Postanesthesia Recovery

Chapter 50


Postanesthesia Recovery



The term perianesthesia patient care reflects a continuum of care, because the patient is moved from the preanesthesia holding or admitting area to the operating room (OR) and then to the postanesthesia care unit (PACU). Postanesthesia recovery refers to those activities undertaken to manage the patient after completion of a surgical or nonsurgical procedure in which anesthesia, analgesia, or sedation was administered. The primary purpose of postanesthesia recovery is critical assessment and stabilization of patients after these procedures, with an emphasis on prevention and detection of complications.1 Care in the postanesthesia Phase I unit centers on providing postanesthesia nursing care and transitioning the patient to the intensive care setting, the surgical floor setting, or Phase II outpatient care.2 The focus of this chapter is on the postanesthesia care of patients with the goals of improving postanesthetic safety and quality of life, reducing postoperative adverse events, providing a uniform assessment of recovery, and streamlining postoperative care and discharge criteria.



Postanesthesia Care Unit Admission


Before the patient is transferred, PACU personnel should be notified not only to expect the transfer but also to have any necessary equipment (e.g., ventilator, nebulizer, invasive monitoring equipment, pharmacologic infusions, capnograph) ready and waiting. Knowledge of the patient’s acuity enables the PACU staff to best plan the patient’s care and assign that care to an appropriately experienced practitioner.


Both the anesthesia provider and the PACU nurse should collaborate in the patient’s admission to the PACU. The immediate priority is evaluation of respiratory and circulatory adequacy. During this initial assessment, any signs of inadequate oxygenation or ventilation are identified, as well as the cause (Boxes 50-1 and 50-2). Although many of the signs of respiratory compromise could have multifactorial explanations, assessment of the adequacy of oxygenation and ventilation ensures that respiratory inadequacy is not contributory. Any evidence of respiratory compromise requires immediate correction.



BOX 50-1   Signs and Symptoms of Inadequate Oxygenation






Modified from Marley RA, Hoyle BL. Respiratory care. In Schick L, Windle PE. PeriAnesthesia Nursing Core Curriculum. 2nd ed. St. Louis: Saunders; 2010:625-693.



BOX 50-2   Causes of Hypoxemia




Modified from Mason RJ, et al. Murray and Nadel’s Textbook of Respiratory Medicine. 5th ed. Philadelphia: Saunders; 2010.


Electrocardiographic (ECG) monitoring is initiated for determination of cardiac rate and rhythm. Any deviation from preoperative or intraoperative findings is noted and evaluated. Also, blood pressure is measured, and adequacy of organ perfusion is determined. Any necessary invasive monitoring, such as an arterial line, is initiated. Any evidence of cardiocirculatory compromise requires immediate correction.


The anesthesia provider should be active during the patient’s transfer and stabilization in the PACU. Assistance in the initiation of oxygen therapy, maintenance or verification of airway adequacy, and assessment of circulatory status familiarizes PACU personnel with the patient and fosters a smooth transfer of care. After initially stabilizing the patient, the anesthesia provider can communicate relevant preoperative and intraoperative data to the PACU nurse.



Anesthesia Report


To ensure patient safety and continuity of care, the anesthesia provider must give a verbal handoff report to the PACU nurse that specifies the details of the surgical and anesthetic course, the preoperative conditions that warrant or influence the surgical and anesthetic outcome, and the PACU treatment plan, including suggested interventions and end-points. Transfer of the patient from the OR to the PACU is a critical patient handoff and should include an opportunity for the PACU nurse to ask questions and the anesthesia provider to respond. Communication errors can occur during the process of a handoff. To decrease these communication errors, handoff information needs to be standardized and communicated in a logical and meaningful manner.3 A coherent order for the presentation of this information is presented in Box 50-3.



