Potential perioperative complications

Chapter 31


Potential perioperative complications



Chapter objectives


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.



Key terms and definitions



Anemia 


Reduction of the number of functioning red blood cells capable of containing enough hemoglobin to transport oxygen.


Anoxia 


Absence of oxygen. (Not synonymous with hypoxia.)


Aspiration 


Entry of gastric, oropharyngeal, or other substance into the lungs.


Atelectasis 


Collapsed or airless lung.


Cardiotonic 


Drug that increases the tone of the heart, such as digitalis.


Coagulopathy 


A disorder of blood clotting.


Dysrhythmia 


Abnormal, disordered, disturbed rhythm.


Embolus 


A blood clot or other substance, such as plaque or fat that occludes a segment of the cardiovascular system.


Hemoglobinopathy 


Any one of a group of blood diseases that are characterized by abnormal forms of hemoglobin in the blood.


Hemorrhage 


Abnormal internal or external loss of blood from an arterial, venous, or capillary source.


Hypertension 


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.


Hypotension 


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.


Hypoventilation 


Reduced rate and depth of breathing that causes an increase in circulating carbon dioxide.


Hypoxia 


Decreased concentration of circulating oxygen.


Metabolic crisis 


Physical and chemical changes that cause catabolic or anabolic activity that may be life threatening.


Anabolism 


Buildup of tissues or properties.


Catabolism 


Breakdown of tissues or properties.


Thrombus 


A blood clot within a blood vessel.


Vasoconstrictor 


A drug that causes narrowing of a blood vessel.


Vasodilator 


A drug that causes relaxation of a blood vessel or causes opening (dilation).



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Potential 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:



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.





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.




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.





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.




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.





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.




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.


Injury to the intima of vessel walls and coagulative changes in blood also are important factors. A prolonged period on the operating bed (OR bed) may decrease blood flow to the lower extremities by more than 50%. Blood flow is impaired further if the knees are raised on a hard rolled towel, putting occlusive pressure on the deep veins of the legs.


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.


Fat embolism occurs primarily after fracture of a long bone, pelvis, or ribs. However, it sometimes occurs after a blood transfusion, cardiopulmonary bypass, or renal transplant. Fat globules enter a venous sinus and become bloodborne. Symptoms develop when globules block pulmonary capillaries, causing interstitial edema and hemorrhage.


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.





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.







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:



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.





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.




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.




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.


image
FIG. 31-1 Premature ventricular contractions.

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.


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FIG. 31-2 Ventricular tachycardia.

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.


image
FIG. 31-3 Ventricular fibrillation.


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.


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:




Internal defibrillation.


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.




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.







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.






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.








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:



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.






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Apr 6, 2017 | Posted by in GENERAL SURGERY | Comments Off on Potential perioperative complications

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