Respiratory Failure

Clues:

Type I Respiratory Failure is due to flooding of the alveole

Type II Respiratory Failure is due to abscence of O2 and acumulation of Co2

Type III Respiratory Failure is due to atelectasis

Type IV Respiratory Failure is due to respiratory muscles hypoperfusion in the context of a shock, in which the needs is near 40% of cardiac output

In hypotensive patients with clinical signs of a reduced CO, an assessment of intravascular and cardiac volume status is appropriate. A hypotensive patient with decreased intravascular and cardiac volume status may have a history suggesting hemorrhage or other volume losses (e.g., vomiting, diarrhea, polyuria). The jugular venous pressure (JVP) is often reduced in such a patient, while the change in pulse pressure as a function of respiration is increased. A hypotensive patient with increased intravascular volume status and cardiac dysfunction may have S₃ and/or S₄ gallops on cardiac examination, increased JVP, extremity edema, and crackles on lung auscultation. The chest x-ray may show cardiomegaly, widening of the vascular pedicle, Kerley B lines, and pulmonary edema. Chest pain and electrocardiographic changes consistent with ischemia may also be noted

Early intubation and mechanical ventilation are often required. Reasons for institution of endotracheal intubation and mechanical ventilation include acute hypoxemic respiratory failure as well as ventilatory failure, which frequently accompany shock. Acute hypoxemic respiratory failure may occur in patients with cardiogenic shock and pulmonary edema (Chap. 266) as well as in those in septic shock with pneumonia or acute respiratory distress syndrome (ARDS) (Chap. 265). Ventilatory failure often occurs as a result of an increased load on the respiratory system. This load may present in the form of acute metabolic acidosis (often lactic acidosis) or decreased compliance of the lungs ("stiff" lungs) as a result of pulmonary edema. Inadequate perfusion to respiratory muscles in the setting of shock may be another reason for early intubation and mechanical ventilation. Normally, the respiratory muscles receive a very small percentage of the CO. However, in patients who are in shock with respiratory distress for the reasons listed above, the percentage of CO dedicated to respiratory muscles may increase tenfold or more. Lactic acid production from inefficient respiratory muscle activity presents an additional ventilatory load.

Respiratory Failure

Type I, or Acute Hypoxemic, Respiratory Failure

This occurs when alveolar flooding and subsequent intrapulmonary shunt physiology occurs. Alveolar flooding may be a consequence of pulmonary edema, pneumonia, or alveolar hemorrhage. Pulmonary edema can be further categorized as occurring due to elevated intravascular pressures seen in heart failure and intravascular volume overload, or acute lung injury ("low-pressure pulmonary edema"; Chap. 266). ARDS (Chap. 262) represents an extreme degree of lung injury. This syndrome is defined by diffuse bilateral airspace edema seen by chest radiography, the absence of left atrial hypertension, and profound shunt physiology (Fig. 262-2), in a clinical setting in which this syndrome is known to occur. This includes sepsis, gastric aspiration, pneumonia, near drowning, multiple blood transfusions, and pancreatitis. The mortality rate of patients with ARDS was traditionally very high (50–70%), though recent changes in ventilator management strategy have led to reports of mortality in the low 30% range (see below)

For many years, physicians have suspected that mechanical ventilation of patients with acute lung injury and ARDS may propagate lung injury. Cyclical collapse and reopening of alveoli may be partly responsible for this. As seen in Fig. 261-3, the pressure-volume relationship of the lung in ARDS is not linear. Alveoli may collapse at very low lung volumes. Animal studies have suggested that stretching and overdistention of injured alveoli during mechanical ventilation can further injure the lung. Concern over this alveolar overdistention, termed ventilator induced "volutrauma," led to a multicenter, randomized, prospective trial to compare traditional ventilator strategies for acute lung injury and ARDS (large tidal volume—12 mL/kg ideal body weight) to a low tidal volume (6 mL/kg ideal body weight). This study showed a dramatic reduction in mortality in the low tidal volume group (large tidal volume—39.8% mortality versus low tidal volume—31% mortality) and confirmed that ventilator management could impact outcomes in these patients. In addition, a "fluid conservative" management strategy [maintaining a relatively low central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP)] is associated with the need for fewer days of mechanical ventilation when compared to a "fluid liberal" management strategy (maintaining a relatively high CVP or PCWP) in acute lung injury and ARDS