BOX 50-3   Anesthesia Admission Report







The importance of the anesthesia report is reflected in the American Association of Nurse Anesthetists (AANA) guideline from the AANA Scope and Standards for Nurse Anesthesia Practice: “Standard VII: Transfer the responsibility for care of the patient to other qualified providers in a manner which assures continuity of care and patient safety.”4 The American Society of Anesthesiologists (ASA) points to the importance of a verbal report to the responsible PACU nurse but also goes on to state, “The member of the Anesthesia Care Team shall remain in the PACU until the PACU nurse accepts responsibility for the nursing care of the patient.”5



Initial Postanesthesia Care Unit Assessment


Many postanesthesia assessment approaches (e.g., head-to-toe, major body systems assessments, and scoring systems) are currently used in PACUs, and each approach has its benefits and limitations. The assessment approach should accomplish the following:



• Determine the patient’s physiologic status at the time of admission to the PACU


• Allow the periodic reexamination of the patient so that physiologic trends become obvious


• Establish the patient’s baseline level so that the effect of previous medical conditions can be assessed and predicted as they affect current physiology


• Assess the ongoing status of the surgical site and its effect on any preexisting conditions and recovery


• Assess the patient’s recovery from anesthesia and note residual effects


• Prevent or immediately treat complications that occur


• Provide a safe environment for the patient who is impaired either physically, mentally, or emotionally


• Allow the compilation and trend analysis of patient-specific characteristics that relate to discharge or transfer criteria1,6


• Anesthesia personnel must assist in management of the patient until PACU providers secure admission vital signs and attach appropriate monitors. To optimize safety, the anesthesia provider cannot shift responsibility to PACU personnel until the patient’s airway status, ventilation, and hemodynamics are appropriate.



Aldrete Scoring System


The most commonly used assessment approach is a combination of the Aldrete scoring system7 and the major body systems assessment. The Aldrete scoring system evaluates the patient’s activity, respiration, circulation, consciousness, and oxygen saturation level (Box 50-4). Patients receive a numeric score of 0, 1, or 2 in each area, with 2 representing the highest level of function.8 The Aldrete postanesthetic scoring system is the most widely used scoring system in PACUs, although its predictive value in determining recovery from anesthesia has not been studied prospectively.



BOX 50-4   Postanesthesia Recovery Score







Modified from Ead H. From Aldrete to PADSS: reviewing discharge criteria after ambulatory surgery. J Perianesth Nurs. 2006;21:259-267.



Major Body Systems


The major body systems assessment systematically evaluates the body systems that are most affected by anesthesia and the surgical procedure. After the patient is admitted to the PACU, an assessment of cardiorespiratory stability and a more in-depth cardiac assessment are performed. Respiratory assessment comprises rate, depth of ventilation, auscultation of breath sounds, and oxygen saturation level. Type of oxygen delivery system and presence of any artificial airway should be noted.9 The heart is auscultated, and the quality of heart sounds, the presence of any adventitious sounds, and any irregularities in rate or rhythm are noted. Unexpected findings are compared with preoperative data. Arterial pulses are evaluated for strength and equality. An ECG strip is obtained on admission to the PACU and compared with the preoperative ECG. In addition, body temperature and skin color and condition are assessed and the findings documented.


After respiratory and cardiac assessments are completed, the neurologic system is evaluated, with a focus on the level of consciousness, orientation, sensory and motor function, and pupil size, equality, and reactivity. The patient is assessed on ability to follow commands and move extremities purposefully and equally.6


The renal system assessment focuses on fluid intake and output (e.g., blood, crystalloids, and colloids), as well as on volume and electrolyte status. The anesthesia provider relates intraoperative fluid totals in the verbal report, and the PACU nurse notes and documents all intravenous (IV) lines, irrigation solutions, and infusions that enter the patient. All output devices, including drains, catheters, and tubes, are inspected, and the color and consistency of any drainage are noted.


The surgical site is examined. The amount and color of any drainage on the bandage are noted. The patient is also assessed for pain or discomfort, such as nausea, with appropriate interventions administered.


All data obtained in the admission assessment should be documented in a manner that facilitates data collection, trend analysis, and retrieval. Recommended criteria for the initial assessment of a patient in the PACU are included in Box 50-5.



