vasodilatory shock or following mitochondrial poisoning demonstrate elevated Scv o 2 (>70%), as the oxygen extraction is severely impaired owing to mitochondrial dysfunction. ,

Despite an adequate hemodynamic status as quantified by Scv o 2 , microcirculatory splanchnic hypoperfusion may be present in patients with shock, resulting in significant morbidity and mortality. The cause of microcirculatory failure is multifactorial and includes physiologic shunting, maldistributed flow, increased microvascular permeability, and microvascular thrombosis. Thus, an increased understanding of microcirculatory aberrations and cellular hypoxia has stimulated a search for a minimally invasive means of sampling regional circulations. Gastric tonometry, , near-infrared spectroscopy, , rectal tonometry, sublingual capnometry, , muscle oxygenation, tissue microdialysis, , and orthogonal polarization spectral imaging , are investigational methods to evaluate regional circulation, but their clinical utility remains unproven at this time. Repeated evaluations and monitoring of the patient in shock by a competent clinician, with appropriate, timely interventions, remains the most effective and sensitive physiologic monitor available.

Contemporary cardiac output monitoring in pediatric shock

The American College of Critical Care Medicine Clinical Practice Parameters for Hemodynamic Support of Pediatric and Neonatal Septic Shock recommend titration of therapy to a cardiac output goal of 3.3 to 6.0 L/min per square meter in patients with persistent catecholamine-resistant shock. Historically, pulmonary catheter-directed treatment was considered the gold standard for assessing cardiac function and optimizing oxygen delivery in the hemodynamically unstable patient. However, the use of the pulmonary catheter has significantly decreased as trials noted the lack of benefit with the use of pulmonary artery catheters in adult patients admitted to the ICU. , For example, in the Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments (SUPPORT) trial, the use of right heart catheterization in more than 5700 patients was associated with increased mortality and increased utilization of resources. Similarly, a meta-analysis also noted a lack of benefit with the use of pulmonary artery catheters in critically ill patients. With the decrease in the use of the pulmonary artery catheter, the search continues for noninvasive cardiac output monitoring devices.

The ideal attributes of such a device would be that it is reliable, noninvasive, cost-effective, and provides continuous cardiac output monitoring. In addition to CI, other variables that help titrate therapy include stroke volume index, indexed systemic vascular resistance, Ca o 2 , and D o 2 . Several noninvasive CO monitoring devices are available; a review of the various technology platforms that support these devices is beyond the scope of this chapter. A detailed review of noninvasive hemodynamic monitoring in the ICU can be found elsewhere in the literature. ,


General principles

Early identification and aggressive, timely treatment improves the outcome in pediatric shock. , The American Heart Association’s Pediatric Advanced Life Support Guidelines provide a systematic approach to assess shock, focusing the primary goal of management on optimizing and balancing oxygen delivery with oxygen consumption. The initial approach for stabilization in a patient with undifferentiated shock is highlighted in Box 34.4 . Treatment begins with an assessment of the patient’s airway and breathing to provide adequate oxygen delivery during resuscitation. Ensuring sufficient cardiac output through assessment of circulation and end-organ perfusion is imperative, allowing for titration of fluid resuscitation and vasoactive administration. During the first hour of resuscitation, attention must be directed to the underlying etiology of the shock state. Efforts to reduce oxygen requirements when oxygen delivery is compromised are essential. Even routine nursing procedures can increase oxygen consumption by up to 20% to 30% in healthy adults. Management should be guided by both the clinical examination and monitoring techniques discussed previously in this chapter and titrated to the desired effect.

May 20, 2021 | Posted by in RHEUMATOLOGY | Comments Off on Shock states

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