Potential perioperative complications
After studying this chapter, the learner will be able to:
• Describe several respiratory complications that are possible in the perioperative period.
• Identify three potential dysrhythmias that may complicate the patient’s perioperative course.
• Demonstrate the procedure for weighing surgical sponges in the operating room.
• List the primary drugs used in the management of an acute malignant hyperthermic crisis.
• Identify three methods for preventing hypothermia in the perioperative patient.
Reduction of the number of functioning red blood cells capable of containing enough hemoglobin to transport oxygen.
Absence of oxygen. (Not synonymous with hypoxia.)
Entry of gastric, oropharyngeal, or other substance into the lungs.
Collapsed or airless lung.
Drug that increases the tone of the heart, such as digitalis.
A disorder of blood clotting.
Abnormal, disordered, disturbed rhythm.
A blood clot or other substance, such as plaque or fat that occludes a segment of the cardiovascular system.
Any one of a group of blood diseases that are characterized by abnormal forms of hemoglobin in the blood.
Abnormal internal or external loss of blood from an arterial, venous, or capillary source.
Elevated blood pressure. If on several occasions the systolic pressure is greater than 140 or the diastolic pressure is greater than 90, the patient is considered hypertensive.
Low blood pressure. If on several occasions the systolic pressure is lower than 100, the patient is considered hypotensive. This should be compared with other assessment parameters.
Reduced rate and depth of breathing that causes an increase in circulating carbon dioxide.
Decreased concentration of circulating oxygen.
Physical and chemical changes that cause catabolic or anabolic activity that may be life threatening.
Buildup of tissues or properties.
Breakdown of tissues or properties.
A blood clot within a blood vessel.
A drug that causes narrowing of a blood vessel.
A drug that causes relaxation of a blood vessel or causes opening (dilation).
WebsitePotential for complications during and after surgery
Many facilities use scoring systems as guidelines to predict the potential for complications during the perioperative care period. The patient receives care from a multidisciplinary team that plans for his or her safety by assessing risks and benefits of the surgical procedure. Preoperatively, the patient is assessed by the anesthesia provider using the American Society of Anesthesiologists (ASA) scoring system. Intraoperatively, the patient’s risk for infection is assessed using the Centers for Disease Control and Prevention (CDC) wound classification scheme. In the postanesthesia care area, the patient’s readiness for discharge is scored according to one of several predictive indicator grids based on his or her physiology. All of the scoring systems add up to a number that is used in decision making concerning the plan of care and progression toward wellness.
The purpose of this chapter is to acquaint the caregiver with the potential complications that patients experience during and after surgery. A satisfactory score in one care period is not always a predictor of how the patient will do in subsequent phases of care after the physical changes associated with surgery.
Each organ system interacts with other organ systems to produce homeostasis in the patient. An alteration in one organ system will affect all of the others, causing the potential for a poor outcome. Morbidity and mortality can be minimized with prompt detection and precise intervention.
Respiratory complications
One of the primary areas of postoperative complications is the respiratory system. The patient’s potential for developing pulmonary problems depends on several factors. Any preexisting lung disease, such as emphysema, infection, or asthma, predisposes the patient. Smokers have the highest risk of succumbing to postoperative pulmonary problems because of chronic irritation of the respiratory tract with consequent production of excess mucus. Chest wall deformities, obesity, and extremes of age are other pertinent preoperative influences. Intraoperative factors include the following:
• Types of preoperative medications
• Type and duration of anesthesia
• Type and duration of assisted ventilation
• Position of the patient during the surgical procedure
Postoperatively, one of the most critical factors is the patient’s ability to mobilize secretions by deep breathing, coughing, and ambulation. Patients undergoing chest and abdominal surgery are likely to breathe shallowly because of pain and therefore may not adequately raise accumulated secretions. Development of one pulmonary complication often predisposes the patient to development of another. Acute respiratory distress syndrome (ARDS), also known as progressive pulmonary insufficiency or shock lung, may develop in the first 24 to 48 hours after a traumatic injury.
Aspiration
Aspiration of gastric contents into the lungs may occur because of decreased throat reflexes when the patient is unconscious or is conscious with the throat anesthetized, as for bronchoscopy. Residual effects impede lung function and blood-gas exchange.
A chemical pneumonitis results from aspiration of highly acidic gastric juices. Edema forms, alveoli collapse, ventilation-perfusion mismatch occurs, and hypoxemia results. Aspiration of solids in emesis results in edema, severe hypoxia, and respiratory obstruction. Bronchospasm and atelectasis may be followed by pneumonitis or bronchopneumonia. Most aspirate is irritating, but it can be infectious if nasopharyngeal or gastric flora are aspirated. Pneumonia or lung abscess may result with necrosis of the pulmonary parenchyma.
Etiology
Every patient who has food in the stomach is a poor risk for anesthesia. Increased intragastric pressure is an aspiration hazard and may result from conditions such as diaphragmatic hernia, gastrointestinal bleeding, intestinal obstruction, or gas forced into the stomach by application of positive pressure ventilation without use of a cuffed endotracheal tube.
Treatment
Most effective treatment occurs during the first minutes after aspiration. The strategy is to remove as much aspirate as possible and limit the spread of what is left in the lung. The head of the operating bed is lowered with a right lateral tilt for postural drainage; the right mainstem bronchus bifurcates slightly higher than the left mainstem bronchus. The oropharynx and tracheobronchial tree are suctioned. If the patient has aspirated particulate matter that causes obstruction of the airways, bronchoscopy must be performed to remove it. Suctioning must be interrupted every 10 to 15 seconds to administer oxygen. Oxygenation and carbon dioxide removal are high priorities.
Aspiration of acid gastric content injures the alveolar capillary interface, resulting in intrapulmonary shunting and pulmonary edema. Intensive pulmonary care is aimed at improving ventilation-perfusion ratios and decreasing abnormal gas exchange. This may require endotracheal intubation for mechanical ventilation with continuous positive pressure. Most cases of severe hypoxemia occur rapidly within the first 30 to 60 minutes after aspiration. Careful cardiovascular monitoring and frequent blood-gas and acid-base determinations guide therapeutic measures to maintain intravascular volume. Prophylactic antibiotics may be given for aspiration of bowel-contaminated fluid to prevent infection, and a bronchodilator may be used to treat spasm. Most cases of permanent injury or death result from the initial hypoxemia.