BOX 50-5   Criteria for Initial Assessment: Phase I Postanesthesia Care Unit


Initial assessment and documentation include:



1. Integration of data received at transfer of care



2. Vital signs



3. Pain level, level of emotional comfort


4. Neurologic function to include level of consciousness; pupillary response as indicated


5. Sensory and motor function as appropriate


6. Position of patient


7. Condition and color of skin


8. Patient safety needs


9. Neurovascular: Peripheral pulses and sensation of extremity(ies) as applicable


10. Condition of dressings and visible incisions


11. Type and patency of drainage tubes, catheters, and receptacles; effectively secured


12. Amount and type of drainage


13. Hydration status/fluid therapy: Location of lines, condition of IV site, and amount of solution infusing


14. Procedure-specific assessment (i.e., firmness of abdomen)


15. Postanesthesia scoring system if used


Modified from American Society of Perianesthesia Nurses (ASPAN). Perianesthesia Nursing Standards and Practice Recommendations 2010-2012. Cherry Hill, NJ. ASPAN; 2010.



Ongoing Assessment


Perioperative and postanesthetic management of the patient includes ongoing assessment and monitoring of the following5:




Respiratory Function


In postoperative patients, airway problems that interfere with oxygenation and ventilation are always related to an increase in the resistance to gas flow in the airway.10 However, the most common cause of airway obstruction in the immediate postoperative phase is the loss of pharyngeal muscle tone in a sedated or obtunded patient.11



Obstruction


In postanesthesia patients, the tongue causes most upper airway obstructions. Obstruction occurs when the tongue falls back into a position that occludes the pharynx and blocks the flow of air into and out of the lungs. Signs and symptoms of an upper airway obstruction include snoring and activation of accessory muscles of ventilation. Intercostal and suprasternal retractions may be noted. However, patients are usually somnolent and may be difficult to arouse. Risk factors for an upper airway obstruction include anatomy (e.g., obesity, large neck, or short neck), poor muscle tone (secondary to opioids, sedation, residual neuromuscular blockade, or neuromuscular disease), or swelling (secondary to surgical manipulation, edema, or anaphylaxis).


The goal for the relief of a tongue obstruction is a patent airway. Treatment consists of a series of interventions. The initial intervention may be as simple as stimulating the patient to take deep breaths, or it may require repositioning of the airway via a jaw thrust or a chin lift. Placement of an oral or a nasal airway may be required. The nasal airway is tolerated much better by patients emerging from general anesthesia, and unlike the oral airway, it is unlikely to cause gagging or vomiting. If the obstruction remains unrelieved, reintubation may be required, with or without adjunctive mechanical ventilation.


Laryngeal obstruction may occlude the airway as a result of partial or complete spasm of the intrinsic or extrinsic muscles of the larynx. Laryngospasm may be the result of a reflex closure of the glottis (intrinsic muscles) or the larynx (extrinsic muscles).10 Glottic closure usually manifests as intermittent obstruction; laryngeal closure manifests as complete obstruction. Airway irritation that predisposes a patient to laryngospasm may be the result of laryngoscopy, secretions, vomitus, blood, artificial airway placement, coughing, bronchospasm, or frequent suctioning. Symptoms that suggest laryngospasm include agitation, decreased oxygen saturation, absent breath sounds, and acute respiratory distress. Incomplete obstruction may manifest as a crowing sound or stridor.


Treatment of laryngospasm must be immediate. Positive-pressure ventilation with 100% oxygen is the initial intervention. If this intervention is ineffective, a subparalytic dose of IV succinylcholine (0.1 mg/kg) may be given by the anesthesia provider. If succinylcholine is administered, assisted ventilation for 5 to 10 minutes is required, even if the obstruction has been relieved. Reintubation should be performed if severe airway edema is present or if the obstruction persists despite treatment interventions. During the crisis, the anesthesia provider should consider medication for sedation, such as midazolam, to alleviate the possibility of an awake or partially awake patient.