Type II Respiratory Failure

This type of respiratory failure occurs as a result of alveolar hypoventilation and results in the inability to eliminate carbon dioxide effectively. Mechanisms by which this occurs are categorized by impaired central nervous system (CNS) drive to breathe, impaired strength with failure of neuromuscular function in the respiratory system, and increased load(s) on the respiratory system. Reasons for diminished CNS drive to breathe include drug overdose, brainstem injury, sleep-disordered breathing, and hypothyroidism. Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis, phrenic nerve injury) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue).

The overall load on the respiratory system can be classified into increased resistive loads (e.g., bronchospasm), loads due to reduced lung compliance [e.g., alveolar edema, atelectasis, intrinsic positive end-expiratory pressure (autoPEEP)—see below], loads due to reduced chest wall compliance (e.g., pneumothorax, pleural effusion, abdominal distention), and loads due to increased minute ventilation requirements (e.g., pulmonary embolus with increased dead space fraction, sepsis).

The mainstays of therapy for type II respiratory failure are treatments directed at reversing the underlying cause(s) of ventilatory failure. Noninvasive positive-pressure ventilation using a mechanical ventilator with a tight-fitting face or nasal mask that avoids endotracheal intubation can often stabilize these patients. This approach has been shown to be beneficial in treating patients with exacerbations of chronic obstructive pulmonary disease. Noninvasive ventilation has been tested less extensively in other types of type II respiratory failure, but may be attempted nonetheless, in the absence of contraindications (hemodynamic instability, inability to protect airway, respiratory arrest).

Type III Respiratory Failure

This form of respiratory failure occurs as a result of lung atelectasis. Because atelectasis occurs so commonly in the perioperative period, this is also called perioperative respiratory failure. After general anesthesia, decreases in functional residual capacity lead to collapse of dependent lung units. Such atelectasis can be treated by frequent changes in position, chest physiotherapy, upright positioning, and aggressive control of incisional and/or abdominal pain. Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis.

Type IV Respiratory Failure

This form occurs due to hypoperfusion of respiratory muscles in patients in shock. Normally, respiratory muscles consume <5%>2 delivery. Patients in shock often suffer respiratory distress due to pulmonary edema (e.g., patients in cardiogenic shock), lactic acidosis, and anemia. In this setting, up to 40% of the CO may be distributed to the respiratory muscles. Intubation and mechanical ventilation can allow redistribution of the CO away from the respiratory muscles and back to vital organs while the shock is treated

CHILD SEPSIS - NELSON TEXTBOOK OF PEDIATRICS 18º

TABLE 176-2 -- International Consensus Definitions for Pediatric Sepsis

Infection: Suspected or proven infection or a clinical syndrome associated with high probability of infection

SIRS: 2 out of 4 criteria, 1 of which must be abnormal temperature or abnormal leukocyte count 1. Core temperature >38.5°C or <36°c> 2. Tachycardia: mean heart rate >2 SD above normal for age in absence of external stimuli, chronic drugs or painful stimuli; OR unexplained persistent elevation over 0.5–4 hr; OR in children <1>β blocker drugs, or congenital heart disease) 3. Respiratory rate >2 SD above normal for age or acute need for mechanical ventilation not related to neuromuscular disease or general anesthesia 4. Leukocyte count elevated or depressed for age (not secondary to chemotherapy) or >10% immature neutrophils