Prevention
Prevention involves adequate preoperative preparation (withholding oral intake 8 to 10 hours before induction) and careful administration of anesthetic agents. The anesthetic is decreased near the end of the surgical procedure, hastening the return of throat reflexes. All trauma and obstetric patients receiving general anesthesia should be treated as if they have full stomachs and should be intubated using cricoid pressure (Sellick’s maneuver). The cricoid pressure should be released after verification of endotracheal tube placement. Gastric evacuation is delayed during labor and by analgesic medications. A nasogastric tube may be inserted preoperatively or intraoperatively.
Laryngospasm and bronchospasm
Laryngospasm is a partial or complete closure of the vocal cords as an involuntary reflex action. Bronchospasm is contraction of smooth muscle in the walls of the bronchi and bronchioles, causing narrowing of the lumen. Spasms or abnormal narrowing is produced by a marked increase in smooth muscle tone of the airway walls. Marked elevation of airway resistance profoundly alters gas flow into and out of the lungs. Accompanying changes result in a decreased ventilation-perfusion ratio with a subsequent reduction in Pao2 and rise in Paco2. Many factors can precipitate spasm.
Etiology
Etiologic factors include mechanical airway obstruction, use of certain anesthetics and drugs, allergic conditions such as asthma, vagal reflex, stimulation of the pharynx and larynx with the patient under light anesthesia, traction on the peritoneum, foreign material in the tracheobronchial tree, movement of the head or neck or traction on the carotid sinus, and painful peripheral stimuli. The degree of spasm varies from mild to severe.
Treatment
Treatment depends on the precipitating factor. Methods generally used include positive pressure ventilation, oxygen, tracheal intubation, and neuromuscular blockers for relaxation. Bronchodilator drugs such as aminophylline, isoetharine, and metaproterenol are given with caution because they act as cardiac stimulators and, in the presence of hypoxia, may contribute to cardiac dysrhythmia and cardiac arrest.
Patients may be refractory (unresponsive) to bronchodilators because of acid-base abnormalities. Correction can reduce the side effects and augment the beneficial effects of bronchodilators. If the etiologic factor is an allergy, steroids and antihistamines may be given. Vagal reflexes are inhibited by atropine. If reflex is the cause, anesthesia is deepened. Drying agents are given for excessive secretions. Immediate effective treatment is mandatory to counteract hypoxia and prevent cardiac arrest.
Airway and respiratory obstruction
An airway is maintained with an oral airway or endotracheal tube. Airway obstruction is the most frequent cause of respiratory difficulty in the immediate postoperative period. The patient may exhibit paradoxic respiration (i.e., downward movement of the diaphragm occurring with contraction rather than expansion of the chest), resulting in hypoxia and carbon dioxide retention. As the condition worsens, the patient becomes restless, diaphoretic, cyanotic, and finally unconscious. If not relieved within seconds, this serious complication may lead to cardiac arrest.
Symptoms
Symptoms of respiratory obstruction include increased respiratory effort with inadequate ventilatory exchange, visible use of accessory muscles, and respiratory motion of the chest and abdomen without audible air movement at the airway. If the airway is totally obstructed, breath sounds will be absent; if it is partially obstructed, a snoring sound will be elicited. The pulse is rapid and thready.
Assessment of oxygenation is essential if the patient’s airway patency is in question. Visual inspection of the patient may reveal peripheral cyanosis (i.e., pallor, duskiness, or bluish color of the nail beds and extremities). This is caused by a decrease in capillary oxygen levels. Peripheral cyanosis is not always indicative of impending danger to the patient. It can be caused by hypothermia, stress, medications, or other physiologic factors that cause peripheral vasoconstriction.
If the patient is in an arterial hypoxemic state, he or she will exhibit central cyanosis—pallor, duskiness, or bluish color of the lips, face, and generalized body surface. Central cyanosis is a serious sign that requires immediate airway and ventilatory assessment followed by emergent treatment. Central cyanosis may develop more slowly if the patient has been breathing a high concentration of oxygen.
Treatment
Suctioning blood, mucus, or emesis, gently hyperextending the neck, and elevating the chin may eliminate the cause of obstruction. Oxygen is administered by positive pressure; a nasal airway or endotracheal intubation may be necessary. If the anesthesia provider has been unable to manually ventilate or intubate the patient in two or three attempts, it may be necessary to establish an indirect airway by opening the patient’s anterior neck; a needle is inserted through the cricoid cartilage for a cricothyrotomy or, if time permits, a tracheotomy.
Hypoventilation
The ability to oxygenate depends on the condition of the lungs, hemoglobin concentration, cardiac output, and oxygen saturation. Inadequate or reduced alveolar ventilation can cause a deficit in oxygenation. This can lead to hypoxia (a decreased level of oxygen in arterial blood and tissues), hypoxemia (a decreased level of oxygen in arterial blood), and hypercapnia, also known as hypercarbia (an elevated level of carbon dioxide in arterial blood).
The body compensates for mild hypoxia with increased heart and respiratory rates, bringing oxygen to the blood and tissues at a faster rate. If hypoxia progresses, this compensation is inadequate. If hypoxia is prolonged, cardiac dysrhythmias or irreversible brain, liver, kidney, and heart damage result. Retention of carbon dioxide also leads to acidosis.
Etiology
Contributing factors to hypoventilation include alveolar impairment, pain, faulty positioning, a full bladder, or a short, thick neck. Inadequate pulmonary ventilation from depression of the medullary center in the brain by narcotics or anesthetics, neurologic effects of spinal or epidural drug administration, reduced cardiac output, severe blood loss, obstruction to the respiratory passages, or abnormality of the ventilation-perfusion ratio also can contribute to hypoxia and hypercapnia.
Symptoms
Symptoms of hypoventilation and hypoxia include an increased pulse rate; pallor or central cyanosis from hypoxia or a flushed or reddened appearance from hypercapnia; decreased volume of respirations; stertorous or labored respirations; and dark blood in the surgical field. The acid-base balance can be affected.
Treatment
The immediate administration of oxygen in the proper dosage is the treatment of choice for hypoventilation and hypoxia. Oxygen is a medication requiring proper dosage for safe, effective administration. In the healthy patient, changes in the concentration of carbon dioxide in the blood stimulate the primary central chemoreceptor (respiratory center) in the medulla of the brain. In response to this stimulation, the patient takes a breath to increase oxygenation.