Steroids and topical or IV lidocaine have been included in the prevention and management of airway irritability. Other preventive strategies include obtaining meticulous hemostasis during surgery, suctioning the oropharynx before extubation to clear any retained blood or secretions, and extubating the patient when he or she is in either a very deep plane of anesthesia or the awake state.10 When obstruction occurs, rapid intervention is imperative because the arterial carbon dioxide pressure (Paco2) increases 6 mmHg in the first minute of total obstruction and an additional 3 to 4 mmHg each minute thereafter.11



Hypoxemia


Hypoxemia, defined as low arterial oxygen pressure (Pao2) (usually less than 60 mmHg), is characterized by nonspecific signs and symptoms ranging from agitation to somnolence, hypertension to hypotension, and tachycardia to bradycardia. Pulse oximetry may confirm low oxygen saturation (less than 90%); arterial blood gas analysis may confirm a Pao2 of less than 60 mmHg. Hypoxemia, if untreated, can result in organ ischemia.


Hypoxemia can be the result of a delivered airway obstruction, low concentration of oxygen, hypoventilation, impaired alveolar-capillary diffusion, ventilation-perfusion mismatches, or increased intrapulmonary shunting.11,12 The most common causes of hypoxemia in the PACU include atelectasis, pulmonary edema, pulmonary embolism, aspiration, bronchospasm, and hypoventilation. A brief explanation of these pathologic states follows.


Clinical issues with pulse oximetry have to be considered when used to determine oxygen saturation levels. The relationship between percent of hemoglobin saturated with oxygen (Sao2) and the partial pressure of oxygen in the blood (Pao2) is symbolized by the oxyhemoglobin dissociation curve (see Figure 26-8). Shifts in the curve are caused by abnormal values of pH, temperature, partial pressure of carbon dioxide, and 2,3-diphosphoglycerate. The patient’s level of hemoglobin must also be considered, because if too low, even fully saturated hemoglobin is not adequate to meet tissue needs.1




Pulmonary Edema


Pulmonary edema, which is caused by fluid accumulation within the alveoli, may be the result of an increase in hydrostatic pressure, a decrease in interstitial pressure, or an increase in capillary permeability.


An increase in hydrostatic pressure is usually the result of fluid overload, left ventricular failure (especially in the presence of systolic hypertension), mitral valve dysfunction, or ischemic heart disease. Increased capillary permeability may be the result of sepsis, aspiration, transfusion reaction, trauma, anaphylaxis, shock, or disseminated intravascular coagulation and is frequently referred to as adult respiratory distress syndrome.10


A decrease in interstitial pressure is often seen after prolonged airway obstruction, such as laryngospasm. Acute pulmonary edema that occurs shortly after relief of severe upper airway obstruction is called postobstruction or negative-pressure pulmonary edema or noncardiogenic pulmonary edema. The airway obstruction causes extreme negative intrapleural pressure that increases the pulmonary transvascular hydrostatic pressure gradient. The rapid movement of fluid from pulmonary vasculature to interstitium exceeds the clearing capacity of the pulmonary lymphatic system, and the alveoli become flooded.14 Other causes of noncardiogenic pulmonary edema are bolus dosing with naloxone, incomplete reversal of neuromuscular blockade, or a significant period of hypoxia.15


Pulmonary edema is characterized by hypoxemia, cough, frothy sputum, rales on auscultation, decreased lung compliance, and pulmonary infiltrates seen on chest radiography. Treatment of pulmonary edema is directed toward identification of the cause and reduction of hydrostatic pressure within the lungs. Oxygenation must be maintained (particularly in the presence of profound hypoxemia) via oxygen mask or continuous positive airway pressure (CPAP) with mask, or if necessary, intubation, mechanical ventilation, and the addition of positive end-expiratory pressure (PEEP) ventilation. Diuretics (most commonly furosemide) and fluid restriction are a part of treatment. Dialysis may be used if the fluid retention results from renal failure. Afterload reduction, which is achieved through the use of nitroglycerin or sodium nitroprusside, may be used to decrease myocardial work.10 Patients with noncardiogenic pulmonary edema usually recover quickly after the acute phase and have no permanent sequelae.15