Sepsis: SIRS plus a suspected or proven infection

Severe Sepsis: Sepsis plus 1 of the following 1. Cardiovascular organ dysfunction defined as Despite >40 mL/kg of isotonic intravenous fluid in 1 hr Hypotension <5th> OR Need for vasoactive drug to maintain blood pressure OR 2 of the following Unexplained metabolic acidosis: base deficit >5 mEq/L Increased arterial lactate >2 times upper limit of normal Oliguria: urine output <0.5> Prolonged capillary refill 5 sec Core to peripheral temperature gap >3°C 2. Acute respiratory distress syndrome (ARDS) as defined by the presence of a Pao2/FiO2 ratio ≤300 mm Hg, bilateral infiltrates on chest radiograph, and no evidence of left heart failure OR Sepsis plus 2 or more organ dysfunctions (respiratory, renal, neurologic, hematologic, or hepatic) Septic Shock: Sepsis plus cardiovascular organ dysfunction as defined above Multiple Organ Dysfunction Syndrome (MODS): Presence of altered organ function such that homeostasis cannot be maintained without medical intervention SIRS, systemic inflammatory response syndrome; SD, standard deviation.

The infectious agents associated with sepsis in pediatric patients vary with the patient's age and immune status. In the neonatal age group, group B streptococcus, Escherichia coli, Listeria monocytogenes, enteroviruses, and herpes simplex virus are the pathogens most commonly associated with sepsis. In older children Streptococcus pneumoniae, Neisseria meningitidis, and Staphylococcus aureus (methicillin-sensitive or resistant) are more common. Toxic shock syndrome from group A streptococcus or S. aureus can also be seen in older children

Infections with gram-negative bacteria (e.g., Escherichia coli, Pseudomonas, Acinetobacter, Klebsiella, Enterobacter, Serratia) and fungi (e.g., Candida, Aspergillus) most often occur in immunocompromised and hospitalized patients colonized with these organisms.

Shock is a state of circulatory dysfunction that occurs from (1) decreased cardiac output and/or maldistribution of regional blood flow and (2) increased metabolic demands with or without impaired oxygen utilization at the cellular level despite adequate oxygen delivery (see Chapter 68 ). Cardiac output may be high, low, or normal. The body has compensatory mechanisms to maintain blood pressure through increased heart rate and peripheral vasoconstriction. Hypotension, a late finding in infants and children, occurs when the compensatory mechanisms are failing and cardiorespiratory arrest is imminent.

Septic shock is a combination of the three classic types of shock: hypovolemic, cardiogenic, and distributive. Hypovolemia from intravascular fluid losses occurs through capillary leak. Cardiogenic shock results from the myocardial-depressant effects of sepsis. Distributive shock is the result of decreased systemic vascular resistance. The degree to which a patient will exhibit each of these responses is variable. Warm shock occurs in some patients with increased cardiac output and decreased systemic vascular resistance. Cold shock occurs in other patients with decreased cardiac output and elevated systemic vascular resistance. In both cases, perfusion to major organ systems may be compromised. Recent data suggest that, unlike adults in septic shock who present with vasodilation and high cardiac output, newborns and children may have fluid refractory shock and develop progressive myocardial dysfunction.

It is important to distinguish between the infection and the host response to the infection, the inflammatory response. The host's immune response, through the actions of the cellular and humoral immune systems, and the reticular endothelium system, prevents the body from developing sepsis in response to breaches in the host defense system. However, this host immune response produces an inflammatory cascade of highly toxic mediators, including hormones, cytokines, and enzymes. If this inflammatory cascade is uncontrolled, SIRS occurs with subsequent organ and cellular dysfunction from derangement of the microcirculatory system