Patients with chronic obstructive pulmonary disease (COPD) have higher than normal levels of circulating carbon dioxide and have a decreased primary chemoreceptor response. They rely on secondary chemoreceptors in the carotid and aortic bodies to sense the changes in carbon dioxide levels in the blood. High concentrations of oxygen decrease the sensitivity of the secondary chemoreceptors in patients with COPD, causing respiratory depression known as carbon dioxide narcosis.
To minimize the risk for respiratory arrest in patients at risk for carbon dioxide narcosis, a 2- to 3-liter per minute (L/min) flow of oxygen per nasal cannula is recommended postoperatively. An endotracheal tube may be left in place postoperatively to support assisted ventilation in select patients.
Patients are encouraged to cough and breathe deeply postoperatively. If a patient received naloxone hydrochloride (Narcan) to reverse the respiratory depressant effect of a narcotic, the patient may awaken rapidly and cough, inadvertently causing extubation. The patient must be watched closely during recovery.
Prevention
A patent airway, appropriate oxygenation, and proper positioning help prevent hypoventilation. Intraoperative measurements of arterial pH, Pco2, and Po2 enable the anesthesia provider to evaluate oxygenation and carbon dioxide gas exchange. To prevent hypoventilation and hypoxia, patients may be given oxygen and assisted ventilation during transport to the recovery area.
Pulmonary embolism (PE)
Pulmonary embolism (PE) is a major cause of death during a surgical procedure and in the immediate postoperative period. Some intraoperative problems may extend into postoperative recovery.8
PE is an obstruction of the pulmonary artery or one of its branches by an embolus, most often a blood clot, but can be fat or other material. The most common cause of PE is stasis of blood, particularly in the low-pressure regions such as deep veins of the legs and pelvis, where the majority of thrombi arise.8 These clots become detached and are carried to the lungs.
Venous stasis also is correlated with obesity, dehydration, congestive heart failure, and atrial fibrillation. Local trauma to a vein or venous disease enhances the chance of thrombus formation. Hypercoagulability may coexist with conditions such as pregnancy, fever, myocardial infarction, and some malignancies and after abrupt cessation of anticoagulant therapy. Prevention consists of a regimen of prophylactic anticoagulants or antiplatelets for high-risk patients and routine measures to prevent venous stasis, such as intermittent compression or antiembolic stockings.
Because of the origin of thrombi in deep veins, it is important to observe the patient postoperatively for thrombophlebitis, evidenced by heat, edema, redness, pain in the calf, or a positive Homans’ sign, which is pain in the calf on forceful dorsiflexion of the foot.
Nonspecific symptoms depend on whether the embolism is mild or massive. The patient may have dyspnea, pleural pain, hemoptysis, tachypnea, crackles, tachycardia, mild fever, or persistent cough. Patients with massive emboli have air hunger, hypotension, shock, and central cyanosis.11 Treatment of pulmonary emboli consists of bed rest, oxygen therapy, anticoagulant therapy, thrombolytic agents, and sometimes a surgical procedure to remove the emboli or place a vena cava filter to prevent additional clots from reaching the lungs.
Frequently, ARDS ensues 24 to 48 hours after injury, with hypoxia and decreased surfactant production, resulting in collapse of the alveolar membrane and microatelectasis. The syndrome develops most frequently in patients older than 10 years, especially those who have traveled long distances with an immobilized fracture. Symptoms include disorientation, increased pulse rate, elevated temperature, tachypnea, dyspnea, crackles, and pleuritic chest pain. Other significant signs are fat in the sputum and urine and a petechial rash on the anterior chest. Treatment is supportive. Mortality is high.
Air embolism may follow incidental injection of air into a body cavity or a bolus of air in an intravenous (IV) or intraarterial infusion. Another means of entry is during transection of large veins with the patient in a sitting or prone position. The pull of gravity on the venous drainage exerts a significant negative pressure that sucks air into the veins and into the right atrium of the heart. The air embolus blocks the tricuspid valve. This can be a complication in handling central venous catheters and using syringes to obtain blood for gas analysis.
Immediate treatment of air embolus is to place the patient into the Trendelenburg’s position with the right side slightly elevated (Durant’s procedure). The anesthesia provider can place a venous catheter into the patient’s jugular and slide it into the right atrium to evacuate the air with a large syringe.
Intrauterine fetal death, abruptio placenta, or placenta previa may precipitate an embolism of amniotic fluid. Also, tumors may cause emboli from primary or metastatic sites. Other material such as plaque or hemostatic material can embolize, causing injury or death to the patient.
Pneumothorax
Although it is rare, insertion of a needle into the thoracic cage can occur during a nerve block or subclavian catheter insertion. Excision of a breast mass close to the chest wall can precipitate pneumothorax. The primary symptoms are pain and shortness of breath. Confirmation is made by x-ray. If the pneumothorax is extensive and the lung fails to reexpand, a chest tube with an underwater seal is required.
Patients with pleural effusion may require thoracentesis which involves draining the chest for relief of symptoms. Careful placement of the needle can prevent pneumothorax.5
Atelectasis (pulmonary collapse)
Partial collapse of a lung is one of the most common postoperative problems. If mucus obstructs a bronchus, air in the alveoli distal to the obstruction is resorbed. That segment of lung then collapses and consolidates. Retained mucus becomes contaminated by inhaled bacteria; the patient may develop bronchopneumonia.
Etiology
Factors that promote increased production of mucus, such as certain irritating anesthetics, and decreased mobilization of mucus, such as from a tight abdominal dressing, predispose the patient to pulmonary collapse. Furthermore, normal respiration includes a deep sigh several times an hour to help keep the lungs expanded. This natural sigh is inhibited by anesthetics, narcotics, and sedatives. Oxygen and carbon dioxide are absorbed into the pulmonary blood flow, and the alveoli collapse. Low tidal volume intensifies the problem. High concentrations of oxygen remove nitrogen from the lungs, leaving oxygen, carbon dioxide, and water in the alveoli.
Symptoms
Atelectasis increases the temperature, pulse, and respiratory rate. The patient may appear cyanotic and uncomfortable, with shallow respirations and pain on coughing. Breath sounds are diminished, with fine crackles. Chest x-ray reveals collapsed areas of the lungs as patch opacities, generally involving the lung bases.