Pulmonary Embolism


Pulmonary embolism is a leading cause of morbidity and mortality, accounting for 50,000 to 90,000 deaths annually in the United States. Most cases of pulmonary embolism are not fatal; however, two thirds of all deaths caused by a pulmonary embolism occur within 30 minutes of an acute event.16


Patients can be considered to be at risk for pulmonary embolism if three conditions, known as Virchow’s triad, exist: venous stasis, hypercoagulability, and abnormalities of the blood vessel wall. These conditions are accentuated in the presence of obesity, varicose veins, immobility, malignancy, congestive heart failure, and increased age and after pelvic or long-bone surgery or injury. However, 90% of all pulmonary emboli arise from deep veins in the legs.16,17 Thrombosis in postoperative patients seems to be related to surgical tissue trauma and liberation of tissue factor that leads to thrombin formation. Leukocyte reactivity and surgery-induced hemostatic changes also may contribute18 (Box 50-6).



BOX 50-6   Surgery-Induced Hemostatic Changes







From Patel K, Chaney MA. Hypercoagulable states: thrombosis and embolism. In Atlee JL. Complications in Anesthesia. 2nd ed. Philadelphia: Saunders; 2007:363.


A pulmonary embolism should be suspected in a patient who complains of or whose presenting signs include acute-onset tachypnea, dyspnea, and tachycardia, particularly when the patient is already receiving oxygen therapy. Signs and symptoms also may include chest pain, hypotension, hemoptysis, dysrhythmias, and congestive heart failure. Although the clinical symptomatology may be suggestive of a pulmonary embolism, confirmation requires pulmonary angiography. Pulmonary angiography is infrequently performed because of its high risk and associated mortality. A ventilation-perfusion scan may also prove useful.


Treatment of a pulmonary embolism is directed toward the correction of hypoxemia and support of hemodynamic stability. Preventive measures may include the use of antiembolic stockings or sequential compression devices. Subcutaneous heparin therapy also may be initiated. Once the occurrence of a pulmonary embolism has been confirmed, IV heparin therapy is started for the prevention of further clot formation. The goal of heparin therapy is an activated partial thromboplastin time that is 1.5 to 2 times the control value. Several new drugs are under development that will have fixed doses and not require laboratory monitoring.19



Aspiration


Aspiration is a potentially serious airway emergency that can compromise patient safety and stability on the induction of, or the emergence from, anesthesia. Aspiration may occur in the OR, in the PACU, or at any time during transfer. Patients may aspirate foreign matter (e.g., a tooth, food), blood, or gastric contents. Each type of material is associated with a characteristic clinical presentation.


Foreign matter aspiration may result in cough, airway obstruction, atelectasis, bronchospasm, and pneumonia. A profound reflex sympathetic nervous system (SNS) response might also cause hypertension, tachycardia, and dysrhythmias. In the absence of complete upper airway obstruction, complications are often localized and treated with supportive care once the foreign matter has been expelled or removed by bronchoscopy.16


Aspiration of blood may result from trauma or surgical manipulation and also may cause minor airway obstruction that is rapidly cleared by cough, resorption, and phagocytosis. Massive blood aspiration interferes with gas exchange through mechanical blockage of airways and leads to chronic fibrinous changes in air spaces or pulmonary hemochromatosis from iron accumulation in phagocytic cells. Aspiration of blood may result in infection, particularly if particles of soft tissue are aspirated along with the blood. Treatment involves correction of hypoxemia, maintenance of airway patency, and initiation of antibiotic therapy, if indicated.15


Aspiration of gastric contents is the most severe form of aspiration and may result in a chemical pneumonitis. Patients have diffuse bronchospasm (secondary to reflex airway closure), hypoxemia (compromised alveolar-capillary membrane), atelectasis (loss of surfactant), interstitial edema (loss of capillary integrity), hemorrhage, and adult respiratory distress syndrome. Gastric aspiration also may cause laryngospasm, infection, and pulmonary edema.