The clinical manifestations of sepsis and shock are mediated through the inflammatory cascade. Hypovolemia, cardiac and vascular failure, acute respiratory distress syndrome, insulin resistance, decreased CYP450 activity (decreased steroid synthesis), coagulopathy, and unresolved or secondary infection are all results of the inflammatory cascade. TNF and other inflammatory mediators increase vascular permeability, leading to diffuse capillary leak, decreased vascular tone, and, at the microcirculatory level, an imbalance between perfusion and metabolic demands of the tissue. TNF and IL-1 stimulate the release of pro-inflammatory and anti-inflammatory mediators causing fever and vasodilatation. Arachidonic acid metabolites lead to the development of fever, tachypnea, ventilation-perfusion abnormalities, and lactic acidosis. Nitric oxide, released from the endothelium or inflammatory cells, is a major contributor to hypotension. Myocardial depression is caused by myocardial depressant factors, TNF, and some interleukins through direct myocardial injury, depleted catecholamines, increased β-endorphin, and production of myocardial nitric oxide.

The initial signs and symptoms of sepsis include alterations in temperature regulation (hyperthermia or hypothermia), tachycardia, and tachypnea. In the early stages (hyperdynamic phase), the cardiac output increases in an attempt to maintain adequate oxygen delivery to meet the increased metabolic demands of tissues. As sepsis progresses, cardiac output falls in response to the effects of numerous mediators. Although hypotension (systolic arterial pressure <2 style="background: yellow none repeat scroll 0% 0%; -moz-background-clip: border; -moz-background-origin: padding; -moz-background-inline-policy: continuous;">Other signs of poor cardiac output include delayed capillary refill, diminished peripheral and central pulses, cool extremities, and decreased urine output. Alterations in mental status, including confusion, agitation, lethargy, anxiety, obtundation, or coma, can also be signs of poor cardiac output. Capillary leak develops from altered vascular permeability. Lactic acidosis occurs as shock progresses and is the consequence of increased tissue production and decreased hepatic clearance

Dx: consist in prove an infection

Laboratory findings often include evidence of hematologic abnormalities and electrolyte disturbances. Hematologic abnormalities include thrombocytopenia, prolonged prothrombin and partial thromboplastin times, reduced serum fibrinogen levels and elevated fibrin split products, and anemia. Also, elevated neutrophil and increased immature forms (bands, myelocytes, promyelocytes), vacuolation of neutrophils, toxic granulations, and Döhle bodies can be seen with infection. Neutropenia is an ominous sign of overwhelming sepsis. Electrolyte abnormalities include hyperglycemia as a stress response or hypoglycemia if glycogen reserves are exhausted. Other electrolyte abnormalities include hypocalcemia, hypoalbuminemia, metabolic acidosis, and low serum bicarbonate. Lactic acidosis can occur if there is significant anaerobic metabolism.

Broad-spectrum bactericidal synergistic antimicrobial agents should be promptly administered to the patient in septic shock. The choice of antimicrobial agents depends on the specific predisposing risk factors ( Table 176-3 ). Neonates should be treated with ampicillin plus cefotaxime or gentamicin. Acyclovir should be added if herpes simplex virus is suspected. Community-acquired infections with N. meningitidis, S. pneumoniae, and Haemophilus influenzae can be treated empirically with a 3rd generation cephalosporin (ceftriaxone or cefotaxime) unless resistant S. pneumoniae or S. aureus is prevalent, which requires the addition of vancomycin. If an intra-abdominal process is suspected, anaerobic coverage should be included with agents such as metronidazole or clindamycin. Nosocomial sepsis should be treated with a 3rd or 4th generation cephalosporin or an extended gram-negative spectrum penicillin (e.g., piperacillin-tazobactam) plus an aminoglycoside. Vancomycin should be added to the regimen if the patient has an indwelling medical device (see Chapter 178 ) and gram-positive cocci are isolated from the blood, if methicillin-resistant S. aureus infection is suspected, and as empiric coverage for S. pneumoniae in patients with meningitis. Empirical use of amphotericin B to treat fungal infections should be considered for selected immunocompromised patients (see Chapter 177 ).

Nelson Textbook of Pediatrics,
18th