Treatment and prevention
Measures to help prevent or treat atelectasis are abstention from smoking, a regimen of coughing and deep breathing, and early ambulation. An upright position allows for better lung expansion. Medication for pain, when appropriate, before breathing exercises or ambulation improves the ability to breathe deeply and cough effectively. Splinting the thoracic or abdominal incision with a pillow also helps decrease the pain of coughing. Repeated vigorous coughing is contraindicated in some patients (e.g., after cataract extraction, craniotomy, herniorrhaphy).
Pulmonary edema
Pulmonary edema may be defined as an abnormal accumulation of water in extravascular portions of the lungs, including both alveolar and interstitial spaces. In surgical patients the most probable cause is increased microvascular pulmonary capillary permeability or capillary endothelial injury. Blood stagnates in the pulmonary circulation. Fluid exudes from capillaries into the alveoli and interstitial spaces. Reduction of capillary membrane perfusion leads to hypoxia. Symptoms, usually seen postoperatively in the postanesthesia care unit (PACU) or intensive care unit (ICU), may include a bounding, rapid pulse; crackles; dyspnea; and engorged peripheral veins.
Cardiovascular complications
The emotional and physical stresses to which a surgical patient is subjected may lead to cardiovascular complications. The patient who fears dying while under anesthesia runs a greater risk of cardiac arrest on the operating bed than do patients with known cardiac disease. Psychologic stress can have physiologic manifestations. Extreme preoperative anxiety predisposes the patient to a difficult induction and intraoperative period and postoperative discomfort.
Patients with a history of cardiovascular problems are prone to develop complications. These may include dysrhythmias, hypotension, thromboembolism and/or thrombophlebitis, myocardial infarction, or congestive heart failure. Cerebral thrombosis or embolism may result in prolonged coma. Patients must be closely monitored for symptoms of cardiovascular complications. Anoxia, the complete or almost total absence of oxygen from inspired gases, arterial blood, or tissues, is a precursor to cardiovascular collapse. Cardiac arrest can result in death in the operating room (OR).
Hypotension
Reduced blood pressure, with resultant inadequate circulation, may accompany depression of the myocardium, depression of the vasomotor center in the brain, a decline in cardiac output, or dilation of the peripheral vessels. Hypotension may occur also when positive pressure is applied to the airway. Progressive deepening of general anesthesia usually produces peripheral vasodilation and diminished myocardial contractility. Adequate blood flow to the brain and heart, the two most vulnerable vascular beds because of their high metabolic demand, must be maintained. If arterial hypotension is uncontrolled, it may cause a cerebrovascular accident, myocardial infarction, or death.
Etiology
Overdosage of general anesthetic agents or rapid vascular absorption of local agents may result from the patient’s receiving an amount of the agent that exceeds his or her tolerance. Tendency for overdosage occurs during prolonged anesthesia with large amounts of drugs absorbed, in age-extreme patients, or with unrecognized hypothermia during lengthy abdominal or thoracic procedures. Circulatory effects of spinal or epidural anesthesia, such as diminished cardiac output or reduced peripheral resistance, also produce hypotension.
Other causes of hypotension include the following:
• Volume depletion and/or hemorrhage
• Circulatory abnormalities (e.g., cardiac tamponade, heart failure)
• Cerebral or pulmonary embolism (fat embolism from fracture sites, amniotic fluid emboli during delivery, or air emboli from introduction of air into the circulation during an infusion or procedure)
• Myocardial ischemia or infarction
• Changes in position, especially if executed rapidly or roughly
• Excessive preanesthetic medication (postural hypotension may follow narcotic administration)
• Epidural or spinal anesthesia above the level of T6 (sympathetic block)
• Potent therapeutic drugs (e.g., tranquilizers, adrenal steroids, antihypertensives) given before the anesthetic
Surgical manipulation may mechanically induce hypotension by obstructing venous return to the heart with packs, retractors, or body rests, or hypotension and bradycardia may result from a vagal-induced reflex precipitated by intraperitoneal traction, manipulation in the chest or neck area, rapid release of either increased intraabdominal pressure or overdistention of the bladder, anorectal stimulation, or stimulation of the periosteum or joint cavities. Other causes are transfusion reaction (suggested by accompanying cyanosis and oozing at the surgical site), septic shock, severe hyperthermia, and anaphylactic reaction.
Symptoms
Early reversible shock is accompanied by unstable blood pressure, vasoconstriction, elevated serum pH, and elevated catecholamine levels. Late manifestations are pallor or central cyanosis, clammy skin, dilated pupils, decreased urinary output, tachycardia, decreased bleeding in the surgical field or pallor of organs caused by compensatory vasoconstriction, nausea, vomiting, sighing respirations, or air hunger in conscious patients.
Diagnosis
Determination of arterial blood pressure and pulse rate and estimation of pulse volume are indicative of the volume of cardiac ejection. Arbitrary figures of measured blood pressure are not as important as individual circulatory status. A specific measurement in a healthy adult may be relatively insignificant, whereas the same figure in a geriatric patient could be hazardous. In critically ill patients, direct arterial pressure, central venous pressure (CVP), and urinary output are monitored.
Treatment
Treatment must be prompt to avoid circulatory collapse. The aim is to increase perfusion of the vital organs and treat any specific cause while giving general supportive therapy. Supportive measures include oxygen by mask with assisted respiration; elevation of the legs to increase blood pressure by draining pooled blood, especially after sympathetic blockade; and rapid IV fluid therapy to increase blood volume.
Because the volume of fluid is more vital than its composition, various solutions are applicable for early treatment in an emergency. If whole blood is not available, crystalloid solutions (e.g., Ringer’s lactate), 5% dextrose in water (D5W), physiologic saline solution (0.9% saline), plasma or serum albumin, or 6% dextran (plasma expander) may be given. Rapid infusion under pressure may be necessary. Vasoactive drugs are given as necessary; these are usually vasopressors to constrict arterioles and veins while increasing the myocardial contractile force. Blood gases should be monitored.