For this reason, the prevention of gastric aspiration, rather than its treatment, is the goal. Patients who are at risk for gastric aspiration (e.g., obese or pregnant patients or those with a history of hiatal hernia, peptic ulcer, or trauma) may be given histamine-2 (H2) blockers, gastrokinetic agents, nonparticulate antacids, or anticholinergics before anesthesia induction. Prophylactic medications are not recommended for those patients who are not at risk.20 Rapid-sequence induction is likely used. Intraoperatively a nasogastric tube may be inserted and is usually then removed to decrease gastric volume and decompress the stomach. Postoperatively the patient should be left intubated until airway reflexes return.


Treatment of gastric aspiration is directed toward correction of hypoxemia and maintenance of hemodynamic stability. Antibiotics are indicated only if signs of infection (e.g., fever, leukocytosis, positive culture results) are present. No beneficial effect of corticosteroids has been determined. Administration of corticosteroids may be indicated with the presence of inflammatory pneumonitis, but the immunosuppressant effect may exacerbate any secondary bacterial pneumonia.21


If aspiration causes hypoxemia, increased airway resistance, atelectasis, or pulmonary edema, institution of support with supplemental oxygen, PEEP, or CPAP and mechanical ventilation is often necessary. Pulmonary edema is usually secondary to increased capillary permeability, so diuretics should not be used to decrease intravascular volume. Bacterial infection does not always occur, so prophylactic antibiotics might merely promote colonization by resistant organisms. If evidence of secondary bacterial infections appears, specific antibiotic therapy is instituted, based on sputum samples obtained for Gram stain and culture or on prevailing colonization experience within the institution.15



Bronchospasm


Bronchospasm results from an increase in bronchial smooth muscle tone, with resultant closure of small airways. As a result of the strong increase in inspiratory force against these closed airways, airway edema develops, causing secretions to build up in the airway. Clinically, the patient demonstrates wheezing, dyspnea, use of accessory muscles, and tachypnea. Airway resistance is increased, and increased peak inspiratory pressures are noted if the patient is receiving mechanical ventilation.10,22


Bronchospasm may result from aspiration, pharyngeal or tracheal suctioning, endotracheal intubation, histamine release secondary to medications, or an allergic response, and it may be seen in greater frequency in patients with a history of asthma or chronic obstructive pulmonary disease.


Treatment of bronchospasm requires confirmation and removal of the precipitating cause. Pharmacotherapy is instituted, with the goals of decreasing airway irritability and promoting bronchodilation. Medications used in the management of bronchospasm include salmeterol (Serevent) and β2-agonists such as albuterol (Proventil, Ventolin), salbutamol, and terbutaline and, if the condition is life threatening, IV epinephrine. Anticholinergics such as atropine sulfate and glycopyrrolate have been given via nebulization to decrease secretions. Both IV and inhaled lidocaine attenuate histamine-induced bronchospasm; however, inhaled lidocaine works at a lower serum level than IV lidocaine.22 Steroids have been used if the underlying cause is an inflammatory disease such as asthma.15



Hypoventilation


Hypoventilation is a common, easily recognizable complication in the PACU. It is manifested clinically by a decrease in respiratory rate that results in an increase in Paco2 secondary to a decrease in alveolar ventilation. This may occur because of a decrease in central respiratory drive, poor respiratory muscle function, or a combination of both.11


Depression of central respiratory drive can occur with both IV and inhalation anesthetics. Central respiratory depression is most profound on admission to the PACU, although the time and route of anesthetic administration may suggest otherwise. For example, an IV dose of fentanyl given just before the patient emerges from anesthesia may not peak until later in the PACU. An intramuscular dose of an opioid takes substantially longer to peak than does an IV dose.16


Patients also may demonstrate a secondary stage of respiratory depression once certain stimuli are removed. For example, a patient may be admitted awake and breathing to the PACU with an endotracheal tube in place. After extubation, because of the loss of stimulation from the endotracheal tube, the patient may become hypercarbic secondary to residual opioid effects and hypoventilation.10 Verbal and tactile stimulation, deep breaths, and repositioning the patient may increase ventilatory function and decrease carbon dioxide. Capnography may be of use in patients at risk.15


Poor respiratory muscle function can result from many conditions. Some of the most common situations are inadequate reversal of neuromuscular blocking agents, surgery involving the upper abdomen, positioning, obesity, and diseases involving the neuromuscular system.