Prevention
The causes must be reversed or avoided. Therefore the patient should be observed constantly throughout anesthesia. In suspected individuals, the cardiovascular response to the desired surgical position should be tested before induction. Overdosage of premedication and anesthetic drugs is avoided. The patient’s position is changed slowly, tissue is manipulated gently, and blood and fluid loss are replaced promptly. The anesthesia provider administers a minimal amount of the anesthetic and takes adequate time to induce and deepen anesthesia so as not to raise the blood level of the anesthetic too rapidly. Positive pressure is applied to the airway prudently.
Some narcotics and anesthetic agents, surgical trauma, anoxia, and blood loss can lead to postoperative hypotension. When combined, these factors interfere with the complex physiologic mechanisms that support blood pressure. Peripheral vessels dilate. A degree of cardiovascular collapse ensues. Vasoconstriction reduces renal blood flow, causing decrease or failure of kidney function. Patients must be monitored postoperatively for sudden drops in blood pressure or other signs of shock. Vasoactive drugs and oxygen may be administered. To avoid hypotension, fluid management is critical to renal function after restoration of systemic blood pressure.
Hypertension
Abnormal elevation of the blood pressure may occur, especially in a hypertensive or arteriosclerotic patient. Even mildly hypertensive patients are prone to myocardial ischemia (inadequate blood flow to the heart) during induction of and emergence from anesthesia. Intubation stimulates the sympathetic nervous system. Other predisposing factors include pain, shivering, hypoxia, hypercapnia, effects of vasopressor drugs, or hypervolemia from excessive replacement of fluid losses. Treatment consists of administration of oxygen, diuretics, and antihypertensive beta-blocker drugs as indicated. If not controlled, hypertension may precipitate a cerebrovascular accident or myocardial infarction. It may cause bleeding from the surgical site or may threaten the integrity of a vascular bypass.
Air embolism
Air embolism may occur intraoperatively with the patient in a sitting position for a craniotomy or posterior cervical operation. Cerebral diploic veins are noncollapsible; venous sinuses in the skull remain open. Air entering a vein is carried rapidly to the right side of the heart and pulmonary circulation, obstructing right atrioventricular flow. Cardiac dysrhythmias and unexplained hypotension are prime signs and symptoms. A characteristic heart murmur may be audible with a precordial stethoscope or Doppler device. Air embolism also may occur during cardiopulmonary bypass, thyroidectomy, or laparoscopy.
Preoperative placement of a central venous catheter allows immediate aspiration of air. To relieve ventricular obstruction if no catheter is in place, the patient is placed in the Trendelenburg’s position with the right side up. Durant’s procedure is performed by placing a venous catheter in the right atrium to remove the air. If cardiac arrest occurs, cardiopulmonary resuscitation (CPR) is begun. Closed heart massage may move an embolus obstructing the coronary artery.
Venous stasis
Venous return of blood from the lower extremities can be slowed by the effects of general or spinal anesthesia and by the position of the legs during prolonged surgical procedures. The venous stasis that develops in most patients during a surgical procedure can be effectively counteracted. To prevent thrombophlebitis and thrombosis in patients with thromboembolic disease, anticoagulants may be administered. Antiembolic stockings, with or without a sequential pneumatic compression device, augment venous flow from the legs. Elevation of the legs as little as 15% above horizontal can assist in venous return.
Postoperatively the patient may be placed in the Trendelenburg’s position with the legs elevated. Flexion and extension of the legs and feet, frequent turning, and early ambulation, unless contraindicated, aid circulation.
Deep vein thrombosis
Venous stasis, changes in clotting factors in the blood, and damage to vessel walls are the primary causes of deep vein thrombosis (DVT) in the lower extremities. Age, obesity, immobility, and a history of thromboembolic or other cardiovascular disease are predisposing factors. The type, location, and extent of the surgical procedure can contribute also. Preoperative prophylactic interventions, including anticoagulants, sequential compression devices, or antiembolic stockings, can reduce the risk of postoperative pulmonary embolism, which is a life-threatening complication of DVT.
Disseminated intravascular coagulation
Although it occurs rarely, disseminated intravascular coagulation (DIC) is a life-threatening syndrome. It is a complex derangement of clotting factors. The hemostatic process involves vasoconstriction with platelet aggregation and clotting. In DIC the normal clotting mechanisms do not function. Instead, a repetitive, overactive cycle of clot formation (coagulopathy) and simultaneous clot breakdown (fibrinolysis) occurs. This leads to consumption of platelets and coagulation factors and release of fibrin degradation products that act as potent anticoagulants.
DIC can follow hemorrhage, thrombi, emboli, infection, or allergic reaction to an incompatible blood transfusion. It may be precipitated by septic shock, abruptio placentae during pregnancy, or massive soft tissue damage of extensive trauma or burns. As blood becomes depleted of platelets and major clotting factors, coagulation is initiated throughout the bloodstream, especially in microcirculation.
Prolonged bleeding may be noted; hematomas and cutaneous petechiae may appear. Massive hemorrhage and ischemia of vital organs may ensue. Bleeding may be noted from various sites, such as through the nasogastric tube.
The patient may have hypotension and oliguria. Postoperatively the patient may have nausea and vomiting, severe muscular pain, and convulsions and may lapse into a coma. Diagnosis is based on laboratory blood studies. Treatment begins with control of the primary condition. Blood, plasma, and dextran can be administered IV. Heparin and clotting factors, if given early, may prevent hemorrhage.
Cardiac dysrhythmias
An alteration of normal cardiac rhythm may decrease cardiac output, exhaust the myocardium, and lead to ventricular fibrillation or cardiac arrest. Bradycardia is the slowing of the heart or pulse rate. Tachycardia is an excessive rapidity of the heart’s action. Ventricular tachycardia and ventricular fibrillation are the dysrhythmias of most serious consequence and thus most feared.
Etiology
Etiologic factors include hypoxia; hypercapnia; acidosis; electrolyte imbalance; coronary disease; myocardial infarction; vagal reflexes; anesthetic agents; toxic doses of digitalis, epinephrine, or other drugs; and laryngospasm and coughing initiated by the presence of secretions in the airway after induction. Other causes may be hypotension, hemorrhage, hypovolemia, pneumothorax, and mechanical injuries.
Ventricular dysrhythmias
An impulse originating in the ventricles must travel to the rest of the myocardium from one ventricle, then proceeding to the other. Because the impulse does not travel via the rapid, specialized conduction system, depolarization of both ventricles takes longer and is not simultaneous. The complexes of dysrhythmias have an abnormal appearance on an electrocardiogram (ECG) as compared with normally initiated and conducted impulses.