Inadequate reversal of neuromuscular blocking agents can result in hypoventilation secondary to respiratory muscle weakness. Factors that can adversely affect neuromuscular blockade and reversal include certain medications, hypokalemia, hypermagnesemia, hypothermia, and acidosis.23


Medications that have been associated with prolongation of blockade include the aminoglycoside antibiotics (e.g., gentamicin, clindamycin, and neomycin), as well as magnesium and lithium. Hypermagnesemia and hypothermia may potentiate neuromuscular blockade. Hypokalemia and respiratory acidosis inhibit reversal.23


Upper abdominal surgery also can affect respiratory muscle function. Hypoventilation occurs because of a reduced vital capacity secondary to poor diaphragmatic function. A reduction in vital capacity of up to 60% has been noted on the first postoperative day.11 Obesity, especially when combined with upper abdominal surgery, further contributes to hypoventilation because of the increased intraabdominal pressure in obese patients.


Diseases of the neuromuscular system also can affect ventilation. Patients with muscular dystrophy, myasthenia gravis, Eaton-Lambert syndrome, Guillain-Barré syndrome, or other muscle diseases can exhibit postoperative muscle weakness. Patients with severe scoliosis also exhibit poor respiratory muscle function. It is often in the best interests of patients with these disorders that they remain intubated in the PACU until complete return of function occurs, and any residual anesthetic effects are absent.



Cardiovascular Function



Hypotension


Classically, hypotension has been defined as a blood pressure of less than 20% of the baseline or preoperative blood pressure. However, the clinical signs of hypoperfusion, rather than numeric values, should be the indicators of compromise. Because the autonomic nervous system preferentially maintains blood flow to the brain, heart, and kidneys, signs of hypoperfusion to these organs (including disorientation, nausea, loss of consciousness, chest pain, oliguria, and anuria) reflect the failure of physiologic compensation. Hypoxia, which results from hypoperfusion, may cause lactic acidosis. Intervention must be implemented in a timely fashion so that cerebral ischemia, cerebrovascular accident (CVA), myocardial infarction or ischemia, renal ischemia, bowel infarction, and spinal cord damage do not develop.24


Hypotension in the PACU is most commonly caused by hypovolemia secondary to inadequate replacement of intraoperative fluid and blood loss. As a result, initial treatment should focus on restoring circulating volume. The patient should be assessed for active bleeding and a 300- to 500-mL fluid bolus of physiologic saline or lactated Ringer’s solution should be given. If no response is noted, myocardial dysfunction should be considered the cause of hypotension.


Primary cardiac dysfunction, as is the case with myocardial infarction, tamponade, or embolism, results in an acute fall in ventricular emptying and cardiac output. Secondary cardiac dysfunction occurs as a result of the negative chronotropic and negative inotropic effects of medications.


Low systemic vascular resistance (SVR) also can contribute to hypotension. Numerous anesthetic agents cause histamine release with subsequent vasodilation (e.g., morphine, atracurium), whereas others cause vasodilation by directly relaxing arterial smooth muscle (e.g., volatile inhalation anesthetics, local anesthetics used for producing spinal anesthesia). Sensitivity to vasodilators such as hydralazine, sodium nitroprusside, and nitroglycerin also can produce profound hypotension. Sepsis may be another cause of low SVR.


Dysrhythmias that interfere with cardiac conduction and subsequently compromise cardiac output also can produce hypotension. Tachydysrhythmias prevent optimal ventricular filling and emptying. Conduction blocks compromise myocardial effectiveness, resulting in a lowered cardiac output and hypotension. See Box 50-7 for a differential diagnosis of hypotension in the postoperative patient.



BOX 50-7   Differential Diagnosis of Hypotension in the Postanesthesia Care Unit


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May 31, 2016 | Posted by in ANESTHESIA | Comments Off on Postanesthesia Recovery

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