Premature ventricular contraction
An ectopic focus in the ventricles stimulates the heart to contract or beat prematurely before the regularly scheduled sinoatrial impulse arrives (Fig. 31-1). Primary precipitating factors are electrolyte or acid-base imbalance, myocardial infarction, digitalis toxicity, and caffeine. The premature ventricular contraction (PVC) must be distinguished from a premature atrial contraction (PAC). Isolated PVCs may not require treatment, but those occurring in clusters of two or more or more than five or six per minute require therapy. The aim is to quiet the irritable myocardium and restore adequate cardiac output.
Treatment consists of a lidocaine bolus followed by a continuous drip by infusion, correction of the cause (e.g., hypoxia), and other antidysrhythmic drugs if indicated (e.g., procainamide, quinidine). Temporary pacing may be used for severe bradycardia. Paired PVCs pose an increased danger of ventricular tachycardia.
Ventricular tachycardia
A rapid heart rate (100 to 220 beats per minute) may be caused by ventricular ischemia or irritability, anoxia, or digitalis intoxication. The heart rate does not allow time for ventricular filling (Fig. 31-2). The resultant reduced cardiac output predisposes the patient to ventricular fibrillation or cardiac failure. Ventricular tachycardia is treated by prompt IV administration of lidocaine or procainamide, or intramuscular quinidine.
Synchronized cardioversion of 10 to 200 joules may be used if the blood pressure is palpable. This is the application of a high-intensity, short-duration electric shock to the chest wall over the heart to produce total cardiac depolarization. This countershock is timed to interrupt an abnormal rhythm in the cardiac cycle, thereby permitting resumption of a normal one. Cardioversion is usually applied in instances of nonarrest for a dangerous ventricular tachycardia. It may be an elective or emergency treatment. Asynchronous cardioversion is used if the patient is pulseless. Treatment includes correction of the underlying cause.
Ventricular fibrillation
The most serious of all dysrhythmias, fibrillation is characterized by total disorganization of ventricular activity (Fig. 31-3). There are rapid and irregular, uncoordinated, random contractions of small myocardial groups without effective ventricular contraction or cardiac output. Circulation ceases. The patient in fibrillation is unconscious and possibly convulsing from cerebral hypoxia.
Treatment.
Because respiratory and cardiac arrest quickly follow, ventricular fibrillation is rapidly fatal unless successful defibrillation is effected as follows:
1. Precordial thump: In a monitored patient a fast, sharp, single blow to the midportion of the sternum (using the nipple line as a landmark) may be delivered with the bottom fleshy part of a closed fist struck from 8 to 12 inches (20 to 30 cm) above the chest. The blow generates a small electrical stimulus in a heart that is reactive. It may be effective in restoring a beat in cases of asystole or recent onset of dysrhythmia.
2. Asynchronous cardioversion: Prompt defibrillation by short-duration electric shock to the heart produces simultaneous depolarization of all muscle fiber bundles, after which spontaneous beating (conversion to spontaneous normal sinus rhythm) may resume if the myocardium is oxygenated and not acidotic. Defibrillation of an anoxic myocardium is difficult. The time that fibrillation is started should be noted. The electric shock is coordinated with controlled ventilation and cardiac compression. CPR begins as soon as fibrillation is identified. Many variables may affect defibrillation, such as body weight, paddle position, electrical waveform, and resistance to electric current flow. Procedures follow an established protocol.
3. Adjunct drug therapy: Drugs are given as necessary: vasopressor, cardiotonic, and myocardial stimulant drugs to maintain a useful heartbeat; vasodilator or antidysrhythmic drugs to prevent recurrence; and sodium bicarbonate to combat acidosis. Continuous monitoring of the heart and laboratory analysis of arterial blood gases is essential.
Defibrillation: equipment and technique.
Necessary equipment for defibrillation includes a defibrillator machine and two paddle electrodes. Defibrillators use direct electric current. Most have integrated monitors; monitor and defibrillator switches may be separate or combined. An operational monitor does not always indicate that the fibrillation power is on.
Many monitor-defibrillator units can monitor the ECG from the paddle electrodes, as well as from separate patient leads. These paddles and patient leads cannot operate simultaneously, however. Depending on the type of defibrillator, the electrical cord must be plugged in or batteries charged. All defibrillators should be checked regularly with suitable test equipment. Paddles must be cleaned immediately and prepared for reuse. This is emergency equipment and must be available at all times.
External defibrillation of the heart is used unless the chest is already open, as for intrathoracic surgery. Standard electrode paste or jelly or saline-soaked 4 × 4–inch gauze pads reduce the resistance of the skin to passage of the electric current. If paste is used on paddles, it should not extend beyond the electrodes or onto any part of the handles.
Gel pads between the paddles and the patient’s skin provide the advantage that if external cardiac compression is resumed after defibrillation, hands will not slip on the chest. The large diameter of the paddles increases the area of skin contact, thus reducing the possibility of skin burns by spreading of the current. The paddles must be held flat against the skin and more than 2 inches (5 cm) apart to prevent electrical arcing. They must be kept scrupulously clean because foreign material reduces the uniformity of the shock. The electrodes must be pressed firmly against the chest wall for good contact. One of two external paddle positions may be used:
1. Standard position: One electrode is placed just to the right of the upper sternum below the clavicle. The other is positioned to the left of the cardiac apex (i.e., left of the nipple at the fifth intercostal space along the left midaxillary line). The delivered current flows through the long axis of the heart.
2. Anterior-posterior position: One electrode is placed anteriorly over the precordium between the left nipple and the sternum. The other is positioned posteriorly behind the heart immediately below the left scapula, avoiding the spinal column. This allows for more energy passage through the heart, but placement is more difficult.
For internal defibrillation, sterile electrodes are placed on the myocardium—one over the right atrium, the other over the left ventricle. If these electrodes are gauze covered, they are dipped in sterile saline solution before use. Minimal current is needed when paddles are placed directly on the heart.
Perioperative team members must understand the functioning of the defibrillator for the patient’s safety and their own. The person holding the electrode paddles delivers the electric charge by pressing a switch on the handle or a foot switch. The safest method is to activate both paddles simultaneously for discharge of electrical energy. The operator should have dry hands and stand on a dry floor.
To avoid possible self-electrocution when using a defibrillator, neither the person holding the electrodes nor anyone else should touch the metal frame of the OR bed or the patient while the current is being applied. No part of the operator’s body should touch the paste or the uninsulated electrodes. Loud verbal warning is given before discharge. Countershock is repeated at intervals if fibrillation persists. Transthoracic impedance falls with repetitive, closely spaced electrical discharges. After each countershock, the ECG and pulse should be reassessed.
Myocardial damage resulting from defibrillation efforts are in direct proportion to the energy used; therefore maximal settings, when not required, may increasingly impair an already damaged myocardium. The energy level delivered through a specific ohm load should be indicated on the front panel of the defibrillator. Delivery output ranges vary among machines.
The strength of the countershock is expressed in energy as joules or watt-seconds—the product of power and duration. If the patient’s chest muscles do not contract, no current has reached the patient. The defibrillator’s connection to the electrical source and the “off” button to the synchronizer circuit should be checked. If the machine is battery operated, the battery must be charged enough to energize the capacitor. Personnel must be familiar with and follow operating instructions for the defibrillator in use.
Prevention.
Appropriate preoperative sedation and skillfully administered anesthetic help prevent hazardous cardiovascular reflexes. Because PVCs are precursors to ventricular fibrillation, in itself a precursor to cardiac arrest, any cardiopulmonary emergency in a prearrest phase requires the following:
1. Monitoring of the heart rhythm and rate: The ability to recognize the rhythms that precede arrest permits intervention that may prevent arrest. If the cardiac status is not under constant monitoring, hypoxia and acidosis may be present and require correction before other therapeutic modalities can be used effectively.
2. Establishment of an IV lifeline: Venous cannulation provides access to peripheral and central venous circulation for administering drugs and fluids, obtaining venous blood specimens for laboratory analysis, and inserting catheters into the right side of the heart and pulmonary arteries for physiologic monitoring and electrical pacing. If cardiac arrest appears imminent or has occurred, cannulation of a peripheral or femoral vein should be attempted first so as not to interrupt CPR. To keep the infusion open, the rate should be kept slow. The usual complications to all IV techniques should be guarded against.
Cardiac arrest
In cardiac arrest there is cessation of circulatory action; the pumping mechanism of the heart ceases. Cardiac standstill represents total absence of electrical cardiac activity (asystole), reflected as a straight line on an ECG rhythm strip. It may occur as primary cardiac failure or secondary to failure of pulmonary ventilation. The types of circulatory arrest are profound cardiovascular collapse, electromechanical dissociation, ventricular fibrillation, and ventricular asystole or standstill. Cardiac arrest may precede or follow failure of the respiratory system, because the systems are interrelated.
Incidence
Arrest may occur during induction of anesthesia, intraoperatively, or postoperatively. Occurrence during cardiac surgery or after massive hemorrhage is not uncommon. Patients more prone to arrest include those at age extremes and those with previously diagnosed paroxysmal dysrhythmias, primary cardiovascular abnormalities, myocarditis, heart block, or digitalis toxicity. An unexpected arrest is one that happens in a patient of general good health who is undergoing a low-risk or relatively routine procedure. These arrests are associated with major morbidity and mortality.
Etiology
A single factor or combination of factors may precipitate arrest, but the general cause is inadequate coronary arterial blood flow. Defective respiratory function produces systemic hypoxemia, causing myocardial hypoxia and depression. It also increases myocardial irritability and the heart’s susceptibility to vagal reflexes.
Some of the specific precipitating factors are dysrhythmias, emboli, extreme hypotension or hypovolemia, respiratory obstruction, aspiration, effects of drugs, anesthetic overdosage, excessively rapid or unsmooth induction, sepsis,6 pharyngeal stimulation, metabolic abnormalities (acidosis, toxemia, electrolyte imbalance), poor cardiac filling caused by positioning, manipulation of the heart, central nervous system trauma, anaphylaxis, and electric shock from ungrounded or faulty electrical equipment.
Symptoms
Symptoms include loss of heartbeat and blood pressure; sudden fixed, dilated pupils; sudden pallor or cyanosis; cold, clammy skin; absence of reflexes; unconsciousness or convulsions in a previously conscious patient; respiratory standstill; and dark blood or absence of bleeding in the surgical field.
Diagnosis
The ECG monitor readily detects arrest during anesthesia, with absence of blood pressure and precordial heart sounds and the lack of a palpable carotid pulse. The onset of pupillary dilation is within 45 seconds after cerebral anoxia; full dilation is reached about 90 to 110 seconds after cessation of cerebral circulation.
Prevention
Optimal psychologic preoperative assessment to identify the level of anxiety and testing for abnormalities and sensitivities is an important preoperative preparation. Intraoperative precautions include the following:
• ECG and temperature monitoring
• No stimulation during induction
• Maintenance of an adequate airway
• Oxygen and carbon dioxide monitoring
• Arterial blood pressure monitoring
• Appropriate positioning and slow position changes with the patient under anesthesia; no weight on the patient
• Gentle handling of tissues with minimal traction and manipulation
Intravenous cardiovascular drugs
An important factor in optimal anesthesia management is prompt recognition of the causes of hypotension, shock, and other complications that could lead to cardiac arrest. Prompt correction of reversible precipitants is critical. Many IV drugs are used to correct hypoxia and metabolic acidosis, manipulate cardiovascular variables, or treat pulmonary edema.
Pharmacodynamics
Uptake, movement, binding, and interactions of drugs vary at the tissue site of their biochemical and physiologic actions. Drug action is determined by how the drug interacts in the body. Some drugs alter body fluids; others, such as anesthetics, interact with cell membranes; most act through receptor mechanisms.
Receptor mechanisms.
Most drugs mimic naturally occurring compounds and interact with specific biologic molecules to produce biologic responses. For example, some cardiovascular drugs are sympathomimetics. They evoke physiologic responses similar to those produced by the sympathetic nervous system. A receptor is a structural protein molecule on a cell surface or within cytoplasm that binds with a drug to produce a biologic response. Three types of receptors are noteworthy in understanding the drugs used to counteract complications that may occur during anesthesia.
Adrenergic receptors.
Adrenergic receptors are innervated by sympathetic nerve fibers and activated by epinephrine or norepinephrine secreted at the postganglionic nerve endings. These receptors are classified as alpha or beta, depending on their sensitivity to specific adrenergic activating and blocking drugs. Alpha1 and alpha2 receptors are located primarily in peripheral and renal arteriolar muscles; beta1 receptors predominate in the heart; beta2 receptors are primarily in smooth muscle of the lungs and blood vessels.
Drug interactions.
No drug has a single action. Each modifies existing functions within the body by interactions to stimulate or inhibit responses. The desired action may be accompanied by side effects or an exaggerated response. An allergic reaction may occur immediately after exposure or may be delayed.
Anaphylaxis is a life-threatening, acute allergic reaction in which cells release histamine or a histamine-like substance. Anaphylaxis, a form of vasogenic shock, causes vasodilation, hypotension, and bronchial constriction. Within seconds, the patient will exhibit edema, wheezing, cyanosis, and dyspnea. Treatment includes epinephrine and antihistamines to control bronchospasm. Isoproterenol, vasopressors, corticosteroids, and aminophylline also may be administered.
In combination with local, regional, or general anesthetics, drugs must be carefully administered and monitored. The action of one drug may counteract the action of another drug. Patients who do not respond to one drug (e.g., a catecholamine) may respond to another. Physicians do not always agree on the use of potent drugs. For example, a vasoconstrictor used to treat hypotension may possibly cause ischemic damage to organs. The physician’s orders should be followed for all drugs.
Intravenous administration.
The speed of administration and dosage will depend on the drug and its intended action. Dosages given in this text vary according to individual patient circumstances. The technique of IV administration also varies.
Continuous intravenous drip.
The drug is diluted in a volume of dextrose or normal saline solution. The rate of administration is regulated by adjusting the number of drops per minute from the solution container into the IV tubing. A drug that might be absorbed by plastic should not be added to solution in a plastic infusion bag.
Bolus.
A bolus is a single rapid injection of the full dosage of a drug that cannot be diluted. It is usually given through an existing IV line, and it may be injected directly into a vein or an intrathecal catheter. Some drugs can be given via an endotracheal tube for absorption through the alveoli or mucous membranes. The drug quickly reaches peak level in the bloodstream.
Titration.
Dosage is calculated on the basis of body surface area (BSA) and hemodynamic parameters. Cardiac output is evaluated in terms of BSA. This may be determined by the ratio of the patient’s height and weight on the BSA scale or by thermodilution. The patient’s physiologic responses also will determine total dosage.
Considerations for drug administration.
Some drugs are inactivated by others. The IV tubing should be flushed or changed to avoid precipitation, such as can occur with sodium bicarbonate. Many potent drugs should be infused through an IV catheter, which is safer than a needle to prevent extravasation. If a drug extravasates at the site of injection, the area must be promptly infiltrated with phentolamine (Regitine) to prevent the necrosis that can result from some vasoactive drugs.
Drugs by classification
Pharmacokinetics includes the mechanisms of absorption, distribution, and metabolism of drugs in the body and elimination from the body. Nurses must have knowledge of drug actions and of how to prepare and administer drugs. The following drugs are classified by their pharmacodynamics to counteract adverse cardiovascular and pulmonary status.
Sympathomimetics are used most often for the following purposes:
• To increase force (inotropic effect), maintain contractility (noninotropic effect), or decrease the stroke volume of myocardial contractions
• To increase or decrease arterial blood pressure
• To increase renal blood flow
• To stimulate the central nervous system
• To prolong the effect of local anesthetics
Patients receiving any of the following drugs must be carefully monitored.
Antidysrhythmics.
Antidysrhythmics control the heart rate and rhythm. They may induce a decreased rate and cardiac output. They may reduce cardiac conduction and increase dilation of peripheral vessels.
Lidocaine (xylocaine).
Lidocaine increases the threshold for ventricular irritability by exerting a focal anesthetic effect on the myocardial cell membrane. It is used for ventricular tachycardia and fibrillation, especially if resistance to defibrillation effort occurs. It can be given IV, intrathecally, or by endotracheal tube. Dosage: 1 mg/kg or 75 to 100 mg by IV push over 30 to 60 seconds, followed by half the initial dose every 8 to 10 minutes to a total of 3 mg/kg if ectopic heartbeats continue. After conversion, a maintenance dose of 2 to 4 mg/min can be given by IV drip. Half these dosages are used to treat shock or pulmonary edema.
Bretylium (bretylol).
Bretylium lowers the defibrillation threshold, permitting otherwise refractory rhythms to be electrically converted. It is indicated for ventricular tachycardia and fibrillation unresponsive to other therapy. Dosage: 5 mg/kg by rapid IV bolus, followed by defibrillation. If fibrillation continues, the dose can be doubled and repeated as necessary. For ventricular fibrillation, 300 to 600 mg may be required. The drug may be diluted for continuous IV drip at a dosage of 1 to 2 mg/min for ventricular tachycardia and to prevent fibrillation. Some degree of hypotension may occur.
Procainamide (pronestyl).
Procainamide suppresses PVCs and recurrent tachycardia. This drug may be used if lidocaine is contraindicated or has not controlled ventricular tachycardia. Dosage: 100 mg by IV push every 5 minutes until dysrhythmia ceases, or to a total of 1 g. Maintenance IV drip is 1 to 4 mg/min. Marked hypotension may occur if infusion is too rapid.
Adenosine (adenocard).
Adenosine slows atrioventricular (AV) node conduction. This action converts supraventricular tachycardia to normal sinus rhythm. Dosage: 6 to 12 mg by IV bolus followed immediately by a saline bolus. Incremental doses of 0.05 mg/kg can be given as necessary. This drug is contraindicated for patients with asthma.
Verapamil (isoptin, calan).
A calcium channel blocker, verapamil inhibits calcium ions to slow myocardial contractility, the heart rate, and the demand for oxygen. It is used as an antidysrhythmic to treat paroxysmal supraventricular tachycardia, acute atrial flutter, and atrial fibrillation. Dosage: 5 to 10 mg (0.075 to 0.15 mg/kg adult body weight) by slow IV push over 2 minutes; may be repeated after 30 minutes. This drug is not given to patients with severe hypotension, malignant hyperthermia, or cardiogenic shock, nor is it given concurrently with an IV beta-adrenergic blocker, such as propranolol.
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